R
Rong Jiang
Researcher at Duke University
Publications - 19
Citations - 348
Rong Jiang is an academic researcher from Duke University. The author has contributed to research in topics: Coronary artery disease & Medicine. The author has an hindex of 9, co-authored 15 publications receiving 219 citations.
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Journal ArticleDOI
Genome-wide analysis identifies novel susceptibility loci for myocardial infarction
Jaana Hartiala,Yi Han,Qiong Jia,James R. Hilser,Pin Huang,Janet Gukasyan,William S Schwartzman,Zhiheng Cai,Subarna Biswas,David-Alexandre Trégouët,Nicholas L. Smith,Nicholas L. Smith,Nicholas L. Smith,Marcus M. Seldin,Calvin Pan,Margarete Mehrabian,Aldons J. Lusis,Peter Bazeley,Yan V. Sun,Chang Liu,Arshed A. Quyyumi,Markus Scholz,Joachim Thiery,Graciela E. Delgado,Marcus E. Kleber,Winfried März,Winfried März,Winfried März,Laurence J. Howe,Folkert W. Asselbergs,Folkert W. Asselbergs,Marion van Vugt,Georgios J. Vlachojannis,Riyaz S. Patel,Riyaz S. Patel,Leo-Pekka Lyytikäinen,Mika Kähönen,Terho Lehtimäki,Tuomo Nieminen,Pekka Kuukasjärvi,Jari Laurikka,Xuling Chang,Xuling Chang,Chew-Kiat Heng,Chew-Kiat Heng,Rong Jiang,William E. Kraus,Elizabeth R. Hauser,Jane F. Ferguson,Muredach P. Reilly,Kaoru Ito,Satoshi Koyama,Yoichiro Kamatani,Yoichiro Kamatani,Issei Komuro,Lindsey K. Stolze,Casey E. Romanoski,Mohammad Daud Khan,Adam W. Turner,Clint L. Miller,Redouane Aherrahrou,Mete Civelek,Lijiang Ma,Johan L.M. Björkegren,Johan L.M. Björkegren,S. Ram Kumar,W.H. Wilson Tang,Stanley L. Hazen,Hooman Allayee +68 more
TL;DR: A large-scale analysis comprising ∼831 000 subjects revealed novel genetic determinants of MI and implicated SLC44A3 in the pathophysiology of vulnerable plaques and thrombus formation as mentioned in this paper.
Journal ArticleDOI
Gene by stress genome-wide interaction analysis and path analysis identify EBF1 as a cardiovascular and metabolic risk gene.
Abanish Singh,Michael A. Babyak,Daniel K Nolan,Beverly H. Brummett,Rong Jiang,Ilene C. Siegler,William E. Kraus,Svati H. Shah,Redford B. Williams,Elizabeth R. Hauser +9 more
TL;DR: Analysis of related phenotypes identified gene-by-stress interaction effects for waist circumference, body mass index (BMI), fasting glucose, type II diabetes status, and common carotid intimal–medial thickness (CCIMT), supporting a proposed model of gene- by- stress interaction that connects cardiovascular disease (CVD) risk factor endophenotypes such as central obesity and increased blood glucose or diabetes to CVD itself.
Journal ArticleDOI
Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism interacts with gender to influence cortisol responses to mental stress.
Rong Jiang,Michael A. Babyak,Beverly H. Brummett,Ilene C. Siegler,Cynthia M. Kuhn,Redford B. Williams +5 more
TL;DR: The present findings indicate the gender differences in the effect of Val66Met genotype on the cortisol responses to stress protocol, and extend the evidence for the importance of gender and the role of Val 66Met in the modulation of stress reactivity and subsequent depression prevalence.
Journal ArticleDOI
Socioeconomic indices as independent correlates of C-reactive protein in the National Longitudinal Study of Adolescent Health.
Beverly H. Brummett,Michael A. Babyak,Abanish Singh,Rong Jiang,Redford B. Williams,Kathleen Mullan Harris,Ilene C. Siegler +6 more
TL;DR: Race and sex play a role in how potential mediators are involved with the SES-CRP relationship, such that BMI and smoking were mediators in white men, whereas BMI was the sole mediator in white women.
Journal ArticleDOI
Brain-derived neurotrophic factor rs6265 (Val66Met) polymorphism is associated with disease severity and incidence of cardiovascular events in a patient cohort
Rong Jiang,Michael A. Babyak,Beverly H. Brummett,Elizabeth R. Hauser,Svati H. Shah,Richard C. Becker,Ilene C. Siegler,Abanish Singh,Carol Haynes,Megan Chryst-Ladd,Damian M. Craig,Redford B. Williams +11 more
TL;DR: The Val66Met genotype was associated with greater severity of CAD and incidence of CVD‐related clinical events in a patient sample, and intervention studies in clinical groups with the Val/Val genotype could be undertaken to prevent disease and improve prognosis.