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  • 751. Wang, Xiaoliang
    et al.
    Dai, James Y
    Albanes, Demetrius
    Arndt, Volker
    Berndt, Sonja I
    Bézieau, Stéphane
    Brenner, Hermann
    Buchanan, Daniel D
    Butterbach, Katja
    Caan, Bette
    Casey, Graham
    Campbell, Peter T
    Chan, Andrew T
    Chen, Zhengyi
    Chang-Claude, Jenny
    Cotterchio, Michelle
    Easton, Douglas F
    Giles, Graham G
    Giovannucci, Edward
    Grady, William M
    Hoffmeister, Michael
    Hopper, John L
    Hsu, Li
    Jenkins, Mark A
    Joshi, Amit D
    Lampe, Johanna W
    Larsson, Susanna C
    Lejbkowicz, Flavio
    Li, Li
    Lindblom, Annika
    Le Marchand, Loic
    Martin, Vicente
    Milne, Roger L
    Moreno, Victor
    Newcomb, Polly A
    Offitt, Kenneth
    Ogino, Shuji
    Pharoah, Paul D P
    Pinchev, Mila
    Potter, John D
    Rennert, Hedy S
    Rennert, Gad
    Saliba, Walid
    Schafmayer, Clemens
    Schoen, Robert E
    Schrotz-King, Petra
    Slattery, Martha L
    Song, Mingyang
    Stegmaier, Christa
    Weinstein, Stephanie J
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Woods, Michael O
    Wu, Anna H
    Gruber, Stephen B
    Peters, Ulrike
    White, Emily
    Mendelian randomization analysis of C-reactive protein on colorectal cancer risk2018Inngår i: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Chronic inflammation is a risk factor for colorectal cancer (CRC). Circulating C-reactive protein (CRP) is also moderately associated with CRC risk. However, observational studies are susceptible to unmeasured confounding or reverse causality. Using genetic risk variants as instrumental variables, we investigated the causal relationship between genetically elevated CRP concentration and CRC risk, using a Mendelian randomization approach.

    Methods: Individual-level data from 30 480 CRC cases and 22 844 controls from 33 participating studies in three international consortia were used: the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colorectal Transdisciplinary Study (CORECT) and the Colon Cancer Family Registry (CCFR). As instrumental variables, we included 19 single nucleotide polymorphisms (SNPs) previously associated with CRP concentration. The SNP-CRC associations were estimated using a logistic regression model adjusted for age, sex, principal components and genotyping phases. An inverse-variance weighted method was applied to estimate the causal effect of CRP on CRC risk.

    Results: Among the 19 CRP-associated SNPs, rs1260326 and rs6734238 were significantly associated with CRC risk (P = 7.5 × 10-4, and P = 0.003, respectively). A genetically predicted one-unit increase in the log-transformed CRP concentrations (mg/l) was not associated with increased risk of CRC [odds ratio (OR) = 1.04; 95% confidence interval (CI): 0.97, 1.12; P = 0.256). No evidence of association was observed in subgroup analyses stratified by other risk factors.

    Conclusions: In spite of adequate statistical power to detect moderate association, we found genetically elevated CRP concentration was not associated with increased risk of CRC among individuals of European ancestry. Our findings suggested that circulating CRP is unlikely to be a causal factor in CRC development.

  • 752.
    Warensjö, Eva
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Melhus, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk farmakologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Gedeborg, Rolf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Mallmin, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Wolk, Alicja
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Dietary calcium intake and risk of fracture and osteoporosis: prospective longitudinal cohort study2011Inngår i: BMJ (British edition), ISSN 1756-1833, Vol. 342, s. d1473-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE:

    To investigate associations between long term dietary intake of calcium and risk of fracture of any type, hip fractures, and osteoporosis.

    DESIGN:

    A longitudinal and prospective cohort study, based on the Swedish Mammography Cohort, including a subcohort, the Swedish Mammography Cohort Clinical.

    SETTING:

    A population based cohort in Sweden established in 1987.

    PARTICIPANTS:

    61,433 women (born between 1914 and 1948) were followed up for 19 years. 5022 of these women participated in the subcohort.

    MAIN OUTCOME MEASURES:

    Primary outcome measures were incident fractures of any type and hip fractures, which were identified from registry data. Secondary outcome was osteoporosis diagnosed by dual energy x ray absorptiometry in the subcohort. Diet was assessed by repeated food frequency questionnaires.

    RESULTS:

    During follow-up, 14,738 women (24%) experienced a first fracture of any type and among them 3871 (6%) a first hip fracture. Of the 5022 women in the subcohort, 1012 (20%) were measured as osteoporotic. The risk patterns with dietary calcium were non-linear. The crude rate of a first fracture of any type was 17.2/1000 person years at risk in the lowest quintile of calcium intake, and 14.0/1000 person years at risk in the third quintile, corresponding to a multivariable adjusted hazard ratio of 1.18 (95% confidence interval 1.12 to 1.25). The hazard ratio for a first hip fracture was 1.29 (1.17 to 1.43) and the odds ratio for osteoporosis was 1.47 (1.09 to 2.00). With a low vitamin D intake, the rate of fracture in the first calcium quintile was more pronounced. The highest quintile of calcium intake did not further reduce the risk of fractures of any type, or of osteoporosis, but was associated with a higher rate of hip fracture, hazard ratio 1.19 (1.06 to 1.32).

    CONCLUSION:

    Gradual increases in dietary calcium intake above the first quintile in our female population were not associated with further reductions in fracture risk or osteoporosis.

  • 753.
    Warensjö, Eva
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Jansson, Jan-Hakan
    Cederholm, Tommy
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Boman, Kurt
    Eliasson, Mats
    Hallmans, Goran
    Johansson, Ingegerd
    Sjögren, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Biomarkers of milk fat and the risk of myocardial infarction in men and women: a prospective, matched case-control study2010Inngår i: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 92, nr 1, s. 194-202Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: High intakes of saturated fat have been associated with cardiovascular disease, and milk fat is rich in saturated fat. Objective: The objective of this study was to investigate the association between the serum milk fat biomarkers pentadecanoic acid (15:0), heptadecanoic acid (17:0), and their sum (15:0+17:0) and a first myocardial infarction (MI). Design: The study design was a prospective case-control study nested within a large population- based cohort in Sweden. Included in the study were 444 cases (307 men) and 556 controls (308 men) matched on sex, age, date of examination, and geographic region. Clinical, anthropometric, biomarker fatty acid, physical activity, and dietary data were collected. The odds of a first MI were investigated by using conditional logistic regression. Results: In women, proportions of milk fat biomarkers in plasma phospholipids were significantly higher (P < 0.05) in controls than in cases and were, in general, negatively, albeit weakly, correlated with risk factors for metabolic syndrome. The crude standardized odds ratios of becoming an MI case were 0.74 (95% CI: 0.58, 0.94) in women and 0.91 (95% CI: 0.77, 1.1) in men. After multivariable adjustment for confounders, the inverse association remained in both sexes and was significant in women. In agreement with biomarker data, quartiles of reported intake of cheese (men and women) and fermented milk products (men) were inversely related to a first MI (P for trend < 0.05 for all). Conclusions: Milk fat biomarkers were associated with a lower risk of developing a first MI, especially in women. This was partly confirmed in analysis of fermented milk and cheese intake. Components of metabolic syndrome were observed as potential intermediates for the risk relations. Am J Clin Nutr 2010; 92:194-202.

  • 754.
    Warensjö, Eva
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Smedman, Annika
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Stegmayr, Birgitta
    Hallmans, Göran
    Weinehall, Lars
    Vessby, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Johansson, Ingegerd
    Stroke and plasma markers of milk fat intake: a prospective nested case-control study2009Inngår i: Nutrition Journal, ISSN 1475-2891, E-ISSN 1475-2891, Vol. 8, s. 21-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Dairy products are high in saturated fat and are traditionally a risk factor for vascular diseases. The fatty acids 15:0 and 17:0 of plasma lipids are biomarkers of milk fat intake. The aim of the present study was to evaluate the risk of a first-ever stroke in relation to the plasma milk fat biomarkers. METHODS: A prospective case-control study was nested within two population based health surveys in Northern Sweden. Among 129 stroke cases and 257 matched controls, plasma samples for fatty acid analyses were available in 108 cases and 216 control subjects. Proportions of 15:0 and 17:0 of plasma lipids, weight, height, blood lipids, blood pressures, and lifestyle data were employed in conditional logistic regression modelling. RESULTS: The proportions of fatty acids 17:0 and 15:0+17:0 of total plasma phospholipids were significantly higher in female controls than cases, but not in men. 17:0 and 15:0+17:0 were significantly and inversely related to stroke in the whole study sample as well as in women. The standardised odds ratio (95% CI) in women to have a stroke was 0.41 (0.24-0.69) for 17:0 in plasma phospholipids. Adjustment for traditional cardiovascular risk factors, physical activity and diet had marginal effects on the odds ratios. A similar, but non-significant, trend was seen in men. CONCLUSION: It is hypothesised that dairy or milk fat intake may be inversely related to the risk of a first event of stroke. The intriguing results of this study should be interpreted with caution. Follow up studies with greater power, and where intakes are monitored both by dietary recordings and fatty acid markers are needed.

  • 755.
    Warensjö Lemming, Eva
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Melhus, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk farmakogenomik och osteoporos.
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Long-term a posteriori dietary patterns and risk of hip fractures in a cohort of women2017Inngår i: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 32, nr 7, s. 605-616Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Dietary pattern analysis is a useful tool to study the importance of food components in the context of a diet and how they relate to health and disease. The association between dietary patterns and fractures is at present uncertain. We aimed to study associations between dietary patterns and risk of hip fracture in the Swedish Mammography Cohort, including 56,736 women (median baseline age 52 years). Diet data was collected in food frequency questionnaires at two investigations and dietary patterns were defined by principal component analysis using 31 food groups. Information on hip fractures was collected from the Swedish National Patient Register. Multivariable adjusted hazard ratios (HR) with 95% confidence intervals (CI) were estimated in Cox proportional hazards regression analysis. The two patterns identified-the healthy and Western/convenience dietary patterns-were time-updated and analysed. During a median follow-up time of 25.5 years, 4997 women experienced a hip fracture. Hip fracture rate was 31% lower in the highest compared to the lowest quartile of the healthy dietary pattern [HR (95% CI) 0.69 (0.64; 0.75)]. In contrast, women in the highest compared to the lowest quartile of the Western/convenience dietary pattern had a 50% higher [HR (95% CI) 1.50 (1.38; 1.62)] hip fracture rate. Further, in each stratum of a Western/convenience dietary pattern a higher adherence to a healthy dietary pattern was associated with less hip fractures. The present results suggest that a varied healthy diet may be beneficial for the prevention of fragility fractures in women.

  • 756.
    Warensjö Lemming, Eva
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Nälsén, Cecilia
    Becker, Wulf
    Ridefelt, Peter
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Mattisson, Iréne
    Lindroos, Anna Karin
    Relative validation of the dietary intake of fatty acids among adults in the Swedish National Dietary Survey using plasma phospholipid fatty acid composition.2015Inngår i: Journal of Nutritional Science, ISSN 2048-6790, E-ISSN 2048-6790, Vol. 4Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aims of a national dietary study are several-fold. One purpose is to monitor the intake of foods and nutrients in the population and to compare intakes with dietary recommendations. It is, however, difficult to measure dietary fat intake and plasma biomarker fatty acid (FA) composition may be used as an objective measure of dietary fat intake. Thus, the relative ability of a diet record to capture habitual fat intake was validated against biomarker FA. Dietary fat intake was measured in a novel self-assisted web-based 4-d food record - the 'Riksmaten' method. Spearman rank correlations between dietary FA, certain food groups (fish-shellfish, dairy products, meat and sausages, and spreads) and the fat content of these food groups and biomarker FA were explored. Participants were 150 women and 129 men, aged 18-80 years, who took part in the Swedish National Dietary Survey, Riksmaten adults 2010-11. Blood samples were collected on average 20 d after the diet record and FA composition was measured in plasma phospholipids by GLC. Total n-3 FA (r 0·31), EPA (r 0·34) and DHA (r 0·42) were correlated between plasma and diet (all P ≤ 0·001). Adjustment for covariates attenuated the relationships. Linoleic acid was only marginally correlated (r 0·15; P = 0·06) in women. Plasma pentadecaenoic acid and heptadecaenoic acid were correlated with dairy product intake as previously reported. In conclusion, the Riksmaten method appears valid for the purpose of collecting data on dietary fat composition, at least in a healthy adult population.

  • 757.
    Warensjö Lemming, Eva
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Liisa, Byberg
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Institute of Environmental Medicine (IMM), C6, Nutritional Epidemiology, Stockholm, Sweden.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    A comparison between two healthy diet scores, the modified Mediterranean diet score and the Healthy Nordic Food Index, in relation to all-cause and cause-specific mortality2018Inngår i: British Journal of Nutrition, ISSN 0007-1145, E-ISSN 1475-2662, Vol. 119, nr 7, s. 836-846Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    High adherence to healthy diets has the potential to prevent disease and prolong life span, and healthy dietary pattern scores have each been associated with disease and mortality. We studied two commonly promoted healthy diet scores (modified Mediterranean diet score (mMED) and the Healthy Nordic Food Index (HNFI)) and the combined effect of the two scores in association with all-cause and cause-specific mortality (cancer, CVD and ischaemic heart disease). The study included 38 428 women (median age of 61 years) from the Swedish Mammography Cohort. Diet and covariate data were collected in a questionnaire. mMED and HNFI were generated and categorised into low-, medium- and high-adherence groups, and in nine combinations of these. Multivariable-adjusted hazard ratios (HR) of register-ascertained mortality and 95 % CI were calculated in Cox proportional hazards regression analysis. During follow-up (median: 17 years), 10 478 women died. In the high-adherence categories compared with low-adherence categories, the HR for all-cause mortality was 0·76 (95 % CI 0·70, 0·81) for mMED and 0·89 (95 % CI 0·83, 0·96) for HNFI. Higher adherence to mMED was associated with lower mortality in each stratum of HNFI in the combined analysis. In general, mMED, compared with HNFI, was more strongly associated with a lower cause-specific mortality. In Swedish women, both mMED and HNFI were inversely associated with all-cause and cardiovascular mortality. The combined analysis, however, indicated an advantage to be adherent to the mMED. The present version of HNFI did not associate with mortality independent of mMED score.

  • 758. Weiss, Rudiger J.
    et al.
    Hailer, Nils P.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Stark, Andre
    Karrholm, Johan
    Survival of uncemented acetabular monoblock cups: Evaluation of 210 hips in the Swedish Hip Arthroplasty Register2012Inngår i: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, Vol. 83, nr 3, s. 214-219Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and purpose

    Monoblock acetabular cups represent a subtype of uncemented cups with the polyethylene liner molded into a metal shell, thus eliminating-or at least minimizing-potential backside wear. We hypothesized that the use of mono block cups could reduce the incidence of osteolysis and aseptic loosening, and thus improve survival compared to modular designs.

    Patients and methods

    We identified all 210 primary total hip arthroplasty (THA) procedures in the Swedish Hip Arthroplasty Register that used uncemented monoblock cups during the period 1999-2010. Kaplan-Meier and Cox regression analyses with adjustment for age, sex, and other variables were used to calculate survival rates and adjusted hazard ratios (HRs) of the revision risk for any reason. 1,130 modular cups, inserted during the same time period, were used as a control group.

    Results

    There was a nearly equal sex distribution in both groups. Median age at the index operation was 47 years in the monoblock group and 56 years in the control group (p < 0.001). The cumulative 5-year survival with any revision as the endpoint was 95% (95% CI: 91-98) for monoblock cups and 97% (CI: 96-98) for modular cups (p = 0.6). The adjusted HR for revision of monoblock cups compared to modular cups was 2 (CI: 0.8-6; p = 0.1). The use of 28-mm prosthesis heads rather than 22-mm heads reduced the risk of cup revision (HR = 0.2, CI: 0.1-0.5; p = 0.001).

    Interpretation

    Both cups showed good medium-term survival rates. There was no statistically significant difference in revision risk between the cup designs. Further review of the current patient population is warranted to determine the long-term durability and risk of revision of monoblock cup designs.

  • 759. Weiss, Rudiger J.
    et al.
    Karrholm, Johan
    Hailer, Nils P.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Beckman, Mats O.
    Stark, Andre
    Salvage of failed trochanteric and subtrochanteric fractures using a distally fixed, modular, uncemented hip revision stem 30 patients followed for a mean of 4 years2012Inngår i: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, Vol. 83, nr 5, s. 488-492Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and purpose Treatment options for failed internal fixation of hip fractures include prosthetic replacement. We evaluated survival, complications, and radiographic outcome in 30 patients who were operated with a specific modular, uncemented hip reconstruction prosthesis as a salvage procedure after failed treatment of trochanteric and subtrochanteric fractures. Patients and methods We used data from the Swedish Hip Arthroplasty Register and journal files to analyze complications and survival. Initially, a high proportion of trochanteric fractures (7/10) were classified as unstable and 12 of 20 subtrochanteric fractures had an extension through the greater trochanter. Modes of failure after primary internal fixation were cutout (n = 12), migration of the femoral neck screw (n = 9), and other (n = 9). Results Mean age at the index operation with the modular prosthesis was 77 (52-93) years and the mean follow-up was 4 (1-9) years. Union of the remaining fracture fragments was observed in 26 hips, restoration of proximal bone defects in 16 hips, and bone ingrowth of the stem in 25 hips. Subsidence was evident in 4 cases. 1 patient was revised by component exchange because of recurrent dislocation, and another 6 patients were reoperated: 5 because of deep infections and 1 because of periprosthetic fracture. The cumulative 3-year survival for revision was 96% (95% CI: 89-100) and for any reoperation it was 83% (68-93). Interpretation The modular stem allowed fixation distal to the fracture system. Radiographic outcome was good. The rate of complications, however-especially infections-was high. We believe that preoperative laboratory screening for low-grade infection and synovial cultures could contribute to better treatment in some of these patients.

  • 760.
    Weiss, Rudiger J.
    et al.
    Karolinska Univ Hosp, Karolinska Inst, Dept Mol Med & Surg, Sect Orthopaed & Sports Med, Stockholm, Sweden;Swedish Hip Arthroplasty Register, Gothenburg, Sweden.
    Karrholm, Johan
    Swedish Hip Arthroplasty Register, Gothenburg, Sweden;Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden.
    Rolfson, Ola
    Swedish Hip Arthroplasty Register, Gothenburg, Sweden;Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden.
    Hailer, Nils P.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Swedish Hip Arthroplasty Register, Gothenburg, Sweden.
    Increased early mortality and morbidity after total hip arthroplasty in patients with socioeconomic disadvantage: a report from the Swedish Hip Arthroplasty Register2019Inngår i: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, Vol. 90, nr 3, s. 264-269Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and purpose

    Socioeconomic status is associated with the outcome of major surgery. We investigated the association of socioeconomic status with the risk of early mortality and readmissions after primary total hip arthroplasty (THA).

    Patients and methods

    We obtained information on income, education, immigration, and cohabiting status as well as comorbidities of 166,076 patients who underwent primary THA due to primary osteoarthritis (OA) from the Swedish Hip Arthroplasty Register, the Swedish National Inpatient Register and Statistics Sweden. Multivariable Cox regression models were fitted to estimate the adjusted risk of mortality or readmissions within 90 days after index surgery.

    Results

    Compared with patients on a low income, the adjusted risk of 30-day mortality was considerably lower in patients on a high income (hazard ratio [HR] 0.5, 95% confidence interval [CI] 0.3-0.7) and in those on a medium income (HR 0.7, CI 0.6-0.9). Similar risk reductions were found for the endpoint 90-day mortality. Patients with a high income had a lower adjusted risk of readmission for cardiovascular reasons than those with a low income (HR 0.7, CI 0.6-0.9), as had those with a higher level of education (adjusted HR 0.7, CI 0.6-0.9). Patients with higher socioeconomic status had a lower degree of comorbidities than socioeconomically disadvantaged patients. However, adjusting for socioeconomic confounders in multivariable models only marginally influenced the predictive ability of the models, as expressed by their area under the curve.

    Interpretation

    Income and level of education are strongly associated with early mortality and readmissions after primary THA, and both parameters are closely connected to health status. Since adjustment for socioeconomic confounders only marginally improved the predictive ability of multivariable regression models our findings indicate that comorbidities may under certain circumstances serve as an acceptable proxy measure of socioeconomic background.

