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A homologue of vertebrate lamin B genes has been identified in Hydra, yet no efforts have been reported addressing the role of Lamin in cnidarian longevity. Here we present detailed analysis of the single Hydra lamin gene (hyLMN), its expression pattern,
and distribution and function of its protein product (HyLMN). We demonstrate that proliferation of stem cells in Hydra is robust against the disturbance of Lamin expression and localization. While Lamin is indispensable for Hydra, the stem cells tolerate
overexpression, downregulation, and mislocalization of Lamin, and disturbances in the nuclear envelope structure. This extraordinary robustness may underlie the indefinite self-renewal capacity of stem cells and the non-senescence of Hydra. A relatively
low complexity of the nuclear envelope architecture might allow for the observed extreme lifespans of Hydra, while an increasing complexity of the nuclear architecture in bilaterians resulted in restricted lifespans.

Alcor Receives 5 Million Donation https://www.fightaging.org/archives/2018/05/alcor-receives-5-million-donation/

Today's good news is that the Alcor Life Extension Foundation, one of the two oldest US cryonics providers, has received a 5 million donation. Like a number of recent donations in our broader community, this originates from an individual who has done
well in the growth of cryptocurrencies. I think that this philanthropy is a sign of things to come; these newly wealthy individuals are, on balance, younger and less set in their ways than those who come to wealth via the slower and more traditional
means. They will be, accordingly, more adventurous, more disruptive, more supportive of causes that have a high utility but are not yet mainstream. This is all to the good, I feel.

This donation is an enormous sum for the non-profit cryonics community - it is a significant fraction of the existing Alcor assets, near all of which are locked up to support the long-term commitments of providing for its members. Cryonics is just as
important to the cause of minimizing human death as the forms of medical biotechnology more usually featured here at Fight Aging! Sadly, it is also far worse off when it comes to the available resources, particular in the very necessary endeavor of
research and development, to improve the state of the art, and produce a viable, self-sustaining industry based on reversible low-temperature storage of tissues. I would like to see this state of affairs change for the better, and this donation is a
sizable first step on that road.

I am delighted to announce that Alcor has received a stunning 5,000,000 contribution to fund cryonics research. Alcor member Brad Armstrong (A-3000), came to visit Alcor in November 2016. After a tour and long and fascinating chat, before he left I
suggested that he finally sit down and sign the membership paperwork. We would provide the witnesses and the Notary Public. 90 minutes later, Brad was done and handed us a check, making him a member. (See? It's not as difficult as you think.)

Fast forward to April 2018. Brad's assistant called to say that Brad wanted to make a major contribution to Alcor for the purposes of cryonics research. When I called Brad, I was immediately reminded that he is a down-to-earth, easygoing fellow who wants
cryonics to work and is eager to fund what he knows matters. Brad is an enthusiast of cryptocurrencies and an admirer of Hal Finney - the first recipient and early developer of Bitcoin - and an Alcor member cryopreserved in August 2014. The 5 million
research contribution is being held in the name of the "Hal Finney Cryonics Research Fund".

On behalf of Alcor and the cryonics effort in general, I want to say thank you. But how can I possibly express those thanks adequately? With a gift of this magnitude comes the responsibility of managing and spending it wisely for maximum impact. Until
the Alcor board and Research Group determine how best to hold and use this funding, I have moved it from Alcor's bank account into a money market fund. Stay tuned as we determine how to use this remarkable influx of funding to boost Alcor's cryonics
research.

A Review of Growth Hormone in Aging https://www.fightaging.org/archives/2018/05/a-review-of-growth-hormone-in-aging/

The author of this open access review of the study of growth hormone in aging is one of the eminent experts in this part of the field, noted for work on various loss of function mutant mice, lacking either functional growth hormone or functional growth
hormone receptor genes. The current record for mouse longevity is held by a growth hormone knockout variant: these mice wouldn't survive in the wild, as they are small and vulnerable to cold, but they live 60-70% longer than their unmodified peers in the
laboratory.

It is well documented that circulating levels of GH decline with age in various mammalian species, including humans, domestic dogs, and laboratory rodents. Yet in laboratory mice, disruption of growth hormone (GH) signaling leads to a remarkable
extension of longevity. These findings were hard to interpret and were originally received with some skepticism because they implied that normal actions of a hormone have significant 'costs' in terms of longevity, and that a gross defect in the
functioning of the endocrine system can have striking benefits for healthy survival. However, the evidence that absence of GH signaling extends longevity of mice is strong, reproducible, and now generally accepted.

Several aspects of the findings in GH-deficient and GH-resistant mice deserve particular emphasis. First, the significant extension of longevity in these animals is reproducible and not limited to a particular laboratory, diet, or genetic background.
Second, lifespan is extended in both females and males. Third, extension of longevity is associated with a similarly striking extension of healthspan. Fourth, the magnitude of the increase in longevity exceeds the effects of most genetic, pharmacological,
or dietary interventions that have anti-aging effects in mice.

