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  • 65351. ZhuoHui, Zhao
    et al.
    Xin, Zhang
    RanRan, Liu
    Norbäck, Dan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Arbets- och miljömedicin.
    Wieslander, Gunilla
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Arbets- och miljömedicin.
    Jie, Chen
    Sundell, Jan
    Prenatal and early life home environment exposure in relation to preschool children's asthma, allergic rhinitis and eczema in Taiyuan, China2013Ingår i: Chinese Science Bulletin, ISSN 1001-6538, E-ISSN 1861-9541, Vol. 58, nr 34, s. 4245-4251Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Prenatal and early life home environment might be related to children's asthma or allergic diseases later in life. A cross-sectional epidemiological study was designed and a questionnaire survey was performed in 3700 preschool children in urban areas in Taiyuan, Shanxi Province, China. Questions on children's asthma and allergic diseases from the International Study on Asthma and Allergies in Childhood (ISAAC) were integrated with questions on home environment from the Swedish Dampness in Buildings and Health (DBH) study, appropriately modified for Chinese life habits. By multivariate regression analyses controlling for age, gender, heredity, location in urban/suburban or rural areas, environmental tobacco smoke (ETS) and breastfeeding, we found that home new furniture (HNF) before birth (referring to 1 year before pregnancy and during pregnancy) was positively associated with wheezing ever (odds ratio(OR) 1.23 with 95% CI of 1.03-1.48) and wheezing last 12 months (1.24,1.00-1.54), allergic rhinitis (AR) (1.26,1.06-1.51), and eczema (1.42,1.01-1.99). HNF between 0-1 years old was also positively associated with wheezing last 12 months. Home new decoration (HND) during 0-1 years old was positively associated with AR symptoms and eczema symptoms, more in the last 12 months. Stronger positive associations were found for signs of home mold and dampness with almost all children's asthmatic and allergic symptoms (OR ranging from 1.23-1.85, P<0.05). By mutual adjustment between HNF before children's birth and home mold or dampness, all the significance remained unchanged. Prenatal HNF and home mold or dampness was independently associated with children's asthmatic and allergic diseases later in life.

  • 65352.
    Zi, Zhike
    et al.
    BIOSS Centre for Biological Signalling Studies and Center for Biological Systems Analysis (ZBSA), University of Freiburg, Freiburg, Germany.
    Feng, Zipei
    Department of Chemistry and Biochemistry, University of Colorado, Boulder, CO, USA.
    Chapnick, Douglas A.
    Department of Chemistry and Biochemistry, University of Colorado, Boulder, CO, USA.
    Dahl, Markus
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning.
    Deng, Difan
    BIOSS Centre for Biological Signalling Studies and Center for Biological Systems Analysis (ZBSA), University of Freiburg, Freiburg, Germany.
    Klipp, Edda
    Theoretical Biophysics, Institute for Biology, Humboldt-Universita¨ t zu Berlin, Berlin, Germany.
    Moustakas, Aristidis
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Liu, Xuedong
    Department of Chemistry and Biochemistry, University of Colorado, Boulder, CO, USA.
    Quantitative analysis of transient and sustained transforming growth factor-beta signaling dynamics2011Ingår i: Molecular Systems Biology, ISSN 1744-4292, E-ISSN 1744-4292, Vol. 7, nr 492Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Mammalian cells can decode the concentration of extracellular transforming growth factor-beta (TGF-beta) and transduce this cue into appropriate cell fate decisions. How variable TGF-beta ligand doses quantitatively control intracellular signaling dynamics and how continuous ligand doses are translated into discontinuous cellular fate decisions remain poorly understood. Using a combined experimental and mathematical modeling approach, we discovered that cells respond differently to continuous and pulsating TGF-beta stimulation. The TGF-beta pathway elicits a transient signaling response to a single pulse of TGF-beta stimulation, whereas it is capable of integrating repeated pulses of ligand stimulation at short time interval, resulting in sustained phospho-Smad2 and transcriptional responses. Additionally, the TGF-beta pathway displays different sensitivities to ligand doses at different time scales. While ligand-induced short-term Smad2 phosphorylation is graded, long-term Smad2 phosphorylation is switch-like to a small change in TGF-beta levels. Correspondingly, the short-term Smad7 gene expression is graded, while long-term PAI-1 gene expression is switch-like, as is the long-term growth inhibitory response. Our results suggest that long-term switch-like signaling responses in the TGF-beta pathway might be critical for cell fate determination.

  • 65353.
    Ziaei, Shirin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Women’s status and child nutrition: Findings from community studies in Bangladesh and Nicaragua2016Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    The importance of women’s status for child nutrition has recently been recognized. However, pathways through which women’s status can affect their caretaking practices and child nutrition have not been fully determined. The aim of this thesis was to evaluate associations between aspects of women’s status – including exposure to domestic violence and level of autonomy and social support – with their level of stress, feeding practices and child nutritional status in two different cultural settings: Bangladesh and Nicaragua.

    Data were acquired from population-based studies. For Study I we used data from the Bangladesh 2007 Demographic and Health Survey, and Study II was embedded in the 2009 Health and Demographic Surveillance System conducted in Los Cuatro Santos, rural Nicaragua. Studies III and IV were part of the MINIMat study, conducted in rural Bangladesh. In-person interviews were conducted and validated questionnaires were used in each of the studies. Anthropometric characteristics of the children were recorded based on standardized World Health Organization techniques.

    In Bangladesh, we found women with lifetime experience of domestic violence to be more likely to report emotional distress during pregnancy, cease exclusive breastfeeding before 6 months and have a stunted child. Further, we found a negative association between experience of domestic violence and duration of excusive breastfeeding to be mitigated with breastfeeding counseling. In Nicaragua, a lower level of maternal autonomy was associated with more appropriate breastfeeding practices such as higher odds of exclusive breastfeeding and longer continuation of breastfeeding. Further, a maternal lower level of social support was associated with better child nutritional status.

    In conclusion, this investigation showed that different dimensions of women’s status were associated with their feeding practices and child nutritional status and also revealed that the strength and direction of these associations may vary by the child’s age, setting and other contextual factors. These findings suggest that women’s status might have an important public health impact on child health and its role should be considered in programs and policies aiming to improve child health and nutrition.

    Delarbeten
    1. Women's exposure to intimate partner violence and child malnutrition: findings from demographic and health surveys in Bangladesh
    Öppna denna publikation i ny flik eller fönster >>Women's exposure to intimate partner violence and child malnutrition: findings from demographic and health surveys in Bangladesh
    2014 (Engelska)Ingår i: Maternal and Child Nutrition, ISSN 1740-8695, E-ISSN 1740-8709, Vol. 10, nr 3, s. 347-359Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Domestic violence, in particular intimate partner violence (IPV), has been recognized as a leading cause of mortality and morbidity among women of reproductive age. The effects of IPV against women on their children's health, especially their nutritional status has received less attention but needs to be evaluated to understand the comprehensive public health implications of IPV. The aim of current study was to investigate the association between women's exposure to IPV and their children's nutritional status, using data from the 2007 Bangladesh Demographic and Health Survey (BDHS). Logistic regression models were used to estimate association between ever-married women's lifetime exposure to physical and sexual violence by their spouses and nutritional status of their children under 5 years. Of 2042 women in the BDHS survey with at least one child under 5 years of age, 49.4% reported lifetime experience of physical partner violence while 18.4% reported experience of sexual partner violence. The prevalence of stunting, wasting and underweight in their children under 5 years was 44.3%, 18.4% and 42.0%, respectively. Women were more likely to have a stunted child if they had lifetime experience of physical IPV [odds ratio n = 2027 (OR)adj, 1.48; 95% confidence interval (CI), 1.23–1.79] or had been exposed to sexual IPV (n = 2027 ORadj, 1.28; 95% CI, 1.02–1.61). The present findings contribute to growing body of evidence showing that IPV can also compromise children's growth, supporting the need to incorporate efforts to address IPV in child health and nutrition programmes and policies.

    Nationell ämneskategori
    Näringslära
    Identifikatorer
    urn:nbn:se:uu:diva-198258 (URN)10.1111/j.1740-8709.2012.00432.x (DOI)000337613300004 ()22906219 (PubMedID)
    Tillgänglig från: 2013-04-11 Skapad: 2013-04-11 Senast uppdaterad: 2017-12-06Bibliografiskt granskad
    2. Women´s autonomy and social support and their associations with infant and young child feeding and nutritional status: community-based survey in rural Nicaragua
    Öppna denna publikation i ny flik eller fönster >>Women´s autonomy and social support and their associations with infant and young child feeding and nutritional status: community-based survey in rural Nicaragua
    Visa övriga...
    2015 (Engelska)Ingår i: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 18, nr 11, s. 1979-1990Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Objective

    To evaluate the associations of women’s autonomy and social support with infant and young child feeding practices (including consumption of highly processed snacks and sugar-sweetened beverages) and nutritional status in rural Nicaragua.

    Design

    Cross-sectional study. Feeding practices and children’s nutritional status were evaluated according to the WHO guidelines complemented with information on highly processed snacks and sugar-sweetened beverages. Women’s autonomy was assessed by a seventeen-item questionnaire covering dimensions of financial independence, household-, child-, reproductive and health-related decision making and freedom of movement. Women’s social support was determined using the Duke-UNC Functional Social Support Questionnaire. The scores attained were categorized into tertiles.

    Setting

    Los Cuatro Santos area, rural Nicaragua.

    Subjects

    A total of 1371 children 0–35 months of age.

    Results

    Children of women with the lowest autonomy were more likely to be exclusively breast-fed and continue to be breast-fed, while children of women with middle level of autonomy had better complementary feeding practices. Children of women with the lowest social support were more likely to consume highly processed snacks and/or sugar-sweetened beverages but also be taller.

    Conclusions

    While lower levels of autonomy and social support were independently associated with some favourable feeding and nutrition outcomes, this may not indicate a causal relationship but rather that these factors reflect other matters of importance for child care.