  • 761.
    Weiss, Rüdiger J.
    et al.
    Karolinska Univ Hosp, Karolinska Inst, Dept Mol Med & Surg, Sect Orthoped & Sports Med, SE-17176 Stockholm, Sweden.; Sahlgrens Univ Hosp, Inst Clin Sci, Dept Orthoped, Gothenburg, Sweden.
    Garellick, Göran
    Sahlgrens Univ Hosp, Inst Clin Sci, Dept Orthoped, Gothenburg, Sweden.
    Kärrholm, Johan
    Sahlgrens Univ Hosp, Inst Clin Sci, Dept Orthoped, Gothenburg, Sweden.
    Hailer, Nils P.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Total Hip Arthroplasty in 6690 Patients with Inflammatory Arthritis: Effect of Medical Comorbidities and Age on Early Mortality2016Inngår i: Journal of Rheumatology, ISSN 0315-162X, E-ISSN 1499-2752, Vol. 43, nr 7, s. 1320-1327Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective. We analyzed early mortality after total hip arthroplasty ( THA) in patients with inflammatory arthritis ( IA), adjusting for medical comorbidities and socioeconomic background.

    Methods. Data on 6690 patients with IA who underwent THA during 1992-2012 were extracted from the Swedish Hip Arthroplasty Register. Data on comorbidity, measured using the Charlson Comorbidity Index ( CCI), and socioeconomic data were gathered from the Swedish National Inpatient Register and Statistics Sweden. The CCI was divided into low ( 0), moderate ( 1-2), and high (> 2). Cox proportional hazards models were fitted to calculate adjusted HR of early mortality, with 95% CI.

    Results. Twenty-five patients ( 0.4%) died within 0-90 days, giving a 90-day unadjusted survival rate of 99.6% ( CI 99.5-99.8). Comorbidity was associated with an increased risk of death within 90 days postoperatively [ high vs low CCI: adjusted HR 9.0 ( CI 1.6-49.9)]. There was a trend toward lower risk of death during the period 1999-2005, although patients operated on during this period had more comorbidities than those operated on from 1992 to 1998. A large proportion of patients was re-admitted to hospital within 90 days after the index procedure ( 30.2%), but rarely for cardiovascular reasons.

    Conclusion. Medical comorbidity and an age above 75 years are associated with a substantial increase in the risk of early death after THA in patients with IA. Awareness of potential risk factors may alert clinicians and thus improve perioperative care.

  • 762. Wejheden, Carolina
    et al.
    Brunnberg, Sara
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Lind, Monica
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Arbets- och miljömedicin.
    Andersson, Göran
    Hanberg, Annika
    Transgenic mice with a constitutively active aryl hydrocarbon receptor (CA-AhR) display a gender specific bone phenotype2010Inngår i: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 114, nr 1, s. 48-58Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Bone tissue homeostasis is governed by hormones, growth factors and cytokines and can be distorted by environmental pollutants such as ligands to the aryl hydrocarbon receptor (AhR). A transgenic mouse expressing a constitutively active AhR (CA-AhR), mimicking continuous low-dose exposure to AhR-ligands, was used to explore potential long-term effects of these ligands on bone The density, content and dimensions of cortical and trabecular bone, as well as physical properties, were significantly altered in female transgenic mice, while almost no alterations were detected in males. Osteoclast volume density and serum level of CTX, reflecting osteoclast activity, were both increased by approximately 60% in female CA-AhR mice, while serum TRAP 5b, reflecting osteoclast numbers, was unchanged. Subsequently, the resorption index (CTX/TRAP 5b) was increased by 90% indicating increased osteoclast activity in female CA-AhR. Moreover, the protein level of the osteoclast collagenase cathepsin K was increased by 40 % in bone extracts of female CA-AhR mice. The mRNA expression of several osteoclast and osteoblast associated genes were altered in female transgenic mice, but not in males. Notably, early markers for osteoclast and osteoblast differentiation were normal, while the expression of functional markers of osteoclasts and osteoblasts were reduced. In conclusion, a low continuous activation of the AhR leads to a skeletal phenotype with increased bone resorption associated with more ductile bones in females but not in males. The results indicate the presence of an interaction between the AhR and a female specific mechanism implicated in inhibition of osteoclast development and function. Female bone tissue appears more susceptible to dioxins and other AhR-ligands than male bone tissue.

  • 763.
    Wiberg, Bernice
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Kilander, Lena
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik.
    Sundström, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    The relationship between executive dysfunction and post-stroke mortality: a population-based cohort study2012Inngår i: BMJ Open, ISSN 2044-6055, E-ISSN 2044-6055, Vol. 2, nr 3, s. e000458-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVES:

    To study the associations of pre-stroke cognitive performance with mortality after first-ever stroke or transient ischaemic attack (TIA).

    DESIGN:

    A prospective cohort study.

    SETTING AND PARTICIPANTS:

    In participants having first-ever stroke or TIA during up to 14 years of post-test follow-up (n=155), we investigated the associations of pre-stroke variables and cognitive test results with post-stroke survival. The study is based on those participants of the Uppsala Longitudinal Study of Adult Men who performed cognitive function tests at approximately age 70 (n=919).

    PRIMARY OUTCOME MEASURES:

    Mortality after first-ever stroke or TIA related to pre-stroke executive performance.

    RESULTS:

    Eighty-four (54%) of the first-ever stroke/TIA patients died under a median follow-up of 2.5 years after the event. In Cox proportional hazard analyses adjusting for age, education, social group and traditional stroke risk factors, poor performance in Trail Making Test (TMT)-A was related to mortality (HR 1.88 per SD, 95% CI 1.31 to 2.71, p=0.001). The risk of mortality was approximately threefold higher in the highest tertile compared with the lowest tertile (HR TMT-A= 2.90 per SD, 95% CI 1.24 to 6.77, p=0.014). A similar pattern was seen for TMT-B, but Mini-Mental State Examination results were not related to risk of post-stroke mortality.

    CONCLUSION:

    Executive performance measured by TMT-A and -B before stroke was independently associated with long-term risk of mortality, after first-ever stroke or TIA in a population-based study of older men.

  • 764. Witasp, Anna
    et al.
    Carrero, Juan Jesús
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Ahlström, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Kullberg, Joel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Adamsson, Viola
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Risérus, Ulf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Larsson, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård.
    Helmersson-Karlqvist, Johanna
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Stenvinkel, Peter
    Ärnlöv, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Inflammatory biomarker pentraxin 3 (PTX3) in relation to obesity, body fat depots, and weight loss2014Inngår i: Obesity, ISSN 1930-7381, E-ISSN 1930-739X, Vol. 22, nr 5, s. 1373-1379Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: The relation between inflammatory markers, adiposity and disease is under extensive study. Here we tested the hypothesis that the immunomodulatory protein pentraxin 3 (PTX3) is associated with adiposity in the general population.

    DESIGN AND METHODS: Serum PTX3 concentrations, body mass index (BMI), waist circumference (WC) and fat depots, as quantified by dual-energy X-ray absorptiometry and magnetic resonance imaging, were assessed in three community-based cohorts: ULSAM, n = 790, mean age 78 years; PIVUS, n = 1003, mean age 70 years, women 50%; and the NORDIET-trial, n = 86, mean age 53 years, women 63%. Participants were re-examined after 5 years (PIVUS, n = 804) or following a 6-week randomized controlled dietary intervention (NORDIET).

    RESULTS: PTX3 levels were inversely associated with BMI and WC as well as with total and visceral fat (P < 0.05 for all; adjusted for age, inflammatory biomarkers and cardiovascular risk factors). The association between PTX3 and BMI appeared even stronger in nonobese individuals. A decrease in BMI over 5 years as well as weight loss following the NORDIET intervention were associated with increased serum PTX3 concentrations (P < 0.001).

    CONCLUSIONS: These consistent data support an inverse association between circulating PTX3 and anthropometrical measures, calling for further mechanistic studies of the link between PTX3 and fat.

  • 765.
    Wolf, Olof
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Osteoarthritis of the Hip and Uncemented Total Hip Arthroplasty: Effects of Immediate Weight Bearing on Implant Stability, Bone Mineral Density, and Body Composition2010Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    The initial recommendation for the postoperative regime after uncemented total hip arthroplasty (THA) was 6-12 weeks of partial weight bearing (PWB) to obtain a stable implant position during bone ingrowth. In recent years patients with uncemented THA have increasingly practiced full weight bearing (FWB) after surgery, which has largely been based on clinical experience rather than on scientific evidence. The aim of this thesis was to investigate the effects of FWB versus PWB for 3 months on the stability of the implants and on bone mineral density (BMD), as well as body composition (BC) of the lower extremities.

    We used radiostereometric analysis (RSA) to measure implant micromotion and dual X-ray absorptiometry (DXA) to measure BMD and BC. Forty-six patients with strictly unilateral osteoarthritis of the hip (OAH) received uncemented THA. These patients were then randomized to the FWB or PWB groups and followed for 5 years.

    In a preoperative cross-sectional study the BMD of the hip and heel were compared between the OAH-affected side and the healthy side. The study showed an increase of BMD at the femoral neck and a decrease at the total hip and trochanter. The results of a RSA study of cup stability showed that there might be minimal movement in medial and proximal directions during the first postoperative week. These results indicate that the RSA baseline investigation of uncemented cups should be performed as early as possible after the first postoperative day. FWB had no adverse effects on the stability of the uncemented press-fit cups or the uncemented cementless Spotorno (CLS) femoral stems after a 5-year follow-up. There was no difference in periprosthetic BMD around the CLS stem regardless of the postoperative weight bearing regime. All zones around the femoral stem indicated a recovery in BMD toward baselines, except the calcar region, which showed progressive loss in BMD to -22% at 5 years post-surgery. FWB had no effect on the changes in BC after surgery.

    In conclusion, FWB is safe in uncemented THA in terms of stability, BMD and BC. Furthermore, THA apparently counteracts age-related changes in BC but not in BMD.

    Delarbeid
    1. Differences in hip bone mineral density may explain the hip fracture pattern in osteoarthritic hips
    Åpne denne publikasjonen i ny fane eller vindu >>Differences in hip bone mineral density may explain the hip fracture pattern in osteoarthritic hips
    Vise andre…
    2009 (engelsk)Inngår i: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, Vol. 80, nr 3, s. 308-313Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Introduction In patients with osteoarthritis of the hip (OAH), trochanteric fractures are much more common than femoral neck fractures. One reason may be altered bone composition in the proximal femurs. OAH often leads to a fixed external rotation of the hip, leading to difficulties in positioning during DXA measurements. We compared BMD in OAH-affected legs and healthy legs. Patients and methods 40 patients with strictly unilateral OAH were cross-sectionally investigated with DXA at the hips and heels bilaterally as well as body composition of the legs. 3 regions of interest in the proximal femur were measured: femoral neck (FN), trochanter (TR), and total hip (TH). The design of the study allowed us to perform paired t-test between the OAH side and the healthy side. Results BMD was increased by 4.1% in FN, and reduced by 8.3% in TR and 4.1% in TH (p < 0.001 for all comparisons). Interpretation The differences in BMD, with decrease in the trochanter and increase in the femoral neck, may offer an explanation for the pattern of hip fractures seen in osteoarthritis. External rotation of the hip cannot explain the differences in BMD.

    HSV kategori
    Forskningsprogram
    Ortopedi
    Identifikatorer
    urn:nbn:se:uu:diva-111771 (URN)10.3109/17453670903039528 (DOI)000268569700009 ()19593721 (PubMedID)
    Tilgjengelig fra: 2009-12-21 Laget: 2009-12-21 Sist oppdatert: 2017-12-12bibliografisk kontrollert
    2. The optimal timing of baseline radiostereometric analysis of uncemented press fit cups
    Åpne denne publikasjonen i ny fane eller vindu >>The optimal timing of baseline radiostereometric analysis of uncemented press fit cups
    Vise andre…
    2010 (engelsk)Inngår i: Scandinavian Journal of Surgery, ISSN 1457-4969, E-ISSN 1799-7267, Vol. 99, nr 4, s. 244-249Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Background and Aims: The baseline Radiostereometric analysis (RSA) is usually performed during the first postoperative week. We investigated the micromotion of two uncemented press fit acetabular cups during the first week after total hip arthroplasty.

    Material and Methods: All study patients had unilateral osteoarthritis of the hip and received an uncemented THA combination consisting of a CLS stem and either an Allofit or an Interop acetabular cup. The study group consisted of 24 patients who underwent RSA within 1 hour after skin closure, and at 1 and 7 days after surgery.

    Results: The upper limit of the 95% confidence interval for micromotion was less than or close to the precision of the method for all studied directions during the first week after surgery. Mean values indicate proximal and medial translation of the uncemented cup at one week.

    Conclusions: We found only minimal micromotion, barely above the precision limit, measured as medial and proximal translations of these uncemented cups. This indicates that the first postoperative RSA measurement following a primary THA with an uncemented press fit acetabular cup should be made as early as possible after the first postoperative day.

    Emneord
    RSA, baseline examination, THA, uncemented cup, optimal timing, micromotion, weight bearing, muscle tonus
    HSV kategori
    Forskningsprogram
    Ortopedi
    Identifikatorer
    urn:nbn:se:uu:diva-131033 (URN)000285817800013 ()
    Tilgjengelig fra: 2010-09-21 Laget: 2010-09-21 Sist oppdatert: 2017-12-12bibliografisk kontrollert
    3. Effects of different weight bearing regimes on stability of press fit cups: A randomized study with 5 years of follow-up using radiostereometry
    Åpne denne publikasjonen i ny fane eller vindu >>Effects of different weight bearing regimes on stability of press fit cups: A randomized study with 5 years of follow-up using radiostereometry
    Vise andre…
    (engelsk)Artikkel i tidsskrift (Fagfellevurdert) Submitted
    Abstract [en]

    There is little evidence supporting immediate weight bearing after uncemented THA. Thirty-seven patients with unilateral osteoarthritis of the hip received a press fit cup. They were randomized to immediate full weight bearing or partial weight bearing for 3 months. At 5 years we found no difference in micromotion as assessed with radiostereometry. Numerically there was more proximal translation and increased inclination with immediate weight bearing, but these values barely exceeded the precision limit for the method. Pooled data for the two groups revealed translations of 0.1-0.3 mm and rotations of 0.2-0.3° over the 5 year follow-up period. To conclude, we found no adverse effects of immediate weight bearing after THA on stability of these press fit cups. Early mobilization might have other advantages.

    HSV kategori
    Identifikatorer
    urn:nbn:se:uu:diva-131035 (URN)
    Tilgjengelig fra: 2010-09-21 Laget: 2010-09-21 Sist oppdatert: 2013-08-16bibliografisk kontrollert
    4. A randomized study using DXA and RSA in 38 patients followed for 5 years
    Åpne denne publikasjonen i ny fane eller vindu >>A randomized study using DXA and RSA in 38 patients followed for 5 years
    Vise andre…
    2010 (engelsk)Inngår i: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, Vol. 81, nr 3, s. 286-291Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Background and purpose: There is no real consensus on the best rehabilitation regime after uncemented total hip arthroplasty. Theoretically, bone ingrowth into the implant should benefit from initial partial weight bearing. We investigated whether the degree of postoperative weight bearing influences the periprosthetic bone mineral density (BMD) and/or the stability of the CLS stem.

    Patients and methods: 38 patients received an uncemented CLS stem and were randomized to either unrestricted postoperative weight bearing or to partial weight bearing for 3 months. Periprosthetic BMD was measured in the 7 Gruen zones with DXA and the stability of the femoral stem was assessed by radiostereometric analyses (RSA) after surgery and at 3, 12, 24, and 60 months.

    Results: Periprosthetic BMD was not influenced by the type of postoperative weight bearing. BMD was reduced by 8-15% in all Gruen zones at 3 months. Restoration toward initial BMD was observed in all zones except in zone 7 (calcar region), where BMD was decreased by 22% at 5 years. Immediate weight bearing after surgery did not influence the stability of the CLS stem, as assessed by RSA.

    Interpretation: Immediate full weight bearing after uncemented total hip arthroplasty is safe. There is no difference in the periprosthetic BMD or stability of the stem as measured with RSA compared to partial weight bearing for 3 months. BMD is decreased by more than 20% in the calcar region around a CLS stem after 5 years.

    Emneord
    weight bearing, DXA, periprosthetic BMD, RSA, uncemented CLS stem
    HSV kategori
    Forskningsprogram
    Ortopedi
    Identifikatorer
    urn:nbn:se:uu:diva-131005 (URN)10.3109/17453674.2010.487238 (DOI)20446828 (PubMedID)
    Tilgjengelig fra: 2010-09-21 Laget: 2010-09-20 Sist oppdatert: 2017-12-12bibliografisk kontrollert
    5. Effects of postoperative weight-bearing on body composition and bone mineral density after uncemented total hip arthroplasty
    Åpne denne publikasjonen i ny fane eller vindu >>Effects of postoperative weight-bearing on body composition and bone mineral density after uncemented total hip arthroplasty
    Vise andre…
    2013 (engelsk)Inngår i: Journal of Rehabilitation Medicine, ISSN 1650-1977, E-ISSN 1651-2081, Vol. 45, nr 5, s. 498-503Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Objective:

    To investigate whether a postoperative weight-bearing regimen affects changes in bone mineral density and body composition after uncemented total hip arthroplasty, and to investigate the changes over a 5-year period after the surgical procedure.

    Design:

    Secondary analysis of a previous randomized controlled trial.

    Methods:

    A total of 39 patients were randomized to immediate full weight-bearing or partial weight-bearing for 3 months. Dual-energy X-ray absorptiometry was used to measure bone mineral density of the contralateral hip and both heels and to measure body composition.

    Results:

    The weight-bearing regimen had no effect on change in bone mineral density or body composition after 3 and 12 months. At 5 years, there was a decrease in bone mineral density of 3% in the total body and 2-3% in the contralateral hip regions. At 5 years we found a decrease in total body bone mineral content of 5%, but no changes in fat mass or lean mass compared with preoperative values.

    Conclusion:

    The postoperative weight-bearing regimen had no effect on changes in body composition or bone mineral density. Five years after total hip arthroplasty there was a decrease in bone mineral content and bone mineral density, but no changes in lean mass or fat mass.

    Emneord
    osteoarthritis of the hip; uncemented total hip arthroplasty; DXA; weight-bearing; body composition; bone mineral density
    HSV kategori
    Identifikatorer
    urn:nbn:se:uu:diva-199774 (URN)10.2340/16501977-1140 (DOI)000320345700012 ()23571688 (PubMedID)
    Tilgjengelig fra: 2013-05-14 Laget: 2013-05-14 Sist oppdatert: 2017-12-06bibliografisk kontrollert
  • 766.
    Wolf, Olof
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mattsson, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Milbrink, Jan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mallmin, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    A randomized study using DXA and RSA in 38 patients followed for 5 years2010Inngår i: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, Vol. 81, nr 3, s. 286-291Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and purpose: There is no real consensus on the best rehabilitation regime after uncemented total hip arthroplasty. Theoretically, bone ingrowth into the implant should benefit from initial partial weight bearing. We investigated whether the degree of postoperative weight bearing influences the periprosthetic bone mineral density (BMD) and/or the stability of the CLS stem.

    Patients and methods: 38 patients received an uncemented CLS stem and were randomized to either unrestricted postoperative weight bearing or to partial weight bearing for 3 months. Periprosthetic BMD was measured in the 7 Gruen zones with DXA and the stability of the femoral stem was assessed by radiostereometric analyses (RSA) after surgery and at 3, 12, 24, and 60 months.

    Results: Periprosthetic BMD was not influenced by the type of postoperative weight bearing. BMD was reduced by 8-15% in all Gruen zones at 3 months. Restoration toward initial BMD was observed in all zones except in zone 7 (calcar region), where BMD was decreased by 22% at 5 years. Immediate weight bearing after surgery did not influence the stability of the CLS stem, as assessed by RSA.

    Interpretation: Immediate full weight bearing after uncemented total hip arthroplasty is safe. There is no difference in the periprosthetic BMD or stability of the stem as measured with RSA compared to partial weight bearing for 3 months. BMD is decreased by more than 20% in the calcar region around a CLS stem after 5 years.

