Jayanta Gupta, M.D., Ph.D.

University of Pennsylvania Perelman School of Medicine

Center for Clinical Epidemiology and Biostatistics

Post-doctoral Researcher

2010

Cincinnati Children’s Hospital Medical Center

Division of Asthma Research, Department of Pediatrics

Post-doctoral Researcher

2008

University of Cincinnati College of Medicine

Ph.D.

Epidemiology: Environmental Health

2008

Assessment of oral health related quality of life among ESRD patients in Southwest Florida – a pilot study

National Oral Health Conference  Memphis, Tennessee

2019-04-13

Association of Variants in Genes Belonging to the Angiogenesis/Wound Repair Pathway with Lower Extremity Amputation: Findings from the CRIC study

ASN Kidney Week 2014 Annual Meeting  Philadelphia, Pennsylvania

2014-11-13

Discovery of Novel Candidate Genetic Markers Associated with Pediatric CKD Progression in the PediGFR Study

ASN Kidney Week 2013 Annual Meeting  Atlanta, Georgia

2013-11-05

African-Americans with atopic dermatitis: Skin barrier and immune-dysregulation

National Institutes of Health

2016
Co-investigator with David J. Margolis, M.D., Ph.D. of the University of Pennsylvania School of Medicine.

Atopic dermatitis (AD) is a highly pruritic chronic episodic inflammatory skin disease that often presents between 3 and 6 months of age but may also present during later childhood or in adulthood. In the US, AD affects roughly 10-20% of all children of all races and ethnic groups. The highest prevalence of AD in the US is among African-Americans. The prevalence of AD is increasing worldwide and it is a major public health burden. The majority of children with AD will also develop asthma and seasonal allergies. From the recent Global Burden of Disease study, AD was among the top 50 most prevalent diseases worldwide and it had the second highest disability rank of all non-malignant skin diseases. Recent studies have established a strong association between loss-of-function mutations in filaggrin (FLG), a gene coding for a protein responsible for maintaining an intact skin barrier and AD. We have already demonstrated that these mutations are also associated with more persistent AD. However, these mutations are rarely noted in children of African ancestry. As a result, there is a gap in our knowledge with respect to the basic biology of AD in African-Americans. We recently found that mutations in filaggrin-2 (FLG2) are associated with persistence of AD in African-American children. We have also shown that genetic variation of the gene that codes thymic stromal lymphopoietin appears to modify the association of FLG with AD. The goals of this proposal are to comprehensively explore the association of FLG2 with AD in African-Americans, to better understand the association of thymic stromal lymphopoietin with the persistence of AD, and to explore how TSLP/FLG2 interact to create the phenotype of persistent AD. We will continue to focus on loss-of- function mutations in skin barrier genes using FLG as a model, a concept that was recently justified by a report that LOF may be a preferred pathway for adaptation to environmental stimuli. We plan to focus our studies on African-Americans. This proposal has two goals. The first goal is to better understand FLG2 loss-of-function mutations in African Americans. The second goal is to better understand TSLP variation and ultimately the interaction between TSLP and barrier dysfunction.

Public Health Relevance
Atopic dermatitis (AD) is a very itchy chronic lifelong skin disease that often begins in early childhood

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Cyanobacterial blooms' impact on human health and potential mitigation strategies

Florida Department of Health

2020-01-01

The Florida Department of Health has funded research on the presence of the potential cyanotoxin, BMAA, in both natural water samples and in aerosols adjacent to waterbodies. In conjunction with the Centers for Disease Control, Dr. Gupta and his FGCU colleague Dr. Barry Rosen will be involved in determining if these aerosols find their way into community members who live adjacent to a lake or other water body and if there is a measurable effect on human health.

Resolving the Etiology of Atopic Disorders by Genetic Analysis of Racial Ancestry

Jayanta Gupta, MD, PhD; Elisabet Johansson, PhD; Jonathan A. Bernstein, MD; Ranajit Chakraborty, PhD; Gurjit K. Khurana Hershey, MD, PhD; Marc E. Rothenberg, MD, PhD; and Tesfaye B. Mersha, PhD