    Nyckelord
    social support, decision making, children, nutrition, Nicaragua
    Nationell ämneskategori
    Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi
    Identifikatorer
    urn:nbn:se:uu:diva-248695 (URN)10.1017/S1368980014002468 (DOI)000357673600009 ()25409706 (PubMedID)
    Tillgänglig från: 2015-04-07 Skapad: 2015-04-07 Senast uppdaterad: 2018-11-28Bibliografiskt granskad
    3. Experiencing lifetime domestic violence: associations with mental health and stress among pregnant women in rural Bangladesh: The MINIMat randomized trial
    Öppna denna publikation i ny flik eller fönster >>Experiencing lifetime domestic violence: associations with mental health and stress among pregnant women in rural Bangladesh: The MINIMat randomized trial
    (Engelska)Artikel i tidskrift (Övrigt vetenskapligt) Submitted
    Ort, förlag, år, upplaga, sidor
    uppsala:
    Nationell ämneskategori
    Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi
    Identifikatorer
    urn:nbn:se:uu:diva-302006 (URN)
    Externt samarbete:
    Tillgänglig från: 2016-08-27 Skapad: 2016-08-27 Senast uppdaterad: 2016-08-28
    4. Breastfeeding counseling mitigates the negative association of domestic violence on exclusive breastfeeding duration in rural Bangladesh: The MINIMat randomized trial
    Öppna denna publikation i ny flik eller fönster >>Breastfeeding counseling mitigates the negative association of domestic violence on exclusive breastfeeding duration in rural Bangladesh: The MINIMat randomized trial
    Visa övriga...
    (Engelska)Artikel i tidskrift (Övrigt vetenskapligt) Submitted
    Nationell ämneskategori
    Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi
    Identifikatorer
    urn:nbn:se:uu:diva-302003 (URN)
    Externt samarbete:
    Tillgänglig från: 2016-08-27 Skapad: 2016-08-27 Senast uppdaterad: 2016-08-28
  • 65354.
    Ziaei, Shirin
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Contreras, Mariela
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Zelaya Blandón, Elmer
    Asociación para el Desarrollo Económico y Social de El Espino (APRODESE).
    Persson, Lars-Åke
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Hjern, Anders
    Centre for Health Equity Studies, Karolinska Institutet/Stockholm University.
    Ekström, Eva-Charlotte
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Women´s autonomy and social support and their associations with infant and young child feeding and nutritional status: community-based survey in rural Nicaragua2015Ingår i: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 18, nr 11, s. 1979-1990Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective

    To evaluate the associations of women’s autonomy and social support with infant and young child feeding practices (including consumption of highly processed snacks and sugar-sweetened beverages) and nutritional status in rural Nicaragua.

    Design

    Cross-sectional study. Feeding practices and children’s nutritional status were evaluated according to the WHO guidelines complemented with information on highly processed snacks and sugar-sweetened beverages. Women’s autonomy was assessed by a seventeen-item questionnaire covering dimensions of financial independence, household-, child-, reproductive and health-related decision making and freedom of movement. Women’s social support was determined using the Duke-UNC Functional Social Support Questionnaire. The scores attained were categorized into tertiles.

    Setting

    Los Cuatro Santos area, rural Nicaragua.

    Subjects

    A total of 1371 children 0–35 months of age.

    Results

    Children of women with the lowest autonomy were more likely to be exclusively breast-fed and continue to be breast-fed, while children of women with middle level of autonomy had better complementary feeding practices. Children of women with the lowest social support were more likely to consume highly processed snacks and/or sugar-sweetened beverages but also be taller.

    Conclusions

    While lower levels of autonomy and social support were independently associated with some favourable feeding and nutrition outcomes, this may not indicate a causal relationship but rather that these factors reflect other matters of importance for child care.

  • 65355.
    Ziaei, Shirin
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Contreras, Mariela
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Zelaya, E.
    Ekström, Eva-Charlotte
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Maternal Decision Making Ability And Social Support: Associations With Infant Young Child Feeding And Nutrition In Rural Nicaragua2013Ingår i: Annals of Nutrition and Metabolism, ISSN 0250-6807, E-ISSN 1421-9697, Vol. 63, nr Suppl. 1, s. 678-678Artikel i tidskrift (Övrigt vetenskapligt)
  • 65356.
    Ziaei, Shirin
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Frith, Amy Lynn
    thaca Coll, Sch Hlth Sci & Human Performance, Ithaca, NY 14850 USA.
    Ekström, Eva-Charlotte
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Naved, Ruchira Tabassum
    Int Ctr Diarrhoeal Dis Res ICDDR B, Dhaka, Bangladesh.
    Experiencing Lifetime Domestic Violence: Associations with Mental Health and Stress among Pregnant Women in Rural Bangladesh: The MINIMat Randomized Trial2016Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 11, nr 12, artikel-id e0168103Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Experience of domestic violence has negative mental health consequences for women. The association of cumulative and specific forms of domestic violence, particularly emotional violence and controlling behavior, with common mental disorders and stress has rarely been studied in pregnant women. The aim of this study is to evaluate associations of specific and multiple forms of lifetime domestic violence and controlling behavior with distress and cortisol level during pregnancy in rural Bangladeshi women.

    METHODS AND FINDINGS: In this observational sub-study of larger MINIMat trial, 3504 pregnant women were interviewed using a shortened Conflict Tactic Scale about their lifetime experience of domestic violence including physical, sexual, emotional domestic violence and controlling behavior. Women's levels of emotional distress were assessed using the self-reported questionnaire (SRQ-20) developed by WHO, and levels of morning salivary cortisol were measured in a subsample (n = 1300) of women during week 28-32 of pregnancy. Regression analyses were used to estimate the associations of lifetime physical, sexual, emotional domestic violence and controlling behavior with levels of distress and cortisol during pregnancy. The prevalence of lifetime domestic violence was 57% and emotional distress was 35% in these pregnant women. All forms of domestic violence were associated with higher levels of emotional distress. Women who experienced either emotional violence or controlling behavior had the highest levels of emotional distress. There was a dose-response relationship between cumulative number of the different forms of domestic violence and women's levels of emotional distress. There was no association between women's experience of domestic violence and level of morning salivary cortisol.

    CONCLUSION: Including emotional violence and controlling behavior as major types of violence in future research and health interventions is warranted. Furthermore, the extent of the negative impacts of domestic violence on pregnant women, multiple forms of violence and their cumulative effects need to be investigated.

  • 65357.
    Ziaei, Shirin
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Naved, Ruchira Tabassum
    ICDDR, Dhaka, Bangladesh.
    Ekström, Eva-Charlotte
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Women's exposure to intimate partner violence and child malnutrition: findings from demographic and health surveys in Bangladesh2014Ingår i: Maternal and Child Nutrition, ISSN 1740-8695, E-ISSN 1740-8709, Vol. 10, nr 3, s. 347-359Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Domestic violence, in particular intimate partner violence (IPV), has been recognized as a leading cause of mortality and morbidity among women of reproductive age. The effects of IPV against women on their children's health, especially their nutritional status has received less attention but needs to be evaluated to understand the comprehensive public health implications of IPV. The aim of current study was to investigate the association between women's exposure to IPV and their children's nutritional status, using data from the 2007 Bangladesh Demographic and Health Survey (BDHS). Logistic regression models were used to estimate association between ever-married women's lifetime exposure to physical and sexual violence by their spouses and nutritional status of their children under 5 years. Of 2042 women in the BDHS survey with at least one child under 5 years of age, 49.4% reported lifetime experience of physical partner violence while 18.4% reported experience of sexual partner violence. The prevalence of stunting, wasting and underweight in their children under 5 years was 44.3%, 18.4% and 42.0%, respectively. Women were more likely to have a stunted child if they had lifetime experience of physical IPV [odds ratio n = 2027 (OR)adj, 1.48; 95% confidence interval (CI), 1.23–1.79] or had been exposed to sexual IPV (n = 2027 ORadj, 1.28; 95% CI, 1.02–1.61). The present findings contribute to growing body of evidence showing that IPV can also compromise children's growth, supporting the need to incorporate efforts to address IPV in child health and nutrition programmes and policies.

  • 65358.
    Ziaei, Shirin
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH), Internationell barnhälsa och nutrition.
    Naved, Ruchira Tabassum
    ICDDR B, Dhaka 1212, Bangladesh.
    Rahman, Anisur
    ICDDR B, Dhaka 1212, Bangladesh.
    Raqib, Rubhana
    ICDDR B, Dhaka 1212, Bangladesh.
    Ekström, Eva-Charlotte
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH), Internationell barnhälsa och nutrition.
    Maternal Experience of Domestic Violence, Associations with Children's Lipid Biomarkers at 10 Years: Findings from MINIMat Study in Rural Bangladesh2019Ingår i: Nutrients, ISSN 2072-6643, E-ISSN 2072-6643, Vol. 11, nr 4, artikel-id 910Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The consequences of maternal experience of Domestic Violence (DV) on their children's cardio-metabolic risk factors are unclear. We aimed to assess if maternal exposure to any or a specific form of DV (i.e., physical, sexual, emotional and controlling behaviors) before and after childbirth was associated with their children's lipid biomarkers at the age of 10 years. A current observational sub-study of a larger MINIMat trial included a cohort of 1167 mothers and their children. The conflict tactic scale was used to record women's experience of lifetime DV before and after childbirth at week 30 of pregnancy and at a 10-year follow up, respectively. Five ml of fasting blood sample was collected from the children to evaluate their lipid profile. Children of women who experienced any DV before childbirth had lower Apo A ((adj) -0.04; 95% CI: -0.08, -0.01). Women who experienced physical DV both before and after childbirth had children with higher triglycerides ((adj) 0.07; 95% CI: 0.01, 0.14). Children whose mother experienced sexual DV before birth had lower Apo A ((adj) -0.05; 95% CI: -0.08, -0.01) and High Density Lipoprotein (HDL) ((adj) -0.05; 95% CI: -0.10, -0.01) as well as higher Low Density Lipoprotein (LDL) ((adj) 0.17; 95% CI: 0.05, 0.29) and LDL/HDL ( 0.24; 95% CI: 0.11, 0.38). However, levels of LDL ((adj) -0.17; 95% CI: -0.28, -0.06), LDL/HDL ((adj) -0.12; 95% CI: -0.25, -0.00) and cholesterol ((adj) -0.13; 95% CI: -0.25, -0.02) were lower among the children of mothers who experienced controlling behavior after childbirth. Results from the current study suggest that maternal experience of physical or sexual DV might negatively affect their children's lipid profile at the age of 10 years.

