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A series of three neuroimaging studies identified a pattern of neural activation involving specific brain regions that differentiates drug users from non-users with 82% accuracy. Researchers named the pattern the Neurobiological Craving Signature (NCS). Their findings have been published in Nature Neuroscience.

Craving is a strong desire to use drugs or eat. It has long been considered a key factor driving substance abuse and overeating. It is one of the criteria used for diagnosing substance use disorders. Craving is often induced by exposure to certain stimuli. In the case of overeating, these include the smell or sight of food. In the case of drugs, craving can be induced by one being in places or situations he/she associates with taking drugs or being offered drugs. This is called cue-induced craving.

Earlier studies of craving have successfully relied on self-reported craving, but recent research has focused on discovering its biological basis. Human neuroimaging studies have identified neural circuits related to the risk of substance abuse. Some brain circuits have been found to be involved in different substance use disorders and risky behaviors. These include specific parts of the ventromedial prefrontal cortex (vmPFC), ventral striatal/nucleus accumbens (VS/NAc) and insula regions of the brain. These regions also appear to play a role in weight gain and obesity.

Australian researchers have uncovered an enzyme capable of transforming air into energy. The study, which was recently published in the prestigious journal Nature, shows that the enzyme utilizes small amounts of hydrogen in the air to generate an electrical current. This breakthrough paves the way for the development of devices that can literally generate energy from thin air.

The discovery was made by a team of scientists led by Dr. Rhys Grinter, Ashleigh Kropp, a Ph.D. student, and Professor Chris Greening from the Monash University Biomedicine Discovery Institute in Melbourne, Australia. The team produced and studied a hydrogen-consuming enzyme sourced from a bacterium commonly found in soil.

Recent work by the team has shown that many bacteria use hydrogen from the atmosphere as an energy source in nutrient-poor environments. “We’ve known for some time that bacteria can use the trace hydrogen in the air as a source of energy to help them grow and survive, including in Antarctic soils, volcanic craters, and the deep ocean,” Professor Greening said. “But we didn’t know how they did this, until now.”

University of Virginia scientists have identified a promising approach to delay aging by detoxifying the body of glycerol and glyceraldehyde, harmful by-products of fat that naturally accumulate over time.

The new findings come from UVA researcher Eyleen Jorgelina O’Rourke, Ph.D., and her team, who are seeking to identify the mechanisms driving healthy aging and longevity. Their new work suggests a potential way to do so by reducing glycerol and glyceraldehyde’s health-draining effects.

“The discovery was unexpected. We went after a very well-supported hypothesis that the secret to longevity was the activation of a cell-rejuvenating process named autophagy and ended up finding an unrecognized mechanism of health and lifespan extension,” said O’Rourke, of UVA’s Department of Biology and the UVA School of Medicine’s Department of Cell Biology.

Recently is has become known that one should not take Metformin unless you have diabetes. But a combo test of Rapamycin and Metformin showed each removed each others side effects. So here we have another combo test showing the effect on stem cells in the gut.


In a new study published in Aging Cell, researchers have shown that two promising anti-aging agents, the antibiotic rapamycin and the anti-diabetic drug metformin, reverse aging in a population of intestinal stem cells [1].

Older people are more prone to gastrointestinal problems [2]. Moreover, aging is a major risk factor for various cancers, including colorectal cancer. Therefore, it is necessary to develop therapeutic approaches to rejuvenate the aging intestine.

The function and structure of the intestinal epithelium, a single cell layer that lines the small intestine and colon, is maintained by the residing stem cells. Intestinal stem cells continuously divide to generate several types of progenitor cells.

A new paper in Nature Communications illuminates how a previously poorly understood enzyme works in the cell. Many diseases are tied to chronic cellular stress, and UMBC’s Aaron T. Smith and colleagues discovered that this enzyme plays an important role in the cellular stress response. Better understanding how this enzyme functions and is controlled could lead to the discovery of new therapeutic targets for these diseases.

The enzyme is named ATE1, and it belongs to a family of enzymes called arginyl-tRNA transferases. These enzymes add arginine (an amino acid) to proteins, which often flags the proteins for destruction in the cell. Destroying proteins that are misfolded, often as a result of cellular stress, is important to prevent those proteins from wreaking havoc with cellular function. An accumulation of malfunctioning proteins can cause serious problems in the body, leading to diseases like Alzheimer’s or cancer, so being able to get rid of these proteins efficiently is key to long-term health.

The new paper demonstrates that ATE1 binds to clusters of iron and sulfur ions, and that the enzyme’s activity increases two-to three-fold when it is bound to one of these iron-sulfur clusters. What’s more, when the researchers blocked cells’ ability to produce the clusters, ATE1 activity decreased dramatically. They also found that ATE1 is highly sensitive to oxygen, which they believe relates to its role in moderating the cell’s stress response through a process known as .

A quick introduction to Yamanaka factors!


The quest for longevity has always been with us. Ever since the ancient kings of old we have been trying everything we can think of in order to stave off death and disease, with most of our efforts unfortunately baring little fruit. However, as it turns out, the power to reverse the aging process has been nestled within us this whole time. Not in the metaphorical sense, but rather in the quite literal sense. For you see, we have been reversing the aging process every single time we have reproduced.

Have you ever wondered how it is that regardless of how old the parents of a child are, the child is never born ‘pre-aged?’. This seems like a ridiculous question, but if the genetic material that came from the parents (especially from the father) has already undergone the aging process, then how is it that ‘genetic aging’ is not passed onto the child? If such a process were to occur, then it would obviously spell doom for our entire species, as we would eventually accumulate age with each subsequent generation and we would very quickly perish. Yet, this obviously does not happen. So the question was asked, why is this?

The future of computing includes biology says an international team of scientists.

The time has come to create a new kind of computer, say researchers from John Hopkins University together with Dr. Brett Kagan, chief scientist at Cortical Labs in Melbourne, who recently led development of the DishBrain project, in which human cells in a petri dish learned to play Pong.

In an article published on February 27 in the journal Frontiers in Science, the team outlines how biological computers could surpass today’s electronic computers for certain applications while using a small fraction of the electricity required by today’s computers and server farms.

A pilot trial by investigators from Brigham and Women’s Hospital, a founding member of the Mass General Brigham health care system, tested the nasal administration of the drug Foralumab, an anti-CD3 monoclonal antibody. Investigators found evidence that the drug dampened the inflammatory T cell response and decreased lung inflammation in patients with COVID-19. Further analysis showed the same gene expression modulation in patients with multiple sclerosis, who experienced decreased brain inflammation, suggesting that Foralumab could be used to treat other diseases. Their results are published in the Proceedings of the National Academy of Sciences.

“We discovered a way to shut down inflammation not only seen in COVID-19, but also in a patient with multiple sclerosis as well as in healthy patients,” said lead author Thais Moreira, Ph.D., an assistant scientist at the Ann Romney Center for Neurologic Diseases at BWH and an instructor in Neurology at Harvard Medical School. “This is very exciting because not only does our study suggest that this new monoclonal antibody drug is safe and can modulate the without major side effects, but it can also decrease inflammation in multiple realms, so it may be useful for treating other diseases.”

“Inflammation is a major cause of many diseases,” said senior author Howard Weiner, MD, founder and director of the Brigham Multiple Sclerosis Center and co-director of the Ann Romney Center for Neurologic Diseases. “Our center has spent decades looking for novel ways to treat disease where there is abnormal inflammation in a way that is safe and effective.”