2016-06-11

Atopic dermatitis (AD), food allergy, allergic rhinitis, and asthma are common atopic disorders of complex etiology. The frequently observed atopic march from early AD to asthma, allergic rhinitis, or both later in life and the extensive comorbidity of atopic disorders suggest common causal mechanisms in addition to distinct ones. Indeed, both disease-specific and shared genomic regions exist for atopic disorders. Their prevalence also varies among races; for example, AD and asthma have a higher prevalence in African Americans when compared with European Americans. Whether this disparity stems from true genetic or race-specific environmental risk factors or both is unknown. Thus far, the majority of the genetic studies on atopic diseases have used populations of European ancestry, limiting their generalizability. Large-cohort initiatives and new analytic methods, such as admixture mapping, are currently being used to address this knowledge gap. Here we discuss the unique and shared genetic risk factors for atopic disorders in the context of ancestry variations and the promise of high-throughput "-omics"-based systems biology approach in providing greater insight to deconstruct their genetic and nongenetic etiologies. Future research will also focus on deep phenotyping and genotyping of diverse racial ancestry, gene-environment, and gene-gene interactions.

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Association Between Albuminuria, Kidney Function, and Inflammatory Biomarker Profile

Jayanta Gupta, Nandita Mitra, Peter A. Kanetsky, Joe Devaney, Maria R. Wing, Muredach Reilly, Vallabh O. Shah, Vaidyanathapura S. Balakrishnan, Nicolas J. Guzman, Matthias Girndt, Brian G. Periera, Harold I. Feldman, John W. Kusek, Marshall M. Joffe, Dominic S. Raj, corresponding author and for the CRIC Study Investigators

2012-09-27

Background and objectives
Increased risk of mortality in patients with CKD has been attributed to inflammation. However, the association between kidney function, albuminuria, and biomarkers of inflammation has not been examined in a large cohort of CKD patients.

Design, setting, participants, & measurements
This study measured the plasma levels of IL-1β, IL-1 receptor antagonist (IL-1RA), IL-6, TNF-α, TGF-β, high-sensitivity C-reactive protein (hs-CRP), fibrinogen, and serum albumin in 3939 participants enrolled in the Chronic Renal Insufficiency Cohort study between June 2003 and September 2008. An inflammation score was established based on plasma levels of IL-1β, IL-6, TNF-α, hs-CRP, and fibrinogen. Estimated GFR (eGFR) and serum cystatin C were used as measures of kidney function. Albuminuria was quantitated by urine albumin to creatinine ratio (UACR).

Results
Plasma levels of IL-1β, IL-1RA, IL-6, TNF-α, hs-CRP, and fibrinogen were higher among participants with lower levels of eGFR. Inflammation score was higher among those with lower eGFR and higher UACR. In regression analysis adjusted for multiple covariates, eGFR, cystatin C, and UACR were strongly associated with fibrinogen, serum albumin, IL-6, and TNF-α. Each unit increase in eGFR, cystatin C, and UACR was associated with a −1.2% (95% confidence interval, −1.4, −1), 64.9% (56.8, 73.3) and 0.6% (0.4, 0.8) change in IL-6, respectively (P

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Intrinsically defective skin barrier function in children with atopic dermatitis correlates with disease severity

Jayanta Gupta, MD; Emilie Grube, BA; Mark B. Ericksen, BS; Michelle D. Stevenson, MD, MS; Anne W. Lucky, MD; Anita P. Sheth, MD; Amal H. Assa'ad, MD; Gurjit K. Khurana Hershey, MD, PhD

2008-03-01

Background
Recent genetic evidence supports that an underlying defect in skin barrier function contributes to the pathogenesis of atopic dermatitis (AD). The integrity of the skin barrier can be assessed objectively by measuring transepidermal water loss (TEWL). Previous investigations of TEWL as a biomarker of skin barrier function have been limited by small sample size, and studies including African American subjects are lacking.

Objective
We sought to determine whether children with AD have inherently altered skin barrier function by comparing TEWL as a measure of skin barrier function in African American and white children with AD with that in control subjects without AD.

Methods
TEWL was measured on nonlesional normal-appearing skin at 4 sites (the volar forearm, dorsal arm, lower leg, and cheek) in (1) children with AD (cases), (2) children with asthma or allergic rhinitis but without AD (allergic control subjects), and (3) nonatopic control subjects. AD severity was assessed by using the objective SCORAD index.

Results
TEWL was increased in children with AD compared with that seen in both control groups at most of the anatomic sites tested (P < .05). TEWL also correlated with objective SCORAD score. The presence of allergic sensitization or other allergic conditions did not affect TEWL among children with AD. TEWL was higher in white than in African American children.

Conclusion
Skin barrier function as assessed by TEWL is intrinsically compromised in children with AD but not in children with other allergic conditions. The magnitude of skin barrier dysfunction correlates with AD disease severity.

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