Chronic pancreatitis (CP) is an irreversible disease characterized by progressive inflammation, fibrosis of pancreas, and loss of pancreatic functions. Epidemiological studies have identified CP to be a major risk factor for pancreatic ductal adenocarcinoma (PDAC). PDAC is one of the most lethal diseases with an incidence rate almost equal to the rate of mortality. Elucidation of the molecu lar mechanism driving the development of the diseases will not only help us understanding the disease biology but also help us identifying key molecules which could be used as potential biomarkers for early detection of the malignant disease. Regulation of gene expression by epigenetic mechanisms has gained much importance due to their important role in disease pathophysiology and my work revolves around delineating the role of key epigenetic factors in the development of chronic pancreatitis and pancreatic ductal adenocarcinoma.
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Nonalcoholic fatty liver disease (NAFLD) is a complex disorder. Both genetic and environmental factors affect disease pathogenesis. NAFLD begins with aberrant accumulation of triglycerides in the liver which is called hepatic steatosis. In some individuals it can lead to inflammatory responses and causes progression to Nonalcoholic steatohepatitis to cirrhosis, and subsequently hepatocellul ar carcinoma. The pathogenicity of the disease is poorly understood and therapeutic options are very limited. My work emphasizes on understanding the molecular mechanisms and the role of related pathways involved in disease progression from mild to advanced stages and validation of the role of some specific genes associated with NAFLD in the Indian population in in vitro and in vivo models.
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Chronic Obstructive pulmonary disease (COPD) is a multifactorial disease characterised by irreversible airway obstruction and progressive deterioration of pulmonary function. COPD is the fifth leading cause of mortality worldwide affecting 251 million lives globally. The disease is characterised by airflow obstruction and inflammation that gives rise to the clinical symptoms. Genetic component an d particulate matters play significant role in COPD progression. Environmental triggers like cigarette smoke, pollen grains, carbon black nanoparticles, dust particles, microbial infection etc. are responsible for COPD exacerbations. NLRP3 inflammasome, a cardinal component of the innate immune system plays significant role in regulating the lung pathophysiology during exacerbations. The aim of my research is to examine the molecular pathway of NLRP3 inflammasome activation, identify the genetic factors associated with the disease in an unexplored heterogenic prototype study of Indian population and design intervention strategies using stem cells and genetically modified T cells. Read less
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Sepsis is a life-threatening organ dysfunction caused by dysregulated host response to infection, accounting for one-fifth of all deaths globally. Many children and adults who have bacterial sepsis develop abnormal coagulation in the intravascular compartment thus impeding oxygen supply to the organs. I am interested in the cellular and molecular underpinning of abnormal coagulation in blood of p atients admitted to intensive care unit (ICU). I am focusing on the phenomenon called Neutrophil extracellular trap (NET), that is produced by neutrophil in response to pathogen. NETs consist primarily of decondensed chromatin of neutrophils and can trigger immune-thrombosis. The study shall have three components: computational (integrated analysis of multi-cohort transcriptomic data), clinical (collection of blood samples from neonates admitted to ICU with sepsis) and experimental (investigation of the molecules that trigger NET formation). Read less
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Anatomically Modern Humans (AMH) originated in Africa around 150,000-190,000 YBP (Years Before Present) and started moving Out of Africa (OoA) about 50,000-100,000 YBP. Following the OoA event, AMH underwent several demographic transitions, e.g., population bottlenecks, population expansion, population split, genetic drift, and evolutionary forces of natural selection in the journey of peopling t he globe. The constant interaction between genotype(G) and environment(E) resulted in the local adaptation of human populations with phenotypic trait differences across populations. Thus, spatially structured populations and spatially varying phenotypic traits provide an opportunity to study the environmental factors which might have acted as selective forces for human populations to adapt to their local environment. My research work focuses on the development of deep learning architecture for modeling genotype-environment interactions to detect genomic regions under natural selection in different human populations. Read less
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Healthy pregnancy outcomes are critical determinants of public health. Preterm birth (PTB), remains the leading cause of neonatal morbidity and mortality. The etiology of PTB is multifactorial, involving complex interactions between genetic, environmental, and physiological factors. The mechanisms by which genomic variants, identified in the genome-wide studies, influence the risk of preterm birt h remain largely unknown. One potential mechanism involves the regulation of gene expression through alterations in DNA methylation at specific CpG sites. My research aims to investigate the role of these genetic variants in modulating biological processes implicated in PTB, with a particular focus on their effects on DNA methylation and cell types of the placenta where these genes are differentially expressed. Thus, this will not only explain how these variants modulate the risk of PTB, but also delineate biological pathways involved in this birth outcome, ultimately providing valuable insights for developing targeted therapeutic interventions Read less
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I am deeply interested in exploring the evolutionary history of modern humans through the lens of population genetics and genomics. My research focuses on analyzing archaic admixture in present-day human populations to unravel the complex migrations, admixture events, and demographic changes that have shaped our species. A key area of my work involves studying the genetic contributions of Neander thals and other archaic hominins to modern human populations, providing insights that complement fossil and archaeological records. My study aims to provide a comprehensive understanding of human prehistory and its implications for contemporary genetic diversity. By bridging computational genomics with evolutionary biology, my work seeks to answer fundamental questions about human origins and adaptation. Read less
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Research in the last decade has shown that the genetic background for pancreatic cancer, especially pancreatic ductal adenocarcinoma (PDAC) accounts for more than 90% of all pancreatic tumours. PDAC has poor prognosis and a rising incidence rate. Late detection and threatening nature are two major causes for treatment failure. In case of treatment, identification of some biomarker molecules helps in proper diagnosis. It has been found that some specific genes accelerate cancer progression rate in multiple pathways. There are some specific genes which act as biomarkers, affecting cell cycle regulation, cell signalling mechanisms etc. My research goal is the functional characterization of specified genes which act as progression biomarker and their interaction with other molecules that help retaining cellular proliferation in pancreatic cancer.
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Pancreatic Ductal Adenocarcinoma (PDAC), the most frequent form of pancreatic cancer, is one of the major causes of cancer-related deaths worldwide. This is an aggressive and devastating cancer with a five-year survival rate of less than 9%, the lowest among common cancers. CP (Chronic Pancreatitis) is one of the major reasons to proceed toward PDAC. The mis-regulation during chronic pancreatitis may induce several epigenetic changes. The consequence of such epigenetic modification in pancreatic cancer is not known completely yet. Moreover, a reliable epigenetic feature of active enhancers is the production of enhancer-directed transcripts (eRNAs). eRNAs are tightly regulated and play important roles in gene regulation, which was previously considered as junk element inside the cell with no function. My interest is to explore the role of eRNA in PDAC and how does eRNA regulate the progression of Chronic Pancreatitis to Pancreatic Cancer. Read less
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Primary angle closure glaucoma(PACG) is a major subtype of glaucoma and its prevalence is higher among South Asians including Indians. My research interest is to investigate the functional role of genomic signatures associated with PACG and related quantitative traits. In a previous case-control GWAS from our lab, TNF-α promoter SNP rs1800629 is found to be associated with PACG in Indian patient s. Interestingly it is already identified to be associated with different glaucoma subtypes across various populations worldwide reporting either G or A as risk allele. Investigating the underlying mechanism of rs1800629 will help in revealing its involvement with neurodegeneration and neuroprotection. In another Quantitative Trait (QT) GWAS on lens thickness we reported the novel association of PTPRM genic region. My research is focused on the functional characterization of PTPRM and understanding the underlying molecular mechanisms. It will facilitate a better understanding of risk factor and disease pathophysiology. Read less
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