PHD

Maulana Abul Kalam Azad University of Technology, West Bengal, India
2022

Research Expertise

• My research expertise encompasses molecular and cellular biology, functional genomics, transcriptomics, computational bioinformatics, and translational biomarker discovery, with a particular emphasis on elucidating the molecular mechanisms underlying complex, multifactorial human diseases.

   

• I specialize in whole-blood transcriptomic profiling, differential gene expression analysis, microRNA (miRNA) and long non-coding RNA (lncRNA) characterization, molecular signaling network analysis, and functional interpretation of disease-associated gene signatures. My research integrates high-throughput molecular profiling with clinical and epidemiological data to investigate disease pathogenesis, identify candidate diagnostic and prognostic biomarkers, and characterize molecular pathways associated with disease progression.

   

• My disease-focused expertise includes metabolic dysfunction-associated steatotic liver disease (MASLD), hepatic fibrogenesis, type 2 diabetes mellitus, Alzheimer's disease, and allergic and immunological disorders. My investigations have particularly emphasized the transcriptional regulation of E2F1, TGF-β1-associated signaling, inflammatory pathways, and non-coding RNA-mediated regulatory mechanisms in metabolic and liver diseases. I also investigate the molecular relationships between metabolic dysfunction and neurodegeneration, including shared transcriptomic alterations associated with type 2 diabetes and Alzheimer's disease.

   

• In allergy and immunology, my current research focuses on the clinical and molecular characterization of food allergies, integrating immunological profiling, clinical phenotyping, genetic investigations, and exploratory multi-omics approaches to identify potential biomarkers of disease susceptibility, severity, and clinical outcomes.

   

• My methodological expertise includes microarray-based transcriptomic analysis, quantitative real-time PCR, TaqMan Low-Density Array (TLDA) validation, molecular pathway enrichment analysis, Ingenuity Pathway Analysis (IPA), and experimental cellular and molecular biology techniques. I also have substantial experience in radiation-induced genotoxicity, DNA double-strand break formation and repair, oxidative stress, chromosomal instability, and cellular toxicity assessment.

   

• A central focus of my research is understanding population-associated molecular heterogeneity and health disparities, particularly among African American and other historically underrepresented populations. Through interdisciplinary clinical and molecular investigations, I aim to advance the development of minimally invasive molecular biomarkers and contribute to precision diagnostics, disease risk stratification, and personalized therapeutic strategies.

Teaching Expertise

• My teaching expertise is centered on evolutionary medicine, molecular and cellular biology, genetics, and interdisciplinary biomedical sciences, with a focus on connecting fundamental biological mechanisms to human disease, adaptation, and population health.

   

• As an instructor at Howard University, I have taught Evolutionary Medicine (BIOL 417) and General Biology (BIOL 003), developing and delivering undergraduate lectures, laboratory instruction, and assessments that emphasize conceptual understanding, scientific reasoning, and the critical interpretation of biological evidence. My teaching in evolutionary medicine integrates evolutionary theory with human physiology, genetics, disease susceptibility, and the evolutionary origins of contemporary health challenges.

   

• My instructional experience also includes Environmental Science and Sustainable Development at Maulana Abul Kalam Azad University of Technology, India, where I incorporated environmental health, ecological principles, and sustainability into interdisciplinary science education.

   

• A significant component of my academic teaching involves research-integrated instruction and scientific mentorship. I provide individualized training in experimental design, molecular and cellular techniques, transcriptomic data interpretation, bioinformatics, statistical analysis, and scientific communication. Through structured research supervision, I guide undergraduate and graduate students in developing research questions, evaluating experimental findings, preparing scientific manuscripts, and presenting research at academic conferences.

   

• My teaching philosophy emphasizes scientific rigor, analytical independence, and the integration of classroom knowledge with practical biomedical research, preparing students to critically evaluate scientific evidence and pursue advanced education and research careers.

2018 – 2020    Senior Research Fellowship from Council of Scientific & Industrial Research (CSIR), India

2013 – 2015    Junior Research Fellowship from Inter-University Accelerator Centre (IUAC), India

2012, 2013      Graduate Aptitude Test in Engineering (GATE), Department of Higher Education, India.

