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Category: genetics – Page 300

Most important part comes at 1:49 where Liza talks about gene therapies for people to stop people from aging, reaching homeostasis, or even exceeding it a little bit.

In this video Liz introduces BioViva Science and how the company works with its partners in delivering gene therapies.

Liz Parrish is the Founder and CEO of BioViva Sciences USA Inc. BioViva is committed to extending healthy lifespans using gene therapy. Liz is known as “the woman who wants to genetically engineer you,” she is a humanitarian, entrepreneur, author and innovator and a leading voice for genetic cures. As a strong proponent of progress and education for the advancement of gene therapy, she serves as a motivational speaker to the public at large for BioViva and the life sciences. She is actively involved in international educational media outreach and is a founding member of the International Longevity Alliance (ILA). She is the founder of the BioTrove Podcasts, found at iTunes, which is committed to offering a meaningful way for people to learn about current technologies. She is also a founding member of the American Longevity Alliance (ALA) a 501©(3) nonprofit trade association that brings together individuals, companies, and organizations who work in advancing the emerging field of cellular & regenerative medicine with the aim to get governments to consider aging a disease.

BioViva https://bioviva-science.com.
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Health claims Disclosure: Information provided on this video is not a substitute for direct, individual medical treatment or advice. It is the responsibility of you and your healthcare providers to make all decisions regarding your health. Products or services mentioned in this video are not a recommendation or medical advice.

Continue reading “Fighting Aging With Gene Therapies | Liz Parrish Interview Series Episode 2” | >

To begin with, why do we use mice in medical and biological research? The answer to this question is fairly straight forward. Mice are cheap, they grow quickly, and the public rarely object to experimentations involving mice. However, mice offer something that is far more important than simple pragmatism, as despite being significantly smaller and externally dissimilar to humans, our two species share an awful lot of similarities. Almost every gene found within mice share functions with genes found within humans, with many genes being essentially identical (with the obvious exception of genetic variation found within all species). This means that anatomically mice are remarkably similar to humans.

Now, this is where for the sake of clarity it would be best to break down biomedical research into two categories. Physiological research and pharmaceutical research, as the success of the mouse model should probably be judges separately depending upon the research that is being carried out. Separating the question of the usefulness of the mouse model down into these two categories also solves the function of more accurately focusing the ire of its critics.

The usefulness of the mouse model in the field of physiological research is largely unquestioned at this point. We have quite literally filled entire textbooks with the information we have gained from studying mice, especially in the field of genetics and pathology. The similarities between humans and mice are so prevalent that it is in fact possible to create functioning human/mouse hybrids, known as ‘genetically engineered mouse models’ or ‘GEMMs’. Essentially, GEMMs are mice that have had the mouse version of a particular gene replaced with its human equivalent. This is an exceptionally powerful tool for medical research, and has led to numerous medical breakthroughs, including most notably our current treatment of acute promyelocytic leukaemia (APL), which was created using GEMMs.

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There’s some really interesting CRISPR news out today, and it’s likely to be a forerunner of much more news to come. A research team has demonstrated what looks like robust, long-lasting effects in a primate model after one injection of the CRISPR enzymatic machinery. There have been plenty of rodent reports on various forms of CRISPR, and there are some human trials underway, but these is the first primate numbers that I’m aware of.

The gene they chose to inactivate is PCSK9, which has been a hot topic in drug discovery for some years now. It’s a target validated by several converging lines of evidence from the human population (see the “History” section of that first link). People with overactive PCSK9 have high LDL lipoproteins and cholesterol, and people with mutations that make it inactive have extremely low LDL and seem to be protected from a lot of cardiovascular disease. There are several drugs and drug candidates out there targeting the protein, as well there might be.

It’s a good proof-of-concept, then, because we know exactly what the effects of turning down the expression of active PCSK9 should look like. It’s also got the major advantage of being mostly a liver target – as I’ve mentioned several times on the blog already, many therapies aimed at gene editing or RNA manipulation have a pharmacokinetic complication. The formulations used to get such agents intact into the body (and in a form that they can penetrate cells) tend to get combed out pretty thoroughly by the liver – which after all, is (among other things) in the business of policing the bloodstream for weird, unrecognized stuff that is then targeted for demolition by hepatocytes. Your entire bloodstream goes sluicing through the liver constantly; you’re not going to able to dodge it if your therapy is out there in the circulation. It happens to our small-molecule drugs all the time: hepatic “first pass” metabolism is almost always a factor to reckon with.

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www.iBiology.org.

Dr. Kate Adamala describes what synthetic cells are and how they can teach us the fundamental principles of life.

Life on Earth evolved once — this means that all biological systems on our planet are rooted in the same fundamental framework. This framework is extremely complex and we have yet to fully understand the processes inside each living cell. One way of understanding complex systems is to break them down into simpler parts. This is the principle of engineering the synthetic cell: to use our current knowledge of biology for building a living cell with the least amount of parts and complexity. Synthetic cells can be used to teach us about the basic principles of life and evolution, and they hold promise for a range of applications including biomaterials and drug development. Dr. Kate Adamala narrates an introduction to this exciting field.

0:00 Introduction.
2:22 How do we build a synthetic cell?
7:12 How can we use synthetic cells?

