Researchers found that cocoa, the basic ingredient in chocolate and one of the most flavanol-rich foods, can actually prevent people from gaining excess weight and lower blood sugar levels.
According to sources, the scientists found that one particular type of antioxidant in cocoa called oligomeric procyanidins, when added to the food fed to laboratory mice, made a big difference in keeping the mice’s weight down and also improved their glucose tolerance level which could potentially help prevent type-2 diabetes.
Researchers reportedly also stated that Oligomeric procyanidins possess the greatest antiobesity and antidiabetic bioactivities of the flavanols in cocoa.
Previous studies have also linked chocolate to health benefits such as improved thinking, decreased appetite and lower blood pressure. The study is published in American Chemical Society’s Journal of Agricultural & Food Chemistry.
A latest research paper shows a diet low in nutrients might help increase the lifespan of humans.
The research conducted on laboratory animals argues that dietary restrictions can result in higher rates of cellular recycling and repair mechanisms in the body. But, according to them, this effect evolved to help organisms during famines.
The authors explain that animals need less food for survival as the stored nutrients in the cells can be recycled and reused.
“This is the most intriguing aspect, from a human health stand point. Although extended lifespan may simply be a side effect of dietary restriction, a better understanding of these cellular recycling mechanisms that drive the effect may hold the promise of longer, healthier lives for humans,” said lead study author, Dr Margo Adler, an evolutionary biologist at UNSW Australia in a press release.
“This effect has been demonstrated in laboratories around the world, in species ranging from yeast to flies to mice. There is also some evidence that it occurs in primates,” Adler said
“But we think that lifespan extension from dietary restriction is more likely to be a laboratory artifact,” said Adler. She further explained that the most commonly believed theory is that this effect evolved to enhance the survival chances during times of famine.
The authors explained why no extension in lifespan is seen in the wild. This is because restricted diets lower the ability of the immune system to fight diseases and reduce the muscle strength necessary to defend against predators.
“Unlike in the benign conditions of the lab, most animals in the wild are killed young by parasites or predators,” Adler explained
“Since dietary restriction appears to extend lifespan in the lab by reducing old-age diseases, it is unlikely to have the same effect on wild animals, which generally don’t live long enough to be affected by cancer and other late-life pathologies,” she added.
The paper is published in the journal ‘BioEssays.’
Around 600 million people worldwide have some kind of kidney ailment and chronic kidney diseases are predicted to increase by 17 per cent over the next decade if not detected early, said a nephrologist in Mumbai on Thursday.
Speaking on the occasion of World Kidney Day, Vivekanand Jha, Executive Director, George Institute for Global Health, India said chronic kidney diseases are considered to be a global health problem but many cases go undiagnosed as people ignore the symptoms of the disease in the early stages.
“In kidney diseases if detected early and treated properly, the deterioration in kidney functioning can be slowed or even stopped,” Jha said.
“Though it is an undeniable fact that chronic kidney disease prevalence rises with age and exceeds 40-50 per cent amongst elders, people should visit doctors at least twice a month for a check up,” said Jha, who is also the secretary of the Indian Society of Nephrology.
“Early detection and prevention will lead not only to improved outcomes, better quality of life, but huge cost-savings on treatment,” said Jha.
Early stage kidney disease is not being identified and diagnosed as early and often as is necessary. Patients are frequently told not to worry until kidney damage has progressed to near failure. Furthermore, patients do not have the necessary education or resources to manage their own risk factors and lifestyle to prevent initial kidney damage and progression of the disease.
Primary care practitioners will know which tests to order and how to recognise early-stage kidney disease, which will increase the total number of diagnoses of kidney disease. In addition, primary care practitioners have the knowledge and tools to treat early-stage kidney disease in order to slow its progression, and refer their patients to nephrologists when they need more specialised care.
WASHINGTON: In a breakthrough, scientists have discovered a new class of antibiotics to fight deadly bacteria such as methicillin-resistant Staphylococcus aureus and other drug-resistant bacteria that threaten public health.
The new class, called oxadiazoles, was discovered by University of Notre Dame researchers led by Mayland Chang and Shahriar Mobashery in silico (by computer) screening and has shown promise in the treatment of MRSA in mouse models of infection.
Researchers who screened 1.2 million compounds found that the oxadiazole inhibits a penicillin-binding protein, PBP2a, and the biosynthesis of the cell wall that enables MRSA to resist other drugs.
