Thursday, 11 August 2016
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
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
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