Lifeboat Foundation

Editor’s note: This article is part of a collection of expert commentaries. You can read the rest of the series here.

It is true that the next pandemic is a matter of “when,” not “if.” The statistical certainty of a future pandemic has led to increasing research into potential pandemic pathogens so that we may create lifesaving countermeasures. Such research, unfortunately, also carries a risk of bringing about exactly what it seeks to prevent. Human error or even deliberate action is as likely to be the cause of the next pandemic as natural origin. Such concerns have intensified after the COVID-19 pandemic, which a significant percentage of the US population, at least, believes began with a research accident, one of the two main pandemic origin theories, with the other being the jump of a virus from animals to people. The question then for governments and the research community is how to build confidence in the valuable work that scientists do through appropriate regulation.

While research with favorable risk-benefit profiles must be facilitated, high-risk research of either limited benefits or benefits for only a limited few must be seen through a different regulatory lens.

A new model, vetted by experiments on lung cancer cells, may help to explain how cancer and other diseases accumulate drug-resistance mutations that can compromise the effectiveness of treatments.

During the past 50 years, researchers have accumulated a massive arsenal in our war on cancer. Well over 500 drugs have been approved to treat tumors, but cancer remains the second leading cause of death in the United States. The problem is partly due to drug resistance—the emergence of treatment-resistant mutants of the original disease. Now a study led by Jeff Maltas of Cleveland Clinic and Case Western Reserve University, both in Ohio, puts forward a model explaining why drug resistance is so common, vetting the model with experiments on lung cancer cells [1]. This model indicates that treatment-resistant mutants can be present in larger-than-expected numbers before treatment begins. The conclusion implies that we cannot understand cancer evolution by looking at individual mutations in isolation; instead, we should consider each tumor as an interacting ecosystem.

Mentally stimulating activities and life experiences can improve cognition in memory clinic patients, but stress undermines this beneficial relationship. This is according to a new study from Karolinska Institutet published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

In the late 1980s, researchers discovered that some individuals who showed no apparent symptoms of dementia during their lifetime had brain changes consistent with an advanced stage of Alzheimer’s disease. Since then it has been postulated that so-called cognitive reserve might account for this differential protective effect in individuals.

Cognitively stimulating and enriching life experiences and behaviors such as higher educational attainment, complex jobs, continued physical and leisure activities, and healthy social interactions help build cognitive reserve. However, high or persistent stress levels are associated with reduced social interactions, impaired ability to engage in leisure and physical activities, and an increased risk of dementia.

Scientists at La Jolla Institute for Immunology (LJI) have developed a new computational method for linking molecular marks on our DNA to gene activity. Their work may help researchers connect genes to the molecular “switches” that turn them on or off.

I disagree with you Dan Breeden. In my openion AI WILL A BETTER FUTURE FOR HUMAN CIVILIZATION.

Doctors and engineers from Massachusetts General Hospital and MIT are trying to revolutionize cancer detection through an artificial intelligence program called Sybil. Their study found that Sybil could accurately predict whether a person will develop lung cancer in the next year up to 94 percent of the time. NBC News’ Dr. John Torres reports.

Continue reading “AI could revolutionize cancer detection, according to MIT, Mass General research” »

Some systems are still down, but medical staff can now use the computer system for patient care after almost four weeks.

“Testing people early, so early interventions are possible, is key to longevity,” she says. “Technology, data and AI, and what we’re starting to be able to do with it, are propelling us to a time of greater understanding which will foster earlier, more effective treatment. Or perhaps even therapies that can delay neurodegenerative diseases, pushing back dementia to beyond our lifespan.”

Mind Over Matter goes out on 29th and 30th June on BBC News and 30th June on BBC One.

Lara Lewington will be hosting a Fireside Chat on AI drug discovery with Alex Zhavoronkov at next week’s Founders Longevity Forum. Register your interest to discover how AI is accelerating drug discovery, commercialization and licensing models HERE.

In what they believe is a solution to a 30-year biological mystery, neuroscientists at Johns Hopkins Medicine say they have used genetically engineered mice to address how one mutation in the gene for the light-sensing protein rhodopsin results in congenital stationary night blindness.

The condition, present from birth, causes poor vision in low-light settings.

The findings, published May 14 in Proceedings of the National Academy of Sciences, demonstrate that the rhodopsin gene mutation, called G90D, produces an unusual background electrical “noise” that desensitizes the eye’s rods, those cells in the retina at the back of the eye responsible for nighttime vision, thus causing night blindness.

Scientists from Nagoya University in Japan have identified the role of serotonin neurons in linking glucose availability to reproductive health. Their research demonstrates how elevated glucose levels stimulate serotonergic neurons, leading to the release of serotonin, which in turn activates kisspeptin neurons responsible for reproductive hormone release. These findings explain why poor nutrition affects fertility and suggest potential treatments for depression-induced infertility through the use of selective serotonin reuptake inhibitors (SSRIs). Credit: SciTechDaily.com.

Scientists from Nagoya University in Japan have clarified the connection between energy levels and fertility in both animals and humans. They discovered that signaling from serotonin neurons plays a crucial role in maintaining reproductive function by detecting glucose availability, which in turn enhances the release of the reproductive hormone gonadotropin. These findings also offer an explanation for the reduced fertility seen in individuals with depression and suggest potential treatments. The study was published in Scientific Reports.

People who lack sufficient nutrition encounter problems with their reproductive health. For example, ballet dancers can experience menstrual disruptions, and women who fast can struggle to conceive. According to a new study led by Designated Associate Professor Sho Nakamura and Professors Hiroko Tsukamura and Satoshi Ohkura, one of the main factors that affect a person’s reproductive health is glucose availability.