Role of Oxidative Stress and Antioxidant Defense Biomarkers in Neurodegenerative Diseases.

Oxidative stress is caused by an imbalance in a redox system. It may involve either excessive production of reactive oxygen species or dysfunction of the antioxidant defense system. Unlike other viscera, the brain is especially highly susceptible to oxidative damage because of it requires a high oxygen level and contains an abundance of peroxida-tion-susceptible lipid cells. Oxidative stress is among the common etiological factors involved in neurodegeneration. To measure The extent of oxidative stress is measured with several indicators or biomarkers that are known to arise from oxidation of major biomolecules, including lipids, proteins, carbohydrates, and nucleic acids. In this review, we will discuss oxidative stress biomarkers associated with neurodegenerative diseases, for instance, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. We will also highlight the biomarkers of antioxidant defense mechanisms that are impaired in these diseases.

Stem Cell Therapy for Diabetes Mellitus: Recent Progress and Hurdles.

Diabetes mellitus (DM) is a devastating metabolic syndrome. Currently, parenteral exogenous insulin is the only therapy available around the world to treat type 1 DM. However, it does not tightly regulate blood glucose levels that ultimately lead to long-term complications. The development of pancreatic transplantation gives some hope in the radical cure of diabetes. A limited number of donors and host immune rejection are two major drawbacks associated with pancreatic transplantation. Stem cells are distinctive cells that can differentiate into any other type of specialized cells. Embryonic stem cells have been studied extensively and proved successful in producing beta cells. The numerous kinds of stem cells, including embryonic stem cells, induced pluripotent stem cells, and adult stem cells, prove to be among the notable candidates to treat DM. However, all stem cell therapies have their own limitations. This review article focuses on the progress and limitations in stem cell research to treat DM.

Therapeutic effect of atorvastatin on kidney functions and urinary excretion of Glimepiride in healthy adult human male subjects.

Glimepiride and atorvastatin in combination are commonly employed for treating the hyperglycemia and dyslipidemia, respectively, in patients of type 2 diabetes. The present study was designed to find out the influence of atorvastatin on urinary excretion and renal clearance of Glimepiride in healthy adult male volunteers. In each experimental subject, Glimepiride 2mg was given orally after an overnight fasting. Samples of blood and urine were taken at different specific time intervals. After a washout period of ten days, Glimepiride 2mg was co-administered with atorvastatin 20mg orally. Post-medication, blood and urine samples were collected following the same sampling schedule as for Glimepiride alone. The samples were analyzed for Glimepiride and creatinine concentration by HPLC-UV and Spectrophotometer, respectively. Mean (±SE) values for blood pH 7.445±0.05 and 7.382±0.05, urine pH 4.972±0.08 and 5.08±0.10, diuresis 0.0207±0.00 and 0.0237±0.00ml/min/kg, endogenous creatinine in plasma 9.048±0.33 and 8.613±0.024µg/ml, endogenous creatinine in urine 512.34±18.20 and 556.72±4.60µg/ml, Glimepiride plasma concentration 0.16069±0.00 and 0.3227±0.01µg/ml, Glimepiride urine concentration 1.5994±0.03 and 0.8665±0.04µg/ml, renal clearance of creatinine 1.224±0.09 and 1.550±0.09ml/min/kg, renal clearance of Glimepiride 0.2064±0.01 and 0.0641±0.00ml/min/kg and clearance ratio 0.1791±0.01 and 0.0414±0.00 were observed for Glimepiride alone and its concurrent administration with atorvastatin, respectively. Atorvastatin decreased the urinary excretion and renal clearance of Glimepiride due to which chances of hypoglycemia provokes and renal handling of Glimepiride involves back diffusion besides glomerular filtration and no influence of atorvastatin was seen on these mechanisms.