Cryo-electron microscopy structures of skeletal F-actin show solvent-driven rearrangements governing actin filament assembly and aging with potential application in design of drugs and small molecules for imaging and therapy.

The overexpression of a gene tied to cell division and the structure and function of neurons may prevent and protect against cognitive decline in both mice and humans with Alzheimer’s disease (AD), according to a new study by scientists at the University of Colorado Anschutz Medical Campus.
The gene, Kinesin-5 or KIF11, does this despite the presence of amyloid beta (Abeta), the main component of plaques in the brains of those with AD. Scientists have traditionally targeted the plaques when looking for treatments for the fatal disease. In this case, they went around them.
The study was published online last week in the journal iScience.
I guess it’s time for Twitter execs to go home, and for me to start using Twitter again. They killed my chamber of commerce account, then when I opened a personal account, they kept asking for my phone number every time I logged in. If I give you my number once and you send me an sms, I’m not giving it to you again, as that’s not safe.
It ends months of bad blood between the two parties regarding the takeover, with Elon Musk complaining about fake accounts on the platform and claims by a whistleblower that Twitter misled regulators about security risks.
Werner Syndrome and Hutchinson Gilford Progeria Syndrome are two examples of the rare genetic disorders known as progeroid syndromes that cause signs of premature aging in children and young adults. Patients with progeroid syndromes have pathologies and symptoms that are often linked to aging, including osteoporosis, cataracts, heart disease, and type II diabetes.
This aging is characterized by the gradual loss of nuclear architecture and an underlying tissue-specific genetic program, but the causes are unclear. Scientists have discovered a potential new target for treating these syndromes by preventing nuclear architecture loss.
New imaging of patients with Alzheimer’s demonstrates how a telltale protein spreads throughout the brain based on the phenotype of the disease, i.e., whether the condition is dominated by forgetfulness, or atrophy in a specific brain region. The research offers a host of illuminating clues that ultimately may inform new treatment strategies.
The protein is known as tau and a large multi-disciplinary team of brain researchers at McGill University in Montreal has been able to trace the protein’s patterns in living patients via magnetic resonance imaging (MRI). Alzheimer’s disease is intimately linked to tau, which can form tangles in the brain that irrevocably damage neurons.
The patterns detected by McGill scientists apparently are unique to the phenotype of Alzheimer’s afflicting the patient. This staggering finding opens an intriguing new window into the molecular mechanisms of the disease. And while many features of Alzheimer’s are the same from one patient to the next, phenotypes are a hallmark of the condition. Tracking tau patterns is a specialty of the scientists at McGill, who found that the intrinsic connectivity of the human brain itself provides the scaffolding for the aggregation of tau in distinct variants of the disease.
Viral DNA in human genomes, embedded there from ancient infections, serves as antivirals that protect human cells against certain present-day viruses, according to new research.
The paper, “Evolution and Antiviral Activity of a Human Protein of Retroviral Origin,” published Oct. 28 in Science, provides proof of principle of this effect.
Previous studies have shown that fragments of ancient viral DNA—called endogenous retroviruses —in the genomes of mice, chickens, cats and sheep provide immunity against modern viruses that originate outside the body by blocking them from entering host cells. Though this study was conducted with human cells in culture in the lab, it shows that the antiviral effect of endogenous retroviruses likely also exists for humans.
The finding is a turning point in cancer research.
Two major studies published in Nature.
Phospho Biomedical Animation.
The revelation shows that epigenetics, cells controlling gene activity, play a crucial role in the development of cancer. Cancers are usually tested for DNA mutations alone, which can miss this level of control, thereby failing to predict how cancers may behave and respond to treatment.
It’s illegal to use the carcinogenic color additive Red 3 in cosmetics, such as lipsticks or blush, or externally applied drugs. Yet the discredited chemical is lurking in common varieties of candy corn, Nerds, Peeps, Pez, SweeTarts, and hundreds of candies, cakes, and other foods, including dozens of seasonal Halloween items. That’s why the Center for Science in the Public Interest and 23 other organizations and prominent scientists are today urging the Food and Drug Administration to formally remove Red 3 from the list of approved color additives in foods, dietary supplements, and oral medicines.
Since the early 1980s FDA had evidence that Red 3 caused cancer in laboratory animals. The National Toxicology Program considered the evidence “convincing.” As a result, in 1990, the agency eliminated certain “provisionally listed” uses of the chemical—meaning cosmetics and externally applied drugs. In 1990, FDA also said it would “take steps” to ban its use in foods, ingested drugs, and supplements. But those steps were never taken.
“Halloween has never been the healthiest holiday, but few parents would believe that the FDA permits the use of a dye it acknowledges as a carcinogen to be used as a common ingredient in candy,” said CSPI consultant Lisa Y. Lefferts. “Fewer still would believe that the FDA prohibits this carcinogen in makeup but allows it in food.”
In a study using specialized imaging techniques, Johns Hopkins Medicine researchers report distinctive changes in the “white matter” and other brain tissue physiology of those with post-treatment Lyme disease, a condition affecting 10% to 20% of the nearly half a million Americans who contract Lyme disease annually.
The study’s findings, published October 26 in the journal PLOS ONE, substantiate and help validate that memory difficulties and other cognitive difficulties experienced long-term by individuals with post-treatment Lyme disease are linked to functional and structural changes in the brain.
Lyme disease, whose early symptoms may include a characteristic rash, flu-like aches and fever, joint pain, and fatigue, is treated using a rigorous course of antibiotics, which usually clears the illness.