inflammation

The global menace of cancer requires supplementary treatments beyond standard medical approaches for effective medical intervention. The Ketogenic Diet (KD) composed of high fats combined with moderate proteins and low carbohydrates has become popular as a metabolic therapy for cancer. The anti-cancer mechanism of KD works through metabolic stress induction in cancer cells, reduced insulin and IGF-1 signaling pathways, improved mitochondrial function, inflammation, and immune regulation. Standard cancer treatments receive enhanced outcomes through KD synergistic action which simultaneously decreases treatment-related side effects. To achieve optimized treatment outcomes in cancer, ketogenic diet practitioners need to use personalized nutritional planning in combination with metabolic tracking and exogenous ketone supplements. It is essential to find solutions for diet adherence issues and nutrient deficiencies because they determine KD’s effectiveness as a cancer treatment. The fight against cancer needs sustained and multipronged clinical research and validation to establish the proper implementation of this method.

Methylenetetrahydrofolate Reductase (MTHFR) is an important enzyme of the folate cycle, which is required to convert 5,10-methyltetrahydrofolate into 5-methyltetrahydrofolate (5-methylTHHF). 5-methyl THF is a methyl group donor for several cellular methylation processes. It also donates methyl group for the conversion of homocysteine into methionine, the higher concentration of which is toxic. MTHFR gene C677T polymorphism is clinically important polymorphism and the variant MTHFR (A222V) enzyme has reduced activity, hence increasing the requirement for folic acid. Less conversion of folate to 5-methyl-THF due to C677T polymorphism results in a higher plasma concentration of homocysteine (hyperhomocysteinemia). Individuals having C677T polymorphism are susceptible to various diseases, including reproductive problems like male infertility, polycystic ovary syndrome, Recurrent Pregnancy Loss (RPL), Preeclampsia (PE), placental abruption, and adverse pregnancy outcomes. MTHFR C677T polymorphism mimics folate deficiency, and folate is required for DNA synthesis, repair, methylation, and proper chromosome segregation, and all these processes are important for foetal growth and normal development. Methylation and demethylation processes control the gene expression of about 45% of human genes. Impaired methylation influences the expression of genes involved in the regulation of hormones, spermatogenesis, and oogenesis. In males, oxidative stress damages sperm DNA decreases sperm motility, and may impair fertilization capability. In pregnant women, hyperhomocysteinemia increases oxidative stress and inflammation within the placenta, which causes damage to placental tissue, impairs its function, and disrupts foetal development. Further, hyperhomocysteinemia (HHcy) is embryotoxic and neurotoxic and is responsible for congenital anomalies in the foetus. This review supports the idea that MTHFR C677T polymorphism is associated with an increased risk for male infertility, PCOS, RPL, PE, and congenital anomalies. This review may provide a clue toward a better understanding of the correlation between the MTHFR C677T polymorphism and its detrimental effects on human reproductive health.

Cystoid Macular Oedema (CMO) is a condition characterized by fluid accumulation in the macular region of the retina, leading to the formation of cyst-like spaces. This edema often results in visual impairment and is associated with various ocular and systemic conditions, including surgery, inflammation, or medication use. The authors present a case where Cystoid Macular Oedema (CMO) occurred after commencing topical bimatoprost in a pseudophakic patient with primary open angle glaucoma. The macular oedema was treated effectively with a combination of non-steroidal and steroidal topical drops. This case report shows a possible correlation between bimatoprost and CMO, in a patient with no recent confounding risk factors known to contribute to CMO . The recommendation from this report is that all patients treated with topical bimatoprost drops should have a baseline macula OCT examination and a repeated OCT examination 8 weeks after initiation of treatment, to facilitate early detection of CMO.

The action of modern emergency care for patients with AP, on the one hand, requires a wait-and-see period, which is unacceptable in cases of rapidly progressing inflammation. On the other hand, it uses methods that do not take into account the features of the disease mechanisms. All this creates conditions for an excess of complications and treatment failures. The accumulated facts on this problem indicate the need to revise the principles of treatment. Consequently, the most important initial step in this direction seems to be the correction of professional views in accordance with the classical provisions of medical science.

Background: Monotherapy for liver dysfunction in diabetes is less effective. This study investigated the effect of combined linagliptin and metformin therapy on liver function in diabetic rats. Methods and materials: Sixty-four mature male (200-300 g) Wistar rats were used. Streptozotocin (35 mg/kgb.wt) was repeatedly injected intraperitoneally to induce diabetes. The rats were grouped into eight groups (n = 8). Group I: control; Group II: control + 10 mg/kgb.wt linagliptin; Group III: control + 200 mg/kgb.wt metformin; Group IV; control + 10 mg/kgb.wt linagliptin + 200 mg/kgb.wt metformin; Group V: diabetic; Group VI: diabetic + 10 mg/kgb.wt linagliptin; Group VII: diabetic + 200 mg/kgb.wt metformin; Group VIII: diabetic + 10 mg/kgb.wt linagliptin + 200 mg/kgb.wt metformin. The animals were sacrificed on the last day of the experiment, blood and liver samples were collected for biochemical assay. Results: Insulin, blood glucose, glycated hemoglobin, total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-cholesterol), liver function biomarkers, liver glucose metabolic enzymes, malondialdehyde and inflammatory markers increased (p < 0.05) significantly. High-density lipoprotein-cholesterol (HDL-cholesterol), liver antioxidant, glycogen, and glycogen synthase were reduced significantly in diabetic rats. Linagliptin and metformin administration single and combined reduced the insulin, blood glucose, glycated hemoglobin, total cholesterol, triglycerides, LDL-cholesterol, liver function biomarkers, liver glucose metabolic enzymes, malondialdehyde, and inflammatory markers, and increased the HDL-cholesterol, liver antioxidant, glycogen and glycogen synthase in diabetic rats.Conclusion: Linagliptin monotherapy alone efficiently controls hyperglycemia and remarkably improves liver functions. Combining linagliptin and metformin could be used as safe and effective therapy for liver dysfunction progression in diabetes.

Microplastics (MPs) pose a significant risk to human health, particularly through seafood consumption. Once ingested, MPs can spread from the digestive system to other organs via phagocytosis and endocytosis, leading to toxicological effects. Accumulation of MPs in tissues causes swelling, blockages, oxidative stress, and Cytotoxicity. Studies show MPs alter metabolism, disrupt immune function, and contribute to autoimmune diseases. Chronic exposure has been linked to neurotoxicity, vascular inflammation, and increased cancer risk due to DNA damage. MPs can cross biological barriers, including the placenta, affecting fetal development. Additionally, they serve as vectors for pollutants and bacteria, further complicating health risks. MPs in the bloodstream can trigger inflammatory responses, endothelial adhesion, and red blood cell coagulation, leading to cardiovascular complications. In vitro studies indicate MPs impair renal function and cause long-term inflammation in distal tissues. Moreover, oxidative stress caused by MPs plays a critical role in carcinogenicity. Despite growing evidence of adverse health effects, further research is necessary to understand the full impact of MPs’ exposure on human health and develop effective mitigation strategies.