The oxadiazoles are also effective when taken orally. This is an important feature as there is only one marketed antibiotic for MRSA that can be taken orally, researchers said.
MRSA has become a global public-health problem since the 1960s because of its resistance to antibiotics.
In the US alone, 278,000 people are hospitalised and 19,000 die each year from infections caused by MRSA, said researchers.
Only three drugs currently are effective treatments, and resistance to each of those drugs already exists.
The researchers have been seeking a solution to MRSA for years.
“Professor Mobashery has been working on the mechanisms of resistance in MRSA for a very long time,” Chang said.
“As we understand what the mechanisms are, we can devise strategies to develop compounds against MRSA,” said Chang.
“Mayland Chang and Shahriar Mobashery’s discovery of a class of compounds that combat drug resistant bacteria such as MRSA could save thousands of lives around the world. We are grateful for their leadership and persistence in fighting drug resistance,” said Greg Crawford, dean of the College of Science at the University of Notre Dame.
The research is published in the Journal of the American Chemical Society.
WASHINGTON: Scientists have discovered how the immune system makes a powerful antibody that blocks HIV infection of cells by targeting a key site, paving way for an effective vaccine for the deadly virus.
Researchers believe that if a vaccine could elicit potent antibodies to a specific conserved site in the V1V2 region of the virus, one of a handful of sites that remains constant on the fast-mutating virus, then the vaccine could protect people from HIV infection.
Analyses of the results of a clinical trial of the only experimental HIV vaccine to date to have modest success in people suggest that antibodies to sites within V1V2 were protective.
The new findings point the way towards a potentially more effective vaccine that would generate V1V2-directed HIV neutralising antibodies, researchers said.
The study led by the National Institute of Allergy and Infectious Diseases ( NIAID) scientists began by identifying an HIV-infected volunteer who naturally developed V1V2-directed HIV neutralising antibodies, named CAP256-VRC26, after several months of infection.
Using techniques similar to those employed in an earlier study of HIV-antibody co-evolution, the researchers analysed blood samples donated by the volunteer between 15 weeks and 4 years after becoming infected.
This enabled the scientists to determine the genetic make-up of the original form of the antibody; to identify and define the structures of a number of the intermediate forms taken as the antibody mutated towards its fullest breadth and potency.
It also allowed them to describe the interplay between virus and antibody that fostered the maturation of CAP256-VRC26 to its final, most powerful HIV-fighting form.
The study showed that after relatively few mutations, even the early intermediates of CAP256-VRC26 can neutralise a significant proportion of known HIV strains.
This improves the chances that a V1V2-directed HIV vaccine developed based on the new findings would be effective, according to scientists, who have begun work on a set of vaccine components designed to elicit V1V2 neutralising antibodies and guide their maturation.
NEW YORK: Facial recognition, fingerprints and iris scans are passe – the latest biometric identification method on the block is, hold your breath, body odour!
Researchers at Spain’s Universidad Politecnica de Madrid, in collaboration with tech firm IIia Sistemas SL, are developing a system that can verify people by their scent signatures.
Recognisable body odour patterns remain constant enough over time to allow people to be identified with an accuracy rate of 85 percent.
Researchers believe this paves the way for creating less aggressive ways to ID people than the intrusive measures currently being used, according to a press release by the university.
While iris and fingerprint scan may have a higher accuracy rate, the researchers contend these techniques are commonly associated with criminal records, perhaps making people reluctant to participate with the process. And facial recognition has a high error rate.
Therefore, the release said, the development of scent sensors that could identify a person as they walk through a system stall could provide less invasive solutions with a relatively high accuracy rate.
Researchers believe such technology could be used in airports, border checkpoints or anyplace where photo identification is required.
Security agents may have reputations for being gruff grouches who love nothing more than to nose through your bags, but their rotten tempers might be because of all the body odour they’re forced to smell, day in, day out.
At least with a scent-detecting security system, someone else could sniff out the bad guys, the release added.
Scientists say two of the deadliest pandemics in history were caused by strains of the same plague and warn that new versions of the bacteria could spark future outbreaks.
Researchers found tiny bits of DNA in the teeth of two German victims killed by the Justinian plague about 1,500 years ago. With those fragments, they reconstructed the genome of the oldest bacteria known.
