Life and Longevity

Sat Apr 02, 2016 11:13 am

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Life & Longevity / Health Sciences / Biotech :
[scholiums , Links and papers] ------------------------------------

Sat Apr 02, 2016 11:30 am

http://www.humanlongevity.com/category/news-alert/

http://www.humanlongevity.com/

Human Longevity, Inc.

(HLI) is the genomics-based, technology-driven company creating the world’s largest and most comprehensive database of whole genome, phenotype and clinical data. HLI is developing and applying large scale computing and machine learning to make novel discoveries to revolutionize the practice of medicine.

Introducing Human Longevity, Inc. Health Nucleus

https://www.youtube.com/channel/UCljpbbkw7cT1VdZ39ETkibg

Sat Apr 02, 2016 11:38 am

Sens Research Foundation

https://www.youtube.com/user/SENSFVideo/videos

Newsletter Archive

http://www.sens.org/outreach/newsletter-archive

Publications : Life and Longevity 655564803

http://www.sens.org/research/publications

Fri Jun 10, 2016 8:04 am

"Everybody wants to live long, but not to be old."
-- Johnathan Swift 1667-1745

I would not live forever, because we should not
live forever, because if we were supposed to live forever, then we would live forever,
but we cannot live forever, which is why I would not live forever.
-- Miss Alabama in the 1994 Miss USA contest .

Thu Jul 07, 2016 7:53 am

Sat Apr 29, 2017 7:17 pm

https://www.youtube.com/watch?v=JLS1T7lZzS8
https://www.youtube.com/watch?v=JLS1T7lZzS8

Tue Jun 27, 2017 2:06 pm

A conserved NAD+ binding pocket that regulates protein-protein interactions during aging.

NAD+ binding modulates protein interactions
An unexpected function of the oxidized form of nicotinamide adenine dinucleotide (NAD+) could underlie some effects of aging and propensity to age-related diseases. Li et al. found that the protein DBC1 (deleted in breast cancer 1) contains a domain that specifically binds NAD+. Binding of NAD+ inhibited the interaction of DBC1 with PARP1 [poly(adenosine diphosphate–ribose) polymerase 1], an enzyme important in DNA repair. Activity of PARP1 is inhibited by interaction with DBC1. Thus, the reduced abundance of NAD+ associated with aging may decrease PARP1 activity by promoting the interaction of PARP1 with DBC1. This mechanism could help explain the reported rejuvenating actions of NAD+ supplementation in older animals.

Science Friday (March 24) p. 1312

Abstract
DNA repair is essential for life, yet its efficiency declines with age for reasons that are unclear. Numerous proteins possess Nudix homology domains (NHDs) that have no known function. We show that NHDs are NAD+ (oxidized form of nicotinamide adenine dinucleotide) binding domains that regulate protein-protein interactions. The binding of NAD+ to the NHD domain of DBC1 (deleted in breast cancer 1) prevents it from inhibiting PARP1 [poly(adenosine diphosphate–ribose) polymerase], a critical DNA repair protein. As mice age and NAD+ concentrations decline, DBC1 is increasingly bound to PARP1, causing DNA damage to accumulate, a process rapidly reversed by restoring the abundance of NAD+. Thus, NAD+ directly regulates protein-protein interactions, the modulation of which may protect against cancer, radiation, and aging.

Life and Longevity Disarm10

Disarming a rogue agent: When the NAD molecule (red) binds
to the DBC1 protein (beige), it prevents DBC1 from attaching to
and incapacitating a protein (PARP1) that is critical for DNA repair.
(credit: David Sinclair)

http://science.sciencemag.org/content/355/6331/1312

https://www.youtube.com/watch?v=AIX_EhnE3gQ

Sat Jul 01, 2017 8:00 am

Once printed, an inlet and outlet own opposite ends are perfused with fluids, nutrients, and cell
growth factors, which control stem cell differentiation and sustain cell functions. By flowing growth
factors through the vasculature, stem cells can be differentiated into a variety of tissue cell types.

Wed Aug 23, 2017 7:47 am

High-Resolution Patterned Cellular Constructs by Droplet-Based 3D Printing

https://www.nature.com/articles/s41598-017-06358-x

Life and Longevity 41598_2017_6358_Fig2_HTML

confocal micrograph of an artificial tissue containing two populations of embryonic kidney cells
(HEK-293T) printed in the form of an arborized structure within a cube

Tue Nov 07, 2017 4:30 pm

Multigenerational silencing dynamics control cell aging

ΑΜΠΣΤΡΑΚΤ
Cellular aging plays an important role in many diseases, such as cancers, metabolic syndromes, and neurodegenerative disorders. There has been steady progress in identifying aging-related factors such as reactive oxygen species and genomic instability, yet an emerging challenge is to reconcile the contributions of these factors with the fact that genetically identical cells can age at significantly different rates. Such complexity requires single-cell analyses designed to unravel the interplay of aging dynamics and cell-to-cell variability. Here we use microfluidic technologies to track the replicative aging of single yeast cells and reveal that the temporal patterns of heterochromatin silencing loss regulate cellular life span. We found that cells show sporadic waves of silencing loss in the heterochromatic ribosomal DNA during the early phases of aging, followed by sustained loss of silencing preceding cell death. Isogenic cells have different lengths of the early intermittent silencing phase that largely determine their final life spans. Combining computational modeling and experimental approaches, we found that the intermittent silencing dynamics is important for longevity and is dependent on the conserved Sir2 deacetylase, whereas either sustained silencing or sustained loss of silencing shortens life span. These findings reveal that the temporal patterns of a key molecular process can directly influence cellular aging, and thus could provide guidance for the design of temporally controlled strategies to extend life span.

