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Antibiotic-resistant superbugs are now killing more people than breast cancer, according to a new data analysis by the UK Sepsis Trust.

According to the British Department of Health, about 5,000 people die each year from drug-resistant infections. But the UK Sepsis Trust and others have criticized these figures for being based on studies conducted in other countries, many of them with flawed methodology.

For the new analysis, the UK Sepsis Trust looked at the Department of Health’s own data to come up with an estimate of 12,000 killed per year by superbugs — more than twice as high as the current estimate.

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Big deal.


Researchers from the Genes and Cancer research group at the Bellvitge Biomedical Research Institute (IDIBELL) have identified inactivating mutations in a number of genes that code for HLA-I histocompatibility complex proteins, which are involved in the immune response and can condition the tesponse of lung cancer patients to immunotherapy. The study is a result of the collaboration between several national and international research centers, and has been published in the journal Clinical Cancer Research.

“Initially, we performed a genetic screening of lung cancer tumors using xenograft models, that is, human tumors that grow in mice, to obtain tumors with a low load of normal human cells,” explains Dr. Montse Sanchez-Cespedes, the last author of the paper. Sequencing of the tumors made it possible to identify several mutated genes, including some oncogenes and known tumor suppressor genes, and others that not previously described. “Among the latter, we were particularly interested in the B2M gene for its involvement in the functioning of the immune system, a target of new therapies developed for this type of cancer.”

This observation was validated at a later stage using a large panel of lung tumors, determining that the frequency of B2M mutations in lung cancer is 6–8%. At the same time, the researchers demonstrated that de novo reintroduction of this gene into cell lines that were deficient in B2M restored the functioning of the HLA-I complex.

Pretty wild.


Researchers of the German Center for Neurodegenerative Diseases (DZNE) have found that “alpha-synuclein,” a protein involved in a series of neurological disorders including Parkinson’s disease, is capable of travelling from brain to stomach and that it does so following a specific pathway. Donato Di Monte and co-workers report on this in the journal Acta Neuropathologica. Their study, carried out in rats, sheds new light on pathological processes that could underlie disease progression in humans.

Alpha-synuclein occurs naturally in the nervous system, where it plays an important role in synaptic function. However, in Parkinson’s disease, dementia with Lewy bodies and other neurodegenerative diseases termed “synucleinopathies,” this protein is accumulated within neurons, forming pathological aggregates. Distinct areas of the brain become progressively affected by this condition. The specific mechanisms and pathways involved in this widespread distribution of alpha-synuclein pathology remain to be fully elucidated. Clinical and experimental evidence suggests however that alpha-synuclein — or abnormal forms of it — could “jump” from one neuron to another and thus spread between anatomically interconnected regions.

Alpha-synuclein lesions have also been observed within neurons of the peripheral nervous system, such as those in the gastric wall. In some Parkinson’s patients, these lesions were detected at early disease stages. “Based on these intriguing observations, it has been hypothesized that the pathological process underlying Parkinson’s disease may actually start in the gastrointestinal tract and then move toward the brain,” Professor Di Monte says. “Our present approach was to look at this long-distance transmission of alpha-synuclein from the opposite perspective, investigating the possibility that alpha-synuclein may travel from the brain to the gut.”

Pretty soon, your smart watch may know you’re sick before you do, according to US scientists. The researchers made an app which tracked health data — such as heart rate and skin temperature — collected by 60 people’s smart watches for up to two years, and found that people’s stats changed when they were getting sick.

The authors say smart watches could also help detect the risk of type 2 diabetes and low oxygen on planes, and that they even helped detect Lyme disease in one of the scientists behind the study.

Smart watches and similar portable devices are commonly used for measuring steps and physiological parameters, but have not generally been used to detect illness.

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The Samsung Galaxy Note 7 exploding battery fiasco has stirred major concerns whether smartphone batteries are really safe. In an effort to prevent these disasters from happening, a group of Stanford scientists have developed a lithium-ion battery pack, which includes a capsule filled with triphenyl phosphate (TPP). Once the battery’s internal temperature reaches a certain point, the capsule will melt releasing the TPP and extinguishing the fire.

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The team working on the project found out that TPP is a type of chemical-fire retardant. The chemical is capable of extinguishing an exploding battery in just 0.4 seconds, according to 9to5Google. The team also set the temperature threshold at 302 degrees Fahrenheit, at that point, the capsule will melt releasing the TPP chemical.

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  • Exploiting the usage of 2 D crystals in methanol fuel cells

ChemEurpoe — Scientists from the School of Chemical Engineering and Analytical Science, in the University of Manchester have come up with a way to utilize 2D materials in an actual operating direct methanol fuel cell. They have shown that the addition of single layer graphene by Chemical vapour deposition, on to the membrane area has significantly reduced the methanol cross over at the same time obtaining negligible resistance to protons thereby enhancing the cell performance by 50%.

Fuel cells count as interesting energy technology of the near future, as they pave the way for the production of sustainable energy using simple hydrocarbons as fuels. They work by a simple operational mechanism with the fuel oxidation on one side, and oxidant reduction on other side, which liberates electrons used for electrical energy generation. A wide variety of fuels, short chain alcohols have been used so far. Methanol remains a favourable candidate due to its high energy density, ease of handling and other operational characteristics.

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I can say that I have seen it all with this for cancer research.


SALT LAKE CITY – Researchers at Huntsman Cancer Institute have successfully used synthetic elephant genes to battle human cancer cells.

The synthetic elephant genes are still in the early phases of research, according to HCI, but show promise.

The HCI said there are 1.6 million new cancer diagnosis every year in the United States. Many across the globe are racing to find a cure, but researchers at Huntsman said elephants already have it figured out.

Noted synthetic life researcher Steven Benner of Foundation for Applied Molecular Evolution is fond of pointing out that gooey tars are the end product of too many experiments in his field. His widely-held view is that the tars, made out of chemicals known to be important in the origin of life, are nonetheless a dead end to be avoided when trying to work out how life began.

But in the changing world of origins of life research, others are asking whether those messy tars might not be a breeding ground for the origin of life, rather than an obstacle to it.

One of those is chemist and astrobiologist Irena Mamajanov of the Earth-Life Science Institute (ELSI) in Tokyo. As she recently explained during an institute symposium, scientists know that tar-like substances were present on early Earth, and that she and her colleagues are now aggressively studying their potential role in the prebiotic chemical transformations that ultimately allowed life to emerge out of non-life.

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