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  • 101.
    Christersson, Albert
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Larsson, Sune
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Östlund, Bengt
    Nyköping Hosp, Dept Orthoped, S-61185 Nyköping, Sweden.
    Sandén, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Radiographic results after plaster cast fixation for 10 days versus 1 month in reduced distal radius fractures: a prospective randomised study2016In: Journal of Orthopaedic Surgery and Research, ISSN 1749-799X, E-ISSN 1749-799X, Vol. 11, article id 145Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The aim of this study was to examine whether reduced distal radius fractures can be treated with early mobilisation without affecting the radiographic results.

    METHODS: In a prospective randomised study, 109 patients (mean age 65.8 (range 50-92)) with moderately displaced distal radius fractures were treated with closed reduction and plaster cast fixation for about 10 days (range 8-13 days) followed by randomisation to one of two groups: early mobilisation (n = 54, active group) or continued plaster cast fixation for another 3 weeks (n = 55, control group).

    RESULTS: For three patients in the active group (6%), treatment proved unsuccessful because of severe displacement of the fracture (n = 2) or perceived instability (n = 1). From 10 days to 1 month, i.e. the only period when the treatment differed between the two groups, the active group displaced significantly more in dorsal angulation (4.5°, p < 0.001), radial angulation (2.0°, p < 0.001) and axial compression (0.5 mm, p = 0.01) compared with the control group. However, during the entire study period (i.e. from admission to 12 months), the active group displaced significantly more than the controls only in radial angulation (3.2°, p = 0.002) and axial compression (0.7 mm, p = 0.02).

    CONCLUSIONS: Early mobilisation 10 days after reduction of moderately displaced distal radius fractures resulted in both an increased number of treatment failures and increased displacement in radial angulation and axial compression as compared with the control group. Mobilisation 10 days after reduction cannot be recommended for the routine treatment of reduced distal radius fractures.

    TRIAL REGISTRATION: ClinicalTrail.gov, NCT02798614 . Retrospectively registered 16 June 2016.

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  • 102.
    Christersson, Albert
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Nysjö, Johan
    Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Division of Visual Information and Interaction. Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Computerized Image Analysis and Human-Computer Interaction.
    Berglund, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Malmberg, Filip
    Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Division of Visual Information and Interaction. Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Computerized Image Analysis and Human-Computer Interaction. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Sintorn, Ida-Maria
    Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Division of Visual Information and Interaction. Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Computerized Image Analysis and Human-Computer Interaction.
    Nyström, Ingela
    Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Division of Visual Information and Interaction. Uppsala University, Disciplinary Domain of Science and Technology, Mathematics and Computer Science, Department of Information Technology, Computerized Image Analysis and Human-Computer Interaction.
    Larsson, Sune
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Comparison of 2D radiography and a semi-automatic CT-based 3D method for measuring change in dorsal angulation over time in distal radius fractures2016In: Skeletal Radiology, ISSN 0364-2348, E-ISSN 1432-2161, Vol. 45, no 6, p. 763-769Article in journal (Refereed)
    Abstract [en]

    Objective The aim of the present study was to compare the reliability and agreement between a computer tomography-based method (CT) and digitalised 2D radiographs (XR) when measuring change in dorsal angulation over time in distal radius fractures. Materials and methods Radiographs from 33 distal radius fractures treated with external fixation were retrospectively analysed. All fractures had been examined using both XR and CT at six times over 6 months postoperatively. The changes in dorsal angulation between the first reference images and the following examinations in every patient were calculated from 133 follow-up measurements by two assessors and repeated at two different time points. The measurements were analysed using Bland-Altman plots, comparing intra- and inter-observer agreement within and between XR and CT. Results The mean differences in intra- and inter-observer measurements for XR, CT, and between XR and CT were close to zero, implying equal validity. The average intra- and inter-observer limits of agreement for XR, CT, and between XR and CT were +/- 4.4 degrees, +/- 1.9 degrees and +/- 6.8 degrees respectively. Conclusions For scientific purpose, the reliability of XR seems unacceptably low when measuring changes in dorsal angulation in distal radius fractures, whereas the reliability for the semi-automatic CT-based method was higher and is therefore preferable when a more precise method is requested.

  • 103.
    Christersson, Albert
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Sandén, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Larsson, Sune
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Prospective randomized feasibility trial to assess the use of rhPDGF-BB in treatment of distal radius fractures2015In: Journal of Orthopaedic Surgery and Research, ISSN 1749-799X, E-ISSN 1749-799X, Vol. 10, article id 37Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Recombinant human platelet-derived growth factor BB (rhPDGF-BB) combined with an osteoconductive scaffold (β-TCP) has been demonstrated to increase bone formation, but rhPDGF-BB has not been studied in human fractures. The purpose of this study was to evaluate the safety and potential use of locally administered rhPDGF-BB/β-TCP (Augment®) in acute wrist fractures.

    METHODS: Forty patients with unstable distal radial fracture were randomized to closed reduction and external fixation alone (n = 20) or combined with injection of rhPDGF-BB/β-TCP (Augment®) into the fracture (n = 20). All patients were followed for 24 weeks. Outcome was based on adverse events, fracture displacement on radiographs, fracture healing, range of motion, grip strength, pain, and the disability of the arm, shoulder and hand (DASH) score.

    RESULTS: There were no serious adverse events in the study, but the pin tract infection rate was significantly lower in the Augment® group. There was no difference between the groups in fracture healing time, based on number of healed cortices or fracture displacement. The Augment® group had an early temporary significant decrease in wrist flexion, but no difference in range of motion at 24 weeks. There were no differences between the two treatment groups for any other outcome variables.

    CONCLUSION: rhPDGF-BB/β-TCP (Augment®) is safe and convenient for local administration into wrist fractures. In this pilot study, we could not detect any reduced healing time in the Augment® group although potential efficacy should be addressed in larger studies.

    CLINICAL TRIAL REGISTRATION NUMBER: The clinical trial registration number for the study protocol is BMPI-2014-02-E.

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  • 104.
    Clewemar, Pantelis
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Endocrine Tumor Biology.
    Hailer, Nils P.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Hailer, Yasmin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Klar, Joakim
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik.
    Kindmark, Andreas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Endocrinology and mineral metabolism.
    Ljunggren, Östen
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Endocrinology and mineral metabolism.
    Stattin, Eva-Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Expanding the phenotypic spectrum of osteogenesis imperfecta type V including heterotopic ossification of muscle origins and attachments2019In: Molecular Genetics & Genomic Medicine, ISSN 2324-9269, Vol. 7, no 7, article id e00723Article in journal (Refereed)
    Abstract [en]

    Background

    Osteogenesis imperfecta (OI) is a clinical and genetic heterogeneous group of connective tissue disorders, characterized by bone fragility and a propensity to fracture.

    Methods

    In this report we describe the clinical phenotype of two patients, a 28‐year‐old woman and her mother (54 years old), both with a history of short stature and multiple fractures.

    Results

    Exome sequencing revealed the recurring IFITM5:c.‐14 C>T variant causing OI type V. Both patients had several fractures during childhood. CT‐scan and scintigraphy showed ossification of the origin and attachment of muscles and hypertrophic callus formation.

    Conclusion

    Ossification of the origin and attachment of muscles seems to be part of the phenotype in patients with OI type V.

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  • 105.
    Cnudde, Peter
    et al.
    Swedish Hip Arthroplasty Register, Gothenburg, Sweden;Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden;Hywel Dda Univ Healthboard, Prince Philip Hosp, Dept Orthopaed, Llanelli, Wales.
    Bulow, Erik
    Swedish Hip Arthroplasty Register, Gothenburg, Sweden;Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden.
    Nemes, Szilard
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden.
    Tyson, Yosef
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Swedish Hip Arthroplasty Register, Gothenburg, Sweden.
    Mohaddes, Maziar
    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.
    Association between patient survival following reoperation after total hip replacement and the reason for reoperation: an analysis of 9,926 patients in the Swedish Hip Arthroplasty Register2019In: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, Vol. 90, no 3, p. 226-230Article in journal (Refereed)
    Abstract [en]

    Background and purpose

    The association between long-term patient survival and elective primary total hip replacement (THR) has been described extensively. The long-term survival following reoperation of THR is less well understood. We investigated the relative survival of patients undergoing reoperation following elective THR and explored an association between the indication for the reoperation and relative survival.

    Patients and methods

    In this observational cohort study we selected the patients who received an elective primary THR and subsequent reoperations during 1999-2017 as recorded in the Swedish Hip Arthroplasty Register. The selected cohort was followed until the end of the study period, censoring or death. The indications for 1st- and eventual 2nd-time reoperations were analyzed and the relative survival ratio of the observed survival and the expected survival was determined.

    Results

    There were 9,926 1st-time reoperations and of these 2,558 underwent further reoperations. At 5 years after the latest reoperation, relative survival following 1st-time reoperations was 0.94% (95% CI 0.93-0.96) and 0.90% (CI 0.87-0.92) following 2nd-time reoperations. At 5 years patients with a 1st-time reoperation for aseptic loosening had higher survival than expected; however, reoperations performed for periprosthetic fracture, dislocation, and infection had lower survival.

    Interpretation

    The relative survival following 1st- and 2nd-time reoperations in elective THR patients differs by reason for reoperation. The impact of reoperation on life expectancy is more obvious for infection/dislocation and periprosthetic fracture.

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  • 106.
    Cnudde, Peter
    et al.
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden;Ctr Registers Vastra Gotaland, Medicinargatan 15G, SE-41345 Gothenburg, Sweden.
    Rolfson, Ola
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden;Ctr Registers Vastra Gotaland, Medicinargatan 15G, SE-41345 Gothenburg, Sweden.
    Timperley, A. John
    Royal Devon & Exeter Hosp, Princess Elizabeth Orthopaed Ctr, Hip Unit, Exeter, Devon, England.
    Garland, Anne
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Ctr Registers Vastra Gotaland, Medicinargatan 15G, SE-41345 Gothenburg, Sweden.
    Kaerrholm, Johan
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden;Ctr Registers Vastra Gotaland, Medicinargatan 15G, SE-41345 Gothenburg, Sweden.
    Garellick, Goeran
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden;Ctr Registers Vastra Gotaland, Medicinargatan 15G, SE-41345 Gothenburg, Sweden.
    Nemes, Szilard
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Orthopaed, Gothenburg, Sweden;Ctr Registers Vastra Gotaland, Medicinargatan 15G, SE-41345 Gothenburg, Sweden.
    Do Patients Live Longer After THA and Is the Relative Survival Diagnosis-specific?2018In: Clinical Orthopaedics and Related Research, ISSN 0009-921X, E-ISSN 1528-1132, Vol. 476, no 6, p. 1166-1175Article in journal (Refereed)
    Abstract [en]

    Background Hip replacements are successful in restoring mobility, reducing pain, and improving quality of life. However, the association between THA and the potential for increased life expectancy (as expressed by mortality rate) is less clear, and any such association could well be influenced by diagnosis and patient-related, socioeconomic, and surgical factors, which have not been well studied. Questions/purposes (1) After controlling for birth year and sex, are Swedish patients who underwent THA likely to survive longer than individuals in the general population? (2) After controlling for relevant patient-related, socioeconomic/demographic factors and surgical factors, does relative survival differ across the various diagnoses for which THAs were performed in Sweden? Methods Data from the Swedish Hip Arthroplasty Register, linked to administrative health databases, were used for this study. We identified 131,808 patients who underwent THA between January 1, 1999, and December 31, 2012. Of these, 21,755 had died by the end of followup. Patient- and surgery-specific data in combination with socioeconomic data were available for analysis. We compared patient survival (relative survival) with age- and sex-matched survival data in the entire Swedish population according to Statistics Sweden. We used multivariable modeling proceeded with a Cox proportional hazards model in transformed time. Results Patients undergoing elective THA had a slightly improved survival rate compared with the general population for approximately 10 years after surgery. At 1 year after surgery, the survival in patients undergoing THA was 1% better than the expected survival (r = 1.01; 95% confidence interval [CI], 1.01-1.02; p < 0.001); at 5 years, this increased to 3% (r = 1.03; 95% CI, 1.03-1.03; p < 0.001); at 10 years, the difference was 2% (r = 1.02; 95% CI, 1.02-1.03; p < 0.001); and by 12 years, there was no difference between patients undergoing THA and the general population (r = 1.01; 95% CI, 0.99-1.02; p = 0.13). Using the diagnosis of primary osteoarthritis as a reference, hip arthroplasties performed for sequelae of childhood hip diseases had a similar survival rate (hazard ratio [HR], 1.02; 95% CI, 0.88-1.18; p = 0.77). Patients undergoing surgery for osteonecrosis of the femoral head (HR, 1.69; 95% CI, 1.60-1.79; p < 0.001), inflammatory arthritis (HR, 1.49; 95% CI, 1.38-1.61; p < 0.001), and secondary osteoarthritis (HR, 2.46; 95% CI, 2.03-2.99; p < 0.001) all had poorer relative survival. Comorbidities and the Elixhauser comorbidity index had a negative association with relative survival. Level of achieved education (middle level of education: HR, 0.90, 95% CI, 0.87-0.93, p < 0.001; high level: 0.76, 95% CI, 0.73-0.80, p < 0.001) and marital status (single status: HR, 1.33; 95% CI, 1.28-1.38; p < 0.001) were also negatively associated with survival. Conclusions Whereas it has been known that in most patients, THA improves quality of life, this study demonstrates that it also is associated with a slightly increased life expectancy that lasts for approximately 10 years after surgery, especially among patients whose diagnosis was primary osteoarthritis. This adds further proof of a health-economic value for this surgical intervention. The reasons for the increase in relative survival are unknown but are probably multifactorial.

  • 107.
    Collins, Gary S.
    et al.
    Univ Oxford, Ctr Stat Med, Wolfson Coll Annexe, Oxford OX2 6UD, England.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Fracture risk assessment: state of the art, methodologically unsound, or poorly reported?2012In: Current osteoporosis reports, ISSN 1544-2241, Vol. 10, no 3, p. 199-207Article in journal (Refereed)
    Abstract [en]

    Osteoporotic fractures, including hip fractures, are a global health concern associated with significant morbidity and mortality as well as a major economic burden. Identifying individuals who are at an increased risk of osteoporotic fracture is an important challenge to be resolved. Recently, multivariable prediction tools have been developed to assist clinicians in the management of their patients by calculating their 10-year risk of fracture (FRAX, QFracture, Garvan) using a combination of known risk factors. These prediction models have revolutionized the way clinicians assess the risk of fracture. Studies evaluating the performance of prediction models in this and other areas of medicine have, however, been characterized by poor design, methodological conduct, and reporting. We examine recently developed fracture prediction models and critically discuss issues in their design, validation, and transparency.

  • 108.
    Cornefjord, Michael
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Henriques, Thomas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Alemany, Montserrat
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology, Radiology.
    Olerud, Claes
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Posterior atlanto-axial fusion with the Olerud cervical fixation system for odontoid fractures and C1-C2 instability in reumathoid arthritis2003In: European spine journal, ISSN 0940-6719, E-ISSN 1432-0932, Vol. 12, no 1, p. 91-96Article in journal (Refereed)
    Abstract [en]

    In posterior C1-C2 fusion, traditional wire fixation gives poor stability. The bone quality is often insufficient to provide the competent structural bone graft that is required, and the introduction of sublaminar wires is somewhat dangerous. The stability is markedly improved by adding transarticular screws, but the drawbacks of structural bone graft and sublaminar wires remain. The C1 claw of the Olerud Cervical Fixation System improves C1-C2 fixation without relying on structural bone graft or compromising the spinal canal. The aim of this study was to evaluate radiological healing and possible complications in a consecutive series of C1-C2 fusions from our department operated with the C1 claw device. Twenty-six patients (14 women) with a mean age of 73 (range 37-93) years were included. The diagnoses were odontoid fracture in 18 patients, rheumatoid instability in 6, and odontoid non-union and os odontoideum in 1 each. The patients were followed clinically and with plain radiographs for an average of 15 (range 3-27) months. There were no neurological or vascular complications, and no secondary displacements or reoperations in the series. Twenty patients followed for 6-27 months were radiographically healed. Six patients died from unrelated causes 1-38 months postoperatively. Three of these patients had no radiographs later than the postoperative control, one had a healed odontoid fracture but resorbed bone graft at 8 months, while the remaining two patients were not healed, but showed no signs of healing disturbance at the time of death. On the basis of the findings of this study, posterior C1-C2 fusion with the Olerud Cervical Fixation System seems promising. No serious complications related to the surgical procedure were encountered. The stability of the implant obviates the use of a solid bone block as a graft and still allows a high frequency of fusion healing.

  • 109. Cornelis, M C
    et al.
    Byrne, E M
    Esko, T
    Nalls, M A
    Ganna, A
    Paynter, N
    Monda, K L
    Amin, N
    Fischer, K
    Renstrom, F
    Ngwa, J S
    Huikari, V
    Cavadino, A
    Nolte, I M
    Teumer, A
    Yu, K
    Marques-Vidal, P
    Rawal, R
    Manichaikul, A
    Wojczynski, M K
    Vink, J M
    Zhao, J H
    Burlutsky, G
    Lahti, J
    Mikkilä, V
    Lemaitre, R N
    Eriksson, J
    Musani, S K
    Tanaka, T
    Geller, F
    Luan, J
    Hui, J
    Mägi, R
    Dimitriou, M
    Garcia, M E
    Ho, W-K
    Wright, M J
    Rose, L M
    Magnusson, P K E
    Pedersen, N L
    Couper, D
    Oostra, B A
    Hofman, A
    Ikram, M A
    Tiemeier, H W
    Uitterlinden, A G
    van Rooij, F J A
    Barroso, I
    Johansson, I
    Xue, L
    Kaakinen, M
    Milani, L
    Power, C
    Snieder, H
    Stolk, R P
    Baumeister, S E
    Biffar, R
    Gu, F
    Bastardot, F
    Kutalik, Z
    Jacobs, D R
    Forouhi, N G
    Mihailov, E
    Lind, Lars
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Lindgren, C
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Morris, A
    Jensen, M
    Khaw, K-T
    Luben, R N
    Wang, J J
    Männistö, S
    Perälä, M-M
    Kähönen, M
    Lehtimäki, T
    Viikari, J
    Mozaffarian, D
    Mukamal, K
    Psaty, B M
    Döring, A
    Heath, A C
    Montgomery, G W
    Dahmen, N
    Carithers, T
    Tucker, K L
    Ferrucci, L
    Boyd, H A
    Melbye, M
    Treur, J L
    Mellström, D
    Hottenga, J J
    Prokopenko, I
    Tönjes, A
    Deloukas, P
    Kanoni, S
    Lorentzon, M
    Houston, D K
    Liu, Y
    Danesh, J
    Rasheed, A
    Mason, M A
    Zonderman, A B
    Franke, L
    Kristal, B S
    Karjalainen, J
    Reed, D R
    Westra, H-J
    Evans, M K
    Saleheen, D
    Harris, T B
    Dedoussis, G
    Curhan, G
    Stumvoll, M
    Beilby, J
    Pasquale, L R
    Feenstra, B
    Bandinelli, S
    Ordovas, J M
    Chan, A T
    Peters, U
    Ohlsson, C
    Gieger, C
    Martin, N G
    Waldenberger, M
    Siscovick, D S
    Raitakari, O
    Eriksson, J G
    Mitchell, P
    Hunter, D J
    Kraft, P
    Rimm, E B
    Boomsma, D I
    Borecki, I B
    Loos, R J F
    Wareham, N J
    Vollenweider, P
    Caporaso, N
    Grabe, H J
    Neuhouser, M L
    Wolffenbuttel, B H R
    Hu, F B
    Hyppönen, E
    Järvelin, M-R
    Cupples, L A
    Franks, P W
    Ridker, P M
    van Duijn, C M
    Heiss, G
    Metspalu, A
    North, K E
    Ingelsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Nettleton, J A
    van Dam, R M
    Chasman, D I
    Genome-wide meta-analysis identifies six novel loci associated with habitual coffee consumption2015In: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 20, no 5, p. 647-656Article in journal (Refereed)
    Abstract [en]

    Coffee, a major dietary source of caffeine, is among the most widely consumed beverages in the world and has received considerable attention regarding health risks and benefits. We conducted a genome-wide (GW) meta-analysis of predominately regular-type coffee consumption (cups per day) among up to 91 462 coffee consumers of European ancestry with top single-nucleotide polymorphisms (SNPs) followed-up in ~30 062 and 7964 coffee consumers of European and African-American ancestry, respectively. Studies from both stages were combined in a trans-ethnic meta-analysis. Confirmed loci were examined for putative functional and biological relevance. Eight loci, including six novel loci, met GW significance (log10Bayes factor (BF)>5.64) with per-allele effect sizes of 0.03-0.14 cups per day. Six are located in or near genes potentially involved in pharmacokinetics (ABCG2, AHR, POR and CYP1A2) and pharmacodynamics (BDNF and SLC6A4) of caffeine. Two map to GCKR and MLXIPL genes related to metabolic traits but lacking known roles in coffee consumption. Enhancer and promoter histone marks populate the regions of many confirmed loci and several potential regulatory SNPs are highly correlated with the lead SNP of each. SNP alleles near GCKR, MLXIPL, BDNF and CYP1A2 that were associated with higher coffee consumption have previously been associated with smoking initiation, higher adiposity and fasting insulin and glucose but lower blood pressure and favorable lipid, inflammatory and liver enzyme profiles (P<5 × 10(-8)).Our genetic findings among European and African-American adults reinforce the role of caffeine in mediating habitual coffee consumption and may point to molecular mechanisms underlying inter-individual variability in pharmacological and health effects of coffee.

