Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog – Page 7

Get the latest international news and world events from around the world.

Log in for authorized contributors

Embryonic transplantation and ischemic memory deficit

Transient forebrain ischemia is associated with selective neuronal vulnerability and persistent memory deficit. This study compares functional outcome and morphological changes in rats subjected to post-ischemic CA1 or hilus/dentate gyrus region hippocampal fetal transplantation. Ischemia was produced by bilateral common carotid artery occlusion with hypotension. Fetal hippocampal neurons were transplanted into both sides of the CA1 or hilus/dentate gyrus region of the dorsal hippocampus, 1 week post-ischemia. Four weeks post transplantation, the rats underwent behavioral testing for 5 consecutive days using the water maze trial. All animals were perfusion fixed for morphological studies. Transplants in the CA1 region of the dorsal hippocampus were associated with memory and morphological recovery, while grafts placed into the hilus/dentate gyrus region of the dorsal hippocampus were not. Similarly, neurons transplanted in the CA1 region of the dorsal hippocampus were morphologically similar to CA1 pyramidal cell neurons and stained positive with calbindin D(28k). In contrast the grafts transplanted into the hilus/dentate gyrus region of the dorsal hippocampus were morphologically heterogeneous and staining with calbindin D(28k) was not as robust. Post-ischemic transplantation in the CA1 region of the dorsal hippocampus is effective in improving memory and morphological function.

PubMed Disclaimer

Reappearance of hippocampal CA1 neurons after ischemia is associated with recovery of learning and memory

The pyramidal neurons of the hippocampal CA1 region are essential for cognitive functions such as spatial learning and memory, and are selectively destroyed after cerebral ischemia. To analyze whether degenerated CA1 neurons are replaced by new neurons and whether such regeneration is associated with amelioration in learning and memory deficits, we have used a rat global ischemia model that provides an almost complete disappearance (to approximately 3% of control) of CA1 neurons associated with a robust impairment in spatial learning and memory at two weeks after ischemia. We found that transient cerebral ischemia can evoke a massive formation of new neurons in the CA1 region, reaching approximately 40% of the original number of neurons at 90 days after ischemia (DAI). Co-localization of the mature neuronal marker neuronal nuclei with 5-bromo-2’-deoxyuridine in CA1 confirmed that neurogenesis indeed had occurred after the ischemic insult. Furthermore, we found increased numbers of cells expressing the immature neuron marker polysialic acid neuronal cell adhesion molecule in the adjacent lateral periventricular region, suggesting that the newly formed neurons derive from this region. The reappearance of CA1 neurons was associated with a recovery of ischemia-induced impairments in spatial learning and memory at 90 DAI, suggesting that the newly formed CA1 neurons restore hippocampal CA1 function. In conclusion, these results show that the brain has an endogenous capacity to form new nerve cells after injury, which correlates with a restoration of cognitive functions of the brain.

PubMed Disclaimer

Laser beam builds cell-like protein networks without chemical modification

Networks of protein fibers play important roles in living cells. To understand the dynamical behavior of these networks, model networks are needed to perform in vitro studies. However, fabrication of protein networks similar to those in cells has proved difficult, as current methods could affect the biological function of these proteins—ultimately impacting our understanding of any findings.

Now, researchers at The University of Osaka and Saitama University have used a laser beam to precisely fabricate a network of protein fibers. Their discovery was recently reported in Advanced Science.

The shape of living cells is determined by an internal network of protein fibers called a cytoskeleton. The cytoskeletal structure is dynamic, as the key nodes for cell function shift over time. One such cell function can be witnessed with motor proteins, which convert chemical energy into mechanical work. These proteins walk along cytoskeletal tracks to drive muscle contraction and transport components across the cell.

Enzymes that assemble into droplets can speed up cellular reactions

Within the past decade, biologists have discovered that one strategy cells use to keep their contents organized is a phenomenon known as phase separation.

