Interesting.
The research, published in Nature Structural and Molecular Biology, explains how the gene encourages the attachment of the protein, ubiquitin, to other proteins and plays a vital role in DNA repair. Should the results be confirmed by further studies, it is possible that patients with certain genetic changes in BRCA1 could be identified as being at higher risk of breast and ovarian cancer.
My new article for Vice Motherboard on extreme biohacking that compares the Uncanny Valley to Speciation Syndrome:
Transhumanism tech like CRISPR, 3D printing, and coming biological regeneration of limbs will not only change lives for those that have deformities, but it will change how we look at things like a person with a three-foot tail and maybe even a second head.
At the core of all this is the ingrained belief that the human being is pre-formed organism, complete with one head, four limbs, and other standard anatomical parts. But in the transhumanist age, the human being should be looked at more like a machine—like a car, if you will: something that comes out a particular way with certain attributes, but then can be heavily modified. In fact, it can be rebuilt from scratch.
In the future, there may even be walk-in clinics where people can go to have various gene treatments done to affect their bodies. Already, we have IVF centers where people can use radical tech to privately get pregnant—and also control and monitor various stages of a child’s birth. Eventually, if government allows it, gene editing centers will also offer a multitude of designer baby traits, some which also would come via CRISPR. We might even eventually use artificial wombs for the whole process.
Economically, a trillion dollar industry could be created by the burgeoning genetic editing industry—one that greatly benefits human health and science innovation. But of course, first we must get over our fears of modifying the human body and the effects of speciation syndrome.
Ubiquitous, mobile supercomputing. Artificially-intelligent robots. Self-driving cars. Neuro-technological brain enhancements. Genetic editing. The evidence of dramatic change is all around us and it’s happening at exponential speed.
Previous industrial revolutions liberated humankind from animal power, made mass production possible and brought digital capabilities to billions of people. This Fourth Industrial Revolution is, however, fundamentally different. It is characterized by a range of new technologies that are fusing the physical, digital and biological worlds, impacting all disciplines, economies and industries, and even challenging ideas about what it means to be human.
Awesome.
Researchers have developed a new gene editing tool that is more efficient and easier to use. CRISPR-EZ addresses the issue of target RNA accuracy and embryo viability in IVF transgenic mice.
( andrew modzelewski/lin he | university of california berkeley )
CRISPR gene editing has been the subject of many researchers around the world because of its great potential in the study human genetic disease. But more than that, scientists have high regard for this tool because it can help cure complex and debilitating diseases like dementia and cancer.
As more fine-tuning is done in the use of CRISPR gene editing, more diseases can be effectively cured. CRISPR-Cas9 has been used to accurately replace or change genes but it is mostly done in early embryos, and there is a need to increase its accuracy and ease of use. With this in mind, researchers from the University of California (UC) Berkeley have developed a new method called CRISPR-EZ (CRISPR ribonucleoprotein electroporation of zygotes) that would make gene editing easier.
Not surprised;
A long line of research links poverty and depression. Now, a study by Duke University scientists shows how biology might underlie the depression experienced by high-risk adolescents whose families are socio-economically disadvantaged.
The study, published May 24, 2016 in the journal Molecular Psychiatry, combined genetics, brain imaging and behavioral data gathered as adolescents were followed for more than three years as part of a larger study.
The results are part of a growing body of work that may lead to biological predictors that could guide individualized depression-prevention strategies.
Treatment with sex hormones recovers serious genetic diseases cells, this is the first demonstration that the lengthening of telomeres is possible in humans with the use of a medication,” says the researcher.
Estudo demostrou que há como estimular a enzima telomerase por meio de hormônios sexuais, tanto masculinos quanto femininos.
Por Redação — Editorias: Ciências, Ciências Biológicas, Ciências da Saúde.
Sea urchins are remarkable organisms. They can quickly regrow damaged spines and feet. Some species also live to extraordinary old ages and—even more remarkably—do so with no signs of poor health, such as a decline in regenerative capacity or an increase in age-related mortality. These ocean Methuselahs even reproduce as if they were still youngsters.