  • 110. Cornelis, M C
    et al.
    Gustafsson, Stefan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Ärnlöv, J
    Elmståhl, S
    Söderberg, S
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Ingelsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Stanford Univ, Sch Med, Dept Med, Div Cardiovasc Med, Stanford, CA 94305 USA.
    Targeted proteomic analysis of habitual coffee consumption.2018In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 283, no 2, p. 200-211Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Coffee drinking has been implicated in mortality and a variety of diseases but potential mechanisms underlying these associations are unclear. Large-scale systems epidemiological approaches may offer novel insights to mechanisms underlying associations of coffee with health.

    OBJECTIVE: We performed an analysis of known and novel protein markers linked to cardiovascular disease and their association with habitual coffee intake in the Prospective Study of the Vasculature in Uppsala Seniors (PIVUS, n = 816) and followed up top proteins in the Uppsala Longitudinal Study of Adult Men (ULSAM, n = 635) and EpiHealth (n = 2418).

    METHODS: In PIVUS and ULSAM, coffee intake was measured by 7-day dietary records whilst a computer-based food frequency questionnaire was used in EpiHealth. Levels of up to 80 proteins were assessed in plasma by a proximity extension assay.

    RESULTS: Four protein-coffee associations adjusted for age, sex, smoking and BMI, met statistical significance in PIVUS (FDR < 5%, P < 2.31 × 10(-3) ): leptin (LEP), chitinase-3-like protein 1 (CHI3L), tumour necrosis factor (TNF) receptor 6 and TNF-related apoptosis-inducing ligand. The inverse association between coffee intake and LEP replicated in ULSAM (β, -0.042 SD per cup of coffee, P = 0.028) and EpiHealth (β, -0.025 SD per time of coffee, P = 0.004). The negative coffee-CHI3L association replicated in EpiHealth (β, -0.07, P = 1.15 × 10(-7) ), but not in ULSAM (β, -0.034, P = 0.16).

    CONCLUSIONS: The current study supports an inverse association between coffee intake and plasma LEP and CHI3L1 levels. The coffee-CHI3L1 association is novel and warrants further investigation given links between CHI3L1 and health conditions that are also potentially influenced by coffee.

  • 111.
    Covaro, Augusto
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Manabe, Nodoka
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Bobinski, Lukas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Olerud, Claes
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Robinson, Yohan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    The importance of the occipitocervical area in patients with ankylosing spondylitis analysis of a cohort of 86 cervical fractures in surgically treated patients2017In: Journal of Craniovertebral Junction and Spine, ISSN 0974-8237, E-ISSN 0976-9285, Vol. 8, no 4, p. 374-377Article in journal (Refereed)
    Abstract [en]

    Study Design: This was a retrospective analysis of prospectively collected data.

    Objective: The effect of C0-C1-C2 cervical ankylosis in patients with ankylosing spondylitis (AS) is not documented. The objective of this study is to describe the radiological characteristics of the occipitocervical junction in patients with AS operated for a cervical fracture and to correlate them with their clinical evolution.

    Materials and Methods: Analysis of patients with ankylosing spondylitis (AS) treated in a single institution of a cervical vertebral fracture between 2007 and 2014 who were prospectively followed through the SWESPINE registry. The integrity of the C0-€“C1-€“C2 joints was determined and classified into fused and nonfused joints. By determining the angle between C0-€“C1 and C1-€“C2 joints in the coronal view of the computed tomography scan (X-angle), the progressive degeneration of these joints was described. Intra- and inter-observer reliability of this test was determined. The instruments of health-related quality of life (QOL) and disability were EQ5D and Oswestry disability index (ODI), respectively.

    Results: A total of 86 patients with AS treated surgically for cervical fracture had complete facet ankylosis between C3 and T1 due to their pathology. Mean age 69.2 years (standard deviation [SD]: 11.7). The most common level of fracture was in C5-C6. In 24 patients, the C0-C1 joint was fused, and in 15 patients, C1-C2 joint was fused. The intra- and inter-class reliabilities for X-angle measurement were very high (intraclass correlation coefficients = 0.94; 0.92). The mean X-angle was 125° (SD: 12) in nonfused patients and 136° (SD: 14) in fused patients (p < 0.001). There were no differences in QOL and disability at 2 years between the two groups: EQ5D-index of 0.54 and 0.55 (p = 0.5), ODI of 26.4 and 24, (p = 0.35) respectively. 

    Conclusions: X-angle is a reliable measure for joint integrity C0-€“C1-€C2 in patients with AS. Total cervical ankylosis including the C0-C1-C2 segments is not related to poorer QOL and disability in these patients.

  • 112. Crippa, Alessio
    et al.
    Larsson, Susanna C
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Discacciati, Andrea
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Orsini, Nicola
    Red and processed meat consumption and risk of bladder cancer: a dose-response meta-analysis of epidemiological studies.2018In: European Journal of Nutrition, ISSN 1436-6207, E-ISSN 1436-6215, Vol. 57, no 2, p. 689-701Article in journal (Refereed)
    Abstract [en]

    BACKGROUND/OBJECTIVES: Several epidemiological studies have analyzed the associations between red and processed meat and bladder cancer risk but the shape and strength of the associations are still unclear. Therefore, we conducted a dose-response meta-analysis to quantify the potential association between red and processed meat and bladder cancer risk.

    METHODS: Relevant studies were identified by searching the PubMed database through January 2016 and reviewing the reference lists of the retrieved articles. Results were combined using random-effects models.

    RESULTS: Five cohort studies with 3262 cases and 1,038,787 participants and 8 cases-control studies with 7009 cases and 27,240 participants met the inclusion criteria. Red meat was linearly associated with bladder cancer risk in case-control studies, with a pooled RR of 1.51 (95% confidence interval (CI) 1.13, 2.02) for every 100 g increase per day, while no association was observed among cohort studies (P heterogeneity across study design = 0.02). Based on both case-control and cohort studies, the pooled relative risk (RR) for every 50 g increase of processed meat per day was 1.20 (95% CI 1.06, 1.37) (P heterogeneity across study design = 0.22).

    CONCLUSIONS: This meta-analysis suggests that processed meat may be positively associated with bladder cancer risk. A positive association between red meat and risk of bladder cancer was observed only in case-control studies, while no association was observe in prospective studies.

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  • 113.
    Cronholm, Felix
    et al.
    Lund Univ, Skane Univ Hosp, Dept Clin Sci & Orthoped, Clin & Mol Osteoporosis Res Unit, Malmo, Sweden.
    Rosengren, Björn E.
    Lund Univ, Skane Univ Hosp, Dept Clin Sci & Orthoped, Clin & Mol Osteoporosis Res Unit, Malmo, Sweden.
    Nilsson, Jan-Åke
    Lund Univ, Skane Univ Hosp, Dept Clin Sci & Orthoped, Clin & Mol Osteoporosis Res Unit, Malmo, Sweden.
    Ohlsson, Claes
    Univ Gothenburg, Sahlgrenska Acad, Ctr Bone & Arthrit Res, Dept Internal Med & Clin Nutr,Inst Med, Gothenburg, Sweden.
    Mellström, Dan
    Univ Gothenburg, Sahlgrenska Acad, Dept Internal Med & Clin Nutr, Geriatr Med,Inst Med, Gothenburg, Sweden.
    Ribom, Eva L
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Karlsson, Magnus K.
    Lund Univ, Skane Univ Hosp, Dept Clin Sci & Orthoped, Clin & Mol Osteoporosis Res Unit, Malmo, Sweden.
    The fracture predictive ability of a musculoskeletal composite score in old men - data from the MrOs Sweden study2019In: BMC Geriatrics, ISSN 1471-2318, E-ISSN 1471-2318, Vol. 19, article id 90Article in journal (Refereed)
    Abstract [en]

    Background: Detection of high-risk individuals for fractures are needed. This study assessed whether level of physical activity (PA) and a musculoskeletal composite score could be used as fracture predictive tools, and if the score could predict fractures better than areal bone mineral density (aBMD).

    Methods: MrOs Sweden is a prospective population-based observational study that at baseline included 3014 men aged 69-81years. We assessed femoral neck bone mineral content (BMC), bone area, aBMD and total body lean mass by dual energy X-ray absorptiometry, calcaneal speed of sound by quantitative ultrasound and hand grip strength by a handheld dynamometer. PA was assessed by the Physical Activity Scale for the Elderly (PASE) questionnaire. We followed the participants until the date of first fracture, death or relocation (median 9.6years). A musculoskeletal composite score was calculated as mean Z-score of the five measured traits. A Cox proportional hazards model was used to analyze the association between the musculoskeletal traits, the composite score and incident fractures (yes/no) during the follow-up period. Data are presented as hazard ratios (HR) with 95% confidence intervals (95% CI) for fracture for a+1 standard deviation (SD) change (+1 Z-score) in the various musculoskeletal traits as well as the composite score. We used a linear regression model to estimate the association between level of PA, measured as PASE-score and the different musculoskeletal traits as well as the composite score.

    Results: A+1 SD higher composite score was associated with an incident fracture HR of 0.61 (0.54, 0.69), however not being superior to aBMD in fracture prediction. A+1 SD higher PASE-score was associated with both a higher composite score and lower fracture incidence (HR 0.83 (0.76, 0.90)).

    Conclusions: The composite score was similar to femoral neck aBMD in predicting fractures, and also low PA predicted fractures. This highlights the need of randomized controlled trials to evaluate if PA could be used as a fracture preventive strategy.

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  • 114. Dadaev, Tokhir
    et al.
    Saunders, Edward J
    Newcombe, Paul J
    Anokian, Ezequiel
    Leongamornlert, Daniel A
    Brook, Mark N
    Cieza-Borrella, Clara
    Mijuskovic, Martina
    Wakerell, Sarah
    Olama, Ali Amin Al
    Schumacher, Fredrick R
    Berndt, Sonja I
    Benlloch, Sara
    Ahmed, Mahbubl
    Goh, Chee
    Sheng, Xin
    Zhang, Zhuo
    Muir, Kenneth
    Govindasami, Koveela
    Lophatananon, Artitaya
    Stevens, Victoria L
    Gapstur, Susan M
    Carter, Brian D
    Tangen, Catherine M
    Goodman, Phyllis
    Thompson, Ian M
    Batra, Jyotsna
    Chambers, Suzanne
    Moya, Leire
    Clements, Judith
    Horvath, Lisa
    Tilley, Wayne
    Risbridger, Gail
    Gronberg, Henrik
    Aly, Markus
    Nordström, Tobias
    Pharoah, Paul
    Pashayan, Nora
    Schleutker, Johanna
    Tammela, Teuvo L J
    Sipeky, Csilla
    Auvinen, Anssi
    Albanes, Demetrius
    Weinstein, Stephanie
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Hakansson, Niclas
    West, Catharine
    Dunning, Alison M
    Burnet, Neil
    Mucci, Lorelei
    Giovannucci, Edward
    Andriole, Gerald
    Cussenot, Olivier
    Cancel-Tassin, Géraldine
    Koutros, Stella
    Freeman, Laura E Beane
    Sorensen, Karina Dalsgaard
    Orntoft, Torben Falck
    Borre, Michael
    Maehle, Lovise
    Grindedal, Eli Marie
    Neal, David E
    Donovan, Jenny L
    Hamdy, Freddie C
    Martin, Richard M
    Travis, Ruth C
    Key, Tim J
    Hamilton, Robert J
    Fleshner, Neil E
    Finelli, Antonio
    Ingles, Sue Ann
    Stern, Mariana C
    Rosenstein, Barry
    Kerns, Sarah
    Ostrer, Harry
    Lu, Yong-Jie
    Zhang, Hong-Wei
    Feng, Ninghan
    Mao, Xueying
    Guo, Xin
    Wang, Guomin
    Sun, Zan
    Giles, Graham G
    Southey, Melissa C
    MacInnis, Robert J
    FitzGerald, Liesel M
    Kibel, Adam S
    Drake, Bettina F
    Vega, Ana
    Gómez-Caamaño, Antonio
    Fachal, Laura
    Szulkin, Robert
    Eklund, Martin
    Kogevinas, Manolis
    Llorca, Javier
    Castaño-Vinyals, Gemma
    Penney, Kathryn L
    Stampfer, Meir
    Park, Jong Y
    Sellers, Thomas A
    Lin, Hui-Yi
    Stanford, Janet L
    Cybulski, Cezary
    Wokolorczyk, Dominika
    Lubinski, Jan
    Ostrander, Elaine A
    Geybels, Milan S
    Nordestgaard, Børge G
    Nielsen, Sune F
    Weisher, Maren
    Bisbjerg, Rasmus
    Røder, Martin Andreas
    Iversen, Peter
    Brenner, Hermann
    Cuk, Katarina
    Holleczek, Bernd
    Maier, Christiane
    Luedeke, Manuel
    Schnoeller, Thomas
    Kim, Jeri
    Logothetis, Christopher J
    John, Esther M
    Teixeira, Manuel R
    Paulo, Paula
    Cardoso, Marta
    Neuhausen, Susan L
    Steele, Linda
    Ding, Yuan Chun
    De Ruyck, Kim
    De Meerleer, Gert
    Ost, Piet
    Razack, Azad
    Lim, Jasmine
    Teo, Soo-Hwang
    Lin, Daniel W
    Newcomb, Lisa F
    Lessel, Davor
    Gamulin, Marija
    Kulis, Tomislav
    Kaneva, Radka
    Usmani, Nawaid
    Slavov, Chavdar
    Mitev, Vanio
    Parliament, Matthew
    Singhal, Sandeep
    Claessens, Frank
    Joniau, Steven
    Van den Broeck, Thomas
    Larkin, Samantha
    Townsend, Paul A
    Aukim-Hastie, Claire
    Gago-Dominguez, Manuela
    Castelao, Jose Esteban
    Martinez, Maria Elena
    Roobol, Monique J
    Jenster, Guido
    van Schaik, Ron H N
    Menegaux, Florence
    Truong, Thérèse
    Koudou, Yves Akoli
    Xu, Jianfeng
    Khaw, Kay-Tee
    Cannon-Albright, Lisa
    Pandha, Hardev
    Michael, Agnieszka
    Kierzek, Andrzej
    Thibodeau, Stephen N
    McDonnell, Shannon K
    Schaid, Daniel J
    Lindstrom, Sara
    Turman, Constance
    Ma, Jing
    Hunter, David J
    Riboli, Elio
    Siddiq, Afshan
    Canzian, Federico
    Kolonel, Laurence N
    Le Marchand, Loic
    Hoover, Robert N
    Machiela, Mitchell J
    Kraft, Peter
    Freedman, Matthew
    Wiklund, Fredrik
    Chanock, Stephen
    Henderson, Brian E
    Easton, Douglas F
    Haiman, Christopher A
    Eeles, Rosalind A
    Conti, David V
    Kote-Jarai, Zsofia
    Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants.2018In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 9, no 1, article id 2256Article in journal (Refereed)
    Abstract [en]

    Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling.

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  • 115.
    Dahlstrand, Henrik
    et al.
    Karolinska Univ Hosp, Karolinska Inst, Sect Orthopaed & Sports Med, Dept Mol Med & Surg, Stockholm, Sweden..
    Stark, Andre
    Karolinska Inst, Danderyd Hosp, Dept Clin Sci, Stockholm, Sweden..
    Wick, Marius C.
    Karolinska Univ Hosp, Karolinska Inst Stockholm, Funct Unit Musculoskeletal Radiol Funct Imaging &, Stockholm, Sweden..
    Anissian, Lucas
    Oregon Hlth & Sci Univ, Dept Orthopaed Surg, Portland, OR USA..
    Hailer, Nils
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Weiss, Rudiger J.
    Karolinska Univ Hosp, Karolinska Inst, Sect Orthopaed & Sports Med, Dept Mol Med & Surg, Stockholm, Sweden..
    Comparison of metal ion concentrations and implant survival after total hip arthroplasty with metal-on-metal versus metal-on-polyethylene articulations: a 16-year follow-up of a prospective randomized study2017In: Acta Orthopaedica, ISSN 1745-3674, E-ISSN 1745-3682, Vol. 88, no 5, p. 490-495Article in journal (Refereed)
    Abstract [en]

    Background and purpose - Large metal-on-metal (MoM) articulations are associated with metal wear and corrosion, leading to increased metal ion concentrations and unacceptable revision rates. There are few comparative studies of 28-mm MoM articulations with conventional metal-on-polyethylene (MoP) couplings. We present a long-term follow-up of a randomized controlled trial comparing MoM versus MoP 28-mm articulations, focused on metal ions and implant survival. Patients and methods - 85 patients with a mean age of 65 years at surgery were randomized to a MoM (Metasul) or a MoP (Protasul) bearing. After 16 years, 38 patients had died and 4 had undergone revision surgery. 13 patients were unavailable for clinical follow-up, leaving 30 patients (n = 14 MoM and n = 16 MoP) for analysis of metal ion concentrations and clinical outcome. Results - 15-year implant survival was similar in both groups (MoM 96% [95% CI 88-100] versus MoP 97% [95% CI 91-100]). The mean serum cobalt concentration was 4-fold higher in the MoM (1.5 mu g/L) compared with the MoP cohort (0.4 mu g/L, p < 0.001) and the mean chromium concentration was double in the MoM (2.2 mu g/L) compared with the MoP cohort (1.0 mu g/L, p = 0.05). Mean creatinine levels were similar in both groups (MoM 93 mu mol/L versus MoP 92 mu mol/L). Harris hip scores differed only marginally between the MoM and MoP cohorts. Interpretation - This is the longest follow-up of a randomized trial on 28-mm MoM articulations, and although implant survival in the 2 groups was similar, metal ion concentrations remained elevated in the MoM cohort even in the long term.

  • 116. Dahlstrand, Henrik
    et al.
    Stark, André
    Anissian, Lucas
    Hailer, Nils P.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Elevated serum concentrations of cobalt, chromium, nickel, and manganese after metal-on-metal alloarthroplasty of the hip: a prospective randomized study2009In: The Journal of Arthroplasty, ISSN 0883-5403, E-ISSN 1532-8406, Vol. 24, no 6, p. 837-845Article in journal (Refereed)
    Abstract [en]

    In this prospective randomized study, we investigate metal ion concentrations and clinical outcome 2 years after metal-on-metal (28 patients) or metal-on-polyethylene (26 patients) hip arthroplasty with 28-mm modular heads. Metal ion concentrations in patient serum were analyzed by high-resolution plasma mass spectrometry. The clinical outcome was almost identical in both groups with respect to the Harris hip score and the Medical Outcome Study Short Form-36; and on plain radiography, no signs of loosening occurred in any group. In the metal-on-metal group, concentrations of all investigated ions increased significantly when compared with preoperative values: cobalt, 15.3-fold (95% confidence interval [CI], 9.4-21.2); chromium, 5.2-fold (CI, 3.5-7.0); nickel, 2.1-fold (CI, 1.2-3.0); and manganese, 1.6-fold (CI, 1.3-2.0). In the metal-on-polyethylene group, a smaller but significant increase in the concentrations of cobalt and nickel occurred, whereas concentrations of the other ions did not change significantly.

  • 117. Dehghani, F.
    et al.
    Sayan, M.
    Conrad, A.
    Evers, J.
    Ghadban, C.
    Blaheta, R.
    Korf, H. -W
    Hailer, Nils P.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Inhibition of microglial and astrocytic inflammatory responses by the immunosuppressant mycophenolate mofetil2010In: Neuropathology and Applied Neurobiology, ISSN 0305-1846, E-ISSN 1365-2990, Vol. 36, no 7, p. 598-611Article in journal (Refereed)
    Abstract [en]

    Aims: Nucleotide depletion induced by the immunosuppressant mycophenolate mofetil (MMF) has been shown to exert neuroprotective effects. It remains unclear whether nucleotide depletion directly counteracts neuronal demise or whether it inhibits microglial or astrocytic activation, thereby resulting in indirect neuroprotection. Methods: Effects of MMF on isolated microglial cells, astrocyte/microglial cell co-cultures and isolated hippocampal neurones were analysed by immunocytochemistry, quantitative morphometry, and elisa. Results: We found that: (i) MMF suppressed lipopolysaccharide-induced microglial secretion of interleukin-1 beta, tumour necrosis factor-alpha and nitric oxide; (ii) MMF suppressed lipopolysaccharide-induced astrocytic production of tumour necrosis factor-alpha but not of nitric oxide; (iii) MMF strongly inhibited proliferation of both microglial cells and astrocytes; (iv) MMF did not protect isolated hippocampal neurones from excitotoxic injury; and (v) effects of MMF on glial cells were reversed after treatment with guanosine. Conclusions: Nucleotide depletion induced by MMF inhibits microglial and astrocytic activation. Microglial and astrocytic proliferation is suppressed by MMF-induced inhibition of the salvage pathway enzyme inosine monophosphate dehydrogenase. The previously observed neuroprotection after MMF treatment seems to be indirectly mediated, making this compound an interesting immunosuppressant in the treatment of acute central nervous system lesions.