Transcriptomic Analysis of Alzheimer's Disease Pathways in a Pakistani Population.

Background: Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder that is most prevalent in elderly individuals, especially in developed countries, and its prevalence is now increasing in developing countries like Pakistan.

Objective: Our goal was to characterize key genes and their levels of expression and related molecular transcriptome networks associated with AD pathogenesis in a pilot case-control study in a Pakistani population.

Methods: To obtain the spectrum of molecular networks associated with pathogenesis in AD patients in Pakistan (comparing cases and controls), we used high-throughput qRT-PCR (TaqMan Low-Density Array; n = 33 subjects) coupled with Affymetrix Arrays (n = 8) and Ingenuity Pathway Analysis (IPA) to identify signature genes associated with Amyloid processing and disease pathways.

Results: We confirmed 16 differentially expressed AD-related genes, including maximum fold changes observed in CAPNS2 and CAPN1. The global gene expression study observed that 61% and 39% of genes were significantly (p-value 0.05) up- and downregulated, respectively, in AD patients compared to healthy controls. The key pathways include, e.g., Amyloid Processing, Neuroinflammation Signaling, and ErbB4 Signaling. The top-scoring networks in Diseases and Disorders Development were Neurological Disease, Organismal Injury and Abnormalities, and Psychological Disorders.

Conclusions: Our pilot study offers a non-invasive and efficient way of investigating gene expression patterns by combining TLDA and global gene expression methods in AD patients by utilizing whole blood. This provides valuable insights into the expression status of genes related to Amyloid Processing, which could play a potential role in future studies to identify sensitive, early biomarkers of AD in general.

Transcriptomics of MASLD Pathobiology in African American Patients in the Washington DC Area†.

Metabolic-dysfunction-associated steatotic liver disease (MASLD) is becoming the most common chronic liver disease worldwide and is of concern among African Americans (AA) in the United States. This pilot study evaluated the differential gene expressions and identified the signature genes in the disease pathways of AA individuals with MASLD. Blood samples were obtained from MASLD patients (n = 23) and non-MASLD controls (n = 24) along with their sociodemographic and medical details. Whole-blood transcriptomic analysis was carried out using Affymetrix Clarion-S Assay. A validation study was performed utilizing TaqMan Arrays coupled with Ingenuity Pathway Analysis (IPA) to identify the major disease pathways. Out of 21,448 genes in total, 535 genes (2.5%) were significantly (p < 0.05) and differentially expressed when we compared the cases and controls. A significant overlap in the predominant differentially expressed genes and pathways identified in previous studies using hepatic tissue was observed. Of note, TGFB1 and E2F1 genes were upregulated, and HMBS was downregulated significantly. Hepatic fibrosis signaling is the top canonical pathway, and its corresponding biofunction contributes to the development of hepatocellular carcinoma. The findings address the knowledge gaps regarding how signature genes and functional pathways can be detected in blood samples ('liquid biopsy') in AA MASLD patients, demonstrating the potential of the blood samples as an alternative non-invasive source of material for future studies.

Insights on the pathogenesis of type 2 diabetes as revealed by signature genomic classifiers in an African American population in the Washington, DC area

Aims: African Americans (AA) in the United States have a high risk of type 2 diabetes mellitus (T2DM) and suffer from disparities in the prevalence, mortality, and comorbidities of the disease compared to other Americans. The present study aimed to shed light on the molecular mechanisms of disease pathogenesis of T2DM among AA in the Washington, DC region.

Methods: We performed TaqMan Low Density Arrays (TLDA) on 24 genes of interest that belong to three categories: metabolic disease and disorders, cancer-related genes, and neurobehavioural disorders genes. The 18 genes, viz. ARNT, CYP2D6, IL6, INSR, RRAD, SLC2A2 (metabolic disease and disorders), APC, BCL2, CSNK1D, MYC, SOD2, TP53 (Cancer-related), APBA1, APBB2, APOC1, APOE, GSK3B, and NAE1 (neurobehavioural disorders), were differentially expressed in T2DM participants compared to controls.

