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  • 1.
    Akhter, Tansim
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Research group (Dept. of women´s and children´s health), Gynecological endocrinology.
    Wikström, Anna-Karin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Research group (Dept. of women´s and children´s health), Clinical Obstetrics. Karolinska Inst, Danderyd Hosp, Dept Clin Sci, Stockholm, Sweden.
    Larsson, Marita
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Obstetrics and Gynaecology.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Wikström, Gerhard
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Naessén, Tord
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Research group (Dept. of women´s and children´s health), Gynecological endocrinology.
    Serum Pentraxin 3 is associated with signs of arterial alteration in women with preeclampsia.2017In: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 241, p. 417-422Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Preeclampsia (PE) in pregnancy is a state of exaggerated inflammation and is associated with an increased risk of cardiovascular disease (CVD) later in life. Levels of pentraxin 3 (PTX3), a novel inflammation marker, are increased during PE and in individuals with CVD. The primary aim of this study was to assess whether serum PTX3 in women with PE is associated with adverse arterial effects; a thicker intima and higher intima/media (I/M) ratio in the common carotid artery (CCA).

    METHODS: Serum PTX3 levels were measured using commercially available enzyme-linked immunosorbent assay kits, and individual CCA intima and media thicknesses were estimated by 22MHz non-invasive ultrasound in 55 women at PE diagnosis and 64 women with normal pregnancies at a similar gestational age, and about one year postpartum. A thick intima, thin media and high I/M ratio indicate a less healthy artery wall.

    RESULTS: During pregnancy serum PTX3 correlated positively with intima thickness and I/M ratio but negatively with media thickness (all p<0.0001), indicating adverse arterial effects. About one year postpartum, PTX3 levels had decreased in both groups and there remained no significant group difference or significant correlation with CCA wall layers.

    CONCLUSIONS: Higher levels of serum PTX3 in women with PE were significantly associated with signs of adverse arterial effects during pregnancy, but not one year postpartum, supporting the rapid dynamics of PTX3.

  • 2. Alehagen, Urban
    et al.
    Aaseth, Jan
    Alexander, Jan
    Svensson, Erland
    Johansson, Peter
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Less fibrosis in elderly subjects supplemented with selenium and coenzyme Q10-A mechanism behind reduced cardiovascular mortality?2018In: Biofactors, ISSN 0951-6433, E-ISSN 1872-8081, Vol. 44, no 2, p. 137-147Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: In an intervention study where 221 healthy elderly persons received selenium and coenzyme Q10 as a dietary supplement, and 222 received placebo for 4 years we observed improved cardiac function and reduced cardiovascular mortality. As fibrosis is central in the aging process, we investigated the effect of the intervention on biomarkers of fibrogenic activity in a subanalysis of this intervention study.

    MATERIAL AND METHODS: In the present subanalysis 122 actively treated individuals and 101 controls, the effect of the treatment on eight biomarkers of fibrogenic activity were assessed. These biomarkers were: Cathepsin S, Endostatin, Galectin 3, Growth Differentiation Factor-15 (GDF-15), Matrix Metalloproteinases 1 and 9, Tissue Inhibitor of Metalloproteinases 1 (TIMP 1) and Suppression of Tumorigenicity 2 (ST-2). Blood concentrations of these biomarkers after 6 and 42 months were analyzed by the use of T-tests, repeated measures of variance, and factor analyses.

    RESULTS: Compared with placebo, in those receiving supplementation with selenium and coenzyme Q10, all biomarkers except ST2 showed significant decreased concentrations in blood. The changes in concentrations, that is, effects sizes as given by partial eta2 caused by the intervention were considered small to medium.

    CONCLUSION: The significantly decreased biomarker concentrations in those on active treatment with selenium and coenzyme Q10 compared with those on placebo after 36 months of intervention presumably reflect less fibrogenic activity as a result of the intervention. These observations might indicate that reduced fibrosis precedes the reported improvement in cardiac function, thereby explaining some of the positive clinical effects caused by the intervention. © 2017 BioFactors, 2017.

  • 3. Barber, RM
    et al.
    Fullman, N
    Sorensen, RJD
    Bollyky, T
    McKee, M
    Nolte, E
    Abajobir, AA
    Abate, KH
    Abbafati, C
    Abbas, KM
    Abd-Allah, F
    Abdulle, AM
    Ärnlöv, Johan
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Younis, MZ
    Yu, C
    Zaidi, Z
    El Sayed Zaki, M
    Zambrana-Torrelio, C
    Zapata, T
    Zenebe, ZM
    Zodpey, S
    Zoeckler, L
    Zuhlke, LJ
    Murray, CJL
    Healthcare Access and Quality Index based on mortality from causes amenable to personal health care in 195 countries and territories, 1990-2015: a novel analysis from the Global Burden of Disease Study 2015.2017In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 390, no 10091, p. 231-266Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: National levels of personal health-care access and quality can be approximated by measuring mortality rates from causes that should not be fatal in the presence of effective medical care (ie, amenable mortality). Previous analyses of mortality amenable to health care only focused on high-income countries and faced several methodological challenges. In the present analysis, we use the highly standardised cause of death and risk factor estimates generated through the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) to improve and expand the quantification of personal health-care access and quality for 195 countries and territories from 1990 to 2015.

    METHODS: We mapped the most widely used list of causes amenable to personal health care developed by Nolte and McKee to 32 GBD causes. We accounted for variations in cause of death certification and misclassifications through the extensive data standardisation processes and redistribution algorithms developed for GBD. To isolate the effects of personal health-care access and quality, we risk-standardised cause-specific mortality rates for each geography-year by removing the joint effects of local environmental and behavioural risks, and adding back the global levels of risk exposure as estimated for GBD 2015. We employed principal component analysis to create a single, interpretable summary measure-the Healthcare Quality and Access (HAQ) Index-on a scale of 0 to 100. The HAQ Index showed strong convergence validity as compared with other health-system indicators, including health expenditure per capita (r=0·88), an index of 11 universal health coverage interventions (r=0·83), and human resources for health per 1000 (r=0·77). We used free disposal hull analysis with bootstrapping to produce a frontier based on the relationship between the HAQ Index and the Socio-demographic Index (SDI), a measure of overall development consisting of income per capita, average years of education, and total fertility rates. This frontier allowed us to better quantify the maximum levels of personal health-care access and quality achieved across the development spectrum, and pinpoint geographies where gaps between observed and potential levels have narrowed or widened over time.

    FINDINGS: Between 1990 and 2015, nearly all countries and territories saw their HAQ Index values improve; nonetheless, the difference between the highest and lowest observed HAQ Index was larger in 2015 than in 1990, ranging from 28·6 to 94·6. Of 195 geographies, 167 had statistically significant increases in HAQ Index levels since 1990, with South Korea, Turkey, Peru, China, and the Maldives recording among the largest gains by 2015. Performance on the HAQ Index and individual causes showed distinct patterns by region and level of development, yet substantial heterogeneities emerged for several causes, including cancers in highest-SDI countries; chronic kidney disease, diabetes, diarrhoeal diseases, and lower respiratory infections among middle-SDI countries; and measles and tetanus among lowest-SDI countries. While the global HAQ Index average rose from 40·7 (95% uncertainty interval, 39·0-42·8) in 1990 to 53·7 (52·2-55·4) in 2015, far less progress occurred in narrowing the gap between observed HAQ Index values and maximum levels achieved; at the global level, the difference between the observed and frontier HAQ Index only decreased from 21·2 in 1990 to 20·1 in 2015. If every country and territory had achieved the highest observed HAQ Index by their corresponding level of SDI, the global average would have been 73·8 in 2015. Several countries, particularly in eastern and western sub-Saharan Africa, reached HAQ Index values similar to or beyond their development levels, whereas others, namely in southern sub-Saharan Africa, the Middle East, and south Asia, lagged behind what geographies of similar development attained between 1990 and 2015.

    INTERPRETATION: This novel extension of the GBD Study shows the untapped potential for personal health-care access and quality improvement across the development spectrum. Amid substantive advances in personal health care at the national level, heterogeneous patterns for individual causes in given countries or territories suggest that few places have consistently achieved optimal health-care access and quality across health-system functions and therapeutic areas. This is especially evident in middle-SDI countries, many of which have recently undergone or are currently experiencing epidemiological transitions. The HAQ Index, if paired with other measures of health-system characteristics such as intervention coverage, could provide a robust avenue for tracking progress on universal health coverage and identifying local priorities for strengthening personal health-care quality and access throughout the world.

    FUNDING: Bill & Melinda Gates Foundation.

  • 4.
    Basu, Samar
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry. Univ Clermont Auvergne, Fac Pharm, Dept Biochem Mol Biol & Nutr, BP 10448, F-63000 Clermont Ferrand, France..
    Kadiiska, Maria B.
    NIEHS, Immun Inflammat & Dis Lab, NIH, Res Triangle Pk, NC 27709 USA..
    Ozone exposure effect on systemic prostaglandin F-2 alpha in rat plasma and urine may not reveal pulmonary damage through inflammation2017In: Prostaglandins, Leukotrienes and Essential Fatty Acids, ISSN 0952-3278, E-ISSN 1532-2823, Vol. 126, p. 79-83Article in journal (Refereed)
    Abstract [en]

    The acute ozone induced lung injury model has been widely used to explore injury and repair processes induced by oxidant overload. The current study evaluated acute ozone exposure effects on prostaglandin F-2 alpha (PGF(2 alpha)) in male Fischer rat plasma and urine with the hypothesis that ozone may induce an inflammatory response in the body that can be measured by the induction of PGF2 alpha. That might then lead to the identification of potential marker for acute lung injury through systemic inflammation. The time and dose-dependent effects of ozone exposure on the plasma and urinary levels of a major PGF(2 alpha) metabolite15-keto-dihydro-PGF(2 alpha) were determined using a radioimmunoassay. No statistically significant differences in the PGF(2 alpha) metabolite were found between the control and the experimental groups at either ozone exposure dose (2 ppm and 5 ppm) or any time point (2 h, 7 h and 16 h) post exposure for plasma and at 7 different post exposure time points (between 2 and 80 h) for urine. It is concluded that acute ozone exposure does not cause changes in plasma and urinary PGF(2 alpha), and therefore their measurement in plasma and urine may not be used to reveal pulmonary inflammation and damage by ozone.

  • 5.
    Bergman, Daniel
    et al.
    Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden..
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Hansson-Hamlin, Helene
    Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden..
    Svensson, Anna
    Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden..
    Holst, Bodil Ström
    Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden..
    Prevalence of interfering antibodies in dogs and cats evaluated using a species-independent assay.2018In: Veterinary clinical pathology, ISSN 0275-6382, E-ISSN 1939-165X, Vol. 47, no 2, p. 205-212Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Interfering antibodies in human serum and plasma are known to react with mammalian antibodies in immunoassays and cause false-positive test results. Although this phenomenon was recently shown in companion animals, knowledge regarding immunoassay interference in veterinary medicine is very limited.

    OBJECTIVES: The aims of this study were to set up a species-independent immunoassay procedure to detect interference in serum samples, to screen for interference in a cross-section of canine and feline patient samples from an animal hospital, and to determine if the detected interference could be neutralized using an immunoassay based on nonmammalian reagents.

    METHODS: A 2-site sandwich-type interference assay was set up using commercially available mouse reagents. A total of 369 serum samples from 320 dogs and 263 samples from 218 cats were analyzed using the interference assay. Multiple samples were submitted from 36 dogs and 39 cats. Nineteen samples identified as interference-positive were analyzed in an assay using chicken antibodies.

    RESULTS: Interference was detected in samples from 28 dogs (9%) and 10 cats (5%) screened with the interference assay. Except for 1 cat, consistent results were obtained for all 75 dogs and cats that submitted more than 1 sample. The interference was eliminated when analyzed in the chicken-based assay (P < .001).

    CONCLUSIONS: Substances with reactivity toward mouse IgG can be detected in serum samples from dog and cat patients using a 2-site interference assay. The detected substances are most likely interfering antibodies, possibly originating from immunization with other mammalian species.

  • 6.
    Blom, Kristin
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    ElShafie, Amir Ibrahim
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology. Alribat Univ Hosp, Dept Clin Pathol & Microbiol, Khartoum, Sudan.
    Jönsson, Ulla-Britt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Rönnelid, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Håkansson, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Venge, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    The genetically determined production of the alarmin eosinophil-derived neurotoxin is reduced in visceral leishmaniasis2018In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 126, no 1, p. 85-91Article in journal (Refereed)
    Abstract [en]

    Visceral leishmaniasis (VL) is the most severe form of leishmaniasis. Recent findings indicate that dendritic cells have a key role in the defense against the Leishmania parasite and that the activity of this cell may be modified by the eosinophil secretory protein eosinophil-derived neurotoxin (EDN). We hypothesized that the interactions between dendritic cells and EDN might be of importance in the disease development. Cellular content of EDN was analyzed by ELISA. The single-nucleotide polymorphisms at positions 405, 416, and 1122 in the EDN gene were analyzed by real-time PCR with TaqMan((R)) reagents. The study cohorts comprised 239 Sudanese subjects (65 healthy controls and 174 with VL) and 300 healthy Swedish controls. The eosinophil content of EDN was lower in VL as compared with controls (p < 0.0001). The EDN405 (G>C) genotype distribution was similar among Swedish and Sudanese controls, whereas VL subjects had a higher prevalence of the EDN405-GG genotype (p < 0.0001). The content of EDN in the eosinophils was closely linked to the EDN405 polymorphism (p = 0.0002). Our findings suggest that the predisposition to acquire VL is related to the genetic polymorphism of the EDN gene and the reduced production by the eosinophil of this gene product.