  • 118. DeLuca, S.
    et al.
    Sitara, D.
    Kang, K.
    Marsell, Richard
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Jonsson, Kenneth B.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Taguchi, T.
    Erben, R. G.
    Razzaque, M. S.
    Lanske, Beate
    Amelioration of the premature ageing-like features of Fgf-23 knockout mice by genetically restoring the systemic actions of FGF-232008In: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896, Vol. 216, no 3, p. 345-355Article in journal (Refereed)
    Abstract [en]

    Genetic ablation of fibroblast growth factor 23 from mice (Fgf-23−/−) results in a short lifespan with numerous abnormal biochemical and morphological features. Such features include kyphosis, hypogonadism and associated infertility, osteopenia, pulmonary emphysema, severe vascular and soft tissue calcifications, and generalized atrophy of various tissues. To determine whether these widespread anomalies in Fgf-23−/− mice can be ameliorated by genetically restoring the systemic actions of FGF-23, we generated Fgf-23−/− mice expressing the human FGF-23 transgene in osteoblasts under the control of the 2.3 kb α1(I) collagen promoter (Fgf-23−/−/hFGF-23-Tg double mutants). This novel mouse model is completely void of all endogenous Fgf-23 activity, but produces human FGF-23 in bone cells that is subsequently released into the circulation. Our results suggest that lack of Fgf-23 activities results in extensive premature ageing-like features and early mortality of Fgf-23−/− mice, while restoring the systemic effects of FGF-23 significantly ameliorates these phenotypes, with the resultant effect being improved growth, restored fertility, and significantly prolonged survival of double mutants. With regard to their serum biochemistry, double mutants reversed the severe hyperphosphataemia, hypercalcaemia, and hypervitaminosis D found in Fgf-23−/− littermates; rather, double mutants show hypophosphataemia and normal serum 1,25-dihydroxyvitamin D3 levels similar to pure FGF-23 Tg mice. These changes were associated with reduced renal expression of NaPi2a and 1α-hydroxylase, compared to Fgf-23−/− mice. FGF-23 acts to prevent widespread abnormal features by acting systemically to regulate phosphate homeostasis and vitamin D metabolism. This novel mouse model provides us with an in vivo tool to study the systemic effects of FGF-23 in regulating mineral ion metabolism and preventing multiple abnormal phenotypes without the interference of native Fgf-23.

  • 119. Donat-Vargas, Carolina
    et al.
    Berglund, Marika
    Glynn, Anders
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Åkesson, Agneta
    Dietary polychlorinated biphenyls, long-chain n-3 polyunsaturated fatty acids and incidence of malignant melanoma.2017In: European Journal of Cancer, ISSN 0959-8049, E-ISSN 1879-0852, Vol. 72, p. 137-143, article id S0959-8049(16)32594-1Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: For malignant melanoma, other risk factors aside from sun exposure have been hardly explored. Polychlorinated biphenyls (PCBs)-mainly from fatty fish- may affect melanogenesis and promote melanoma progression, while long-chain n-3 polyunsaturated fatty acids seem to exert antineoplastic actions in melanoma cells.

    OBJECTIVES: We aimed to assess the association of validated estimates of dietary PCB exposure as well as the intake of eicosapentaenoic acid and docosahexaenoic acid (EPA-DHA), accounting for sun habits and skin type, with the risk of malignant melanoma in middle-aged and elderly women.

    METHODS: We included 20,785 women at baseline in 2009 from the prospective population-based Swedish Mammography Cohort. Validated estimates of dietary PCB exposure and EPA-DHA intake were obtained via a food frequency questionnaire. Incident melanoma cases were ascertained through register-linkage.

    RESULTS: During 4.5 years of follow-up, we ascertained 67 incident cases of melanoma. After multivariable adjustments, exposure to dietary PCBs was associated with four-fold increased risk of malignant melanoma (hazard ratio [HR], 4.0 [95% confidence interval {CI}, 1.2-13; P for trend = 0.02]), while EPA-DHA intake was associated with 80% lower risk (HR, 0.2 [95% CI, 0.1-0.8; P for trend = 0.03]), comparing the highest exposure tertiles with the lowest.

    CONCLUSION: While we found a direct association between dietary PCB exposure and risk of melanoma, EPA-DHA intake showed to have a substantial protective association. Question of benefits and risk from fish consumption is very relevant and further prospective studies in the general population verifying these findings are warranted.

  • 120. Dormagen, Johann B.
    et al.
    Tötterman, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Røise, Olav
    Sandvik, Leiv
    Kløw, Nils-E.
    Efficacy of plain radiography and computer tomography in localizing the site of pelvic arterial bleeding in trauma patients2010In: Acta Radiologica, ISSN 0284-1851, E-ISSN 1600-0455, Vol. 51, no 1, p. 107-16Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Immediate angiography is warranted in pelvic trauma patients with suspected arterial injury (AI) in order to stop ongoing bleeding. Prior to angiography, plain pelvic radiography (PPR) and abdominopelvic computer tomography (CT) are performed to identify fracture and hematoma sites. PURPOSE: To investigate if PPR and CT can identify the location of AI in trauma patients undergoing angiography. MATERIAL AND METHODS: 95 patients with pelvic fractures on PPR (29 women, 66 men), at a mean age of 44 (9-92) years, underwent pelvic angiography for suspected AI. Fifty-six of them underwent CT additionally. Right and left anterior and posterior fractures on PPR were registered, and fracture displacement was recorded for each quadrant. Arterial blush on CT was registered, and the size of the hematoma in each region was measured in cm(2). AIs were registered for anterior and posterior segments of both internal iliac arteries. Presence of fractures, arterial blush, and hematomas were correlated with AI. RESULTS: Presence of fracture in the corresponding skeletal segment on PPR showed sensitivity and specificity of 0.86 and 0.58 posteriorly, and 0.87 and 0.44 anteriorly. The area under the curve (AUC) was 0.77 and 0.69, respectively. Fracture displacement on PPR >0.9 cm posteriorly and >1.9 cm anteriorly revealed specificity of 0.84. Sensitivities of arterial blush and hematoma on CT were 0.38 and 0.82 posteriorly, and 0.24 and 0.82 anteriorly. The specificities were 0.96 and 0.58 posteriorly, and 0.79 and 0.53 anteriorly, respectively. For hematomas, the AUC was 0.79 posteriorly and 0.75 anteriorly. Size of hematoma >22 cm(2) posteriorly and >29 cm(2) anteriorly revealed specificity of 0.85 and 0.86, respectively. CONCLUSION: CT findings of arterial blush and hematoma predicted site of arterial bleeding on pelvic angiography. Also, PPR predicted the site of bleeding using location of fracture and size of displacement. In the hemodynamically unstable patient, PPR may contribute equally to effective assessment of injured arteries.

  • 121.
    Dorner, Thomas E.
    et al.
    Med Univ Vienna, Ctr Publ Hlth, Dept Social & Prevent Med, Kinderspitalgasse 15-1, A-1090 Vienna, Austria.
    Helgesson, Magnus
    Karolinska Inst, Div Insurance Med, Dept Clin Neurosci, Berzeliusv 3, S-17177 Stockholm, Sweden.
    Nilsson, Kerstin
    Karolinska Inst, Div Insurance Med, Dept Clin Neurosci, Berzeliusv 3, S-17177 Stockholm, Sweden.
    Pazarlis, Konstantinos A.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Ropponen, Annina
    Karolinska Inst, Div Insurance Med, Dept Clin Neurosci, Berzeliusv 3, S-17177 Stockholm, Sweden;Finnish Inst Occupat Hlth, POB 18, Helsinki 00390, Finland.
    Svedberg, Pia
    Karolinska Inst, Div Insurance Med, Dept Clin Neurosci, Berzeliusv 3, S-17177 Stockholm, Sweden.
    Mittendorfer-Rutz, Ellenor
    Karolinska Inst, Div Insurance Med, Dept Clin Neurosci, Berzeliusv 3, S-17177 Stockholm, Sweden.
    Course and characteristics of work disability 3 years before and after lumbar spine decompression surgery: a national population-based study2018In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 11811Article in journal (Refereed)
    Abstract [en]

    Despite decompression surgery being a widespread intervention for patients with dorsopathies (i.e. back pain) affecting the lumbar spine, the scientific knowledge on patterns and characteristics of work disability before and after the surgery is limited. Sickness absence (SA) and disability pension (DP) were examined three years before and after surgery in 8558 patients aged 25-60 years who underwent lumbar spine decompression surgery in Sweden. They were compared to individuals with diagnosed dorsopathies but no surgery and individuals from the general population as matched comparison groups. According to Group Based Trajectory models, in patients with decompression surgery, 39% had low levels of SA/DP during the entire study period and 15% started with low levels of SA/DP, which increased in the year before, and declined to almost zero in the second year after surgery. Three trajectory groups (12%, 17%, and 18%) started at different levels of SA/DP, which increased in the years before, and declined in the third year after surgery. The trajectory groups in the comparison groups showed lower levels of work disability. Sex, education, and the use of antidepressants and analgesics the year before surgery played an important role to explain the variance of trajectory groups in patients with surgery.

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  • 122. Downer, Mary K
    et al.
    Batista, Julie L
    Mucci, Lorelei A
    Stampfer, Meir J
    Epstein, Mara Meyer
    Håkansson, Niclas
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Johansson, Jan-Erik
    Andrén, Ove
    Fall, Katja
    Andersson, Sven-Olof
    Dairy intake in relation to prostate cancer survival.2017In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 140, no 9, p. 2060-2069Article in journal (Refereed)
    Abstract [en]

    Dairy intake has been associated with increased risk of advanced prostate cancer. Two US cohort studies reported increased prostate cancer-specific mortality with increased high-fat milk intake. We examined whether dairy and related nutrient intake were associated with prostate cancer progression in a Swedish patient population with high dairy consumption. We prospectively followed 525 men with newly diagnosed prostate cancer (diagnosed 1989-1994). We identified and confirmed deaths through February 2011 (n = 222 prostate cancer-specific, n = 268 from other causes). Cox proportional hazards regression was used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for the associations between food or nutrient intake and prostate cancer-specific death. On average, patients consumed 5.0 servings/day of total dairy products at diagnosis. In the whole population, high-fat milk intake was not associated with prostate cancer-specific death (95% CI: 0.78, 2.10; p-trend = 0.32; multivariate-adjusted model). However, among patients diagnosed with localized prostate cancer, compared to men who consumed <1 servings/day of high-fat milk, those who drank ≥3 servings/day had an increased hazard of prostate cancer mortality (HR = 6.10; 95% CI: 2.14, 17.37; p-trend = 0.004; multivariate-adjusted model). Low-fat milk intake was associated with a borderline reduction in prostate cancer death among patients with localized prostate cancer. These associations were not observed among patients diagnosed with advanced stage prostate cancer. Our data suggest a positive association between high-fat milk intake and prostate cancer progression among patients diagnosed with localized prostate cancer. Further studies are warranted to investigate this association and elucidate the mechanisms by which high-fat milk intake may promote prostate cancer progression.

  • 123. Drca, Nikola
    et al.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Jensen-Urstad, Mats
    Larsson, Susanna C.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Physical activity is associated with a reduced risk of atrial fibrillation in middle-aged and elderly women2015In: Heart, ISSN 1355-6037, E-ISSN 1468-201X, Vol. 101, no 20, p. 1627-1630Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Previous studies have found that regular participation in intense physical activity increases the risk of developing atrial fibrillation (AF) in men, but it remains unclear how physical activity influences the risk of AF in women. We aimed to examine whether physical activity of different types and at different ages influences the development of AF in women.

    METHODS: In the population-based Swedish Mammography Cohort, information about physical activity was obtained from 36 513 AF-free women (49-83 years old, median age 60 years) who had completed a questionnaire at study entry (1997). Participants reported their time spent on leisure-time exercise and on walking or bicycling throughout their lifetime (at study entry, and at 30 and 50 years of age). We used the Swedish National Inpatient Register (IPR) to determine whether the participants were diagnosed with AF. Cox proportional hazards regression models were used to estimate relative risks (RR) with 95% CI, adjusted for potential confounders.

    RESULTS: During a median follow-up of 12 years (10th percentile 7.5 years, 90th percentile 12.0 years), 2915 cases of AF were diagnosed. The risk of AF decreased with increasing levels of leisure-time exercise at study entry (RR 0.85, 95% CI 0.75 to 0.95 for ≥4 h/week vs <1 h/week) and walking/bicycling (RR 0.81, 95% CI 0.72 to 0.92, for ≥40 min/day vs almost never).

    CONCLUSIONS: Physical activity is associated with a reduced risk of AF in women. Moderate amount of physical activity was sufficient to significantly reduce AF risk.

