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Category: biotech/medical – Page 998

There needs to be a radical change to biological wetware in order to handle viruses. What is needed is either nanoparticles or an immunity to all diseases. Crispr is the main path for the biological singularity but it needs to be perfected first as the human body is still a black box due to restrictions. I do believe that mass spectrometry will essentially be key to see the inner world of human biology. Then crispr can make new parts essentially to evolve past our current limits. But either way the biological singularity is needed for survival of human beings for better health.

The coronavirus revealed flaws in the nation’s pandemic plans. The spread of monkeypox shows that the problems remain deeply entrenched.

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Foresight Biotech & Health Extension Meeting sponsored by 100 Plus Capital.
Program & apply to join: https://foresight.org/biotech-health-extension-program/

Jennifer Garrison, Buck Institute.
Reframing Health and Aging through the Lens of Reproduct.

Jennifer Garrison is an assistant professor at the Buck Institute for Research on Aging and also holds appointments in the Department of Cellular and Molecular Pharmacology at University of California, San Francisco (UCSF) and the Davis School of Gerontology at the University of Southern California. During her doctoral studies at UCSF with Jack Taunton, she discovered the molecular target of a natural product and elucidated a novel mechanism by which small molecules can regulate protein biogenesis.

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Brain-age (BA) estimates based on deep learning are increasingly used as neuroimaging biomarker for brain health; however, the underlying neural features have remained unclear. We combined ensembles of convolutional neural networks with Layer-wise Relevance Propagation (LRP) to detect which brain features contribute to BA. Trained on magnetic resonance imaging (MRI) data of a population-based study (n = 2,637, 18–82 years), our models estimated age accurately based on single and multiple modalities, regionally restricted and whole-brain images (mean absolute errors 3.37–3.86 years). We find that BA estimates capture ageing at both small and large-scale changes, revealing gross enlargements of ventricles and subarachnoid spaces, as well as white matter lesions, and atrophies that appear throughout the brain. Divergence from expected ageing reflected cardiovascular risk factors and accelerated ageing was more pronounced in the frontal lobe. Applying LRP, our study demonstrates how superior deep learning models detect brain-ageing in healthy and at-risk individuals throughout adulthood.

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CHICAGO, Sept 30 (Reuters) — Clear evidence this week that Eisai (4523.T) and Biogen’s (BIIB.O) drug lecanemab slows cognitive decline in early stage dementia has galvanized efforts among Alzheimer’s researchers toward a tantalizing goal — preventing dementia even before symptoms start.

Lecanemab is an antibody that targets and removes toxic clumps of a protein called amyloid beta that accumulate in the brains of patients with Alzheimer’s. Results from the companies’ 1,800-patient trial released on Tuesday showed convincingly that doing so also slows the advance of the mind-robbing disease.

In volunteers with mild cognitive impairment and early stage dementia, the drug showed a 27% reduction in cognitive decline after 18 months compared with those who got a placebo.

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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.

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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.

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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.

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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.

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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 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 . 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 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.

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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 —and their manifestation as dementia—are not an inevitable consequence of aging.

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

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