  • 65359.
    Ziaei, Shirin
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    Rahman, Anisur
    ICDDR B, Dhaka, Bangladesh.
    Raqib, Rubhana
    ICDDR B, Dhaka, Bangladesh.
    Lönnerdal, Bo
    Univ Calif Davis, Dept Nutr, Davis, CA 95616 USA.
    Ekström, Eva-Charlotte
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Internationell mödra- och barnhälsovård (IMCH).
    A Prenatal Multiple Micronutrient Supplement Produces Higher Maternal Vitamin B-12 Concentrations and Similar Folate, Ferritin, and Zinc Concentrations as the Standard 60-mg Iron Plus 400-μg Folic Acid Supplement in Rural Bangladeshi Women.2016Ingår i: Journal of Nutrition, ISSN 0022-3166, E-ISSN 1541-6100, Vol. 146, nr 12, s. 2520-2529Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The effects of prenatal food and micronutrient supplementation on maternal micronutrient status are not well known.

    OBJECTIVE: We compared the efficacy and effectiveness of 3 different micronutrient supplements on maternal micronutrient status when combined with food supplementation.

    METHODS: In the MINIMat (Maternal and Infant Nutrition Intervention, Matlab) trial in Bangladesh, 4436 pregnant women were randomly assigned to daily intake of 3 types of micronutrient capsules: 30 mg Fe and 400 μg folic acid (Fe30F), 60 mg Fe and 400 μg folic acid (Fe60F), or multiple micronutrient supplements (MMNs) combined with early (week 9 of pregnancy) or usual (week 20 of pregnancy) food supplementation in a 2 by 3 factorial design. Plasma concentrations of vitamin B-12, folate, ferritin, and zinc were analyzed before the start of micronutrient supplementation (week 14) and at week 30 of pregnancy in 641 randomly selected women. An electronic monitoring device was used to measure the number of capsules taken. The effectiveness of food and micronutrient regimens as well as efficacy per capsule in maternal micronutrient status were analyzed by ANOVA and general linear models.

    RESULTS: At week 30 of pregnancy, women in the MMN group had higher geometric mean concentrations of vitamin B-12 than women in the Fe60F group (119 compared with 101 pmol/L, respectively); no other differences in effectiveness of micronutrient and food regimens were observed. A dose-response relation between the number of capsules taken and concentrations of folate and ferritin was observed for all micronutrient supplements. Fe30F had lower efficacy per capsule in increasing ferritin concentrations within the first tertile of capsule intake than did Fe60F and MMNs. Because ferritin reached a plateau for all types of micronutrient supplements, there was no difference between the regimens in their effectiveness.

    CONCLUSION: Compared with Fe60F, MMNs produced higher maternal vitamin B-12 and similar ferritin and folate concentrations in Bangladeshi women. The MINIMat trial was registered at isrctn.org as ISRCTN16581394.

  • 65360. Zickert, A.
    et al.
    Amoudruz, P.
    Rönnelid, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Malmström, V.
    Gunnarsson, I.
    Cytokines in lupus nephritis, levels of IL-17 and IL-23 in association to histopathology and response to treatment2012Ingår i: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 71, s. A4-A5Artikel i tidskrift (Övrigt vetenskapligt)
  • 65361. Zickert, Agneta
    et al.
    Amoudruz, Petra
    Sundstrom, Yvonne
    Rönnelid, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Malmstrom, Vivianne
    Gunnarsson, Iva
    IL-17 and IL-23 in lupus nephritis - association to histopathology and response to treatment2015Ingår i: BMC Immunology, ISSN 1471-2172, E-ISSN 1471-2172, Vol. 16, artikel-id 7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Recent studies indicate a central role for the IL-23/IL-17 axis in the pathogenesis of lupus nephritis (LN) but the importance in the context of treatment outcome is unknown. We studied various cytokines, including the IL-23/IL-17 axis, in association to histopathology and response to therapy. Methods: Fifty-two patients with active LN were included. Renal biopsies were performed at baseline and after immunosuppressive treatment. Serum levels of TNF-alpha, IFN-gamma, IL-6, IL-10, IL-17, IL-23 and TGF-beta were analysed at both biopsy occasions and in 13 healthy controls. IL-17 expression in renal tissue was assessed by immunohistochemistry. Biopsies were evaluated regarding WHO-classification and renal disease activity was estimated using the BILAG-index. Improvement of 2 grades in renal BILAG was regarded complete response, and 1 grade partial response. Results: At baseline, all patients had high disease activity (BILAG A/B). Baseline levels of IL-6, IL-10, IL-17, IL-23 (p < 0.001) and IFN-gamma (p = 0.03) were increased in patients vs. controls. In contrast, TGF-beta was lower in patients compared to controls (p < 0.001). Baseline levels of IL-17 were higher in patients with persisting active nephritis (WHO III, IV, V) after treatment, i.e. a poor histological response, vs. WHO I-II (p < 0.03). At follow-up, IL-23 were higher in BILAG-non-responders vs. responders (p < 0.05). Immunostaining of renal tissue revealed IL-17 expression in inflammatory infiltrates. Conclusions: High baseline IL-17 predicted an unfavourable histopathological response, and BILAG-non-responders had high IL-23, indicating that that a subset of LN-patients has a Th-17 phenotype that may influence response to treatment and could be evaluated as a biomarker for poor therapeutic response.

  • 65362.
    Zidar, Josefina
    et al.
    Linkoping Univ, Dept Phys Chem & Biol, IFM Biol, SE-58183 Linkoping, Sweden.
    Campderrich, Irene
    Swedish Univ Agr Sci, Dept Anim Environm & Hlth, SE-75007 Uppsala, Sweden;Neiker Tecnalia, Dept Anim Prod, Vitoria 01080, Spain.
    Jansson, Emelie
    Linkoping Univ, Dept Phys Chem & Biol, IFM Biol, SE-58183 Linkoping, Sweden.
    Wichman, Anette
    Swedish Univ Agr Sci, Dept Anim Environm & Hlth, SE-75007 Uppsala, Sweden.
    Winberg, Svante
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Fysiologi.
    Keeling, Linda
    Swedish Univ Agr Sci, Dept Anim Environm & Hlth, SE-75007 Uppsala, Sweden.
    Løvlie, Hanne
    Linkoping Univ, Dept Phys Chem & Biol, IFM Biol, SE-58183 Linkoping, Sweden.
    Environmental complexity buffers against stress-induced negative judgement bias in female chickens2018Ingår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, artikel-id 5404Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cognitive processes are often biased by emotions. In humans, affective disorders are accompanied by pessimistic judgement, while optimistic judgement is linked to emotional stability. Similar to humans, animals tend to interpret ambiguous stimuli negatively after experiencing stressful events, although the long-lasting impact on judgement bias has rarely been investigated. We measure judgement bias in female chicks (Gallus gallus domesticus) after exposure to cold stress, and before and after exposure to additional unpredictable stressors. Additionally, we explore if brain monoamines can explain differences in judgement bias. Chicks exposed to cold stress did not differ in judgement bias compared to controls, but showed sensitivity to additional stressors by having higher motivation for social reinstatement. Environmental complexity reduced stress-induced negative judgement bias, by maintaining an optimistic bias in individuals housed in complex conditions even after stress exposure. Moreover, judgement bias was related to dopamine turnover rate in mesencephalon, with higher activity in individuals that had a more optimistic response. These results demonstrate that environmental complexity can buffer against negative effects of additive stress and that dopamine relates to judgement bias in chicks. These results reveal that both internal and external factors can mediate emotionally biased judgement in animals, thus showing similarities to findings in humans.

  • 65363.
    Zidar, Maria Norfjord
    et al.
    Malardalen Univ, Sch Hlth Care & Social Welf, Div Publ Hlth Sci, SE-72123 Vasteras, Sweden..
    Larm, Peter
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centrum för klinisk forskning, Västerås. Malardalen Univ, Sch Hlth Care & Social Welf, Div Publ Hlth Sci, SE-72123 Vasteras, Sweden..
    Tillgren, Per
    Malardalen Univ, Sch Hlth Care & Social Welf, Div Publ Hlth Sci, SE-72123 Vasteras, Sweden..
    Akhavan, Sharareh
    Malardalen Univ, Sch Hlth Care & Social Welf, Div Publ Hlth Sci, SE-72123 Vasteras, Sweden..
    Non-attendance of mammographic screening: the roles of age and municipality in a population-based Swedish sample2015Ingår i: International Journal for Equity in Health, ISSN 1475-9276, E-ISSN 1475-9276, Vol. 14, artikel-id 157Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Inequality in health and health care is increasing in Sweden. Contributing to widening gaps are various factors that can be assessed by determinants, such as age, educational level, occupation, living area and country of birth. A health care service that can be used as an indicator of health inequality in Sweden is mammographic screening. The non-attendance rate is between 13 and 31 %, while the average is about 20 %. This study aims to shed light on three associations: between municipality and non-attendance, between age and non-attendance, and the interaction of municipality of residence and age in relation to non-attendance. Methods: The study is based on data from the register that identifies attenders and non-attenders of mammographic screening in a Swedish county, namely the Radiological Information System (RIS). Further, in order to provide a socio-demographic profile of the county's municipalities, aggregated data for women in the age range 40-74 in 2012 were retrieved from Statistics Sweden (SCB), the Public Health Agency of Sweden, the National Board of Health and Welfare, and the Swedish Social Insurance Agency. The sample consisted of 52,541 women. Analysis conducted of the individual data were multivariate logistic regressions, and pairwise chi-square tests. Results: The results show that age and municipality of residence associated with non-attendance of mammographic screening. Municipality of residence has a greater impact on non-attendance among women in the age group 70 to 74. For most of the age categories there were differences between the municipalities in regard to non-attendance to mammographic screening. Conclusions: Age and municipality of residence affect attendance of mammographic screening. Since there is one sole and pre-selected mammographic screening facility in the county, distance to the screening facility may serve as one explanation to non-attendance which is a determinant of inequity. From an equity perspective, lack of equal access to health and health care influences facility utilization.

  • 65364.
    Zieba, Agata
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg.
    Application of Proximity Ligation Assay for Multidirectional Studies on Transforming Growth Factor-β Pathway2012Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    A comprehensive understanding of how the body and all its components function is essential when this knowledge is exploited for medical purposes. The achievements in biological and medical research during last decades has provided us with the complete human genome and identified signaling pathways that governs the cellular processes that facilitates the development and maintenance of higher order organisms. This has brought about the realization that diseases such as cancer is a consequence of genomic aberrations that effects these signaling pathways, endowing cancer cells with the capacity to circumvent homeostasis by acquiring features like self-sustained proliferation and insensitivity to apoptosis. The increased understanding of biology and medicine has been made possible by the development of advanced methods to carry out biological and clinical analyses. The demands of a method often differ regarding in what context it will be applied. It may be acceptable for method to be laborious and time consuming if it is used in basic research, but for medical purposes molecular methods need to be fast and straightforward to perform. Innovative technologies should preferentially address the demands of both researchers and clinicians and provide data not possible to obtain by other methods. An example of such a method is the in situ proximity ligation assay (in situ PLA). In this thesis I have used this method to determine the activity status, at the single-cell level, of the transforming growth factor-β (TGF-β) signaling pathway and activating protein-1 (AP-1) family of transcription factors.  Both of these pathways are frequently involved in cancer development and progression. In addition to this research I herein also present further modifications of in situ PLA, and analyses thereof, to increase the utility and resolution of this assay.