  • 124.
    Dörk, Thilo
    et al.
    Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany.
    Peterlongo, Paolo
    IFOM FIRC Inst Mol Oncol, Genome Diagnost Program, Milan, Italy.
    Mannermaa, Arto
    Univ Eastern Finland, Translat Canc Res Area, Kuopio, Finland;Univ Eastern Finland, Inst Clin Med Pathol & Forens Med, Kuopio, Finland;Kuopio Univ Hosp, Imaging Ctr, Dept Clin Pathol, Kuopio, Finland.
    Bolla, Manjeet K.
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Wang, Qin
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Dennis, Joe
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Ahearn, Thomas
    NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
    Andrulis, Irene L.
    Lunenfeld Tanenbaum Res Inst Mt Sinai Hosp, Fred A Litwin Ctr Canc Genet, Toronto, ON, Canada;Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
    Anton-Culver, Hoda
    Univ Calif Irvine, Dept Epidemiol, Genet Epidemiol Res Inst, Irvine, CA USA.
    Arndt, Volker
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, C070, Heidelberg, Germany.
    Aronson, Kristan J.
    Queens Univ, Dept Publ Hlth Sci, Kingston, ON, Canada;Queens Univ, Canc Res Inst, Kingston, ON, Canada.
    Augustinsson, Annelie
    Lund Univ, Dept Canc Epidemiol, Clin Sci, Lund, Sweden.
    Freeman, Laura E. Beane
    NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
    Beckmann, Matthias W.
    Friedrich Alexander Univ Erlangen Nuremberg, Univ Hosp Erlangen, Comprehens Canc Ctr ER EMN, Dept Gynecol & Obstet, Erlangen, Germany.
    Beeghly-Fadiel, Alicia
    Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Div Epidemiol,Dept Med,Vanderbilt Epidemiol Ctr, Nashville, TN 37212 USA.
    Behrens, Sabine
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
    Bermisheva, Marina
    Russian Acad Sci, Ufa Fed Res Ctr, Inst Biochem & Genet, Ufa, Russia.
    Blomqvist, Carl
    Univ Helsinki, Helsinki Univ Hosp, Dept Oncol, Helsinki, Finland;Orebro Univ Hosp, Dept Oncol, Orebro, Sweden.
    Bogdanova, Natalia, V
    Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany;Hannover Med Sch, Dept Radiat Oncol, Hannover, Germany;NN Alexandrov Res Inst Oncol & Med Radiol, Minsk, BELARUS.
    Bojesen, Stig E.
    Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Copenhagen Gen Populat Study, Herlev, Denmark;Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Dept Clin Biochem, Herlev, Denmark;Univ Copenhagen, Fac Hlth & Med Sci, Copenhagen, Denmark.
    Brauch, Hiltrud
    Dr Margarete Fischer Bosch Inst Clin Pharmacol, Stuttgart, Germany;German Canc Res Ctr, German Canc Consortium DKTK, Heidelberg, Germany;Univ Tubingen, iFIT Cluster Excellence, Tubingen, Germany.
    Brenner, Hermann
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, C070, Heidelberg, Germany;German Canc Res Ctr, German Canc Consortium DKTK, Heidelberg, Germany;German Canc Res Ctr, Div Prevent Oncol, Heidelberg, Germany;Natl Ctr Tumor Dis NCT, Heidelberg, Germany.
    Burwinkel, Barbara
    German Canc Res Ctr, Mol Epidemiol Grp, C080, Heidelberg, Germany;Heidelberg Univ, Univ Womens Clin Heidelberg, Mol Biol Breast Canc, Heidelberg, Germany.
    Canzian, Federico
    German Canc Res Ctr, Genom Epidemiol Grp, Heidelberg, Germany.
    Chan, Tsun L.
    Canc Genet Ctr, Hong Kong Hereditary Breast Canc Family Registry, Happy Valley, Hong Kong, Peoples R China;Hong Kong Sanat & Hosp, Dept Pathol, Happy Valley, Hong Kong, Peoples R China.
    Chang-Claude, Jenny
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany;Univ Med Ctr Hamburg Eppendorf, UCCH, Canc Epidemiol Grp, Hamburg, Germany.
    Chanock, Stephen J.
    NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
    Choi, Ji-Yeob
    Seoul Natl Univ, Dept Biomed Sci, Grad Sch, Seoul, South Korea;Seoul Natl Univ, Canc Res Inst, Seoul, South Korea.
    Christiansen, Hans
    Hannover Med Sch, Dept Radiat Oncol, Hannover, Germany.
    Clarke, Christine L.
    Univ Sydney, Westmead Inst Med Res, Sydney, NSW, Australia.
    Couch, Fergus J.
    Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
    Czene, Kamila
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Daly, Mary B.
    Fox Chase Canc Ctr, Dept Clin Genet, 7701 Burholme Ave, Philadelphia, PA 19111 USA.
    dos-Santos-Silva, Isabel
    London Sch Hyg & Trop Med, Dept Noncommunicable Dis Epidemiol, London, England.
    Dwek, Miriam
    Univ Westminster, Fac Sci & Technol, Dept Biomed Sci, London, England.
    Eccles, Diana M.
    Univ Southampton, Canc SciencesAcad Unit, Fac Med, Southampton, Hants, England.
    Ekici, Arif B.
    Friedrich Alexander Univ Erlangen Nuremberg, Univ Hosp Erlangen, Comprehens Canc Ctr Erlangen EMN, Inst Human Genet, Erlangen, Germany.
    Eriksson, Mikael
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Evans, D. Gareth
    Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Biol, Sch Biol Sci,Div Evolut & Genom Sci, Manchester, Lancs, England;Manchester Univ Hosp NHS Fdn Trust, St Marys Hosp, Manchester Acad Hlth Sci Ctr, Manchester Ctr Genom Med, Manchester, Lancs, England.
    Fasching, Peter A.
    Friedrich Alexander Univ Erlangen Nuremberg, Univ Hosp Erlangen, Comprehens Canc Ctr ER EMN, Dept Gynecol & Obstet, Erlangen, Germany;Univ Calif Los Angeles, Dept Med, David Geffen Sch Med, Div Hematol & Oncol, Los Angeles, CA 90024 USA.
    Figueroa, Jonine
    NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA;Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Med Sch, Edinburgh, Midlothian, Scotland;Canc Res UK Edinburgh Ctr, Edinburgh, Midlothian, Scotland.
    Flyger, Henrik
    Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Dept Breast Surg, Herlev, Denmark.
    Fritschisl, Lin
    Curtin Univ, Sch Publ Hlth, Perth, WA, Australia.
    Gabrielson, Marike
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Gago-Dominguez, Manuela
    Complejo Hosp Univ Santiago, SERGAS, Inst Invest Sanitaria Santiago de Compostela IDIS, Genom Med Grp,Galician Fdn Genom Med, Santiago De Compostela, Spain;Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
    Gao, Chi
    Harvard TH Chan Sch Publ Hlth, Program Genet Epidemiol & Stat Genet, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Gapstur, Susan M.
    Amer Canc Soc, Behav & Epidemiol Res Grp, Atlanta, GA 30329 USA.
    Garcia-Closas, Montserrat
    NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA;Inst Canc Res, Div Genet & Epidemiol, London, England.
    Garcia-Saenz, Jose A.
    Ctr Invest Biomed Red Canc CIBERONC, Inst Invest Sanitaria San Carlos IdISSC, Hosp Clin San Carlos, Med Oncol Dept, Madrid, Spain.
    Gaudet, Mia M.
    Amer Canc Soc, Behav & Epidemiol Res Grp, Atlanta, GA 30329 USA.
    Giles, Graham G.
    Canc Council Victoria, Canc Epidemiol Div, Melbourne, Vic, Australia;Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia;Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic, Australia.
    Goldberg, Mark S.
    McGill Univ, Dept Med, Montreal, PQ, Canada;McGill Univ, Royal Victoria Hosp, Div Clin Epidemiol, Montreal, PQ, Canada.
    Goldgar, David E.
    Univ Utah, Sch Med, Huntsman Canc Inst, Dept Dermatol, Salt Lake City, UT USA.
    Guenel, Pascal
    Univ Paris Sud, Univ Paris Saclay, INSERM, Canc & Environm Grp,Ctr Res Epidemiol & Populat H, Villejuif, France.
    Haeberle, Lothar
    Friedrich Alexander Univ Erlangen Nuremberg, Comprehens Canc Ctr Erlangen EMN, Univ Hosp Erlangen, Dept Gynaecol & Obstet, Erlangen, Germany.
    Haiman, Christopher A.
    Univ Southern Calif, Dept Prevent Med, Keck Sch Med, Los Angeles, CA USA.
    Hakansson, Niclas
    Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Hall, Per
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden;Soder Sjukhuset, Dept Oncol, Stockholm, Sweden.
    Hamann, Ute
    German Canc Res Ctr, Mol Genet Breast Canc, Heidelberg, Germany.
    Hartman, Mikael
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore;Natl Univ Hlth Syst, Dept Surg, Singapore, Singapore.
    Hauke, Jan
    Univ Cologne, Fac Med, Ctr Familial Breast & Ovarian Canc, Cologne, Germany;Univ Cologne, Univ Hosp Cologne, Cologne, Germany;Univ Cologne, Fac Med, CMMC, Cologne, Germany;Univ Cologne, Fac Med, CIO, Cologne, Germany.
    Hein, Alexander
    Friedrich Alexander Univ Erlangen Nuremberg, Univ Hosp Erlangen, Comprehens Canc Ctr ER EMN, Dept Gynecol & Obstet, Erlangen, Germany.
    Hillemanns, Peter
    Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany.
    Hogervorst, Frans B. L.
    Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Family Canc Clin, Amsterdam, Netherlands.
    Hooning, Maartje J.
    Erasmus MC Canc Inst, Dept Med Oncol, Family Canc Clin, Rotterdam, Netherlands.
    Hopper, John L.
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia.
    Howell, Tony
    Univ Manchester, Div Canc Sci, Manchester, Lancs, England.
    Huo, Dezheng
    Univ Chicago, Ctr Clin Canc Genet, Chicago, IL 60637 USA.
    Ito, Hidemi
    Aichi Canc Ctr Res Inst, Div Canc Epidemiol & Prevent, Nagoya, Aichi, Japan;Nagoya Univ, Div Canc Epidemiol, Grad Sch Med, Nagoya, Aichi, Japan.
    Iwasaki, Motoki
    Natl Canc Ctr, Ctr Publ Hlth Sci, Div Epidemiol, Tokyo, Japan.
    Jakubowska, Anna
    Pomeranian Med Univ, Dept Genet & Pathol, Szczecin, Poland;Pomeranian Med Univ, Lab Mol Biol & Genet Diagnost, Szczecin, Poland.
    Janni, Wolfgang
    Univ Hosp Ulm, Dept Gynaecol & Obstet, Ulm, Germany.
    John, Esther M.
    Stanford Univ, Sch Med, Stanford Canc Inst, Div Oncol,Dept Med, Stanford, CA USA.
    Jung, Audrey
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
    Kaaks, Rudolf
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
    Kang, Daehee
    Seoul Natl Univ, Dept Biomed Sci, Grad Sch, Seoul, South Korea;Seoul Natl Univ, Canc Res Inst, Seoul, South Korea;Seoul Natl Univ, Dept Prevent Med, Coll Med, Seoul, South Korea.
    Kapoor, Pooja Middha
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany;Heidelberg Univ, Fac Med, Heidelberg, Germany.
    Khusnutdinova, Elza
    Russian Acad Sci, Ufa Fed Res Ctr, Inst Biochem & Genet, Ufa, Russia;Bashkir State Univ, Dept Genet & Fundamental Med, Ufa, Russia.
    Kim, Sung-Won
    Daer St Marys Hosp, Dept Surg, Seoul, South Korea.
    Kitahara, Cari M.
    NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
    Koutros, Stella
    NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
    Kraft, Peter
    Harvard TH Chan Sch Publ Hlth, Program Genet Epidemiol & Stat Genet, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Kristensen, Vessela N.
    Oslo Univ Hosp, Radiumhosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway;Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway.
    Kwon, Ava
    Canc Genet Ctr, Hong Kong Hereditary Breast Canc Family Registry, Happy Valley, Hong Kong, Peoples R China;Univ Hong Kong, Dept Surg, Pok Fu Lam, Hong Kong, Peoples R China;Hong Kong Sanat & Hosp, Dept Surg, Happy Valley, Hong Kong, Peoples R China.
    Lambrechts, Diether
    VIB, VIB Ctr Canc Biol, Leuven, Belgium;Univ Leuven, Dept Human Genet, Lab Translat Genet, Leuven, Belgium.
    Le Marchand, Loic
    Univ Hawaii, Epidemiol Program, Canc Ctr, Honolulu, HI 96822 USA.
    Li, Jingmei
    Genome Inst Singapore, Human Genet Div, Singapore, Singapore.
    Lindstrom, Sara
    Univ Washington, Dept Epidemiol, Sch Publ Hlth, Seattle, WA 98195 USA;Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
    Linet, Martha
    NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
    Lo, Wing-Yee
    Dr Margarete Fischer Bosch Inst Clin Pharmacol, Stuttgart, Germany;Univ Tubingen, Tubingen, Germany.
    Long, Jirong
    Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Div Epidemiol,Dept Med,Vanderbilt Epidemiol Ctr, Nashville, TN 37212 USA.
    Lophatananon, Artitaya
    Univ Manchester, Fac Biol Med & Hlth, Sch Hlth Sci, Div Populat Hlth,Hlth Serv Res & Primary Care, Manchester, Lancs, England.
    Lubinski, Jan
    Pomeranian Med Univ, Dept Genet & Pathol, Szczecin, Poland.
    Manoochehri, Mehdi
    German Canc Res Ctr, Mol Genet Breast Canc, Heidelberg, Germany.
    Manoukian, Siranoush
    Fdn IRCCS Ist Nazl Tumori Milano, Dept Med Oncol & Hematol, Unit Med Genet, Milan, Italy.
    Margolin, Sara
    Soder Sjukhuset, Dept Oncol, Stockholm, Sweden;Karolinska Inst, Sodersjukhuset, Dept Clin Sci & Educ, Stockholm, Sweden.
    Martinez, Elena
    Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA;Univ Calif San Diego, Dept Family Med & Publ Hlth, La Jolla, CA 92093 USA.
    Matsuo, Keitaro
    Aichi Canc Ctr Res Inst, Div Canc Epidemiol & Prevent, Nagoya, Aichi, Japan;Nagoya Univ, Div Canc Epidemiol, Grad Sch Med, Nagoya, Aichi, Japan.
    Mavroudis, Dimitris
    Univ Hosp Heraklion, Dept Med Oncol, Iraklion, Greece.
    Meindl, Alfons
    Ludwig Maximilian Univ Munich, Dept Gynecol & Obstet, Munich, Germany.
    Menon, Usha
    UCL, Inst Clin Trials & Methodol, MRC Clin Trials Unit, London, England.
    Milne, Roger L.
    Canc Council Victoria, Canc Epidemiol Div, Melbourne, Vic, Australia;Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia;Monash Univ, Sch Clin Sci, Precis Med, Monash Hlth, Clayton, Vic, Australia.
    Taib, Nur Aishah Mohd
    Univ Malaya, UM Canc Res Inst, Breast Canc Res Unit, Med Ctr, Kuala Lumpur, Malaysia.
    Muir, Kenneth
    Univ Warwick, Warwick Med Sch, Div Hlth Sci, Coventry, W Midlands, England;Univ Manchester, Fac Biol Med & Hlth, Sch Hlth Sci, Div Populat Hlth,Hlth Serv Res & Primary Care, Manchester, Lancs, England.
    Mulligan, Anna Marie
    Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada;Univ Hlth Network, Lab Med Program, Toronto, ON, Canada.
    Neuhausen, Susan L.
    City Hope Natl Med Ctr, Dept Populat Sci, Beckman Res Inst, Duarte, CA USA.
    Nevanlinna, Heli
    Univ Helsinki, Helsinki Univ Hosp, Dept Obstet & Gynecol, Helsinki, Finland.
    Neven, Patrick
    Univ Hosp Leuven, Leuven Multidisciplinary Breast Ctr, Leuven Canc Inst, Dept OfOncol, Leuven, Belgium.
    Newman, William G.
    Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Biol, Sch Biol Sci,Div Evolut & Genom Sci, Manchester, Lancs, England;Manchester Univ Hosp NHS Fdn Trust, St Marys Hosp, Manchester Acad Hlth Sci Ctr, Manchester Ctr Genom Med, Manchester, Lancs, England.
    Offit, Kenneth
    Mem Sloan Kettering Canc Ctr, Clin Genet Res Lab, Dept Canc Biol & Genet, 1275 York Ave, New York, NY 10021 USA;Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, 1275 York Ave, New York, NY 10021 USA.
    Olopade, Olufunmilayo, I
    Univ Chicago, Ctr Clin Canc Genet, Chicago, IL 60637 USA.
    Olshan, Andrew F.
    Univ North Carolina Chapel Hill, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA;Univ North Carolina Chapel Hill, UNC Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA.
    Olson, Janet E.
    Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
    Olsson, Hakan
    Lund Univ, Dept Canc Epidemiol, Clin Sci, Lund, Sweden.
    Park, Sue K.
    Seoul Natl Univ, Dept Biomed Sci, Grad Sch, Seoul, South Korea;Seoul Natl Univ, Canc Res Inst, Seoul, South Korea;Seoul Natl Univ, Dept Prevent Med, Coll Med, Seoul, South Korea.
    Park-Simon, Tjoung-Won
    Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany.
    Peto, Julian
    London Sch Hyg & Trop Med, Dept Noncommunicable Dis Epidemiol, London, England.
    Plaseska-Karanfilska, Dijana
    Macedonian Acad Sci & Arts, Res Ctr Genet Engn & Biotechnol Georgi D Efremov, Skopje, Macedonia.
    Pohl-Rescigno, Esther
    Univ Cologne, Fac Med, Ctr Familial Breast & Ovarian Canc, Cologne, Germany;Univ Cologne, Univ Hosp Cologne, Cologne, Germany;Univ Cologne, Fac Med, CMMC, Cologne, Germany;Univ Cologne, Fac Med, CIO, Cologne, Germany.
    Presneau, Nadege
    Univ Westminster, Fac Sci & Technol, Dept Biomed Sci, London, England.
    Rack, Brigitte
    Univ Hosp Ulm, Dept Gynaecol & Obstet, Ulm, Germany.
    Radice, Paolo
    Fdn IRCCS Ist Nazl Tumori INT, Dept Res, Unit Mol Bases Genet Risk & Genet Testing, Milan, Italy.
    Rashid, Muhammad U.
    German Canc Res Ctr, Mol Genet Breast Canc, Heidelberg, Germany;Shaukat Khanum Mem Canc Hosp & Res Ctr SKMCH & RC, Dept Basic Sci, Lahore, Pakistan.
    Rennert, Gad
    Carmel Hosp, Clalit Natl Canc Control Ctr, Haifa, Israel;Technion Fac Med, Haifa, Israel.
    Rennert, Hedy S.
    Carmel Hosp, Clalit Natl Canc Control Ctr, Haifa, Israel;Technion Fac Med, Haifa, Israel.
    Romero, Atocha
    Hosp Univ Puerta Hierro, Med Oncol Dept, Madrid, Spain.
    Ruebner, Matthias
    Friedrich Alexander Univ Erlangen Nuremberg, Comprehens Canc Ctr Erlangen EMN, Univ Hosp Erlangen, Dept Gynaecol & Obstet, Erlangen, Germany.
    Saloustros, Emmanouil
    Univ Hosp Larissa, Dept Oncol, Larisa, Greece.
    Schmidt, Marjanka K.
    Antoni von Leeuwenhoek Hosp, Div Mol Pathol, Netherlands Canc Inst, Amsterdam, Netherlands;Antoni von Leeuwenhoek Hosp, Div Psychosocial Res & Epidemiol, Netherlands Canc Inst, Amsterdam, Netherlands.
    Schmutzler, Rita K.
    Univ Cologne, Fac Med, Ctr Familial Breast & Ovarian Canc, Cologne, Germany;Univ Cologne, Univ Hosp Cologne, Cologne, Germany;Univ Cologne, Fac Med, CMMC, Cologne, Germany;Univ Cologne, Fac Med, CIO, Cologne, Germany.
    Schneider, Michael O.
    Friedrich Alexander Univ Erlangen Nuremberg, Comprehens Canc Ctr Erlangen EMN, Univ Hosp Erlangen, Dept Gynaecol & Obstet, Erlangen, Germany.
    Schoemaker, Minouk J.
    Inst Canc Res, Div Genet & Epidemiol, London, England.
    Scott, Christopher
    Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
    Shen, Chen-Yang
    Acad Sinica, Inst Biomed Sci, Taipei, Taiwan;China Med Univ, Sch Publ Hlth, Taichung, Taiwan.
    Shu, Xiao-Ou
    Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Div Epidemiol,Dept Med,Vanderbilt Epidemiol Ctr, Nashville, TN 37212 USA.
    Simard, Jacques
    Univ Laval, CHU Quebec, Res Ctr, Genom Ctr, Quebec City, PQ, Canada.
    Slager, Susan
    Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
    Smichkoska, Snezhana
    Ss Cyril & Methodius Univ Skopje, Med Fac, Univ Clin Radiotherapy & Oncol, Skopje, Macedonia.
    Southey, Melissa C.
    Monash Univ, Sch Clin Sci, Precis Med, Monash Hlth, Clayton, Vic, Australia;Univ Melbourne, Dept Clin Pathol, Melbourne, Vic, Australia.
    Spinelli, John J.
    BC Canc, Populat Oncol, Vancouver, BC, Canada;Univ British Columbia, Sch Populat & Publ Hlth, Vancouver, BC, Canada.
    Stone, Jennifer
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia;Curtin Univ, Curtin UWA Ctr Genet Origins Hlth & Dis, Perth, WA, Australia;Univ Western Australia, Perth, WA, Australia.
    Surowy, Harald
    German Canc Res Ctr, Mol Epidemiol Grp, C080, Heidelberg, Germany;Heidelberg Univ, Univ Womens Clin Heidelberg, Mol Biol Breast Canc, Heidelberg, Germany.
    Swerdlow, Anthony J.
    Inst Canc Res, Div Genet & Epidemiol, London, England;Inst Canc Res, Div Breast Canc Res, London, England.
    Tamimi, Rulla M.
    Harvard TH Chan Sch Publ Hlth, Program Genet Epidemiol & Stat Genet, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA 02115 USA.
    Tapper, William J.
    Univ Southampton, Fac Med, Southampton, Hants, England.
    Teo, Soo H.
    Univ Malaya, UM Canc Res Inst, Breast Canc Res Unit, Med Ctr, Kuala Lumpur, Malaysia;Canc Res Malaysia, Subang Jaya, Selangor, Malaysia.
    Terry, Mary Beth
    Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA.
    Toland, Amanda E.
    Ohio State Univ, Dept Canc Biol & Genet, Columbus, OH 43210 USA.
    Tollenaar, Rob A. E. M.
    Leiden Univ, Dept Surg, Med Ctr, Leiden, Netherlands.
    Torres, Diana
    German Canc Res Ctr, Mol Genet Breast Canc, Heidelberg, Germany;Pontificia Univ Javeriana, Inst Human Genet, Bogota, Colombia.
    Torres-Mejia, Gabriela
    Natl Inst Publ Hlth, Ctr Populat Hlth Res, Mexico City, DF, Mexico.
    Troester, Melissa A.
    Univ North Carolina Chapel Hill, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA;Univ North Carolina Chapel Hill, UNC Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA.
    Truong, Therese
    Univ Paris Sud, Univ Paris Saclay, INSERM, Canc & Environm Grp,Ctr Res Epidemiol & Populat H, Villejuif, France.
    Tsugane, Shoichiro
    Natl Canc Ctr, Ctr Publ Hlth Sci, Tokyo, Japan.
    Untch, Michael
    Helios Clin Berlin Buch, Dept Gynecol & Obstet, Berlin, Germany.
    Vachon, Celine M.
    Mayo Clin, Div Epidemiol, Dept Hlth Sci Res, Rochester, MN USA.
    van den Ouweland, Ans M. W.
    Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands.
    van Veen, Elke M.
    Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Biol, Sch Biol Sci,Div Evolut & Genom Sci, Manchester, Lancs, England;Manchester Univ Hosp NHS Fdn Trust, St Marys Hosp, Manchester Acad Hlth Sci Ctr, Manchester Ctr Genom Med, Manchester, Lancs, England.
    Vijai, Joseph
    Mem Sloan Kettering Canc Ctr, Clin Genet Res Lab, Dept Canc Biol & Genet, 1275 York Ave, New York, NY 10021 USA;Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, 1275 York Ave, New York, NY 10021 USA.
    Wendt, Camilla
    Karolinska Inst, Sodersjukhuset, Dept Clin Sci & Educ, Stockholm, Sweden.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Yu, Jyh-Cherng
    Triserv Gen Hosp, Natl Def Med Ctr, Dept Surg, Taipei, Taiwan.
    Zheng, Wei
    Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Div Epidemiol,Dept Med,Vanderbilt Epidemiol Ctr, Nashville, TN 37212 USA.
    Ziogas, Argyrios
    Univ Calif Irvine, Dept Epidemiol, Genet Epidemiol Res Inst, Irvine, CA USA.
    Ziv, Elad
    Univ Calif San Francisco, UCSF Helen Diller Family Comprehens Canc Ctr, Inst Human Genet, Dept Med, San Francisco, CA 94143 USA.
    Dunning, Alison M.
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Oncol, Cambridge, England.
    Pharoah, Paul D. P.
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England;Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Oncol, Cambridge, England.
    Schindler, Detlev
    Univ Wurzburg, Bioctr, Inst Human Genet, Wurzburg, Germany.
    Devilee, Peter
    Leiden Univ, Dept Pathol, Med Ctr, Leiden, Netherlands;Leiden Univ, Dept Human Genet, Med Ctr, Leiden, Netherlands.
    Easton, Douglas F.
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England;Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Oncol, Cambridge, England.
    Balleine, Rosemary
    Pathol West ICPMR, Sydney, NSW, Australia.
    Baxter, Robert
    Univ Sydney, Royal North Shore Hosp, Kollig Inst Med Res, Sydney, NSW, Australia.
    Braye, Stephen
    John Hunter Hosp, Pathol North, Newcastle, NSW, Australia.
    Carpenter, Jane
    Univ Sydney, Westmead Inst Med Res, Sydney, NSW, Australia.
    Dahlstrom, Jane
    Canberra Hosp, Dept Anat Pathol, ACT Pathol, Canberra, ACT, Australia;Australian Natl Univ, ANU Med Sch, Canberra, ACT, Australia.
    Forbes, John
    Univ Newcastle, Dept Surg Oncol, Calvary Mater Newcastle Hosp, Australian New Zealand Breast Canc Trials Grp, Newcastle, NSW, Australia;Univ Newcastle, Sch Med & Publ Hlth, Newcastle, NSW, Australia.
    Lee, C. Soon
    Univ Western Sydney, Sch Sci & Hlth, Sydney, NSW, Australia.
    Marsh, Deborah
    Univ Sydney, Royal North Shore Hosp, Kolling Inst Med Res, Hormones & Canc Grp, Sydney, NSW, Australia.
    Morey, Adrienne
    Syd Path St Vincents Hosp, Sydney, NSW, Australia.
    Pathmanathan, Nirmala
    Westmead Hosp, Westmead Breast Canc Inst, Dept Tissue Pathol & Diagnost Oncol, Pathol West, Sydney, NSW, Australia.
    Scott, Rodney
    Hunter Med Res Inst, Ctr Informat Based Med, Newcastle, NSW, Australia;Univ Newcastle, Fac Hlth, Prior Res Ctr Canc, Sch Biomed Sci & Pharm, Newcastle, NSW, Australia.
    Simpson, Peter
    Univ Queensland, UQ Ctr Clin Res & Sch Med, Brisbane, Qld, Australia.
    Spigelman, Allan
    St Vincents Hosp, Kinghorn Canc Ctr, Hereditary Canc Clin, Sydney, NSW, Australia.
    Wilcken, Nicholas
    Westmead Hosp, Crown Princess Mary Canc Ctr, Sydney, NSW, Australia;Univ Sydney, Sydney Med Sch Westmead, Sydney, NSW, Australia.
    Yip, Desmond
    Australian Natl Univ, ANU Med Sch, Canberra, ACT, Australia;Canberra Hosp, Dept Med Oncol, Canberra, ACT, Australia.
    Zeps, Nikolajs
    St John God Perth Northern Hosp, Perth, WA, Australia.
    Borresen-Dale, Anne-Lise
    Oslo Univ Hosp, Radiumhosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway;Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway.
    Alnaes, Grethe I. Grenaker
    Oslo Univ Hosp, Radiumhosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway.
    Sahlberg, Kristine K.
    Oslo Univ Hosp, Radiumhosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway;Vestre Viken Hosp, Dept Res, Drammen, Norway;Oslo Univ Hosp, Breast Canc Res Consortium, Oslo, Norway.
    Ottestad, Lars
    Oslo Univ Hosp, Radiumhosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway.
    Karesen, Rolf
    Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway;Oslo Univ Hosp Ulleval, Div Surg Canc & Transplantat Med, Dept Canc, Sect Breast & Endocrine Surg, Oslo, Norway.
    Schlichting, Ellen
    Oslo Univ Hosp Ulleval, Div Surg Canc & Transplantat Med, Dept Canc, Sect Breast & Endocrine Surg, Oslo, Norway.
    Holmen, Marit Muri
    Oslo Univ Hosp, Dept Radiol & Nucl Med, Oslo, Norway.
    Sauer, Toril
    Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway;Akershus Univ Hosp, Dept Pathol, Lorenskog, Norway.
    Haakensen, Vilde
    Oslo Univ Hosp, Radiumhosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway.
    Engebraten, Olav
    Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway;Oslo Univ Hosp, Inst Canc Res, Dept Tumor Biol, Oslo, Norway;Oslo Univ Hosp, Dept Oncol, Div Surg Canc & Transplantat Med, Radiumhosp, Oslo, Norway.
    Naume, Bjorn
    Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway;Oslo Univ Hosp, Dept Oncol, Div Surg Canc & Transplantat Med, Radiumhosp, Oslo, Norway.
    Fossa, Alexander
    Oslo Univ Hosp, Dept Oncol, Div Surg Canc & Transplantat Med, Radiumhosp, Oslo, Norway;Oslo Univ Hosp, Natl Advisory Unit Late Effects Canc Treatment, Radiumhosp, Oslo, Norway.
    Kiserud, Cecile E.
    Oslo Univ Hosp, Dept Oncol, Div Surg Canc & Transplantat Med, Radiumhosp, Oslo, Norway;Oslo Univ Hosp, Natl Advisory Unit Late Effects Canc Treatment, Radiumhosp, Oslo, Norway.
    Reinertsen, Kristin, V
    Oslo Univ Hosp, Dept Oncol, Div Surg Canc & Transplantat Med, Radiumhosp, Oslo, Norway;Oslo Univ Hosp, Natl Advisory Unit Late Effects Canc Treatment, Radiumhosp, Oslo, Norway.
    Helland, Aslaug
    Oslo Univ Hosp, Radiumhosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway;Oslo Univ Hosp, Dept Oncol, Div Surg Canc & Transplantat Med, Radiumhosp, Oslo, Norway.
    Riis, Margit
    Oslo Univ Hosp Ulleval, Div Surg Canc & Transplantat Med, Dept Canc, Sect Breast & Endocrine Surg, Oslo, Norway.
    Geisler, Juergen
    Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway;Akershus Univ Hosp, Dept Oncol, Lorenskog, Norway.
    Two truncating variants in FANCC and breast cancer risk2019In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 9, article id 12524Article in journal (Refereed)
    Abstract [en]

