King George''s Medical University

The Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) gene has emerged as a pivotal player in regulating glucose and lipid metabolism. This review aimed to provide a comprehensive overview of the PPARγ gene, its functions, its polymorphic association with diabetes mellitus and other associated complications, and its role in the response to antidiabetic drugs. A narrative comprehensive review was conducted using peer-reviewed literatures on PPARγ which were published during 2015 to 2025. Relevant studies were retrieved from databases including Pubmed, Scopus, World Health Organization (WHO) and International Diabetes Federation (IDF) and were considered in our studies. PPARγ is a nuclear receptor that modulates gene expression upon binding to specific ligands, primarily thiazolidinediones (TZDs). These ligands have been extensively used as antidiabetic drugs due to their ability to improve insulin sensitivity and glucose homeostasis. However, genetic variations in the PPARγ gene can influence drug response and efficacy, leading to variations in therapeutic outcomes. This review explored the molecular mechanisms of PPARγ, its role in diabetes, and the interplay between genetic variations and drug response. A deeper understanding of these interactions holds the potential to personalize antidiabetic therapies based on an individual's genetic makeup.

Thyroid nodules with indeterminate cytology represent a clinical challenge owing to uncertain malignancy risk, often leading to diagnostic surgery. Molecular testing has emerged as a promising adjunct to improve risk stratification and guide surgical decision-making. However, the clinical utility and impact of different molecular platforms remain debated. The present study evaluates the impact of molecular testing on surgical decision-making in indeterminate thyroid nodules and compares outcomes between first- and second-generation molecular platforms. A PRISMA-guided systematic review and meta-analysis identified 132 studies including 66,448 thyroid nodules, of which 30,292 (45.6

We conducted a comprehensive analysis of spectrum of neuroimaging findings in Subacute Sclerosing Panencephalitis (SSPE) across case reports and cohort studies. A systematic review was conducted as per PRISMA guidelines. Electronic databases were searched from inception using predefined terms related to SSPE and neuroimaging. Eligible studies included confirmed cases with reported imaging findings from case reports, case series, and cohort studies. Among 461 reported cases, neuroimaging was performed in 456 (98.9

Acquired aplastic anemia (AA) is a life-threatening bone marrow failure syndrome characterized by immune-mediated destruction of hematopoietic stem cells, resulting in profound pancytopenia. Historically fatal, the disease is now manageable through advancements in immunosuppressive therapy and hematopoietic stem cell transplantation. Clinically, AA follows a bimodal distribution, peaking at ages 10–25 and over 60. Patients typically present with features of pallor, mucocutaneous hemorrhage, and infections. In very severe cases, traditional signs of infection like fever may be absent; clinicians must instead monitor for tachycardia, tachypnea, and hypotension.As a diagnosis of exclusion, AA requires the systematic ruling out of inherited bone marrow failure syndromes (IBMFS), hypoplastic myelodysplastic syndromes (hMDS), and nutritional deficiencies. Severity is stratified using the Modified Camitta criteria into non-severe, severe (SAA), and very severe (VSAA) categories, which dictates the urgency and type of intervention. Accurate classification and rapid risk assessment remain essential to improving survival outcomes in this complex hematological disorder. Diagnostic Strategy: Acquired AA is a diagnosis of exclusion requiring a thorough history and physical examination to rule out secondary causes. Demographic Peaks: The disease follows a bimodal distribution with peaks at 10–25 years and over 60 years of age. Grading: The Modified Camitta classification is used to stratify patients into non-severe (NSAA), severe (SAA), and very severe (VSAA) categories, which serves as the primary determinant for the urgency of definitive intervention. Clinical Triad: Presentation typically involves pallor from anemia, mucocutaneous hemorrhages from thrombocytopenia, and an increased risk of bacterial or fungal infections due to profound neutropenia. Atypical Presentations: AA may initially present as isolated lineage cytopenia; practitioners must remain alert to evolving AA where megakaryocytic suppression helps distinguish it from primary Immune Thrombocytopenia (ITP). Masked Sepsis: In cases of severe neutropenia, traditional inflammatory responses like fever may be absent; tachycardia, tachypnea, and hypotension must be treated as signs of infection with clinical urgency. Screening for Mimics: Systematic examination for congenital stigmata of inherited bone marrow failure syndromes (IBMFS) or signs of nutritional deficiencies like Vitamin B12 and folate is mandatory to identify reversible or genetic conditions. Historical and Occupational Context: History should prioritize ancestry, duration of cytopenia, and exposure to cytotoxic agents or environmental toxins such as benzene.

To evaluate the polymorphisms of RETN + 62 and RETN + 420 genes in different grades of oral submucous fibrosis (OSMF) in a North Indian population. Thirty OSMF patients of various grades were recruited at a tertiary healthcare centre in Northern India. Blood samples were analyzed for RETN + 62 and RETN + 420 gene variants using Polymerase Chain Reaction (PCR). Chi-square (χ2) tests assessed associations between genotypes and factors such as age, habits, and OSMF grades. Stepwise linear regression evaluated the influence of independent variables on RETN polymorphisms. The RETN + 62 GG genotype was the most prevalent (66.67