    Delarbeten
    1. Intercellular variation in signaling through the TGF-β pathway and its relation to cell densityand cell cycle phase
    Öppna denna publikation i ny flik eller fönster >>Intercellular variation in signaling through the TGF-β pathway and its relation to cell densityand cell cycle phase
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    2012 (Engelska)Ingår i: Molecular & Cellular Proteomics, ISSN 1535-9476, E-ISSN 1535-9484, Vol. 11, nr 7, artikel-id M111.013482Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Fundamental open questions in signal transduction remain concerning the sequence and distribution of molecular signaling events among individual cells. In this work we have characterized the intercellular variability of transforming growth factor β-induced Smad interactions, providing essential information about TGF-β signaling and its dependence on the density of cell populations and the cell-cycle phase. By employing the recently developed in situ proximity ligation assay, we investigated the dynamics of interactions and modifications of Smad proteins and their partners under native and physiological conditions. We analyzed the kinetics of assembly of Smad complexes and the influence of cellular environment and relation to mitosis. We report rapid kinetics of formation of Smad complexes, including native Smad2-Smad3-Smad4 trimeric complexes, in a manner influenced by the rate of proteasomal degradation of these proteins, and we found a striking cell to cell variation of signaling complexes. The single-cell analysis of TGF-β signaling in genetically unmodified cells revealed previously unknown aspects of regulation of this pathway, and it provided a basis for analysis of these signaling events to diagnose pathological perturbations in patient samples, and to evaluate their susceptibility to drug treatment.

    Ort, förlag, år, upplaga, sidor
    American Society for Biochemistry and Molecular Biology, 2012
    Nationell ämneskategori
    Cellbiologi
    Forskningsämne
    Molekylär cellbiologi
    Identifikatorer
    urn:nbn:se:uu:diva-171949 (URN)10.1074/mcp.M111.013482 (DOI)000306411300017 ()22442258 (PubMedID)
    Tillgänglig från: 2012-03-29 Skapad: 2012-03-29 Senast uppdaterad: 2017-12-07Bibliografiskt granskad
    2. Specific interactions between Smad proteins and AP-1 components determine TGFβ-induced breast cancer cell invasion
    Öppna denna publikation i ny flik eller fönster >>Specific interactions between Smad proteins and AP-1 components determine TGFβ-induced breast cancer cell invasion
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    2013 (Engelska)Ingår i: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 32, nr 31, s. 3606-3615Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Deregulation of the transforming growth factor β (TGFβ) signal transduction cascade is functionally linked to cancer. In early phases, TGFβ acts as a tumor suppressor by inhibiting tumor cell proliferation, whereas in late phases, it can act as a tumor promoter by stimulating tumor cell invasion and metastasis. Smad transcriptional effectors mediate TGFβ responses, but relatively little is known about the Smad-containing complexes that are important for epithelial-mesenchymal transition and invasion. In this study, we have tested the hypothesis that specific members of the AP-1 transcription factor family determine TGFβ signaling specificity in breast cancer cell invasion. Using a 3D model of collagen-embedded spheroids of MCF10A-MII premalignant human breast cancer cells, we identified the AP-1 transcription factor components c-Jun, JunB, c-Fos and Fra1 as essential factors for TGFβ-induced invasion and found that various mesenchymal and invasion-associated TGFβ-induced genes are co-regulated by these proteins. In situ proximity ligation assays showed that TGFβ signaling not only induces complexes between Smad3 and Smad4 in the nucleus but also complexes between Smad2/3 and Fra1, whereas complexes between Smad3, c-Jun and JunB could already be detected before TGFβ stimulation. Finally, chromatin immunoprecipitations showed that c-Jun, JunB and Fra1, but not c-Fos, are required for TGFβ-induced binding of Smad2/3 to the mmp-10 and pai-1 promoters. Together these results suggest that in particular formation of Smad2/3-Fra1 complexes may reflect activation of the Smad/AP-1-dependent TGFβ-induced invasion program.

    Nationell ämneskategori
    Medicin och hälsovetenskap
    Identifikatorer
    urn:nbn:se:uu:diva-180124 (URN)10.1038/onc.2012.370 (DOI)000322638400005 ()22926518 (PubMedID)
    Anmärkning

    Agata Zieba & Eleftheria Vasilaki contributed equally to this work.

    Tillgänglig från: 2012-08-30 Skapad: 2012-08-30 Senast uppdaterad: 2017-12-07Bibliografiskt granskad
    3. A detailed analysis of 3D subcellular signal localization
    Öppna denna publikation i ny flik eller fönster >>A detailed analysis of 3D subcellular signal localization
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    2009 (Engelska)Ingår i: Cytometry Part A, ISSN 1552-4922, Vol. 75A, nr 4, s. 319-328Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Detection and localization of fluorescent signals in relation to other subcellular structures is an important task in various biological studies. Many methods for analysis of fluorescence microscopy image data are limited to 2D. As cells are in fact 3D structures, there is a growing need for robust methods for analysis of 3D data. This article presents an approach for detecting point-like fluorescent signals and analyzing their subnuclear position. Cell nuclei are delineated using marker-controlled (seeded) 3D watershed segmentation. User-defined object and background seeds are given as input, and gradient information defines merging and splitting criteria. Point-like signals are detected using a modified stable wave detector and localized in relation to the nuclear membrane using distance shells. The method was applied to a set of biological data studying the localization of Smad2-Smad4 protein complexes in relation to the nuclear membrane. Smad complexes appear as early as 1 min after stimulation while the highest signal concentration is observed 45 min after stimulation, followed by a concentration decrease. The robust 3D signal detection and concentration measures obtained using the proposed method agree with previous observations while also revealing new information regarding the complex formation.

    Nyckelord
    3D image analysis, fluorescence signal segmentation, subcellular positioning, Smad detection
    Nationell ämneskategori
    Data- och informationsvetenskap
    Identifikatorer
    urn:nbn:se:uu:diva-98014 (URN)10.1002/cyto.a.20663 (DOI)000264513800006 ()
    Tillgänglig från: 2009-02-05 Skapad: 2009-02-05 Senast uppdaterad: 2018-01-13Bibliografiskt granskad
    4. Bright-Field Microscopy Visualization of Proteins and Protein Complexes by In Situ Proximity Ligation with Peroxidase Detection
    Öppna denna publikation i ny flik eller fönster >>Bright-Field Microscopy Visualization of Proteins and Protein Complexes by In Situ Proximity Ligation with Peroxidase Detection
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    2010 (Engelska)Ingår i: Clinical Chemistry, ISSN 0009-9147, E-ISSN 1530-8561, Vol. 56, nr 1, s. 99-110Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    BACKGROUND:

    The in situ proximity ligation assay (PLA) allows a protein or protein complex to be represented as an amplifiable DNA molecule. Recognition is mediated by proximity probes consisting of antibodies coupled with oligonucleotides. Upon dual binding of the proximity probes, the oligonucleotides direct the formation of a circular DNA molecule, which is then amplified by rolling-circle replication. The localized concatemeric product is then detected with fluorescent probes. The in situ PLA enables localized detection of individual native proteins or interacting protein pairs in fixed cells or tissue sections, thus providing an important tool for basic and clinical research.

    METHODS:

    We used horseradish peroxidase (HRP)conjugated oligonucleotides to couple in situ PLA with enzymatic visualization of the localized detection event.

    RESULTS:

    We demonstrate the detection of protein complexes, both in cells and in tissue sections, and show that we can quantify the complexes with image-analysis software specially developed for recognizing HRP signals in bright-field microscopy images. We show that fluorescence and HRP signals produce equivalent results, both ill cultured cells and in tissue samples.

    CONCLUSIONS:

    The combination of in situ PLA with bright-field detection and automated image analysis allows the signals present to be Counted in an automated fashion and thus provides a sensitive and specific method for quantification of proteins and protein complexes with bright-field microscopy. With this approach, in situ PLA can be used without the requirement for expensive fluorescence microscopes, thereby avoiding problems with nonspecific fluorescence while maintaining compatibility with conventional histologic staining.

    Nationell ämneskategori
    Medicinsk genetik Bioinformatik och systembiologi
    Forskningsämne
    Klinisk genetik; Datoriserad bildanalys
    Identifikatorer
    urn:nbn:se:uu:diva-111499 (URN)10.1373/clinchem.2009.134452 (DOI)000273466300016 ()
    Tillgänglig från: 2009-12-15 Skapad: 2009-12-15 Senast uppdaterad: 2018-01-12Bibliografiskt granskad
  • 65365.
    Zieba, Agata
    et al.
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylär och morfologisk patologi.
    Grannas, Karin
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg.
    Söderberg, Ola
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg.
    Gullberg, Mats
    Nilsson, Mats
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg.
    Landegren, Ulf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Molecular tools for companion diagnostics2012Ingår i: New Biotechnology, ISSN 1871-6784, E-ISSN 1876-4347, Vol. 29, nr 6, s. 634-640Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The heterogeneous nature of cancer results in highly variable therapeutic responses even among patients with identical stages and grades of a malignancy. The move towards personalised medicine in cancer therapy has therefore been motivated by a need to customise therapy according to molecular features of individual tumours. Companion diagnostics serves to support early drug development, it can provide surrogate markers in clinical trials, and also guide selection of individual therapies and monitoring of responses in routine clinical care. The era of companion diagnostics can be said to have begun with the introduction of the HercepTest - a first-of-a-kind diagnostic tool developed by DakoCytomation in 1998 to select patients for therapy with the anticancer drug Herceptin (trastuzumab). Herceptin and the paired test proved that companion diagnostics can help guide patient-tailored therapies. We will discuss herein technologies to analyse companion diagnostics markers at the level of DNA, RNA or protein, focusing on a series of methods developed in our laboratory that can facilitate drug development and help stratify patients for therapy.