  • 767.
    Wolf, Olof
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mattsson, Per
    Milbrink, Jan
    Larsson, Sune
    Mallmin, Hans
    Effects of different weight bearing regimes on stability of press fit cups: A randomized study with 5 years of follow-up using radiostereometryArtikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    There is little evidence supporting immediate weight bearing after uncemented THA. Thirty-seven patients with unilateral osteoarthritis of the hip received a press fit cup. They were randomized to immediate full weight bearing or partial weight bearing for 3 months. At 5 years we found no difference in micromotion as assessed with radiostereometry. Numerically there was more proximal translation and increased inclination with immediate weight bearing, but these values barely exceeded the precision limit for the method. Pooled data for the two groups revealed translations of 0.1-0.3 mm and rotations of 0.2-0.3° over the 5 year follow-up period. To conclude, we found no adverse effects of immediate weight bearing after THA on stability of these press fit cups. Early mobilization might have other advantages.

  • 768.
    Wolf, Olof
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mattsson, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Milbrink, Jan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mallmin, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Effects of postoperative weight-bearing on body composition and bone mineral density after uncemented total hip arthroplasty2013Inngår i: Journal of Rehabilitation Medicine, ISSN 1650-1977, E-ISSN 1651-2081, Vol. 45, nr 5, s. 498-503Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective:

    To investigate whether a postoperative weight-bearing regimen affects changes in bone mineral density and body composition after uncemented total hip arthroplasty, and to investigate the changes over a 5-year period after the surgical procedure.

    Design:

    Secondary analysis of a previous randomized controlled trial.

    Methods:

    A total of 39 patients were randomized to immediate full weight-bearing or partial weight-bearing for 3 months. Dual-energy X-ray absorptiometry was used to measure bone mineral density of the contralateral hip and both heels and to measure body composition.

    Results:

    The weight-bearing regimen had no effect on change in bone mineral density or body composition after 3 and 12 months. At 5 years, there was a decrease in bone mineral density of 3% in the total body and 2-3% in the contralateral hip regions. At 5 years we found a decrease in total body bone mineral content of 5%, but no changes in fat mass or lean mass compared with preoperative values.

    Conclusion:

    The postoperative weight-bearing regimen had no effect on changes in body composition or bone mineral density. Five years after total hip arthroplasty there was a decrease in bone mineral content and bone mineral density, but no changes in lean mass or fat mass.

  • 769.
    Wolf, Olof
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mattsson, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Milbrink, Jan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mallmin, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    The effects of different weight-bearing regimes on press-fit cup stability: a randomised study with five years of follow-up using radiostereometry2012Inngår i: International Orthopaedics, ISSN 0341-2695, E-ISSN 1432-5195, Vol. 36, nr 4, s. 735-740Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    PURPOSE:

    There is little evidence to support immediate weight bearing after uncemented total hip arthroplasty (THA).

    METHODS:

    Thirty-seven patients with unilateral osteoarthritis of the hip received a press-fit cup. Cup stability was assessed with radiostereometry (RSA) over five years. Patients were randomised to immediate full weight bearing, or partial weight bearing for three months.

    RESULTS:

    At five years, we found no difference in micromotion as assessed with radiostereometry. Numerically, there was more proximal translation and increased inclination with immediate weight bearing, but these values barely exceeded the precision limit for the method. Pooled data for the two groups revealed translations of 0.1-0.3 mm and rotations of 0.2-0.3° over the five year follow-up period.

    CONCLUSIONS:

    We found no adverse effects of immediate weight bearing after THA in relation to stability of these press-fit cups. Early mobilisation might have other advantages.

  • 770.
    Wolf, Olof
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Milbrink, Jan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mattson, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mallmin, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    The optimal timing of baseline radiostereometric analysis of uncemented press fit cups2010Inngår i: Scandinavian Journal of Surgery, ISSN 1457-4969, E-ISSN 1799-7267, Vol. 99, nr 4, s. 244-249Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and Aims: The baseline Radiostereometric analysis (RSA) is usually performed during the first postoperative week. We investigated the micromotion of two uncemented press fit acetabular cups during the first week after total hip arthroplasty.

    Material and Methods: All study patients had unilateral osteoarthritis of the hip and received an uncemented THA combination consisting of a CLS stem and either an Allofit or an Interop acetabular cup. The study group consisted of 24 patients who underwent RSA within 1 hour after skin closure, and at 1 and 7 days after surgery.

    Results: The upper limit of the 95% confidence interval for micromotion was less than or close to the precision of the method for all studied directions during the first week after surgery. Mean values indicate proximal and medial translation of the uncemented cup at one week.

    Conclusions: We found only minimal micromotion, barely above the precision limit, measured as medial and proximal translations of these uncemented cups. This indicates that the first postoperative RSA measurement following a primary THA with an uncemented press fit acetabular cup should be made as early as possible after the first postoperative day.

  • 771.
    Wolf, Olof
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Ström, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Milbrink, Jan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mallmin, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Differences in hip bone mineral density may explain the hip fracture pattern in osteoarthritic hips2009Inngår i: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, Vol. 80, nr 3, s. 308-313Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Introduction In patients with osteoarthritis of the hip (OAH), trochanteric fractures are much more common than femoral neck fractures. One reason may be altered bone composition in the proximal femurs. OAH often leads to a fixed external rotation of the hip, leading to difficulties in positioning during DXA measurements. We compared BMD in OAH-affected legs and healthy legs. Patients and methods 40 patients with strictly unilateral OAH were cross-sectionally investigated with DXA at the hips and heels bilaterally as well as body composition of the legs. 3 regions of interest in the proximal femur were measured: femoral neck (FN), trochanter (TR), and total hip (TH). The design of the study allowed us to perform paired t-test between the OAH side and the healthy side. Results BMD was increased by 4.1% in FN, and reduced by 8.3% in TR and 4.1% in TH (p < 0.001 for all comparisons). Interpretation The differences in BMD, with decrease in the trochanter and increase in the femoral neck, may offer an explanation for the pattern of hip fractures seen in osteoarthritis. External rotation of the hip cannot explain the differences in BMD.

  • 772.
    Wolf, Olof
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Åberg, Henrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Tornberg, Ulrika
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Jonsson, Kenneth B.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Do Orthogeriatric Inpatients Have a Correct Medication List?: A Pharmacist-Led Assessment of 254 Patients in a Swedish University Hospital2016Inngår i: Geriatric Orthopaedic Surgery & Rehabilitation, E-ISSN 2151-4585, Vol. 7, nr 1, s. 18-22Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Introduction: Comorbidities and polypharmacy complicate the treatment of geriatric patients with acute orthopedic injuries. A correct medication history and an updated medication list are a prerequisite for safe treatment of these debilitated patients. Published evidence suggests favorable outcomes with comanaged care. The aim of this study was to assess the accuracy of the inpatient medication lists generated at admission and investigate the efficacy of a dedicated ward-based pharmacist to find and correct mistakes in these lists. Methods: A total of 254 patients were enrolled. The ward-based pharmacist performed the assessment regarding the accuracy of the medication list generated at admission by the method of medication reconciliation. Number of discrepancies and types of discrepancy were noted. Results: The 254 patients (176 women) had a mean age of 85 years (standard deviation 7.4 years, range 42-100 years). The most common reason for orthopedic admission was hip fracture. The mean number of discrepancies was 2.1 for all patients (range 0-13). Omission of a prescribed drug was the most common mistake. Fifty-six (22%) of the 254 assessed patients had a correct medication list. Discussion: The many discrepancies in our study may have several explanations but highlight the difficulties in taking a correct medication history of patients in a stressful environment with an extremely high workload. Moreover, electronic medication lists create challenges. Implementing new electronic tools for health care requires feedback, redesign, and adaptation to meet various needs of the users. Conclusion: In conclusion, orthogeriatric patients have an unsatisfactory high number of discrepancies in their medication lists. Clinical pharmacists can accurately identify many of these mistakes.

  • 773.
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Potential health hazards of eating red meat.2017Inngår i: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 281, nr 2, s. 106-122Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Red meat (beef, veal, pork, lamb and mutton) consumption contributes several important nutrients to the diet, for example essential amino acids, vitamins (including B12) and minerals (including iron and zinc). Processed red meat (ham, sausages, bacon, frankfurters, salami, etc.) undergoes treatment (curing, smoking, salting or the use of chemical preservatives and additives) to improve its shelf life and/or taste. During recent decades, consumption of red meat has been increasing globally, especially in developing countries. At the same time, there has been growing evidence that high consumption of red meat, especially of processed meat, may be associated with an increased risk of several major chronic diseases. Here, a comprehensive summary is provided of the accumulated evidence based on prospective cohort studies regarding the potential adverse health effects of red meat consumption on major chronic diseases, such as diabetes, coronary heart disease, heart failure, stroke and cancer at several sites, and mortality. Risk estimates from pooled analyses and meta-analyses are presented together with recently published findings. Based on at least six cohorts, summary results for the consumption of unprocessed red meat of 100 g day-1 varied from nonsignificant to statistically significantly increased risk (11% for stroke and for breast cancer, 15% for cardiovascular mortality, 17% for colorectal and 19% for advanced prostate cancer); for the consumption of 50 g day-1 processed meat, the risks were statistically significantly increased for most of the studied diseases (4% for total prostate cancer, 8% for cancer mortality, 9% for breast, 18% for colorectal and 19% for pancreatic cancer, 13% for stroke, 22% for total and 24% for cardiovascular mortality and 32% for diabetes). Potential biological mechanisms underlying the observed risks and the environmental impact of red meat production are also discussed. The evidence-based integrated message is that it is plausible to conclude that high consumption of red meat, and especially processed meat, is associated with an increased risk of several major chronic diseases and preterm mortality. Production of red meat involves an environmental burden. Therefore, some European countries have already integrated these two issues, human health and the 'health of the planet', into new dietary guidelines and recommended limiting consumption of red meat.

  • 774. Wu, Huaxing
    et al.
    Mhd Omar, Nor Adila
    Håkansson, Niclas
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Landberg, Rikard
    Evaluation of alkylresorcinols in adipose tissue biopsies as a long-term biomarker of whole-grain wheat and rye intake in free-living Swedish men and women.2018Inngår i: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 21, nr 10, s. 1933-1942Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: Wheat and rye, the most consumed whole grains (WG) in the Nordic countries, contain alkylresorcinols (AR) in their bran. AR concentrations in human adipose tissue might reflect long-term WG rye and wheat intake. We aimed to evaluate AR concentrations in adipose tissue biopsies as a long-term biomarker of WG wheat and rye intake in free-living Swedish men and women.

    DESIGN: Cross-sectional study. AR concentrations in adipose tissue biopsies were analysed and compared with long-term WG intake assessed by three FFQ (repeated over a period of 14 years in men, 17 years in women) and with plasma AR concentrations.

    SETTING: The Cohort of Swedish Men between 1997 and 2010 and the Swedish Mammography Cohort between 1987 and 2003, Sweden.

    SUBJECTS: Men (n 149) and women (n 109).

    RESULTS: Long-term WG rye intake estimated with repeated FFQ correlated (r=0·31-0·41, P<0·01) with adipose-tissue AR concentrations, while WG wheat intake correlated only weakly (r=0·17-0·33, P<0·05). Total AR concentration in adipose tissue was 61 % lower in women than in men at similar energy-adjusted WG wheat and rye intakes, but plasma concentrations were similar. AR concentrations in adipose tissue correlated well with plasma concentrations (r=0·49-0·81, P<0·001).

    CONCLUSIONS: AR in adipose tissue reflected long-term WG rye but not WG wheat intake, probably due to poor precision in estimating WG wheat intake by FFQ. AR in adipose tissue appears promising as a biomarker of long-term WG rye intake but should be adjusted for sex.

  • 775. Wu, Lang
    et al.
    Shi, Wei
    Long, Jirong
    Guo, Xingyi
    Michailidou, Kyriaki
    Beesley, Jonathan
    Bolla, Manjeet K
    Shu, Xiao-Ou
    Lu, Yingchang
    Cai, Qiuyin
    Al-Ejeh, Fares
    Rozali, Esdy
    Wang, Qin
    Dennis, Joe
    Li, Bingshan
    Zeng, Chenjie
    Feng, Helian
    Gusev, Alexander
    Barfield, Richard T
    Andrulis, Irene L
    Anton-Culver, Hoda
    Arndt, Volker
    Aronson, Kristan J
    Auer, Paul L
    Barrdahl, Myrto
    Baynes, Caroline
    Beckmann, Matthias W
    Benitez, Javier
    Bermisheva, Marina
    Blomqvist, Carl
    Bogdanova, Natalia V
    Bojesen, Stig E
    Brauch, Hiltrud
    Brenner, Hermann
    Brinton, Louise
    Broberg, Per
    Brucker, Sara Y
    Burwinkel, Barbara
    Caldés, Trinidad
    Canzian, Federico
    Carter, Brian D
    Castelao, J Esteban
    Chang-Claude, Jenny
    Chen, Xiaoqing
    Cheng, Ting-Yuan David
    Christiansen, Hans
    Clarke, Christine L
    Collée, Margriet
    Cornelissen, Sten
    Couch, Fergus J
    Cox, David
    Cox, Angela
    Cross, Simon S
    Cunningham, Julie M
    Czene, Kamila
    Daly, Mary B
    Devilee, Peter
    Doheny, Kimberly F
    Dörk, Thilo
    Dos-Santos-Silva, Isabel
    Dumont, Martine
    Dwek, Miriam
    Eccles, Diana M
    Eilber, Ursula
    Eliassen, A Heather
    Engel, Christoph
    Eriksson, Mikael
    Fachal, Laura
    Fasching, Peter A
    Figueroa, Jonine
    Flesch-Janys, Dieter
    Fletcher, Olivia
    Flyger, Henrik
    Fritschi, Lin
    Gabrielson, Marike
    Gago-Dominguez, Manuela
    Gapstur, Susan M
    García-Closas, Montserrat
    Gaudet, Mia M
    Ghoussaini, Maya
    Giles, Graham G
    Goldberg, Mark S
    Goldgar, David E
    González-Neira, Anna
    Guénel, Pascal
    Hahnen, Eric
    Haiman, Christopher A
    Håkansson, Niclas
    Hall, Per
    Hallberg, Emily
    Hamann, Ute
    Harrington, Patricia
    Hein, Alexander
    Hicks, Belynda
    Hillemanns, Peter
    Hollestelle, Antoinette
    Hoover, Robert N
    Hopper, John L
    Huang, Guanmengqian
    Humphreys, Keith
    Hunter, David J
    Jakubowska, Anna
    Janni, Wolfgang
    John, Esther M
    Johnson, Nichola
    Jones, Kristine
    Jones, Michael E
    Jung, Audrey
    Kaaks, Rudolf
    Kerin, Michael J
    Khusnutdinova, Elza
    Kosma, Veli-Matti
    Kristensen, Vessela N
    Lambrechts, Diether
    Le Marchand, Loic
    Li, Jingmei
    Lindström, Sara
    Lissowska, Jolanta
    Lo, Wing-Yee
    Loibl, Sibylle
    Lubinski, Jan
    Luccarini, Craig
    Lux, Michael P
    MacInnis, Robert J
    Maishman, Tom
    Kostovska, Ivana Maleva
    Mannermaa, Arto
    Manson, JoAnn E
    Margolin, Sara
    Mavroudis, Dimitrios
    Meijers-Heijboer, Hanne
    Meindl, Alfons
    Menon, Usha
    Meyer, Jeffery
    Mulligan, Anna Marie
    Neuhausen, Susan L
    Nevanlinna, Heli
    Neven, Patrick
    Nielsen, Sune F
    Nordestgaard, Børge G
    Olopade, Olufunmilayo I
    Olson, Janet E
    Olsson, Håkan
    Peterlongo, Paolo
    Peto, Julian
    Plaseska-Karanfilska, Dijana
    Prentice, Ross
    Presneau, Nadege
    Pylkäs, Katri
    Rack, Brigitte
    Radice, Paolo
    Rahman, Nazneen
    Rennert, Gad
    Rennert, Hedy S
    Rhenius, Valerie
    Romero, Atocha
    Romm, Jane
    Rudolph, Anja
    Saloustros, Emmanouil
    Sandler, Dale P
    Sawyer, Elinor J
    Schmidt, Marjanka K
    Schmutzler, Rita K
    Schneeweiss, Andreas
    Scott, Rodney J
    Scott, Christopher G
    Seal, Sheila
    Shah, Mitul
    Shrubsole, Martha J
    Smeets, Ann
    Southey, Melissa C
    Spinelli, John J
    Stone, Jennifer
    Surowy, Harald
    Swerdlow, Anthony J
    Tamimi, Rulla M
    Tapper, William
    Taylor, Jack A
    Terry, Mary Beth
    Tessier, Daniel C
    Thomas, Abigail
    Thöne, Kathrin
    Tollenaar, Rob A E M
    Torres, Diana
    Truong, Thérèse
    Untch, Michael
    Vachon, Celine
    Van Den Berg, David
    Vincent, Daniel
    Waisfisz, Quinten
    Weinberg, Clarice R
    Wendt, Camilla
    Whittemore, Alice S
    Wildiers, Hans
    Willett, Walter C
    Winqvist, Robert
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Xia, Lucy
    Yang, Xiaohong R
    Ziogas, Argyrios
    Ziv, Elad
    Dunning, Alison M
    Pharoah, Paul D P
    Simard, Jacques
    Milne, Roger L
    Edwards, Stacey L
    Kraft, Peter
    Easton, Douglas F
    Chenevix-Trench, Georgia
    Zheng, Wei
    A transcriptome-wide association study of 229,000 women identifies new candidate susceptibility genes for breast cancer.2018Inngår i: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 50, nr 7, s. 968-978Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    , including 14 genes at loci not yet reported for breast cancer. We silenced 13 genes and showed an effect for 11 on cell proliferation and/or colony-forming efficiency. Our study provides new insights into breast cancer genetics and biology.