They concluded the Justinian plague was caused by a strain of Yersinia pestis, the same pathogen responsible for the Black Death that struck medieval Europe. The study was published online Tuesday in the journal, Lancet Infectious Diseases.
The two plagues packed quite a punch. The Justinian Plague is thought to have wiped out half the globe as it spread across Asia, North Africa, the Middle East and Europe. And the Black Death killed about 50 million Europeans in just four years during the 14th century.
“What this shows is that the plague jumped into humans on several different occasions and has gone on a rampage,” said Tom Gilbert, a professor at the Natural History Museum of Denmark who wrote an accompanying commentary. “That shows the jump is not that difficult to make and wasn’t a wild fluke.”
The plague is usually spread to humans by rodents whose fleas carry the bacteria.
“Humans are infringing on rodents’ territory, so it’s only a matter of time before we get more exposure to them,” Gilbert said.
Still, he and other experts doubted a modern plague epidemic would be as devastating.
“Plague is something that will continue to happen but modern-day antibiotics should be able to stop it,” said Hendrik Poinar, director of the Ancient DNA Centre at McMaster University in Canada, who led the new research. He said about 200 rodent species carry the plague and could potentially infect other animals or humans.
Poinar warned that if the plague transforms into an airborne version _ which can happen if the bacteria reaches the lungs and its droplets are spread by coughing _ it would be much harder to snuff out. That type of plague can kill people within 24 hours of being infected.
Poinar said scientists need to sharpen their surveillance of plague in rodent populations to try averting future human infections.
“If we happen to see a massive die-off of rodents somewhere with (the plague), then it would become alarming,” he said.
There are several thousand human cases of plague every year, most often in central and Eastern Europe, Africa, Asia and parts of the Americas.
Scientists have discovered a mechanism that helps HIV evade antibodies and stabilise key proteins, a finding that could pave way for more effective vaccine for the deadly virus.
National Institutes of Health (NIH) scientists found the mechanism involved in stabilising key HIV proteins and thereby concealing sites where some of the most powerful HIV neutralising antibodies bind.
Numerous spikes jut out of the surface of HIV, each containing a set of three identical, bulb-shaped proteins called gp120 that can be closed together or spread apart like the petals of a flower, researchers said.
Some of the most important sites targeted by HIV neutralising antibodies are hidden when the three gp120s, or the trimer, are closed, and the gp120 trimer remains closed until the virus binds to a cell, they said.
The researchers discovered that certain amino acids located on the gp120 protein undergo a process that stabilises the trimer in its closed position.
In this process, called sulfation, the amino acids acquire a sulfur atom surrounded by four oxygen atoms.
By either blocking or increasing sulfation of these amino acids, the researchers changed the sensitivity of the virus to different neutralising antibodies, indicating that the trimer was being either opened or closed.
The scientists suggest that if the synthesised gp120 widely used in HIV research were fully sulfated during manufacture, the resulting product would adopt a more true-to-life structure and more closely mirror the way the immune system sees unbound HIV.
This might help generate a more effective HIV vaccine, NIH researchers said.
They added that full sulfation of gp120 may enable scientists to crystallise the molecule more readily, which also could advance HIV vaccine design.
Vitamin D had been gaining a reputation as a ”wonder supplement.” Studies have suggested it can help bone and heart health, ease mild depression, and lower the risk of cancer. Others have suggested it might help people with fibromyalgia, multiple sclerosis, and other chronic diseases.
Now comes a different finding. Researchers who looked at dozens of studies say that vitamin D supplements do not lower the risks of heart attacks, strokes, cancer, or fractures by more than 15% in generally healthy people. This was true whether or not the supplements included calcium.
Bottom line: For most healthy adults, vitamin D supplements are not worth it, the researchers say in The Lancet Diabetes & Endocrinology.
Not everyone agrees, and the debate is far from done. Here, two experts address the most common questions about vitamin D supplements.
Are vitamin D supplements losing their luster?
“I believe so,” says Doug Campos-Outcalt, MD, of the University of Arizona College of Medicine, Phoenix. He recently wrote a review of vitamin D for The Journal of Family Practice.
Evidence shows that vitamin D helps bone health, he says. But early studies that show vitamin D may help in other areas, such as heart health and cancer prevention, are not convincing.
“Information on the health benefits of vitamin D is difficult to sort out,” he writes in the review. He cites a report from the Institute of Medicine, an independent organization that provides health advice. The institute looked at studies of vitamin D to protect against cancer, heart disease, diabetes, and autoimmune diseases such as lupus. Except for bone health, it found no evidence that vitamin D helped with any other diseases.