  • 65366.
    Zieba, Agata
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Pardali, Katerina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Söderberg, Ola
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Lindbom, Lena
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Nyström, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Moustakas, Aristidis
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Heldin, Carl-Henrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Landegren, Ulf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Intercellular variation in signaling through the TGF-β pathway and its relation to cell densityand cell cycle phase2012Ingår i: Molecular & Cellular Proteomics, ISSN 1535-9476, E-ISSN 1535-9484, Vol. 11, nr 7, artikel-id M111.013482Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Fundamental open questions in signal transduction remain concerning the sequence and distribution of molecular signaling events among individual cells. In this work we have characterized the intercellular variability of transforming growth factor β-induced Smad interactions, providing essential information about TGF-β signaling and its dependence on the density of cell populations and the cell-cycle phase. By employing the recently developed in situ proximity ligation assay, we investigated the dynamics of interactions and modifications of Smad proteins and their partners under native and physiological conditions. We analyzed the kinetics of assembly of Smad complexes and the influence of cellular environment and relation to mitosis. We report rapid kinetics of formation of Smad complexes, including native Smad2-Smad3-Smad4 trimeric complexes, in a manner influenced by the rate of proteasomal degradation of these proteins, and we found a striking cell to cell variation of signaling complexes. The single-cell analysis of TGF-β signaling in genetically unmodified cells revealed previously unknown aspects of regulation of this pathway, and it provided a basis for analysis of these signaling events to diagnose pathological perturbations in patient samples, and to evaluate their susceptibility to drug treatment.

  • 65367.
    Zieba, Agata
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Ponten, Fredrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Uhlen, Mathias
    KTH Royal Inst Technol, Sci Life Lab, Stockholm, Sweden..
    Landegren, Ulf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    In situ protein detection with enhanced specificity using DNA-conjugated antibodies and proximity ligation2018Ingår i: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 31, nr 2, s. 253-263Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Antibodies are important tools in anatomical pathology and research, but the quality of in situ protein detection by immunohistochemistry greatly depends on the choice of antibodies and the abundance of the targeted proteins. Many antibodies used in scientific research do not meet requirements for specificity and sensitivity. Accordingly, methods that improve antibody performance and produce quantitative data can greatly advance both scientific investigations and clinical diagnostics based on protein expression and in situ localization. We demonstrate here protocols for antibody labeling that allow specific protein detection in tissues via bright-field in situ proximity ligation assays, where each protein molecule must be recognized by two antibodies. We further demonstrate that single polyclonal antibodies or purified serum preparations can be used for these dual recognition assays. The requirement for protein recognition by pairs of antibody conjugates can significantly improve specificity of protein detection over single-binder assays.

  • 65368.
    Zieba, Agata
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg.
    Sjöstedt, Evelina
    KTH Royal Inst Technol, Sci Life Lab, Stockholm, Sweden..
    Olovsson, Matts
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa, Obstetrik & gynekologi. Uppsala Univ, Dept Womens & Childrens Hlth, S-75185 Uppsala, Sweden..
    Fagerberg, Linn
    KTH Royal Inst Technol, Sci Life Lab, Stockholm, Sweden..
    Hallström, Björn M.
    KTH Royal Inst Technol, Sci Life Lab, Stockholm, Sweden..
    Oskarsson, Linda
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi.
    Edlund, Karolina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi.
    Tolf, Anna
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi.
    Uhlen, Mathias
    KTH Royal Inst Technol, Sci Life Lab, Stockholm, Sweden..
    Pontén, Fredrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi.
    The Human Endometrium-Specific Proteome Defined by Transcriptomics and Antibody-Based Profiling2015Ingår i: Omics, ISSN 1536-2310, E-ISSN 1557-8100, Vol. 19, nr 11, s. 659-668Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The human uterus includes the complex endometrial mucosa, the endometrium that undergoes dynamic, hormone-dependent alterations throughout the life of fertile females. Here we have combined a genome-wide transcriptomics analysis with immunohistochemistry-based protein profiling to analyze gene expression patterns in the normal endometrium. Human endometrial tissues from five women were used for deep sequencing (RNA-Seq). The mRNA and protein expression data from the endometrium were compared to 31 (RNA) and 44 (protein) other normal tissue types, to identify genes with elevated expression in the endometrium and to localize the expression of corresponding proteins at a cellular resolution. Based on the expression levels of transcripts, we could classify all putative human protein coding genes into categories defined by expression patterns and found altogether 101 genes that showed an elevated pattern of expression in the endometrium, with only four genes showing more than five-fold higher expression levels in the endometrium compared to other tissues. In conclusion, our analysis based on transcriptomics and antibody-based protein profiling reports here comprehensive lists of genes with elevated expression levels in the endometrium, providing important starting points for a better molecular understanding of human reproductive biology and disease.

  • 65369.
    Zieba, Agata
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Wählby, Carolina
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Matematisk-datavetenskapliga sektionen, Centrum för bildanalys. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Hjelm, Fredrik
    Jordan, Lee
    Berg, Jonathan
    Landegren, Ulf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Pardali, Katerina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Bright-Field Microscopy Visualization of Proteins and Protein Complexes by In Situ Proximity Ligation with Peroxidase Detection2010Ingår i: Clinical Chemistry, ISSN 0009-9147, E-ISSN 1530-8561, Vol. 56, nr 1, s. 99-110Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND:

    The in situ proximity ligation assay (PLA) allows a protein or protein complex to be represented as an amplifiable DNA molecule. Recognition is mediated by proximity probes consisting of antibodies coupled with oligonucleotides. Upon dual binding of the proximity probes, the oligonucleotides direct the formation of a circular DNA molecule, which is then amplified by rolling-circle replication. The localized concatemeric product is then detected with fluorescent probes. The in situ PLA enables localized detection of individual native proteins or interacting protein pairs in fixed cells or tissue sections, thus providing an important tool for basic and clinical research.

    METHODS:

    We used horseradish peroxidase (HRP)conjugated oligonucleotides to couple in situ PLA with enzymatic visualization of the localized detection event.

    RESULTS:

    We demonstrate the detection of protein complexes, both in cells and in tissue sections, and show that we can quantify the complexes with image-analysis software specially developed for recognizing HRP signals in bright-field microscopy images. We show that fluorescence and HRP signals produce equivalent results, both ill cultured cells and in tissue samples.

    CONCLUSIONS:

    The combination of in situ PLA with bright-field detection and automated image analysis allows the signals present to be Counted in an automated fashion and thus provides a sensitive and specific method for quantification of proteins and protein complexes with bright-field microscopy. With this approach, in situ PLA can be used without the requirement for expensive fluorescence microscopes, thereby avoiding problems with nonspecific fluorescence while maintaining compatibility with conventional histologic staining.

  • 65370. Zieden, B
    et al.
    Kaminskas, A
    Kristenson, M
    Kucinskiene, Z
    Vessby, B
    Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap.
    Olsson, AG
    Diczfalusy, U
    Increased plasma 7 beta-hydroxycholesterol concentrations in a population with a high risk for cardiovascular disease1999Ingår i: Arterioscler. Thromb. Vasc. Biol., Vol. 19, s. 967-Artikel i tidskrift (Refereegranskat)
  • 65371.
    Ziegler, Nicole
    et al.
    Goethe Univ Frankfurt, Edinger Inst, Inst Neurol, Sch Med, D-60528 Frankfurt, Germany..
    Awwad, Khader
    Goethe Univ Frankfurt, Inst Vasc Signaling, D-60596 Frankfurt, Germany..
    Fisslthaler, Beate
    Goethe Univ Frankfurt, Inst Vasc Signaling, D-60596 Frankfurt, Germany.;German Ctr Cardiovasc Res, Partner Site Rhine Main, D-60528 Frankfurt, Germany..
    Reis, Marco
    Roche Diagnost GmbH, Roche Innovat Ctr Penzberg, Oncol, Pharma Res & Early Dev, D-82377 Penzberg, Germany..
    Devraj, Kavi
    Goethe Univ Frankfurt, Edinger Inst, Inst Neurol, Sch Med, D-60528 Frankfurt, Germany..
    Corada, Monica
    FIRC Inst Mol Oncol, I-20139 Milan, Italy..
    Minardi, Simone Paolo
    FIRC Inst Mol Oncol, I-20139 Milan, Italy..
    Dejana, Elisabetta
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Vaskulärbiologi. FIRC Inst Mol Oncol, I-20139 Milan, Italy.; Univ Milan, Dipartimento Biosci, I-20133 Milan, Italy..
    Plate, Karl H.
    Goethe Univ Frankfurt, Edinger Inst, Inst Neurol, Sch Med, D-60528 Frankfurt, Germany.;German Ctr Cardiovasc Res, Partner Site Rhine Main, D-60528 Frankfurt, Germany..
    Fleming, Ingrid
    Goethe Univ Frankfurt, Inst Vasc Signaling, D-60596 Frankfurt, Germany.;German Ctr Cardiovasc Res, Partner Site Rhine Main, D-60528 Frankfurt, Germany..
    Liebner, Stefan
    Goethe Univ Frankfurt, Edinger Inst, Inst Neurol, Sch Med, D-60528 Frankfurt, Germany.;German Ctr Cardiovasc Res, Partner Site Rhine Main, D-60528 Frankfurt, Germany..
    beta-Catenin Is Required for Endothelial Cyp1b1 Regulation Influencing Metabolic Barrier Function2016Ingår i: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 36, nr 34, s. 8921-8935Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The canonical Wnt/beta-catenin signaling pathway is crucial for blood-brain barrier (BBB) formation in brain endothelial cells. Although glucose transporter 1, claudin-3, and plasmalemma vesicular-associated protein have been identified as Wnt/beta-catenin targets in brain endothelial cells, further downstream targets relevant to BBB formation and function are incompletely explored. By Affymetrix expression analysis, we show that the cytochrome P450 enzyme Cyp1b1 was significantly decreased in beta-catenin-deficient mouse endothelial cells, whereas its close homolog Cyp1a1 was upregulated in an aryl hydrocarbon receptor-dependent manner, hence indicating that beta-catenin is indispensable for Cyp1b1 but not for Cyp1a1 expression. Functionally, Cyp1b1 could generate retinoic acid from retinol leading to cell-autonomous induction of the barrier-related ATP-binding cassette transporter P-glycoprotein. Cyp1b1 could also generate 20-hydroxyeicosatetraenoic acid from arachidonic acid, decreasing endothelial barrier function in vitro. In mice in vivo pharmacological inhibition of Cyp1b1 increased BBB permeability for small molecular tracers, and Cyp1b1 was downregulated in glioma vessels in which BBB function is lost. Hence, we propose Cyp1b1 as a target of beta-catenin indirectly influencing BBB properties via its metabolic activity, and as a potential target for modulating barrier function in endothelial cells.