  • 776.
    Wu, Lang
    et al.
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37203 USA;Univ Hawaii Manoa, Canc Epidemiol Div, Populat Sci Pacific Program, Univ Hawaii Canc Ctr, Honolulu, HI 96822 USA.
    Wang, Jifeng
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37203 USA;Fifth Peoples Hosp Shanghai, Dept Urol, Shanghai, Peoples R China.
    Cai, Qiuyin
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37203 USA.
    Cavazos, Taylor B.
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37203 USA.
    Emami, Nima C.
    Univ Calif San Francisco, Program Biol & Med Informat, San Francisco, CA 94143 USA;Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
    Long, Jirong
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37203 USA.
    Shu, Xiao-Ou
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37203 USA.
    Lu, Yingchang
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37203 USA.
    Guo, Xingyi
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37203 USA.
    Bauer, Joshua A.
    Vanderbilt Univ, Dept Biochem, Sch Med, Nashville, TN 37203 USA;Vanderbilt Univ, Sch Med, Vanderbilt Inst Chem Biol, High Throughput Screening Facil, Nashville, TN 37203 USA.
    Pasaniuc, Bogdan
    Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA;Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA.
    Penney, Kathryn L.
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Harvard Med Sch, Channing Div Network Med, Dept Med, Brigham & Womens Hosp, Boston, MA 02115 USA.
    Freedman, Matthew L.
    Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA;Broad Inst, Cambridge, MA USA.
    Kote-Jarai, Zsofia
    Inst Canc Res, Div Genet & Epidemiol, London, England;Royal Marsden NHS Fdn Trust, London, England;Inst Canc Res, London, England.
    Witte, John S.
    Univ Calif San Francisco, Program Biol & Med Informat, San Francisco, CA 94143 USA;Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
    Haiman, Christopher A.
    Univ Southern Calif, Dept Prevent Med, Los Angeles, CA USA;Univ Southern Calif, Dept Prevent Med, Keck Sch Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
    Eeles, Rosalind A.
    Inst Canc Res, Div Genet & Epidemiol, London, England;Royal Marsden NHS Fdn Trust, London, England;Inst Canc Res, London, England.
    Zheng, Wei
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med,Vanderbilt Epidemiol Ctr,Vanderbilt Ingr, Nashville, TN 37203 USA.
    Benlloch, Sara
    Inst Canc Res, London, England;Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Strangeways Res Lab, Cambridge, England.
    Henderson, Brian E.
    Univ Southern Calif, Dept Prevent Med, Keck Sch Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
    Conti, David, V
    Univ Southern Calif, Dept Prevent Med, Keck Sch Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
    Schumacher, Fredrick R.
    Case Western Reserve Univ, Dept Populat & Quantitat Hlth Sci, Cleveland, OH 44106 USA;Univ Hosp Cleveland, Seidman Canc Ctr, Cleveland, OH 44106 USA.
    Easton, Douglas
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Strangeways Res Lab, Cambridge, England.
    Al Olama, Ali Amin
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Strangeways Res Lab, Cambridge, England;Univ Cambridge, Dept Clin Neurosci, Cambridge, England.
    Muir, Kenneth
    Univ Manchester, Div Populat Hlth Hlth Serv Res & Primary Care, Oxford Rd, Manchester, Lancs, England;Univ Warwick, Warwick Med Sch, Coventry, W Midlands, England.
    Berndt, Sonja, I
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Chanock, Stephen
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Albanes, Demetrius
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Weinstein, Stephanie
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Koutros, Stella
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Wildund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Gapstur, Susan M.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
    Stevens, Victoria L.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
    Tangen, Catherine M.
    Fred Hutchinson Canc Res Ctr, SWOG Stat Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
    Batra, Jyotsna
    Queensland Univ Technol, Inst Hlth & Biomed Innovat, Brisbane, Qld 4059, Australia;Queensland Univ Technol, Sch Biomed Sci, Brisbane, Qld 4059, Australia;Queensland Univ Technol, Australian Prostate Canc Res Ctr Qld, Inst Hlth & Biomed Innovat, Brisbane, Qld, Australia.
    Clements, Judith
    Australian Prostate Canc Res Ctr BioResource APCB, Translat Res Inst, Brisbane, Qld, Australia.
    Pashayan, Nora
    UCL, Dept Appl Hlth Res, London, England;Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Oncol, Strangeways Lab, Cambridge, England.
    Schleutker, Johanna
    Univ Turku, Inst Biomed, Kiinamyllynkatu 10, FI-20014 Turku, Finland;Turku Univ Hosp, Tyks Microbiol & Genet, Dept Med Genet, Turku, Finland.
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Div Nutr Epidemiol, Inst Environm Med, Stockholm, Sweden.
    West, Catharine
    Univ Manchester, Christie Hosp NHS Fdn Trust, Manchester Acad Hlth Sci,Div Canc Sci, Radiotherapy Related Res,Manchester NIHR Biomed R, Manchester, Lancs, England.
    Mucci, Lorelei
    Harvard Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Cancel-Tassin, Geraldine
    Tenon Hosp, CeRePP, Paris, France;UPMC Sorbonne Univ, GRC ONCOTYPE URO 5, Tenon Hosp, 4 Rue Chine, Paris, France.
    Sorensen, Karina Dalsgaard
    Aarhus Univ Hosp, Dept Mol Med, Aarhus, Denmark;Aarhus Univ, Dept Clin Med, Aarhus, Denmark.
    Grindedal, Eli Marie
    Oslo Univ Hosp, Dept Med Genet, Oslo, Norway.
    Neal, David E.
    Univ Cambridge, Dept Oncol, Addenbrookes Hosp, Cambridge, England;Canc Res UK Cambridge Res Inst, Li Ka Shing Ctr, Cambridge, England.
    Hamdy, Freddie C.
    Univ Oxford, Nuffield Dept Surg Sci, Oxford, England;Univ Oxford, Fac Med Sci, John Radcliffe Hosp, Oxford, England.
    Donovan, Jenny L.
    Univ Bristol, Sch Social & Community Med, Bristol, Avon, England.
    Travis, Ruth C.
    Univ Oxford, Canc Epidemiol Unit, Nuffield Dept Populat Hlth, Oxford, England.
    Hamilton, Robert J.
    Princess Margaret Canc Ctr, Dept Surg Oncol, Toronto, ON, Canada.
    Rosenstein, Bany S.
    Icahn Sch Med Mt Sinai, Dept Radiat Oncol, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
    Lu, Yong-Jie
    Queen Mary Univ London, Ctr Mol Oncol, Barts Canc Inst, John Vane Sci Ctr, London, England.
    Giles, Graham G.
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia;Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia.
    Kibel, Adam S.
    Brigham & Womens Hosp, Div Urol Surg, 75 Francis St, Boston, MA 02115 USA.
    Vega, Ana
    IDIS, Fdn Publ Galega Med Xenom SERGAS, Grp Med Xenom, CIBERER, Santiago De Compostela, Spain.
    Kogevinas, Manolis
    Barcelona Inst Global Hlth ISGlobal, Ctr Res Environm Epidemiol CREAL, Barcelona, Spain;CIBERESP, Madrid, Spain;IMIM Hosp del Mar Res Inst, Barcelona, Spain;Univ Pompeu Fabra, Barcelona, Spain.
    Park, Jong Y.
    H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL USA.
    Stanford, Janet L.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
    Newcomb, Lisa F.
    Univ Washington, Dept Epidemiol, Sch Publ Hlth, Seattle, WA 98195 USA;Univ Washington, Dept Urol, Seattle, WA 98195 USA.
    Cybulski, Cezary
    Pomeranian Med Univ, Int Hereditary Canc Ctr, Dept Genet & Pathol, Szczecin, Poland.
    Nordestgaard, Borge G.
    Univ Copenhagen, Fac Hlth & Med Sci, Copenhagen, Denmark;Copenhagen Univ Hosp, Dept Clin Biochem, Herlev & Gentofte Hosp, Herlev, Denmark.
    Brenner, Hermann
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany;German Canc Res Ctr, German Canc Consortium DKTZ, Heidelberg, Germany;German Canc Res Ctr, Div Prevent Oncol, Heidelberg, Germany;Natl Ctr Tumor Dis NCT, Heidelberg, Germany.
    Maier, Christian
    Univ Hosp Ulm, Inst Human Genet, Ulm, Germany.
    Kim, Jeri
    Univ Texas MD Anderson Canc Ctr, Dept Genitourinary Med Oncol, Houston, TX 77030 USA.
    John, Esther M.
    Stanford Univ, Dept Med Oncol, Sch Med, Stanford, CA USA;Stanford Univ, Sch Med, Stanford Canc Inst, Stanford, CA 94305 USA.
    Teixeira, Manuel R.
    Portuguese Oncol Inst Porto, Dept Genet, Porto, Portugal;Univ Porto, Biomed Sci Inst ICBAS, Porto, Portugal.
    Neuhausen, Susan L.
    City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Duarte, CA USA.
    De Ruyck, Kim
    Univ Ghent, Fac Med & Hlth Sci, Basic Med Sci, Ghent, Belgium.
    Razack, Azad
    Univ Malaya, Dept Surg, Fac Med, Kuala Lumpur, Malaysia.
    Gamulin, Marija
    Univ Med Ctr Hamburg Eppendorf, Inst Human Genet, Hamburg, Germany.
    Kaneva, Radka
    Med Univ, Mol Med Ctr, Dept Med Chem & Biochem, Sofia, Bulgaria.
    Usmani, Nawaid
    Univ Alberta, Dept Oncol, Cross Canc Inst, Edmonton, AB, Canada;Cross Canc Inst, Div Radiat Oncol, Edmonton, AB, Canada.
    Claessens, Frank
    Katholieke Univ Leuven, Mol Endocrinol Lab, Dept Cellular & Mol Med, Leuven, Belgium.
    Townsend, Paul A.
    Univ Manchester, Manchester Canc Res Ctr, Hlth Innovat Manchester,Fac Biol Med & Hlth,Div C, Manchester Acad Hlth Sci Ctr,NIHR Manchester Biom, Manchester, Lancs, England.
    Gago Dominguez, Manuela
    Complejo Hosp Univ Santiago, Genom Med Grp, Serv Galego Saude,Galician Fdn Genom Med,SERGAS, Inst Invest Sanitaria Santiago de Compostela IDIS, Santiago De Compostela, Spain;Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
    Roobol, Monique J.
    Erasmus MC, Dept Urol, Rotterdam, Netherlands.
    Menegaux, Florence
    Univ Paris Saclay, Univ Paris Sud, Canc & Environm Grp, Ctr Res Epidemiol & Populat Hlth CESP,INSERM, Villejuif, France.
    Khaw, Kay-Tee
    Univ Cambridge, Clin Gerontol Unit, Cambridge, England.
    Cannon-Albright, Lisa
    Univ Utah, Sch Med, Dept Med, Div Genet Epidemiol, Salt Lake City, UT USA;Vet Affairs Med Ctr, George E Wahlen Dept, Salt Lake City, UT 84148 USA.
    Thibodeau, Stephen N.
    Univ Surrey, Guildford, Surrey, England;Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
    Hunter, David J.
    Harvard TH Chan Sch Publ Hlth, Program Genet Epidemiol & Stat Genet, Dept Epidemiol, Boston, MA USA.
    Blot, William J.
    Vanderbilt Univ, Med Ctr, Div Epidemiol, Dept Med, Nashville, TN 37203 USA;Int Epidemiol Inst, Rockville, MD USA.
    Riboli, Elio
    Imperial Coll London, Dept Epidemiol & Biostat, Sch Publ Hlth, London, England.
    Identification of Novel Susceptibility Loci and Genes for Prostate Cancer Risk: A Transcriptome-Wide Association Study in over 140,000 European Descendants2019Inngår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 79, nr 13, s. 3192-3204Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Genome-wide association study-identified prostate cancer risk variants explain only a relatively small fraction of its familial relative risk, and the genes responsible for many of these identified associations remain unknown. To discover novel prostate cancer genetic loci and possible causal genes at previously identified risk loci, we performed a transcriptome-wide association study in 79,194 cases and 61,112 controls of European ancestry. Using data from the Genotype-Tissue Expression Project, we established genetic models to predict gene expression across the transcriptome for both prostate models and cross-tissue models and evaluated model performance using two independent datasets. We identified significant associations for 137 genes at P < 2.61 x 10(-6), a Bonferroni-corrected threshold, including nine genes that remained significant at P < 2.61 x 10(-6) after adjusting for all known prostate cancer risk variants in nearby regions. Of the 128 remaining associated genes, 94 have not yet been reported as potential target genes at known loci. We silenced 14 genes and many showed a consistent effect on viability and colony-forming efficiency in three cell lines. Our study provides substantial new information to advance our understanding of prostate cancer genetics and biology. Significance: This study identifies novel prostate cancer genetic loci and possible causal genes, advancing our understanding of the molecular mechanisms that drive prostate cancer.

  • 777. Wulaningsih, W.
    et al.
    Van Hemelrijck, M.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Kanarek, N.
    Nelson, W. G.
    Ix, J. H.
    Platz, E. A.
    Rohrmann, S.
    Association of serum inorganic phosphate with sex steroid hormones and vitamin D in a nationally representative sample of men2014Inngår i: Andrology, ISSN 2047-2919, E-ISSN 2047-2927, Vol. 2, nr 6, s. 967-976Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Defects in bone regulatory pathways have been linked to chronic diseases including cardiovascular disease and cancer. In men, a link between bone metabolism and gonadal hormones has been suggested. However, to date, there is lack of evidence on the association between serum inorganic phosphate (Pi) and sex steroid hormones. The objective of this study was to investigate the association between Pi, sex steroid hormones and a known Pi metabolic regulator, vitamin D, in men in the National Health and Nutrition Examination Survey III (NHANES III). From NHANES III, we selected 1412 men aged 20+ who participated in the morning session of Phase I (1988-1991) with serum measurements of Pi, sex hormones, and vitamin D. Multivariable linear regression was used to calculate crude and geometric mean Pi by total and estimated free testosterone and estradiol, sex hormone-binding globulin, androstanediol glucuronide (AAG), and vitamin D. Similar analyses were performed while stratifying by race/ethnicity and vitamin D levels. We found a lack of statistically significant difference in geometric means of Pi across quintiles of concentrations of sex hormones, indicating a tight regulation of Pi. However, Pi levels were inversely associated with calculated free testosterone in non-Hispanic black men, with geometric mean levels of Pi of 1.16 and 1.02ng/mL for those in the lowest and highest quintiles of free testosterone, respectively (p-trend<0.05). A similar but weaker pattern was seen between total testosterone and Pi. An inverse association was also seen between AAG and Pi in men with vitamin D concentration below the median (<24.2ng/mL). No associations were observed among men with vitamin D levels at or above the median. Our findings suggest a weak link among sex hormones, vitamin D, and Pi in men. The observed effects of race/ethnicity and vitamin D indicate a complex association involving various regulators of Pi homeostasis.

  • 778. Wulaningsih, Wahyu
    et al.
    Michaelsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Garmo, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Hammar, Niklas
    Jungner, Ingmar
    Walldius, Goran
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi.
    Van Hemelrijck, Mieke
    Inorganic phosphate and the risk of cancer in the Swedish AMORIS study2013Inngår i: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 13, s. UNSP 257-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Both dietary and serum levels of inorganic phosphate (Pi) have been linked to development of cancer in experimental studies. This is the first population-based study investigating the relation between serum Pi and risk of cancer in humans. Methods: From the Swedish Apolipoprotein Mortality Risk (AMORIS) study, we selected all participants (>20 years old) with baseline measurements of serum Pi, calcium, alkaline phosphatase, glucose, and creatinine (n = 397,292). Multivariable Cox proportional hazards regression analyses were used to assess serum Pi in relation to overall cancer risk. Similar analyses were performed for specific cancer sites. Results: We found a higher overall cancer risk with increasing Pi levels in men (HR: 1.02 (95% CI: 1.00-1.04) for every SD increase in Pi), and a negative association in women (HR: 0.97 (95% CI: 0.96-0.99) for every SD increase in Pi). Further analyses for specific cancer sites showed a positive link between Pi quartiles and the risk of cancer of the pancreas, lung, thyroid gland and bone in men, and cancer of the oesophagus, lung, and nonmelanoma skin cancer in women. Conversely, the risks for developing breast and endometrial cancer as well as other endocrine cancer in both men and women were lower in those with higher Pi levels. Conclusions: Abnormal Pi levels are related to development of cancer. Furthermore, the inverse association between Pi levels and risk of breast, endometrial and other endocrine cancers may indicate the role of hormonal factors in the relation between Pi metabolism and cancer.

  • 779. Wulaningsih, Wahyu
    et al.
    Michaelsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Garmo, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Hammar, Niklas
    Jungner, Ingmar
    Walldius, Goran
    Lambe, Mats
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Van Hemelrijck, Mieke
    Serum calcium and risk of gastrointestinal cancer in the Swedish AMORIS study2013Inngår i: BMC Public Health, ISSN 1471-2458, E-ISSN 1471-2458, Vol. 13, s. 663-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background:

    Observational studies have indicated that high calcium intake may prevent colorectal cancer, but as for randomized trials the results are inconclusive. Meanwhile, limited data on the link between serum calcium and cancer risk is available. We investigated the relation between serum calcium and risk of different gastrointestinal cancers in a prospective study.

    Methods:

    A cohort based on 492,044 subjects with baseline information on calcium (mmol/L) and albumin (g/L) was selected from the Swedish Apolipoprotein MOrtality RISk (AMORIS) study. Multivariable Cox proportional hazard models were used to analyse associations between standardised levels, quartiles and age/sex-specific categories of serum calcium and risk of oesophageal, stomach, colon, rectal cancer and also colorectal cancer combined, while taking into account serum albumin and other comorbidities.

    Results:

    During 12 years of follow-up, we identified 323 incident oesophageal cancers, 782 stomach cancers, 2519 colon cancers, and 1495 rectal cancers. A positive association was found between albumin-adjusted serum calcium and risk of oesophageal [HR: 4.82 (95% CI: 2.07 - 11.19) for high compared to normal age-specific calcium levels] and colon cancer [e.g. HR: 1.07 (95% CI: 1.00 - 1.14) for every SD increase of calcium] as well as colorectal cancer [e.g. HR: 1.06 (95% CI: 1.02-1.11) for every SD increase of calcium] in women. In men there were similar but weaker non-statistically significant trends.

    Conclusion:

    The positive relation between serum calcium, oesophageal cancer and colorectal cancer calls for further studies including calcium regulators to evaluate whether there is a true link between calcium metabolism and development of gastrointestinal cancer.

  • 780.
    Xia, Wei
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Carlsson, Elin
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Hulsart-Billström, Gry
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Ott, Marjam
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Engqvist, Håkan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Evaluation of CaP spherical particles on rat osteoblasts2012Inngår i: 4th NanoImpactNet Integrating Conference and the 1st QNano Integrating Conference, "From theory to practice - development, training and enabling nanosafety and health research", UCD Dublin, Ireland, 27 February - 2 March, 2012 / [ed] Michael Riediker, 2012, s. 120-120Konferansepaper (Fagfellevurdert)
  • 781.
    Yan, Hongji
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - Ångström, Polymerkemi.
    Casalini, Tommaso
    Hulsart Billström, Gry
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Wang, Shujiang
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - Ångström, Polymerkemi.
    Oommen, Oommen P.
    Salvalaglio, Matteo
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Hilborn, Jöns
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - Ångström, Polymerkemi.
    Varghese, Oommen P.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - Ångström, Polymerkemi.
    Synthetic design of growth factor sequestering extracellular matrix mimetic hydrogel for promoting in vivo bone formation2018Inngår i: Biomaterials, ISSN 0142-9612, E-ISSN 1878-5905, Vol. 161, s. 190-202Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Synthetic scaffolds that possess an intrinsic capability to protect and sequester sensitive growth factors is a primary requisite for developing successful tissue engineering strategies. Growth factors such as recombinant human bone morphogenetic protein-2 (rhBMP-2) is highly susceptible to premature degradation and to provide a meaningful clinical outcome require high doses that can cause serious side effects. We discovered a unique strategy to stabilize and sequester rhBMP-2 by enhancing its molecular interactions with hyaluronic acid (HA), an extracellular matrix (ECM) component. We found that by tuning the initial protonation state of carboxylic acid residues of HA in a covalently crosslinked hydrogel modulate BMP-2 release at physiological pH by minimizing the electrostatic repulsion and maximizing the Van der Waals interactions. At neutral pH, BMP-2 release is primarily governed by Fickian diffusion, whereas at acidic pH both diffusion and electrostatic interactions between HA and BMP-2 become important as confirmed by molecular dynamics simulations. Our results were also validated in an in vivo rat ectopic model with rhBMP-2 loaded hydrogels, which demonstrated superior bone formation with acidic hydrogel as compared to the neutral counterpart. We believe this study provides new insight on growth factor stabilization and highlights the therapeutic potential of engineered matrices for rhBMP-2 delivery and may help to curtail the adverse side effects associated with the high dose of the growth factor.

  • 782. Yang, Fei
    et al.
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Håkansson, Niclas
    Pedersen, Nancy L
    Wirdefeldt, Karin
    Dietary antioxidants and risk of Parkinson's disease in two population-based cohorts.2017Inngår i: Movement Disorders, ISSN 0885-3185, E-ISSN 1531-8257, Vol. 32, nr 11, s. 1631-1636Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: A neuroprotective effect of dietary antioxidants on Parkinson's disease (PD) risk has been suggested, but epidemiological evidence is limited.

    OBJECTIVES: To examine the associations between intake of dietary antioxidant vitamins and total antioxidant capacity and risk of PD.

    METHODS: We prospectively assessed the relationships of dietary antioxidant vitamins C and E, ß-carotene, and total antioxidant capacity with PD risk in two population-based cohorts (38,937 women and 45,837 men).

    RESULTS: During a mean 14.9-year follow-up period, 1,329 PD cases were identified. Dietary intake of ß-carotene was associated with a lower risk of PD (hazard ratio: 0.86; 95% confidence interval: 0.78-0.95; Ptrend  < 0.01 for women and hazard ratio: 0.91; 95% confidence interval: 0.84-0.99; Ptrend  = 0.05 for men). An inverse association between dietary vitamin E and PD risk was found in women (hazard ratio: 0.87; 95% confidence interval: 0.79-0.96; Ptrend  = 0.02). Dietary intake of vitamin C was inversely associated with PD risk in women at borderline significance (hazard ratio: 0.91; 95% confidence interval: 0.83-1.00; Ptrend  = 0.04). There was no association between dietary total antioxidant capacity and PD risk in either women (hazard ratio: 0.93; 95% confidence interval: 0.84-1.02; Ptrend  = 0.35) or men (hazard ratio: 1.00; 95% confidence interval: 0.93-1.07; Ptrend  = 0.97).