  • 7. Bäckryd, Emmanuel
    et al.
    Lind, Anne-Li
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care. Uppsala Berzelii Technology Center for Neurodiagnostics, Uppsala University, Uppsala, Sweden.
    Thulin, Måns
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Statistics.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Gerdle, Björn
    Gordh, Torsten
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care. Uppsala Berzelii Technology Center for Neurodiagnostics, Uppsala University, Uppsala, Sweden.
    High levels of cerebrospinal fluid chemokines point to the presence of neuroinflammation in peripheral neuropathic pain: a cross-sectional study of 2 cohorts of patients compared with healthy controls2017In: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 158, no 12, p. 2487-2495Article in journal (Refereed)
    Abstract [en]

    Animal models suggest that chemokines are important mediators in the pathophysiology of neuropathic pain. Indeed, these substances have been called "gliotransmitters," a term that illustrates the close interplay between glial cells and neurons in the context of neuroinflammation and pain. However, evidence in humans is scarce. The aim of the study was to determine a comprehensive cerebrospinal fluid (CSF) inflammatory profile of patients with neuropathic pain. Our hypothesis was that we would thereby find indications of a postulated on-going process of central neuroinflammation. Samples of CSF were collected from 2 cohorts of patients with neuropathic pain (n = 11 and n = 16, respectively) and healthy control subjects (n = 11). The samples were analyzed with a multiplex proximity extension assay in which 92 inflammation-related proteins were measured simultaneously (Proseek Multiplex Inflammation I; Olink Bioscience, Uppsala, Sweden). Univariate testing with control of false discovery rate, as well as orthogonal partial least squares discriminant analysis, were used for statistical analyses. Levels of chemokines CXCL6, CXCL10, CCL8, CCL11, CCL23 in CSF, as well as protein LAPTGF-beta-1, were significantly higher in both neuropathic pain cohorts compared with healthy controls, pointing to neuroinflammation in patients. These 6 proteins were also major results in a recent similar study in patients with fibromyalgia. The findings need to be confirmed in larger cohorts, and the question of causality remains to be settled. Because it has been suggested that prevalent comorbidities to chronic pain (eg, depression, anxiety, poor sleep, and tiredness) also are associated with neuroinflammation, it will be important to determine whether neuroinflammation is a common mediator.

  • 8.
    Carlsson, Axel C
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology. Centre for Family Medicine, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Jansson, Jan-Håkan
    Department of Public Health and Clinical Medicine, Research Unit Skellefteå, Umeå University, Umeå, Sweden.
    Söderberg, Stefan
    Department of Public Health and Clinical Medicine, Heart Centre, Umeå University, Umeå, Sweden.
    Ruge, Toralph
    Dept of Medicine Solna, Karolinska Institutet and Function of Emergency Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Ärnlöv, Johan
    Centre for Family Medicine, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden; School of Health and Social Sciences, Dalarna University, Falun, Sweden.
    Levels of soluble tumor necrosis factor receptor 1 and 2, gender, and risk of myocardial infarction in Northern Sweden2018In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 272, p. 41-46Article in journal (Refereed)
    Abstract [en]

    BACKGROUND AND AIMS:

    Soluble receptors for tumor necrosis factor alpha (sTNFR1 and sTNFR2) have been associated with cardiovascular diseases, and some evidence points towards a difference in associated risk between men and women. We aimed to study the association between sTNFR1 and sTNFR2 and incident myocardial infarctions (MI) and to explore the influence of established cardiovascular risk factors in men and women.

    METHODS:

    We conducted a nested case control study in three large Swedish cohorts, including 533 myocardial infarction cases, and 1003 age-, sex- and cohort-matched controls. Odds ratios (OR) with 95% confidence intervals (CI) were calculated.

    RESULTS:

    An association between circulating sTNFR1 and sTNFR2 and an increased risk for MI was found when comparing cases and controls. The odds ratios were significant after adjustment for established cardiovascular risk factors and C-reactive protein in women (OR 1.44, 95% CI 1.08-1.93 for TNFR1, and 1.61, 95% CI 1.11-2.34 for TNFR2), but was abolished in men. Women with a combination of elevated CRP and values in the upper quartile of TNFR1 or TNFR2 had a 5-fold higher risk of myocardial infarction versus those with normal CRP and values in the lower three quartiles of TNFR1 or TNFR2.

    CONCLUSIONS:

    As the risk estimates for TNFR1 and TNFR2 were higher and remained significant after adjustments for established cardiovascular risk factors in women but not in men, a potential role for TNFR1 and TNFR2 in identifying women with a higher MI risk is possible. The future clinical role of TNFR1 and TNFR2 in combination with CRP to identify high risk patients for coronary heart disease has yet to be determined.

  • 9.
    Carlsson, Axel C
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Ruge, Toralph
    Kjøller, Erik
    Hilden, Jørgen
    Kolmos, Hans Jørn
    Sajadieh, Ahmad
    Kastrup, Jens
    Jensen, Gorm Boje
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Nowak, Christoph
    Jakobsen, Janus Christian
    Winkel, Per
    Gluud, Christian
    Ärnlöv, Johan
    10-Year Associations between Tumor Necrosis Factor Receptors 1 and 2 and Cardiovascular Events in Patients with Stable Coronary Heart Disease: A CLARICOR (Effect of Clarithromycin on Mortality and Morbidity in Patients With Ischemic Heart Disease) Trial Substudy.2018In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, ISSN 2047-9980, E-ISSN 2047-9980, Vol. 7, no 9, article id e008299Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: We aimed to assess the associations and predictive powers between the soluble receptors for tumor necrosis factor (TNF)-α (TNFR1 and TNFR2) and cardiovascular outcomes in patients with stable coronary heart disease.

    METHODS AND RESULTS: CLARICOR (Effect of Clarithromycin on Mortality and Morbidity in Patients With Ischemic Heart Disease) is a randomized clinical trial comparing clarithromycin with placebo in patients with stable coronary heart disease. The primary outcome was a composite of nonfatal acute myocardial infarction, unstable angina pectoris, cerebrovascular disease, and all-cause mortality. Patients were followed up for 10 years; discovery sample, those assigned placebo (1204 events in n=1998); and replication sample, those assigned clarithromycin (1220 events in n=1979). We used Cox regression adjusted for C-reactive protein level, established cardiovascular risk factors, kidney function, and cardiovascular drugs. After adjustments, higher serum levels of TNFR1 and TNFR2 were associated with the composite outcome in the discovery sample (hazard ratio per SD increase, 1.13; 95% confidence interval, 1.05-1.22; P=0.001 for TNFR1; hazard ratio, 1.16; 95% confidence interval, 1.08-1.24; P<0.001 for TNFR2). The associations were similar in the replication sample. The associations with the composite outcome were mainly driven by acute myocardial infarction, cardiovascular mortality, and noncardiovascular mortality. The addition of TNFR1 and TNFR2 to established cardiovascular risk factors improved prediction only modestly (<1%).

    CONCLUSIONS: Increased concentrations of circulating TNFR1 and TNFR2 were associated with increased risks of cardiovascular events and mortality in patients with stable coronary heart disease. Yet, the utility of measuring TNFR1 and TNFR2 to improve risk prediction in these patients appears limited.

    CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT00121550.

  • 10.
    Cedervall, Jessica
    et al.
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
    Dragomir, Anca
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical and experimental pathology.
    Saupe, Falk
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
    Zhang, Yanyu
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
    Ärnlöv, Johan
    Karolinska Inst, Dept Neurobiol Care Sci & Soc, Divis Family Med, Huddinge, Sweden.
    Larsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical and experimental pathology.
    Dimberg, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Olsson, Anna-Karin
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
    Pharmacological targeting of peptidylarginine deiminase 4 prevents cancer-associated kidney injury in mice.2017In: Oncoimmunology, ISSN 2162-4011, E-ISSN 2162-402X, Vol. 6, no 8, article id e1320009Article in journal (Refereed)
    Abstract [en]

    Renal insufficiency is a frequent cancer-associated problem affecting more than half of all cancer patients at the time of diagnosis. To minimize nephrotoxic effects the dosage of anticancer drugs are reduced in these patients, leading to sub-optimal treatment efficacy. Despite the severity of this cancer-associated pathology, the molecular mechanisms, as well as therapeutic options, are still largely lacking. We here show that formation of intravascular tumor-induced neutrophil extracellular traps (NETs) is a cause of kidney injury in tumor-bearing mice. Analysis of clinical biomarkers for kidney function revealed impaired creatinine clearance and elevated total protein levels in urine from tumor-bearing mice. Electron microscopy analysis of the kidneys from mice with cancer showed reversible pathological signs such as mesangial hypercellularity, while permanent damage such as fibrosis or necrosis was not observed. Removal of NETs by treatment with DNase I, or pharmacological inhibition of the enzyme peptidylarginine deiminase 4 (PAD4), was sufficient to restore renal function in mice with cancer. Tumor-induced systemic inflammation and impaired perfusion of peripheral vessels could be reverted by the PAD4 inhibitor. In conclusion, the current study identifies NETosis as a previously unknown cause of cancer-associated renal dysfunction and describes a novel promising approach to prevent renal failure in individuals with cancer.

  • 11.
    Christersson, Christina
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Lindahl, Bertil
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Berglund, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Siegbahn, Agneta
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Oldgren, Jonas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    The utility of coagulation activity for prediction of risk of mortality and cardiovascular events in guideline-treated myocardial infarction patients2017In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 122, no 4, p. 224-233Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Despite improved treatment of myocardial infarction (MI), real-world patients still suffer substantial risk for subsequent cardiovascular events. Little is known about coagulation activity shortly after MI and whether coagulation activity markers may identify patients at increased risk despite contemporary treatment.

    OBJECTIVE: To evaluate D-dimer concentration and thrombin generation potential shortly after discharge after MI and evaluate if these markers could predict the risk of future cardiovascular and bleeding events.

    METHODS: Unselected MI patients (n = 421) were included in the observational REBUS study (NCT01102933) and followed for two years. D-dimer concentrations, thrombin peak, and endogenous thrombin potential (ETP) were analyzed at inclusion (3-5 days after MI) and at early follow-up (after 2-3 weeks).

    RESULTS: Seventy-five patients (17.8%) experienced the composite endpoint (all-cause death, MI, congestive heart failure, or all-cause stroke), and 31 patients (7.4%) experienced a clinically relevant bleeding event. D-dimer concentrations at early follow-up were associated with the composite endpoint (HR [per SD increase] 1.51 [95% CI 1.22-1.87]) and with clinically relevant bleeding (HR [per SD increase] 1.80 [95% CI 1.32-2.44]). Thrombin generation potential was not significantly associated with either the composite endpoint or with clinically relevant bleeding. Higher thrombin peak and ETP at early follow-up were both inversely associated with stroke (HR [per SD increase] 0.50 [95% CI 0.30-0.81] and 0.43 [95% CI 0.22-0.83], respectively).

    CONCLUSION: In unselected MI patients treated according to contemporary guidelines, D-dimer measurements may identify patients at increased risk of new cardiovascular and bleeding events. The inverse association of thrombin generation potential and risk of stroke has to be further investigated.

  • 12.
    Christersson, Christina
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Thulin, Åsa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Siegbahn, Agneta
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Microparticles during long-term follow-up after acute myocardial infarction: Association to atherosclerotic burden and risk of cardiovascular events2017In: Thrombosis and Haemostasis, ISSN 0340-6245, Vol. 117, no 8, p. 1571-1581Article in journal (Refereed)
    Abstract [en]

    Microparticles (MPs) are formed from platelets (PMPs), endothelial cells (EMPs) and monocytes (MMPs), and in acute myocardial infarction (MI), there is an increase of MPs in the culprit artery. In this study MPs were evaluated in whole blood in 105 patients with MI at five time-points during a two-year follow-up (FU). Patients with non-ST elevated MI had higher concentrations of CD41+MPs compared to ST elevated MI patients (p=0.024). The concentrations of PMPs in whole blood increased during the time period (p<0.001), but no significant change over time was found for EMPs and MMPs. CD62P+MP counts were higher in MI patients with diabetes (p=0.020), and patients with hypertension had increased levels of CD14+MPs (p=0.004). The amount of CD62P+TF+MPs increased significantly during FU (p<0.001). Patients with atherosclerosis in three arterial beds, i.e. coronary, carotid and peripheral arteries, had lower concentrations of CD62P+TF+MPs (p=0.035) and CD144+TF+MPs (p=0.004) compared to patients with atherosclerosis in one or two arterial beds. Higher concentrations of CD62P+MPs early after MI were associated with an increased risk of cardiovascular events during FU, hazard ratio 3.32 (95 %C11.20-9.31). Only small variations in PMP, EMP and MMP concentrations were found during long-term FU after MI and their levels seem to reflect the underlying cardiovascular disease rather than the acute MI. PMPs expressing P-selectin might be a promising biomarker for predicting future cardiovascular events, but further studies are needed to confirm these results.