  • 65372. Ziegler-Heitbrock, Loems
    et al.
    Frankenberger, Marion
    Heimbeck, Irene
    Burggraf, Dorothe
    Wjst, Matthias
    Haeussinger, Karl
    Brightling, Chris
    Gupta, Sumit
    Parr, David
    Subramanian, Deepak
    Singh, Dave
    Kolsum, Umme
    Boschetto, Piera
    Potena, Alfredo
    Gorecka, Dorota
    Nowinski, Adam
    Barta, Imre
    Doeme, Balazs
    Strausz, Janos
    Greulich, Timm
    Vogelmeier, Claus
    Bals, Robert
    Hohlfeld, Jens M.
    Welte, Tobias
    Venge, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Biokemisk struktur och funktion.
    Gut, Ivo
    Boland, Anne
    Olaso, Robert
    Hager, Joerg
    Hiemstra, Pieter
    Rabe, Klaus F.
    Unmuessig, Martina
    Mueller-Ouernhelm, Joachim
    Prasse, Antje
    The EvA study: aims and strategy2012Ingår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 40, nr 4, s. 823-829Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The EvA study is a European Union-funded project under the Seventh Framework Programme (FP7), which aims at defining new markers for chronic obstructive pulmonary disease (COPD) and its subtypes. The acronym is derived from emphysema versus airway disease, indicating that the project targets these two main phenotypes of the disease. The EvA study is based on the concept that emphysema and airway disease are governed by different pathophysiological processes, are driven by different genes and have differential gene expression in the lung. To define these genes, patients and non-COPD controls are recruited for clinical examination, lung function analysis and computed tomography (CT) of the lung. CT scans are used to define the phenotypes based on lung density and airway wall thickness. This is followed by bronchoscopy in order to obtain samples from the airways and the alveoli. These tissue samples, along with blood samples, are then subjected to genome-wide expression and association analysis and markers linked to the phenotypes are identified. The population of the EvA study is different from other COPD study populations, since patients with current oral glucocorticoids, antibiotics and exacerbations or current smokers are excluded, such that the signals detected in the molecular analysis are due to the distinct inflammatory process of emphysema and airway disease in COPD.

  • 65373. Zielin„ski, Rafal
    et al.
    Hellman, Ulf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning.
    Kubinski, Konrad
    Szyszka, Ryszard
    Fip1 - an essential component of the Saccharomyces cerevisiae polyadenylation machinery is phosophorylated by protein kinase CK22006Ingår i: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 286, nr 1-2, s. 191-197Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Since Fip1 is phosphoprotein we investigated whether it is a substrate for protein kinase CK2. According to the amino acid sequence Fip1 harbours twenty putative CK2 phosphorylation sites. Here we have report characterization of Fip1 as a substrate for both forms of CK2. Fip1 serves as a substrate for both the recombinant CK2α ′ (K m 1.28 μM) and holoenzyme (K m 1.4 μM) but not for CK1. By MALDI-MS we identified the two serine residues at positions 73 and 77 as the possible in vitro phosphorylation sites. These data may help to elucidate the role of Fip1 in the mRNA 3'-OH polyadenylation process and the involvement of CK2 mediated phosphorylation in regulation of interactions and activity members of cleavage/polyadenylation factor (CPF) complex.

  • 65374. Zielinski, Rafał
    et al.
    Pilecki, Marek
    Kubin„ski, Konrad
    Zien, Piotr
    Hellman, Ulf
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning.
    Szyszka, Ryszard
    Inhibition of yeast ribosomal stalk phosphorylation by Cu-Zn superoxide dismutase2002Ingår i: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 296, nr 5, s. 1310-1316Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Reversible phosphorylation of acidic ribosomal proteins of Saccharomyces cerevisiae is an important mechanism, regulating the number of active ribosomes. The key role in regulation of this process is played by specific, second messenger-independent protein kinases. A new protein-inhibitor regulating activity of PK60S kinase has been purified from yeast extracts and characterised. Peptide mass fingerprinting (PMF) and amino-acid sequence analysis by Post Source Decay (PSD) have identified the inhibitor as a Cu-Zn superoxide dismutase (SOD). Inhibition by SOD is competitive with respect to protein substrates-P proteins and 80S ribosome-with K(i) values of 3.7 microM for P2A protein and 0.6 microM for 80S ribosomes. A close correlation was found between the state of phosphorylation of P proteins in diauxic shift and logarithmic growth yeast cells and activity of SOD. The possible mechanism of regulation of PK60S activity, and participation of SOD protein in regulation of 80S-ribosome activity in stress conditions, is discussed.

