Lifeboat Foundation

Since 2020, the condition known as long COVID-19 has become a widespread disability affecting the health and quality of life of millions of people across the globe and costing economies billions of dollars in reduced productivity of employees and an overall drop in the work force.

The intense scientific effort that long COVID sparked has resulted in more than 24,000 scientific publications, making it the most researched health condition in any four years of recorded human history.

Long COVID is a term that describes the constellation of long-term health effects caused by infection with the SARS-CoV-2 virus. These range from persistent respiratory symptoms, such as shortness of breath, to debilitating fatigue or brain fog that limits people’s ability to work, and conditions such as heart failure and diabetes, which are known to last a lifetime.

In a recent study published in Science Advances, researchers from the University of California, Berkeley, used the nematode model Caenorhabditis elegans to determine whether the olfactory nervous system could non-autonomously control the mitochondrial unfolded protein response in response to cellular stress.

A critical part of maintaining a state of cellular homeostasis is coordinating responses to environmental stress across tissues. Substantial evidence now supports the fact that the central nervous system regulates stress across all tissues. Furthermore, cell non-autonomous induction of stress responses occurs in peripheral tissues when unfolded protein responses (UPR) in the mitochondria and the endoplasmic reticulum are activated in the neurons.

Stressed cells undergo misfolding or unfolding of proteins, and UPR transmits protein folding status information to the nucleus to enable cellular stress responses or induce apoptotic cell death. The non-autonomous control of cellular stress responses is believed to be essential for the organism to survive toxic environmental conditions.

According to the World Health Organization, antibiotic resistance is a top public health risk that was responsible for 1.27 million deaths across the globe in 2019. When repeatedly exposed to antibiotics, bacteria rapidly learn to adapt their genes to counteract the drugs—and share the genetic tweaks with their peers—rendering the drugs ineffective.

Superpowered bacteria also torpedo medical procedures—surgery, chemotherapy, C-sections—adding risk to life-saving therapies. With antibiotic resistance on the rise, there are very few new drugs in development. While studies in petri dishes have zeroed in on potent candidates, some of these also harm the body’s cells, leading to severe side effects.

What if there’s a way to retain their bacteria-fighting ability, but with fewer side effects? This month, researchers used AI to reengineer a toxic antibiotic. They made thousands of variants and screened for the ones that maintained their bug-killing abilities without harming human cells.

which is widely believed to be the root cause of many age-related diseases.

The study, published today in the journal npj Aging, raises the exciting possibility of a protective agent that could dampen age-related inflammation and restore normal immune function in older adults.

PEPITEM (Peptide Inhibitor of Trans-Endothelial Migration) was initially identified at the University of Birmingham in 2015. While the role of the PEPITEM pathway has already been demonstrated in immune-mediated diseases, this is the first data showing that PEPITEM has the potential to increase healthspan in an aging population.

We’re closer to a cure for HIV than ever before. This half hour, Scripps News examines the fight against a virus that has killed millions of people around the world in the last generation.

In 2023 there were nearly 40 million people living with HIV. Some 30.7 million of them receive antiretroviral treatment. Despite recent advances in preventing infections, more than a million people are expected to become newly infected in 2024. More than 600,000 will die of HIV/AIDS.

But a handful of people have now been cured, thanks to recent breakthroughs in treatment.

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Scientists looking to tackle our ongoing obesity crisis have made an important discovery: Intermittent calorie restriction leads to significant changes both in the gut and the brain, which may open up new options for maintaining a healthy weight.

Researchers from China studied 25 volunteers classed as obese over a period of 62 days, during which they took part in an intermittent energy restriction (IER) program – a regime that involves careful control of calorie intake and relative fasting on some days.

Not only did the participants in the study lose weight – 7.6 kilograms (16.8 pounds) or 7.8 percent of their body weight on average – there was also evidence of shifts in the activity of obesity-related regions of the brain, and in the make-up of gut bacteria.

Increasing serotonin can change how people learn from negative information, as well as improving how they respond to it, according to a new study published in the journal Nature Communications.

The study by scientists at the University of Oxford’s Department of Psychiatry and the National Institute of Health and Care Research (NIHR) Oxford Health Biomedical Research Center (OH BRC) found people with increased serotonin levels had reduced sensitivity to punishing outcomes (for example, losing money in a game) without significantly affecting sensitivity to rewarding ones (winning money).

The study involved 26 participants who were given the drug to increase serotonin, with a further 27 in a control group, who were asked to do a series of tasks measuring learning and behavioral control. State-of-the-art models were then used to understand participant behavior.