Robert R. Recker, MD, director of osteoporosis research at Creighton University School of Medicine in Nebraska, disagrees. He cites research finding vitamin D lowers the risks of colon, breast, and other cancers, and improves how the immune system works.
On the other hand, other experts say low vitamin D levels may be a result of illness, not the cause.
What do we know for sure about vitamin D?
What it does: Experts agree on the basics. Vitamin D helps the body absorb calcium, and that is good for bone health. Vitamin D also helps reduce inflammation in our cells. Inflammation can trigger disease.
What are the main areas of disagreement about Vitamin D?
How much is needed: At the center of the debate is how much vitamin D is enough. “We need more vitamin D than what we are getting [from diet and sun exposure],” Recker says. “What is not agreed upon is how much more.”
The Institute of Medicine recommends that most Americans need no more than 600 international units (IU) of vitamin D a day. People 71 and older may need 800 IU, it says. This level is enough for bone health, it says.
Vitamin D is found in some foods, including fatty fish like salmon and tuna, beef liver, fortified dairy products, cheese, and egg yolks. Except for those, getting enough vitamin D from your diet isn’t easy. As examples, a 3-ounce serving of salmon provides 447 IU, and 3 ounces of tuna fish offer 154 IU.
Meanwhile, our skin makes vitamin D when exposed to natural sunlight. This helps vitamin D levels in our blood. But Recker says only people who live at the equator get a large amount of D from sunlight.
Testing: Experts disagree on whether healthy people need routine testing to detect low vitamin D blood levels.
How much is enough: Experts also disagree on how much vitamin D we need in our blood to be healthy.
Which groups of people might benefit more from higher levels of D?
Older adults who are frail, Campos-Outcalt says. Getting 800 IU a day may help them prevent falls and fractures.
Recker says older people who are healthy can also benefit from the higher levels, ”because the skin loses the ability to make vitamin D” as people age. Some older people also stay indoors more as they age, he says.
Other people may also need to pay close attention to vitamin D in their foods. Among them are people on corticosteroids and other medications that can affect bone health, Recker says.
What are the potential harms of excess vitamin D supplements?
Very high doses of vitamin D can cause extremely high levels of calcium in your blood, which can lead to heart rhythm problems, kidney stones and damage, and severe muscle weakness. This calcium excess usually happens if you take 40,000 IU per day for a couple of months or longer, or take a very large one-time dose.
WASHINGTON — A new study shows that a combination of drugs can be used in targeted therapy against a common type of lung cancer.
Lung adenocarcinomas, the most common genetic subtype of lung cancer which has long defied treatment with targeted therapies, has had its growth halted by a combination of two already-in-use drugs in laboratory and animal studies, setting the stage for clinical trials of the drugs on patients, researchers at Dana-Farber Cancer Institute in Boston, Massachusetts and other scientists report in a new study.
The study, published in the journal Cancer Discovery, describes a new tack in the treatment of lung adenocarcinomas which account for about 40 percent of all lung cancers that carry mutations in the gene KRAS.
While most efforts to target KRAS directly with drugs have not proved successful, the authors of the current study took a more circuitous approach, targeting KRAS’s accomplices, the genes that carry out its instructions rather than KRAS itself, reports Science Daily.
“About 30 percent of lung adenocarcinomas have mutations in KRAS which amount to nearly 30,000 of all patients diagnosed with lung cancer each year in the United States,” says the study’s senior author, David Barbie, MD, of the Lowe Centre for Thoracic Oncology at Dana-Farber and the Broad Institute of Harvard and Massachusetts Institute of Technology.
“That represents the single biggest subset of lung cancer patients, if grouped by the mutations within their tumour cells. Unfortunately, there has not been a reliable way of striking at the genetic mechanism that causes these cells to proliferate.”
Mutations in KRAS cause cancer cells to grow and divide in a wildly disordered way. The lack of drugs able to block KRAS safely has led investigators to look for ways of stifling its effects “downstream” by interfering with the signals it sends to other genes.
“The next step will be to take these results to the clinic where the combination can be tested on lung cancer patients,” says Wong.
“We’re in the process of developing a clinical trial. Because KRAS mutations are also common in colon and pancreatic cancer, we’re hopeful that trials will be organised for these patients as well.”