Similar to the way oil forms droplets that float in a vinegar solution, proteins inside cells can phase separate to form highly concentrated droplets that keep them organized within the cell. In a new study, MIT researchers have now shown that this droplet formation is critical for controlling the function of a class of enzymes called kinases.

Severe obesity in human HFpEF alters contractile protein function and organization

Heart failure with preserved ejection fraction (HFpEF) causes substantial morbidity and mortality and has few effective therapies. Its phenotype has changed over time, with morbid obesity and metabolic defects supplanting hypertension and cardiac hypertrophy. We reveal that cardiomyocytes from patients with severe obesity and HFpEF have very depressed contractile reserve, including reduced calcium-and length-stimulated tension, power, and myosin activation compared with less-obese HFpEF and nonfailing (NF) controls with or without obesity but similar to those with advanced HF and reduced ejection fraction. Myocyte defects correlate with body mass index and exercise hemodynamics in patients with HFpEF but not NF and appear reversible upon weight loss. Increased troponin I phosphorylation at threonine 181 occurs only in heart failure with obesity, contributing to sarcomere dysfunction.

An ensemble pipeline, PhageHost, for phage tail fiber discovery and accurate Klebsiella pneumoniae host prediction using protein language models

Wu et al. present an ensemble pipeline, PhageHost, comprising a protein language model, TailSeek, for tail fiber detection from phage and prophage genomes and a deep learning model, HostBuster, that integrates tail fiber features with host information to predict the lytic potential of phage–K. pneumoniae pairs.

AI ‘super-antigen’ vaccine could protect against whole families of viruses

A groundbreaking new vaccine technology using artificial intelligence could offer immunity against entire families of viruses and protect against future mutations with a single injection.

Researchers say this could prevent future pandemics before they emerge, saving millions of lives and sparing countries from the necessity of lockdowns.

A “super-antigen” has been developed through AI machine learning that meticulously analyses past and current outbreaks to pinpoint the essential elements for the survival of viruses.

Robin Hanson (part 2): Social Science or Extremist Politics in Disguise?!

What happens when an economist starts designing a future society?

Thirteen years ago, I sat down with Robin Hanson for a second time. It became the most vigorous debate ever recorded.

I rarely disagree with a guest. With Robin, I disagreed more than I ever had.

Here is what unsettled me. His work on the Em Economy reads like social science. It uses the language of markets, incentives, and equilibrium. But underneath the economic reasoning sit choices that are not economic at all. Policies of social discrimination. The full privatization of law and punishment. Minds run a thousand times faster, and handed a thousand times more voting power. Emulations deleted when they cannot pay their storage fees.

These are not technical footnotes. They are ethical and political decisions wearing the costume of impartial analysis.

Adam Smith, the father of economics, was first a moral philosopher. He understood where the tools of his discipline stop being useful and start being dangerous.

Continue reading “Robin Hanson (part 2): Social Science or Extremist Politics in Disguise?!” | >

Why energy fades with age: Missing membrane lipid may destabilize mitochondria

Why do cells age—and why do we lose our energy and vitality as we get older? This question is one of the central challenges of modern biomedicine. The focus is particularly on mitochondria—tiny cellular organelles long known as the cell’s powerhouses but now understood as dynamic control centers that not only produce energy, but also coordinate cellular communication, adaptation, and many of the processes essential for life.

They supply us with the energy that our body needs for movement, growth, and repair processes. But as we age, these powerhouses begin to slow down. It has long been known that their function declines with age. But until now, the mechanisms driving this gradual decline have been poorly understood.

Focus on membrane lipids For a long time, it was assumed that genetic damage within the mitochondria themselves was primarily responsible. A study now published in Nature Communications by an international research team led by Dr. Maria Ermolaeva of the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena provides a surprising answer to this question: A key factor appears to be the imbalance in the structure of the mitochondrial network, which is caused by the absence of a major lipid in the membrane composition.

/* */