    CONCLUSION: Intake of dietary vitamin E and ß-carotene was associated with a lower risk of PD. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

  • 783.
    Yang, Yaohua
    et al.
    Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Wu, Lang
    Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Shu, Xiang
    Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Lu, Yingchang
    Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Shu, Xiao-Ou
    Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Cai, Qiuyin
    Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Beeghly-Fadiel, Alicia
    Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Li, Bingshan
    Vanderbilt Univ, Vanderbilt Genet Inst, Dept Mol Physiol & Biophys, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Ye, Fei
    Vanderbilt Univ, Med Ctr, Dept Biostat, Div Canc Biostat, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Berchuck, Andrew
    Duke Univ, Med Ctr, Dept Obstet & Gynecol, Durham, NC 27710 USA.
    Anton-Culver, Hoda
    Univ Calif Irvine, Genet Epidemiol Res Instl, Dept Epidemiol, Irvine, CA USA.
    Banerjee, Susana
    Royal Marsden Hosp, Gynaecol Unit, London, England.
    Benitez, Javier
    Spanish Natl Canc Res Ctr, CNIO, Human Canc Genet Programme, Madrid, Spain;CIBERER, Biomed Network Rare Dis, Madrid, Spain.
    Bjorge, Line
    Haukeland Hosp, Dept Gynecol & Obstet, Bergen, Norway;Univ Bergen, Dept Clin Sci, Ctr Canc Biomarkers CCBIO, Bergen, Norway.
    Brenton, James D.
    Univ Cambridge, Canc Res UK Cambridge Inst, Cambridge, England.
    Butzow, Ralf
    Univ Helsinki, Helsinki Univ Hosp, Dept Pathol, Helsinki, Finland.
    Campbell, Ian G.
    Peter MacCallum Canc Inst, Melbourne, Vic, Australia;Univ Melbourne, Sir Peter MacCallum Dept Oncol, Melbourne, Vic, Australia.
    Chang-Claude, Jenny
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany;Univ Med Ctr Hamburg Eppendorf, UCCH, Canc Epidemiol Grp, Hamburg, Germany.
    Chen, Kexin
    Tianjin Med Univ Canc Inst & Hosp, Dept Epidemiol, Tianjin, Peoples R China.
    Cook, Linda S.
    Univ New Mexico, Hlth Sci Ctr, Albuquerque, NM 87131 USA;Alberta Hlth Serv, Dept Canc Epidemiol & Prevent Res, Calgary, AB, Canada.
    Cramer, Daniel W.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Brigham & Womens Hosp, Obstetr & Gynecol Epidemiol Ctr, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA USA.
    defazio, Anna
    Univ Sydney, Westmead Inst Med Res, Ctr Canc Res, Sydney, NSW, Australia;Westmead Hosp, Dept Gynaecol Oncol, Sydney, NSW, Australia.
    Dennis, Joe
    Univ Cambridge, Dept Publ Hlth & Primary Care, Ctr Canc Genet Epidemiol, Cambridge, England.
    Doherty, Jennifer A.
    Univ Utah, Dept Populat Hlth Sci, Huntsman Canc Inst, Salt Lake City, UT USA.
    Doerk, Thilo
    Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany.
    Eccles, Diana M.
    Univ Southampton, Fac Med, Canc Sci Acad Unit, Southampton, Hants, England.
    Edwards, Digna Velez
    Vanderbilt Univ, Med Ctr, Dept Obstet & Gynecol, Vanderbilt Genet Inst,Vanderbilt Epidemol Ctr, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Fasching, Peter A.
    Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Hematol & Oncol, Los Angeles, CA 90095 USA;Friedrich Alexander Univ Erlangen Nuremberg, Univ Hosp Erlangen, Comprehens Canc Ctr ER EMN, Dept Gynecol & Obstet, Erlangen, Germany.
    Fortner, Renee T.
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
    Gayther, Simon A.
    Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Ctr Bioinformat & Funct Genom, Los Angeles, CA 90048 USA.
    Giles, Graham G.
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia;Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia;Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic, Australia.
    Glasspool, Rosalind M.
    Beatson West Scotland Canc Ctr, Glasgow, Lanark, Scotland.
    Goode, Ellen L.
    Mayo Clin, Div Epidemiol, Dept Hlth Sci Res, Rochester, MN USA.
    Goodman, Marc T.
    Cedars Sinai Med Ctr, Canc Prevent & Genet Program, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
    Gronwald, Jacek
    Pomeranian Med Univ, Dept Genet & Pathol, Szczecin, Poland.
    Harris, Holly R.
    Fred Hutchinson Canc Res Ctr, Program Epidemiol, Div Publ Hlth Sci, Seattle, WA 98104 USA;Univ Washington, Dept Epidemiol, Seattle, WA USA.
    Heitz, Florian
    Dr Horst Schmidt Kliniken Wiesbaden, Dept Gynecol & Gynecol Oncol, Wiesbaden, Germany;Huyssens Stiftung Knappschaft GmbH, Kliniken Essen Mitte Evang, Dept Gynecol & Gynecol Oncol, Essen, Germany.
    Hildebrandt, Michelle A.
    Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
    Hogdall, Estrid
    Danish Canc Soc Res Ctr, Dept Virus Lifestyle & Genes, Copenhagen, Denmark;Univ Copenhagen, Herlev Hosp, Dept Pathol, Mol Unit, Copenhagen, Denmark.
    Hogdall, Claus K.
    Univ Copenhagen, Rigshosp, Dept Gynecol, Juliane Marie Ctr, Copenhagen, Denmark.
    Huntsman, David G.
    BC Canc Res Ctr, Dept Mol Oncol, Vancouver, BC, Canada;Univ British Columbia, Dept Pathol & Lab Med, Vancouver, BC, Canada;Univ British Columbia, Dept Obstet & Gynaecol, Vancouver, BC, Canada;Vancouver Gen Hosp, OVCARE, Vancouver Coastal Hlth Res Ctr, Vancouver, BC, Canada;Univ British Columbia, Vancouver, BC, Canada.
    Kar, Siddhartha P.
    Univ Cambridge, Dept Publ Hlth & Primary Care, Ctr Canc Genet Epidemiol, Cambridge, England.
    Karlan, Beth Y.
    Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Womens Canc Program, Los Angeles, CA 90048 USA.
    Kelemen, Linda E.
    Med Univ South Carolina, Hollings Canc Ctr, Charleston, SC 29425 USA;Med Univ South Carolina, Dept Publ Hlth Sci, Charleston, SC 29425 USA.
    Kiemeney, Lambertus A.
    Radboud Univ Nijmegen, Med Ctr, Radboud Inst Hlth Sci, Nijmegen, Netherlands.
    Kjaer, Susanne K.
    Danish Canc Soc Res Ctr, Dept Virus Lifestyle & Genes, Copenhagen, Denmark;Univ Copenhagen, Rigshosp, Dept Gynaecol, Copenhagen, Denmark.
    Koushik, Anita
    Univ Montreal, CHUM Res Ctr CRCHUM, Montreal, PQ, Canada;Univ Montreal, Dept Med Social & Prevent, Montreal, PQ, Canada.
    Lambrechts, Diether
    Univ Leuven, VIB Ctr Canc Biol, VIB, Dept Human Genet, Leuven, Belgium;Univ Leuven, Lab Translat Genet, Dept Human Genet, Leuven, Belgium.
    Le, Nhu D.
    BC Canc Agcy, Canc Control Res, Vancouver, BC, Canada.
    Levine, Douglas A.
    Mem Sloan Kettering Canc Ctr, Dept Surg, Gynecol Serv, New York, NY 10021 USA;NYU, Langone Med Ctr, Laura & Isaac Pearlmutter Canc Ctr, Gynecol Oncol, New York, NY USA.
    Massuger, Leon F.
    Radboud Univ Nijmegen, Med Ctr, Radboud Inst Mol Life Sci, Dept Gynaecol, Nijmegen, Netherlands.
    Matsuo, Keitaro
    Aichi Canc Ctr, Res Inst, Div Mol Med, Nagoya, Aichi, Japan;Nagoya Univ, Grad Sch Med, Dept Epidemiol, Nagoya, Aichi, Japan.
    May, Taymaa
    Univ Hlth Network, Princess Margaret Hosp, Div Gynecol Oncol, Toronto, ON, Canada.
    McNeish, Iain A.
    Imperial Coll London, Dept Surg & Canc, London, England;Univ Glasgow, Beatson Inst Canc Res, Wolfson Wohl Canc Res Ctr, Inst Canc Sci, Glasgow, Lanark, Scotland.
    Menon, Usha
    UCL, Inst Clin Trials & Methodol, MRC Clin Trials Unit, London, England.
    Modugno, Francesmary
    Womens Canc Res Ctr, Magee Womens Res Inst, Pittsburgh, PA USA;Hillman Canc Ctr, Pittsburgh, PA USA;Univ Pittsburgh, Sch Med, Dept Obstet Gynecol & Reprod Sci, Div Gynecol Oncol, Pittsburgh, PA USA.
    Monteiro, Alvaro N.
    H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL USA.
    Moorman, Patricia G.
    Duke Univ, Med Ctr, Dept Community & Family Med, Durham, NC 27710 USA.
    Moysich, Kirsten B.
    Roswell Pk Canc Inst, Div Canc Prevent & Control, Buffalo, NY 14263 USA.
    Ness, Roberta B.
    Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, UTHlth, Houston, TX 77030 USA.
    Nevanlinna, Heli
    Univ Helsinki, Helsinki Univ Hosp, Dept Obstet & Gynecol, Helsinki, Finland.
    Olsson, Hakan
    Lund Univ, Clin Sci, Dept Canc Epidemiol, Lund, Sweden.
    Onland-Moret, N. Charlotte
    Univ Utrecht, UMC Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
    Park, Sue K.
    Seoul Natl Univ, Coll Med, Dept Prevent Med, Seoul, South Korea;Seoul Natl Univ, Grad Sch, Dept Biomed Sci, Seoul, South Korea;Seoul Natl Univ, Canc Res Inst, Seoul, South Korea.
    Paul, James
    Beatson West Scotland Canc Ctr, Glasgow, Lanark, Scotland.
    Pearce, Celeste L.
    Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA;Univ Southern Calif, Keck Sch Med, Norris Comprehen Canc Ctr, Dept Prevent Med, Los Angeles, CA 90033 USA.
    Pejovic, Tanja
    Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA;Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
    Phelan, Catherine M.
    H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL USA.
    Pike, Malcolm C.
    Univ Southern Calif, Keck Sch Med, Norris Comprehen Canc Ctr, Dept Prevent Med, Los Angeles, CA 90033 USA;Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
    Ramus, Susan J.
    Univ New South Wales Sydney, Fac Med, Sch Womens & Childrens Hlth, Sydney, NSW, Australia;Garvan Inst Med Res, Kinghorn Canc Ctr, Sydney, NSW, Australia.
    Riboli, Elio
    Imperial Coll London, London, England.
    Rodriguez-Antona, Cristina
    Spanish Natl Canc Res Ctr, CNIO, Human Canc Genet Programme, Madrid, Spain;CIBERER, Biomed Network Rare Dis, Madrid, Spain.
    Romieu, Isabelle
    IARC, WHO, Nutrit & Metab Sect, Lyon, France.
    Sandler, Dale P.
    NIEHS, Epidemiol Branch, NIH, Res Triangle Pk, NC 27709 USA.
    Schildkraut, Joellen M.
    Univ Virginia, Dept Publ Hlth Sci, Charlottesville, VA USA.
    Setiawan, Veronica W.
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
    Shan, Kang
    Hebei Med Univ, Hosp 4, Dept Obstet & Gynaecol, Shijiazhuang, Hebei, Peoples R China.
    Siddiqui, Nadeem
    Glasgow Royal Infirm, Dept Gynaecolo Oncol, Glasgow, Lanark, Scotland.
    Sieh, Weiva
    Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Dept Hlth Sci & Policy, New York, NY 10029 USA.
    Stampfer, Meir J.
    Harvard Med Sch, Boston, MA USA;Brigham & Womens Hosp, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.
    Sutphen, Rebecca
    Univ S Florida, Coll Med, Epidemiol Ctr, Tampa, FL USA.
    Swerdlow, Anthony J.
    Inst Canc Res, Div Genet & Epidemiol, London, England;Inst Canc Res, Div Breast Canc Res, London, England.
    Szafron, Lukasz M.
    Maria Sklodowska Curie Inst, Oncol Ctr, Dept Immunol, Warsaw, Poland.
    Teo, Soo Hwang
    Canc Res Malaysia, Subang Jaya, Selangor, Malaysia;Univ Malaya, Med Ctr, Canc Res Inst, Breast Canc Res Unit, Kuala Lumpur, Malaysia.
    Tworoger, Shelley S.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL USA;Harvard TH Chan Sch Publ Hlth, Res Inst, Boston, MA USA.
    Tyrer, Jonathan P.
    Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Cambridge, England.
    Webb, Penelope M.
    QIMR Berghofer Med Res Inst, Populat Hlth Dept, Brisbane, Qld, Australia.
    Wentzensen, Nicolas
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
    White, Emily
    Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA;Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
    Willett, Walter C.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Harvard Med Sch, Boston, MA USA;Brigham & Womens Hosp, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA;Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Woo, Yin Ling
    Univ Malaya, Med Ctr, Dept Obstet & Gynaecol, Kuala Lumpur, Malaysia.
    Wu, Anna H.
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
    Yan, Li
    Hebei Med Univ, Hosp 4, Dept Mol Biol, Shijiazhuang, Hebei, Peoples R China.
    Yannoukakos, Drakoulis
    NCSR Demokritos, INRASTES, Mol Diagnos Lab, Athens, Greece.
    Chenevix-Trench, Georgia
    QIMR Berghofer Med Res Inst, Dept Genet & Computat Biol, Brisbane, Qld, Australia.
    Sellers, Thomas A.
    H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL USA.
    Pharoah, Paul D. P.
    Univ Cambridge, Dept Publ Hlth & Primary Care, Ctr Canc Genet Epidemiol, Cambridge, England;Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Cambridge, England.
    Zheng, Wei
    Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Long, Jirong
    Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr,Dept Med,Div Epidemiol, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Genetic Data from Nearly 63,000 Women of European Descent Predicts DNA Methylation Biomarkers and Epithelial Ovarian Cancer Risk2019Inngår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 79, nr 3, s. 505-517Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    DNA methylation is instrumental for gene regulation. Global changes in the epigenetic landscape have been recognized as a hallmark of cancer. However, the role of DNA methylation in epithelial ovarian cancer (EOC) remains unclear. In this study, high-density genetic and DNA methylation data in white blood cells from the Framingham Heart Study (N = 1,595) were used to build genetic models to predict DNA methylation levels. These prediction models were then applied to the summary statistics of a genome-wide association study (GWAS) of ovarian cancer including 22,406 EOC cases and 40,941 controls to investigate genetically predicted DNA methylation levels in association with EOC risk. Among 62,938 CpG sites investigated, genetically predicted methylation levels at 89 CpG were significantly associated with EOC risk at a Bonferroni-corrected threshold of P < 7.94 x 10(-7). Of them, 87 were located at GWAS-identified EOC susceptibility regions and two resided in a genomic region not previously reported to be associated with EOC risk. Integrative analyses of genetic, methylation, and gene expression data identified consistent directions of associations across 12 CpG, five genes, and EOC risk, suggesting that methylation at these 12 CpG may influence EOC risk by regulating expression of these five genes, namely MAPT, HOXB3, ABHD8, ARHGAP27, and SKAP1. We identified novel DNA methylation markers associated with EOC risk and propose that methylation at multiple CpG may affect EOC risk via regulation of gene expression. Significance: Identification of novel DNA methylation markers associated with EOC risk suggests that methylation at multiple CpG may affect EOC risk through regulation of gene expression.

  • 784. Zelano, Johan
    et al.
    Berg, Alexander
    Thams, Sebastian
    Hailer, Nils P.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Cullheim, Staffan
    SynCAM1 expression correlates with restoration of central synapses on spinal motoneurons after two different models of peripheral nerve injury2009Inngår i: Journal of Comparative Neurology, ISSN 0021-9967, E-ISSN 1096-9861, Vol. 517, nr 5, s. 670-82Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    SynCAM1 and neuroligins (NLGs) are adhesion molecules that govern synapse formation in vitro. In vivo, the molecules are expressed during synaptogenesis, and altered NLG function is linked to synapse dysfunction in autism. Less is known about SynCAM1 and NLGs in adult synapse remodeling. CNS synapse elimination occurs after peripheral nerve injury, which causes a transient decrease in synapse number on spinal motoneurons. Here we have studied the expression of SynCAM1 and NLGs in relation to changes in synaptic covering on spinal motoneurons. We performed sciatic nerve transection (SNT) or crush (SNC), axotomy models that result in poor or good conditions for axon regeneration, respectively. The two lesions resulted in similar synapse elimination and in poor (SNT) and good (SNC) return of synapses after 70 days. Functional recovery was good after SNC but absent after SNT. SynCAM1 mRNA decreased after 14 days in both models and was restored 70 days after SNC, but not after SNT. NLG2 and -3 mRNAs decreased to a smaller degree after SNC than after SNT. Synaptophysin immunoreactivity correlated with SynCAM1 mRNA 70 days after SNT and NLG2 mRNA 70 days after SNC. Surprisingly, an inverse correlation was seen between NLG3 mRNA and Vglut2, a marker for excitatory synapses, 70 days after SNT. We conclude that 1) SynCAM1 mRNA levels seem to reflect the loss and restoration of synapses on motoneurons, 2) down-regulation of NLGs is not a prerequisite for synapse elimination, and 3) expression of SynCAM1 and NLGs is regulated by different mechanisms during regeneration.

  • 785. Zelano, Johan
    et al.
    Plantman, Stefan
    Hailer, Nils P.
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Cullheim, Staffan
    Altered expression of nectin-like adhesion molecules in the peripheral nerve after sciatic nerve transection2009Inngår i: Neuroscience Letters, ISSN 0304-3940, E-ISSN 1872-7972, Vol. 449, nr 1, s. 28-33Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Following axotomy several processes involving cell-cell interaction occur, such as loss of synapses, axon guidance, and remyelination. Two recently discovered families of cell-cell adhesion molecules, nectins and nectin-like molecules (necls) are involved in such processes in vitro and during development, but their roles in nerve injury have been largely unknown until recently. We have previously shown that axotomized motoneurons increase their expression of nectin-1 and nectin-3 and maintain a high expression of necl-1. We here investigate the expression of potential binding partners for motoneuron nectins and necls in the injured peripheral nerve. In situ hybridization (ISH) revealed a decreased signal for necl-1 mRNA in the injured nerve, whereas no signal for necl-2 was detected before or after injury. The signals for necl-4 and necl-5 mRNA both increased in the injured nerve and necl immunoreactivity displayed a close relation to axon and Schwann cell markers. Finally, signal for mRNA encoding necl-5 increased in axotomized spinal motoneurons. We conclude that peripheral axotomy results in altered expression of several necls in motoneurons and Schwann cells, suggesting involvement of the molecules in regeneration.

  • 786. Zelano, Johan
    et al.
    Wallquist, Wilhelm
    Hailer, Nils P.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Cullheim, Staffan
    Down-regulation of mRNAs for synaptic adhesion molecules neuroligin-2 and -3 and synCAM1 in spinal motoneurons after axotomy2007Inngår i: Journal of Comparative Neurology, ISSN 0021-9967, E-ISSN 1096-9861, Vol. 503, nr 2, s. 308-318Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    After peripheral axotomy, synapses are eliminated from the somata of spinal motoneurons. Recent evidence indicates that synaptic adhesion molecules play a role in maintenance of synaptic contacts, but so far such molecules have not been investigated in the context of synapse elimination after injury. In vitro, the neuroligins (NLGs) and SynCAM1 drive formation of synapses, and RNAi of NLGs results in decreased synaptic input, indicating an important role for these molecules in synaptic biology. To address potential involvement of NLGs and SynCAMs in postinjury synapse elimination, we investigated the mRNA expression of NLG1, -2, and -3; SynCAM1 and -3; and PSD-95 - an intracellular NLG-binding scaffolding protein - in rat spinal motoneurons in control animals and after sciatic nerve transection (SNT). mRNA signals for NLG2, NLG3, SynCAM1, and SynCAM3, but not NLG1, were seen in uninjured motoneurons. Immunoreactivity for SynCAM was seen in close relation to synaptophysin immunoreactivity on the surface of motoneurons and in close relation to neurofilament immunoreactivity in the sciatic nerve. After axotomy, the signals for NLG2, NLG3, and SynCAM1 mRNAs decreased, whereas the signal for NLG1 mRNA remained undetectable and that for SynCAM3 remained at control levels. The signal for PSD-95 mRNA decreased gradually and reached approximately 50% of control values 2 weeks after axotomy. Thus the retrograde response to axotomy of spinal motoneurons involves a rapid down-regulation of NLG2, NLG3, and SynCAM1 mRNAs and a gradual decrease in PSD-95 mRNA. This indicates that down-regulation of synaptic adhesion molecules plays a role in postinjury synapse elimination.

