Monday, 18 February 2019

When 8-year olds look like 80: Researchers describe mechanism behind premature aging disease

Progeria, a premature aging disease, is the research focus of Roland Foisner's team at the Max F. Perutz Laboratories of the University of Vienna and the Medical University of Vienna. Children suffering from progeria die at an average age of 14 to 15 years, often from heart attacks and strokes. So far, there is no cure for the disease, and though researchers identified the abnormal protein behind the disease -- progerin -- the exact way in which it causes the accelerated aging remains elusive. In their latest publication in Genes & Development, Roland Foisner and his group describe a yet unknown mechanism behind progeria that may provide new approaches for therapy.
Children suffering from progeria are born normal, but from age one to two their disease starts to resemble premature aging in some aspects. So by the time they reach their teens they have typical age-related conditions such as brittle bones, stiff joints and severe cardiovascular disease. In the end many die from strokes and heart attacks before reaching their twenties. Presently, there is no cure for progeria. Patients can be treated with drugs called FTIs (farnesyltransferase inhibitors), which were initially developed to treat cancer. These drugs improve some aspects of the disease, such as bone structure, arterial stiffness, and increase estimated lifespan by at least 1.6 years.
Progerin: the protein behind the aging disease progeria
Progerin, a protein present in very high concentration in progeria cells, is known to be responsible for many of the characteristics of the disease. It is a mutant version of lamin A, a protein crucial for the stability of the nucleus and involved in many essential nuclear functions. How progerin exerts its effects exactly is the reseach interest of Roland Foisner and his team at the Max F. Perutz Laboratories -- a joint venture of the University of Vienna and the Medical University of Vienna. They investigate the molecular functions of nuclear lamins and their mutated forms such as progerin and associated diseases.
"A few years ago, we and others found that progeria cells have much less LAP2α than normal cells. LAP2α is a protein that interacts with lamin A to regulate cell proliferation, the process that produces new cells. Interestingly, LAP2α levels also decrease during normal aging," explains Roland Foisner, Deputy Director of the Department of Medical Biochemistry of the Medical University of Vienna. Supported by an Innovator Award from The Progeria Research Foundation, senior postdoc Thomas Dechat and PhD student Sandra Vidak in collaboration with Tom Misteli from the NIH National Cancer Institute (USA) developed a cell line that allows studying the molecular mechanisms behind progeria in the lab.

Source: Medical University of Vienna

Welcome to the 2nd World Congress on Infectious and Rare Diseases

Theme : Treating Diseases with Advanced Techniques

We cordially invite you all the participants from all over the world to attend "2nd World Congress on Infectious and Rare Diseases" Scheduled During September 09-10, 2019 in Bangkok, Thailand. Which includes prompt Keynote Presentations, Special Sessions, Workshops, Symposiums, Oral talks, Poster Presentations and Exhibitions.
This medical conference will give a magnificent forum for you to update your insight and investigate the advancements in Infectious and Rare Diseases.

Wednesday, 13 February 2019

Fighting deadly drug resistant bacteria in intestines with new antibiotic

A new antibiotic developed by a Flinders University researcher is being heralded as a breakthrough in the war against a drug resistant superbug.
Bacteria are winning the fight against antibiotics as they evolve to fight off traditional treatments, threatening decades of advancements in modern medicine, with predictions they will kill over 10 million people by 2050.
The scientific development of new, effective and safe antibiotics is crucial in addressing the ever-growing threat posed by drug resistant bacteria around the world.
Clostridium difficile infection (CDI) is a potentially deadly infection in the large intestine most common in people who need to take antibiotics for a long period of time, particularly in Australia's ageing population.
Dr Ramiz Boulos, adjunct research associate at Flinders University and CEO of Boulos & Cooper Pharmaceuticsals, says the fact CDI is becoming resistant to traditional antibiotics is alarming and highlights the need to develop more effective treatments.
"Cases of CDI disease are rising and the strains are becoming more lethal. If there is an imbalance in your intestines it can begin to grow and release toxins that attack the lining of the intestines which leads to symptoms," says Dr Boulos.
Over the past ten years, various strains of C. difficile have emerged, and are associated with outbreaks of severe infections worldwide. One particular strain is easily transmitted between people and has been responsible for large outbreaks in hospitals in the United States and Europe.
"It's concerning when you consider CDI is one of the most common infections acquired during hospital visits in the Western hemisphere, and the most likely cause of diarrhea for patients and staff in hospitals."
But when doses of a new antibiotic called Ramizol were given to hamsters infected with a lethal dose of the bacteria, a significant proportion of hamsters survived the infection.
In a recent safety study in rats evaluating the effect of repeated exposure of the antibiotic, no rats experienced serious side effects or changes in weight.
"Our research indicates Ramizol is an extremely well-tolerated antibiotic in rats, with good microbiology and antioxidant properties. It also has high chemical stability and is scalable because of the low cost of manufacturing, which could make it a viable treatment option."
Forty-eight rats were given a high dose of a new class of antibiotic for 14 days to assess its safety.
Source: Flinders University