Kewl… ~~~ “Led by Associate Professor Alfredo Franco-Obregón from the NUS Institute for Health Innovation and Technology (iHealthtech), the team found that a protein known as TRPC1 responds to weak oscillating magnetic fields. Such a response is normally activated when the body exercises. This responsiveness to magnets could be used to stimulate muscle recovery, which could improve the life quality for patients with impaired mobility, in an increasingly aging society.”

---

As people age, they progressively lose muscle mass and strength, and this can lead to frailty and other age-related diseases. As the causes for the decline remain largely unknown, promoting muscle health is an area of great research interest. A recent study led by the researchers from NUS has shown how a molecule found in muscles responds to weak magnetic fields to promote muscle health.

Led by Associate Professor Alfredo Franco-Obregón from the NUS Institute for Health Innovation and Technology (iHealthtech), the team found that a protein known as TRPC1 responds to weak oscillating magnetic fields. Such a response is normally activated when the body exercises. This responsiveness to magnets could be used to stimulate muscle recovery, which could improve the life quality for patients with impaired mobility, in an increasingly aging society.

“The use of pulsed magnetic fields to simulate some of the effects of exercise will greatly benefit patients with muscle injury, stroke, and frailty as a result of advanced age,” said lead researcher Assoc Prof Franco-Obregón, who is also from the NUS Department of Surgery.

According to new research from CCR scientists, embryonic stem cells have a unique way of protecting their telomeres, the structures at the ends of chromosomes that shorten with every cell division. A research team led by Eros Lazzerini Denchi, Ph.D., an NIH Stadtman investigator in CCR’s Laboratory of Genomic Integrity, has found that rather than treating exposed telomeres as damaged DNA as most cells do, embryonic stem cells call on genes typically used only during the earliest stage of development to stave off unwanted DNA repair. The team’s findings, which come from studies of mouse embryonic stem cells, are reported November 25, 2020, in Nature.

By revealing an unexpected way cells can protect their telomeres, the new findings may help explain a survival strategy employed by some cancer cells, which must find a way to circumvent growth limits imposed by the natural shortening of telomeres that occurs as we age.

Embryonic stem cells, which arise early in an embryo’s development, have a unique capacity to become virtually any of the body’s specialized cell types. Lazzerini Denchi and colleagues first discovered their unusual approach to protecting telomeres when they found that the cells can survive without a protein called TRF2, which binds to and protects chromosome tips. The protein is absolutely essential for hundreds of different types of cells. Without it, exposed chromosome tips trigger faulty activation of DNA damage repair pathways, which stitch the unprotected ends together. Chromosomes fuse together and cells lose the ability to divide. But when Lazzerini Denchi’s team removed TRF2 from embryonic stem cells, chromosomes maintained their integrity and the cells continued to proliferate.

Here’s my latest video!

---

Meta-analysis for the association between HDL with all-cause mortality risk has identified HDL levels 55 — 60 mg/dL range as optimal. However, that data includes subjects up to 85y-in the video, I present data for 85y — 115yr olds that additionally suggests HDL in the 55 — 60 mg/dL range as optimal. In addition, I show my own HDL data over the past 15 years (n=34), the correlation for HDL with my diet, and how I plan on consistently increasing my 15-year average HDL of ~44 mg/dL to the 50’s.