Background/Aim: There has been a progressive rise in the incidence and prevalence of End Stage Renal Disease (ESRD). It has also been observed that the most important reasons for a rapid increase in Chronic Kidney Disease (CKD) patients are the rapidly increasing worldwide incidence of diabetes and hypertension. The present study evaluates the effect of diabetes, hypertension, and comorbid state of hypertension and diabetes (hypertensive-diabetic) on renal function using serum creatinine and urea as markers. Method: A total number of 120 persons were recruited for the research; 30 controls, 30 hypertensive, 30 diabetic, and 30 hypertensive-diabetic persons. Of the 30 control persons, 18 were females and 12 were males; of the 30 hypertensive subjects, 17 were females and 13 were males; of the 30 diabetics subjects, 20 were females and 10 were males, whereas of the 30 hypertensive-diabetic subjects, 21 were females and 9 were males. In total, there were seventy-six (76) females and 44 males. The respondents were pulled from Central Hospital (Auchi) Diabetic and General Clinic and Auchi Polytechnic Cottage Hospital. Verbal consent was sort and questionnaires were used to extract information regarding biodata and patients’ history of diabetes and hypertension. Height and weight were measured, and blood pressure was determined taken. Blood samples were collected into fluoride oxalate and lithium heparin bottle for the assessment of FBS and (serum urea and creatinine) respectively. Results: The mean (±SD) serum creatinine was higher in the hypertensive-diabetic group (2.08 ± 1.06) and declined as follows: diabetic group (1.75 ± 1.01), hypertensive group (1.34 ± 0.96) and control group (0.70 ± 0.14). The mean (±SD) serum urea was also found to be higher in the hypertensive-diabetic group (17.5 ± 9.06) and declined as follows: diabetic group (14.5 ± 6.13), hypertensive group (12.7 ± 6.23) and control group (7.18 ± 5.06). There was a positive correlation between serum creatinine and fasting blood sugar The study also established a positive correlation between serum creatinine and blood pressure but not between serum urea and blood pressure with r values of 0.31 and 0.16 respectively. Conclusion: Good control of blood glucose and blood pressure levels reduces the likelihood of the development of renal impairment which is usually associated with both diabetes and hypertension. Co-morbidity of diabetes and hypertension poses a higher risk of developing renal disease than individual problems of diabetes and hypertension. Serum creatinine and serum urea are important biomarkers for renal impairment hence the two should be monitored on a regular basis for diabetic and hypertensive patients and much more frequently for hypertensive-diabetic patients.

Kidney transplantation is the therapy of choice for patients with end-stage kidney disease (ESKD). Nevertheless, the main limitation for long-term graft survival is immune-mediated rejection. Some authors have proposed that differences in immune effector mechanisms are influenced by underlying molecular mechanisms; thereby, the identification of differentially expressed genes in acute or chronic rejection in non-invasive samples such as urine may be essential for the identification of potential biomarkers and biological processes associated with allograft outcomes. Our aim was to explore differences in gene expression and functional categories associated with acute and chronic kidney rejection in blood, biopsy, and urine of kidney transplant patients using RNA-Seq. RNA was isolated and sequenced implementing standard protocols. Analyses were addressed to identify differentially expressed genes (DEGs) and Functional Categories of Gene Ontology comparing between samples. Then we focused on immune genes and pathways to identify their association with the allograft. We identified a significant transcriptional similarity between biopsy and urine, in comparison with blood in acute and chronic rejection. Functional analyses suggested an enrichment of immune processes such as antigen processing and presentation, and regulation of B cell receptor signaling pathway in blood of acute and chronic rejection, respectively. Additionally, we observed an increase in expression of chemokines in biopsy and urine of both outcomes along with an increase in chemokine receptors in blood. Our findings suggest that urine is suitable for identifying potential biomarkers and biological processes related to renal allograft rejection, as it shares a significant number of regulated genes with biopsy.