A recent study examined longevity of mice lacking both GH and functional GH receptors. While these tiny 'double mutants' were remarkably long-lived compared to their normal siblings, they did not live significantly longer than mice lacking only GH or
only GH receptors. In females, survival curves of GH-deficient Ames dwarf, GH-resistant GHRKO, and 'double mutant' (df/KO) animals were nearly identical.

The importance of GH signaling in the control of murine lifespan is further emphasized by the evidence that disruption of signaling events 'downstream' from GH and its receptor also extends longevity. Early findings of extended longevity of female mice
heterozygous for the deletion of IGF-1 receptor were confirmed and extended in further studies. Major increase of longevity was seen in mice in which amount of bioavailable IGF-1 was reduced at the tissue level by germline or adult disruption of the gene
coding for pregnancy associated plasma protein A, an enzyme degrading IGF-1 binding protein. Significant and reproducible extension of longevity was also produced by pharmacological suppression of the activity of mechanistic target of rapamycin, a kinase
regulated by GH and IGF1.

Importantly, conclusions concerning pro-aging effects of normal or elevated GH based on studies in mutant, gene knockout, transgenic, or drug treated mice appear to apply to genetically normal mice and to other mammalian species. Multiple studies
reported negative association of adult body size (a strongly GH- and IGF-1-dependent trait) with longevity in comparisons of different mouse strains, selected lines, and individual animals.

The Damage Done by a Lack of Exercise, and Digging Yourself Out of the Hole https://www.fightaging.org/archives/2018/05/the-damage-done-by-a-lack-of-exercise-and-digging-yourself-out-of-the-hole/

How much harm is done - and how quickly - by failing to maintain an exercise program? How long does it take to reverse those consequences? No-one has the final answer to those questions, firm numbers derived from the way in which the human body functions.
We can look at the results of studies such as this one with some interest, however. We might compare this with studies of weight and mortality, in which the evidence suggests that lasting harm is done by carrying excess fat tissue over years, even if
lost later.

By analyzing reported physical activity levels over time in more than 11,000 American adults, researchers conclude that increasing physical activity to recommended levels over as few as six years in middle age is associated with a significantly decreased
risk of heart failure. The same analysis found that as little as six years without physical activity in middle age was linked to an increased risk of the disorder. "In everyday terms our findings suggest that consistently participating in the recommended
150 minutes of moderate to vigorous activity each week, such as brisk walking or biking, in middle age may be enough to reduce your heart failure risk by 31 percent. Additionally, going from no exercise to recommended activity levels over six years in
middle age may reduce heart failure risk by 23 percent."

The researchers caution that their study was observational, meaning the results can't and don't show a direct cause-and-effect link between exercise and heart failure. But the trends observed in data gathered on middle-aged adults suggest that it may
never be too late to reduce the risk of heart failure with moderate exercise. "Unlike other heart disease risk factors like high blood pressure or high cholesterol, we don't have specifically effective drugs to prevent heart failure, so we need to
identify and verify effective strategies for prevention and emphasize these to the public." There are drugs used to treat heart failure, such as beta blockers and ACE inhibitors, but they are essentially "secondary" prevention drugs, working to reduce
the heart's workload after dysfunction is already there.

The researchers used data already gathered from 11,351 participants in the long term Atherosclerosis Risk in Communities (ARIC) study, recruited from 1987 to 1989. The participants' average age was 60, and 57 percent were women. Participants were
monitored annually for an average of 19 years for cardiovascular disease events such as heart attack, stroke, and heart failure using telephone interviews, hospital records and death certificates. Over the course of the study there were 1,693
hospitalizations and 57 deaths due to heart failure.

In addition to those measures, at the first and third ARIC study visits (six years apart), each participant filled out a questionnaire, which asked them to evaluate their physical activity levels, which were then categorized as poor, intermediate or "
recommended," in alignment with guidelines issued by the American Heart Association. The "recommended" amount is at least 75 minutes per week of vigorous intensity or at least 150 minutes per week of moderate intensity exercise. One to 74 minutes per
week of vigorous intensity or one to 149 minutes per week of moderate exercise per week counted as intermediate level activity. And physical activity qualified as "poor" if there was no exercise at all.

Heart failure risk decreased by about 12 percent in the 2,702 participants who increased their physical activity category from poor to intermediate or recommended, or from intermediate to recommended, compared with those with consistently poor or
intermediate activity ratings. Conversely, heart failure risk increased by 18 percent in the 2,530 participants who reported decreased physical activity from visit one to visit three, compared with those with consistently recommended or intermediate
activity levels.

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