    Fanconi anemia (FA) is a genetically heterogeneous disorder with 22 disease-causing genes reported to date. In some FA genes, monoallelic mutations have been found to be associated with breast cancer risk, while the risk associations of others remain unknown. The gene for FA type C, FANCC, has been proposed as a breast cancer susceptibility gene based on epidemiological and sequencing studies. We used the Oncoarray project to genotype two truncating FANCC variants (p.R185X and p.R548X) in 64,760 breast cancer cases and 49,793 controls of European descent. FANCC mutations were observed in 25 cases (14 with p.R185X, 11 with p.R548X) and 26 controls (18 with p.R185X, 8 with p.R548X). There was no evidence of an association with the risk of breast cancer, neither overall (odds ratio 0.77, 95% CI 0.44-1.33, p = 0.4) nor by histology, hormone receptor status, age or family history. We conclude that the breast cancer risk association of these two FANCC variants, if any, is much smaller than for BRCA1, BRCA2 or PALB2 mutations. If this applies to all truncating variants in FANCC it would suggest there are differences between FA genes in their roles on breast cancer risk and demonstrates the merit of large consortia for clarifying risk associations of rare variants.

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  • 125.
    Ekman, Anna
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Petren-Mallmin, M.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Ljunghall, Sverker
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Mallmin, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    DXA of the hip and heel ultrasound but not densitometry of the fingers can discriminate female hip fracture patients from controls: a comparison between four different methods2001In: Osteoporosis International, ISSN 0937-941X, E-ISSN 1433-2965, Vol. 12, no 3, p. 185-191Article in journal (Refereed)
    Abstract [en]

    Dual-energy X-ray absorptiometry (DXA) of the proximal femur and in more recent years quantitative ultrasound (QUS) of the heel are the most established methods for assessing hip fracture risk. Measurement of the fingers offers a new approach. We performed DXA of the proximal femur, QUS of the heel and fingers, and radiographic absorptiometry (RA) of the fingers in 87 non-institutionalized women, 65-85 years of age, with a first hip fracture and compared them with 195 randomly selected age-matched controls. Bone mineral density (BMD) of the femoral neck and heel Stiffness Index were significantly lower among cases than among controls (by 15% and 17%, respectively; p < 0.0001), whereas no significant differences were found for finger measurements. When applying the WHO criterion of osteoporosis, 62-98% of the patients were classified as osteoporotic, compared with 19-85% of the controls, depending on method and site. The risks of hip fracture, estimated as odds ratios for every 1 SD reduction in femoral neck BMD, heel Stiffness Index, finger QUS and finger RA, were: 3.6 (95% CI 2.4-5.5), 3.4 (95% CI 2.2-5.0), 1.0 (95% CI 0.7-1.3) and 1.2 (95% CI 0.8-1.6), respectively. Compared with women with normal BMD of the femoral neck, those classified as osteopenic had an odds ratio of hip fracture of 14 (95% CI 2-110), whereas those classified as osteoporotic had an odds ratio of 63 (95% CI 8-501). We conclude that hip DXA and heel QUS have similar capacities to discriminate the risk of a first hip fracture, whereas QUS and RA of the phalanges seem inferior techniques for differentiating female hip fracture patients from controls.

  • 126.
    Ekman, Anna
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Petrén-Mallmin, M.
    Ljunghall, Sverker
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Mallmin, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Dual X-ray absorptiometry of hip, heel ultrasound, and densitometry of fingers can discriminate male patients with hip fracture from control subjects: a comparison of four different methods2002In: Journal of clinical densitometry, ISSN 1094-6950, E-ISSN 1559-0747, Vol. 5, no 1, p. 79-85Article in journal (Refereed)
    Abstract [en]

    Few studies have examined different bone densitometry techniques to determine male hip fracture risk. We conducted a case-control study of 31 noninstitutionalized men, mean age 77 yr, with a first hip fracture and compared the results with 68 randomly selected age-matched control subjects. The methods used were dual X-ray absorptiometry (DXA) of the proximal femur, quantitative ultrasound (QUS) of the heel and fingers, and radiographic absorptiometry of the fingers. Case patients had significantly lower values (4-17%; p < 0.01) for all methods. The odds ratios for every SD reduction in bone values were 4.8 (95% confidence interval [CI]: 2.3-9.9) for DXA of the femoral neck, 2.2 (95% CI: 1.2-3.9) for QUS of the heel, 2.0 (95% CI: 1.2-3.3) for QUS of the phalanges, and 3.1 (95% CI: 1.5-6.6) for radiographic absorptiometry of the phalanges. The results indicate a strong capability of DXA of the femoral neck to distinguish between men with a first hip fracture and control subjects. Furthermore, ultrasound of the heel and fingers as well as radiographic absorptiometry proved capable of discriminating men with hip fractures from control subjects.

  • 127. Ekström, Wilhelmina
    et al.
    Karlsson-Thur, Charlotte
    Larsson, Sune
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Ragnarsson, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Alberts, Karl-Akke
    Functional outcome in treatment of unstable trochanteric and subtrochanteric fractures with the proximal femoral nail and the Medoff sliding plate2007In: Journal of Orthopaedic Trauma, ISSN 0890-5339, E-ISSN 1531-2291, Vol. 21, no 1, p. 18-25Article in journal (Refereed)
    Abstract [en]

    Objective: To compare outcome between the proximal femoral nail (PFN) and the Medoff sliding plate (MSP) in patients with unstable trochanteric or subtrochanteric fractures.

    Methods: This was a consecutive prospective randomized clinical study. In all, 203 patients admitted to two university hospitals with an unstable trochanteric or a subtrochanteric fracture type were included. Surgery was performed with a short intramedullary nail or a dual-sliding plate device. Follow up visits occurred at 6 weeks, 4 months, and 12 months. Functional outcome was measured by walking ability, rising from a chair, curb test, and additional assessments of abductor strength, pain, living conditions, and complications.

    Results: The ability to walk 15 m at 6 weeks was significantly better in the PFN group compared to the MSP group with an odds ratio 2.2 (P = 0.04, 95% confidence limits 1.03-4.67). No statistical difference in walking ability could be found between trochanteric and subtrochanteric fractures. The major complication rate (8% in the PFN group and 4% in the MSP group) did not differ statistically (P = 0.50) but reoperations were more frequent in the PFN group (9%) compared to the MSP group (1%; P < 0.02).

    Conclusions: There were no major differences in functional outcome or major complications between the treatment groups. Reasons other than the operated fracture seem to be equally important in determining the long-term functional ability of the patients in our study. An advantage with the MSP was the lower reoperation rate.

  • 128.
    Eliasson, Pernilla
    et al.
    Linkoping Univ, Dept Clin & Expt Med, Fac Hlth Sci, Linkoping, Sweden.
    Dietrich-Zagonel, Franciele
    Linkoping Univ, Dept Clin & Expt Med, Fac Hlth Sci, Linkoping, Sweden.
    Lundin, Anna-Carin
    Linkoping Univ, Dept Clin & Expt Med, Fac Hlth Sci, Linkoping, Sweden.
    Aspenberg, Per
    Linkoping Univ, Dept Clin & Expt Med, Fac Hlth Sci, Linkoping, Sweden.
    Wolk, Alicja
    Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Statin treatment increases the clinical risk of tendinopathy through matrix metalloproteinase release - a cohort study design combined with an experimental study2019In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 9, article id 17958Article in journal (Refereed)
    Abstract [en]

    Recent experimental evidence indicates potential adverse effects of statin treatment on tendons but previous clinical studies are few and inconclusive. The aims of our study were, first, to determine whether statin use in a cohort design is associated with tendinopathy disorders, and second, to experimentally understand the pathogenesis of statin induced tendinopathy. We studied association between statin use and different tendon injuries in two population-based Swedish cohorts by time-dependent Cox regression analysis. Additionally, we tested simvastatin in a 3D cell culture model with human tenocytes. Compared with never-users, current users of statins had a higher incidence of trigger finger with adjusted hazard ratios (aHRs) of 1.50 for men (95% confidence interval [CI] 1.21-1.85) and 1.21 (1.02-1.43) for women. We also found a higher incidence of shoulder tendinopathy in both men (aHR 1.43; 1.24-1.65) and women (aHR 1.41; 0.97-2.05). Former users did not confer a higher risk of tendinopathies. In vitro experiments revealed an increased release of matrix metalloproteinase (MMP)-1 and MMP-13 and a weaker, disrupted matrix after simvastatin exposure. Current statin use seems to increase the risk of trigger finger and shoulder tendinopathy, possibly through increased MMP release, and subsequently, a weakened tendon matrix which will be more prone to injuries.

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  • 129.
    Elmekaty, Mohamed
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Tanta Univ, Tanta, Egypt.
    ElMehy, Emad
    Tanta Univ, Orthoped & Traumatol Dept, Tanta, Egypt.
    Försth, Peter
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    MacDowall, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    El Elemi, Ahmed
    Tanta Univ, Orthoped & Traumatol Dept, Tanta, Egypt.
    Hosni, Mohamed
    Tanta Univ, Orthoped & Traumatol Dept, Tanta, Egypt.
    Robinson, Yohan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Safety of a novel modular cage for transforaminal lumbar interbody fusion: clinical cohort study in 20 patients with degenerative disc disease2018In: SICOT-J, ISSN 2426-8887, Vol. 4, article id 24Article in journal (Refereed)
    Abstract [en]

    Introduction: Transforaminal lumbar interbody fusion (TLIF) is used to reconstruct disc height and reduce degenerative deformity in spinal fusion. Patients with osteoporosis are at high risk of TLIF cage subsidence; possibly due to the relatively small footprint compared to anterior interbody devices. Recently, modular TLIF cage with an integral rail and slot system was developed to reduce cage subsidence and allow early rehabilitation. Objective: To study the safety of a modular TLIF device in patients with degenerative disc disorders (DDD) with regard to surgical complications, non-union, and subsidence. Methods: Patients with DDD treated with a modular TLIF cage (Polyetheretherketone(PEEK), VTI interfuse S) were analysed retrospectively with one-year follow-up. Lumbar sagittal parameters were collected preoperatively, postoperatively and at one year follow-up. Cage subsidence, fusion rate, screw loosening and proportion of endplate coverage were assessed in computed tomography scan. Results: 20 patients (age 66 +/- 10 years, 65% female, BMI 28 +/- 5 kg/m(2)) with a total of 37 fusion levels were included. 15 patients had degenerative spondylosis and 5 patients had degenerative scoliosis. The cages covered >60% of the vertebral body diameters. Lumbar lordosis angle and segmental disc angle increased from 45.2 +/- 14.5 and 7.3 +/- 3.6 to 52.7 +/- 9.1 and 10.5 +/- 3.5 (p=0.029 and 0.0002) postoperatively for each parameter respectively without loss of correction at one year follow up. One case of deep postoperative infection occurred (5%). No cage subsidence occurred. No non-union or screw loosening occurred. Conclusions: The modular TLIF cage was safe with regard to subsidence and union-rate. It restored and maintained lumbar lordosis angle, segmental disc angle and disc height, which can be attributed to the large footprint of this modular cage.

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  • 130.
    Elmekaty, Mohamed
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Steel Mem Muroran Hosp, Spine & Spinal Cord Ctr, Muroran, Hokkaido, Japan;Tanta Univ, Fac Med, Dept Orthoped Surg, Tanta, Egypt.
    Kotani, Yoshihisa
    Steel Mem Muroran Hosp, Spine & Spinal Cord Ctr, Muroran, Hokkaido, Japan.
    El Mehy, Emad
    Tanta Univ, Fac Med, Dept Orthoped Surg, Tanta, Egypt.
    Robinson, Yohan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    El Tantawy, Ahmed
    Tanta Univ, Fac Med, Dept Orthoped Surg, Tanta, Egypt.
    Sekiguchi, Ivan
    Steel Mem Muroran Hosp, Spine & Spinal Cord Ctr, Muroran, Hokkaido, Japan.
    Fujita, Ryo
    Steel Mem Muroran Hosp, Spine & Spinal Cord Ctr, Muroran, Hokkaido, Japan.
    Clinical and Radiological Comparison between Three Different Minimally Invasive Surgical Fusion Techniques for Single-Level Lumbar Isthmic and Degenerative Spondylolisthesis: Minimally Invasive Surgical Posterolateral Fusion versus Minimally Invasive Surgical Transforaminal Lumbar Interbody Fusion versus Midline Lumbar Fusion2018In: Asian Spine Journal, ISSN 1976-1902, E-ISSN 1976-7846, Vol. 12, no 5, p. 870-879Article in journal (Refereed)
    Abstract [en]

    Study Design: Retrospective cohort study.

    Purpose: Comparison between three different minimally invasive surgical (MIS) fusion techniques for single-level lumbar spondylolisthesis.

    Overview of Literature: There has been an increase in the development and utilization of MIS techniques for lumbar spine fusion. No study has compared the efficacy of MIS-posterolateral fusion (MIS-PLF), MIS-transforaminal lumbar interbody fusion (MIS-TLIF), and midline lumbar fusion (MIDLF) with modified cortical bone trajectory screws for lumbar spondylolisthesis.

    Methods: Fifty-nine patients with single-level lumbar spondylolisthesis and a minimum follow-up period of 1 year were included in this study. The MIS-PLF, MIS-TLIF, and MIDLF groups included 22, 15, and 22 patients, respectively. The average age of the groups was 70.6, 49.3, and 62.7 years, respectively. The evaluation parameters were operation time, intraoperative bleeding, serum C-reactive protein (CAP) value, creatine kinase (CK) value, and overall functional outcome as per the Japanese Orthopedic Association Back Pain Evaluation Questionnaire (JOABPEQ) score. The changes in the lumbar lordosis angle (LLA), segmental disc angle (SDA), and disc height were measured. Fusion rate, screw loosening, and loss of correction were also assessed.

    Results: MIDLF showed a significantly shorter operation time (111 min), less bleeding amount (112.5 mL), and lower values of CRP and CK than the other two techniques. There was no significant difference in the JOABPEQ scores of the three groups. MIDLF resulted in a greater increase in the LLA and SDA postoperatively. MIDLF and MIS-TLIF resulted in a significant increase in the middle disc height compared with MIS-PLF. MIDLF showed a lower loss of correction after 6 months postoperatively (2.6%) than MIS-PLF (5.2%) and MIS-TLIF (4.2%). The fusion rate was 100% in the MIDLF and MIS-TLIF groups and 90% in the MIS-PLF group. Screw loosening occurred in 10% of the MIS-PLF cases, 7.14% of the MIS-TLIF cases, and 4.76% of the MIDLF cases.

    Conclusions: MIDLF was the least invasive, and there was no significant difference between the three groups in terms of fusion, screw loosening, and clinical outcomes.

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  • 131. Engstrom, Annette
    et al.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Vahter, Marie
    Julin, Bettina
    Wolk, Alicja
    Akesson, Agneta
    Associations between dietary cadmium exposure and bone mineral density and risk of osteoporosis and fractures among women2012In: Bone, ISSN 8756-3282, E-ISSN 1873-2763, Vol. 50, no 6, p. 1372-1378Article in journal (Refereed)
    Abstract [en]

    Osteoporosis and its main health outcome, fragility fractures, are large and escalating public health problems. Cadmium, a widespread food contaminant, is a proposed risk factor; still the association between estimated dietary cadmium exposure and bone mineral density (BMD) has never been assessed. Within a sub-cohort of the Swedish Mammography Cohort, we assessed dietary cadmium exposure based on a food frequency questionnaire (1997) and urinary cadmium (2004-2008) in relation to total-body BMD and risk of osteoporosis and fractures (1997-2009) among 2676 women (aged 56-69 years). In multivariable-adjusted linear regression, dietary cadmium was inversely associated with BMD at the total body and lumbar spine. After further adjustment for dietary factors important for bone health and cadmium bioavailability-calcium, magnesium, iron and fiber, the associations became more pronounced. A 32% increased risk of osteoporosis (95% Cl: 2-71%) and 31% increased risk for any first incident fracture (95% Cl; 2-69%) were observed comparing high dietary cadmium exposure (>= 13 mu g/day, median) with lower exposures (<13 mu g/day). By combining high dietary with high urinary cadmium (>= 0.50 mu g/g creatinine), odds ratios among never-smokers were 2.65 (95% Cl: 1.43-4.91) for osteoporosis and 3.05 (95% Cl; 1.66-5.59) for fractures. In conclusion, even low-level cadmium exposure from food is associated with low BMD and an increased risk of osteoporosis and fractures. The partial masking of the associations by essential nutrients indicates important interplay between dietary factors and contaminants present in food. In separate analyses, dietary and urinary cadmium underestimated the association with bone effects.

