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Ruim 900.000 euro voor nieuwe behandeling tegen slagaderverkalking

How do we slow down atherosclerosis? Researcher Amanda Foks believes this is possible by eliminating aging immune cells. This would represent a completely new treatment for heart attacks and strokes. For this research, she has received the Established Investigator Dekker Grant from the Dutch Heart Foundation.


Hoe remmen we slagaderverkalking af? Onderzoeker Amanda Foks denkt dat dit mogelijk is door verouderde afweercellen uit te schakelen. Dat zou een geheel nieuwe behandeling tegen hart-en herseninfarcten zijn. Voor dit onderzoek ontvangt ze de Established Investigator Dekkerbeurs van de Hartstichting.

Slagaderverkalking ontstaat doordat vetten en cellen zich jarenlang ophopen in de vaatwand. Vaak merk je daar niets van, totdat zo’n verdikking plotseling scheurt. Dan kan er acuut een hart-of herseninfarct ontstaan.

Met de leeftijd neemt het risico toe: bloedvaten worden minder soepel en het afweersysteem werkt minder goed, waardoor ontstekingen ontstaan. Die ontstekingen versnellen juist weer de slagaderverkalking.

TMAO Is Bad For Health, But Can Be Reduced (21-Test Analysis)

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Discount Links/Affiliates:
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At-Home Metabolomics: https://www.iollo.com?ref=michael-lustgarten.
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NAD+ Quantification: https://www.jinfiniti.com/intracellular-nad-test/

Muscle dysmorphia in adolescents and young adults

Body image concerns among adolescent boys and young men are increasingly recognised as societal ideals shift towards a lean, muscular physique. In severe cases, these pressures can lead to muscle dysmorphia, a specifier of body dysmorphic disorder marked by preoccupation with being too small or insufficiently muscular. Adolescents and young adults are developmentally vulnerable and might be at higher risk for a variety of eating-related and body image-related concerns, including muscle dysmorphia.

New Breakthrough to Restore Aging Joints Could Help Treat Osteoarthritis

A study in mice by researchers from Stanford University has traced the loss of cartilage that comes with aging to a single protein, pointing to treatments that may one day restore mobility and ease discomfort in seniors.

The protein 15-PGDH has previously been extensively linked to aging: it becomes more abundant as we get older, and interferes with the molecules that repair tissue and reduce inflammation.

That led scientists to consider whether 15-PGDH might be involved in osteoarthritis, where stress on joints leads to the breakdown of collagen in cartilage, causing inflammation and pain.

Discrimination of normal from slow-aging mice by plasma metabolomic and proteomic features

Tests that can predict whether a drug is likely to extend mouse lifespan could speed up the search for anti-aging drugs. We have applied a machine learning algorithm, XGBoost regression, to seek sets of plasma metabolites (n = 12,000) and peptides (n = 17,000) that can discriminate control mice from mice treated with one of five anti-aging interventions (n = 278 mice). When the model is trained on any four of these five interventions, it predicts significantly higher lifespan extension in mice exposed to the intervention which was not included in the training set. Plasma peptide data sets also succeed at this task. Models trained on drug-treated normal mice also discriminate long-lived mutant mice from their respective controls, and models trained on males can discriminate drug-treated from control females.

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