Multigenerational silencing dynamics control cell aging

periodic switching during aging

Sat Jul 07, 2018 10:00 am

some new stats from elizabetta barbi.[italia]

http://science.sciencemag.org/content/360/6396/1459

Logarithmic plot of the exponential “hazard” from ages 65 to 115
starting at age 80, the range of risks of death (blue bars) starts to increase
it’s no longer a fixed probability, as in the traditional “Gompertz” model (black line).
However by age 105, based on data from the new Italian ISTAT model, the risk
actually stops increasing, as shown in dashed black line with orange background)
[[suggesting there’s no known upper limit for h-lifespan.*]]
and the odds of someone surviving from one birthday to the next are roughly 50:50.
(credit: E. Barbi et al., Science)
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Wed Jul 11, 2018 3:00 pm

Keith Lynch remembers 1979-1980

http://space.mit.edu/home/tegmark/everett/everett.html#e23

According to Lynch, Everett's desktop computer, a Radio Shack (Tandy) TRS-80, would occasionally be running something when Everett wasn't around. Lynch gained the impression that this work wasn't business-related but had something to do with physics or math or sheer curiosity.
To Lynch Everett appeared aloof, off doing his own thing, not involved with the day-to-day business of DBS, which included analyzing statistics to look for patterns of racial discrimination, sex discrimination, police brutality, etc., mostly for the Department of Health, Education, and Welfare (though Lynch admits that he could be mistaken, since he was very new to the world of business then).Everett's digital alarm clock played a short synthesized tune at 11:30 every morning, and everybody at DBS had to drop whatever he or she was doing (unless it was very urgent) and eat. What makes Lynch's recollections especially valuable to the reader is that Lynch, more than any other DBS employee, shared with Everett many interests and views in physics, math, logic, paradoxes and religion.Everett's "political philosophy" was very similar to what Harry Browne has stated : One shouldn't waste one's time trying to change the government, since no matter how restrictive government becomes, there will always be ways for a clever person to find loopholes. In fact, the more restrictive it becomes, the more loopholes there will be.Everett was a committed atheist. He once claimed he had a disproof of the Catholic faith. (He chose not to share this "disproof" with Lynch. He said he had shared it once with someone who was strongly Catholic and also strongly committed to logic, and that person was driven to suicide. Everett was afraid that Lynch would promptly use it on Catholics.) Atheist or not, Everett firmly believed that his many-worlds theory guaranteed him immortality: His consciousness, he argued, is bound at each branching to follow whatever path does not lead to death —and so on ad infinitum. (Sadly, Everett's daughter Liz, in her later suicide note, said she was going to a parallel universe to be with her father.Everett believed deeply in the many-worlds theory, and when Lynch argued that this theory was not falsifiable, and therefore was not scientific, he replied that it would be falsified if standard quantum mechanics was falsified.Everett took a great interest in the notorious "unexpected hanging" paradox .[]..Everett, according to Lynch, was great fun to talk with.

Sat Aug 18, 2018 8:30 pm

What have you or I to do with the superstitions of our age? No: we have given up our belief in the soul.[] I am only ten years older than you are, and I am wrinkled, and worn, and yellow.[] I wish you would tell me your secret. To get back my youth I would do anything in the world, except take exercise, get up early, or be respectable. Youth! There is nothing like it. It's absurd to talk of the ignorance of youth. The only people to whose opinions I listen now with any respect are people much younger than myself. They seem in front of me. Life has revealed to them her latest wonder. As for the aged, I always contradict the aged. I do it on principle. If you ask them their opinion on something that happened yesterday, they solemnly give you the opinions current in 1820, when people wore high stocks, believed in everything, and knew absolutely nothing. []
The tragedy of old age is not that one is old, but that one is young.

the picture of Dorian Gray 1889 .

Fri Aug 09, 2019 5:00 pm

Cerebrospinal fluid (CSF) clears toxic metabolites from intercellular spaces in the brain, much as the lymphatic system does in the rest of the body.
The first regions of the brain to be impacted by Alzheimer's disease are cleared by CSF that drains across a porous bone called the cribriform plate.
Aging and life events can occlude the cribriform plate and reduce the CSF-mediated clearance of toxic metabolites from those regions of the brain,
thereby causing plaques and tangles formation. Leucadia’s Arethusta

technology restores CSF flow across the cribriform plate, improving
the clearance of toxic metabolites from the earliest regions of the brain to be affected by Alzheimer's disease.

Doug Ethell - Leucadia Therapeutics Presentation

https://www.youtube.com/watch?v=dhSU7J0QHgk&t=425