  • 132. Engström, Annette
    et al.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , UCR-Uppsala Clinical Research Center.
    Suwazono, Yasushi
    Wolk, Alicja
    Vahter, Marie
    Åkesson, Agneta
    Long-term cadmium exposure and the association with bone mineral density and fractures in a population-based study among women2011In: Journal of Bone and Mineral Research, ISSN 0884-0431, E-ISSN 1523-4681, Vol. 26, no 3, p. 486-495Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:: All people are exposed to cadmium (Cd) via food, smokers are additionally exposed. High Cd exposure is associated with severe bone damage, but the public health impact in relation to osteoporosis and fractures at low environmental exposure remains to be clarified. METHODS:: Within the population-based Swedish Mammography Cohort, we assessed urinary Cd (U-Cd, mug/g creatinine, cr) as a marker of life-time exposure and bone mineral density (BMD) by DXA among 2,688 women. Register-based information on fractures was retrieved from 1997 to 2009. Associations were evaluated by multivariable regression analyses. RESULTS:: In linear regression U-Cd was inversely associated with BMD at the total body (p<0.001), femoral neck (p=0.025), total hip (p=0.004), lumbar spine (p=0.088), and volumetric femoral neck (p=0.013). In comparison to women with U-Cd <0.50 mug/g cr, those with U-Cd >/=0.75 mug/g cr had OR 2.45 (95% CI, 1.51-3.97) and 1.97 (95% CI, 1.24-3.14) for osteoporosis at the femoral neck and lumbar spine, respectively. Among never-smokers, the corresponding ORs were 3.45 (95% CI, 1.46-8.23) and 3.26 (95% CI, 1.44-7.38). For any first fracture (n=395) OR was 1.16 (95% CI, 0.89-1.50) comparing U-Cd >/=0.5 mug/g cr with lower levels. Among never-smokers, the ORs (95% CIs) were 2.03 (1.33-3.09) for any first fracture, 2.06 (1.28-3.32) for first osteoporotic fracture, 2.18 (1.20-3.94) for first distal forearm fracture and 1.89 (1.25-2.85) for multiple incident fractures. CONCLUSIONS:: U-Cd at low environmental exposure from food in a general population of women showed modest but significant association with both BMD and fractures especially in never smokers indicating a larger concern than previously known.

  • 133.
    Engström, Joakim
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Reinius, Henrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Ström, Jennie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Bergström, Monica Frick
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Education in Nursing.
    Larsson, Ing-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Borg, Tomas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Lung complications are common in intensive care treated patients with pelvis fractures: a retrospective cohort study2016In: Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, ISSN 1757-7241, E-ISSN 1757-7241, Vol. 24, article id 52Article in journal (Refereed)
    Abstract [en]

    Background: The incidence of severe respiratory complications in patients with pelvis fractures needing intensive care have not previously been studied. Therefore, the aims of this registry study were to 1) determine the number of ICU patients with pelvis fractures who had severe respiratory complications 2) whether the surgical intervention in these patients is associated with the pulmonary condition and 3) whether there is an association between lung complications and mortality. We hypothesized that acute hypoxic failure (AHF) and acute respiratory distress syndrome (ARDS) 1) are common in ICU treated patients with pelvis fractures, 2) are not related to the reconstructive surgery, or to 3) to mortality. Methods: All patients in the database cohort (n = 112), scheduled for surgical stabilization of pelvis ring and/or acetabulum fractures, admitted to the general ICU at Uppsala University Hospital between 2007 and 2014 for intensive care were included. Results: The incidence of AHF/ARDS was 67 % (75/112 patients), i.e., the percentage of patients that at any period during the ICU stay fulfilled the AHF/ARDS criteria. The incidence of AHF was 44 % and incidence of ARDS was 23 %. The patients with AHF/ARDS had more lung contusions and pneumonia than the patients without AHF/ARDS. Overall, there were no significant changes in oxygenation variables associated with surgery. However, 23 patients with pre-operative normal lung status developed AHF/ARDS in relation to the surgical procedure, whereas 12 patients with AHF/ARDS normalized their lung condition. The patients who developed AHF/ARDS had a higher incidence of lung contusion (P = 0.04) and the surgical stabilization was performed earlier (5 versus 10 days) in these patients (P = 0.03). Conclusions: We found that the incidence of respiratory failure in ICU treated patients with pelvis fractures was high, that the procedure around surgical stabilization seems to be associated with a worsening in the respiratory function in patients with lung contusion, and that mortality was low and was probably not related to the respiratory condition.

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  • 134.
    Engström, Joakim
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Reinius, Henrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Ström, Jennie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Frick Bergström, Monica
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Larsson, Ing-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Borg, Tomas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Lung complications in intensive care treated patients with pelvis fractures - common but probably not fatal: a retrospective cohort studyArticle in journal (Other academic)
  • 135.
    Eriksson, Hannah K.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Ahadpour, David
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Hailer, Nils
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Lazarinis, Stergios
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Järhult, Josef D.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Infectious Diseases.
    Linezolid in the treatment of periprosthetic joint infection caused by coagulase-negative staphylococci2019In: Infectious Diseases, ISSN 2374-4235, E-ISSN 2374-4243, Vol. 51, no 9, p. 683-690Article in journal (Refereed)
    Abstract [en]

    Background: Periprosthetic joint infection (PJI) caused by coagulase-negative staphylococci (CoNS) is increasingly common and is sometimes treated with off-label use of linezolid.

    Methods: We conducted a retrospective study of patients with PJI caused by CoNS treated with surgical intervention and orally administrated linezolid during the period 1995-2014 (n = 28). Clinical outcomes and adverse events related to linezolid administration were evaluated. Mean time to follow-up was 4.3 years (range: 0.2-12).

    Results: Twenty-two of 28 patients were infection-free at follow-up. No CoNS strain was resistant to vancomycin, but 16 of 28 were resistant to rifampicin, 23 of 28 to clindamycin and 20 of 27 to quinolones. The mean duration of linezolid treatment was 4.2 weeks (range: 1-12). Eleven of 28 patients had an adverse event related to the antimicrobial treatment, and four had to discontinue linezolid, but all adverse events were reversible within 2 months after discontinuation.

    Conclusions: Oral linezolid administration combined with adequate surgical treatment may be useful for the treatment of PJIs caused by CoNS.

  • 136.
    Eriksson, Hannah K.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Nordström, Jakob
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Gabrysch, Katja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Hailer, Nils P.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Lazarinis, Stergios
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Does the Alpha-defensin Immunoassay or the Lateral Flow Test Have Better Diagnostic Value for Periprosthetic Joint Infection?: A Systematic Review2018In: Clinical Orthopaedics and Related Research, ISSN 0009-921X, E-ISSN 1528-1132, Vol. 476, no 5, p. 1065-1072Article, review/survey (Refereed)
    Abstract [en]

    Background: Measuring alpha-defensin concentrations in synovial fluid may help to diagnose periprosthetic joint infection (PJI). There are two commercially available methods for measuring alpha-defensin in synovial fluid: the enzyme-linked immunosorbent assay-based Synovasure (R) alpha-defensin immunoassay, which gives a numeric readout within 24 hours, and the Synovasure lateral flow test, which gives a binary readout within 20 minutes. There is no compilation of the existing literature to support the use of one of these two tests over the other.

    Questions/purposes: Does the immunoassay or the lateral flow test have better diagnostic value (sensitivity and specificity) in diagnosing PJI?

    Methods: We followed PRISMA guidelines and identified all studies on alpha-defensin concentration in synovial fluid as a PJI diagnostic marker, indexed to April 14, 2017, in PubMed, JSTOR, Google Scholar, and OVID databases. The search retrieved 1578 records. All prospective and retrospective studies on alpha-defensin as a PJI marker (PJI classified according to the criteria of the Musculoskeletal Infection Society) after THA or TKA were included in the analysis. All studies used only one of the two commercially available test methods, but none of them was comparative. After excluding studies with overlapping patient populations, four studies investigating the alpha-defensin immunoassay and three investigating the lateral flow test remained. Alpha-defensin immunoassay studies included 482 joints and lateral flow test studies included 119. The quality of the trials was assessed according to the Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) tool. The heterogeneity among studies was evaluated by the I-2 index, indicating that the heterogeneity of the included studies was low. Pooled sensitivity, specificity, positive and negative likelihood ratios, and receiver operating curves were calculated for each method and compared with each other.

    Results: The alpha-defensin immunoassay had superior overall diagnostic value compared with the lateral flow test (area under the curve, 0.98 versus 0.75) with higher sensitivity (96% [90%-98%] versus 71% [55%-83%], p < 0.001), but no difference in specificity with the numbers available (96% [93%-97%] versus 90% [81%-95%], p = 0.060).

    Conclusions: Measurement of alpha-defensin in synovial fluid is a valuable complement to existing diagnostic criteria, and the immunoassay test detects PJI more accurately than the lateral flow test. The lateral flow test has lower sensitivity, making it difficult to rule out infection, but its relatively high specificity combined with the advantage of a quick response time can make it useful to rule in infection perioperatively.

    Level of Evidence: Level III, diagnostic study.

  • 137.
    Eriksson, Thomas
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Berg, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Olerud, Claes
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Shalabi, Adel
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Hänni, Mari
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Low-dose CT of postoperative pelvic fractures: a comparison with radiography2019In: Acta Radiologica, ISSN 0284-1851, E-ISSN 1600-0455, Vol. 60, no 1, p. 85-91Article in journal (Refereed)
    Abstract [en]

    Background Computed tomography (CT) is superior to conventional radiography (CR) for assessing internal fixation of pelvic fractures, but with a higher radiation exposure. Low-dose CT (LDCT) could possibly have a sufficient diagnostic accuracy but with a lower radiation dose. Purpose To compare postoperative diagnostic accuracy of LDCT and CR after open reduction and internal fixation of pelvic fracture. Material and Methods Twenty-one patients were examined with LDCT and CR 0-9 days after surgery. The examinations were reviewed by two musculoskeletal radiologists. Hardware, degree of fracture reduction, image quality, and reviewing time were assessed, and effective radiation dose was calculated. Inter-reader agreement was calculated. Results LDCT was significantly better than CR in determining whether hardware positioning was assessable ( P < 0.001). Acetabular congruence was assessable in all fractured patients with LDCT. In 12 of the 32 assessments with CR of patients with an acetabular fracture, joint congruence was not assessable due to overlapping hardware ( P = 0.001). Image quality was significantly higher for LDCT. Median time to review was 240 s for LDCT compared to 180 s for CR. Effective dose was 0.79 mSv for LDCT compared to 0.32 mSv for CR ( P < 0.001). Conclusion LDCT is more reliable than CR in assessing hardware position and fracture reduction. Joint congruency is sometimes not possible to assess with CR, due to overlapping hardware. The image quality is higher, but also the effective dose, with LDCT than with CR.

  • 138.
    Escala-Garcia, Maria
    et al.
    Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Divi Mol Pathol, Amsterdam, Netherlands.
    Abraham, Jean
    Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Cambridge, England;Cambridge Expt Canc Med Ctr, Cambridge, England;Univ Cambridge NHS Fdn Hosp, NIHR Cambridge Biomed Res Ctr, Cambridge, England;Univ Cambridge NHS Fdn Hosp, Cambridge Breast Unit, Cambridge, England.
    Andrulis, Irene L.
    Lunenfeld Tanenbaum Res Inst Mt Sinai Hosp, Fred A Litwin Ctr Canc Genet, Toronto, ON, Canada;Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
    Anton-Culver, Hoda
    Univ Calif Irvine, Genet Epidemiol Res Inst, Dept Epidemiol, Irvine, CA USA.
    Arndt, Volker
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany.
    Ashworth, Alan
    Univ Calif San Francisco, UCSF Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
    Auer, Paul L.
    Fred Hutchinson Canc Res Ctr, Canc Prevent Program, Seattle, WA USA;Univ Wisconsin Milwaukee, Zilber Sch Publ Hlth, Milwaukee, WI USA.
    Auvinen, Paivi
    Kuopio Univ Hosp, Canc Ctr, Kuopio, Finland;Univ Eastern Finland, Inst Clin Med, Oncol, Kuopio, Finland;Univ Eastern Finland, Translat Canc Res Area, Kuopio, Finland.
    Beckmann, Matthias W.
    Friedrich Alexander Univ Erlangen Nuremberg, Univ Hosp Erlangen, Comprehens Canc Ctr ER EMN, Dept Gynecol & Obstet, Erlangen, Germany.
    Beesley, Jonathan
    QIMR Berghofer Med Res Inst, Dept Genet & Computat Biol, Brisbane, Qld, Australia.
    Behrens, Sabine
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
    Benitez, Javier
    Spanish Natl Canc Res Ctr CNIO, Human Canc Genet Programme, Madrid, Spain;Biomed Network Rare Dis CIBERER, Madrid, Spain.
    Bermisheva, Marina
    Ufa Sci Ctr Russian Acad Sci, Inst Biochem & Genet, Ufa, Russia.
    Blomqvist, Carl
    Univ Helsinki, Helsinki Univ Hosp, Dept Oncol, Helsinki, Finland;Orebro Univ Hosp, Dept Oncol, Orebro, Sweden.
    Blot, William
    Vanderbilt Univ Sch Med, Vanderbilt Ingram Canc Ctr, Vanderbilt Epidemiol Ctr, Dept Med,Div Epidemiol, Nashville, TN USA;Int Epidemiol Inst, Rockville, MD USA.
    Bogdanova, Natalia V.
    Hannover Med Sch, Dept Radiat Oncol, Hannover, Germany;Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany;NN Alexandrov Res Inst Oncol & Med Radiol, Minsk, BELARUS.
    Bojesen, Stig E.
    Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Copenhagen Gen Populat Study, Herlev, Denmark;Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Dept Clin Biochem, Herlev, Denmark;Univ Copenhagen, Fac Hlth & Med Sci, Copenhagen, Denmark.
    Bolla, Manjeet K.
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Borresen-Dale, Anne-Lise
    Oslo Univ Hosp Radiumhosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway;Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway.
    Brauch, Hiltrud
    Dr Margarete Fischer Bosch Inst Clin Pharmacol, Stuttgart, Germany;Univ Tubingen, iFIT Cluster Excellence, Tubingen, Germany;German Canc Consortium DKTK, German Canc Res Ctr DKFZ, Heidelberg, Germany.
    Brenner, Hermann
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany;German Canc Consortium DKTK, German Canc Res Ctr DKFZ, Heidelberg, Germany;Natl Ctr Tumor Dis NCT, Heidelberg, Germany;German Canc Res Ctr, Div Prevent Oncol, Heidelberg, Germany.
    Brucker, Sara Y.
    Univ Tubingen, Dept Gynecol & Obstet, Tubingen, Germany.
    Burwinkel, Barbara
    German Canc Res Ctr, Mol Epidemiol Grp, C080, Heidelberg, Germany;Heidelberg Univ, Univ Womens Clin Heidelberg, Mol Biol Breast Canc, Heidelberg, Germany.
    Caldas, Carlos
    Univ Cambridge, Li Ka Shing Ctr, Canc Res UK Cambridge Inst, Dept Oncol, Cambridge, England;CRUK Cambridge Canc Ctr, Breast Canc Programme, Cambridge, England;Cambridge Univ Hosp NHS Fdn Trust, NIHR Biomed Res Ctr, Cambridge, England.
    Canzian, Federico
    German Canc Res Ctr, Gen Epidemiol Grp, Heidelberg, Germany.
    Chang-Claude, Jenny
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany;Univ Med Ctr Hamburg Eppendorf, Univ Canc Ctr Hamburg UCCH, Canc Epidemiol Grp, Hamburg, Germany.
    Chanock, Stephen J.
    Natl Canc Inst, Natl Inst Hlth, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet, Bethesda, MD USA.
    Chin, Suet-Feung
    Univ Cambridge, Canc Res UK Cambridge Inst, Cambridge, England.
    Clarke, Christine L.
    Univ Sydney, Westmead Inst Med Res, Sydney, NSW, Australia.
    Couch, Fergus J.
    Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
    Cox, Angela
    Univ Sheffield, Sheffield Inst Nucle Acids SInFoNiA, Dept Oncol & Metab, Sheffield, S Yorkshire, England.
    Cross, Simon S.
    Univ Sheffield, Dept Neurosci, Acad Unit Pathol, Sheffield, S Yorkshire, England.
    Czene, Kamila
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Daly, Mary B.
    Fox Chase Canc Ctr, Dept Clin Genet, Philadelphia, PA USA.
    Dennis, Joe
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Devilee, Peter
    Leiden Univ Med Ctr, Dept Pathol, Leiden, Netherlands;Leiden Univ Med Ctr, Dept Human Genet, Leiden, Netherlands.
    Dunn, Janet A.
    Univ Warwick, Warwick Clin Trials Unit, Coventry, W Midlands, England.
    Dunning, Alison M.
    Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Cambridge, England.
    Dwek, Miriam
    Univ Westminster, Fac Sci & Technol, Dept Biomed Sci, London, England.
    Earl, Helena M.
    Univ Cambridge NHS Fdn Hosp, NIHR Cambridge Biomed Res Ctr, Cambridge, England;Univ Cambridge NHS Fdn Hosp, Cambridge Breast Unit, Cambridge, England;Univ Cambridge, Dept Oncol, Cambridge, England.
    Eccles, Diana M.
    Univ Southampton, Fac Med, Canc Sci Acad Unit, Southampton, Hants, England.
    Eliassen, A. Heather
    Harvard Med Sch, Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Ellberg, Carolina
    Lund Univ, Dept Canc Epidemiol Clin Sci, Lund, Sweden.
    Evans, D. Gareth
    Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Biol Med & Hlth, Sch Biol Sci,Div Evolut & Genom Med, Manchester, Lancs, England;Manchester Univ Hosp NHS Fdn Trust, Manchester Acad Hlth Sci Ctr, Manchester Ctr Genom Med, St Marys Hosp,Genom Med, Manchester, Lancs, England;Manchester Univ NHS Fdn Trust, Manchester Acad Hlth Sci Ctr, NIHR Manchester Biomed Res Ctr, Manchester, Lancs, England.
    Fasching, Peter A.
    Friedrich Alexander Univ Erlangen Nuremberg, Univ Hosp Erlangen, Comprehens Canc Ctr ER EMN, Dept Gynecol & Obstet, Erlangen, Germany;Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Hematol & Oncol, Los Angeles, CA USA.
    Figueroa, Jonine
    Natl Canc Inst, Natl Inst Hlth, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet, Bethesda, MD USA;Univ Edinburgh Med Sch, Usher Inst Populat Hlth Sci & Informat, Edinburgh, Midlothian, Scotland;Canc Res UK Edinburgh Ctr, Edinburgh, Midlothian, Scotland.
    Flyger, Henrik
    Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Dept Breast Surg, Herlev, Denmark.
    Gago-Dominguez, Manuela
    Complejo Hospitalario Univ Santiago, SERGAS, Inst Invest Sanitaria Santiago Compostela IDIS, Galician Fdn Genom Med,Genom Med Grp, Santiago De Compostela, Spain;Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA USA.
    Gapstur, Susan M.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA USA.
    Garcia-Closas, Montserrat
    Natl Canc Inst, Natl Inst Hlth, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet, Bethesda, MD USA;Inst Canc Res, Div Genet & Epidemiol, London, England.
    Garcia-Saenz, Jose A.
    Hosp Clino San Carlos, Inst Invest Sanitaria San Carlos IdISSC, Ctr Invest Biomed Red Canc CIBERONC, Madrid, Spain.
    Gaudet, Mia M.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA USA.
    George, Angela
    Inst Canc Res, Div Genet & Epidemiol, London, England.
    Giles, Graham G.
    Canc Council Victoria, Canc Epidemiol 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.
    Goldgar, David E.
    Univ Utah Sch Med Salt, Huntsman Canc Inst, Dept Dermatol, Salt Lake City, UT USA.
    Gonzalez-Neira, Anna
    Spanish Natl Canc Res Ctr CNIO, Human Canc Genet Programme, Madrid, Spain.
    Grip, Mervi
    Univ Oulu, Oulu Univ Hosp, Dept Surg, Oulu, Finland.
    Guenel, Pascal
    Univ Paris Sud, INSERM, Univ Paris Saclay, Ctr Res Epidemiol & Populat Hlth CESP,Canc & Envi, Villejuif, France.
    Guo, Qi
    Univ Cambridge, Dept Publ Hlth & Primary Care, Cardiovasc Epidemiol Unit, Cambridge, England.
    Haiman, Christopher A.
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA.
    Hakansson, Niclas
    Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Hamann, Ute
    German Canc Res Ctr, Mol Genet Breast Canc, Heidelberg, Germany.
    Harrington, Patricia A.
    Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Cambridge, England.
    Hiller, Louise
    Univ Warwick, Warwick Clin Trials Unit, Coventry, W Midlands, England.
    Hooning, Maartje J.
    Erasmus MC Canc Inst, Family Canc Clin, Dept Med Oncol, Rotterdam, Netherlands.
    Hopper, John L.
    Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia.
    Howell, Anthony
    Univ Manchester, Div Canc Sci, Manchester, Lancs, England.
    Huang, Chiun-Sheng
    Natl Taiwan Univ Hosp, Dept Surg, Taipei, Taiwan;Natl Taiwan Univ Coll Med, Taipei, Taiwan.
    Huang, Guanmengqian
    German Canc Res Ctr, Mol Genet Breast Canc, Heidelberg, Germany.
    Hunter, David J.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Program Genet Epidemiol & Stat Genet, Boston, MA USA;Univ Oxford, Nuffield Dept Populat Hlth, Oxford, England.
    Jakubowska, Anna
    Pomeranian Med Univ, Dept Genet & Pathol, Szczecin, Poland;Pomeranian Med Univ, Independent Lab Mol Biol & Genet Diagnost, Szczecin, Poland.
    John, Esther M.
    Stanford Univ Sch Med, Stanford Canc Inst, Dept Med, Div Oncol, Stanford, CA USA.
    Kaaks, Rudolf
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
    Kapoor, Pooja Middha
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany;Heidelberg Univ, Fac Med, Heidelberg, Germany.
    Keeman, Renske
    Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Divi Mol Pathol, Amsterdam, Netherlands.
    Kitahara, Cari M.
    Natl Canc Inst, Div Canc Epidemiol & Genet, Radiat Epidemiol Branch, Bethesda, MD USA.
    Koppert, Linetta B.
    Erasmus MC Canc Inst, Family Canc Clin, Dept Surg Oncol, Rotterdam, Netherlands.
    Kraft, Peter
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Program Genet Epidemiol & Stat Genet, Boston, MA USA.
    Kristensen, Vessela N.
    Oslo Univ Hosp Radiumhosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway;Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway.
    Lambrechts, Diether
    VIB Ctr Canc Biol, VIB, Leuven, Belgium;Univ Leuven, Lab Translat Genet, Dept Human Genet, Leuven, Belgium.
    Le Marchand, Loic
    Univ Hawaii Canc Ctr, Epidemiol Program, Honolulu, HI USA.
    Lejbkowicz, Flavio
    Clalit Natl Canc Control Ctr, Technion Fac Med, Haifa, Israel;Carmel Hosp, Haifa, Israel.
    Lindblom, Annika
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden;Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden.
    Lubinski, Jan
    Pomeranian Med Univ, Dept Genet & Pathol, Szczecin, Poland.
    Mannermaa, Arto
    Univ Eastern Finland, Translat Canc Res Area, Kuopio, Finland;Univ Eastern Finland, Inst Clin Med Pathol & Forens Med, Kuopio, Finland;Kuopio Univ Hosp, Dept Clin Pathol, Imaging Ctr, Kuopio, Finland.
    Manoochehri, Mehdi
    German Canc Res Ctr, Mol Genet Breast Canc, Heidelberg, Germany.
    Manoukian, Siranoush
    Fdn IRCCS Ist Nazl Tumori Milano INT, Dept Med Oncol & Hematol, Unit Med Genet, Milan, Italy.
    Margolin, Sara
    Ssdersjukhuset, Dept Oncol, Stockholm, Sweden;Karolinska Inst, Ssdersjukhuset, Dept Clin Sci & Educ, Stockholm, Sweden.
    Martinez, Maria Elena
    Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA USA;Univ Calif San Diego, Dept Family Med & Publ Hlth, La Jolla, CA USA.
    Maurer, Tabea
    Univ Med Ctr Hamburg Eppendorf, Univ Canc Ctr Hamburg UCCH, Canc Epidemiol Grp, Hamburg, Germany.
    Mavroudis, Dimitrios
    Univ Hosp Herakl, Dept Med Oncol, Iraklion, Greece.
    Meindl, Alfons
    Ludwig Maximilian Univ Munich, Dept Gynecol & Obstet, Munich, Germany.
    Milne, Roger L.
    Canc Council Victoria, Canc Epidemiol Div, Melbourne, Vic, Australia;Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia;Monash Univ, Sch Clin Sci Monash Hlth, Precis Med, Clayton, Vic, Australia.
    Mulligan, Anna Marie
    Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada;Univ Hlth Network, Lab Med Program, Toronto, ON, Canada.
    Neuhausen, Susan L.
    Beckman Res Inst City Hope, Dept Populat Sci, Duarte, CA USA.
    Nevanlinna, Heli
    Univ Helsinki, Helsinki Univ Hosp, Dept Obstet & Gynecol, Helsinki, Finland.
    Newman, William G.
    Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Biol Med & Hlth, Sch Biol Sci,Div Evolut & Genom Med, Manchester, Lancs, England;Manchester Univ Hosp NHS Fdn Trust, Manchester Acad Hlth Sci Ctr, Manchester Ctr Genom Med, St Marys Hosp,Genom Med, Manchester, Lancs, England.
    Olshan, Andrew F.
    Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Epidemiol, Chapel Hill, NC USA.
    Olson, Janet E.
    Olsson, Hakan
    Lund Univ, Dept Canc Epidemiol Clin Sci, Lund, Sweden.
    Orr, Nick
    Queens Univ Belfast, Ctr Canc Res & Cell Biol, Belfast, Antrim, North Ireland.
    Peterlongo, Paolo
    Inst Mol Oncol, IFOM FIRC Italian Fdn Canc Research, Genome Diagnost Program, Milan, Italy.
    Petridis, Christos
    Guys Hosp, Kings Coll London, Res Oncol, London, England.
    Prentice, Ross L.
    Fred Hutchinson Canc Res Ctr, Canc Prevent Program, Seattle, WA USA.
    Presneau, Nadege
    Univ Westminster, Fac Sci & Technol, Dept Biomed Sci, London, England.
    Punie, Kevin
    Univ Hosp Leuven, Leuven Canc Inst, Leuven Multidisciplinary Breast Ctr, Dept Oncol, Leuven, Belgium.
    Ramachandran, Dhanya
    Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany.
    Rennert, Gad
    Clalit Natl Canc Control Ctr, Technion Fac Med, Haifa, Israel;Carmel Hosp, Haifa, Israel.
    Romero, Atocha
    Hosp Univ Puerta Hierro, Med Oncol Dept, Madrid, Spain.
    Sachchithananthan, Mythily
    Univ Sydney, Westmead Inst Med Res, Sydney, NSW, Australia.
    Saloustros, Emmanouil
    Univ Hosp Larissa, Dept Oncol, Larisa, Greece.
    Sawyer, Elinor J.
    Guys Hosp, Kings Coll London, Res Oncol, London, England.
    Schmutzler, Rita K.
    Univ Hosp Cologne, Ctr Hereditary Breast & Ovarian Canc, Cologne, Germany;Univ Cologne, Ctr Mol Med Cologne CMMC, Cologne, Germany.
    Schwentner, Lukas
    Univ Hosp Ulm, Dept Gynaecol & Obstet, Ulm, Germany.
    Scott, Christopher
    Simard, Jacques
    Univ Laval, Ctr Hosp Univ Quebec, Res Ctr, Gen Ctr, Quebec City, PQ, Canada.
    Sohn, Christof
    Heidelberg Univ, Natl Ctr Tumor Dis, Heidelberg, Germany.
    Southey, Melissa C.
    Monash Univ, Sch Clin Sci Monash Hlth, Precis Med, Clayton, Vic, Australia;Univ Melbourne, Dept Clin Pathol, Melbourne, Vic, Australia.
    Swerdlow, Anthony J.
    Inst Canc Res, Div Genet & Epidemiol, London, England;Inst Canc Res, Div Breast Canc Res, London, England.
    Tamimi, Rulla M.
    Harvard Med Sch, Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Program Genet Epidemiol & Stat Genet, Boston, MA USA.
    Tapper, William J.
    Univ Southampton, Fac Med, Southampton, Hants, England.
    Teixeira, Manuel R.
    Portuguese Oncol Inst, Dept Genet, Porto, Portugal;Univ Porto, Biomed Sci Inst ICBAS, Porto, Portugal.
    Terry, Mary Beth
    Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA.
    Thorne, Heather
    Peter MacCallum Canc Ctr, Melbourne, Vic, Australia;Univ Melbourne, Sir Peter MacCallum Dept Oncol, Melbourne, Vic, Australia.
    Tollenaar, Rob A. E. M.
    Leiden Univ Med Ctr, Dept Surg, Leiden, Netherlands.
    Tomlinson, Ian
    Univ Birmingham, Inst Canc & Genom Sci, Birmingham, W Midlands, England;Univ Oxford, Oxford NIHR Biomed Res Ctr, Oxford, England;Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
    Troester, Melissa A.
    Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Epidemiol, Chapel Hill, NC USA.
    Truong, Therese
    Univ Paris Sud, INSERM, Univ Paris Saclay, Ctr Res Epidemiol & Populat Hlth CESP,Canc & Envi, Villejuif, France.
    Turnbull, Clare
    Inst Canc Res, Div Genet & Epidemiol, London, England.
    Vachon, Celine M.
    van der Kolk, Lizet E.
    Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Family Canc Clin, Amsterdam, Netherlands.
    Wang, Qin
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Winqvist, Robert
    Univ Oulu, Lab Canc Genet & Tumor Biol, Canc & Translat Med Res Unit, Bioctr Oulu, Oulu, Finland;Northern Finland Lab Ctr Oulu, Lab Canc Genet & Tumor Biol, Oulu, Finland.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Yang, Xiaohong R.
    Natl Canc Inst, Natl Inst Hlth, Dept Hlth & Human Serv, Div Canc Epidemiol & Genet, Bethesda, MD USA.
    Ziogas, Argyrios
    Univ Calif Irvine, Genet Epidemiol Res Inst, Dept Epidemiol, Irvine, CA USA.
    Pharoah, Paul D. P.
    Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Cambridge, England;Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Hall, Per
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden;Ssdersjukhuset, Dept Oncol, Stockholm, Sweden.
    Wessels, Lodewyk F. A.
    Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Div Mol Carcinogenesis, Amsterdam, Netherlands;Delft Univ Technol, Fac EEMCS, Delft, Netherlands.
    Chenevix-Trench, Georgia
    QIMR Berghofer Med Res Inst, Dept Genet & Computat Biol, Brisbane, Qld, Australia.
    Bader, Gary D.
    Univ Toronto, Dept Mol Genet, Toronto, ON, Canada;Univ Toronto, Donnelly Ctr, Toronto, ON, Canada.
    Doerk, Thilo
    Hannover Med Sch, Gynaecol Res Unit, Hannover, Germany.
    Easton, Douglas F.
    Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Cambridge, England;Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Canisius, Sander
    Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Divi Mol Pathol, Amsterdam, Netherlands;Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Div Mol Carcinogenesis, Amsterdam, Netherlands.
    Schmidt, Marjanka K.
    Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Divi Mol Pathol, Amsterdam, Netherlands;Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Div Psychosocial Res & Epidemiol, Amsterdam, Netherlands.
    A network analysis to identify mediators of germline-driven differences in breast cancer prognosis2020In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 11, no 1, article id 312Article in journal (Refereed)
    Abstract [en]

