Thursday, 11 August 2016

By
Mrs. K. Pavithra
Assistant Professor

New Insight into How Diabetes Leads to Blindness
Diabetic retinopathy is the leading cause of vision impairment and blindness. Retinopathy is caused by high blood glucose levels that lead to the abnormal development of tiny blood vessels in the eye. A number of landmark studies have demonstrated that intensive glycemic control reduces the development and progression of diabetic retinopathy. However, exactly how high blood glucose levels disrupt blood vessel development in the eye is not completely understood.
By
V. V. Sathibabu Uddandrao
JRF-DST & Ph. D Research Scholar 
Department of Biochemistry
Microvascular outcomes with empagliflozin in patients with type 2 diabetes
-Kathryn A Martin et al., 2016

There are few trials evaluating microvascular outcomes in patients taking sodium-glucose co-transporter 2 (SGLT2) inhibitors. Microvascular disease was a prespecified secondary outcome in a recent trial designed specifically to evaluate cardiovascular morbidity and mortality in patients with type 2 diabetes and established cardiovascular disease (CVD). In this trial, 7028 patients with type 2 diabetes and established CVD were randomly assigned to empagliflozin or placebo once daily; the majority of patients were also taking metformin, antihypertensives, and lipid-lowering agents. Incident or worsening nephropathy occurred in 12.7 and 18.8 percent of patients in the empagliflozin and placebo groups, respectively. The reduction in nephropathy drove the improved composite microvascular endpoint (the initiation of retinal photocoagulation, vitreous hemorrhage, diabetes-related blindness, or incident or worsening nephropathy) for empagliflozin. The mechanism behind the reduction in incident or worsening nephropathy with empagliflozin is likely multifactorial, but is thought to be largely related to a direct renovascular effect of empagliflozin. Whether other SGLT2 inhibitors have similar renal effects is unknown. There have been reports of acute kidney injury, some requiring hospitalization and dialysis, in patients taking canagliflozin or dapagliflozin. 
By 
Dr. G. Saravanan
Associate Professor & Head
Department of Biochemistry

Wednesday, 10 August 2016




Aging and DNA damage by Oxidants
The human body is in a constant battle to prevent aging. Many of the pathological changes in diseases as well as the aging process itself, show a link to these reactive and potentially destructive free radicals. The mechanism of aging attributes to DNA or the accumulation of cellular mitochondria. As the body ages, the cells struggle to recycle the mitochondria also called the “powerhouse of the cell. Mitophagy is the process by which the damaged mitochondria are removed. This process becomes less efficient and the cells end up cluttered with old and poorly functioning mitochondria. The accumulation of dysfunctional mitochondria affects the health of many tissues and muscles and also plays a role in aging. The increasing age-related oxidative stress seems to be a consequence of the imbalance between the free radical production and antioxidant effect. Oxidative modifications have been shown to occur in of DNA, protein, and lipid molecules. Elevated levels of both oxidant-damaged DNA and protein have been found in aged organisms.


By
Dr. A. Praveena
Assistant Professor
Diabetes mellitus Complication
By
V. V. Sathibabu Uddandrao
JRF-DST
Diabetes Mellitus types
By
V. V. Sathibabu Uddandrao
JRF-DST

Tuesday, 9 August 2016

Cancer treatments based on laser irridation of tiny nanoparticles that are injected directly into the cancer tumor are working and can destroy the cancer from within. Researchers from the Niels Bohr Institute and the Faculty of Health Sciences at the University of Copenhagen have developed a method that kills cancer cells using nanoparticles and lasers. The treatment has been tested on mice and it has been demonstrated that the cancer tumors are considerably damaged. The results are published in the scientific journal,Scientific Reports.
By
Dr. A. Praveena
Assistant Professor