  • 65375.
    Zillikens, M. Carola
    et al.
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;NCHA, NCI, NL-2593 Leiden, Netherlands..
    Demissie, Serkalem
    Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA..
    Hsu, Yi-Hsiang
    Inst Aging Res, HebrewSenior Life, Roslindale, MA 02131 USA.;Harvard Med Sch, Boston, MA 02115 USA.;Harvard Sch Publ Hlth, Mol & Integrat Physiol Sci Program, Boston, MA 02115 USA..
    Yerges-Armstrong, Laura M.
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA..
    Chou, Wen-Chi
    Inst Aging Res, HebrewSenior Life, Roslindale, MA 02131 USA.;Harvard Med Sch, Boston, MA 02115 USA.;Broad Inst, Cambridge, MA 02142 USA..
    Stolk, Lisette
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;NCHA, NCI, NL-2593 Leiden, Netherlands..
    Livshits, Gregory
    Tel Aviv Univ, Sackler Fac Med, Dept Anat & Anthropol, IL-6997801 Tel Aviv, Israel.;Kings Coll London, Dept Twin Res & Genet Epidemiol, St Thomas Campus, London WC2R 2LS, England..
    Broer, Linda
    Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Johnson, Toby
    Univ Lausanne, Dept Med Genet, CH-1011 Lausanne, Switzerland.;Swiss Inst Bioinformat, CH-1015 Lausanne, Switzerland.;Univ Inst Social & Prevent Med, Ctr Hosp Univ CHUV, CH-1010 Lausanne, Switzerland..
    Koller, Daniel L.
    Indiana Univ, Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA..
    Kutalik, Zoltyn
    Univ Lausanne, Dept Med Genet, CH-1011 Lausanne, Switzerland.;Swiss Inst Bioinformat, CH-1015 Lausanne, Switzerland.;Univ Inst Social & Prevent Med, Ctr Hosp Univ CHUV, CH-1010 Lausanne, Switzerland..
    Luan, Jian'an
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge Biomed Campus, Cambridge CB2 OQQ, England..
    Malkin, Ida
    Tel Aviv Univ, Sackler Fac Med, Dept Anat & Anthropol, IL-6997801 Tel Aviv, Israel..
    Ried, Janina S.
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany..
    Smith, Albert V.
    Iceland Heart Assoc, IS-201 Kopavogur, Iceland..
    Thorleifsson, Gudmar
    Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.;deCODE Genet, IS-101 Reykjavik, Iceland..
    Vandenput, Liesbeth
    Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Internal Med, SE-40530 Gothenburg, Sweden..
    Zhao, Jing Hua
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge Biomed Campus, Cambridge CB2 OQQ, England..
    Zhang, Weihua
    Imperial Coll, Sch Publ Hlth, Dept Epidemiol & Biostat, London SW7 2AZ, England.;Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England..
    Aghdassi, Ali
    Ernst Moritz Arndt Univ Greifswald, Dept Med A, D-17489 Greifswald, Germany..
    Akesson, Kristina
    Lund Univ, Dept Clin Sci, S-22362 Malmo, Sweden.;Skane Univ Hosp, Dept Orthoped, S-20502 Malmo, Sweden..
    Amin, Najaf
    Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Baier, Leslie J.
    NIH, Phoenix Epidemiol & Clin Res Branch, Natl Inst Diabet & Digest & Kidney Dis, Phoenix, AZ 85014 USA..
    Barroso, Ines
    Wellcome Trust Sanger Inst, Wellcome Trust Genome Campus, Saffron Walden CB10 1SA, Essex, England.;Addenbrookes Hosp, NIHR Cambridge Biomed Res Ctr, Inst Met Sci, Cambridge CB2 OQQ, England.;Univ Cambridge, Addenbrookes Hosp, Inst Met Sci, Metab Res Labs, Cambridge CB2 OQQ, England..
    Bennett, David A.
    Rush Univ, Med Ctr, Rush Alzheimers Dis Ctr, Chicago, IL 60612 USA..
    Bertram, Lars
    Univ Lubeck, Lubeck Interdisciplinary Platform Genome Analyt, Inst Neurogenet & Expt & Integrat Gen, D-23562 Lubeck, Germany.;Imperial Coll London, Fac Med, Sch Publ Hlth, London W6 8RP, England..
    Biffar, Rainer
    Ernst Moritz Arndt Univ Greifswald, Ctr Oral Hlth, Dept Prosthet Dent Gerodontol & Biomat, D-17489 Greifswald, Germany..
    Bochud, Murielle
    Swiss Inst Bioinformat, CH-1015 Lausanne, Switzerland.;Univ Inst Social & Prevent Med, Ctr Hosp Univ CHUV, CH-1010 Lausanne, Switzerland..
    Boehnke, Michael
    Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.;Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA..
    Borecki, Ingrid B.
    Washington Univ, Div Stat Gen, Dept Genet, Sch Med, St Louis, MO 63110 USA.;Washington Univ, Div Biostat, Sch Med, St Louis, MO 63110 USA..
    Buchman, Aron S.
    Rush Univ, Med Ctr, Rush Alzheimers Dis Ctr, Chicago, IL 60612 USA..
    Byberg, Liisa
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Campbell, Harry
    Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Edinburgh EH8 9AG, Midlothian, Scotland..
    Obanda, Natalia Campos
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands..
    Cauley, Jane A.
    Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15261 USA..
    Cawthon, Peggy M.
    Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA..
    Cederberg, Henna
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Chen, Zhao
    Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Tucson, AZ 85714 USA..
    Cho, Nam H.
    Ajou Univ, Sch Med, Dept Prevent Med, Suwon 16499, South Korea..
    Choi, Hyung Jin
    Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 03080, South Korea.;Chungbuk Natl Univ Hosp, Dept Internal Med, Cheongju, South Korea..
    Claussnitzer, Melina
    Inst Aging Res, HebrewSenior Life, Roslindale, MA 02131 USA.;Harvard Med Sch, Boston, MA 02115 USA.;Broad Inst, Cambridge, MA 02142 USA.;MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.;Tech Univ Munich, Inst Human Genet, MRI, D-81675 Munich, Germany.;Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA..
    Collins, Francis
    Natl Human Genome Res Inst, Med Genom & Metab Genet Branch, Bethesda, MD 20892 USA..
    Cummings, Steven R.
    Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA..
    De Jager, Philip L.
    Harvard Med Sch, Boston, MA 02115 USA.;Brigham & Womens Hosp, Dept Neurol, Program Translat NeuroPsychiatr Genom, Boston, MA 02115 USA.;Broad Inst, Program Med & Populat Genet, Cambridge, MA 02142 USA..
    Demuth, Ilja
    Charite, Res Grp Geriatr, Berlin Aging Study 2, D-13353 Berlin, Germany.;Charite, Inst Med & Human Genet, D-13353 Berlin, Germany..
    Dhonukshe-Rutten, Rosalie A. M.
    Wageningen Univ, Dept Human Nutr, POB 17, NL-6700 AA Wageningen, Netherlands..
    Diatchenko, Luda
    McGill Univ, Alan Edwards Ctr Res Pain, Montreal H3A 0G1, PQ, Canada.;Univ N Carolina, Sch Dent, Reg Ctr Neurosensory Disorders, Chapel Hill, NC 27599 USA..
    Eiriksdottir, Gudny
    Iceland Heart Assoc, IS-201 Kopavogur, Iceland..
    Enneman, Anke W.
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands..
    Erdos, Mike
    Natl Human Genome Res Inst, Med Genom & Metab Genet Branch, Bethesda, MD 20892 USA..
    Eriksson, Johan G.
    Univ Helsinki, Dept Gen Practice & Primary Hlth Care, Helsinki 00014, Finland.;Univ Helsinki, Cent Hosp, Unity Gen Practice, Helsinki 00014, Finland.;Folkhalsan Res Ctr, Helsinki 00250, Finland.;Vasa Cent Hosp, Vaasa 65130, Finland.;Nat Inst Hlth & Welf, Helsinki 00271, Finland..
    Eriksson, Joel
    Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Internal Med, SE-40530 Gothenburg, Sweden..
    Estrada, Karol
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Evans, Daniel S.
    Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA..
    Feitosa, Mary F.
    Washington Univ, Div Stat Gen, Dept Genet, Sch Med, St Louis, MO 63110 USA..
    Fu, Mao
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA..
    Garcia, Melissa
    Natl Inst Aging, Intramural Res Program, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA..
    Gieger, Christian
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, Inst Genet Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany..
    Girke, Thomas
    Univ Calif Riverside, Inst Integrat Genome Biol, Dept Bot & Plant Sci, Riverside, CA 92521 USA.;Univ Calif Riverside, Dept Bot & Plant Sci, Riverside, CA 92521 USA..
    Glazer, Nicole L.
    Boston Univ, Sch Med & Publ Hlth, Dept Med, Boston, MA 02118 USA.;Boston Univ, Sch Med & Publ Hlth, Dept Epidemiol, Boston, MA 02118 USA..
    Grallert, Harald
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany.;Univ Calif Riverside, Dept Bot & Plant Sci, Riverside, CA 92521 USA.;German Ctr Diabet Res DZD, Neuherberg, Germany.;Helmholtz Zentrum Munchen, CCG Type Diabet 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, CCG Nutrigen & Type Diabet 2, D-85764 Neuherberg, Germany..
    Grewal, Jagvir
    Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England.;Imperial Coll London, Natl Heart & Lung Inst, London SW3 6LY, England..
    Han, Bok-Ghee
    Osong Hlth Technol Adm Complex, Ctr Genome Sci, Natl Inst Hlth, Chungcheongbuk Do 28159, South Korea..
    Hanson, Robert L.
    NIH, Phoenix Epidemiol & Clin Res Branch, Natl Inst Diabet & Digest & Kidney Dis, Phoenix, AZ 85014 USA..
    Hayward, Caroline
    Univ Edinburgh, IGMM, MRC Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland..
    Hofman, Albert
    NCHA, NCI, NL-2593 Leiden, Netherlands.;Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Hoffman, Eric P.
    SUNY Binghamton, Dept Pharmaceut Sci, Binghamton, NY 13902 USA..
    Homuth, Georg
    Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Gen, D-17487 Greifswald, Germany..
    Hsueh, Wen-Chi
    NIH, Phoenix Epidemiol & Clin Res Branch, Natl Inst Diabet & Digest & Kidney Dis, Phoenix, AZ 85014 USA..
    Hubal, Monica J.
    George Washington Univ, Dept Exercise & Nutr Sci, Washington, DC 20052 USA.;Childrens Natl Med Ctr, Res Ctr Genet Med, Washington, DC 20052 USA..
    Hubbard, Alan
    Univ Calif Berkeley, Div Biostat, Sch Publ Hlth, Berkeley, CA 94720 USA..
    Huffman, Kim M.
    Duke Univ, Sch Med, Div Rheumatol, Dept Med,Duke Mol Physiol Inst, Durham, NC 27710 USA..
    Husted, Lise B.
    Aarhus Univ Hosp, Endocrinol & Internal Med, DK-8000 Aarhus, Denmark..
    Illig, Thomas
    Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany.;Hannover Med Sch, Dept Human Genet, D-30625 Hannover, Germany.;Hannover Med Sch, Hannover Unified Biobank, D-30625 Hannover, Germany..
    Ingelsson, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Molekylär epidemiologi. Stanford Univ, Dept Med, Div Cardiovasc Med, Sch Med, Stanford, CA 94305 USA..
    Ittermann, Till
    Ernst Moritz Arndt Univ Greifswald, Inst Community Med, D-17489 Greifswald, Germany..
    Jansson, John-Olov
    Univ Gothenburg, Dept Physiol, Inst Neurosci & Physiol, Sahlgrenska Acad, SE-40530 Gothenburg, Sweden..
    Jordan, Joanne M.
    Univ N Carolina, Thurston Arthrit Res Ctr, Chapel Hill, NC 27517 USA..
    Jula, Antti
    Nat Inst Hlth & Welf, Helsinki 00271, Finland..
    Karlsson, Magnus
    Lund Univ, Dept Clin Sci & Orthopaed, Skane Univ Hosp SUS, S-22362 Malmo, Sweden..
    Khaw, Kay-Tee
    Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge CB1 8RN, England..
    Kilpainen, Tuomas O.
    Univ Cambridge, Sch Clin Med, MRC Epidemiol Unit, Cambridge Biomed Campus, Cambridge CB2 OQQ, England.;Univ Copenhagen, Novo Nordisk Fdn Ctr Basic Metab Res, Sect Metab Genet, DK-2100 Copenhagen, Denmark.;Icahn Sch Med Mt Sinai, Dept Environm Med & Publ Hlth, New York, NY 10029 USA..
    Klopp, Norman
    Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany.;Hannover Med Sch, Hannover Unified Biobank, D-30625 Hannover, Germany..
    Kloth, Jacqueline S. L.
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands..
    Koistinen, Heikki A.
    Univ Helsinki, Dept Med, Helsinki 00029, Finland.;Helsinki Univ Cent Hosp, Helsinki 00029, Finland.;Univ Helsinki, Abdominal Ctr, Endocrinol, Helsinki 00029, Finland.;Natl Inst Hlth & Welf, Dept Hlth, Helsinki 00271, Finland.;Minerva Fdn, Helsinki 00290, Finland..