  • 787. Zelano, Johan
    et al.
    Wallquist, Wilhelm
    Hailer, Nils P.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Cullheim, Staffan
    Expression of nectin-1, nectin-3, N-cadherin, and NCAM in spinal motoneurons after sciatic nerve transection2006Inngår i: Experimental Neurology, ISSN 0014-4886, E-ISSN 1090-2430, Vol. 201, nr 2, s. 461-469Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    We here study the expression patterns of the cell adhesion molecules nectin-1, nectin-3, N-cadherin, and neural cell adhesion molecule (NCAM) in motoneurons after sciatic nerve transection (SNT). Nectins are a newly discovered family of adhesion molecules that colocalize with N-cadherin in synapses and are expressed in axons during development. By in situ hybridization (ISH), we found nectin-3, N-cadherin, and NCAM mRNA in uninjured motoneurons. In uninjured animals, nectin-3 mRNA was present in a few vesicular acetylcholine transporter (VAChT)-positive cells of small motoneuron size in lamina IX of the spinal cord. SNT induced a significant increase of nectin-1, nectin-3, and NCAM mRNA, but the signal for N-cadherin mRNA was not affected. After SNT, signal for nectin-3 mRNA appeared over most motoneurons. We next investigated the presence of N-cadherin and nectin protein in synapses on spinal motoneurons by immunohistochemistry. Only N-cadherin immunoreactivity was seen in close relation to synaptophysin staining, while nectin-1 and nectin-3 immunoreactivity did not display such proximity. SNT resulted in decreased immunoreactivity for N-cadherin around the motoneuron soma, while nectin-1 and nectin-3 immunoreactivity remained unchanged. In the peripheral sciatic nerve, nectin-3 immunoreactivity was observed both in controls and following injury and nectin-3 colocalized with both neurofilament and the Schwann cell marker S100. In addition, an increased ISH signal for nectin-3 mRNA could be seen over the proximal stump of the sciatic nerve after SNT. We conclude that motoneuron injury induces complex changes in the spatiotemporal expression pattern of the investigated cell adhesion molecules.

  • 788.
    Zhou, Ang
    et al.
    Univ South Australia, Australian Ctr Precis Hlth, Adelaide, SA, Australia.
    Taylor, Amy E.
    Univ Bristol, MRC Integrat Epidemiol Unit IEU, Bristol, Avon, England;Univ Bristol, UKCTAS, Bristol, Avon, England;Univ Bristol, Sch Expt Psychol, Bristol, Avon, England.
    Karhunen, Ville
    Univ Oulu, Ctr Life Course Hlth Res, Oulu, Finland;Oulu Univ Hosp, Oulu, Finland.
    Zhan, Yiqiang
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Rovio, Suvi P.
    Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland.
    Lahti, Jari
    Helsinki Collegium Adv Studies, Helsinki, Finland;Univ Helsinki, Dept Psychol & Logoped, Fac Med, Helsinki, Finland.
    Sjögren, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Lyall, Donald M.
    Univ Glasgow, Inst Hlth & Wellbeing, Glasgow, Lanark, Scotland.
    Auvinen, Juha
    Univ Oulu, Ctr Life Course Hlth Res, Oulu, Finland;Oulu Univ Hosp, Unit Primary Hlth Care, Oulu, Finland.
    Lehtimaki, Terho
    Univ Tampere, Fac Med & Life Sci, Fimlab Labs, Dept Clin Chem, Tampere, Finland;Univ Tampere, Fac Med & Life Sci, Finnish Cardiovasc Res Ctr Tampere, Tampere, Finland.
    Kahonen, Mika
    Univ Tampere, Dept Clin Physiol, Tampere Univ Hosp, Tampere, Finland;Univ Tampere, Fac Med & Life Sci, Tampere, Finland.
    Hutri-Kahonen, Nina
    Univ Tampere, Fac Med & Life Sci, Tampere, Finland;Univ Tampere, Tampere Univ Hosp, Dept Pediat, Tampere, Finland.
    Perala, Mia Maria
    Natl Inst Hlth & Welf, Dept Publ Hlth Solut, Helsinki, Finland.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mahajan, Anubha
    Wellcome Ctr Human Genet, Nuffield Dept Med, Oxford OX3 7BN, England.
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi.
    Power, Chris
    UCL Great Ormond St Inst Child Hlth, Populat Policy & Practice, London WC1N 1EH, England.
    Eriksson, Johan G.
    Univ Helsinki, Dept Gen Practice & Primary Hlth Care, Helsinki, Finland;Helsinki Univ Hosp, Helsinki, Finland;Folkhalsan Res Ctr, Helsinki, Finland.
    Raitakari, Olli T.
    Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland;Turku Univ Hosp, Dept Clin Physiol & Nucl Med, Turku, Finland.
    Hagg, Sara
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Pedersen, Nancy L.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Veijola, Juha
    Univ Oulu, Dept Psychiat, Res Unit Clin Neurosci, Oulu, Finland;Univ Hosp Oulu, Dept Psychiat, Oulu, Finland.
    Jarvelin, Marjo-Riitta
    Univ Oulu, Ctr Life Course Hlth Res, Oulu, Finland;Oulu Univ Hosp, Unit Primary Hlth Care, Oulu, Finland;Imperial Coll London, Sch Publ Hlth, Dept Epidemiol & Biostat, MRC PHE Ctr Environm & Hlth, London, England;Univ Oulu, Bioctr Oulu, Oulu, Finland.
    Munafo, Marcus R.
    Univ Bristol, MRC Integrat Epidemiol Unit IEU, Bristol, Avon, England;Univ Bristol, UKCTAS, Bristol, Avon, England;Univ Bristol, Sch Expt Psychol, Bristol, Avon, England.
    Ingelsson, Erik
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Stanford Univ, Div Cardiovasc Med, Dept Med, Sch Med, Stanford, CA 94305 USA;Stanford Univ, Stanford Cardiovasc Inst, Stanford, CA 94305 USA.
    Llewellyn, David J.
    Univ Exeter, Med Sch, Exeter, Devon, England.
    Hypponen, Elina
    Univ South Australia, Australian Ctr Precis Hlth, Adelaide, SA, Australia;UCL Great Ormond St Inst Child Hlth, Populat Policy & Practice, London WC1N 1EH, England;South Australian Hlth & Med Res Inst, Adelaide, SA, Australia.
    Habitual coffee consumption and cognitive function: a Mendelian randomization meta-analysis in up to 415,530 participants2018Inngår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, artikkel-id 7526Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Coffee's long-term effect on cognitive function remains unclear with studies suggesting both benefits and adverse effects. We used Mendelian randomization to investigate the causal relationship between habitual coffee consumption and cognitive function in mid-to later life. This included up to 415,530 participants and 300,760 coffee drinkers from 10 meta-analysed European ancestry cohorts. In each cohort, composite cognitive scores that capture global cognition and memory were computed using available tests. A genetic score derived using CYP1A1/2 (rs2472297) and AHR (rs6968865) was chosen as a proxy for habitual coffee consumption. Null associations were observed when examining the associations of the genetic score with global and memory cognition (beta = -0.0007, 95% C.I. -0.009 to 0.008, P = 0.87; beta = -0.001, 95% C.I. -0.005 to 0.002, P = 0.51, respectively), with high consistency between studies (P-heterogeneity > 0.4 for both). Domain specific analyses using available cognitive measures in the UK Biobank also did not support effects by habitual coffee intake for reaction time, pairs matching, reasoning or prospective memory (P >= 0.05 for all). Despite the power to detect very small effects, our meta-analysis provided no evidence for causal long-term effects of habitual coffee consumption on global cognition or memory.