  • 13.
    Dubois, Louise
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Occurrence of purinergic receptors in human prostasomes (prostate epithelial cell derived exosomes)Manuscript (preprint) (Other academic)
  • 14.
    Dubois, Louise
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Occurrence of purinergic receptors in human prostasomes (prostate epithelial cell-derived exosomes)2018In: Article in journal (Refereed)
  • 15.
    Dubois, Louise
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Löf, Lisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Hultenby, K
    Waldenström, Anders
    Kamali-Moghaddam, M,
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Ronquist, G
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Ronquist, KG
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Human erythrocyte-derived nanovesicles can readily be loaded with doxorubicin and act as anticancer agents.2018In: Cancer Research Frontiers, Vol. 4, no 1, p. 13-26Article in journal (Refereed)
  • 16.
    Dubois, Louise
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Manouchehri Doulabi, Ehsan
    Uppsala University, Science for Life Laboratory, SciLifeLab.
    Löf, Liza
    Uppsala University, Science for Life Laboratory, SciLifeLab.
    Kamali-Moghaddam, Masood
    Uppsala University, Science for Life Laboratory, SciLifeLab.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Stålhandske, Per
    Biovica International AB.
    Increased Levels of Thymidine Kinase 1 in Malignant Cell-derived ExosomesManuscript (preprint) (Other academic)
  • 17.
    Dubois, Louise
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Manouchehri Doulabi, Ehsan
    Uppsala University, Science for Life Laboratory, SciLifeLab.
    Löf, Liza
    Uppsala University, Science for Life Laboratory, SciLifeLab.
    Kamali-Moghaddam, Masood
    Uppsala University, Science for Life Laboratory, SciLifeLab.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Stålhandske, Per
    Biovica International AB.
    Increased levels of thymidine kinase 1 in malignant cell-derived exosomesManuscript (preprint) (Other academic)
  • 18.
    Eggers, Kai M.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Lindahl, Bertil
    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.
    Venge, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Predictors of 10-year changes in levels of N-terminal pro B-type natriuretic peptide and cardiac troponin I in the elderly2018In: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 257, p. 300-305Article in journal (Refereed)
    Abstract [en]

    Background: Measurement of N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) might be useful for monitoring of cardiovascular disease in the elderly. However, it is not clear whether changes in these biomarkers are associated with changes in the cardiovascular risk profile and if this pattern could be modified by changes in lifestyle habits or medications.

    Methods: We measured levels of NT-proBNP and cTnI in community-dwelling subjects (PIVUS study) upon visits scheduled at age 70 (n = 1007), 75 (n = 825) and 80 (n = 602). The associations of these biomarkers with repeated measurements of clinical variables (risk factors, lifestyle habits, echocardiographic data and medications) were investigated using sex-adjusted linear mixed random effect models.

    Results: NT-proBNP and cTnI were positively associated with increasing age. NT-proBNP, but not cTnI, was affected by changes of renal function and the degree of obesity. NT-proBNP was more closely related than cTnI to changes in echocardiographic estimates of cardiac geometry and function. Biomarker levels and/or their changes were inversely associated with a physically more active lifestyle (both NT-proBNP and cTnI) and statin treatment at age 70 (only cTnI). Changes in smoking status or antihypertensive treatment had no effect on biomarker levels.

    Conclusions: Changes in NT-proBNP and cTnI levels are associated with different patterns of cardiovascular disease burden when using a longitudinal approach. However, levels of both biomarkers and their changes also reflect changes in the cardiovascular risk profile that might be modifiable. This is an important aspect for the use of any cardiovascular biomarker in an elderly population.

  • 19.
    Emami Khoonsari, Payam
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Proteomics Studies of Subjects with Alzheimer’s Disease and Chronic Pain2017Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Alzheimer’s disease (AD) is a neurodegenerative disease and the major cause of dementia, affecting more than 50 million people worldwide. Chronic pain is long-lasting, persistent pain that affects more than 1.5 billion of the world population. Overlapping and heterogenous symptoms of AD and chronic pain conditions complicate their diagnosis, emphasizing the need for more specific biomarkers to improve the diagnosis and understand the disease mechanisms.

    To characterize disease pathology of AD, we measured the protein changes in the temporal neocortex region of the brain of AD subjects using mass spectrometry (MS). We found proteins involved in exo-endocytic and extracellular vesicle functions displaying altered levels in the AD brain, potentially resulting in neuronal dysfunction and cell death in AD.

    To detect novel biomarkers for AD, we used MS to analyze cerebrospinal fluid (CSF) of AD patients and found decreased levels of eight proteins compared to controls, potentially indicating abnormal activity of complement system in AD.

    By integrating new proteomics markers with absolute levels of Aβ42, total tau (t-tau) and p-tau in CSF, we improved the prediction accuracy from 83% to 92% of early diagnosis of AD. We found increased levels of chitinase-3-like protein 1 (CH3L1) and decreased levels of neurosecretory protein VGF (VGF) in AD compared to controls.

    By exploring the CSF proteome of neuropathic pain patients before and after successful spinal cord stimulation (SCS) treatment, we found altered levels of twelve proteins, involved in neuroprotection, synaptic plasticity, nociceptive signaling and immune regulation.

    To detect biomarkers for diagnosing a chronic pain state known as fibromyalgia (FM), we analyzed the CSF of FM patients using MS. We found altered levels of four proteins, representing novel biomarkers for diagnosing FM. These proteins are involved in inflammatory mechanisms, energy metabolism and neuropeptide signaling.

    Finally, to facilitate fast and robust large-scale omics data handling, we developed an e-infrastructure. We demonstrated that the e-infrastructure provides high scalability, flexibility and it can be applied in virtually any fields including proteomics. This thesis demonstrates that proteomics is a promising approach for gaining deeper insight into mechanisms of nervous system disorders and find biomarkers for diagnosis of such diseases.

    List of papers
    1. Increased levels of extracellular microvesicle markers and decreased levels of endocytic/exocytic proteins in the Alzheimer’s disease brain
    Open this publication in new window or tab >>Increased levels of extracellular microvesicle markers and decreased levels of endocytic/exocytic proteins in the Alzheimer’s disease brain
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    2016 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 54, no 4, p. 71p. 1671-1686Article in journal (Refereed) Published
    Abstract [en]

    Background: Alzheimer's disease (AD) is a chronic neurodegenerative disorder accounting for more than 50% of all dementia cases. AD neuropathology is characterized by the formation of extracellular plaques and intracellular neurofibrillary tangles consisting of aggregated amyloid-beta and tau, respectively. The disease mechanism has only been partially elucidated and is believed to also involve many other proteins.

    Objective: This study intended to perform a proteomic profiling of post mortem AD brains and compare it with control brains as well as brains from other neurological diseases to gain insight into the disease pathology.

    Methods: Here we used label-free shotgun mass spectrometry to analyze temporal neocortex samples from AD, other neurological disorders, and non-demented controls, in order to identify additional proteins that are altered in AD. The mass spectrometry results were verified by antibody suspension bead arrays.

    Results: We found 50 proteins with altered levels between AD and control brains. The majority of these proteins were found at lower levels in AD. Pathway analyses revealed that several of the decreased proteins play a role in exocytic and endocytic pathways, whereas several of the increased proteins are related to extracellular vesicles. Using antibody-based analysis, we verified the mass spectrometry results for five representative proteins from this group of proteins (CD9, HSP72, PI42A, TALDO, and VAMP2) and GFAP, a marker for neuroinflammation.

    Conclusions: Several proteins involved in exo-endocytic pathways and extracellular vesicle functions display altered levels in the AD brain. We hypothesize that such changes may result in disturbed cellular clearance and a perturbed cell-to-cell communication that may contribute to neuronal dysfunction and cell death in AD.

    Publisher
    p. 71
    Keywords
    Brain, Proteomics, Mass spectrometry, Alzheimer's disease
    National Category
    Analytical Chemistry Geriatrics Neurosciences
    Research subject
    Chemistry with specialization in Analytical Chemistry
    Identifiers
    urn:nbn:se:uu:diva-277617 (URN)10.3233/JAD-160271 (DOI)000386749900034 ()27636840 (PubMedID)
    Funder
    VINNOVALars Hierta Memorial FoundationSwedish Research Council, P29797-1; 621-2011-4423Knut and Alice Wallenberg FoundationStiftelsen Gamla Tjänarinnor
    Available from: 2016-02-22 Created: 2016-02-22 Last updated: 2018-01-10Bibliographically approved
    2. Analysis of the Cerebrospinal Fluid Proteome in Alzheimer's Disease
    Open this publication in new window or tab >>Analysis of the Cerebrospinal Fluid Proteome in Alzheimer's Disease
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    2016 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 11, no 3, article id e0150672Article in journal (Refereed) Published
    Abstract [en]

    Alzheimer's disease is a neurodegenerative disorder accounting for more than 50% of cases of dementia. Diagnosis of Alzheimer's disease relies on cognitive tests and analysis of amyloid beta, protein tau, and hyperphosphorylated tau in cerebrospinal fluid. Although these markers provide relatively high sensitivity and specificity for early disease detection, they are not suitable for monitor of disease progression. In the present study, we used label-free shotgun mass spectrometry to analyse the cerebrospinal fluid proteome of Alzheimer's disease patients and non-demented controls to identify potential biomarkers for Alzheimer's disease. We processed the data using five programs (DecyderMS, Maxquant, OpenMS, PEAKS, and Sieve) and compared their results by means of reproducibility and peptide identification, including three different normalization methods. After depletion of high abundant proteins we found that Alzheimer's disease patients had lower fraction of low-abundance proteins in cerebrospinal fluid compared to healthy controls (p<0.05). Consequently, global normalization was found to be less accurate compared to using spiked-in chicken ovalbumin for normalization. In addition, we determined that Sieve and OpenMS resulted in the highest reproducibility and PEAKS was the programs with the highest identification performance. Finally, we successfully verified significantly lower levels (p<0.05) of eight proteins (A2GL, APOM, C1QB, C1QC, C1S, FBLN3, PTPRZ, and SEZ6) in Alzheimer's disease compared to controls using an antibody-based detection method. These proteins are involved in different biological roles spanning from cell adhesion and migration, to regulation of the synapse and the immune system.

    National Category
    Neurology Geriatrics
    Identifiers
    urn:nbn:se:uu:diva-283774 (URN)10.1371/journal.pone.0150672 (DOI)000371990100049 ()26950848 (PubMedID)
    Funder
    Knut and Alice Wallenberg FoundationMarianne and Marcus Wallenberg FoundationThe Swedish Brain FoundationSwedish Research Council FormasSwedish Research Council, P29797-1Swedish Research Council, 621-2011-4423
    Available from: 2016-04-14 Created: 2016-04-14 Last updated: 2017-11-30Bibliographically approved
    3. Chitinase-3-like protein 1 (CH3L1) and Neurosecretory protein VGF (VGF) as two novel CSF biomarker candidates for improved diagnostics in Alzheimer’s disease
    Open this publication in new window or tab >>Chitinase-3-like protein 1 (CH3L1) and Neurosecretory protein VGF (VGF) as two novel CSF biomarker candidates for improved diagnostics in Alzheimer’s disease
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    (English)Manuscript (preprint) (Other academic)
    Abstract [en]

    Alzheimer’s disease (AD) is a chronic neurodegenerative disorder characterized by amyloid-β (Aβ) plaque deposition and accumulation of intracellular neurofibrillary tangles. This pathology is mirrored in the cerebrospinal fluid (CSF), where decreased Aβ42 together with increased total (t-tau) and phospho-tau (p-tau) today is used as a diagnostic marker. Although these biomarkers have a fairly good sensitivity and specificity, additional biomarkers are needed to further improve the accuracy for early disease detection and to monitor disease development. In this study, we used mass spectrometry-based shotgun proteomics to investigate the CSF proteome of patients with AD and mild cognitive impairment (MCI) as well as of non-demented controls. By combining the diagnostic markers (Aβ42, total t-tau, and p-tau) with a selection of proteomics biomarkers, the accuracy of predicting MCI to AD conversion increased from 83% to 92% with a specificity of 1.0 and sensitivity of 0.86. Among these markers, the levels of protein chitinase-3-like protein 1 (CH3L1) were significantly higher in AD and MCI converters compared to controls. In addition to Aβ42, t-tau, and p-tau the protein CH3L1 contributed mostly to the prediction accuracy. We also found statistically significant lower CSF levels of the neurosecretory protein VGF (VGF) in AD compared to controls. Taken together, our findings suggest that incorporating new CSF biomarkers can further enhance early diagnosis of AD.

