Lifeboat Foundation

First of all, they have to have survived the impact. Laboratory tests have shown that frozen specimens of the Hypsibius dujardini species travelling at 3,000 km/h in a vacuum were fatally damaged when they smashed into sand. However, they survived impacts of 2,600 km/h or less – and their “hard landing” on the Moon, unwanted or not, was far slower.

The Moon’s surface is not protected from solar particles and cosmic rays, particularly gamma rays, but here too, the tardigrades would be able to resist. In fact, Robert Wimmer-Schweingruber, professor at the University of Kiel in Germany, and his team have shown that the doses of gamma rays hitting the lunar surface were permanent but low compared with the doses mentioned above – 10 years’ exposure to Lunar gamma rays would correspond to a total dose of around 1 Gy.

But then there’s the question of “life” on the Moon. The tardigrades would have to withstand a lack of water as well as temperatures ranging from −170 to −190°C during the lunar night and 100 to 120°C during the day. A lunar day or night lasts a long time, just under 15 Earth days. The probe itself wasn’t designed to withstand such extremes and even if it hadn’t crashed, it would have ceased all activity after just a few Earth days.

Your immune system should ideally recognize and attack infectious invaders and cancerous cells. But the system requires safety mechanisms, or brakes, to keep it from damaging healthy cells. To do this, T cells—the immune system’s most powerful attackers—rely on immune “checkpoints” to turn immune activation down when they receive the right signal. While these interactions have been well studied, a research team supported in part by NIH has made an unexpected discovery into how a key immune checkpoint works, with potentially important implications for therapies designed to boost or dampen immune activity to treat cancer and autoimmune diseases.¹

The checkpoint in question is a protein called programmed cell death-1 (PD-1). Here’s how it works: PD-1 is a receptor on the surface of T cells, where it latches onto certain proteins, known as PD-L1 and PD-L2, on the surface of other cells in the body. When this interaction occurs, a signal is sent to the T cells that stops them from attacking these other cells.

Cancer cells often take advantage of this braking system, producing copious amounts of PD-L1 on their surface, allowing them to hide from T cells. An effective class of immunotherapy drugs used to treat many cancers works by blocking the interaction between PD-1 and PD-L1, to effectively release the brakes on the immune system to allow the T cells to unleash an assault on cancer cells. Researchers have also developed potential treatments for autoimmune diseases that take the opposite tact: stimulating PD-1 interaction to keep T cells inactive. These PD-1 “agonists” have shown promise in clinical trials as treatments for certain autoimmune diseases.

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Researchers Prof. Judith Haendeler from the Medical Faculty and the molecular biologist Prof. Joachim Altschmied from the Department of Biology, together with their teams, have shown for the first time in the cardiovascular system that telomerase reverse transcriptase (TERT) within the mitochondria, the powerhouses of the cells, has a protective function in myocardial infarction. This work, which was performed together with other groups from the University Hospital Düsseldorf and the University Hospital Essen within the frame of the Collaborative Research Center 1,116, was recently published in the journal Circulation.

Cardiac muscle cells benefit from the increased mitochondrial function and are protected from cell death. Other cell types also profit from increased mitochondrial function such as fibroblasts, which are essential for stable scarring after an infarction, and endothelial cells, which are needed for vascularization and thus blood supply in the infarct area.

Continue reading “‘Immortality protein’ within the mitochondria offers protection in myocardial infarction” »

Aging reversed in living cells through rejuvenation techniques.

Rejuvenation and partial reprogramming are two frontier areas in the field of aging. Here, the authors summarize advances in these fields and suggest future directions for research and therapy.

face_with_colon_three year 2023 The ultimate goal is to use crispr to modify genetic programming for eternal life this an example of heart age reversal.

An anti-aging gene found in centenarians has been shown to reverse the heart’s biological age by 10 years. This groundbreaking discovery, published in the journal Cardiovascular Research and led by scientists from the University of Bristol and MultiMedica Group in Italy, offers a potential target for heart failure patients.

Individuals who carry healthy mutant genes, commonly found in populations known for exceptional longevity such as the “blue zones,” often live to 100 years or more and remain in good health. These carriers are also less susceptible to cardiovascular complications. Scientists funded by the British Heart Foundation believe the gene helps keep their hearts youthful by guarding against diseases related to aging, such as heart failure.

Continue reading “Anti-Aging Gene Shown To Rewind Heart Age by 10 Years” »

Gene therapy may be the best hope for curing retinitis pigmentosa (RP), an inherited condition that usually leads to severe vision loss and blinds 1.5 million people worldwide.

But there’s a huge obstacle: RP can be caused by mutations in over 80 different genes. To treat most RP patients with gene therapy, researchers would have to create a therapy for each gene—a nearly impractical task using current gene therapy strategies.

A more universal treatment may be forthcoming. Using CRISPR-based genome engineering, scientists at Columbia University Vagelos College of Physicians and Surgeons are designing a gene therapy with the potential to treat RP patients regardless of the underlying genetic defect.

Valter Longo grew up in Italy and has been studying longevity for 35 years. Here’s what he says is the No. 1 contributing factor to a long life.

Certain RNA molecules in the nerve cells in the brain last a life time without being renewed. Neuroscientists from Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) have now demonstrated that this is the case together with researchers from Germany, Austria and the USA. RNAs are generally short-lived molecules that are constantly reconstructed to adjust to environmental conditions. With their findings that have now been published in the journal Science, the research group hopes to decipher the complex aging process of the brain and gain a better understanding of related degenerative diseases.

Most cells in the human body are regularly renewed, thereby retaining their vitality. However, there are exceptions: the heart, the pancreas and the brain consist of cells that do not renew throughout the whole lifespan, and yet still have to remain in full working order. “Aging neurons are an important risk factor for neurodegenerative illnesses such as Alzheimer’s,” says Prof. Dr. Tomohisa Toda, Professor of Neural Epigenomics at FAU and at the Max Planck Center for Physics and Medicine in Erlangen. “A basic understanding of the aging process and which key components are involved in maintaining cell function is crucial for effective treatment concepts:”

In a joint study conducted together with neuroscientists from Dresden, La Jolla (USA) and Klosterneuburg (Austria), the working group led by Toda has now identified a key component of brain aging: the researchers were able to demonstrate for the first time that certain types of ribonucleic acid (RNA) that protect genetic material exist just as long as the neurons themselves. “This is surprising, as unlike DNA, which as a rule never changes, most RNA molecules are extremely short-lived and are constantly being exchanged,” Toda explains.