  • 789.
    Zillikens, M. Carola
    et al.
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;NCHA, NCI, NL-2593 Leiden, Netherlands..
    Demissie, Serkalem
    Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA..
    Hsu, Yi-Hsiang
    Inst Aging Res, HebrewSenior Life, Roslindale, MA 02131 USA.;Harvard Med Sch, Boston, MA 02115 USA.;Harvard Sch Publ Hlth, Mol & Integrat Physiol Sci Program, Boston, MA 02115 USA..
    Yerges-Armstrong, Laura M.
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA..
    Chou, Wen-Chi
    Inst Aging Res, HebrewSenior Life, Roslindale, MA 02131 USA.;Harvard Med Sch, Boston, MA 02115 USA.;Broad Inst, Cambridge, MA 02142 USA..
    Stolk, Lisette
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;NCHA, NCI, NL-2593 Leiden, Netherlands..
    Livshits, Gregory
    Tel Aviv Univ, Sackler Fac Med, Dept Anat & Anthropol, IL-6997801 Tel Aviv, Israel.;Kings Coll London, Dept Twin Res & Genet Epidemiol, St Thomas Campus, London WC2R 2LS, England..
    Broer, Linda
    Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Johnson, Toby
    Univ Lausanne, Dept Med Genet, CH-1011 Lausanne, Switzerland.;Swiss Inst Bioinformat, CH-1015 Lausanne, Switzerland.;Univ Inst Social & Prevent Med, Ctr Hosp Univ CHUV, CH-1010 Lausanne, Switzerland..
    Koller, Daniel L.
    Indiana Univ, Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA..
    Kutalik, Zoltyn
    Univ Lausanne, Dept Med Genet, CH-1011 Lausanne, Switzerland.;Swiss Inst Bioinformat, CH-1015 Lausanne, Switzerland.;Univ Inst Social & Prevent Med, Ctr Hosp Univ CHUV, CH-1010 Lausanne, Switzerland..
    Luan, Jian'an
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge Biomed Campus, Cambridge CB2 OQQ, England..
    Malkin, Ida
    Tel Aviv Univ, Sackler Fac Med, Dept Anat & Anthropol, IL-6997801 Tel Aviv, Israel..
    Ried, Janina S.
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany..
    Smith, Albert V.
    Iceland Heart Assoc, IS-201 Kopavogur, Iceland..
    Thorleifsson, Gudmar
    Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.;deCODE Genet, IS-101 Reykjavik, Iceland..
    Vandenput, Liesbeth
    Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Internal Med, SE-40530 Gothenburg, Sweden..
    Zhao, Jing Hua
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge Biomed Campus, Cambridge CB2 OQQ, England..
    Zhang, Weihua
    Imperial Coll, Sch Publ Hlth, Dept Epidemiol & Biostat, London SW7 2AZ, England.;Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England..
    Aghdassi, Ali
    Ernst Moritz Arndt Univ Greifswald, Dept Med A, D-17489 Greifswald, Germany..
    Akesson, Kristina
    Lund Univ, Dept Clin Sci, S-22362 Malmo, Sweden.;Skane Univ Hosp, Dept Orthoped, S-20502 Malmo, Sweden..
    Amin, Najaf
    Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Baier, Leslie J.
    NIH, Phoenix Epidemiol & Clin Res Branch, Natl Inst Diabet & Digest & Kidney Dis, Phoenix, AZ 85014 USA..
    Barroso, Ines
    Wellcome Trust Sanger Inst, Wellcome Trust Genome Campus, Saffron Walden CB10 1SA, Essex, England.;Addenbrookes Hosp, NIHR Cambridge Biomed Res Ctr, Inst Met Sci, Cambridge CB2 OQQ, England.;Univ Cambridge, Addenbrookes Hosp, Inst Met Sci, Metab Res Labs, Cambridge CB2 OQQ, England..
    Bennett, David A.
    Rush Univ, Med Ctr, Rush Alzheimers Dis Ctr, Chicago, IL 60612 USA..
    Bertram, Lars
    Univ Lubeck, Lubeck Interdisciplinary Platform Genome Analyt, Inst Neurogenet & Expt & Integrat Gen, D-23562 Lubeck, Germany.;Imperial Coll London, Fac Med, Sch Publ Hlth, London W6 8RP, England..
    Biffar, Rainer
    Ernst Moritz Arndt Univ Greifswald, Ctr Oral Hlth, Dept Prosthet Dent Gerodontol & Biomat, D-17489 Greifswald, Germany..
    Bochud, Murielle
    Swiss Inst Bioinformat, CH-1015 Lausanne, Switzerland.;Univ Inst Social & Prevent Med, Ctr Hosp Univ CHUV, CH-1010 Lausanne, Switzerland..
    Boehnke, Michael
    Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.;Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA..
    Borecki, Ingrid B.
    Washington Univ, Div Stat Gen, Dept Genet, Sch Med, St Louis, MO 63110 USA.;Washington Univ, Div Biostat, Sch Med, St Louis, MO 63110 USA..
    Buchman, Aron S.
    Rush Univ, Med Ctr, Rush Alzheimers Dis Ctr, Chicago, IL 60612 USA..
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Campbell, Harry
    Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Edinburgh EH8 9AG, Midlothian, Scotland..
    Obanda, Natalia Campos
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands..
    Cauley, Jane A.
    Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15261 USA..
    Cawthon, Peggy M.
    Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA..
    Cederberg, Henna
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Chen, Zhao
    Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Tucson, AZ 85714 USA..
    Cho, Nam H.
    Ajou Univ, Sch Med, Dept Prevent Med, Suwon 16499, South Korea..
    Choi, Hyung Jin
    Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 03080, South Korea.;Chungbuk Natl Univ Hosp, Dept Internal Med, Cheongju, South Korea..
    Claussnitzer, Melina
    Inst Aging Res, HebrewSenior Life, Roslindale, MA 02131 USA.;Harvard Med Sch, Boston, MA 02115 USA.;Broad Inst, Cambridge, MA 02142 USA.;MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.;Tech Univ Munich, Inst Human Genet, MRI, D-81675 Munich, Germany.;Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA..
    Collins, Francis
    Natl Human Genome Res Inst, Med Genom & Metab Genet Branch, Bethesda, MD 20892 USA..
    Cummings, Steven R.
    Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA..
    De Jager, Philip L.
    Harvard Med Sch, Boston, MA 02115 USA.;Brigham & Womens Hosp, Dept Neurol, Program Translat NeuroPsychiatr Genom, Boston, MA 02115 USA.;Broad Inst, Program Med & Populat Genet, Cambridge, MA 02142 USA..
    Demuth, Ilja
    Charite, Res Grp Geriatr, Berlin Aging Study 2, D-13353 Berlin, Germany.;Charite, Inst Med & Human Genet, D-13353 Berlin, Germany..
    Dhonukshe-Rutten, Rosalie A. M.
    Wageningen Univ, Dept Human Nutr, POB 17, NL-6700 AA Wageningen, Netherlands..
    Diatchenko, Luda
    McGill Univ, Alan Edwards Ctr Res Pain, Montreal H3A 0G1, PQ, Canada.;Univ N Carolina, Sch Dent, Reg Ctr Neurosensory Disorders, Chapel Hill, NC 27599 USA..
    Eiriksdottir, Gudny
    Iceland Heart Assoc, IS-201 Kopavogur, Iceland..
    Enneman, Anke W.
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands..
    Erdos, Mike
    Natl Human Genome Res Inst, Med Genom & Metab Genet Branch, Bethesda, MD 20892 USA..
    Eriksson, Johan G.
    Univ Helsinki, Dept Gen Practice & Primary Hlth Care, Helsinki 00014, Finland.;Univ Helsinki, Cent Hosp, Unity Gen Practice, Helsinki 00014, Finland.;Folkhalsan Res Ctr, Helsinki 00250, Finland.;Vasa Cent Hosp, Vaasa 65130, Finland.;Nat Inst Hlth & Welf, Helsinki 00271, Finland..
    Eriksson, Joel
    Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Internal Med, SE-40530 Gothenburg, Sweden..
    Estrada, Karol
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Evans, Daniel S.
    Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA..
    Feitosa, Mary F.
    Washington Univ, Div Stat Gen, Dept Genet, Sch Med, St Louis, MO 63110 USA..
    Fu, Mao
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA..
    Garcia, Melissa
    Natl Inst Aging, Intramural Res Program, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA..
    Gieger, Christian
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, Inst Genet Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany..
    Girke, Thomas
    Univ Calif Riverside, Inst Integrat Genome Biol, Dept Bot & Plant Sci, Riverside, CA 92521 USA.;Univ Calif Riverside, Dept Bot & Plant Sci, Riverside, CA 92521 USA..
    Glazer, Nicole L.
    Boston Univ, Sch Med & Publ Hlth, Dept Med, Boston, MA 02118 USA.;Boston Univ, Sch Med & Publ Hlth, Dept Epidemiol, Boston, MA 02118 USA..
    Grallert, Harald
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany.;Univ Calif Riverside, Dept Bot & Plant Sci, Riverside, CA 92521 USA.;German Ctr Diabet Res DZD, Neuherberg, Germany.;Helmholtz Zentrum Munchen, CCG Type Diabet 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, CCG Nutrigen & Type Diabet 2, D-85764 Neuherberg, Germany..
    Grewal, Jagvir
    Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England.;Imperial Coll London, Natl Heart & Lung Inst, London SW3 6LY, England..
    Han, Bok-Ghee
    Osong Hlth Technol Adm Complex, Ctr Genome Sci, Natl Inst Hlth, Chungcheongbuk Do 28159, South Korea..
    Hanson, Robert L.
    NIH, Phoenix Epidemiol & Clin Res Branch, Natl Inst Diabet & Digest & Kidney Dis, Phoenix, AZ 85014 USA..
    Hayward, Caroline
    Univ Edinburgh, IGMM, MRC Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland..
    Hofman, Albert
    NCHA, NCI, NL-2593 Leiden, Netherlands.;Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Hoffman, Eric P.
    SUNY Binghamton, Dept Pharmaceut Sci, Binghamton, NY 13902 USA..
    Homuth, Georg
    Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Gen, D-17487 Greifswald, Germany..
    Hsueh, Wen-Chi
    NIH, Phoenix Epidemiol & Clin Res Branch, Natl Inst Diabet & Digest & Kidney Dis, Phoenix, AZ 85014 USA..
    Hubal, Monica J.
    George Washington Univ, Dept Exercise & Nutr Sci, Washington, DC 20052 USA.;Childrens Natl Med Ctr, Res Ctr Genet Med, Washington, DC 20052 USA..
    Hubbard, Alan
    Univ Calif Berkeley, Div Biostat, Sch Publ Hlth, Berkeley, CA 94720 USA..
    Huffman, Kim M.
    Duke Univ, Sch Med, Div Rheumatol, Dept Med,Duke Mol Physiol Inst, Durham, NC 27710 USA..
    Husted, Lise B.
    Aarhus Univ Hosp, Endocrinol & Internal Med, DK-8000 Aarhus, Denmark..
    Illig, Thomas
    Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany.;Hannover Med Sch, Dept Human Genet, D-30625 Hannover, Germany.;Hannover Med Sch, Hannover Unified Biobank, D-30625 Hannover, Germany..
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Stanford Univ, Dept Med, Div Cardiovasc Med, Sch Med, Stanford, CA 94305 USA..
    Ittermann, Till
    Ernst Moritz Arndt Univ Greifswald, Inst Community Med, D-17489 Greifswald, Germany..
    Jansson, John-Olov
    Univ Gothenburg, Dept Physiol, Inst Neurosci & Physiol, Sahlgrenska Acad, SE-40530 Gothenburg, Sweden..
    Jordan, Joanne M.
    Univ N Carolina, Thurston Arthrit Res Ctr, Chapel Hill, NC 27517 USA..
    Jula, Antti
    Nat Inst Hlth & Welf, Helsinki 00271, Finland..
    Karlsson, Magnus
    Lund Univ, Dept Clin Sci & Orthopaed, Skane Univ Hosp SUS, S-22362 Malmo, Sweden..
    Khaw, Kay-Tee
    Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge CB1 8RN, England..
    Kilpainen, Tuomas O.
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge Biomed Campus, Cambridge CB2 OQQ, England.;Univ Copenhagen, Novo Nordisk Fdn Ctr Basic Metab Res, Sect Metab Genet, DK-2100 Copenhagen, Denmark.;Icahn Sch Med Mt Sinai, Dept Environm Med & Publ Hlth, New York, NY 10029 USA..
    Klopp, Norman
    Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany.;Hannover Med Sch, Hannover Unified Biobank, D-30625 Hannover, Germany..
    Kloth, Jacqueline S. L.
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands..
    Koistinen, Heikki A.
    Univ Helsinki, Dept Med, Helsinki 00029, Finland.;Helsinki Univ Cent Hosp, Helsinki 00029, Finland.;Univ Helsinki, Abdominal Ctr, Endocrinol, Helsinki 00029, Finland.;Natl Inst Hlth & Welf, Dept Hlth, Helsinki 00271, Finland.;Minerva Fdn, Helsinki 00290, Finland..
    Kraus, William E.
    Duke Univ, Sch Med, Div Cardiol, Dept Med,Duke Mol Physiol Inst, Durham, NC 27710 USA..
    Kritchevsky, Stephen
    Sticht Ctr Aging, Wake Forest Sch Med, Winston Salem, NC 27157 USA..
    Kuulasmaa, Teemu
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Kuusisto, Johanna
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Laakso, Markku
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Lahti, Jari
    Univ Helsinki, Inst Behav Sci, FI-00014 Helsinki, Finland..
    Lang, Thomas
    Univ Calif San Francisco, San Francisco, CA 94143 USA..
    Langdahl, Bente L.
    Aarhus Univ Hosp, Endocrinol & Internal Med, DK-8000 Aarhus, Denmark..
    Launer, Lenore J.
    Natl Inst Aging, Intramural Res Program, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA..
    Lee, Jong-Young
    Osong Hlth Technol Adm Complex, Ctr Genome Sci, Natl Inst Hlth, Chungcheongbuk Do 28159, South Korea..
    Lerch, Markus M.
    Ernst Moritz Arndt Univ Greifswald, Dept Med A, D-17489 Greifswald, Germany..
    Lewis, Joshua R.
    Univ Western Australia, Sch Med & Pharmacol, Perth, WA 6009, Australia.;Univ Sydney, Ctr Kidney Res, Sch Publ Hlth, Sydney, NSW 2006, Australia..
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Uppsala Univ, Dept Med Sci, S-75185 Uppsala, Sweden..
    Lindgren, Cecilia
    Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England..
    Liu, Yongmei
    Wake Forest Sch Med, Dept Epidemiol & Prevent, Winston Salem, NC 27517 USA..
    Liu, Tian
    Max Planck Inst Mol Genet, D-14195 Berlin, Germany.;Max Planck Inst Human Dev, D-14195 Berlin, Germany..
    Liu, Youfang
    Univ N Carolina, Thurston Arthrit Res Ctr, Chapel Hill, NC 27517 USA..
    Ljunggren, Östen
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Endokrinologi och mineralmetabolism.
    Lorentzon, Mattias
    Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Internal Med, SE-40530 Gothenburg, Sweden..
    Luben, Robert N.
    Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge CB1 8RN, England..
    Maixner, William
    Univ N Carolina, Sch Dent, Reg Ctr Neurosensory Disorders, Chapel Hill, NC 27599 USA..
    McGuigan, Fiona E.
    Lund Univ, Dept Clin Sci, S-22362 Malmo, Sweden..
    Medina-Gomez, Carolina
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Meitinger, Thomas
    Tech Univ Munich, Inst Human Genet, MRI, D-81675 Munich, Germany.;Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Human Genet, D-85764 Neuherberg, Germany..
    Melhus, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk farmakogenomik och osteoporos.
    Mellstrom, Dan
    Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Internal Med, SE-40530 Gothenburg, Sweden..
    Melov, Simon
    Buck Inst Res Aging, Novato, CA 94945 USA.;Univ Southern Calif, Leonard Davis Sch Gerontol, Los Angeles, CA 90089 USA..
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mitchell, Braxton D.
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA.;Baltimore Vet Adm Med Ctr, Geriatr Res & Educ Clin Ctr, Baltimore, MD 21201 USA..
    Morris, Andrew P.
    Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England.;Univ Liverpool, Inst Tradit Med, Liverpool L69 3BX, Merseyside, England..
    Mosekilde, Leif
    Aarhus Univ Hosp, Endocrinol & Internal Med, DK-8000 Aarhus, Denmark..
    Newman, Anne
    Univ Pittsburgh, Ctr Aging & Populat Hlth, Pittsburgh, PA 15261 USA..
    Nielson, Carrie M.
    Oregon Hlth & Sci Univ, Portland, OR 97239 USA..
    O'Connell, Jeffrey R.
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA..
    Oostra, Ben A.
    Erasmus MC, Dept Clin Genet, NL-300 CA Rotterdam, Netherlands.;Ctr Med Syst Biol & Netherlands Consortium Hlth A, RC-2300 Leiden, Netherlands..
    Orwoll, Eric S.
    Oregon Hlth & Sci Univ, Portland, OR 97239 USA..
    Palotie, Aarno
    Harvard Med Sch, Boston, MA 02115 USA.;Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland.;Univ Helsinki, Dept Med Genet, FI-00014 Helsinki, Finland.;Univ Cent Hosp, FI-00014 Helsinki, Finland..
    Parker, Stephan
    Univ Michigan, Human Genet & Computat Med & Bioinformat, Ann Arbor, MI 48109 USA..
    Peacock, Munro
    Indiana Univ, Dept Med, Sch Med, Indianapolis, IN 46202 USA..
    Perola, Markus
    Nat Inst Hlth & Welf, Helsinki 00271, Finland.;Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland.;Univ Helsinki, Diabet & Obes Res Program, FI-00014 Helsinki, Finland.;Univ Tartu, Estonian Genome Ctr, Tartu, Estonia..
    Peters, Annette
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany..
    Polasek, Ozren
    Univ Split, Fac Med, Dept Publ Hlth, Split 21000, Croatia..
    Prince, Richard L.
    Univ Western Australia, Sch Med & Pharmacol, Perth, WA 6009, Australia.;Sir Charles Gairdner Hosp, Dept Endocrinol & Diabet, Perth, WA 6009, Australia..
    Raikkonen, Katri
    Univ Helsinki, Inst Behav Sci, FI-00014 Helsinki, Finland..
    Ralston, Stuart H.
    Western Gen Hosp, Mol Med Ctr, MRC Inst Genet & Mol Med, Edinburgh EH4 2XU, Midlothian, Scotland..
    Ripatti, Samuli
    Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland.;Univ Helsinki, Hjelt Inst, Helsinki, Finland.;Wellcome Trust Sanger Inst, Wellcome Trust Genome Campus, Hinxton CB10 1SA, England..
    Robbins, John A.
    Univ Calif Davis, Dept Med, Sacramento, CA 95817 USA..
    Rotter, Jerome I.
    Harbor UCLA Med Ctr, Inst Translat Genom & Populat Sci, Los Angeles Biomed Res Inst, Torrance, CA 90502 USA.;Harbor UCLA Med Ctr, Dept Pediat, Torrance, CA 90502 USA..
    Rudan, Igor
    Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Edinburgh EH8 9AG, Midlothian, Scotland..
    Salomaa, Veikko
    Nat Inst Hlth & Welf, Helsinki 00271, Finland..
    Satterfield, Suzanne
    Univ Tennessee, Dept Prevent Med, Hlth Sci Ctr, Memphis, TN 38163 USA..
    Schadt, Eric E.
    Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, Inst Genom & Multiscale Biol, New York, NY 10029 USA..
    Schipf, Sabine
    Ernst Moritz Arndt Univ Greifswald, Inst Community Med, D-17489 Greifswald, Germany..
    Scott, Laura
    Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.;Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA..
    Sehmi, Joban
    Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England.;Imperial Coll London, Natl Heart & Lung Inst, London SW3 6LY, England..
    Shen, Jian
    Oregon Hlth & Sci Univ, Portland, OR 97239 USA..
    Shin, Chan Soo
    Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 03080, South Korea..
    Sigurdsson, Gunnar
    Natl Univ Hosp Iceland, Landspitali, Dept Endocrinol & Metab, IS-101 Reykjavik, Iceland..
    Smith, Shad
    Duke Univ, Med Ctr, Ctr Translat Pain Med, Dept Anesthesiol, Durham, NC 27110 USA..
    Soranzo, Nicole
    Wellcome Trust Sanger Inst, Wellcome Trust Genome Campus, Hinxton CB10 1SA, England..
    Stancakova, Alena
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Steinhagen-Thiessen, Elisabeth
    Charite, Res Grp Geriatr, Berlin Aging Study 2, D-13353 Berlin, Germany..
    Streeten, Elizabeth A.
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA.;Vet Adm Med Ctr, GRECC, Baltimore, MD 21201 USA..
    Styrkarsdottir, Unnur
    Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.;deCODE Genet, IS-101 Reykjavik, Iceland..
    Swart, Karin M. A.
    Vrije Univ Amsterdam Med Ctr, Dept Epidemiol & Biostat, BT-1081 Amsterdam, Netherlands.;Vrije Univ Amsterdam Med Ctr, EMGO Inst, BT-1081 Amsterdam, Netherlands..
    Tan, Sian-Tsung
    Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England.;Imperial Coll London, Natl Heart & Lung Inst, London SW3 6LY, England..
    Tarnopolsky, Mark A.
    McMaster Univ, Med Ctr, Dept Med, Hamilton, ON L8N 3Z5, Canada..
    Thompson, Patricia
    Stony Brook Sch Med, Dept Pathol, Stony Brook, NY 11794 USA..
    Thomson, Cynthia A.
    Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Tucson, AZ 85714 USA..
    Thorsteinsdottir, Unnur
    Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.;deCODE Genet, IS-101 Reykjavik, Iceland..
    Tikkanen, Emmi
    Nat Inst Hlth & Welf, Helsinki 00271, Finland.;Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland.;Western Gen Hosp, Mol Med Ctr, MRC Inst Genet & Mol Med, Edinburgh EH4 2XU, Midlothian, Scotland..
    Tranah, Gregory J.
    Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA..
    Tuomilehto, Jaakko
    Vasa Cent Hosp, Vaasa 65130, Finland.;Danube Univ Krems, Dept Neurosci & Prevent Med, A-3500 Krems, Austria.;King Abdulaziz Univ, Diabet Res Grp, Jeddah 12589, Saudi Arabia.;Dasman Diabet Inst, Dasman 15462, Kuwait..
    van Schoor, Natasja M.
    Vrije Univ Amsterdam Med Ctr, Dept Epidemiol & Biostat, BT-1081 Amsterdam, Netherlands.;Vrije Univ Amsterdam Med Ctr, EMGO Inst, BT-1081 Amsterdam, Netherlands..
    Verma, Arjun
    Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England..
    Vollenweider, Peter
    CHU Vaudois, Dept Med & Internal Med, CH-1011 Lausanne, Switzerland..
    Voelzke, Henry
    Ernst Moritz Arndt Univ Greifswald, Inst Community Med, D-17489 Greifswald, Germany..
    Wactawski-Wende, Jean
    SUNY Buffalo, Univ Buffalo, Dept Epidemiol & Environm Hlth, Buffalo, NY 14214 USA..
    Walker, Mark
    Newcastle Univ, Inst Cellular Med, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England..
    Weedon, Michael N.
    Univ Exeter, Med Sch, Genet Complex Traits, Exeter EX1 2LU, Devon, England..
    Welch, Ryan
    Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.;Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA..
    Wichman, H. -Erich
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Ludwig Maximilians Univ Munchen, Inst Med Informat Biometry & Epidemiol, Chair Epidemiol, D-81377 Munich, Germany.;Tech Univ, Inst Med Stat & Epidemiol, D-81675 Munich, Germany..
    Widen, Elisabeth
    Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland..
    Williams, Frances M. K.
    Kings Coll London, Dept Twin Res & Genet Epidemiol, St Thomas Campus, London WC2R 2LS, England..
    Wilson, James F.
    Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Edinburgh EH8 9AG, Midlothian, Scotland.;Univ Edinburgh, IGMM, MRC Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland..
    Wright, Nicole C.
    Univ Alabama Birmingham, Dept Epidemiol, Birmingham, AL 35294 USA..
    Xie, Weijia
    Univ Exeter, Med Sch, Genet Complex Traits, Exeter EX1 2LU, Devon, England..
    Yu, Lei
    Rush Univ, Med Ctr, Rush Alzheimers Dis Ctr, Chicago, IL 60612 USA..
    Zhou, Yanhua
    Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA..
    Chambers, John C.
    Imperial Coll, Sch Publ Hlth, Dept Epidemiol & Biostat, London SW7 2AZ, England.;Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England.;Royal Brompton & Harefield NHS Fdn Trust, NIHR Cardiovasc Biomed Res Unit, London SW3 6NP, England.;Imperial Coll, London SW3 6NP, England.;Imperial Coll Healthcare NHS Trust, London W2 1NY, England..
    Doring, Angela
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 1, D-85764 Neuherberg, Germany..
    van Duijn, Cornelia M.
    Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands.;Ctr Med Syst Biol & Netherlands Consortium Hlth A, RC-2300 Leiden, Netherlands..
    Econs, Michael J.
    Indiana Univ Sch Med, Dept Med, Indianapolis, IN 46202 USA.;Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA..
    Gudnason, Vilmundur
    Iceland Heart Assoc, IS-201 Kopavogur, Iceland..
    Kooner, Jaspal S.
    Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England.;Imperial Coll London, Natl Heart & Lung Inst, London SW3 6LY, England.;Imperial Coll Healthcare NHS Trust, London W2 1NY, England..
    Psaty, Bruce M.
    Univ Washington, Cardiovasc Hlth Res Unit, Dept Med, Seattle, WA 98101 USA.;Univ Washington, Cardiovasc Hlth Res Unit, Dept Epidemiol, Seattle, WA 98101 USA.;Univ Washington, Cardiovasc Hlth Res Unit, Dept Med Hlth Serv, Seattle, WA 98101 USA.;Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA 98101 USA..
    Spector, Timothy D.
    Kings Coll London, Dept Twin Res & Genet Epidemiol, St Thomas Campus, London WC2R 2LS, England..
    Stefansson, Kari
    Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.;deCODE Genet, IS-101 Reykjavik, Iceland..
    Rivadeneira, Fernando
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;NCHA, NCI, NL-2593 Leiden, Netherlands.;Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Uitterlinden, Andre G.
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;NCHA, NCI, NL-2593 Leiden, Netherlands.;Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Wareham, Nicholas J.
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge Biomed Campus, Cambridge CB2 OQQ, England..
    Ossowski, Vicky
    NIH, Phoenix Epidemiol & Clin Res Branch, Natl Inst Diabet & Digest & Kidney Dis, Phoenix, AZ 85014 USA..
    Waterworth, Dawn
    GlaxoSmithKline, Med Genet, Philadelphia, PA 19112 USA..
    Loos, Ruth J. F.
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge Biomed Campus, Cambridge CB2 OQQ, England.;Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA.;Icahn Sch Med Mt Sinai, Inst Child Hlth & Dev, New York, NY 10029 USA.;Icahn Sch Med Mt Sinai, Genet Obes & Related Traits Program, New York, NY 10029 USA.;Icahn Sch Med Mt Sinai, Dept Prevent Med, New York, NY 10029 USA..
    Karasik, David
    Inst Aging Res, HebrewSenior Life, Roslindale, MA 02131 USA.;Harvard Med Sch, Boston, MA 02115 USA.;Bar Ilan Univ, Fac Med Galilee, IL-1311502 Safed, Israel..
    Harris, Tamara B.
    Natl Inst Aging, Intramural Res Program, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA..
    Ohlsson, Claes
    Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Internal Med, SE-40530 Gothenburg, Sweden..
    Kiel, Douglas P.
    Inst Aging Res, HebrewSenior Life, Roslindale, MA 02131 USA.;Harvard Med Sch, Boston, MA 02115 USA.;Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA..
    Large meta-analysis of genome-wide association studies identifies five loci for lean body mass2017Inngår i: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 8, artikkel-id 80Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Lean body mass, consisting mostly of skeletal muscle, is important for healthy aging. We performed a genome-wide association study for whole body (20 cohorts of European ancestry with n = 38,292) and appendicular (arms and legs) lean body mass (n = 28,330) measured using dual energy X-ray absorptiometry or bioelectrical impedance analysis, adjusted for sex, age, height, and fat mass. Twenty-one single-nucleotide polymorphisms were significantly associated with lean body mass either genome wide (p < 5 x 10(-8)) or suggestively genome wide (p < 2.3 x 10(-6)). Replication in 63,475 (47,227 of European ancestry) individuals from 33 cohorts for whole body lean body mass and in 45,090 (42,360 of European ancestry) subjects from 25 cohorts for appendicular lean body mass was successful for five single-nucleotide polymorphisms in/ near HSD17B11, VCAN, ADAMTSL3, IRS1, and FTO for total lean body mass and for three single-nucleotide polymorphisms in/ near VCAN, ADAMTSL3, and IRS1 for appendicular lean body mass. Our findings provide new insight into the genetics of lean body mass.

  • 790. Zillikens, M Carola
    et al.
    Demissie, Serkalem
    Hsu, Yi-Hsiang
    Yerges-Armstrong, Laura M
    Chou, Wen-Chi
    Stolk, Lisette
    Livshits, Gregory
    Broer, Linda
    Johnson, Toby
    Koller, Daniel L
    Kutalik, Zoltán
    Luan, Jian'an
    Malkin, Ida
    Ried, Janina S
    Smith, Albert V
    Thorleifsson, Gudmar
    Vandenput, Liesbeth
    Hua Zhao, Jing
    Zhang, Weihua
    Aghdassi, Ali
    Åkesson, Kristina
    Amin, Najaf
    Baier, Leslie J
    Barroso, Inês
    Bennett, David A
    Bertram, Lars
    Biffar, Rainer
    Bochud, Murielle
    Boehnke, Michael
    Borecki, Ingrid B
    Buchman, Aron S
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Campbell, Harry
    Campos Obanda, Natalia
    Cauley, Jane A
    Cawthon, Peggy M
    Cederberg, Henna
    Chen, Zhao
    Cho, Nam H
    Jin Choi, Hyung
    Claussnitzer, Melina
    Collins, Francis
    Cummings, Steven R
    De Jager, Philip L
    Demuth, Ilja
    Dhonukshe-Rutten, Rosalie A M
    Diatchenko, Luda
    Eiriksdottir, Gudny
    Enneman, Anke W
    Erdos, Mike
    Eriksson, Johan G
    Eriksson, Joel
    Estrada, Karol
    Evans, Daniel S
    Feitosa, Mary F
    Fu, Mao
    Garcia, Melissa
    Gieger, Christian
    Girke, Thomas
    Glazer, Nicole L
    Grallert, Harald
    Grewal, Jagvir
    Han, Bok-Ghee
    Hanson, Robert L
    Hayward, Caroline
    Hofman, Albert
    Hoffman, Eric P
    Homuth, Georg
    Hsueh, Wen-Chi
    Hubal, Monica J
    Hubbard, Alan
    Huffman, Kim M
    Husted, Lise B
    Illig, Thomas
    Ingelsson, Erik
    Ittermann, Till
    Jansson, John-Olov
    Jordan, Joanne M
    Jula, Antti
    Karlsson, Magnus
    Khaw, Kay-Tee
    Kilpeläinen, Tuomas O
    Klopp, Norman
    Kloth, Jacqueline S L
    Koistinen, Heikki A
    Kraus, William E
    Kritchevsky, Stephen
    Kuulasmaa, Teemu
    Kuusisto, Johanna
    Laakso, Markku
    Lahti, Jari
    Lang, Thomas
    Langdahl, Bente L
    Launer, Lenore J
    Lee, Jong-Young
    Lerch, Markus M
    Lewis, Joshua R
    Lind, Lars
    Lindgren, Cecilia
    Liu, Yongmei
    Liu, Tian
    Liu, Youfang
    Ljunggren, Östen
    Lorentzon, Mattias
    Luben, Robert N
    Maixner, William
    McGuigan, Fiona E
    Medina-Gomez, Carolina
    Meitinger, Thomas
    Melhus, Håkan
    Mellström, Dan
    Melov, Simon
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mitchell, Braxton D
    Morris, Andrew P
    Mosekilde, Leif
    Newman, Anne
    Nielson, Carrie M
    O'Connell, Jeffrey R
    Oostra, Ben A
    Orwoll, Eric S
    Palotie, Aarno
    Parker, Stephen C J
    Peacock, Munro
    Perola, Markus
    Peters, Annette
    Polasek, Ozren
    Prince, Richard L
    Räikkönen, Katri
    Ralston, Stuart H
    Ripatti, Samuli
    Robbins, John A
    Rotter, Jerome I
    Rudan, Igor
    Salomaa, Veikko
    Satterfield, Suzanne
    Schadt, Eric E
    Schipf, Sabine
    Scott, Laura
    Sehmi, Joban
    Shen, Jian
    Soo Shin, Chan
    Sigurdsson, Gunnar
    Smith, Shad
    Soranzo, Nicole
    Stančáková, Alena
    Steinhagen-Thiessen, Elisabeth
    Streeten, Elizabeth A
    Styrkarsdottir, Unnur
    Swart, Karin M A
    Tan, Sian-Tsung
    Tarnopolsky, Mark A
    Thompson, Patricia
    Thomson, Cynthia A
    Thorsteinsdottir, Unnur
    Tikkanen, Emmi
    Tranah, Gregory J
    Tuomilehto, Jaakko
    van Schoor, Natasja M
    Verma, Arjun
    Vollenweider, Peter
    Völzke, Henry
    Wactawski-Wende, Jean
    Walker, Mark
    Weedon, Michael N
    Welch, Ryan
    Wichmann, H-Erich
    Widen, Elisabeth
    Williams, Frances M K
    Wilson, James F
    Wright, Nicole C
    Xie, Weijia
    Yu, Lei
    Zhou, Yanhua
    Chambers, John C
    Döring, Angela
    van Duijn, Cornelia M
    Econs, Michael J
    Gudnason, Vilmundur
    Kooner, Jaspal S
    Psaty, Bruce M
    Spector, Timothy D
    Stefansson, Kari
    Rivadeneira, Fernando
    Uitterlinden, André G
    Wareham, Nicholas J
    Ossowski, Vicky
    Waterworth, Dawn
    Loos, Ruth J F
    Karasik, David
    Harris, Tamara B
    Ohlsson, Claes
    Kiel, Douglas P
    Erratum: Large meta-analysis of genome-wide association studies identifies five loci for lean body mass.2017Inngår i: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 8, nr 1, artikkel-id 1414Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    A correction to this article has been published and is linked from the publisher´s HTML version of the article.