    Identifying the underlying genetic drivers of the heritability of breast cancer prognosis remains elusive. We adapt a network-based approach to handle underpowered complex datasets to provide new insights into the potential function of germline variants in breast cancer prognosis. This network-based analysis studies similar to 7.3 million variants in 84,457 breast cancer patients in relation to breast cancer survival and confirms the results on 12,381 independent patients. Aggregating the prognostic effects of genetic variants across multiple genes, we identify four gene modules associated with survival in estrogen receptor (ER)-negative and one in ER-positive disease. The modules show biological enrichment for cancer-related processes such as G-alpha signaling, circadian clock, angiogenesis, and Rho-GTPases in apoptosis.

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  • 139.
    Fang, Fang
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Box 281, S-17177 Stockholm, Sweden.
    Hållmarker, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Mora Hosp, Dept Internal Med, Mora, Sweden.
    James, Stefan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Ingre, Caroline
    Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden.; Karolinska Inst, Dept Clin Neurosci, S-17177 Stockholm, Sweden.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Ahlbom, Anders
    Karolinska Inst, Inst Environm Med, S-17177 Stockholm, Sweden.
    Feychting, Maria
    Karolinska Inst, Inst Environm Med, S-17177 Stockholm, Sweden.
    Amyotrophic lateral sclerosis among cross-country skiers in Sweden.2016In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 31, no 3, p. 247-253Article in journal (Refereed)
    Abstract [en]

    A highly increased risk of amyotrophic lateral sclerosis (ALS) has been suggested among professional athletes. We aimed to examine whether long distance cross-country skiers have also a higher risk of ALS and whether the increased risk was modified by skiing performance. We followed 212,246 cross-country skiers in the Swedish Vasaloppet cohort and a random selection of 508,176 general Swedes not participating in the Vasaloppet during 1989-2010. The associations between cross-country skiing as well as skiing performance (i.e., type of race, finishing time and number of races) and the consequent risk of ALS were estimated through hazard ratios (HRs) derived from Cox model. During the study, 39 cases of ALS were ascertained among the skiers. The fastest skiers (100-150 % of winner time) had more than fourfold risk of ALS (HR 4.31, 95 % confidence interval [CI] 1.78-10.4), as compared to skiers that finished at >180 % of winner time. Skiers who participated >4 races during this period had also a higher risk (HR 3.13, 95 % CI 1.37-7.17) than those participated only one race. When compared to the non-skiers, the fastest skiers still had a higher risk (HR 2.08, 95 % CI 1.12-3.84), as skiers who had >4 races (HR 1.88, 95 % CI 1.05-3.35), but those finishing at >180 % of winner time had a lower risk (HR 0.46, 95 % CI 0.24-0.87). In conclusion, long distance cross-country skiing is associated with a higher risk of ALS, but only among the best skiers; recreational skiers appear to have a largely reduced risk.

  • 140.
    Farrokhnia, Nasim
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Castrén, Maaret
    Ehrenberg, Anna
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Oredsson, Sven
    Jonsson, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Asplund, Kjell
    Göransson, Katarina E.
    Emergency Department Triage Scales and Their Components: A Systematic Review of the Scientific Evidence2011In: Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, ISSN 1757-7241, E-ISSN 1757-7241, Vol. 19, p. 42-Article, review/survey (Refereed)
    Abstract [en]

    Emergency department (ED) triage is used to identify patients' level of urgency and treat them based on their triage level. The global advancement of triage scales in the past two decades has generated considerable research on the validity and reliability of these scales. This systematic review aims to investigate the scientific evidence for published ED triage scales. The following questions are addressed: 1. Does assessment of individual vital signs or chief complaints affect mortality during the hospital stay or within 30 days after arrival at the ED? 2. What is the level of agreement between clinicians' triage decisions compared to each other or to a gold standard for each scale (reliability)? 3. How valid is each triage scale in predicting hospitalization and hospital mortality? A systematic search of the international literature published from 1966 through March 31, 2009 explored the British Nursing Index, Business Source Premier, CINAHL, Cochrane Library, EMBASE, and PubMed. Inclusion was limited to controlled studies of adult patients (>= 15 years) visiting EDs for somatic reasons. Outcome variables were death in ED or hospital and need for hospitalization (validity). Methodological quality and clinical relevance of each study were rated as high, medium, or low. The results from the studies that met the inclusion criteria and quality standards were synthesized applying the internationally developed GRADE system. Each conclusion was then assessed as having strong, moderately strong, limited, or insufficient scientific evidence. If studies were not available, this was also noted. We found ED triage scales to be supported, at best, by limited and often insufficient evidence. The ability of the individual vital signs included in the different scales to predict outcome is seldom, if at all, studied in the ED setting. The scientific evidence to assess interrater agreement (reliability) was limited for one triage scale and insufficient or lacking for all other scales. Two of the scales yielded limited scientific evidence, and one scale yielded insufficient evidence, on which to assess the risk of early death or hospitalization in patients assigned to the two lowest triage levels on a 5-level scale (validity).

  • 141. Farvid, Maryam S
    et al.
    Stern, Mariana C
    Norat, Teresa
    Sasazuki, Shizuka
    Vineis, Paolo
    Weijenberg, Matty P
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Wu, Kana
    Stewart, Bernard W
    Cho, Eunyoung
    Consumption of red and processed meat and breast cancer incidence: A systematic review and meta-analysis of prospective studies.2018In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 143, no 11, p. 2787-2799Article in journal (Refereed)
    Abstract [en]

    = 44.4%). In addition, we identified two nested case-control studies evaluating the association between red meat and breast cancer stratified by N-acetyltransferase 2 acetylator genotype. We did not observe any association among those with either fast (per 25 g/day pooled odds ratio (OR), 1.18; 95%CI, 0.93-1.50) or slow N-acetyltransferase 2 acetylators (per 25 g/day pooled OR, 0.99; 95%CI, 0.91-1.08). In the prospective observational studies, high processed meat consumption was associated with increased breast cancer risk.

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  • 142. Felici, N
    et al.
    Marcoccio, I
    Giunta, R
    Haerle, M
    Leclercq, C
    Pajardi, G
    Wilbrand, Stephan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Georgescu, A V
    Pess, G
    Dupuytren contracture recurrence project: reaching consensus on a definition of recurrence2014In: Handchirurgie, Mikrochirurgie, Plastische Chirurgie, ISSN 0722-1819, E-ISSN 1439-3980, Vol. 46, no 6, p. 350-354Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to determine a definition of recurrence of Dupuytren disease that could be utilized for the comparison of the results independently from the treatment used. 24 hand surgeons from 17 countries met in an international consensus conference. The participants used the Delphi method to evaluate a series of statements: (1) the need for defining recurrence, (2) the concept of recurrence applied to the Tubiana staging system, (3) the concept of recurrence applied to each single treated joint, and (4) the concept of recurrence applied to the finger ray. For each item, the possible answer was given on a scale of 1-5: 1=maximum disagreement; 2=disagreement; 3=agreement; 4=strong agreement; 5=absolute agreement. There was consensus on disagreement if 1 and 2 comprised at least 66% of the recorded answers and consensus on agreement if 3, 4 and 5 comprised at least 66% of the recorded answers. If a threshold of 66% was not reached, the related statement was considered "not defined". A need for a definition of recurrence was established. The presence of nodules or cords without finger contracture was not considered an indication of recurrence. The Tubiana staging system was considered inappropriate for reporting recurrence. Recurrence was best determined by the measurement of a specific joint, rather than a total ray. Time 0 occurred between 6 weeks and 3 months. Recurrence was defined as a PED of more than 20° for at least one of treated joint, in the presence of a palpable cord, compared to the result obtained at time 0. This study determined the need for a standard definition of recurrence and reached consensus on that definition, which we should become the standard for the reporting of recurrence. If utilized in subsequent publications, this will allow surgeons to compare different techniques and make is easier to help patients make an informed choice.

  • 143. Ferro, Ana
    et al.
    Morais, Samantha
    Rota, Matteo
    Pelucchi, Claudio
    Bertuccio, Paola
    Bonzi, Rossella
    Galeone, Carlotta
    Zhang, Zuo-Feng
    Matsuo, Keitaro
    Ito, Hidemi
    Hu, Jinfu
    Johnson, Kenneth C
    Yu, Guo-Pei
    Palli, Domenico
    Ferraroni, Monica
    Muscat, Joshua
    Malekzadeh, Reza
    Ye, Weimin
    Song, Huan
    Zaridze, David
    Maximovitch, Dmitry
    Aragonés, Nuria
    Castaño-Vinyals, Gemma
    Vioque, Jesus
    Navarrete-Muñoz, Eva M
    Pakseresht, Mohammadreza
    Pourfarzi, Farhad
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Orsini, Nicola
    Bellavia, Andrea
    Håkansson, Niclas
    Mu, Lina
    Pastorino, Roberta
    Kurtz, Robert C
    Derakhshan, Mohammad H
    Lagiou, Areti
    Lagiou, Pagona
    Boffetta, Paolo
    Boccia, Stefania
    Negri, Eva
    La Vecchia, Carlo
    Peleteiro, Bárbara
    Lunet, Nuno
    Tobacco smoking and gastric cancer:: meta-analyses of published data versus pooled analyses of individual participant data (StoP Project).2018In: European Journal of Cancer Prevention, ISSN 0959-8278, E-ISSN 1473-5709, Vol. 27, no 3, p. 197-204Article in journal (Refereed)
    Abstract [en]

    Tobacco smoking is one of the main risk factors for gastric cancer, but the magnitude of the association estimated by conventional systematic reviews and meta-analyses might be inaccurate, due to heterogeneous reporting of data and publication bias. We aimed to quantify the combined impact of publication-related biases, and heterogeneity in data analysis or presentation, in the summary estimates obtained from conventional meta-analyses. We compared results from individual participant data pooled-analyses, including the studies in the Stomach Cancer Pooling (StoP) Project, with conventional meta-analyses carried out using only data available in previously published reports from the same studies. From the 23 studies in the StoP Project, 20 had published reports with information on smoking and gastric cancer, but only six had specific data for gastric cardia cancer and seven had data on the daily number of cigarettes smoked. Compared to the results obtained with the StoP database, conventional meta-analyses overvalued the relation between ever smoking (summary odds ratios ranging from 7% higher for all studies to 22% higher for the risk of gastric cardia cancer) and yielded less precise summary estimates (SE ≤2.4 times higher). Additionally, funnel plot asymmetry and corresponding hypotheses tests were suggestive of publication bias. Conventional meta-analyses and individual participant data pooled-analyses reached similar conclusions on the direction of the association between smoking and gastric cancer. However, published data tended to overestimate the magnitude of the effects, possibly due to publication biases and limited the analyses by different levels of exposure or cancer subtypes.

