Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: genetics – Page 353

Grey hair seems to be driven by stem cell exhaustion, one of the suggested reasons we age. One researcher believes we can turn back the clock on greying hair.

rep melissa harris 550px

Melissa Harris’s research points to a new paradigm for hair graying. “We thought that once you go gray the stem cells are all lost — there’s no going back,” Harris said. “But presumably they can be reactivated.”

Molecular biology is not usually the kind of science you can do with the naked eye. Sure enough, Melissa Harris, Ph.D., runs a lab that leans into CRISPR gene-editing tools, single-cell sequencing studies and network-analysis algorithms. But all she needs is a glance to diagnose the state of your melanocyte stem cells.

Read more | >

If you are interested in superlongevity, I have a spectacular book for you: Lifespan — Why We Age and Why We Don’t Have To, by David Sinclair PhD.

Sinclair has written a book about all the various ways in which humans can extend their lifespan and their healthspan.

One of the best aspects of this book is that Sinclair has a way of writing that is clear and insightful. It is so rare for me to read a book about scientific experiments in which it is easy to follow the methodology, but it is unique to also have an explanation of the application of the results that is crystal clear. Sinclair does both simply and easily.

Sinclair writes about all of the avenues that I’ve heard of for life extension. Metformin. NAD+. NMN. NR. Diet. Exercise. Resveratrol. Senolytics.

However, the most gripping aspect of this book is Sinclair’s Information Theory of Aging. Here is one excerpt from the book:

Continue reading “Lifespan: Why We Age—and Why We Don’t Have To” | >

CHICAGO/LONDON (Reuters) — When a newly organized vaccine research group at the U.S. National Institutes of Health (NIH) met for the first time this week, its members had expected to be able to ease into their work. But their mandate is to conduct human trials for emerging health threats — and their first assignment came at shocking speed.

Read more | >

To better understand the dynamics of bats and potential threats to human health, Goldberg and his colleagues explored the relationship of an African forest bat, a novel virus and a parasite. Their work, described in a report published July 13 in Nature Scientific Reports, identifies all three players as potentially new species, at least at the molecular level as determined by their genetic sequences.

Many viral pathogens often have more than one or two hosts or intermediate hosts needed to complete their life cycles. The role of bat parasites in maintaining chains of viral infection is little studied, and the new Wisconsin study serves up some intriguing insights into how viruses co-opt parasites to help do the dirty work of disease transmission.

The parasite in the current study is an eyeless, wingless fly, technically an ectoparasite. It depends on the bat to be both its eyes and wings. And it plays host to a virus, as the current study shows. For the virus, the fly plays the role of chauffeur. “From a virus’s perspective, an ectoparasite is like Uber. It’s a great way to get around — from animal to animal — at minimal expense and effort,” Goldberg explains.

Read more | >

The Tasmanian devil (Sarcophilus harrisii), the largest marsupial carnivore, is endangered due to a transmissible facial cancer spread by direct transfer of living cancer cells through biting. Here we describe the sequencing, assembly, and annotation of the Tasmanian devil genome and whole-genome sequences for two geographically distant subclones of the cancer. Genomic analysis suggests that the cancer first arose from a female Tasmanian devil and that the clone has subsequently genetically diverged during its spread across Tasmania. The devil cancer genome contains more than 17,000 somatic base substitution mutations and bears the imprint of a distinct mutational process. Genotyping of somatic mutations in 104 geographically and temporally distributed Tasmanian devil tumors reveals the pattern of evolution and spread of this parasitic clonal lineage, with evidence of a selective sweep in one geographical area and persistence of parallel lineages in other populations.

Read more | >

Circa 2013

In a feat of “molecular time travel,” the researchers resurrected and analyzed the functions of the ancestors of genes that play key roles in modern human reproduction, development, immunity and cancer. By re-creating the same DNA changes that occurred during those genes’ ancient history, the team showed that two mutations set the stage for hormones like estrogen, testosterone and cortisol to take on their crucial present-day roles.

“Changes in just two letters of the genetic code in our deep evolutionary past caused a massive shift in the function of one protein and set in motion the evolution of our present-day hormonal and reproductive systems,” said Joe Thornton, PhD, professor of human genetics and ecology & evolution at the University of Chicago, who led the study.

“If those two mutations had not happened, our bodies today would have to use different mechanisms to regulate pregnancy, libido, the response to stress, kidney function, inflammation, and the development of male and female characteristics at puberty,” Thornton said.

Read more | >

Circa 2011 essentially cancer could help with evolution as it can challenge the immune system to be more strong. Essentially a symbiotic relationship to evolve with it and grow stronger with it then like it can be used as a good thing to make sure that evolution has stronger genetic code.

