¿Pueden unas nanopartículas de sílice frenar el cáncer de próstata? #CancerDeProstata #Nanoparticulas #Oncologia #Inmunoterapia #Ferroptosis #InvestigacionMedica #Ciencia #Salud #Medicina #InvestigacionContraElCancer #Tumores #felizmiercoles #17dejunio
https://donporque.com/nanoparticulas-contra-el-cancer-de-prostata/
Agenzia Nova: Iran: ministero Esteri Qatar, false le voci su presunte offerte di denaro a Teheran per accettare accordo
26 mag 04:40 - (Agenzia Nova) - Il Qatar ha respinto le indiscrezioni secondo cui all'Iran sarebbe stato offerto un pagamento in denaro per... (Res)
Iran, Trump “Enriched uranium must be delivered to the US or destroyed on the spot”
ROME (ITALPRESS) – “Enriched uranium will be immediately delivered to the United States to be returned home and destroyed or, preferably, in collaboration and coordination with the Islamic Republic of Iran, destroyed on site or, in another acceptable location, with the Atomic Energy Commission, or its equivalent, witness to this process and event.” This was announced on Truth by the President of the United States, Donald Trump. (ITALPRESS).
Why does the Greenland shark live longer?
Great White Shark - The Greenland shark, considered the longest-lived vertebrate known with an estimated lifespan of almost 400 years, possesses genetic characteristics that could explain its extraordinary resistance to aging and disease.
This emerges from a study published in the journal Proceedings of the National Academy of Sciences (PNAS) by Kaiqiao Yang, Kazuya Nishiwaki, Hideaki Mizobata and Shigeharu Kinoshita of the University of Tokyo, together with an international group of researchers.
The Greenland Shark Genome
The researchers have carried out the first complete chromosomal-level genomic assembly of the Greenland shark, a species adapted to the deep, cold environments of the Arctic and characterized by an extremely slow metabolism. The reconstructed genome measures approximately 5.9 gigabases, with a high level of genetic completeness of 96.7 percent.
Biological Mechanisms of Longevity
The analyses highlighted several biological mechanisms associated with extreme longevity, including strengthening of immune defenses, resistance to tumors, and particularly efficient DNA repair systems.
The Role of Histone H1.0
The researchers also identified specific amino acid modifications in the histone protein H1.0, involved in chromatin stability, which could contribute to protecting genetic material from accumulated molecular damage over centuries.
Protection from Cellular Degradation
According to the authors, these characteristics could help the Greenland shark overcome the normal biological limits of lifespan. “The amino acid substitutions observed in the globular domain of histone H1.0 could improve chromatin stability,” explain the researchers, indicating a possible mechanism of protection against age-related cellular degradation.
Longevity and Ferroptosis
The study also suggests a possible link between longevity and ferroptosis, a particular form of cell death regulated by iron and oxidative processes. The distinctive genetic repertoire of the species, the researchers observe, provides a foundation for future hypotheses on the role of ferroptosis in aging processes.
Evolution and Populations
In addition to aspects related to the biology of longevity, the work also reconstructs the historical dynamics of Greenland shark populations and the closely related species *Somniosus pacificus*, offering new information on the evolution of cartilaginous sharks.
A Resource for Future Research
According to the authors, the availability of this genome represents an important resource for evolutionary studies as well as research into the genetic mechanisms of aging. “These genomic analyses offer new perspectives on the molecular basis of the Greenland shark’s exceptional longevity,” the researchers conclude, emphasizing how the results can contribute to the development of future research on human aging and age-related diseases.
