An imbalance between the generation of reactive oxygen species (ROS) and antioxidant defense systems is known as oxidative stress, and it is a major factor in diseases like atherosclerosis, vascular inflammation, endothelial dysfunction, and others that are largely caused by elevated oxidative stress. Interestingly, oxidative stress has also been implicated in the progression of prediabetes to type 2 diabetes (T2DM). Prediabetes, characterized by increased blood glucose levels than the diabetes threshold, impacts a substantial portion of the global population. In India alone, the estimated prevalence of prediabetes by 2023 is approximately 15.3 %. Hyperglycaemia, a hallmark of prediabetes, can promote vascular dysfunction by increasing ROS formation and upregulating chronic inflammatory markers. Additionally, oxidative stress contributes to insulin resistance and impaired beta cell function. Various risk factors of oxidative stress are associated with prediabetes development. This review focuses on ROS's role in prediabetes pathogenesis and its risk factors increasing the effect of oxidative stress. Various ROS scavengers were used as oxidative stress indicators, and ROS scavenging has a deleterious impact on disease progression. Lack of study has reported on role of oxidative stress in prediabetes development and this will be the first review covers pathogenesis and impact of oxidative stress biomarker in prediabetes. This review comprises managing the risk factors of oxidative stress would pave the way for the management of prediabetes progression to T2DM.

The functioning of the human immune system is highly dependent on the sex of the individual, which comes by virtue of sex chromosomes and hormonal differences. Epigenetic mechanisms such as X chromosome inactivation, mosaicism, skewing, and dimorphism in X chromosome genes and Y chromosome regulatory genes create a sex-based variance in the immune response between males and females. This leads to differential susceptibility in immune-related disorders like infections, autoimmunity, and malignancies. Various naturally available immunomodulators are also available which target immune pathways containing X chromosome genes.

Head and neck cancers (HNC) are extremely complex disease types and it is likely that chromosomal instability is involved in the genetic mechanisms of its genesis. However, there is little information regarding the background levels of chromosome instability in these patients. In this pilot study, we examined spontaneous chromosome instability in short-term lymphocyte cultures (72 hours) from 72 study subjects - 36 newly diagnosed HNC squamous cell carcinoma patients and 36 healthy ethnic controls. We estimated chromosome instability (CIN) using chromosomal aberration (CA) analysis and nuclear level anomalies using the Cytokinesis Block Micronucleus Cytome Assay (CBMN Cyt Assay). The proliferation rates in cultures of peripheral blood lymphocytes (PBL) were assessed by calculating the Cytokinesis Block Proliferation Index (CBPI). Our results showed a significantly higher mean level of spontaneous chromosome type aberrations (CSAs), chromatid type aberration (CTAs) dicentric chromosomes (DIC) and chromosome aneuploidy (CANEUP) in patients (CSAs, 0.0294±0.0038; CTAs, 0.0925±0.0060; DICs, 0.0213±0.0028; and CANEUPs, 0.0308±0.0035) compared to controls (CSAs, 0.0005±0.0003; CTAs, 0.0058±0.0015; DICs, 0.0005±0.0003; and CANEUPs, 0.0052±0.0013) where p<0.001. Similarly, spontaneous nuclear anomalies showed significantly higher mean level of micronuclei (MNi), nucleoplasmic bridges (NPBs) and nuclear buds (NBUDs) among cases (MNi, 0.01867±0.00108; NPBs, 0.01561±0.00234; NBUDs, 0.00658±0.00068) compared with controls (MNi, 0.00027±0.00009; NPBs, 0.00002±0.00002; NBUDs, 0.00011±0.00007).The evaluation of CBPI supported genomic instability in the peripheral blood lymphocytes showing a significantly lower proliferation rate in HNC patients (1.525±0.005552) compared to healthy subjects (1.686±0.009520 ) (p<0.0001). In conclusion, our preliminary results showed that visible spontaneous genomic instability and low rate proliferation in the cultured peripheral lymphocytes of solid tumors could be biomarkers to predict malignancy in early stages.

Prediabetes is characterized by elevated blood glucose levels that are higher than normal but below the threshold for diabetes mellitus. While AI models have been used for prediabetes prediction, most rely solely on standard clinical and biochemical markers. This study introduces a novel Pattern Neural Network (PNN) model that uniquely integrates total antioxidant scavenging potential with traditional risk factors, providing new insights into the role of oxidative stress in prediabetes risk stratification among Indian adults. A total of 199 individuals aged 18 to 60 years were recruited and classified based on HbA1c levels into Control ( n = 99) and Prediabetes ( n = 100) groups. Fourteen input features including age, gender, total antioxidant status, HbA1c, FBG, OGTT, TGL, HDL, LDL, VLDL, TC, WC, Hb, and BMI were used to train a PNN with 14 input nodes, 10 hidden nodes, and one output node. The dataset was randomly divided into training, validation, and testing subsets. Model performance was compared against SVM, KNN, and LR classifiers. Feature importance analysis was conducted to interpret the model’s clinical relevance. The PNN model achieved superior validation performance with an accuracy of 98.3%, outperforming SVM (96%), KNN (83%), and LR (71%). Notably, antioxidant scavenging potential and waist circumference emerged as the most influential predictors. The model’s output value of 0.8770 (threshold > 0.5) effectively identified individuals at increased risk of developing diabetes. By incorporating oxidative stress markers, this study provides the first AI model in an Indian cohort to link antioxidant status to prediabetes risk. The PNN model demonstrates excellent accuracy and interpretability, offering a clinically actionable tool for early disease detection and personalized intervention.

The association of Vitamin D and children with asthma is known and there are several individual studies on Vitamin D polymorphisms. However, systematic reviews on all vitamin D associated gene polymorphisms have not been done in children with asthma. To investigate the association of Vitamin D associated gene polymorphisms and asthma in children (0–18 years) by systematic review and meta-analytic approach. Our search included 20 full text articles of which 15 were case control studies and 5 used family based linkage disequilibrium method. Total of 2491cases and 3682 controls were included in case control studies, with mean age of 9.58 years and 10.16 years respectively. Quantitative and qualitative analysis were done. Quantitative analysis revealed significant association with protective effect of Apa1 polymorphism in allele (OR 0.81 (0.71,0.91) and homozygous major form (OR 0.83 (0.70,0.98) and Taq 1 minor allele in homozygous form (OR 0.73 (0.58,0.92) in children with asthma. However, the minor allele of Apa1(OR 1.21 (1.07,1.37), Bsm 1 in heterozygous (OR 1.35 (1.07,1.71) and homozygous minor form (OR 1.95 (1.59,2.39), major allele of Fok1(OR1.34 (1.17,1.52) and Taq1 (OR 1.22 (1.08,1.38) were found to be increasing the odds of asthma. Ethnic variations were noted in subgroup analysis. Qualitative analysis of the polymorphisms of the Vitamin D associated metabolic genes also showed significant associations. Our review shows significant associations with VDR polymorphisms - Apa1, Bsm1, Fok 1, Taq 1, polymorphisms of Vitamin D metabolic genes – CYP27A1, CYP 2R1, CYP 24A1, GC and genes related to Vitamin D response element (VDRE) in children with asthma. Conducting large studies involving various ethnic regions will strengthen our knowledge on the association and aid in targeted interventions for control of asthma in children.