Lifeboat Foundation

Researchers from CNRS, the Curie Institute, and Sorbonne University have successfully physically acted on chromosomes in live cells for the first time. They found that, outside of cell division phases, chromosomes are actually very fluid—almost liquid—by subjecting to different forces using magnets. The study was recently published in the prestigious journal Science.

When they are not in their division phases, chromosomes are fluid, though not quite liquid. This discovery was made possible by the first-ever direct mechanical manipulation of chromosomes in the nucleus of live cells.

Previously, chromosomes, which are extraordinarily long DNA.

When cancer develops in the body, it begins with tumor cells that rapidly multiply and divide before spreading. But how are these nascent tumor cells able to evade the body’s immune system, which is designed to recognize and defend against such faulty cells? The answer to this long-unsolved topic may hold the key to more successful cancer treatments — medications that block tumors’ subversive moves and allow the immune system to do its job.

Researchers at Harvard Medical School have now discovered a mechanism through which tumor cells can disable the immune system, enabling the tumor to spread unchecked. The study, which was conducted primarily in mice and published today in Science, demonstrates that tumor cells with a certain mutation generate a chemical, known as a metabolite, that weakens adjacent immune cells, making them less capable of eliminating cancer cells.

The results underscore the crucial roles played by tumor metabolites in the deactivation of the immune system by malignancies. The findings also highlight the crucial part that the tumor microenvironment—the region around the tumor—plays in the development of cancer.

Summary: Oxytocin, a hormone connected with bonding and love, could help to heal damage following a heart attack. Researchers found oxytocin stimulates stem cells from the heart’s outer layer and migrates into the middle layer where it develops into muscle cells that generate heart contractions. This could be used to promote the regeneration of heart cells following a heart attack.

Source: Frontiers.

The neurohormone oxytocin is well-known for promoting social bonds and generating pleasurable feelings, for example from art, exercise, or sex. But the hormone has many other functions, such as the regulation of lactation and uterine contractions in females, and the regulation of ejaculation, sperm transport, and testosterone production in males.

In a recent study published in The Lancet Microbe, researchers assessed the role of gut bacterial microbiome assembly and the gut mycobiome in relation to health, pathology, and clinical applications.

Studies have built a framework for investigating how gut fungi are connected to—or perhaps cause—different diseases and how to alter gut fungi to treat diseases by revealing the landscape of gut mycobiome composition in humans. Importantly, available mycobiome discoveries are not extensively applied to clinical practice, and gut fungi are still widely ignored in the context of treatments based on the microbiota.

According to studies conducted on mice, altering the intestinal fungi through oral administration of antifungal medications worsened allergic rhinitis and colitis, indicating that an imbalance in the gut mycobiome may play a role in the pathogenesis of intestinal as well as extra-intestinal diseases. Similar comparisons between the gut mycobiomes of healthy people and patients with various intestinal and extra-intestinal disorders have been documented in many studies.

A team of researchers affiliated with several institutions in Switzerland and the U.S. reports evidence that the genetics of longevity are influenced by both gender and age. In their paper published in the journal Science, the group describes their study of aging in mice and humans. João Pedro de Magalhães, with the University of Birmingham, has published a Perspective piece in the same journal issue outlining the technical challenges to understanding how aging works and the work done by the team on this new effort.

Scientists have been studying the aging process for many years but still do not have a good explanation for why organisms age and why some live longer than others. In this new effort, the researchers wondered if something in the genome plays a role in how long a species lives on average.

Noting that another team had created a very large dataset of information regarding aging in nearly 3,000 mice, the researchers found that it also contained genetic information. After obtaining access to the database, they analyzed that genetic information—more specifically, they conducted quantitative trait locus mapping. They found multiple loci that they could associate with longevity, some that were specific to one or the other gender. They also found that mice who weighed more during their early years or who had small litter sizes tended to die younger. They suggest the same genes that were associated with aging may have also played a role in the other two traits. The researchers also found that the aging-related genes they isolated appeared to remain dormant until the latter stages of a given individual’s life.

With more of us living into old age than at any other time, dementia is increasing steadily worldwide, with major individual, family, societal and economic consequences.

Treatment remains largely ineffective and aspects of the underlying pathophysiology are still unclear. But there is good evidence that neurodegenerative diseases —and their manifestation as dementia—are not an inevitable consequence of aging.

Many causes of dementia, including viral infections, are preventable.

Without altering the genetic code in the DNA, epigenetic modifications can change how genes are expressed, affecting an organism’s health and development. The once radical idea that such changes in gene expression can be inherited now has a growing body of evidence behind it, but the mechanisms involved remain poorly understood.

A new study by researchers at UC Santa Cruz shows how a common type of epigenetic modification can be transmitted via sperm not only from parents to offspring, but to the next generation (“grandoffspring”) as well. This is called “transgenerational epigenetic inheritance,” and it may explain how a person’s health and development could be influenced by the experiences of his or her parents and grandparents.

The study, published the week of September 26 in the Proceedings of the National Academy of Sciences (PNAS), focused on a particular modification of a histone protein that changes the way DNA is packaged in the chromosomes. This widely studied epigenetic mark (called H3K27me3) is known to turn off or “repress” the affected genes and is found in all multicellular animals—from humans to the nematode worm C. elegans used in this study.

Robotics and wearable devices might soon get a little smarter with the addition of a stretchy, wearable synaptic transistor developed by Penn State engineers. The device works like neurons in the brain to send signals to some cells and inhibit others in order to enhance and weaken the devices’ memories.

Led by Cunjiang Yu, Dorothy Quiggle Career Development Associate Professor of Engineering Science and Mechanics and associate professor of biomedical engineering and of materials science and engineering, the team designed the synaptic transistor to be integrated in robots or wearables and use artificial intelligence to optimize functions. The details were published Sept. 29 in Nature Electronics.

“Mirroring the human brain, robots and wearable devices using the synaptic transistor can use its artificial neurons to ‘learn’ and adapt their behaviors,” Yu said. “For example, if we burn our hand on a stove, it hurts, and we know to avoid touching it next time. The same results will be possible for devices that use the synaptic transistor, as the artificial intelligence is able to ‘learn’ and adapt to its environment.”

Sept 27 (Reuters) — An experimental Alzheimer’s drug made by Eisai Co Ltd (4523.T) and Biogen (BIIB.O) slowed cognitive and functional decline in a large trial of patients in the early stages of the disease, they said on Tuesday, potentially a rare win in a field littered with failed drugs.

Multiple drugmakers have so far tried and failed to find an effective treatment for the brain-wasting disease that affects about 55 million people globally. A breakthrough would be a major boost to similar studies being run by Roche and Eli Lilly.

Speaking of the Eisai-Biogen drug results announced late on Tuesday night, Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center in Rochester, Minnesota said: “It’s not a huge effect, but it’s a positive effect”.