  • 791.
    Åberg, Jonas
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Pankotai, Eszter
    Weszl, Miklós
    Forster-Horváth, Casba
    Hulsart Billström, Gry
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Lacza, Zombor
    Engqvist, Håkan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    In vivo evaluation of an injectable premixed radiopaque calcium phosphate cement2011Inngår i: EFORT, 2011Konferansepaper (Fagfellevurdert)
  • 792.
    Åberg, Jonas
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Persson, Cecilia
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Hulsart Billström, Gry
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Brisby, Helena
    Thomsen, Peter
    Engqvist, Håkan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Evaluation of a radio-opaque premixed calcium phosphate cement2010Inngår i: Scandinavian Society or Biomaterials Annual Meeting, 2010Konferansepaper (Fagfellevurdert)
  • 793.
    Åberg, Jonas
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Persson, Cecilia
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Hulsart, Gry
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Thomsen, Peter
    Avdelningen för Biomaterial, Göteborgs Universitet.
    Brisby, Helena
    Avdelningen för Ortopedi, Göteborgs Universitet.
    Engqvist, Håkan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Setting time and initial compressive strength of a radiopaque premixed calcium phosphate cement2010Inngår i: GRIBOI, Turin, 2010, 2010Konferansepaper (Fagfellevurdert)
  • 794. Ödquist, Magnus
    et al.
    Hallberg, Kristofer
    Rahme, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Salomonsson, Björn
    Rosso, Aldana
    Lower age increases the risk of revision for stemmed and resurfacing shoulder hemi arthroplasty.2017Inngår i: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, s. 1-7Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and purpose - The number of patients where shoulder hemiarthroplasty (SHA) is an option is still substantial. Descriptive analyses performed by the Swedish Shoulder Arthroplasty Registry (SSAR) showed that while patients receiving SHA designs, i.e. resurfacing hemi (RH) and stemmed hemi (SH), reported similar shoulder functionality and quality of life, the revision rate for RH (12%) was larger than for SH (6.7%); this difference was studied. Patients and methods - All primary SHA (n = 1,140) for OA reported to SSAR between 1999 and 2009 were analyzed regarding risk factors for revision and PROM outcome, 950 shoulders with primary OA (POA), and 190 secondary OA (SOA). Mean age was 67.4 years (SD 10.8). PROM including WOOS and EQ-5D were collected at 5 years, until December 31, 2014. Results - 76/950 prostheses because of POA and 16/190 prosthesis because of SOA were revised. Age at primary surgery was the main factor that influenced the risk of revision, lower age increased the risk of revision, and was also the explanation for the difference between SH and RH. We also found that SH and RH had similar outcomes measured by PROM, but the POA group had higher scores than the SOA group with a clinically relevant difference of 10% in WOOS. Interpretation - The risk of revision for SH and RH is similar when adjusted for age and does not depend on primary diagnosis or sex. A lower age increases the risk of revision. Patients suffering from POA experience better shoulder functionality than SOA patients irrespective of implant type.

  • 795.
    Öhman, Caroline
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Hulsart-Billström, Gry
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Particelli, Francesca
    Laboratorio di Tecnologia Medica, Istituto Ortopedico Rizzoli, Italy.
    Baruffaldi, Fabio
    Laboratorio di Tecnologia Medica, Istituto Ortopedico Rizzoli, Italy.
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Engqvist, Håkan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Premixed calcium phosphate cement as a carrier of bone morphogenetic protein2013Konferansepaper (Fagfellevurdert)
  • 796.
    Öhman, Caroline
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Nouhi, Shirin
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Hulsart-Billström, Gry
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Engqvist, Håkan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Tillämpad materialvetenskap.
    Larsson, Sune
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Facilitating separation of bone from bonelike materials in micro-computed tomography images2014Konferansepaper (Fagfellevurdert)
  • 797.
    Östman, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Influence of Oxidative Stress on Muscle and Bone2009Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Reactive oxygen species (ROS) induce oxidative stress and although are primarily recognized for playing a deleterious biological role, they can be beneficial to cell systems. ROS are extremely short-lived and normally tightly regulated by antioxidant defence systems. Cells react to oxidative stress in different ways, which primarily depends on cell type, stress severity, or both. There is a general limitation in extrapolating to humans conclusions drawn from in vitro and animal studies because of important species-specific differences. Therefore, the general aim of this thesis was to study the influence of oxidative stress on human muscle and bone in vivo.

    In paper I we presented a one-step HPLC method optimized for the simultaneous determination of purine degradation products in small microdialysis samples. The clinical utility of the method was successfully tested in a patient with traumatic brain injury. In paper II we evaluated microdialysis as an in vivo method to characterize the relative kinetics of ROS-related metabolites in human skeletal muscle exposed to ischaemia-reperfusion. Results indicated that microdialysis was feasible and safe to use in monitoring metabolic events during tourniquet-assisted surgery. In paper III we investigated the association between an oxidative stress marker (urinary 8-iso-PGF) and bone mineral density (BMD) and whether α-tocopherol modified the association. The main finding was the negative association between 8-iso-PGF and BMD and that the association was further dependent on serum α-tocopherol level. In paper IV we performed a randomized controlled trial to evaluate the influence of Q10 supplementation on exercise performance and metabolites of muscular damage. We did not observe any effects on exercise capacity after 8 weeks of Q10 administration. Nor did we find a significant effect on serum markers related to oxidative stress.

    In conclusion we have studied the influence of oxidative stress on muscle and bone in vivo in humans. The oxidative stress was triggered by four different causes (trauma, ischemia-reperfusion, ageing, and exercise exhaustion).

    Delarbeid
    1. Hypoxanthine, uric acid and allantoin as indicators of in vivo free radical reactions. Description of a HPLC method and human brain microdialysis data.
    Åpne denne publikasjonen i ny fane eller vindu >>Hypoxanthine, uric acid and allantoin as indicators of in vivo free radical reactions. Description of a HPLC method and human brain microdialysis data.
    Vise andre…
    2000 (engelsk)Inngår i: Acta Neurochir (Wien), Vol. 142Artikkel i tidsskrift (Fagfellevurdert) Published
    Identifikatorer
    urn:nbn:se:uu:diva-56099 (URN)
    Tilgjengelig fra: 2008-10-17 Laget: 2008-10-17 Sist oppdatert: 2011-01-14
    2. Tourniquet-induced ischemia and reperfusion in human skeletal muscle
    Åpne denne publikasjonen i ny fane eller vindu >>Tourniquet-induced ischemia and reperfusion in human skeletal muscle
    2004 (engelsk)Inngår i: Clinical Orthopaedics and Related Research, ISSN 0009-921X, E-ISSN 1528-1132, Vol. 418, s. 260-265Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Microdialysis conceivably enables longitudinal and simultaneous investigation of several metabolites by repeated measurements in skeletal muscle. We used and evaluated microdialysis as an in vivo method to characterize the time-course and relative kinetics of pyruvate, glucose, lactate, glycerol, hypoxanthine, uric acid, and urea, in skeletal muscles, exposed to ischemia and reperfusion, in eight patients having arthroscopic-assisted anterior cruciate ligament reconstruction. A dialysis probe was implanted before surgery in the rectus femoris muscle. Dialysate samples were collected at 10-minute intervals at a flow rate of 1 microL/minute until 2 hours after tourniquet deflation. Ninety minutes of ischemia resulted in accumulation of lactate (234% +/- 38%), hypoxanthine (582% +/- 166%), and glycerol (146% +/- 46%), consumption of glucose (54% +/- 9%) and pyruvate (16% +/- 44%), and a slight decrease of urea (78% +/- 11%) compared with baseline (100%). Uric acid was unchanged (95% +/- 12%). Within 90 minutes after tourniquet deflation the concentrations were virtually normalized for all measured metabolites, suggesting that the duration of ischemia was well tolerated by the patients. The results indicate that the use of microdialysis for monitoring energy metabolic events during orthopaedic surgery that requires ischemia and reperfusion is feasible and safe.

    HSV kategori
    Identifikatorer
    urn:nbn:se:uu:diva-82225 (URN)15043128 (PubMedID)
    Tilgjengelig fra: 2006-09-22 Laget: 2006-09-22 Sist oppdatert: 2017-12-14bibliografisk kontrollert
    3. Oxidative stress and bone mineral density in elderly men: antioxidant activity of alpha-tocopherol
    Åpne denne publikasjonen i ny fane eller vindu >>Oxidative stress and bone mineral density in elderly men: antioxidant activity of alpha-tocopherol
    Vise andre…
    2009 (engelsk)Inngår i: Free Radical Biology & Medicine, ISSN 0891-5849, E-ISSN 1873-4596, Vol. 47, nr 5, s. 668-673Artikkel i tidsskrift, Letter (Fagfellevurdert) Published
    Abstract [en]

    Oxidative stress has recently been identified as a pivotal pathogenetic factor of bone loss in mice, but its importance in humans is not clear. We aimed to investigate the association between urinary 8-iso-PGF(2 alpha) levels, a major F(2)-isoprostane and a reliable in vivo biomarker of oxidative stress, and bone mineral density (BMD), and to study whether vitamin E in the form of serum alpha-tocopherol, a scavenger of peroxyl radicals, modifies the association. In 405 men, urinary 8-iso-PGF(2 alpha) and serum alpha-tocopherol were measured at age 77 years and BMD at age 82 years. One SD increase in 8-iso-PGF(2 alpha) corresponded to an approximately 2-4% decrease in average adjusted BMD values of total body, lumbar spine, and proximal femur (all P<0.001). Serum alpha-tocopherol levels seemed to modify the association between urinary 8-iso-PGF(2 alpha) and BMD. Men with alpha-tocopherol levels below the median combined with high oxidative stress, i.e., 8-iso-PGF(2 alpha) above the median, had 7% (95% CI 3-11%) lower BMD at the lumbar spine and 5% (95% CI 2-9%) lower BMD at the proximal femur. In elderly men high oxidative stress is associated with reduced BMD, which is more pronounced in individuals with low serum levels of the antioxidant vitamin E.

    Emneord
    BMD, Bone, Isoprostanes, Prostaglandins, Osteoporosis, Vitamin E, α-Tocopherol
    HSV kategori
    Forskningsprogram
    Ortopedi
    Identifikatorer
    urn:nbn:se:uu:diva-109406 (URN)10.1016/j.freeradbiomed.2009.05.031 (DOI)000268995900024 ()19500667 (PubMedID)
    Tilgjengelig fra: 2009-10-15 Laget: 2009-10-15 Sist oppdatert: 2017-12-12bibliografisk kontrollert
    4. Coenzyme Q10 supplementation and exercise-induced oxidative stress in humans
    Åpne denne publikasjonen i ny fane eller vindu >>Coenzyme Q10 supplementation and exercise-induced oxidative stress in humans
    2012 (engelsk)Inngår i: Nutrition (Burbank, Los Angeles County, Calif.), ISSN 0899-9007, E-ISSN 1873-1244, Vol. 28, nr 4, s. 403-417Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Objective: The theoretically beneficial effects of coenzyme Q10 (Q10) on exercise-related oxidative stress and physical capacity have not been confirmed to our knowledge by interventional supplementation studies. Our aim was to investigate further whether Q10 supplementation at a dose recommended by manufacturers influences these factors. Methods: Using a randomized, double-blind, controlled design, we investigated the effect on physical capacity of 8 wk of treatment with a daily dose of 90 mg of Q10 (n = 12) compared with placebo (n = 11) in moderately trained healthy men 19 to 44 y old. Two days of individualized performance tests to physical exhaustion were performed before and after the intervention. Primary outcomes were maximal oxygen uptake, workload, and heart rate at the lactate threshold. Secondary outcomes were creatine kinase, hypoxanthine, and uric acid. Results: No significant differences between the groups were discerned after the intervention for maximal oxygen uptake (-0.11 L/min, 95% confidence interval 0.31 to 0.08, P = 0.44), workload at lactate threshold (6.3 W, 13.4 to 25.9, P = 0.36), or heart rate at lactate threshold (2.0 beats/min, -4.9 to 8.9, P = 0.41). No differences between the groups were detected for hypoxanthine or uric acid (serum markers of oxidative stress) or creatine kinase (a marker of skeletal muscle damage). Conclusion: Although in theory Q10 could be beneficial for exercise capacity and in decreasing oxidative stress, the present study could not demonstrate that such effects exist after supplementation with a recommended dose. 

    HSV kategori
    Forskningsprogram
    Ortopedi
    Identifikatorer
    urn:nbn:se:uu:diva-110356 (URN)10.1016/j.nut.2011.07.010 (DOI)000302395800011 ()
    Tilgjengelig fra: 2009-11-12 Laget: 2009-11-12 Sist oppdatert: 2018-08-24
  • 798.
    Östman, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniskt forskningscentrum (UCR).
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniskt forskningscentrum (UCR).
    Helmersson, Johanna
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Oxidativ stress och inflammation.
    Basu, Samar
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Oxidativ stress och inflammation.
    Gedeborg, Rolf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Anestesiologi och intensivvård. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniskt forskningscentrum (UCR).
    Melhus, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniskt forskningscentrum (UCR).
    Oxidative stress and bone mineral density in elderly men: antioxidant activity of alpha-tocopherol2009Inngår i: Free Radical Biology & Medicine, ISSN 0891-5849, E-ISSN 1873-4596, Vol. 47, nr 5, s. 668-673Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Oxidative stress has recently been identified as a pivotal pathogenetic factor of bone loss in mice, but its importance in humans is not clear. We aimed to investigate the association between urinary 8-iso-PGF(2 alpha) levels, a major F(2)-isoprostane and a reliable in vivo biomarker of oxidative stress, and bone mineral density (BMD), and to study whether vitamin E in the form of serum alpha-tocopherol, a scavenger of peroxyl radicals, modifies the association. In 405 men, urinary 8-iso-PGF(2 alpha) and serum alpha-tocopherol were measured at age 77 years and BMD at age 82 years. One SD increase in 8-iso-PGF(2 alpha) corresponded to an approximately 2-4% decrease in average adjusted BMD values of total body, lumbar spine, and proximal femur (all P<0.001). Serum alpha-tocopherol levels seemed to modify the association between urinary 8-iso-PGF(2 alpha) and BMD. Men with alpha-tocopherol levels below the median combined with high oxidative stress, i.e., 8-iso-PGF(2 alpha) above the median, had 7% (95% CI 3-11%) lower BMD at the lumbar spine and 5% (95% CI 2-9%) lower BMD at the proximal femur. In elderly men high oxidative stress is associated with reduced BMD, which is more pronounced in individuals with low serum levels of the antioxidant vitamin E.

  • 799.
    Östman, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Rahme, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Hillered, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
    Tourniquet-induced ischemia and reperfusion in human skeletal muscle2004Inngår i: Clinical Orthopaedics and Related Research, ISSN 0009-921X, E-ISSN 1528-1132, Vol. 418, s. 260-265Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Microdialysis conceivably enables longitudinal and simultaneous investigation of several metabolites by repeated measurements in skeletal muscle. We used and evaluated microdialysis as an in vivo method to characterize the time-course and relative kinetics of pyruvate, glucose, lactate, glycerol, hypoxanthine, uric acid, and urea, in skeletal muscles, exposed to ischemia and reperfusion, in eight patients having arthroscopic-assisted anterior cruciate ligament reconstruction. A dialysis probe was implanted before surgery in the rectus femoris muscle. Dialysate samples were collected at 10-minute intervals at a flow rate of 1 microL/minute until 2 hours after tourniquet deflation. Ninety minutes of ischemia resulted in accumulation of lactate (234% +/- 38%), hypoxanthine (582% +/- 166%), and glycerol (146% +/- 46%), consumption of glucose (54% +/- 9%) and pyruvate (16% +/- 44%), and a slight decrease of urea (78% +/- 11%) compared with baseline (100%). Uric acid was unchanged (95% +/- 12%). Within 90 minutes after tourniquet deflation the concentrations were virtually normalized for all measured metabolites, suggesting that the duration of ischemia was well tolerated by the patients. The results indicate that the use of microdialysis for monitoring energy metabolic events during orthopaedic surgery that requires ischemia and reperfusion is feasible and safe.

  • 800.
    Östman, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Sjödin, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Klinisk nutrition och metabolism.
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Coenzyme Q10 supplementation and exercise-induced oxidative stress in humans2012Inngår i: Nutrition (Burbank, Los Angeles County, Calif.), ISSN 0899-9007, E-ISSN 1873-1244, Vol. 28, nr 4, s. 403-417Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: The theoretically beneficial effects of coenzyme Q10 (Q10) on exercise-related oxidative stress and physical capacity have not been confirmed to our knowledge by interventional supplementation studies. Our aim was to investigate further whether Q10 supplementation at a dose recommended by manufacturers influences these factors. Methods: Using a randomized, double-blind, controlled design, we investigated the effect on physical capacity of 8 wk of treatment with a daily dose of 90 mg of Q10 (n = 12) compared with placebo (n = 11) in moderately trained healthy men 19 to 44 y old. Two days of individualized performance tests to physical exhaustion were performed before and after the intervention. Primary outcomes were maximal oxygen uptake, workload, and heart rate at the lactate threshold. Secondary outcomes were creatine kinase, hypoxanthine, and uric acid. Results: No significant differences between the groups were discerned after the intervention for maximal oxygen uptake (-0.11 L/min, 95% confidence interval 0.31 to 0.08, P = 0.44), workload at lactate threshold (6.3 W, 13.4 to 25.9, P = 0.36), or heart rate at lactate threshold (2.0 beats/min, -4.9 to 8.9, P = 0.41). No differences between the groups were detected for hypoxanthine or uric acid (serum markers of oxidative stress) or creatine kinase (a marker of skeletal muscle damage). Conclusion: Although in theory Q10 could be beneficial for exercise capacity and in decreasing oxidative stress, the present study could not demonstrate that such effects exist after supplementation with a recommended dose. 

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