Evolutionary theories are critical for understanding cancer development at the level of species as well as at the level of cells and tissues, and for developing effective therapies. Animals have evolved potent tumor suppressive mechanisms to prevent cancer development. These mechanisms were initially necessary for the evolution of multi-cellular organisms, and became even more important as animals evolved large bodies and long lives. Indeed, the development and architecture of our tissues were evolutionarily constrained by the need to limit cancer. Cancer development within an individual is also an evolutionary process, which in many respects mirrors species evolution. Species evolve by mutation and selection acting on individuals in a population; tumors evolve by mutation and selection acting on cells in a tissue. The processes of mutation and selection are integral to the evolution of cancer at every step of multistage carcinogenesis, from tumor genesis to metastasis. Factors associated with cancer development, such as aging and carcinogens, have been shown to promote cancer evolution by impacting both mutation and selection processes. While there are therapies that can decimate a cancer cell population, unfortunately, cancers can also evolve resistance to these therapies, leading to the resurgence of treatment-refractory disease. Understanding cancer from an evolutionary perspective can allow us to appreciate better why cancers predominantly occur in the elderly, and why other conditions, from radiation exposure to smoking, are associated with increased cancers. Importantly, the application of evolutionary theory to cancer should engender new treatment strategies that could better control this dreaded disease.

We expect that the public generally views evolutionary biology as a science about the past, with stodgy old professors examining dusty fossils in poorly lit museum basements. Evolution must certainly be a field well-separated from modern medicine and biomedical research, right? If the public makes a connection between evolution and medicine, it is typically in the example of bacteria acquiring antibiotic resistance. But what does evolution have to do with afflictions like heart disease, obesity, and cancer? As it turns out, these diseases are intricately tied to our evolutionary histories, and understanding evolution is essential for preventing, managing and treating these diseases (1, 2). This review will focus on cancer: how evolutionary theories can be used to understand cancer development at the level of species as well as at the level of cells and tissues. We will also discuss the implications and benefits of an evolutionary perspective towards cancer prevention and therapies.

For almost all animals, old age is associated with a general decline in tissue structure and function. This decline is thought to reflect the lack of selective pressure to maintain tissues beyond an age when the animal would be likely to contribute genetically to future generations (3−5). Similarly, there is little selective pressure to limit cancer in old animals who are substantially beyond their reproductive years. For example, while mice can live 2–4 years in the lab, and tend to develop cancer in their second and third years, it is rare to find a mouse greater than 1 year old in the wild. Most wild mice will be dead from other causes, such as cold, hunger, disease or predators, well before the age when cancer would be a likely cause of their demise. Thus, evolution has favored a “breed early, breed often” strategy for mice.

Continue reading “How cancer shapes evolution, and how evolution shapes cancer” | >

The Měnglà virus can infect human cells but the risk of its transmission from bats to humans is unknown.

Zheng-Li Shi at the Chinese Academy of Sciences in Wuhan and their colleagues examined a Rousettus fruit bat caught in southern China. The bat’s liver contained a new type of filovirus that the researchers named Měnglà virus for the county where the bat was captured. Měnglà is substantially different from both Ebola and Marburg virus, highlighting the genetic diversity of filoviruses in bats.

Read more | >

Study reveals interplay of an African bat, a parasite and a virus

Since the emergence of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) and Middle East Respiratory Syndrom Coronavirus (MERS-CoV) it has become increasingly clear that bats are important reservoirs of CoVs. Despite this, only 6% of all CoV sequences in GenBank are from bats. The remaining 94% largely consist of known pathogens of public health or agricultural significance, indicating that current research effort is heavily biased towards describing known diseases rather than the ‘pre-emergent’ diversity in bats. Our study addresses this critical gap, and focuses on resource poor countries where the risk of zoonotic emergence is believed to be highest. We surveyed the diversity of CoVs in multiple host taxa from twenty countries to explore the factors driving viral diversity at a global scale. We identified sequences representing 100 discrete phylogenetic clusters, ninety-one of which were found in bats, and used ecological and epidemiologic analyses to show that patterns of CoV diversity correlate with those of bat diversity. This cements bats as the major evolutionary reservoirs and ecological drivers of CoV diversity. Co-phylogenetic reconciliation analysis was also used to show that host switching has contributed to CoV evolution, and a preliminary analysis suggests that regional variation exists in the dynamics of this process. Overall our study represents a model for exploring global viral diversity and advances our fundamental understanding of CoV biodiversity and the potential risk factors associated with zoonotic emergence.

Read more | >