#Greenland #KaiqiaoYang #KazuyaNishiwaki #Mizobata #ShigeharuKinoshita #first #Arctic #967percent #Ferroptosis #Somniosus
https://www.agi.it/scienza/news/2026-05-26/squalo-genoma-longevo-37225681/
Vitamin B2 Supports Cancer Cells by Protecting Them from Ferroptosis, Study Finds
📰 Original title: Scientists discover vitamin B2 may help cancer cells survive
🤖 IA: It's clickbait ⚠️
👥 Users: It's clickbait ⚠️
View full AI summary: https://en.killbait.com/vitamin-b2-supports-cancer-cells-by-protecting-them-from-ferroptosis-study-finds.html?utm_source=mastodon_world&utm_medium=social&utm_campaign=killbait.mastodon_world
Researchers at the University of Würzburg have found that vitamin B2, also known as riboflavin, may inadvertently help cancer cells survive. While essential for human health and normally protective against cellular oxidative damage, riboflavin metabolism appears to shield cancer cells from ferroptosis, a form of programmed cell death that helps prevent tumor growth. The study, published in Nature Cell Biology, shows that vitamin B2 supports a protein called FSP1, which protects cells from oxidative stress, allowing tumors to resist destruction. In laboratory experiments, scientists tested roseoflavin, a naturally occurring compound similar to vitamin B2, and found it could successfully trigger ferroptosis in cancer cells, even at low concentrations. The research suggests that inhibiting vitamin B2 metabolism could be a potential strategy for new cancer therapies. Beyond oncology, the findings may also improve understanding of diseases involving excessive or insufficient cell death, such as neurodegenerative disorders and tissue damage after organ transplants or ischemic injuries. Future work will focus on developing more effective inhibitors of riboflavin metabolism and testing them in preclinical cancer models, offering a promising avenue for targeted cancer treatments.
Vitamin B2 Supports Cancer Cells by Protecting Them from Ferroptosis, Study Finds
📰 Original title: Scientists discover vitamin B2 may help cancer cells survive
🤖 IA: It's clickbait ⚠️
👥 Users: It's clickbait ⚠️
View full AI summary: https://en.killbait.com/vitamin-b2-supports-cancer-cells-by-protecting-them-from-ferroptosis-study-finds.html?utm_source=mastodon_social&utm_medium=social&utm_campaign=killbait.mastodon_social
Researchers at the University of Würzburg have found that vitamin B2, also known as riboflavin, may inadvertently help cancer cells survive. While essential for human health and normally protective against cellular oxidative damage, riboflavin metabolism appears to shield cancer cells from ferroptosis, a form of programmed cell death that helps prevent tumor growth. The study, published in Nature Cell Biology, shows that vitamin B2 supports a protein called FSP1, which protects cells from oxidative stress, allowing tumors to resist destruction. In laboratory experiments, scientists tested roseoflavin, a naturally occurring compound similar to vitamin B2, and found it could successfully trigger ferroptosis in cancer cells, even at low concentrations. The research suggests that inhibiting vitamin B2 metabolism could be a potential strategy for new cancer therapies. Beyond oncology, the findings may also improve understanding of diseases involving excessive or insufficient cell death, such as neurodegenerative disorders and tissue damage after organ transplants or ischemic injuries. Future work will focus on developing more effective inhibitors of riboflavin metabolism and testing them in preclinical cancer models, offering a promising avenue for targeted cancer treatments.
Ferroptosis, an iron-dependent form of regulated cell death (RCD) driven by lipid peroxidation, has been extensively studied since its conceptualization in 2012 and has been suggested as a therapeutic target in many cancers and degenerative diseases. However, three fundamental questions remain unanswered about ferroptosis. First, the mechanisms by which cells execute death during ferroptosis remain elusive: The key role of lipid peroxides in triggering ferroptosis is established, but how this results in the death of a cell remains unclear. Second, the physiological role of ferroptosis throughout the human life cycle is unclear; currently, there is evidence for ferroptosis in early development, immunity, aging, and tumor suppression, but not in many other aspects of physiology. Third, and finally, the intersection between ferroptosis and other RCD modalities, such as apoptosis, necroptosis, pyroptosis, and autophagic cell death, is necessary for understanding how ferroptosis integrates into networks controlling cellular fate. Addressing these gaps in knowledge is essential for building a comprehensive understanding of this mode of cell death, as well as translating ferroptosis knowledge into effective therapeutics.
Researchers show how a defect in the #enzyme #GPX4 can trigger #ferroptosis and lead to neuronal loss in certain forms of #dementia. The work provides new insights into cell protection mechanisms: http://go.tum.de/142494
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