Frank Jennings Tipler is a mathematical physicist and cosmologist, holding a joint appointment in the Departments of Mathematics and Physics at Tulane University. He holds a BS in Physics from MIT and a PhD from the University of Maryland.
Watch his interview below on eternal life. To watch more interviews on this topic, click here: https://bit.ly/2wcTT1N
A molecule produced by the body during fasting or calorie restriction has anti-aging effects on the vascular system, which could reduce the occurrence and severity of human diseases related to blood vessels, such as cardiovascular disease, according to a study led by Georgia State University.
“As people become older, they are more susceptible to disease, like cancer, cardiovascular disease and Alzheimer’s disease,” said Dr. Ming-Hui Zou, senior author of the study. “Age is the most important so-called risk factor for human disease. How to actually delay aging is a major pathway to reducing the incidence and severity of human disease.
A new Cornell University-led study finds that the genome for a widely researched worm, on which countless studies are based, was flawed. Now, a fresh genome sequence will set the record straight and improve the accuracy of future research.
When scientists study the genetics of an organism, they start with a standard genome sequenced from a single strain that serves as a baseline. It’s like a chess board in a chess game: every board is fundamentally the same.
One model organism that scientists use in research is a worm called Caenorhabditis elegans. The worm—the first multicellular eukaryote (animal, plant or fungus) to have its genome sequenced—is easy to grow and has simple biology with no bones, heart or circulatory system. At the same time, it shares many genes and molecular pathways with humans, making it a go-to model for studying gene function, drug treatments, aging and human diseases such as cancer and diabetes.
Regenerative medicine and stem cells are often uttered within the same breath, for good reason.
In animal models, stem cells have reliably reversed brain damage from Parkinson’s disease, repaired severed spinal cords, or restored damaged tissue from diabetes, stroke, blood cancers, heart disease, or aging-related tissue damage. With the discovery of induced pluripotent stem cells (iPSCs), in which skin and other tissue can be reversed into a stem cell-like state, the cells have further been adapted into bio-ink for 3D printing brand new organs.
Yet stem cells are hard to procure, manufacture, and grow. And unless they’re made from the patient’s own cell supply—massively upping production costs—they’re at risk of immune rejection or turning cancerous inside their new hosts.
A number of physiological and psychological changes occur as we age, and many studies have shown that our gut microbiome also changes as we grow older. A fascinating new study is suggesting that a shift in gut bacteria in our middle-age could trigger a process that plays a role in cognitive decline in our later years. And diet may be the key to encouraging the growth of beneficial bacteria that benefit healthy brain aging.
UCLA researchers have discovered a new way to activate the stem cells in the hair follicle to make hair grow. The research, led by scientists Heather Christofk and William Lowry, may lead to new drugs that could promote hair growth for people with baldness or alopecia, which is hair loss associated with such factors as hormonal imbalance, stress, aging or chemotherapy treatment.
The research was published in the journal Nature Cell Biology.
Hair follicle stem cells are long-lived cells in the hair follicle; they are present in the skin and produce hair throughout a person’s lifetime. They are “quiescent,” meaning they are normally inactive, but they quickly activate during a new hair cycle, which is when new hair growth occurs. The quiescence of hair follicle stem cells is regulated by many factors. In certain cases they fail to activate, which is what causes hair loss.
Choriocapillary loss is a major cause of neovascular age-related macular degeneration (NV-AMD). Although vascular endothelial growth factor (VEGF) blockade for NV-AMD has shown beneficial outcomes, unmet medical needs for patients refractory or tachyphylactic to anti-VEGF therapy exist. In addition, the treatment could exacerbate choriocapillary rarefaction, necessitating advanced treatment for fundamental recovery from NV-AMD. In this study, Tie2 activation by angiopoietin-2–binding and Tie2-activating antibody (ABTAA) presents a therapeutic strategy for NV-AMD. Conditional Tie2 deletion impeded choriocapillary maintenance, rendering eyes susceptible to NV-AMD development. Moreover, in a NV-AMD mouse model, ABTAA not only suppressed choroidal neovascularization (CNV) and vascular leakage but also regenerated the choriocapillaris and relieved hypoxia. Conversely, VEGF blockade degenerated the choriocapillaris and exacerbated hypoxia, although it suppressed CNV and vascular leakage. Together, we establish that angiopoietin-Tie2 signaling is critical for choriocapillary maintenance and that ABTAA represents an alternative, combinative therapeutic strategy for NV-AMD by alleviating anti-VEGF adverse effects.
Neovascular age-related macular degeneration (NV-AMD) is a leading cause of irreversible vision loss among elderly persons in developed countries. NV-AMD is characterized by the formation of choroidal neovascularization (CNV), an ingrowth of abnormal blood vessels from the choroid through Bruch’s membrane into the sub-retinal pigment epithelium (RPE) or subretinal space. Throughout this ingrowth, abnormal leakages of fluids and bloods occur into the retina, causing vision distortion and loss of central vision (2, 3). To treat neovascular eye diseases including NV-AMD, anti–vascular endothelial growth factor A (VEGF) therapy has largely been used based on the fact that an excessive production of VEGF from hypoxic cells in the retino-choroidal complex is critical in the pathogenesis and features of neovascular eye diseases (3, 4).