    Keywords
    Alzheimer's disease, cerebrospinal fluid, biomarker, diagnostics, neurodegenerative disorder, dementia
    National Category
    Geriatrics Neurosciences
    Research subject
    Geriatrics; Medical Science; Neurology
    Identifiers
    urn:nbn:se:uu:diva-331711 (URN)
    Available from: 2017-10-17 Created: 2017-10-17 Last updated: 2018-01-13
    4. Spinal Cord Stimulation Alters Protein Levels in the Cerebrospinal Fluid of Neuropathic Pain Patients: A Proteomic Mass Spectrometric Analysis
    Open this publication in new window or tab >>Spinal Cord Stimulation Alters Protein Levels in the Cerebrospinal Fluid of Neuropathic Pain Patients: A Proteomic Mass Spectrometric Analysis
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    2016 (English)In: Neuromodulation (Malden, Mass.), ISSN 1094-7159, E-ISSN 1525-1403, Vol. 19, no 6, p. 549-562Article in journal (Refereed) Published
    Abstract [en]

    ObjectivesElectrical neuromodulation by spinal cord stimulation (SCS) is a well-established method for treatment of neuropathic pain. However, the mechanism behind the pain relieving effect in patients remains largely unknown. In this study, we target the human cerebrospinal fluid (CSF) proteome, a little investigated aspect of SCS mechanism of action. MethodsTwo different proteomic mass spectrometry protocols were used to analyze the CSF of 14 SCS responsive neuropathic pain patients. Each patient acted as his or her own control and protein content was compared when the stimulator was turned off for 48 hours, and after the stimulator had been used as normal for three weeks. ResultsEighty-six proteins were statistically significantly altered in the CSF of neuropathic pain patients using SCS, when comparing the stimulator off condition to the stimulator on condition. The top 12 of the altered proteins are involved in neuroprotection (clusterin, gelsolin, mimecan, angiotensinogen, secretogranin-1, amyloid beta A4 protein), synaptic plasticity/learning/memory (gelsolin, apolipoprotein C1, apolipoprotein E, contactin-1, neural cell adhesion molecule L1-like protein), nociceptive signaling (neurosecretory protein VGF), and immune regulation (dickkopf-related protein 3). ConclusionPreviously unknown effects of SCS on levels of proteins involved in neuroprotection, nociceptive signaling, immune regulation, and synaptic plasticity are demonstrated. These findings, in the CSF of neuropathic pain patients, expand the picture of SCS effects on the neurochemical environment of the human spinal cord. An improved understanding of SCS mechanism may lead to new tracks of investigation and improved treatment strategies for neuropathic pain.

    Keywords
    Cerebrospinal fluid, mechanism of action, neuropathic pain, spinal cord stimulation
    National Category
    Neurology Radiology, Nuclear Medicine and Medical Imaging
    Identifiers
    urn:nbn:se:uu:diva-304434 (URN)10.1111/ner.12473 (DOI)000382755300001 ()27513633 (PubMedID)
    Funder
    VINNOVASwedish Research Council
    Available from: 2016-10-05 Created: 2016-10-05 Last updated: 2017-10-17Bibliographically approved
    5. Systematic Analysis of the Cerebrospinal Fluid Proteome of Fibromyalgia patients
    Open this publication in new window or tab >>Systematic Analysis of the Cerebrospinal Fluid Proteome of Fibromyalgia patients
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    (English)Manuscript (preprint) (Other academic)
    Abstract [en]

    Fibromyalgia (FM) is a syndrome characterized by widespread muscular pain, fatigue and functional symptoms, which is known to be difficult to diagnose as the various symptoms overlap with many other conditions. Currently, there are no biomarkers for FM, and the diagnosis is made subjectively by the clinicians. We have performed shotgun proteomics on cerebrospinal fluid (CSF) from FM patients and non-pain controls to find potential biomarker candidates for this syndrome. Based on our multivariate and univariate analyses, we found that the relative differences in the CSF proteome between FM patients and controls were moderate. Four proteins, important to discriminate FM patients from non-pain controls, were found: Apolipoprotein C-III, Galectin-3-binding protein, Malate dehydrogenase cytoplasmic and the neuropeptide precursor protein ProSAAS. These proteins are involved in lipoprotein lipase (LPL) activity, inflammatory signaling, energy metabolism and neuropeptide signaling.

    Keywords
    cerebrospinal fluid, biomarker, chronic pain, fibromyalgia, inflammation, neuroinflammation, mass spectrometry
    National Category
    Health Sciences Neurosciences Clinical Laboratory Medicine Biomedical Laboratory Science/Technology
    Research subject
    Bioinformatics; Biology with specialization in Molecular Biology; Chemistry with specialization in Analytical Chemistry; Medical Science; Clinical Chemistry
    Identifiers
    urn:nbn:se:uu:diva-331615 (URN)
    Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13
    6. Interoperable and scalable metabolomics data analysis with microservices
    Open this publication in new window or tab >>Interoperable and scalable metabolomics data analysis with microservices
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    (English)Manuscript (preprint) (Other academic)
    Abstract [en]

    Developing a robust and performant data analysis workflow that integrates all necessary components whilst still being able to scale over multiple compute nodes is a challenging task. We here present a generic method based on microservice architecture, where software tools are encapsulated as Docker containers that can be connected into scientific workflows and executed in parallel using the Kubernetes container orchestrator. The method was developed within the PhenoMeNal consortium to support flexible metabolomics data analysis and was designed as a virtual research environment which can be launched on-demand on cloud resources and desktop computers. IT-expertise requirements on the user side are kept to a minimum, and established workflows can be re-used effortlessly by any novice user. We validate our method on two mass spectrometry studies, one nuclear magnetic resonance spectroscopy study and one fluxomics study, showing that the method scales dynamically with increasing availability of computational resources. We achieved a complete integration of the major software suites resulting in the first turn-key workflow encompassing all steps for mass-spectrometry-based metabolomics including preprocessing, multivariate statistics, and metabolite identification. Microservices is a generic methodology that can serve any scientific discipline and opens up for new types of large-scale integrative data analysis.

    Keywords
    Bioinformatics, e-infrastructure, microservices, metabolomics, kubernetes, Docker, container
    National Category
    Bioinformatics (Computational Biology)
    Research subject
    Bioinformatics
    Identifiers
    urn:nbn:se:uu:diva-331658 (URN)
    Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13
  • 20. Feigin, VL
    et al.
    Abate, KH
    Abd-Allah, F
    Abdulle, AM
    Abera, SF
    Abyu, GY
    Ahmed, MB
    Aichour, AN
    Aichour, I
    Aichour, MTE
    Akinyemi, RO
    Alabed, S
    Al-Raddadi, R
    Alvis-Guzman, N
    Amare, AT
    Ärnlöv, Johan
    Karolinska institute; Dalarna university.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Yimam, HH, ,
    Yonemoto, N,
    Yu, C,
    Zaidi, Z
    El Sayed Zaki, M
    Zunt, JR
    Murray, CJL
    Vos, T
    Global, regional, and national burden of neurological disorders during 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015.2017In: Lancet Neurology, ISSN 1474-4422, E-ISSN 1474-4465, Vol. 16, no 11, p. 877-897Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Comparable data on the global and country-specific burden of neurological disorders and their trends are crucial for health-care planning and resource allocation. The Global Burden of Diseases, Injuries, and Risk Factors (GBD) Study provides such information but does not routinely aggregate results that are of interest to clinicians specialising in neurological conditions. In this systematic analysis, we quantified the global disease burden due to neurological disorders in 2015 and its relationship with country development level.

    METHODS: We estimated global and country-specific prevalence, mortality, disability-adjusted life-years (DALYs), years of life lost (YLLs), and years lived with disability (YLDs) for various neurological disorders that in the GBD classification have been previously spread across multiple disease groupings. The more inclusive grouping of neurological disorders included stroke, meningitis, encephalitis, tetanus, Alzheimer's disease and other dementias, Parkinson's disease, epilepsy, multiple sclerosis, motor neuron disease, migraine, tension-type headache, medication overuse headache, brain and nervous system cancers, and a residual category of other neurological disorders. We also analysed results based on the Socio-demographic Index (SDI), a compound measure of income per capita, education, and fertility, to identify patterns associated with development and how countries fare against expected outcomes relative to their level of development.

    FINDINGS: Neurological disorders ranked as the leading cause group of DALYs in 2015 (250·7 [95% uncertainty interval (UI) 229·1 to 274·7] million, comprising 10·2% of global DALYs) and the second-leading cause group of deaths (9·4 [9·1 to 9·7] million], comprising 16·8% of global deaths). The most prevalent neurological disorders were tension-type headache (1505·9 [UI 1337·3 to 1681·6 million cases]), migraine (958·8 [872·1 to 1055·6] million), medication overuse headache (58·5 [50·8 to 67·4 million]), and Alzheimer's disease and other dementias (46·0 [40·2 to 52·7 million]). Between 1990 and 2015, the number of deaths from neurological disorders increased by 36·7%, and the number of DALYs by 7·4%. These increases occurred despite decreases in age-standardised rates of death and DALYs of 26·1% and 29·7%, respectively; stroke and communicable neurological disorders were responsible for most of these decreases. Communicable neurological disorders were the largest cause of DALYs in countries with low SDI. Stroke rates were highest at middle levels of SDI and lowest at the highest SDI. Most of the changes in DALY rates of neurological disorders with development were driven by changes in YLLs.

    INTERPRETATION: Neurological disorders are an important cause of disability and death worldwide. Globally, the burden of neurological disorders has increased substantially over the past 25 years because of expanding population numbers and ageing, despite substantial decreases in mortality rates from stroke and communicable neurological disorders. The number of patients who will need care by clinicians with expertise in neurological conditions will continue to grow in coming decades. Policy makers and health-care providers should be aware of these trends to provide adequate services.

    FUNDING: Bill & Melinda Gates Foundation.

  • 21.
    Frithiof, Robert
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Bandert, Anna
    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 Medical Sciences, Clinical Chemistry.
    Lipcsey, Miklos
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Smekal, David
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Central Venous Line and Dialysis Catheter Position Affects Drug Clearance during Continuous Renal Replacement Therapy in an Animal Model.2018In: ASAIO journal (1992), ISSN 1058-2916, E-ISSN 1538-943XArticle in journal (Refereed)
    Abstract [en]

    In intensive care, drugs are commonly administered through central venous catheters (CVC). These catheters and central venous dialysis catheters (CVDC) are often placed in the same vessel for practical reasons. The aim of this experimental study was to investigate if the position of CVC and CVDC influences the elimination of infused drugs, during continuous renal replacement therapy (CRRT). In a randomized, cross-over model, anesthetized piglets received both a CVC and a CVDC in a jugular vein. Another CVDC was placed in a femoral vein for comparison. After baseline measurements, CRRT was performed in either of the CVDC, each CRRT-period separated by another baseline period. Hypotension was induced by peripherally given sodium nitroprusside. In the CVC, both gentamicin and noradrenaline were administered. Noradrenaline was titrated to reach a target blood pressure. When CRRT was performed using the CVDC in the same vessel as the drugs were infused, the plasma concentration of gentamicin was reduced compared with when the infusion and CVDC were in different vessels (5.66 [standard deviation (SD) ± 1.23] vs. 7.76 [SD ± 2.30] mg/L [p = 0.02]). The noradrenaline infusion rate needed to reach the target blood pressure was more than doubled (0.32 [SD ± 0.16] vs. 0.15 [SD ± 0.08] µg/kg/min [p = 0.006]). This experimental study indicates that the removal of drugs is increased if infusion is in close vicinity of the CVDC, during CRRT.

  • 22. Fullman, N
    et al.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Murray, Christopher J L
    Measuring progress and projecting attainment on the basis of past trends of the health-related Sustainable Development Goals in 188 countries: an analysis from the Global Burden of Disease Study 2016.2017In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 390, no 10100, p. 1423-1459Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The UN's Sustainable Development Goals (SDGs) are grounded in the global ambition of "leaving no one behind". Understanding today's gains and gaps for the health-related SDGs is essential for decision makers as they aim to improve the health of populations. As part of the Global Burden of Diseases, Injuries, and Risk Factors Study 2016 (GBD 2016), we measured 37 of the 50 health-related SDG indicators over the period 1990-2016 for 188 countries, and then on the basis of these past trends, we projected indicators to 2030.

    METHODS: We used standardised GBD 2016 methods to measure 37 health-related indicators from 1990 to 2016, an increase of four indicators since GBD 2015. We substantially revised the universal health coverage (UHC) measure, which focuses on coverage of essential health services, to also represent personal health-care access and quality for several non-communicable diseases. We transformed each indicator on a scale of 0-100, with 0 as the 2·5th percentile estimated between 1990 and 2030, and 100 as the 97·5th percentile during that time. An index representing all 37 health-related SDG indicators was constructed by taking the geometric mean of scaled indicators by target. On the basis of past trends, we produced projections of indicator values, using a weighted average of the indicator and country-specific annualised rates of change from 1990 to 2016 with weights for each annual rate of change based on out-of-sample validity. 24 of the currently measured health-related SDG indicators have defined SDG targets, against which we assessed attainment.

    FINDINGS: Globally, the median health-related SDG index was 56·7 (IQR 31·9-66·8) in 2016 and country-level performance markedly varied, with Singapore (86·8, 95% uncertainty interval 84·6-88·9), Iceland (86·0, 84·1-87·6), and Sweden (85·6, 81·8-87·8) having the highest levels in 2016 and Afghanistan (10·9, 9·6-11·9), the Central African Republic (11·0, 8·8-13·8), and Somalia (11·3, 9·5-13·1) recording the lowest. Between 2000 and 2016, notable improvements in the UHC index were achieved by several countries, including Cambodia, Rwanda, Equatorial Guinea, Laos, Turkey, and China; however, a number of countries, such as Lesotho and the Central African Republic, but also high-income countries, such as the USA, showed minimal gains. Based on projections of past trends, the median number of SDG targets attained in 2030 was five (IQR 2-8) of the 24 defined targets currently measured. Globally, projected target attainment considerably varied by SDG indicator, ranging from more than 60% of countries projected to reach targets for under-5 mortality, neonatal mortality, maternal mortality ratio, and malaria, to less than 5% of countries projected to achieve targets linked to 11 indicator targets, including those for childhood overweight, tuberculosis, and road injury mortality. For several of the health-related SDGs, meeting defined targets hinges upon substantially faster progress than what most countries have achieved in the past.

