A novel drug based on capsaicin, the compound that gives chili peppers their spicy burn, caused long term weight loss and improved metabolic health in mice eating a high fat diet, in new studies from the University of Wyoming School of Pharmacy. The drug, Metabocin, was designed to slowly release capsaicin throughout the day so it can exert its anti-obesity effect without producing inflammation or adverse side effects.
Treatments using antibiotics should stop as soon as possible to prevent patients passing the tipping point of becoming resistant to their effects, new research has shown.
A team of researchers, led by Professor Robert Beardmore from the University of Exeter, has uncovered new evidence that suggests reducing the length of the antibiotic course reduces the risk of resistance.
For the study, the researchers examined how microbial communities - groups of microorganisms that share a common living space in the body - reacted to different antibiotic cycling patterns, which sees the medication restricted or increased, under laboratory conditions.
They found that changes both in the duration and dose of antibiotics used and in sugar levels (which mimics the variable sugar levels in human patients) could push these microbial communities beyond a "tipping point" - creating an irreversible shift to becoming drug resistant.
The researchers insist this new study demonstrates that resistant species can increase within the body even after an antibiotic is withdrawn - if a tipping point was unwittingly passed during treatment.
Professor Beardmore, a mathematical biosciences expert from the University of Exeter, said: "It's a sensible idea that when you take an antibiotic away, resistance goes away too, but we wondered what kinds of antibiotic treatments don't behave like that. After all, in some clinical studies, resistance didn't disappear when the antibiotic did."
Antibiotic resistance occurs when microbes develop the ability to defeat the drugs designed to kill them, and so they multiply unhindered. Antibiotics are the most effective treatment for a wide-range of microbial infections, including strep throat and pneumonia.
For decades, patients have been instructed to complete courses of antibiotics because the perceived wisdom had been that taking too few tablets would allow bacteria to mutate and become resistant. However, more recently it has been suggested that the longer microbes are exposed to antibiotics, the more likely it is that resistance will develop.
Little research has been conducted to show how the length of a course of antibiotics impacts resistance, which, despite differences in patients, for example in their blood sugar levels, are recommended to be the same for all.
In the new study, the researchers examined how microbial communities containing Candida albicans and Candida glabrata reacted to different doses of an antimicrobial when fed with sugar.
Both species are commonly found together in healthy people, but are also opportunistic pathogens which can cause infection.
The study showed that as the antimicrobial was introduced, the communities were reduced, while the removal of the treatment allowed them to flourish again.
Crucially, the researchers showed that if sugar levels dropped in the community, it could reach a "tipping point" whereby resistance would persist even after the antimicrobial had stopped being used.
The new research opens up the possibilities for further studies to better understand when the best time would be to stop antibiotic treatment, to prevent resistance occurring.
Co-author Professor Ivana Gudelj added: "Our body is a mother ship for microbial communities but we've still expected to understand drug resistance by studying microbial species one at a time, in the lab.
"We show this can be misleading because microbes have intricate relationships that the drugs make even more complicated, and yet our theories of antibiotic resistance have ignored this, until now. So that's the first surprise: even sugars can affect antibiotic resistance."
People with multiple sclerosis (MS) can find an abundance of conflicting advice suggesting that special diets - everything from avoiding processed foods to going low-carb - will ease their symptoms. But the evidence is scanty that dietary changes can improve fatigue or other MS symptoms.
A drug used to treat altitude sickness - as well as glaucoma, epilepsy, heart failure and seizures - may also offer significant gains for patients with a fast-growing brain tumor known as glioblastoma, according to a study.
McMaster University researchers have developed a new theory on Huntington's disease which is being welcomed for showing promise to open new avenues of drug development for the condition. Huntington's disease is caused by a mutation in the gene that makes the protein called huntingtin.
Cochrane Library shows that human papilloma virus (HPV) vaccines protect against cervical lesions in young women, particularly in those who are vaccinated between the ages of 15 and 26. It also summarizes findings on harms that have been assessed in randomized controlled trials.
New findings suggest that the molecule triggers a pathway that is normally used by the immune system to prevent excessive damage but may contribute to chronic white matter injury by completely blocking repair operations.
A drug combination aimed at preventing transmission of HIV from a pregnant woman to her fetus likely does not increase the risk for preterm birth and early infant death, according to a re-analysis of two studies funded by the National Institutes of Health. The research appears in the New England Journal of Medicine.
Transplanted livers change the profile of blood cells in the recipients, reducing the potential for organ rejection, Mayo Clinic research shows. The findings are published in Kidney International.
Researchers at LSTM's Alistair Reid Venom Research Unit are looking at treatment for snakebite in a completely different way and have shown that it is possible to treat the bite from one snake with antivenom produced from a completely different species that causes the same pathology in humans.
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