    Kraus, William E.
    Duke Univ, Sch Med, Div Cardiol, Dept Med,Duke Mol Physiol Inst, Durham, NC 27710 USA..
    Kritchevsky, Stephen
    Sticht Ctr Aging, Wake Forest Sch Med, Winston Salem, NC 27157 USA..
    Kuulasmaa, Teemu
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Kuusisto, Johanna
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Laakso, Markku
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Lahti, Jari
    Univ Helsinki, Inst Behav Sci, FI-00014 Helsinki, Finland..
    Lang, Thomas
    Univ Calif San Francisco, San Francisco, CA 94143 USA..
    Langdahl, Bente L.
    Aarhus Univ Hosp, Endocrinol & Internal Med, DK-8000 Aarhus, Denmark..
    Launer, Lenore J.
    Natl Inst Aging, Intramural Res Program, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA..
    Lee, Jong-Young
    Osong Hlth Technol Adm Complex, Ctr Genome Sci, Natl Inst Hlth, Chungcheongbuk Do 28159, South Korea..
    Lerch, Markus M.
    Ernst Moritz Arndt Univ Greifswald, Dept Med A, D-17489 Greifswald, Germany..
    Lewis, Joshua R.
    Univ Western Australia, Sch Med & Pharmacol, Perth, WA 6009, Australia.;Univ Sydney, Ctr Kidney Res, Sch Publ Hlth, Sydney, NSW 2006, Australia..
    Lind, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Kardiovaskulär epidemiologi. Uppsala Univ, Dept Med Sci, S-75185 Uppsala, Sweden..
    Lindgren, Cecilia
    Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England..
    Liu, Yongmei
    Wake Forest Sch Med, Dept Epidemiol & Prevent, Winston Salem, NC 27517 USA..
    Liu, Tian
    Max Planck Inst Mol Genet, D-14195 Berlin, Germany.;Max Planck Inst Human Dev, D-14195 Berlin, Germany..
    Liu, Youfang
    Univ N Carolina, Thurston Arthrit Res Ctr, Chapel Hill, NC 27517 USA..
    Ljunggren, Östen
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Endokrinologi och mineralmetabolism.
    Lorentzon, Mattias
    Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Internal Med, SE-40530 Gothenburg, Sweden..
    Luben, Robert N.
    Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge CB1 8RN, England..
    Maixner, William
    Univ N Carolina, Sch Dent, Reg Ctr Neurosensory Disorders, Chapel Hill, NC 27599 USA..
    McGuigan, Fiona E.
    Lund Univ, Dept Clin Sci, S-22362 Malmo, Sweden..
    Medina-Gomez, Carolina
    Erasmus MC, Dept Internal Med, NL-3000 Rotterdam, Netherlands.;Erasmus MC, Dept Epidemiol, NL-3000 DR Rotterdam, Netherlands..
    Meitinger, Thomas
    Tech Univ Munich, Inst Human Genet, MRI, D-81675 Munich, Germany.;Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Human Genet, D-85764 Neuherberg, Germany..
    Melhus, Håkan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk farmakogenomik och osteoporos.
    Mellstrom, Dan
    Univ Gothenburg, Sahlgrenska Acad, Inst Med, Dept Internal Med, SE-40530 Gothenburg, Sweden..
    Melov, Simon
    Buck Inst Res Aging, Novato, CA 94945 USA.;Univ Southern Calif, Leonard Davis Sch Gerontol, Los Angeles, CA 90089 USA..
    Michaëlsson, Karl
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi.
    Mitchell, Braxton D.
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA.;Baltimore Vet Adm Med Ctr, Geriatr Res & Educ Clin Ctr, Baltimore, MD 21201 USA..
    Morris, Andrew P.
    Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England.;Univ Liverpool, Inst Tradit Med, Liverpool L69 3BX, Merseyside, England..
    Mosekilde, Leif
    Aarhus Univ Hosp, Endocrinol & Internal Med, DK-8000 Aarhus, Denmark..
    Newman, Anne
    Univ Pittsburgh, Ctr Aging & Populat Hlth, Pittsburgh, PA 15261 USA..
    Nielson, Carrie M.
    Oregon Hlth & Sci Univ, Portland, OR 97239 USA..
    O'Connell, Jeffrey R.
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA..
    Oostra, Ben A.
    Erasmus MC, Dept Clin Genet, NL-300 CA Rotterdam, Netherlands.;Ctr Med Syst Biol & Netherlands Consortium Hlth A, RC-2300 Leiden, Netherlands..
    Orwoll, Eric S.
    Oregon Hlth & Sci Univ, Portland, OR 97239 USA..
    Palotie, Aarno
    Harvard Med Sch, Boston, MA 02115 USA.;Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland.;Univ Helsinki, Dept Med Genet, FI-00014 Helsinki, Finland.;Univ Cent Hosp, FI-00014 Helsinki, Finland..
    Parker, Stephan
    Univ Michigan, Human Genet & Computat Med & Bioinformat, Ann Arbor, MI 48109 USA..
    Peacock, Munro
    Indiana Univ, Dept Med, Sch Med, Indianapolis, IN 46202 USA..
    Perola, Markus
    Nat Inst Hlth & Welf, Helsinki 00271, Finland.;Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland.;Univ Helsinki, Diabet & Obes Res Program, FI-00014 Helsinki, Finland.;Univ Tartu, Estonian Genome Ctr, Tartu, Estonia..
    Peters, Annette
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, Rese Unit Mol Epidemiol, German Res Ctr Environm Hlth, D-85764 Neuherberg, Germany..
    Polasek, Ozren
    Univ Split, Fac Med, Dept Publ Hlth, Split 21000, Croatia..
    Prince, Richard L.
    Univ Western Australia, Sch Med & Pharmacol, Perth, WA 6009, Australia.;Sir Charles Gairdner Hosp, Dept Endocrinol & Diabet, Perth, WA 6009, Australia..
    Raikkonen, Katri
    Univ Helsinki, Inst Behav Sci, FI-00014 Helsinki, Finland..
    Ralston, Stuart H.
    Western Gen Hosp, Mol Med Ctr, MRC Inst Genet & Mol Med, Edinburgh EH4 2XU, Midlothian, Scotland..
    Ripatti, Samuli
    Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland.;Univ Helsinki, Hjelt Inst, Helsinki, Finland.;Wellcome Trust Sanger Inst, Wellcome Trust Genome Campus, Hinxton CB10 1SA, England..
    Robbins, John A.
    Univ Calif Davis, Dept Med, Sacramento, CA 95817 USA..
    Rotter, Jerome I.
    Harbor UCLA Med Ctr, Inst Translat Genom & Populat Sci, Los Angeles Biomed Res Inst, Torrance, CA 90502 USA.;Harbor UCLA Med Ctr, Dept Pediat, Torrance, CA 90502 USA..
    Rudan, Igor
    Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Edinburgh EH8 9AG, Midlothian, Scotland..
    Salomaa, Veikko
    Nat Inst Hlth & Welf, Helsinki 00271, Finland..
    Satterfield, Suzanne
    Univ Tennessee, Dept Prevent Med, Hlth Sci Ctr, Memphis, TN 38163 USA..
    Schadt, Eric E.
    Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, Inst Genom & Multiscale Biol, New York, NY 10029 USA..
    Schipf, Sabine
    Ernst Moritz Arndt Univ Greifswald, Inst Community Med, D-17489 Greifswald, Germany..
    Scott, Laura
    Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.;Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA..
    Sehmi, Joban
    Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England.;Imperial Coll London, Natl Heart & Lung Inst, London SW3 6LY, England..
    Shen, Jian
    Oregon Hlth & Sci Univ, Portland, OR 97239 USA..
    Shin, Chan Soo
    Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 03080, South Korea..
    Sigurdsson, Gunnar
    Natl Univ Hosp Iceland, Landspitali, Dept Endocrinol & Metab, IS-101 Reykjavik, Iceland..
    Smith, Shad
    Duke Univ, Med Ctr, Ctr Translat Pain Med, Dept Anesthesiol, Durham, NC 27110 USA..
    Soranzo, Nicole
    Wellcome Trust Sanger Inst, Wellcome Trust Genome Campus, Hinxton CB10 1SA, England..
    Stancakova, Alena
    Univ Eastern Finland, Dept Med, Kuopio 70210, Finland.;Kuopio Univ Hosp, Kuopio 70210, Finland..
    Steinhagen-Thiessen, Elisabeth
    Charite, Res Grp Geriatr, Berlin Aging Study 2, D-13353 Berlin, Germany..
    Streeten, Elizabeth A.
    Univ Maryland, Program Personalized & Genom Med, Baltimore, MD 21201 USA.;Univ Maryland, Div Endocrinol Diabet & Nutr, Dept Med, Baltimore, MD 21201 USA.;Vet Adm Med Ctr, GRECC, Baltimore, MD 21201 USA..
    Styrkarsdottir, Unnur
    Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.;deCODE Genet, IS-101 Reykjavik, Iceland..
    Swart, Karin M. A.
    Vrije Univ Amsterdam Med Ctr, Dept Epidemiol & Biostat, BT-1081 Amsterdam, Netherlands.;Vrije Univ Amsterdam Med Ctr, EMGO Inst, BT-1081 Amsterdam, Netherlands..
    Tan, Sian-Tsung
    Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England.;Imperial Coll London, Natl Heart & Lung Inst, London SW3 6LY, England..
    Tarnopolsky, Mark A.
    McMaster Univ, Med Ctr, Dept Med, Hamilton, ON L8N 3Z5, Canada..
    Thompson, Patricia
    Stony Brook Sch Med, Dept Pathol, Stony Brook, NY 11794 USA..
    Thomson, Cynthia A.
    Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Tucson, AZ 85714 USA..
    Thorsteinsdottir, Unnur
    Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.;deCODE Genet, IS-101 Reykjavik, Iceland..
    Tikkanen, Emmi
    Nat Inst Hlth & Welf, Helsinki 00271, Finland.;Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland.;Western Gen Hosp, Mol Med Ctr, MRC Inst Genet & Mol Med, Edinburgh EH4 2XU, Midlothian, Scotland..
    Tranah, Gregory J.
    Calif Pacific Med Ctr, Res Inst, San Francisco, CA 94107 USA..
    Tuomilehto, Jaakko
    Vasa Cent Hosp, Vaasa 65130, Finland.;Danube Univ Krems, Dept Neurosci & Prevent Med, A-3500 Krems, Austria.;King Abdulaziz Univ, Diabet Res Grp, Jeddah 12589, Saudi Arabia.;Dasman Diabet Inst, Dasman 15462, Kuwait..
    van Schoor, Natasja M.
    Vrije Univ Amsterdam Med Ctr, Dept Epidemiol & Biostat, BT-1081 Amsterdam, Netherlands.;Vrije Univ Amsterdam Med Ctr, EMGO Inst, BT-1081 Amsterdam, Netherlands..
    Verma, Arjun
    Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England..
    Vollenweider, Peter
    CHU Vaudois, Dept Med & Internal Med, CH-1011 Lausanne, Switzerland..
    Voelzke, Henry
    Ernst Moritz Arndt Univ Greifswald, Inst Community Med, D-17489 Greifswald, Germany..
    Wactawski-Wende, Jean
    SUNY Buffalo, Univ Buffalo, Dept Epidemiol & Environm Hlth, Buffalo, NY 14214 USA..
    Walker, Mark
    Newcastle Univ, Inst Cellular Med, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England..
    Weedon, Michael N.
    Univ Exeter, Med Sch, Genet Complex Traits, Exeter EX1 2LU, Devon, England..
    Welch, Ryan
    Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.;Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA..
    Wichman, H. -Erich
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Ludwig Maximilians Univ Munchen, Inst Med Informat Biometry & Epidemiol, Chair Epidemiol, D-81377 Munich, Germany.;Tech Univ, Inst Med Stat & Epidemiol, D-81675 Munich, Germany..
    Widen, Elisabeth
    Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki 00251, Finland..
    Williams, Frances M. K.
    Kings Coll London, Dept Twin Res & Genet Epidemiol, St Thomas Campus, London WC2R 2LS, England..
    Wilson, James F.
    Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Edinburgh EH8 9AG, Midlothian, Scotland.;Univ Edinburgh, IGMM, MRC Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland..
    Wright, Nicole C.
    Univ Alabama Birmingham, Dept Epidemiol, Birmingham, AL 35294 USA..
    Xie, Weijia
    Univ Exeter, Med Sch, Genet Complex Traits, Exeter EX1 2LU, Devon, England..
    Yu, Lei
    Rush Univ, Med Ctr, Rush Alzheimers Dis Ctr, Chicago, IL 60612 USA..
    Zhou, Yanhua
    Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA..
    Chambers, John C.
    Imperial Coll, Sch Publ Hlth, Dept Epidemiol & Biostat, London SW7 2AZ, England.;Ealing Hosp NHS Trust, Cardiol Dept, Middlesex UB1 3HW, England.;Royal Brompton & Harefield NHS Fdn Trust, NIHR Cardiovasc Biomed Res Unit, London SW3 6NP, England.;Imperial Coll, London SW3 6NP, England.;Imperial Coll Healthcare NHS Trust, London W2 1NY, England..
    Doring, Angela
    Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 2, D-85764 Neuherberg, Germany.;Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 1, D-85764 Neuherberg, Germany..
    van Duijn, Cornelia M.