    INTERPRETATION: GBD 2016 provides an updated and expanded evidence base on where the world currently stands in terms of the health-related SDGs. Our improved measure of UHC offers a basis to monitor the expansion of health services necessary to meet the SDGs. Based on past rates of progress, many places are facing challenges in meeting defined health-related SDG targets, particularly among countries that are the worst off. In view of the early stages of SDG implementation, however, opportunity remains to take actions to accelerate progress, as shown by the catalytic effects of adopting the Millennium Development Goals after 2000. With the SDGs' broader, bolder development agenda, multisectoral commitments and investments are vital to make the health-related SDGs within reach of all populations.

  • 23.
    Fullman, Nancy
    et al.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Yearwood, Jamal
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Abay, Solomon M.
    Addis Ababa Univ, Addis Ababa, Ethiopia.
    Abbafati, Cristiana
    Univ Roma La Sapienza, Rome, Italy.
    Abd-Allah, Foad
    Cairo Univ, Dept Neurol, Cairo, Egypt.
    Abdela, Jemal
    Haramaya Univ, Coll Hlth & Med Sci, Harar, Ethiopia.
    Abdelalim, Ahmed
    Cairo Univ, Dept Neurol, Cairo, Egypt.
    Abebe, Zegeye
    Univ Gondar, Gondar, Ethiopia.
    Abebo, Teshome Abuka
    Hawassa Univ, Coll Med & Hlth Sci, Hawassa, Ethiopia.
    Aboyans, Victor
    Dupuytren Univ Hosp, Limoges, France.
    Abraha, Haftom Niguse
    Mekelle Univ, Mekelle, Ethiopia.
    Abreu, Daisy M. X.
    Univ Fed Minas Gerais, Belo Horizonte, MG, Brazil.
    Abu-Raddad, Laith J.
    Weill Cornell Med Coll Qatar, Infect Dis Epidemiol Grp, Doha, Qatar.
    Adane, Akilew Awoke
    Univ Gondar, Gondar, Ethiopia;Univ Queensland, Brisbane, Qld, Australia.
    Adedoyin, Rufus Adesoji
    Obafemi Awolowo Univ, Dept Med Rehabil, Ife, Nigeria.
    Adetokunboh, Olatunji
    Stellenbosch Univ, Cape Town, South Africa.
    Adhikari, Tara Ballav
    Univ Southern Denmark, Fac Hlth Sci, Unit Hlth Promot Res, Esbjerg, Denmark.
    Afarideh, Mohsen
    Univ Tehran Med Sci, Endocrinol & Metab Res Ctr, Tehran, Iran.
    Afshin, Ashkan
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Agarwal, Gina
    McMaster Univ, Hamilton, ON, Canada;CSIR, Inst Genom & Integrat Biol, Delhi, India;Baylor Coll Med, Dept Internal Med, Houston, TX 77030 USA;Indian Inst Publ Hlth, Gurugram, India;Publ Hlth Fdn India, Gurugram, India.
    Agius, Dominic
    Directorate Hlth Informat & Res, Pieta, Malta;Malta Coll Family Doctors, Gzira, Malta.
    Agrawal, Anurag
    Agrawal, Sutapa
    Kiadaliri, Aliasghar Ahmad
    Lund Univ, Skane Univ Hosp, Dept Clin Sci Lund, Dept Clin Sci Lund,Orthoped,Clin Epidemiol Unit,N, Lund, Sweden.
    Aichour, Miloud Taki Eddine
    High Natl Sch Vet Med, Algiers, Algeria.
    Akibu, Mohammed
    Debere Berhan Univ, Debre Berhan, Ethiopia.
    Akinyemi, Rufus Olusola
    Univ Ibadan, Ibadan, Nigeria;Newcastle Univ, Newcastle Upon Tyne, Tyne & Wear, England.
    Akinyemiju, Tomi F.
    Univ Alabama Birmingham, Dept Epidemiol, Birmingham, AL USA.
    Akseer, Nadia
    Hosp Sick Children, Ctr Global Child Hlth, Toronto, ON, Canada;Univ Toronto, Fac Med, Dalla Lana Sch Publ Hlth, Dept Nutr Sci, Toronto, ON, Canada.
    Al Lami, Faris Hasan
    Baghdad Coll Med, Baghdad, Iraq.
    Alahdab, Fares
    Mayo Clin, Fdn Med Educ & Res, Rochester, MN USA;Syrian Amer Med Soc, Washington, DC USA.
    Al-Aly, Ziyad
    Washington Univ St Louis, St Louis, MO USA.
    Alam, Khurshid
    Univ Western Australia, Sch Populat & Global Hlth, Perth, WA, Australia.
    Alam, Tahiya
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Alasfoor, Deena
    Minist Hlth, Int Relat Div, Al Khuwair, Oman.
    Albittar, Mohammed I.
    Alene, Kefyalew Addis
    Univ Gondar, Inst Publ Hlth, Dept Epidemiol & Biostat, Gondar, Ethiopia;Australian Natl Univ, Res Sch Populat Hlth, Dept Global Hlth, Canberra, ACT, Australia.
    Al-Eyadhy, Ayman
    King Saud Univ, Riyadh, Saudi Arabia;King Faisal Specialist Hosp & Res Ctr, Riyadh, Saudi Arabia.
    Ali, Syed Danish
    Univ London, London, England;SIR Management Consultants, Oxford, England;Inst & Fac Actuaries, Oxford, England.
    Alijanzadeh, Mehran
    Qazvin Univ Med Sci, Qavin, Iran.
    Aljunid, Syed M.
    Kuwait Univ, Fac Publ Hlth, Kuwait, Kuwait;Natl Univ Malaysia, Int Ctr Casemix & Clin Coding, Kuala Lumpur, Malaysia.
    Alkerwi, Ala'a
    Luxembourg Inst Hlth, Strassen, Luxembourg.
    Alla, Francois
    Univ Lorraine, Sch Publ Hlth, Nancy, France.
    Allebeck, Peter
    Karolinska Inst, Dept Publ Hlth Sci, Stockholm, Sweden.
    Allen, Christine
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Alomari, Mahmoud A.
    Jordan Univ Sci & Technol, Fac Appl Med Sci, Dept Rehabil Sci, Div Phys Therapy, Irbid, Jordan.
    Al-Raddadi, Rajaa
    King Abdulaziz Univ, Dept Family & Community Med, Coll Med, Jeddah, Saudi Arabia.
    Alsharif, Ubai
    Charite Univ Med Berlin, Berlin, Germany.
    Altirkawi, Khalid A.
    King Saud Univ, Riyadh, Saudi Arabia.
    Alvis-Guzman, Nelson
    Univ Cartagena, Cartagena De Indias, Colombia.
    Amare, Azmeraw T.
    Bahir Dar Univ, Coll Med & Hlth Sci, Bahir Dar, Ethiopia.
    Amenu, Kebede
    Ammar, Walid
    Minist Publ Hlth, Beirut, Lebanon.
    Amoako, Yaw Ampem
    Komfo Anokye Teaching Hosp, Dept Med, Kumasi, Ghana.
    Anber, Nahla
    Andrei, Catalina Liliana
    Carol Davila Univ Med & Pharm, Bucharest, Romania.
    Androudi, Sofia
    Univ Thessaly, Larisa, Greece.
    Antonio, Carl Abelardo T.
    Univ Philippines Manila, Coll Publ Hlth, Manila, Philippines;Univ Philippines Manila, Coll Publ Hlth, Dept Hlth Policy & Adm, Manila, Philippines.
    Araujo, Valdelaine E. M.
    Univ Fed Minas Gerais, Belo Horizonte, MG, Brazil;Minist Hlth Brazil, Brasilia, DF, Brazil.
    Aremu, Olatunde
    Birmingham City Univ Dept Publ Hlth & Therapies, Birmingham, W Midlands, England.
    Arnlov, Johan
    Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Family Med & Primary Care, Stockholm, Sweden;Dalama Univ, Sch Hlth & Social Studies, Falun, Sweden.
    Artaman, Al
    Univ Manitoba, Winnipeg, MB, Canada.
    Aryal, Krishna Kumar
    Nepal Hlth Res Council, Kathmandu, Nepal;Univ Oslo, Oslo, Norway.
    Asayesh, Hamid
    Qom Univ Med Sci, Sch Paramed, Dept Emergency Med, Qom, Iran.
    Asfaw, Ephrem Tsegay
    Mekelle Univ, Coll Hlth Sci, Mekelle, Ethiopia;Mekelle Univ, Inst Biomed Sci, Mekelle, Ethiopia.
    Asgedom, Solomon Weldegebreal
    Mekelle Univ, Mekelle, Ethiopia.
    Asghar, Rana Jawad
    South Asian Publ Hlth Forum, Islamabad, Pakistan.
    Ashebir, Mengistu Mitiku
    Mekelle Univ, Sch Publ Hlth, Mekelle, Ethiopia.
    Asseffa, Netsanet Abera
    Atey, Tesfay Mehari
    Atre, Sachin R.
    Johns Hopkins Univ, Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Clin Global Hlth Educ, Baltimore, MD USA;Dr D Y Patil Vidyapeeth Pune, Pune, Maharashtra, India.
    Atteraya, Madhu S.
    Keimyung Univ, Daegu, South Korea.
    Avila-Burgos, Leticia
    Natl Inst Publ Hlth, Cuemavaca, Mexico.
    Avokpaho, Euripide Frinel G. Arthur
    Inst Rech Clin Benin, Cotonou, Benin;Lab Etudes & Rech Act St LERAS Afrique, Parakou, Benin.
    Awasthi, Ashish
    Indian Inst Publ Hlth, Gandhinagar, India.
    Quintanilla, Beatriz Paulina Ayala
    La Trobe Univ, Judith Lumley Ctr Mother Infant & Family Hlth Res, Melbourne, Vic, Australia;Peruvian Natl Inst Hlth, Lima, Peru.
    Ayalew, Animut Alebel
    Debre Markos Univ, Debre Markos, Ethiopia.
    Ayele, Henok Tadesse
    McGill Univ, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ, Canada;Dilla Univ, Dilla, Ethiopia.
    Ayer, Rakesh
    Univ Tokyo, Tokyo, Japan.
    Ayuk, Tambe Betrand
    Inst Med Res & Plant Med Studies Cameroon, Yaounde, Cameroon;Univ South Africa, Pretoria, South Africa.
    Azzopardi, Peter
    Burnet Inst, Melbourne, Vic, Australia;Univ Melbourne, Dept Paediat, Melbourne, Vic, Australia;Univ Melbourne, Murdoch Childrens Res Inst, Melbourne, Vic, Australia;South Australian Hlth & Med Res Inst, Wardliparingga Aboriginal Res Unit, Adelaide, SA, Australia.
    Azzopardi-Muscat, Natasha
    Directorate Hlth Informat & Res, Pieta, Malta;Univ Malta, Isl & Small States Inst, Dept Hlth Serv Management, Msida, Malta.
    Babalola, Tesleem Kayode
    Univ Lagos, Dept Community Hlth & Primary Care, Lagos, Nigeria.
    Badali, Hamid
    Invas Fungi Res Ctr, Sari, Iran;Ctr Expertise Mycol Radboudumc CWZ, Nijmegen, Netherlands.
    Badawi, Alaa
    Univ Toronto, Fac Med, Dalla Lana Sch Publ Hlth, Dept Nutr Sci, Toronto, ON, Canada;Publ Hlth Agcy Canada, Toronto, ON, Canada.
    Banach, Maciej
    Med Univ Lodz, Dept Hypertens, Lodz, Poland.
    Banerjee, Amitava
    UCL, Inst Hlth Informat, Farr Inst Hlth Informat Res, London, England.
    Banstola, Amrit
    Publ Hlth Perspect Nepal, Pokhara, Nepal.
    Barber, Ryan M.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Barboza, Miguel A.
    Hosp Dr Rafael A Calderon Guardia, CCSS, San Jose, Costa Rica;Univ Costa Rica, San Pedro, Costa Rica.
    Barker-Collo, Suzanne L.
    Univ Auckland, Sch Psychol, Auckland, New Zealand.
    Baernighausen, Till
    Barquera, Simon
    Natl Inst Publ Hlth, Cuemavaca, Mexico.
    Barrero, Lope H.
    Pontificia Univ Javeriana, Sch Engn, Dept Ind Engn, Bogota, Colombia.
    Bassat, Quique
    Univ Barcelona, Barcelona Inst Global Hlth, Barcelona, Spain;ICREA, Barcelona, Spain.
    Basu, Sanjay
    Stanford Univ, Stanford, CA USA.
    Baune, Bernhard T.
    Univ Adelaide, Sch Med, Discipline Psychiat, Adelaide, SA, Australia.
    Bazargan-Hejazi, Shahrzad
    Charles R Drew Univ Med & Sci, Coll Med, Los Angeles, CA USA;Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
    Bedi, Neeraj
    Jazan Univ, Coll Publ Hlth & Trop Med, Jazan, Saudi Arabia.
    Beghi, Ettore
    IRCCS, Ist Ric Farmacol Mario Negri, Milan, Italy.
    Behzadifar, Masoud
    Lorestan Univ Med Sci, Social Determinants Hlth Res Ctr, Khorramabad, Iran;Lorestan Univ Med Sci, Khorramabad, Iran;Iran Univ Med Sci, Hlth Management & Econ Res Ctr, Tehran, Iran.
