Lifeboat Foundation

NYU Abu Dhabi (NYUAD) researchers have uncovered a code that sets the genome of the liver to account for the remarkable ability for this organ to regenerate. This finding offers new insight into how the specific genes that promote regeneration can be activated when part of the liver is removed. These findings have the potential to inform the development of a new form of regenerative medicine that could help non-regenerative organs regrow in mice and humans.

While other animals can regenerate most organs, humans, mice, and other mammals can only regenerate their liver in response to an injury or when a piece is removed. NYUAD researchers hypothesized that the genes that drive regeneration in the liver would be controlled by a specific code that allows them to be activated in response to injury or resection. They home in on the epigenome, which is the modifications on the DNA that alter the gene expression, as opposed to changing the genetic code itself.

Using a mouse liver model, the team of NYUAD researchers, led by Professor of Biology Kirsten Sadler Edepli, identified the elements of the epigenetic code present in quiescent liver cells—cells that are currently not replicating but have the ability to proliferate under the right conditions—that activate specific genes to regenerate. Genes involved in liver cell proliferation are silenced in livers that are not regenerating, but the surprising finding was that they reside in parts of the genome where most genes are active. The researchers found that these pro-regenerative genes were marked with a specific modification—H3K27me3. During regeneration, H3K27me3 is depleted from these genes, enabling their dynamic expression and driving proliferation.

A new $7.9 million seed round boosts Butlr Technologies’ ability to apply its real-time people-sensing technology beyond commercial real estate and retail uses to monitor falls and other movements for active seniors who are aging in place.

Hyperplane led the round, with Founder Collective, Union Labs, 500 Startups, SOSV, E14 Fund, Tectonic Ventures, Scott Belsky, Chad Laurans and Sunny Vu participating.

The new funding comes one year after the Burlingame, California-based proptech company raised $1.2 million in convertible notes, which is included in the $7.9 million. It is developing a platform and Heatic sensors that detect someone’s body heat anonymously to determine occupancy, headcount and activity.

Interested in living longer? You are probably going to get TPE at some point. The Conboys are looking for funding for human trials to produce a product in 3–4 years. Here we have infor on what it is and how it works plus actual human results to date (starting at 10 minutes).

In Part III, Dr Kiprov, discusses the history of moving from the Conboy’s experiments in the lab to the process used in the clinic and reasons for the choices made. He also covers the benefits that he has seen with plasma exchange in the clinic.

Continue reading “Plasma Dilution Potential Benefits & Real Cases Part III | Dr Dobri Kiprov Interview Series” »

A potentially life-saving treatment for heart attack victims has been discovered from a very unlikely source — the venom of one of the world’s deadliest spiders.

A drug candidate developed from a molecule found in the venom of the Fraser Island (K’gari) funnel web spider can prevent damage caused by a heart attack and extend the life of donor hearts used for organ transplants. The discovery was made by a team led by Dr Nathan Palpant and Professor Glenn King from The University of Queensland (UQ) and Professor Peter Macdonald from the Victor Chang Cardiac Research Institute.

Dr Palpant, from UQ’s Institute for Molecular Bioscience (IMB), said the drug candidate worked by stopping a ‘death signal’ sent from the heart in the wake of an attack.

Timestamps:

0:00 How the Rose lab more than doubled the lifespan of Drosophila.
17:20 Use of machine learning (ML) and multi-‘omics to characterize aging, and use of ML to develop interventions.
37:04 Adherence to an ancestral diet in Drosophila extends healthspan relative to their evolutionary recent diet.
40:35 The importance of measuring objective markers of health to determine if one’s diet is best for them.
44:04 Does aging stop, and use of biomarker testing to help decipher/optimize that.
53:33 The importance of characterizing aging for both Drosophila and its co-associated microbiome.
1:00:35 Why a massive, wide-scale, Manhattan-project approach for increasing human lifespan is necessary.