  • 144.
    Ferro, Ana
    et al.
    Univ Porto, Inst Saude Publ, EPIUnit, Rua Taipas 135, P-4050600 Porto, Portugal.
    Morais, Samantha
    Univ Porto, Inst Saude Publ, EPIUnit, Rua Taipas 135, P-4050600 Porto, Portugal.
    Rota, Matteo
    Univ Milan, Dept Biomed & Clin Sci, Milan, Italy;Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Pelucchi, Claudio
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Bertuccio, Paola
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Bonzi, Rossella
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Galeone, Carlotta
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Zhang, Zuo-Feng
    UCLA, Dept Epidemiol, Fielding Sch Publ Hlth, Los Angeles, CA USA;Jonsson Comprehens Canc Ctr, Los Angeles, CA 90034 USA.
    Matsuo, Keitaro
    Aichi Canc Ctr, Div Mol Med, Res Inst, Nagoya, Aichi, Japan.
    Ito, Hidemi
    Aichi Canc Ctr, Div Mol Med, Res Inst, Nagoya, Aichi, Japan.
    Hu, Jinfu
    Harbin Med Univ, Dept Epidemiol, Harbin, Heilongjiang, Peoples R China.
    Johnson, Kenneth C.
    Univ Ottawa, Fac Med, Sch Epidemiol Publ Hlth & Prevent Med, Ottawa, ON, Canada.
    Yu, Guo-Pei
    Peking Univ, Med Informat Ctr, Beijing, Peoples R China.
    Palli, Domenico
    ISPO, Canc Res & Prevent Inst, Mol & Nutr Epidemiol Unit, Florence, Italy.
    Ferraroni, Monica
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Muscat, Joshua
    Penn State Univ, Coll Med, Penn State Hershey Med Ctr, Dept Publ Hlth Sci, Hershey, PA USA.
    Malekzadeh, Reza
    Univ Tehran Med Sci, Digest Dis Res Inst, Digest Oncol Res Ctr, Tehran, Iran.
    Ye, Weimin
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Song, Huan
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden;Univ Iceland, Fac Med, Ctr Publ Hlth Sci, Reykjavik, Iceland.
    Zaridze, David
    Russian NN Blokhin Canc Res Ctr, Dept Epidemiol & Prevent, Moscow, Russia.
    Maximovitch, Dmitry
    Russian NN Blokhin Canc Res Ctr, Dept Epidemiol & Prevent, Moscow, Russia.
    Fernandez de Larrea, Nerea
    Inst Salud Carlos III, Natl Ctr Epidemiol, Environm & Canc Epidemiol Unit, Madrid, Spain;CIBERESP, Madrid, Spain.
    Kogevinas, Manolis
    CIBERESP, Madrid, Spain;Ctr Res Environm Epidemiol CREAL, ISGlobal, Barcelona, Spain;Hosp del Mar, Med Res Inst, IMIM, Barcelona, Spain;UPF, Barcelona, Spain.
    Vioque, Jesus
    Miguel Hernandez Univ, Campus San Juan, Alicante, Spain;ISABIAL FISABIO Fdn, Campus San Juan, Alicante, Spain.
    Navarrete-Munoz, Eva M.
    Miguel Hernandez Univ, Campus San Juan, Alicante, Spain;ISABIAL FISABIO Fdn, Campus San Juan, Alicante, Spain.
    Pakseresht, Mohammadreza
    Univ Tehran Med Sci, Digest Dis Res Inst, Digest Oncol Res Ctr, Tehran, Iran;Univ Alberta, Dept Agr Food & Nutr Sci, Edmonton, AB, Canada;Univ Leeds, Ctr Epidemiol & Biostat, Nutr Epidemiol Grp, Leeds, W Yorkshire, England.
    Pourfarzi, Farhad
    Univ Tehran Med Sci, Digest Dis Res Inst, Digest Oncol Res Ctr, Tehran, Iran;Ardabil Univ Med Sci, Digest Dis Res Ctr, Ardebil, Iran.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Orsini, Nicola
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Bellavia, Andrea
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Håkansson, Niclas
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Mu, Lina
    Univ Buffalo, Sch Publ Hlth & Hlth Profess, Dept Epidemiol & Environm Hlth, Buffalo, NY USA.
    Pastorino, Roberta
    Univ Cattolica Sacro Cuore, IRCCS Fdn Policlin Agostino Gemelli, Inst Publ Hlth, Sect Hyg, Lgo F Vito 1, I-00168 Rome, Italy.
    Kurtz, Robert C.
    Mem Sloan Kettering Canc Ctr, Dept Med, 1275 York Ave, New York, NY 10021 USA.
    Derakhshan, Mohammad H.
    Univ Tehran Med Sci, Digest Dis Res Inst, Digest Oncol Res Ctr, Tehran, Iran;Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.
    Lagiou, Areti
    Athens Technol Educ Inst, Sch Hlth Profess, Dept Publ Hlth & Community Hlth, Athens, Greece.
    Lagiou, Pagona
    Univ Athens, Sch Med, Dept Hyg Epidemiol & Med Stat, Athens, Greece;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Boffetta, Paolo
    Icahn Sch Med Mt Sinai, Tisch Canc Inst, New York, NY 10029 USA.
    Boccia, Stefania
    Univ Cattolica Sacro Cuore, IRCCS Fdn Policlin Agostino Gemelli, Inst Publ Hlth, Sect Hyg, Lgo F Vito 1, I-00168 Rome, Italy.
    Negri, Eva
    Univ Milan, Dept Biomed & Clin Sci, Milan, Italy.
    La Vecchia, Carlo
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Peleteiro, Barbara
    Univ Porto, Inst Saude Publ, EPIUnit, Rua Taipas 135, P-4050600 Porto, Portugal;Univ Porto, Fac Med, Dept Ciencias Saude Publ & Forenses & Educ Med, Al Prof Hernani Monteiro, P-4200319 Porto, Portugal.
    Lunet, Nuno
    Univ Porto, Inst Saude Publ, EPIUnit, Rua Taipas 135, P-4050600 Porto, Portugal;Univ Porto, Fac Med, Dept Ciencias Saude Publ & Forenses & Educ Med, Al Prof Hernani Monteiro, P-4200319 Porto, Portugal.
    Alcohol intake and gastric cancer: Meta-analyses of published data versus individual participant data pooled analyses (StoP Project)2018In: Cancer Epidemiology, ISSN 1877-7821, E-ISSN 1877-783X, Vol. 54, p. 125-132Article in journal (Refereed)
    Abstract [en]

    Background: Individual participant data pooled analyses allow access to non-published data and statistical reanalyses based on more homogeneous criteria than meta-analyses based on systematic reviews. We quantified the impact of publication-related biases and heterogeneity in data analysis and presentation in summary estimates of the association between alcohol drinking and gastric cancer.

    Methods: We compared estimates obtained from conventional meta-analyses, using only data available in published reports from studies that take part in the Stomach Cancer Pooling (StoP) Project, with individual participant data pooled analyses including the same studies.

    Results: A total of 22 studies from the StoP Project assessed the relation between alcohol intake and gastric cancer, 19 had specific data for levels of consumption and 18 according to cancer location; published reports addressing these associations were available from 18, 5 and 5 studies, respectively. The summary odds ratios [OR, (95%CI)] estimate obtained with published data for drinkers vs. non-drinkers was 10% higher than the one obtained with individual StoP data [18 vs. 22 studies: 1.21 (1.07-1.36) vs. 1.10 (0.99-1.23)] and more heterogeneous (1(2): 63.6% vs 54.4%). In general, published data yielded less precise summary estimates (standard errors up to 2.6 times higher). Funnel plot analysis suggested publication bias.

    Conclusion: Meta-analyses of the association between alcohol drinking and gastric cancer tended to overestimate the magnitude of the effects, possibly due to publication bias. Additionally, individual participant data pooled analyses yielded more precise estimates for different levels of exposure or cancer subtypes.

  • 145.
    Figlioli, Gisella
    et al.
    IFOM FIRC Inst Mol Oncol, Genome Diagnost Program, Milan, Italy.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Young, Mary Ann
    Genome One, Darlinghurst, NSW, Australia.
    The FANCM:p.Arg658* truncating variant is associated with risk of triple-negative breast cancer2019In: NPJ BREAST CANCER, ISSN 2374-4677, Vol. 5, article id 38Article in journal (Refereed)
    Abstract [en]

    Breast cancer is a common disease partially caused by genetic risk factors. Germline pathogenic variants in DNA repair genes BRCA1, BRCA2, PAM, ATM, and CHEK2 are associated with breast cancer risk. FANCM, which encodes for a DNA translocase, has been proposed as a breast cancer predisposition gene, with greater effects for the ER-negative and triple-negative breast cancer (TNBC) subtypes. We tested the three recurrent protein-truncating variants FANCM:p.Arg658*, p.Gln1701*, and pArg1931* for association with breast cancer risk in 67,112 cases, 53,766 controls, and 26,662 carriers of pathogenic variants of BRCA1 or BRCA2. These three variants were also studied functionally by measuring survival and chromosome fragility in FANCM(-/-) patient-derived immortalized fibroblasts treated with diepoxybutane or olaparib. We observed that FANCM:p.Arg658* was associated with increased risk of ER-negative disease and TNBC (OR = 2.44, P = 0.034 and OR = 3.79; P = 0.009, respectively). In a country-restricted analysis, we confirmed the associations detected for FANCM:p.Arg658* and found that also FANCM:p.Arg1931* was associated with ER-negative breast cancer risk (OR = 1.96; P = 0.006). The functional results indicated that all three variants were deleterious affecting cell survival and chromosome stability with FANCM:p.Arg658* causing more severe phenotypes. In conclusion, we confirmed that the two rare FANCM deleterious variants p.Arg658* and p.Arg1931* are risk factors for ER-negative and TNBC subtypes. Overall our data suggest that the effect of truncating variants on breast cancer risk may depend on their position in the gene. Cell sensitivity to olaparib exposure, identifies a possible therapeutic option to treat FANCM-associated tumors.

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  • 146.
    Forsgren, Johan
    et al.
    Uppsala University, Disciplinary Domain of Science and Technology, Technology, Department of Engineering Sciences, Nanotechnology and Functional Materials. Uppsala University, Disciplinary Domain of Science and Technology, Technology, Department of Engineering Sciences, Applied Materials Sciences.
    Brohede, Ulrika
    Sandvik AB, Stockholm.
    Piskounova, Sonya
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Materials Chemistry, Polymer Chemistry.
    Mihranyan, Albert
    Uppsala University, Disciplinary Domain of Science and Technology, Technology, Department of Engineering Sciences, Nanotechnology and Functional Materials.
    Larsson, Sune
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Maria, Strømme
    Uppsala University, Disciplinary Domain of Science and Technology, Technology, Department of Engineering Sciences, Nanotechnology and Functional Materials.
    Engqvist, Håkan
    Uppsala University, Disciplinary Domain of Science and Technology, Technology, Department of Engineering Sciences, Applied Materials Sciences.
    In Vivo Evaluation of Functionalized Biomimetic Hydroxyapatite for Local Delivery of Active Agents2011In: Journal of Biomaterials and Nanobiotechnology, ISSN 2158-7027, 2158-7043, Vol. 2, no 2, p. 149-154Article in journal (Refereed)
    Abstract [en]

    This study was carried out to investigate the biological response in vivo to biomimetic hydroxyapatite implant coatings functionalized with bisphosphonates and bone morphogenetic proteins. The functionalization was carried out by a simple soaking procedure in the operating room immediately prior to surgery. Cylindrical titanium samples with and without coatings were implanted in the distal femoral epiphysis of sheep and retrieved after 6 weeks. The histological analysis proved that all samples were integrated well in the tissue with no signs of intolerance. Fewer osteoclasts were observed in the vicinity of bisphosphonate-functionalized samples and the bone was denser around these samples compared to the other samples. Samples functionalized with bone morphogenetic protein induced more bone/implant contact but showed a more inconsistent outcome with reduced bone density around the samples. This study demonstrates a simple method to functionalize implant coatings, which provides surgeons with an option of patient-specific functionalization of implants. The observed biological impact due to the delivery of active molecules from the coatings suggests that this strategy may also be employed to deliver antibiotics from similar coatings.

  • 147.
    Fox, Glen A
    et al.
    Canadian Wildlife Service, National Wildlife Research Centre, Carleton University, Ottawa, Ontario, Canada.
    Lundberg, Rebecca
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Wejheden, Carolina
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Larsson, Sune
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Örberg, Jan
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Environmental Toxicology.
    Lind, Monica
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Health of herring gulls (Larus argentatus) in relation to breeding location in the early 1990s: III. Effects on the bone tissue2008In: Journal of Toxicology and Environmental Health, ISSN 1528-7394, E-ISSN 1087-2620, Vol. 71, no 21, p. 1448-1456Article in journal (Refereed)
    Abstract [en]

    Health effects associated with the Great Lakes environment were assessed in adult herring gulls (Larus argentatus) in the early 1990s, including the size and quality of their bones. Femurs were excised from 140 individuals from 10 colonies distributed throughout the Great Lakes and 2 reference colonies in Lake Winnipeg (freshwater) and the Bay of Fundy (marine). Femurs of gulls from the Great Lakes differed from the freshwater or marine reference for 9 of 12 variables of size, composition, and strength assessed using peripheral quantitative computed tomography (pQCT) and biomechanical testing. Femurs of Great Lakes gulls were significantly smaller in length (-2.9%), periosteal circumference (-2.4%), and cross-sectional area (-5.4%) than freshwater reference birds. Femurs of the Great Lakes gulls had a lower significant cortical bone mineral content (-8.1%) and density (-2%) than the marine reference. A significant increase in the amount the bone could bend before it broke (+34%) and the energy required to break it (+44%) and a significant decrease (-16.3%) in stiffness during three-point biomechanical bending test were also detected in Great Lakes versus the freshwater gulls. These differences are indicative of impaired mineralization. When divided into high and low 2,3,7,8-tetrachlorodibenzo-p-dioxin toxicity equivalent (TCDD-TEQ) colonies, the amount the bone could bend before it broke and the energy required to break it were significantly higher in the high TEQ colonies, but not high polychlorinated biphenyl (PCB) colonies. Breeding location and dietary choices of Great Lakes herring gulls in the early 1990s resulted in modulations of physiological processes that affected the size, mineralization, and biomechanical properties of bone.

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  • 148.
    Franzon, Kristin
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Byberg, Liisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Sjögren, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Zethelius, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. Med Prod Agcy, Uppsala, Sweden.
    Cederholm, Tommy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Kilander, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Predictors of Independent Aging and Survival: A 16-Year Follow-Up Report in Octogenarian Men2017In: Journal of The American Geriatrics Society, ISSN 0002-8614, E-ISSN 1532-5415, Vol. 65, no 9, p. 1953-1960Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: To examine the longitudinal associations between aging with preserved functionality, i.e. independent aging and survival, and lifestyle variables, dietary pattern and cardiovascular risk factors.

    DESIGN: Cohort study.

    SETTING: Uppsala Longitudinal Study of Adult Men, Sweden.

    PARTICIPANTS: Swedish men (n = 1,104) at a mean age of 71 (range 69.4-74.1) were investigated, 369 of whom were evaluated for independent aging 16 years later, at a mean age of 87 (range 84.8-88.9).

    MEASUREMENTS: A questionnaire was used to obtain information on lifestyle, including education, living conditions, and physical activity. Adherence to a Mediterranean-like diet was assessed according to a modified Mediterranean Diet Score derived from 7-day food records. Cardiovascular risk factors were measured. Independent aging at a mean age of 87 was defined as lack of diagnosed dementia, a Mini-Mental State Examination score of 25 or greater, not institutionalized, independence in personal activities of daily living, and ability to walk outdoors alone. Complete survival data at age 85 were obtained from the Swedish Cause of Death Register.

    RESULTS: Fifty-seven percent of the men survived to age 85, and 75% of the participants at a mean age of 87 displayed independent aging. Independent aging was associated with never smoking (vs current) (odds ratio (OR) = 2.20, 95% confidence interval (CI) = 1.05-4.60) and high (vs low) adherence to a Mediterranean-like diet (OR = 2.69, 95% CI = 1.14-6.80). Normal weight or overweight and waist circumference of 102 cm or less were also associated with independent aging. Similar associations were observed with survival.

    CONCLUSION: Lifestyle factors such as never smoking, maintaining a healthy diet, and not being obese at age 71 were associated with survival and independent aging at age 85 and older in men.

  • 149. Fritzell, Peter
    et al.
    Knutsson, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Sandén, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Strömqvist, Björn
    Hägg, Olle
    Recurrent Versus Primary Lumbar Disc Herniation Surgery: Patient-reported Outcomes in the Swedish Spine Register Swespine2015In: Clinical Orthopaedics and Related Research, ISSN 0009-921X, E-ISSN 1528-1132, Vol. 473, no 6, p. 1978-1984Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Lumbar disc herniation (LDH) is a common indication for lumbar spine surgery. The proportion of patients having a second surgery within 2 years varies in the literature between 0.5% and 24%, with recurrent herniation being the most common cause. Several studies have not found any relevant outcome differences between patients undergoing surgery for primary LDH and patients undergoing reoperation for a recurrent LDH, but these studies have limitations, including small sample size and retrospective design.

    QUESTIONS/PURPOSES:

    We (1) compared patient-reported outcomes between patients operated on for primary LDH and patients reoperated on for recurrent LDH within 1 year after index surgery and (2) determined risk factors for worse outcomes.

    METHODS:

    We obtained data from the Swedish National Spine Register, Swespine, where patient-reported outcomes are collected using mailed protocols at 1, 2, 5, and 10 years after surgery. Of the 13,562 patients identified who underwent LDH between January 2000 and May 2011, 13,305 (98%) underwent primary surgery for LDH and 257 (2%) underwent reoperation for a recurrent LDH within the first year. Patient-reported outcomes at 1 to 2 years were available for 8497 patients (63%), 8350 of 13,305 (63%) in the primary LDH group and 147 of 257 (57%) in the recurrent LDH group (p = 0.068). We compared leg and back pain (VAS: 0-100), function (Oswestry Disability Index [ODI]: 0-100), quality of life (EQ-5D: -0.59 to 1.0), patient satisfaction, and global assessment of leg pain between groups. We also analyzed rsik factors for worse global assessment and satisfaction.

    RESULTS:

    Mean (95% CI) differences in improvement between groups favoring patients with primary LDH were VAS leg pain 9 (4-14), ODI 6 (3-9), and EQ-5D 0.09 (0.04-0.15). While statistically significant, these effect sizes may be lower than the minimal clinically important differences often referred to. Percentage of satisfied patients was 79% and 58% in the primary and recurrent LDH groups, respectively (p < 0.001), and percentage of patients with no or better leg pain (global assessment) was 74% and 65%, respectively (p = 0.008). Reoperation for recurrent LDH represented the largest independent risk for dissatisfaction; this factor and smoking represented similar risks for less improvement in leg pain.

    CONCLUSIONS:

    Repeat surgery for a recurrent LDH was performed with good probability for improvement, although not as good as for primary LDH surgery, and patients undergoing repeated surgery were less satisfied. Studies on risk factors for recurrence are warranted.

    LEVEL OF EVIDENCE:

    Level II, therapeutic study. See Instructions for Authors for a complete description of levels of evidence.

  • 150. Försth, P
    et al.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Sandén, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Does fusion improve the outcome after decompressive surgery for lumbar spinal stenosis?: a two-year follow-up study involving 5390 patients2013In: The Bone & Joint Journal, ISSN 2049-4408, Vol. 95-B, no 7, p. 960-965Article in journal (Refereed)
    Abstract [en]

    Whether to combine spinal decompression with fusion in patients with symptomatic lumbar spinal stenosis remains controversial. We performed a cohort study to determine the effect of the addition of fusion in terms of patient satisfaction after decompressive spinal surgery in patients with and without a degenerative spondylolisthesis.                  

    The National Swedish Register for Spine Surgery (Swespine) was used for the study. Data were obtained for all patients in the register who underwent surgery for stenosis on one or two adjacent lumbar levels. A total of 5390 patients fulfilled the inclusion criteria and completed a two-year follow-up. Using multivariable models the results of 4259 patients who underwent decompression alone were compared with those of 1131 who underwent decompression and fusion. The consequence of having an associated spondylolisthesis in the operated segments pre-operatively was also considered.                

    At two years there was no significant difference in patient satisfaction between the two treatment groups for any of the outcome measures, regardless of the presence of a pre-operative spondylolisthesis. Moreover, the proportion of patients who required subsequent further lumbar surgery was also similar in the two groups.                  

    In this large cohort the addition of fusion to decompression was not associated with an improved outcome.

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