ABSTRACT
Diabetes mellitus is a global health issue with numerous complications, and SGLT-2 inhibitors can slow kidney disease progression, reduce heart failure, and lower the risk of kidney failure and death in individuals with CKD. This study evaluated the impact of Sodium-glucose co-transporter 2 (SGLT2) inhibitors, specifically dapagliflozin and empagliflozin, on cardiovascular and renal health in Type 2 Diabetes Mellitus (T2DM) patients at Benghazi Diabetes Center (BDC). The study involved 600 T2DM patients initiating dapagliflozin or empagliflozin, and collected data from interviews, structured questionnaires, and electronic medical records. After three months of treatment, the analysis showed significant improvements in glycemic control, weight management, blood pressure, and lipid profiles, reduced albuminuria, and improved estimated glomerular filtration rate (eGFR) and ejection fraction (EF). However, drug- and sex-specific nuances were revealed. Dapagliflozin showed numerically greater improvements in BP, postprandial glucose, lipid parameters, plasma urea, and albuminuria, while empagliflozin demonstrated numerically greater reductions in weight, body mass index, fasting plasma glucose, and eGFR. Females showed greater reductions in PPG, weight, BMI, BP, and plasma urea, while males demonstrated more pronounced improvements in FPG, triglycerides, low-density lipoprotein cholesterol, albuminuria, and EF. Combined SGLT2 inhibitor use with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers did not show statistically significant differences in clinical parameters compared to SGLT2 inhibitor monotherapy. SGLT2 inhibitors show beneficial effects on cardiorenal and metabolic parameters in T2DM patients, with variations based on drug and sex, emphasizing personalized treatment plans and urging further research.

ABSTRACT
Migration is a fundamental demographic process with profound consequences for population health globally. Increasingly driven by economic inequality, conflict, environmental change, and social transformation, migration shapes the distribution of health risks and opportunities across populations. While migration can improve socioeconomic conditions, enhance access to services, and contribute to economic development, it also introduces complex vulnerabilities related to infectious diseases, non-communicable diseases, mental health, maternal and child health, and occupational hazards. This paper provides an expanded examination of the multifaceted relationship between migration and health, analyzing underlying determinants, health system responses, and the lived experiences of migrants across different contexts. Drawing on contemporary scholarship and international frameworks, this review explores the health implications of migration in low-, middle-, and high-income countries, emphasizing structural drivers, health inequities, and the role of policy in shaping outcomes. The findings demonstrate that migrant health outcomes are shaped by interconnected social, political, and economic factors and require multisectoral and rights-based approaches to ensure equitable access to healthcare and protection of vulnerable populations. Drawing on evidence from global studies and country-specific experiences, including Nigeria, the European Union, and the United States, the article highlights key pathways through which migration influences population health. It concludes with recommendations for policy, health systems strengthening, and future research directions.

ABSTRACT
The article discusses about the virulent bacterium Shigella, its clinical manifestations, the related epidemiology, treatment options that includes both preventive & curative approaches. It also discusses the supportive therapy. The public health dimension of the Shigella bacterium is also dealt with. The article discusses the role that homoeopathic therapeutics can play in the absence of any treatment options to deal with the chronic cases. Homoeopathy can be a supportive therapy that can reduce not only the morbidity but also the fatality of Shigella cases due to all the strains. Homoeopathy has repeatedly proved its efficacy in chronic bowel diseases since the last two and half centuries.

ABSTRACT
Persistent infection with high-risk human papillomavirus (HR-HPV) is the primary driver of cervical cancer; however, viral presence alone is insufficient to induce malignancy. The progression from initial infection to invasive carcinoma requires a coordinated series of alterations in both the viral genome and the host cell's regulatory machinery. This review focuses on three principal mechanisms by which HR-HPV bypasses host regulatory controls: epigenetic modifications, immune evasion, and endocrine signaling. Specifically, we describe how the viral oncoproteins E6 and E7 recruit host DNA methyltransferases—particularly DNMT1, DNMT3A, and DNMT3B—to silence tumor suppressor genes such as CCNA, hTERT, and E-cadherin via promoter hypermethylation. Beyond DNA methylation, HPV disrupts histone acetylation and methylation patterns through interactions with p300/CBP, the NuRD complex, and Polycomb group proteins, while simultaneously dysregulating non-coding RNAs and specific microRNAs to reinforce this transcriptionally silenced state. The review further details how HPV escapes immune clearance by driving a Th1-to-Th2 cytokine shift, downregulating MHC class I expression, and recruiting myeloid-derived suppressor cells and regulatory T cells to the cervical microenvironment. Additionally, we discuss the role of cofactors, focusing on the synergistic interaction between estradiol and HPV oncogenes; this interaction promotes local immunosuppression via estrogen receptor alpha signaling on stromal fibroblasts and infiltrating immune cells. We also examine the contribution of high parity as a key epidemiological risk factor. A comparative analysis of patient data across three distinct studies is presented to illustrate how demographic and reproductive variables correlate with cervical lesion severity in different populations. Ultimately, cervical carcinogenesis stems from multi-pathway interactions where viral oncogenes, epigenetic changes, immune escape, and hormonal factor