MDI Biological Laboratory Associate Professor James A. Coffman, Ph.D., is studying the regenerative capacity of sea urchins in hopes that a deeper understanding of the process of regeneration, which governs the regeneration of aging tissues as well as lost or damaged body parts, will lead to a deeper understanding of the aging process in humans, with whom sea urchins share a close genetic relationship.
In a paper recently published in Aging Cell, a leading journal in the field of aging biology, with Andrea G. Bodnar, Ph.D., of the Bermuda Institute of Ocean Studies, the scientists shed new light on the aging process in sea urchins, raising the prospect that the physical decline that typically accompanies aging is not inevitable.
The visible impacts of depression and stress that can be seen in a person’s face—and contribute to shorter lives—can also be found in alterations in genetic activity, according to newly published research.
In a series of studies involving both C. elegans worms and human cohorts, researchers from the Indiana University School of Medicine and the Scripps Research Institute have identified a series of genes that may modulate the effects of good or bad mood and response to stress on lifespan. In particular, the research pointed to a gene known as ANK3 as playing a key role in affecting longevity. The research was published May 24, 2016 in the Nature Publishing Group journal Molecular Psychiatry, the top ranked journal in the field of psychiatry.
“We were looking for genes that might be at the interface between mood, stress and longevity”, said Alexander B. Niculescu III, M.D., Ph.D., professor of psychiatry and medical neuroscience at the IU School of Medicine. “We have found a series of genes involved in mood disorders and stress disorders which also seem to be involved in longevity.
(Medical Xpress)—A large team of researchers from a host of research facilities across Japan has found some genetic variants in some cancer cells that lead to enhanced PD-L1 protein production—which results in increased protection against attacks by the immune system. In their paper published in the journal Nature, the team describes their sequencing study involving adult T-cell leukemia/lymphoma cases, what they found and the possibility that such variants could be used as identifying markers in cancer patients.
Prior studies have shown that an increase in the expression of the protein PD-L1 by cancer cells confers enhanced protection against attacks by the human immune system—PD-1 receptors on T cells bind with PD-L1 causing the immune cells to become unresponsive, preventing them from attacking tumors. In this new effort, the researchers conducted a genetic analysis of a particular type of cancer cell to learn more about the genetic process involved in causing an increase in expression of PD-L1.
The team conducted whole-genome sequencing on samples given by 49 adult patients suffering from leukemia or lymphoma, looking specifically for variations that might account for an increase in expression of PD-L1. In so doing, they found that variations such as duplications, inversions or translocations in 13 of the samples, representing 27 percent of those tested, existed on a certain part of chromosome 9, which prior research had found was the part of the genome responsible for the expression of PD-L1. They report that such alterations seemed to cut off the gene’s 3’ untranslated region of the protein and in some cases led to rearranging the gene’s open reading frame, which allowed more of the protein to be expressed.
“The possibility to selectively activate genes using various engineered variants of the CRISPR-Cas9 system left many researchers questioning which of the available synthetic activating Cas9 proteins to use for their purposes. The main challenge was that all had been uniquely designed and tested in different settings; there was no side-by-side comparison of their relative potentials,” said George Church, Ph.D., who is Core Faculty Member at the Wyss Institute for Biologically Inspired Engineering at Harvard University, leader of its Synthetic Biology Platform, and Professor of Genetics at Harvard Medical School. “We wanted to provide that side-by-side comparison to the biomedical research community.”
In a study published on 23 May in Nature Methods, the Wyss Institute team reports how it rigorously compared and ranked the most commonly used artificial Cas9 activators in different cell types from organisms including humans, mice and flies. The findings provide a valuable guide to researchers, allowing them to streamline their endeavors.
The team also included Wyss Core Faculty Member James Collins, Ph.D., who also is the Termeer Professor of Medical Engineering & Science and Professor of Biological Engineering at the Massachusetts Institute of Technology (MIT)’s Department of Biological Engineering and Norbert Perrimon, Ph.D., a Professor of Genetics at Harvard Medical School.