    Behzadifar, Meysam
    Bekele, Bayu Begashaw
    Univ Gondar, Coll Med & Hlth Sci, Gondar, Ethiopia;Mizan Tepi Univ, Mizan Aman, Ethiopia.
    Belachew, Abate Bekele
    Mekelle Univ, Sch Publ Hlth, Mekelle, Ethiopia.
    Belay, Saba Abraham
    Dr Tewelde Legesse Hlth Sci Coll, Mekelle, Ethiopia.
    Belay, Yihalem Abebe
    Debre Markos Univ, Debre Markos, Ethiopia.
    Bell, Michelle L.
    Yale Univ, New Haven, CT USA.
    Bello, Aminu K.
    Univ Alberta, Edmonton, AB, Canada.
    Bennett, Derrick A.
    Univ Oxford, Nuffield Dept Populat Hlth, Oxford, England.
    Bennett, James R.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Bensenor, Isabela M.
    Univ Sao Paulo, Sao Paulo, Brazil.
    Berhe, Derbew Fikadu
    Mekelle Univ, Sch Pharm, Mekelle, Ethiopia;Univ Groningen, Univ Med Ctr Groningen, Groningen, Netherlands.
    Bernabe, Eduardo
    Kings Coll London, London, England.
    Bernstein, Robert Steven
    Emory Univ, Rollins Sch Publ Hlth, Dept Global Hlth, Atlanta, GA 30322 USA;Univ South Honda, Coll Publ Hlth, Dept Global Hlth, Tampa, FL USA.
    Beuran, Mircea
    Carol Davila Univ Med & Pharm, Bucharest, Romania;Emergency Hosp Bucharest, Bucharest, Romania.
    Bhalla, Ashish
    Postgrad Inst Med Educ & Res, Chandigarh, India.
    Bhatt, Paurvi
    Medtron Philanthropy, Minneapolis, MN USA.
    Bhaumik, Soumyadeep
    Publ Hlth Fdn India, Gurugram, India.
    Bhutta, Zulfiqar A.
    Hosp Sick Children, Ctr Global Child Hlth, Toronto, ON, Canada;Aga Khan Univ, Ctr Excellence Women & Child Hlth, Karachi, Pakistan.
    Biadgo, Belete
    Univ Gondar, Gondar, Ethiopia.
    Bijani, Ali
    Babol Univ Med Sci, Social Determinants Hlth Res Ctr, Hlth Res Inst, Babol Sar, Iran.
    Bikbov, Boris
    IRCCS, Ist Ric Farmacol Mario Negri, Milan, Italy.
    Birungi, Charles
    UCL, London, England.
    Biryukov, Stan
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Bizuneh, Hailemichael
    St Pauls Hosp, Millennium Med Coll, Addis Ababa, Ethiopia;Jigjiga Univ, Jigjiga, Ethiopia.
    Bolliger, Ian W.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Bolt, Kaylin
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Bou-Orm, Ibrahim R.
    Minist Publ Hlth, Beirut, Lebanon.
    Bozorgmehr, Kayvan
    Univ Heidelberg Hosp, Dept Gen Practice & Hlth Serv Res, Heidelberg, Germany.
    Brady, Oliver Jerome
    London Sch Hyg & Trop Med, London, England.
    Brazinova, Alexandra
    Comenius Univ, Inst Epidemiol, Fac Med, Bratislava, Slovakia.
    Breitborde, Nicholas J. K.
    Ohio State Univ, Columbus, OH 43210 USA.
    Brenner, Hermann
    German Canc Res Ctr, Heidelberg, Germany.
    Britton, Gabrielle
    INDICASAT AIP, Panama City, Panama.
    Brugha, Traolach S.
    Univ Leicester, Leicester, Leics, England.
    Butt, Zahid A.
    Al Shifa Trust Eye Hosp, Rawalpindi, Pakistan.
    Cahuana-Hurtado, Lucero
    Natl Inst Publ Hlth, Cuemavaca, Mexico.
    Campos-Nonato, Ismael Ricardo
    Natl Inst Publ Hlth, Cuemavaca, Mexico;Harvard Univ, Harvard T H Chan Sch Publ Hlth, Boston, MA 02115 USA. Africa Hlth Res Inst, Mtubatuba, South Africa.
    Campuzano, Julio Cesar
    Natl Inst Publ Hlth, Cuemavaca, Mexico.
    Car, Josip
    Nanyang Technol Univ, LKCMed, Singapore, Singapore;Imperial Coll London, London, England.
    Car, Mate
    Imperial Coll London, London, England;Minist Hlth Republ Croatia, Zagreb, Croatia.
    Cardenas, Rosario
    Metropolitan Autonomous Univ, Mexico City, DF, Mexico.
    Carrero, Juan Jesus
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden;Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Family Med & Primary Care, Stockholm, Sweden.
    Carvalho, Felix
    Univ Porto, Fac Pharm, Porto, Portugal.
    Castaneda-Orjuela, Carlos A.
    Inst Nacl Salud, Colombian Natl Hlth Observ, Bogota, Colombia;Univ Nacl Colombia, Publ Hlth Dept, Epidemiol & Publ Hlth Evaluat Grp, Bogota, Colombia.
    Rivas, Jacqueline Castillo
    Univ Costa Rica, San Pedro, Costa Rica;Caja Costarricense Seguro Social, San Jose, Costa Rica.
    Catala-Lopez, Ferran
    Univ Valencia, INCLIVA Hlth Res Inst, Dept Med, Valencia, Spain;Univ Valencia, CIBERSAM, Dept Med, Valencia, Spain;Ottawa Hosp Res Inst, Clin Epidemiol Program, Ottawa, ON, Canada.
    Cercy, Kelly
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Chalek, Julian
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Chang, Hsing-Yi
    Natl Hlth Res Inst, Zgunan Town, Taiwan;Natl Yang Ming Univ, Taipei, Taiwan.
    Chang, Jung-Chen
    Natl Taiwan Univ, Coll Med, Sch Nursing, Taipei, Taiwan.
    Chattopadhyay, Aparajita
    Int Inst Populat Sci, Mumbai, Maharashtra, India.
    Chaturvedi, Pankaj
    Tata Mem Hosp, Mumbai, Maharashtra, India.
    Chiang, Peggy Pei-Chia
    Gold Coast Hlth, Clin Governance Unit, Southport, Qld, Australia.
    Chisumpa, Vesper Hichilombwe
    Univ Zambia, Lusaka, Zambia;Univ Witwatersrand, Johannesburg, South Africa.
    Choi, Jee-Young J.
    Seoul Natl Univ, Seoul, South Korea;Seoul Natl Univ, Med Lib, Seoul, South Korea.
    Christensen, Hanne
    Bispebjerg Hosp, Copenhagen, Denmark.
    Christopher, Devasahayam Jesudas
    Christian Med Coll & Hosp, Vellore, Tamil Nadu, India.
    Chung, Sheng-Chia
    UCL, Inst Hlth Informat, Farr Inst Hlth Informat Res, London, England.
    Ciobanu, Liliana G.
    Univ Adelaide, Sch Med, Discipline Psychiat, Adelaide, SA, Australia.
    Cirillo, Massimo
    Univ Salerno, Baronissi, Italy.
    Colombara, Danny
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Conti, Sara
    Univ Milano Bicocca, Monza, Italy.
    Cooper, Cyrus
    Univ Oxford, NIHR Musculoskeletal Biomed Res Ctr, Oxford, England;Univ Southampton, MRC Lifecourse Epidemiol Unit, Southampton, Hants, England.
    Cornaby, Leslie
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Cortesi, Paolo Angelo
    Univ Milano Bicocca, Res Ctr Publ Hlth, Monza, Italy.
    Cortinovis, Monica
    IRCCS, Ist Ric Farmacol Mario Negri, Milan, Italy.
    Pereira, Alexandre Costa
    Univ Sao Paulo, Inst Heart, Sao Paulo, Brazil.
    Cousin, Ewerton
    Univ Fed Rio Grande do Sul, Porto Alegre, RS, Brazil.
    Criqui, Michael H.
    Univ Calif San Diego, San Diego, CA 92103 USA.
    Cromwell, Elizabeth A.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Crowe, Christopher Stephen
    Univ Washington, Seattle, WA 98195 USA.
    Crump, John A.
    Univ Otago, Dunedin Sch Med, Ctr Int Hlth, Dunedin, New Zealand.
    Daba, Alemneh Kabeta
    Hawassa Univ, Hawassa, Ethiopia.
    Dachew, Berihun Assefa
    Univ Gondar, Inst Publ Hlth, Gondar, Ethiopia;Univ Queensland, Brisbane, Qld, Australia;Wolaita Sodo Univ, Wolaita Sodo, Ethiopia.
    Dadi, Abel Fekadu
    Univ Gondar, Gondar, Ethiopia;Flinders Univ S Australia, Adelaide, SA, Australia.
    Dandona, Lalit
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA;Publ Hlth Fdn India, Gurugram, India.
    Dandona, Rakhi
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA;Publ Hlth Fdn India, Gurugram, India.
    Dargan, Paul I.
    Guys & St Thomas NHS Fdn Trust, London, England.
    Daryani, Ahmad
    Mazandaran Univ Med Sci, Toxoplasmosis Res Ctr, Sari, Iran.
    Daryani, Maryam
    Mazandaran Univ Med Sci, Sari, Iran.
    Das, Jai
    Aga Khan Univ, Dept Paediat & Child Hlth, Karachi, Pakistan.
    Das, Siddharth Kumar
    KG Med Univ, Lucknow, Uttar Pradesh, India.
    das Neves, Jose
    Univ Porto, INEB Inst Engn Biomed, Porto, Portugal;Univ Porto, Inst Invest & Inovacao Sande I3S, Porto, Portugal.
    Weaver, Nicole Davis
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Davletov, Kairat
    Kazakh Natl Med Univ, Sch Publ Hlth, Alma Ata, Kazakhstan.
    de Courten, Barbora
    Monash Univ, Melbourne, Vic, Australia;Monash Med Ctr, Clayton, Vic, Australia.
    De Leo, Diego
    Griffith Univ, Brisbane, Qld, Australia.
    De Neve, Jan-Walter
    Heidelberg Inst Publ Hlth, Heidelberg, Germany.
    Dellavalle, Robert P.
    Univ Colorado, Sch Med, Aurora, CO USA;Colorado Sch Publ Hlth, Aurora, CO USA.
    Demoz, Gebre
    Addis Ababa Univ, Addis Ababa, Ethiopia;Aksum Univ, Aksum, Ethiopia.
    Deribe, Kebede
    Addis Ababa Univ, Sch Publ Hlth, Addis Ababa, Ethiopia;Brighton & Sussex Med Sch, Brighton, E Sussex, England.
    Des Jarlais, Don C.
    Mt Sinai Beth Israel, New York, NY USA;Icahn Sch Med Mt Sinai, New York, NY 10029 USA.
    Dey, Subhojit
    Indian Inst Publ Hlth, Gurugram, India.
    Dharmaratne, Samath D.
    Univ Peradeniya, Fac Med, Dept Community Med, Peradeniya, Sri Lanka.
    Dhimal, Meghnath
    Govt Nepal, Nepal Hlth Res Council, Kathmandu, Nepal.
    Djalalinia, Shirin
    Minist Hlth & Med Educ, Res & Technol, Tehran, Iran.
    Doku, David Teye
    Univ Cape Coast, Cape Coast, Ghana;Univ Tampere, Tampere, Finland.
    Dolan, Kate
    UNSW, Sydney, NSW, Australia.
    Dorsey, E. Ray
    Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
    Bender dos Santos, Kadine Priscila
    Univ Estado Santa Catarina, Florianopolis, SC, Brazil.
    Doyle, Kerrie E.
    Australian Natl Univ, Res Sch Populat Hlth, Dept Global Hlth, Canberra, ACT, Australia;RMIT Univ, Bundoora, Vic, Australia.
    Driscoll, Tim R.
    Univ Sydney, Sydney Sch Publ Hlth, Sydney, NSW, Australia.
    Dubey, Manisha
    Int Inst Populat Sci, Mumbai, Maharashtra, India.
    Dubljanin, Eleonora
    Univ Belgrade, Inst Microbiol & Immunol, Belgrade, Serbia.
    Duncan, Bruce Bartholow
    Univ Fed Rio Grande do Sul, Porto Alegre, RS, Brazil;Univ N Carolina, Chapel Hill, NC 27515 USA.
    Echko, Michelle
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Edessa, Dumessa
    Haramaya Univ, Harar, Ethiopia.
    Edvardsson, David
    La Trobe Univ, Bundoora, Vic, Australia;Umea Univ, Umea, Sweden.
    Ehrlich, Joshua R.
    Univ Michigan, Ann Arbor, MI 48109 USA.
    Eldrenkamp, Erika
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    El-Khatib, Ziad
    Karolinska Inst, Dept Publ Hlth Sci, Stockholm, Sweden;Harvard Med Sch, Dept Global Hlth & Social Med, Kigali, Rwanda.
    Endres, Matthias
    Charite Univ Med Berlin, Berlin, Germany.
    Endries, Aman Yesuf
