Aster clinical transplant nursing program

Published on Sep 11, 2017 by Nii in In the News

The three month certificate course(9 June 2017 to 9 sept 2017)in transplantation nursing concluded today. 30 nurses from four hospitals in three states attended. There was a two month online didactic program with live lectures from within India and abroad followed by a one month competency and skills assessment, as well as peer initiated teaching and shadowing senior nurses in icu. Lalita and Sumana from Mohan foundation conducted the soft skills and communication course.Mohan foundation conducted the grief counseling and communications skills course.

This is the first course of its kind in India it combines a unique hybrid format of online + immersion for short periods of intense training. Training was imparted by doctors and nursing tutors. Soft skills communication and grief counseling are integral skills to medicine today’s, and were part of the curriculum

Addressing the group Dr Nitish Shetty, CEO said that it is increasingly recognized that nurses also need subspecialty skills and training to meet the demands of quarter nary specialties such as transplant.

A fatty liver leads to a broken heart?

Published on Jun 15, 2016 by Nii in In the News

Strict Monitoring of Cardiovascular Disease Recommended When Managing Nonalcoholic Fatty Liver Disease

Cardiovascular disease (CVD) is primarily the cause of death of patients with nonalcoholic fatty liver disease (NAFLD). The extent to which NAFLD itself, rather than associated conditions such as diabetes, obesity, or dyslipidemia, is responsible for increased cardiovascular death has been a matter of debate. In a new study, investigators from the Pitié-Salpêtrière Hospital, Pierre and Marie Curie University conclude that NAFLD is an independent risk factor for atherosclerosis and therefore CVD. Their findings, published in the Journal of Hepatology, recommend strict monitoring of cardiovascular health and metabolic complications in patients with NAFLD.

Fatty liver is an increasingly common condition in patients with obesity, type 2 diabetes, dyslipidemia and hypertension. Evidence indicates that the fatty and inflamed liver expresses several pro-inflammatory and procoagulant factors, as well as genes involved in accelerated atherogenesis. This raises the possibility that the link between NAFLD and cardiovascular mortality might not simply be mediated by shared, underlying, common risk factors, but rather that fatty liver independently contributes to increasing this risk.

Close to 6000 patients were examined using carotid ultrasound with measurement of carotid intima-media thickness and carotid plaques. Using the Fatty Liver Index (FLI) a well-validated biomarker panel, researchers observed that steatosis (fatty liver) is associated with carotid intima-media thickness (C-IMT), a pre-atherosclerotic lesion that predicts cardiovascular events. C-IMT increased proportionally with FLI, and this association was independent of traditional cardio-metabolic risk factors.

The team concluded that in patients with metabolic syndrome at risk for cardiovascular events, NAFLD contributes to early atherosclerosis and its progression, independent of traditional cardiovascular risk factors.

“Regardless of the mechanisms involved, the clinical implications are of critical importance since patients at cardiovascular risk presenting with one or more metabolic syndrome characteristics are at even greater risk if they have steatosis. It was also found that patients with steatosis, but not overweight, not type 2 diabetic, or without arterial hypertension are at higher risk of developing these complications than individuals without steatosis. This indicates that NAFLD is a precursor of metabolic syndrome. It follows that the diagnosis of steatosis is extremely important and therefore a thorough cardiovascular and metabolic work-up and strict monitoring of CVD or metabolic complications are needed in the clinical management of NAFLD.

Researchers convert cirrhosis-causing cells to healthy liver cells

Published on Jun 15, 2016 by Nii in In the News

Advances in stem cell research have made it possible to convert patients’ skin cells into heart cells, kidney cells, liver cells and more in the lab dish, giving researchers hope that one day such cells could replace organ transplantation for patients with organ failure. But successfully grafting these cells into patients’ failing organs remains a major clinical challenge.

Now a team of researchers led by UC San Francisco scientists has demonstrated in mice that it is possible to generate healthy new liver cells within the organ itself, making engraftment unnecessary. What’s more, they did it by converting the very cells that drive liver disease, thereby reducing liver damage and improving liver function at the same time. The technique takes advantage of a viral gene delivery technology that has gone through early validation in patients for liver-directed gene therapies, suggesting it could be readily translated into a therapy for patients with liver disease, said Holger Willenbring, MD, PhD, a professor of surgery at UCSF and senior author of the new study, published in the journal Cell Stem Cell.

“Part of why this works is that the liver is a naturally regenerative organ, so it can deal with new cells very well. What we see is that the converted cells are not only functionally integrated in the liver tissue, but also divide and expand, leading to patches of new liver tissue,” said Willenbring, who is also associate director of the Liver Center at UCSF and a member of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research.

The new approach specifically targets liver fibrosis, the progressive scarring of the liver that is a primary driver of liver disease. Fibrosis develops when liver cells called hepatocytes can’t regenerate fast enough to keep up with damage caused by toxins such as alcohol or diseases such as hepatitis B, hepatitis C or fatty liver disease. Cells called myofibroblasts fill in gaps left by dying hepatocytes with scar-like fibrotic tissue. It’s a bit like patching a flat tire: at first the patches help maintain the liver’s structural integrity, but eventually a liver that is more patches than functional tissue starts to fail.

Fibrotic liver disease has a slow fuse, but leads to catastrophic failure: someone who contracts hepatitis C at age 25 may feel just fine for decades, then suddenly at age 50 start experiencing fatigue, nausea, bruising, and jaundice that indicate the onset of end-stage liver disease. The reason is that the liver can adapt as long as at least 20 percent of it is functional, but once it dips below that critical threshold, patients are often dead within two years.

The team showed in mice with liver disease that viruses packed with the cell fate-changing cocktail indeed infected myofibroblasts and converted them into functional hepatocytes. The number of new cells was relatively small – less than one percent of all hepatocytes in the treated mice – but this was sufficient to reduce fibrosis and improve liver function. The viral approach was also effective in converting human myofibroblasts in a dish into working hepatocytes, but more work is certainly needed to prepare this approach for use in human patients, the researchers say. In particular, the lab is working to package the treatment into a single virus, reducing potential side effects and streamlining clinical development. The team is also working to make the viruses more specific to myofibroblasts – in the current paper muscle cells and some cells of the immune system were also infected, though without converting them into liver cells or obviously impacting their function.