Speaker Biography:
Dr. Kate Adamala is a synthetic biologist and a McKnight Land-Grant Assistant Professor in the Department of Genetics, Cell Biology and Development at the University of Minnesota. Her research interests include astrobiology, synthetic cell engineering and biocomputing. Adamala is a co-founder and steering group member of the international Build-a-Cell Initiative, which seeks to broaden the impact of synthetic cell engineering. Find more information on Adamala’s lab at:
http://www.protobiology.org.

Credits:

Continue reading “Kate Adamala (U of M) 1: Synthetic Cells: Building Life to Understand It” | >

And cells from people with mutations in KMT2D, which results in Kabuki syndrome, showed similar patterns of activity to the EHMT1 cells. Kabuki syndrome often results in intellectual disability but is not typically linked to autism.

Cells that carry mutations in ARID1B showed a distinct pattern of network activity, with short, small bursts occurring at an unusually high rate.

Moving forward, Nadif Kasri and his colleagues plan to test other genes that increase a person’s likelihood of being autistic. They also plan to explore how these activity patterns compare at the individual level, and how they relate to other autism-linked traits, he says.

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“Gene editing offers unique opportunities to make food production more sustainable and to further improve the quality, but also the safety, of food. With the help of these new molecular tools, more robust plants can be developed that deliver high yields for high-quality nutrition, even with less fertiliser,” says co-author Stephan Clemens, Professor of Plant Physiology at the University of Bayreuth and founding Dean of the new Faculty of Life Sciences: Food, Nutrition & Health on the Kulmbach campus.

For more sustainability on a global level, EU legislation should be changed to allow the use of gene editing in organic farming. This is what an international research team involving the Universities of Bayreuth and Göttingen demands in a paper published in the journal “Trends in Plant Science”.

In May 2020, the EU Commission presented its “Farm-to-Fork” strategy, which is part of the “European Green Deal”. The aim is to make European agriculture and its food system more sustainable. In particular, the proportion of organic farming in the EU’s total agricultural land is to be increased to 25 percent by 2030. However, if current EU legislation remains in place, this increase will by no means guarantee more sustainability, as the current study by scientists from Bayreuth, Göttingen, Düsseldorf, Heidelberg, Wageningen, Alnarp, and Berkeley shows.

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Large swaths of U.S. military land are covered with munitions components, including the explosive chemical RDX. This molecule is toxic to people and can cause cancer. It also doesn’t naturally break down and can contaminate groundwater. Now researchers have genetically engineered a grass commonly used to fight soil erosion so that it can remove RDX from the soil, according to a new paper published May 3 in Nature Biotechnology.

A team, which includes researchers from the University of Washington, demonstrated that over the course of three years, a genetically engineered switchgrass could break down an explosive chemical in…

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Humans are distinguished from other species by several aspects of cognition. While much comparative evolutionary neuroscience has focused on the neocortex, increasing recognition of the cerebellum’s role in cognition and motor processing has inspired considerable new research. Comparative molecular studies, however, generally continue to focus on the neocortex. We sought to characterize potential genetic regulatory traits distinguishing the human cerebellum by undertaking genome-wide epigenetic profiling of the lateral cerebellum, and compared this to the prefrontal cortex of humans, chimpanzees, and rhesus macaque monkeys. We found that humans showed greater differential CpG methylation–an epigenetic modification of DNA that can reflect past or present gene expression–in the cerebellum than the prefrontal cortex, highlighting the importance of this structure in human brain evolution. Humans also specifically show methylation differences at genes involved in neurodevelopment, neuroinflammation, synaptic plasticity, and lipid metabolism. These differences are relevant for understanding processes specific to humans, such as extensive plasticity, as well as pronounced and prevalent neurodegenerative conditions associated with aging.

Citation: Guevara EE, Hopkins WD, Hof PR, Ely JJ, Bradley BJ, Sherwood CC (2021) Comparative analysis reveals distinctive epigenetic features of the human cerebellum. PLoS Genet 17: e1009506. https://doi.org/10.1371/journal.pgen.

Editor: Takashi Gojobori, National Institute of Genetics, JAPAN.

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You know you’re a little different when the family tags along for your run in an RV fully equipped for a multi-day road trip.

Have you tried pulling an all-nighter recently? It hurts. A once-common event in college – thanks to studying or partying or midnight hikes that turned into sunrise missions – becomes increasingly debilitating the older you get. It’s like your first run after some time off: You might feel okay doing it, but you’ll pay the next day.

Unless you’re the genetically blessed aberration that is Dean Karnazes, 53, one of the most well known runners of our time.

In 1992, after taking a 15-year break from running, it wasn’t enough for Karnazes’ first run to be 30 miles. Winning the infamous, 135-mile Badwater Ultramarathon across Death Valley in 120-degree heat didn’t cut it. Nor did pushing the opposite end of spectrum of human suffering by running a marathon to the South Pole, at-13-degrees F.

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Great new episode with renowned geneticist Christopher Mason who talks about his book on how we will need to bioengineer our own species in order to expand beyond our solar system.

Geneticist Christopher Mason chats about his new book, “The Next 500 Years: Engineering Life to Reach New Worlds” from MIT Press. We discuss both the nuts and bolts and the philosophy driving our expansion offworld. Mason’s goal is to preserve our species by expanding to an Earth 2.0 in order to avoid our star’s own Red Giant endgame.

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