    Arba Minch Univ, Arba Minch, Ethiopia.
    Eshrati, Babak
    Minist Hlth & Med Educ, Tehran, Iran;Arak Univ Med Sci, Arak, Iran.
    Eskandarieh, Sharareh
    Multiple Sclerosis Res Ctr, Tehran, Iran.
    Esteghamati, Alireza
    Univ Tehran Med Sci, Endocrinol & Metab Res Ctr, Tehran, Iran.
    Fakhar, Mahdi
    Mazandaran Univ Med Sci, Sch Med, Mol & Cell Biol Res Ctr, Sari, Iran.
    Farag, Tamer
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Faramarzi, Mahbobeh
    Babol Univ Med Sci, Babol Sar, Iran.
    Faraon, Emerito Jose Aquino
    Univ Philippines Manila, Coll Publ Hlth, Manila, Philippines;Univ Philippines Manila, Coll Publ Hlth, Dept Hlth Policy & Adm, Manila, Philippines;Dept Hlth, Manila, Philippines.
    Faro, Andre
    Univ Fed Sergipe, Aracaju, Brazil.
    Farzadfar, Farshad
    Univ Tehran Med Sci, Noncommun Dis Res Ctr, Tehran, Iran.
    Fatusi, Adesegun
    Obafemi Awolowo Univ, Coll Hlth Sci, Dept Community Hlth, Ife, Nigeria.
    Fazeli, Mir Sohail
    Doctor Evidence, Santa Monica, CA USA.
    Feigin, Valery L.
    Auckland Univ Technol, Natl Inst Stroke & Appl Neurosci, Auckland, New Zealand.
    Feigl, Andrea B.
    Harvard Univ, Harvard T H Chan Sch Publ Hlth, Dept Global Hlth & Populat, Boston, MA 02115 USA.
    Fentahun, Netsanet
    Jimma Univ, Inst Hlth, Fac Publ Hlth, Dept Hlth Behav & Soc, Jimma, Ethiopia.
    Fereshtehnejad, Seyed-Mohammad
    Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Family Med & Primary Care, Stockholm, Sweden.
    Fernandes, Eduarda
    Univ Porto, Dept Chem Sci, Porto, Portugal.
    Fernandes, Joao C.
    Catholic Univ Portugal, Fac Biotechnol, CBQF Ctr Biotechnol & Fine Chem Associate Lab, Porto, Portugal.
    Fijabi, Daniel Obadare
    Brandeis Univ, Heller Grad Sch, Waltham, MA USA.
    Filip, Irina
    Kaiser Permanente, Fontana, CA USA.
    Fischer, Florian
    Univ Bielefeld, Sch Publ Hlth, Bielefeld, Germany.
    Fitzmaurice, Christina
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA;Univ Washington, Dept Med, Div Hematol, Seattle, WA 98195 USA;Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
    Flaxman, Abraham D.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Flor, Luisa Sorio
    Escola Nacl Sande Publ Sergio Arouca, Rio De Janeiro, Brazil;Univ Fed Espirito Santo, Vitoria, Brazil.
    Foigt, Nataliya
    Acad Med Sci, Inst Gerontol, Kiev, Ukraine. Swiss Trop & Publ Hlth Inst, Dept Epidemiol & Publ Hlth, Basel, Switzerland.
    Foreman, Kyle J.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA;Imperial Coll London, London, England.
    Frostad, Joseph J.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Fuerst, Thomas
    Futran, Neal D.
    Univ Washington, Seattle, WA 98195 USA.
    Gakidou, Emmanuela
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Gallus, Silvano
    IRCCS, Ist Ric Farmacol Mario Negri, Milan, Italy;Univ Fed Santa Catarina, Florian6poliss, Brazil.
    Gambashidze, Ketevan
    Natl Ctr Dis Control & Publ Hlth, Tbilisi, Rep of Georgia.
    Gamkrelidze, Amiran
    Natl Ctr Dis Control & Publ Hlth, Tbilisi, Rep of Georgia.
    Ganji, Morsaleh
    Univ Tehran Med Sci, Endocrinol & Metab Res Ctr, Tehran, Iran.
    Gebre, Abadi Kahsu
    Mekelle Univ, Mekelle, Ethiopia.
    Gebrehiwot, Tsegaye Tewelde
    Jimma Univ, Jimma, Ethiopia.
    Gebremedhin, Amanuel Tesfay
    Jimma Univ, Jimma, Ethiopia;Ludwig Maximilians Univ Munchen, Munich, Germany.
    Gelaw, Yalemzewod Assefa
    Univ Gondar, Inst Publ Hlth, Gondar, Ethiopia;Univ Queensland, Sch Publ Hlth, Brisbane, Qld, Australia.
    Geleijnse, Johanna M.
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands.
    Geremew, Demeke
    Univ Gondar, Gondar, Ethiopia.
    Gething, Peter W.
    Univ Oxford, Dept Zool, Oxford, England.
    Ghadimi, Reza
    Babol Univ Med Sci, Hlth Res Inst, Babol Sar, Iran;Dept Nutr, Babol Sar, Iran.
    Falavarjani, Khalil Ghasemi
    Ghasemi-Kasman, Maryam
    Babol Univ Med Sci, Babol Sar, Iran.
    Gill, Paramjit Singh
    Univ Warwick, Warwick Med Sch, Coventry, W Midlands, England.
    Giref, Ababi Zergaw
    Addis Ababa Univ, Addis Ababa, Ethiopia.
    Giroud, Maurice
    Univ Hosp Dijon, Dijon, France.
    Gishu, Melkamu Dedefo
    Haramaya Univ, Harar, Ethiopia;Kersa Hlth & Demog Surveillance Syst, Harar, Ethiopia.
    Giussani, Giorgia
    IRCCS, Ist Ric Farmacol Mario Negri, Milan, Italy.
    Godwin, William W.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Goli, Srinivas
    Jawaharlal Nehru Univ, New Delhi, India.
    Gomez-Dantes, Hector
    Natl Inst Publ Hlth, Cuemavaca, Mexico.
    Gona, Philimon N.
    Univ Massachusetts, Boston, MA 02125 USA.
    Goodridge, Amador
    Inst Invest Cient Serv Alta Tecnol INDICASAT AIP, Ciudad Saber, Panama.
    Gopalani, Sameer Vali
    Govt Federated States Micronesia, Dept Hlth & Social Affairs, Palikir, Micronesia.
    Goryakin, Yevgeniy
    Org Econ Cooperat & Dev, Paris, France.
    Goulart, Alessandra Carvalho
    Univ Sao Paulo, Univ Hosp, Ctr Clin, Sao Paulo, Brazil;Univ Sao Paulo, Univ Hosp, Epidemiol Res Ctr, Sao Paulo, Brazil.
    Grada, Ayman
    Boston Univ, Sch Med, Boston, MA 02215 USA.
    Griswold, Max
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Grosso, Giuseppe
    Univ Hosp Policlin Vittorio Emanuele, Catania, Italy;NNEdPro Global Ctr Nutr & Hlth, Cambridge, England.
    Gugnani, Harish Chander
    St James Sch Med, Dept Microbiol, Quarter, Anguilla;St James Sch Med, Dept Epidemiol & Biostat, Quarter, Anguilla.
    Guo, Yuming
    Univ Queensland, Brisbane, Qld, Australia.
    Gupta, Rahul
    West Virginia Bur Publ Hlth, Charleston, WV USA.
    Gupta, Rajeev
    Eternal Heart Care Ctr, Jaipur, Rajasthan, India;Res Inst, Jaipur, Rajasthan, India.
    Gupta, Tanush
    Montefiore Med Ctr, Bronx, NY 10467 USA;Albert Einstein Coll Med, Bronx, NY 10467 USA.
    Gupta, Tarun
    Indian Inst Technol Kanpur, Kanpur, Uttar Pradesh, India.
    Gupta, Vipin
    Univ Delhi, Dept Anthropol, Delhi, India.
    Haagsma, Juanita A.
    Univ Med Ctr Rotterdam, Erasmus MC, Rotterdam, Netherlands.
    Hachinski, Vladimir
    Western Univ, London, ON, Canada.
    Hafezi-Nejad, Nima
    Univ Tehran Med Sci, Endocrinol & Metab Res Ctr, Tehran, Iran.
    Hailu, Gessessew Bugssa
    Mekelle Univ, Mekelle, Ethiopia;Kilte Awlaelo Hlth & Demog Surveillance Syst, Mekelle, Ethiopia.
    Hamadeh, Randah Ribhi
    Arabian Gulf Univ, Manama, Bahrain.
    Hamidi, Samer
    Hamdan Bin Mohammed Smart Univ, Abu Dhabi, U Arab Emirates.
    Hankey, Graeme J.
    Univ Western Australia, Sch Med & Pharmacol, Perth, WA, Australia;Harry Perkins Inst Med Res, Nedlands, WA, Australia;Western Australian Neurosci Res Inst, Nedlands, WA, Australia.
    Harb, Hilda L.
    Harewood, Heather C.
    Eunice Gibson Polyclin, Bridgetown, Barbados.
    Harikrishnan, Sivadasanpillai
    Sree Chitra Tirunal Inst Med Sci & Technol, Trivandrum, Kerala, India.
    Haro, Josep Maria
    Parc Sanitari St Joan Deu CIBERSAM, Barcelona, Spain.
    Hassen, Hamid Yimam
    Mizan Tepi Univ, Mizan Aman, Ethiopia.
    Havmoeller, Rasmus
    Hawley, Caitlin
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Hay, Simon I.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA;Univ Oxford, Li Ka Shing Ctr Hlth Informat & Discovery, Oxford Big Data Inst, Oxford, England.
    He, Jiawei
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Hearps, Stephen J. C.
    Murdoch Childrens Res Hosp, Child Neuropsychol, Parkville, Vic, Australia.
    Hegazy, Mohamed I.
    Cairo Univ, Fac Med, Cairo, Egypt.
    Heibati, Behzad
    Iran Univ Med Sci, Air Pollut Res Ctr, Tehran, Iran.
    Heidari, Mohsen
    Hormozgan Univ Med Sci, Fac Hlth, Bandar Abbas, Iran.
    Hendrie, Delia
    Curtin Univ, Sch Publ Hlth, Perth, WA, Australia.
    Henry, Nathaniel J.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Herrera Ballesteros, Victor Hugo
    Gorgas Mem Inst Studies Hlth, Panama City, Panama;Univ Panama, Panama City, Panama.
    Herteliu, Claudiu
    Bucharest Univ Econ Studies, Dept Stat & Econometr, Bucharest, Romania.
    Hibstu, Desalegn Tsegaw
    Hawassa Univ, Coll Med & Hlth Sci, Hawassa, Ethiopia.
    Hiluf, Molla Kahssay
    Samara Univ, Samara, Ethiopia.
    Hoek, Hans W.
    Univ Groningen, Univ Med Ctr Groningen, Dept Psychiat, Groningen, Netherlands;Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10027 USA.
    Rad, Enayatollah Homaie
    Guilan Univ Med Sci, Guilan Rd Trauma Res Ctr, Rasht, Iran.
    Horita, Nobuyuki
    Yokohama City Univ, Grad Sch Med, Dept Pulmonol, Yokohama, Kanagawa, Japan.
    Hosgood, H. Dean
    Albert Einstein Coll Med, Bronx, NY 10467 USA.
    Hosseini, Mostafa
    Hosseini, Seyed Reza
    Babol Univ Med Sci, Social Determinants Hlth Res Ctr, Hlth Res Inst, Babol Sar, Iran.
    Hostiuc, Mihaela
    Carol Davila Univ Med & Pharm, Bucharest, Romania.
    Hostiuc, Sorin
    Carol Davila Univ Med & Pharm, Bucharest, Romania.
    Hoy, Damian G.
    Pacific Community, Publ Hlth Div, Noumea, New Caledonia.
    Hsairi, Mohamed
    Salah Azaiz Inst, Dept Epidemiol, Tunis, Tunisia.
    Htet, Aung Soe
    Univ Oslo, Oslo, Norway.
    Hu, Guoqing
    Cent S Univ, Sch Publ Hlth, Dept Epidemiol & Hlth Stat, Changsha, Peoples R China.
    Huang, John J.
    Yale Univ, New Haven, CT USA.
    Iburg, Kim Moesgaard
    Aarhus Univ, Aarhus, Denmark.
    Idris, Fachmi
    Sriwijaya Univ, Palembang, Indonesia;Social Secur Administering Body Hlth, Jakarta, Indonesia.
    Igumbor, Ehimario Uche
    US Ctr Dis Control & Prevent, Pretoria, South Africa;Univ Western Cape, Sch Publ Hlth, Cape Town, South Africa.
    Ikeda, Chad
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Ileanu, Bogdan Vasile
    Bucharest Univ Econ Studies, Bucharest, Romania.
    Ilesanmi, Olayinka S.
    Natl Publ Hlth Inst, Monrovia, CA, Liberia.
    Innos, Kaire
    Natl Inst Hlth Dev, Tallinn, Estonia.
    Irvani, Seyed Sina Naghibi
    Prevent Metab Disorders Res Ctr, Res Inst Endocrine Sci, Tehran, Iran;Shahid Beheshti Univ Med Sci, Tehran, Iran.
    Irvine, Caleb M. S.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Islami, Farhad