Now researchers have used US economic, health, and demographic data to put a price on just how valuable such an intervention could be. In a paper in Nature Aging, they showed that treatments that slow down aging could be worth US$38 trillion for every extra year of life they give people.

This isn’t the first time someone has tried to pin a number on the benefits of slowing aging. The authors reference a 2013 study in Health Affairs, which estimated that a 2.2-year increase in life expectancy could be worth as much as $7.1 trillion over 50 years.

The new study uses a different methodology, though, known as value of statistical life. This is the measure used by various US agencies and represents how much people would be willing to pay to reduce their risk of dying. It incorporates concepts like health, consumption, and leisure, and therefore measures not just quantity but quality of life.

Immortality DNA strands found in humans.

Distributed stem cells (DSCs), which continuously divide asymmetrically to replenish mature tissue cells, adopt a special form of mitotic chromosome segregation. Chromosome segregation is nonrandom instead of random. DSCs cosegregate the set of sister chromosomes with the older of the two template DNA strands used for semiconservative DNA replication during the preceding S phase. Neither the responsible molecular mechanisms nor the cellular function of nonrandom segregation are known. Here, we report evidence that immortal strand chromosomes have a higher level of cytosine 5-hydroxymethylation than mortal chromosomes, which contain the younger DNA template strands. We propose that asymmetric chromosomal 5-hydroxymethylation is a key element of a cellular mechanism by which DSCs distinguish older DNA template strands from younger ones.

Immortal strands are the targeted chromosomal DNA strands of nonrandom sister chromatid segregation, a mitotic chromosome segregation pattern unique to asymmetrically self-renewing distributed stem cells (DSCs). By nonrandom segregation, immortal DNA strands become the oldest DNA strands in asymmetrically self-renewing DSCs. Nonrandom segregation of immortal DNA strands may limit DSC mutagenesis, preserve DSC fate, and contribute to DSC aging. The mechanisms responsible for specification and maintenance of immortal DNA strands are unknown. To discover clues to these mechanisms, we investigated the 5-methylcytosine and 5-hydroxymethylcytosine (5hmC) content on chromosomes in mouse hair follicle DSCs during nonrandom segregation. Although 5-methylcytosine content did not differ significantly, the relative content of 5hmC was significantly higher in chromosomes containing immortal DNA strands than in opposed mitotic chromosomes containing younger mortal DNA strands.

Given this idea could be scaled up to revive even deceased humans essentially like the tardigrade does.

Arctic ice dating to 24000 years ago held frozen microscopic animals called rotifers. Scientists just brought them back to life.

Circa 2010

In this review, we consider the evidence that a reduction in neurogenesis underlies aging-related cognitive deficits, and impairments in disorders such as Alzheimer’s disease (AD). The molecular and cellular alterations associated with impaired neurogenesis in the aging brain are discussed. Dysfunction of presenilin-1, misprocessing of amyloid precursor protein and toxic effects of hyperphosphorylated tau and β-amyloid likely contribute to impaired neurogenesis in AD. Since factors such as exercise, enrichment and dietary energy restriction enhance neurogenesis, and protect against age-related cognitive decline and AD, knowledge of the underlying neurogenic signaling pathways could lead to novel therapeutic strategies for preserving brain function. In addition, manipulation of endogenous neural stem cells and stem cell transplantation, as stand-alone or adjunct treatments, seem promising.

There is a progressive decline in the regenerative capacity of most organs with increasing age, resulting in functional decline and poor repair from injury and disease. Once thought to exist only in high turnover tissues, such as the intestinal lining or bone marrow, it now appears that most tissues harbor stem cells that contribute to tissue integrity throughout life. In many cases, stem cell numbers decrease with age, suggesting stem cell aging may be of fundamental importance to the biology of aging (for review, see Ref. [1]). Therefore, understanding the regulation of stem cell maintenance and/or activation is of considerable relevance to understanding the age-related decline in maintaining tissue integrity, function, and regenerative response.

Continue reading “When Neurogenesis Encounters Aging and Disease” »