Results: Our results suggest that factors including gender, smoking habits, and the severity or lack of control of T2DM (as indicated by HbA1c levels) were significantly associated with differential gene expression. APBA1 was significantly (p-value <0.05) downregulated in all diabetes participants. Upregulation of APOE and CYP2D6 genes and downregulation of the INSR gene were observed in the majority of diabetes patients.

Conclusions: Tobacco smoking and gender were significantly associated with case-control differences in expression of the APBA1 and APOE genes (connected with Alzheimer's disease) and the INSR and CYP2D6 (associated with metabolic disorders). The results highlight the need for more effective management of T2DM and for tobacco smoking cessation interventions in this community, and further research on the associations of T2DM with other disease processes, including cancer and neurobehavioral pathways.

Gene expression signatures in PCB-exposed Slovak children in relation to their environmental exposures and socio-physical characteristics.

Our previous gene expression studies in a PCB-exposed cohort of young children in Slovakia revealed that early-life exposures to PCBs and other organochlorine compounds were associated with significant alterations across several pathogenetic pathways. The present study was undertaken to further explore the high-throughput qRT-PCR-based gene expression effects by using TaqMan low-density array (TLDA) for selected genes in a sample of 55 children from the cohort. We analyzed the transcriptional changes of 11 genes in relation to PCB and organochlorine pesticide exposure levels (including DDT, DDE, HCH, and HCB), and to BMI and ethnicity in this cohort. The results indicated an overall downregulation of expression of these genes. Maximum downregulation (in fold change) was observed in the ENTPD3 gene, and the minimum level of downregulation was in CYP2D6. As per our multinomial regression model study, downregulation of LEPR gene was significantly directly correlated with all the exposure variables. Downregulation of APC, ARNT, CYP2D6, LEPR, LRP12, and MYC genes was directly correlated with BMI (kg/m2) of the individuals. Gender-specific differences in gene expression were observed in CYP2D6 (p-value 0.0001) and LEPR (p-value 0.028), while downregulation of CYP2D6 (p-value 0.01), LEPR (p-value 0.02), LRP12 (p-value 0.04), and MYC (p-value 0.02) genes was consistently observed in Roma children compared to Caucasians. The investigation of such health disparities must be emphasized in future research, together with interventions to reduce the health consequences of PCB exposures. In this context, we emphasize the importance of biomarker-based approaches to future research on genetic susceptibility to the effects of these compounds.

An evaluation of DNA double strand break formation and excreted guanine species post whole body PET/CT procedure

Ionizing radiation-induced oxidation and formation of deoxyribonucleic acid (DNA) double strand breaks (DSBs) are considered the exemplar of genetic lesions. Guanine bases are most prone to be oxidized when DNA and Ribonucleic acid (RNA) are damaged. The repair processes that are initiated to correct this damage release multiple oxidized guanine species into the urine. Hence, the excretion of guanine species can be related with the total repair process. Our study quantified the total DSBs formation and the amount of guanine species in urine to understand the DNA break and repair process after whole body (WB) exposure to 18F-FDG positron emission tomography/computed tomography (PET/CT). A total of 37 human participants were included with control and test groups and the average radiation dose was 27.50 ± 2.91 mSv. γ-H2AX foci assay in the collected blood samples was performed to assess the DSBs, and excreted guanine species in urine were analyzed by a competitive ELISA method. We observed a significant increase of DNA damage that correlated well with the increasing dose (p-value 0.009) and body weight (p-value 0.05). In the test group, excreted guanine species in urine sample significantly increased (from 24.29 ± 5.82 to 33.66 ± 7.20 mg/mmol creatinine). A minimum (r2 = 0.0488) correlation was observed between DSBs formation and excreted guanine species. A significant difference of DNA damage and 8-OHdG formation was seen in the test group compared to controls. Larger population studies are needed to confirm these observations, describe the fine-scale timing of changes in the biomarker levels after exposure, and further clarify any potential risks to patients from PET/CT procedures.