With the increase in incidence and prevalence of myeloid neoplasms in India, it has become a necessity to understand its molecular mechanisms, acquisition of genomic alterations, and understand its primary and secondary resistance pathways which ultimately impact the decision of therapeutics. The objective of this review is to investigate the molecular aspects of this disease type and identify the biomarkers that help with diagnosis, risk assessment, prognosis, and selecting the best line of treatment for a specific myeloid neoplasm. Advancements and innovations in molecular technologies from simplest Real-Time PCR to high throughput next-generation sequencing have played a vital role in screening the most common mutations and fusions to the novel and rare. Molecular technologies have helped to enumerate the genomic landscape of myeloid malignancies. The understanding of both- the mechanisms and the technology is a strong combination as it has helped revolutionize precision oncology and helped in giving better therapeutic choices with better clinical outcomes. The importance of cellular morphology, clinical symptoms, and molecular pathology in assessing the risk of myeloid malignancies is emphasized and summarized in the review. The review concludes that understanding molecular pathogenesis can be improved by using clinical-pathological-molecular strategies for diagnosis and therapy decision-making.

Neurologic diseases are recognized to have multifactorial origins well beyond mere genetic predisposition. Nutritional burdens have been identified to contribute to neurodegeneration. Healthy diets are becoming increasingly appreciated to potentially play key roles in both the developing and developed world of reducing incidences of neurologic diseases, while unhealthy diets are acknowledged to be contributing to their rise.

Sepsis, a life-threatening condition triggered by infection, poses a significant healthcare challenge with high mortality rates. The interplay between genetics and the immune response in sepsis, particularly in surgical and trauma patients, is complex and critical. Genetic polymorphisms, particularly in cytokine genes like TNF-α, IL-6, and IL-8, have been extensively studied for their influence on sepsis susceptibility, severity, and outcomes. Polymorphisms can alter gene expression and cytokine production, leading to variations in immune responses. Studies have also explored polymorphisms concerning sepsis in genes encoding CD86, TLR4, and SIRT6. This review highlights the association between genetic polymorphisms and inflammatory responses, focusing on their impact on sepsis outcomes in surgical and trauma patients. Genetic variations play a significant role in sepsis risk, severity, and prognosis, with potential implications for personalized therapeutic strategies. Biomarkers such as cytokine gene polymorphisms may aid in predicting sepsis risk and guiding treatment decisions. Complementary therapies like acupuncture and novel biomarkers like microvesicles carrying mitochondrial content provide additional avenues for personalized sepsis management. Furthermore, multiomics approaches offer promise in predicting postoperative outcomes in surgical patients. Understanding the genetic basis of sepsis is essential for improving prevention, diagnosis, and treatment, ultimately leading to better clinical outcomes. Combining genomics, bioinformatics, and clinical expertise, precision medicine can revolutionize sepsis management by tailoring interventions to individual genetic profiles, thus enhancing patient care and outcomes.

Background: Effective medication to manage diabetes mellitus-related organ complications with minimal adverse drug toxicity is still in pursuit by scientists worldwide. This study investigated the cardio-protective of Rida herbal bitter (RHB) in a high-fat diet/streptozotocin (STZ)-induced diabetic rats.Methods: Thirty-two matured male Wistar rats (250 ± 20g) were used. The animals were fed with high-fat diet (HFD) for 6 weeks before diabetes induction. A single dose of (35 mg/kgb.wt) freshly prepared STZ was injected intraperitoneally to induce diabetes. The animals were allocated into four groups, 8rats/group. Group I: control; Group II: HFD/STZ-induced diabetic rats; Groups III & IV: HFD/STZ-induced diabetic rats treated with 0.3 ml RHB & 200 mg/kgb.wt metformin respectively. At the end of the experiment, the animals were sacrificed, blood was sample collected via cardiac puncture and the heart was excised and homogenized. The blood samples and cardiac homogenates tissue were centrifuged to retrieve clear supernatant plasma for biochemical assay.Results: Diabetic rats exhibited significant (p < 0.05) elevated blood glucose, insulin, glycated hemoglobin (HbA1c), cardiac biomarkers, lipid profile, malondialdehyde (MDA), pro-inflammatory cytokines, food, and water intake levels with a reduction in body weight, cardiac antioxidant activity, and total protein. RHB administration significantly (p < 0.05) diminished the blood glucose, insulin, HbA1c, cardiac biomarkers, MDA, pro-inflammatory cytokines, lipid profile, food, and water intake, and improved the body weight cardiac antioxidant activity, and total protein.Conclusion: Rida herbal bitter possesses a cardio-protective effect from this study and could be a better alternative medication for managing diabetes and its related cardiovascular complications.