    Amer Canc Soc, Surveillance & Hlth Serv Res, Atlanta, GA 30329 USA.
    Jacobs, Troy A.
    USAID Global Hlth Bur, HIDN, MCH Div, Washington, DC USA.
    Jacobsen, Kathryn H.
    George Mason Univ, Dept Global & Community Hlth, Fairfax, VA 22030 USA.
    Jahanmehr, Nader
    Shahid Beheshti Univ Med Sci, Sch Publ Hlth, Tehran, Iran.
    Jain, Rajesh
    Jain Hosp MSS, Kanpur, Uttar Pradesh, India.
    Jain, Sudhir Kumar
    Natl Ctr Dis Control Delhi, Delhi, India.
    Jakovljevic, Mihajlo M.
    Univ Washington, Ctr Hlth Trends & Forecasts, Seattle, WA 98195 USA;Univ Kragujevac, Fac Med Sci, Kragujevac, Serbia.
    Jalu, Moti Tolera
    Haramaya Univ, Harar, Ethiopia;St Pauls Hosp, Millennium Med Coll, Addis Ababa, Ethiopia.
    Jamal, Amr A.
    Javanbakht, Mehdi
    Univ Aberdeen, Aberdeen, Scotland.
    Jayatilleke, Achala Upendra
    Postgrad Inst Med, Colombo, Sri Lanka;Inst Violence & Injury Prevent, Colombo, Sri Lanka.
    Jeemon, Panniyammakal
    Ctr Control Chron Condit, Gurugram, India;Ctr Chron Dis Control, New Delhi, India.
    Jha, Ravi Prakash
    Banaras Hindu Univ, Varanasi, Uttar Pradesh, India.
    Jha, Vivekanand
    Univ Oxford, Oxford, England;George Inst Global Hlth, New Delhi, India.
    Jozwiak, Jacek
    Czestochowa Tech Univ, Inst Hlth & Nutr Sci, Czestochowa, Poland.
    John, Oommen
    George Inst Global Hlth, New Delhi, India.
    Johnson, Sarah Charlotte
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Jonas, Jost B.
    Heidelberg Univ, Med Fac Mannheim, Dept Ophthalmol, Mannheim, Germany.
    Joshua, Vasna
    Indian Council Med Res, Natl Inst Epidemiol, Chennai, Tamil Nadu, India.
    Juerisson, Mikk
    Univ Tartu, Inst Family Med & Publ Hlth, Tartu, Estonia.
    Kabir, Zubair
    Univ Coll Cork, Cork, Ireland.
    Kadel, Rajendra
    London Sch Econ & Polit Sci, London, England.
    Kahsay, Amaha
    Mekelle Univ, Mekelle, Ethiopia.
    Kalani, Rizwan
    Univ Washington, Seattle, WA 98195 USA.
    Kar, Chittaranjan
    SCB Med Coll, Cuttack, Orissa, India.
    Karanikolos, Marina
    European Observ Hlth Syst & Policies, London, England.
    Karch, Andre
    Helmholtz Ctr Infect Res, Epidemiol & Stat Methods Res Grp, Braunschweig, Germany;German Ctr Infect Res, Hannover, Germany.
    Karema, Corine Kakizi
    Swiss Trop & Publ Hlth Inst, Basel, Switzerland. Univ Basel, Basel, Switzerland;Qual & Equity Hlth Care, Kigali, Rwanda.
    Karimi, Seyed M.
    Univ Washington Tacoma, Tacoma, WA USA.
    Kasaeian, Amir
    Univ Tehran Med Sci, Hematol Malignancies Res Ctr, Tehran, Iran;Univ Tehran Med Sci, Hematol Oncol & Stem Cell Transplantat Res Ctr, Tehran, Iran.
    Kassa, Dessalegn Haile
    Debre Markos Univ, Debre Markos, Ethiopia.
    Kassa, Getachew Mullu
    Debre Markos Univ, Debre Markos, Ethiopia.
    Kassa, Tesfaye Dessale
    Mekelle Univ, Mekelle, Ethiopia.
    Kassebaum, Nicholas J.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA;Seattle Childrens Hosp, Dept Anesthesiol & Pain Med, Seattle, WA USA.
    Katikireddi, Srinivasa Vittal
    Univ Glasgow, MRC CSO Social Publ Hlth Sci Unit, Glasgow, Lanark, Scotland.
    Kaul, Anil
    Oklahoma State Univ, Tulsa, OK USA.
    Kawakami, Norito
    Univ Tokyo, Sch Publ Hlth, Tokyo, Japan.
    Kazanjan, Konstantin
    Natl Ctr Dis Control & Publ Hlth, Tbilisi, Rep of Georgia.
    Kebede, Seifu
    Mekelle Univ, Mekelle, Ethiopia.
    Keiyoro, Peter Njenga
    Inst Trop & Infect Dis, Nairobi, Kenya;Sch Continuing & Distance Educ, Nairobi, Kenya.
    Kemp, Grant Rodgers
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Kengne, Andre Pascal
    South African Med Res Council, UKZN Gastrointestinal Canc Res Ctr, Cape Town, South Africa;Univ Cape Town, Fac Hlth Sci, Hatter Inst Cardiovasc Res Africa, Dept Psychiat, Cape Town, South Africa.
    Kereselidze, Maia
    Natl Ctr Dis Control & Publ Hlth, Tbilisi, Rep of Georgia.
    Ketema, Ezra Belay
    Mekelle Univ, Mekelle, Ethiopia.
    Khader, Yousef Saleh
    Jordan Univ Sci & Technol, Dept Community Med Publ Hlth & Family Med, Irbid, Jordan;Jordan Univ Sci & Technol, Fac Appl Med Sci, Dept Rehabil Sci, Div Phys Therapy, Irbid, Jordan.
    Khafaie, Morteza Abdullatif
    Ahvaz Jundishapur Univ Med Sci, Ahwaz, Iran.
    Khajavi, Alireza
    Shahid Beheshti Univ Med Sci, Tehran, Iran.
    Khalil, Ibrahim A.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Khan, Ejaz Ahmad
    Hlth Serv Acad, Islamabad, Pakistan.
    Khan, Gulfaraz
    United Arab Emirates Univ, Coll Med Hlth Sci, Dept Microbiol & Immunol, Al Ain, U Arab Emirates.
    Khan, Md Nuruzzaman
    Univ Newcastle, Newcastle, NSW, Australia;Jatiya Kabi Kazi Nazrul Islam Univ, Mymensingh, Bangladesh.
    Khan, Muhammad Ali
    Univ Alabama Birmingham, Dept Epidemiol, Birmingham, AL USA;Univ Tennessee, Hlth Sci Ctr, Memphis, TN 38163 USA.
    Khanal, Mukti Nath
    Dept Hlth Serv Hlth Management Informat Syst, Kathmandu, Nepal.
    Khang, Young-Ho
    Seoul Natl Univ, Dept Hlth Policy & Management, Coll Hlth Sci, Seoul, South Korea;Seoul Natl Univ, Med Ctr, Inst Hlth Policy & Management, Seoul, South Korea.
    Khater, Mona M.
    Cairo Univ, Fac Med, Cairo, Egypt;Cairo Univ, Cairo, Egypt.
    Khoja, Abdullah Tawfih Abdullah
    Johns Hopkins Univ, Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Clin Global Hlth Educ, Baltimore, MD USA;Mohammed Ibn Saudi Univ, Coll Med, Dept Publ Hlth, Riyadh, Saudi Arabia;Mohammed Ibn Saudi Univ, Coll Med, Dept Family Med, Riyadh, Saudi Arabia.
    Khosravi, Ardeshir
    Univ Tehran Med Sci, Noncommun Dis Res Ctr, Tehran, Iran;Iranian Minist Hlth & Med Educ, Tehran, Iran.
    Khubchandani, Jagdish
    Ball State Univ, Dept Nutr & Hlth Sci, Muncie, IN 47306 USA.
    Kibret, Getiye Dejenu
    Addis Ababa Univ, Coll Vet Med & Agr, Addis Ababa, Ethiopia;Debre Markos Univ, Debre Markos, Ethiopia.
    Kiirithio, Daniel Ngari
    Kenya Revenue Author, Nairobi, Kenya;Synotech Consultants, Nairobi, Kenya.
    Kim, Daniel
    Northeastern Univ, Dept Hlth Sci, Boston, MA 02115 USA.
    Kim, Yun Jin
    Xiamen Univ, Sch Med, Malaysia Campus, Sepang, Malaysia.
    Kimokoti, Ruth W.
    Simmons Coll, Boston, MA 02115 USA.
    Kinfu, Yohannes
    Univ Canberra, Ctr Res & Action Publ Hlth, Canberra, ACT, Australia.
    Kinra, Sanjay
    London Sch Hyg & Trop Med, London, England.
    Kisa, Adnan
    Univ Oslo, Oslo, Norway.
    Kissoon, Niranjan
    Univ British Columbia, Fac Med, Sch Populat & Publ Hlth, Vancouver, BC, Canada.
    Kochhar, Sonali
    Univ Washington, Dept Global Hlth, Seattle, WA 98195 USA;Global Healthcare Consulting, New Delhi, India.
    Kokubo, Yoshihiro
    Natl Cerebral & Cardiovasc Ctr, Dept Prevent Cardiol, Suita, Osaka, Japan.
    Kopec, Jacek A.
    Univ British Columbia, Fac Med, Sch Populat & Publ Hlth, Vancouver, BC, Canada.
    Kosen, Soewarta
    Natl Inst Hlth Res Dev, Ctr Community Empowerment Hlth Policy & Humanitie, Jakarta, Indonesia.
    Koul, Parvaiz A.
    Sher Kashmir Inst Med Sci, Srinagar, Jammu & Kashmir, India.
    Koyanagi, Ai
    Parc Sanitari St Joan Deu CIBERSAM, Res & Dev Unit, Barcelona, Spain.
    Kravchenko, Michael
    Res Ctr Neurol, Moscow, Russia.
    Krishan, Kewal
    Panjab Univ, Chandigarh, India.
    Krohn, Kristopher J.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Defo, Barthelemy Kuate
    Univ Montreal, Sch Publ Hlth, Dept Demog, Montreal, PQ, Canada;Univ Montreal, Sch Publ Hlth, Publ Hlth Res Inst, Montreal, PQ, Canada;Univ Montreal, Sch Publ Hlth, Dept Social & Prevent Med, Montreal, PQ, Canada.
    Kumar, G. Anil
    Publ Hlth Fdn India, Gurugram, India.
    Kumar, Pushpendra
    Int Inst Populat Sci, Mumbai, Maharashtra, India.
    Kutz, Michael
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Kuzin, Igor
    Minist Hlth Ukraine, State Inst Publ Hlth Ctr, Kiev, Ukraine.
    Kyu, Hmwe H.
    Univ Washington, Inst Hlth Metr & Evaluat, Seattle, WA 98195 USA.
    Lad, Deepesh Pravinkumar
    Postgrad Inst Med Educ & Res, Chandigarh, India.
    Lafranconi, Alessandra
    Univ Milano Bicocca, Monza, Italy.
    Lal, Dharmesh Kumar
    Publ Hlth Fdn India, Gurugram, India.
    Lalloo, Ratilal
    Univ Queensland, Sch Dent, Brisbane, Qld, Australia.
    Lam, Hilton
    NHLBI, Ctr Translat Res & Implementat Sci, Inst Hlth Policy & Dev Studies, Natl Inst Hlth, Manila, Philippines.
    Lan, Qing
    NCI, Rockville, MD USA.
    Lang, Justin J.
    Publ Hlth Agcy Canada, Toronto, ON, Canada;Childrens Hosp, Eastern Ontario Res Inst, Ottawa, ON, Canada.
    Lansingh, Van C.
    Help Me See Inc, New York, NY USA;Inst Mexicano Oftalmol, Queretaro, Mexico.
    Lansky, Sonia
    Univ Fed Minas Gerais, Sch Med, Belo Horizonte, MG, Brazil;Secretaria Municipal Sande, Belo Horizonte, MG, Brazil.
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Chemistry.
    Latifi, Arman
    Maragheh Univ Med Sci, Managerial Epidemiol Res Ctr, Sch Nursing & Midwifery, Dept Publ Hlth, Maragheh, Iran.
    Lazarus, Jeffrey Victor
    Univ Barcelona, Hosp Clin, ISGlobal, Barcelona, Spain;Univ Copenhagen, Rigshosp, CHIP, Copenhagen, Denmark.
    Leasher, Janet L.
    Nova Southeastern Univ, Coll Optometry, Ft Lauderdale, FL 33314 USA.
    Lee, Paul H.
    Hong Kong Polytech Univ, Hong Kong, Hong Kong, Peoples R China.
    Legesse, Yirga
    Mekelle Univ, Mekelle, Ethiopia.
    Leigh, James
    Univ Sydney, Sydney, NSW, Australia.
    Leshargie, Cheru Tesema
    Debre Markos Univ, Debre Markos, Ethiopia.
    Leta, Samson
    Addis Ababa Univ, Addis Ababa, Ethiopia.
    Leung, Janni
    Univ Washington, Seattle, WA 98195 USA;Univ Queensland, Sch Publ Hlth, Brisbane, Qld, Australia.
    Leung, Ricky
    SUNY Albany, Albany, NY 12222 USA.
    Levi, Miriam
    Tuscany Reg Ctr Occupat Injuries & Dis, Florence, Italy.
    Li, Yongmei
    San Francisco VA Med Ctr, San Francisco, CA USA.
    Liang, Juan
    Sichuan Univ, West China Univ Hosp 2, Natl Off Maternal & Child Hlth Surveillance, Chengdu, Sichuan, Peoples R China.
    Liben, Misgan Legesse
    Samara Univ, Samara, Ethiopia.
    Lim, Lee-Ling
    Univ Malaya, Kuala Lumpur, Malaysia;Chinese Univ Hong Kong, Shatin, Hong Kong, Peoples R China.
    Lim, St