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International research team isolates DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

The cumulative effect of reduced PTPN2 activity on both mechanisms was an elevated fluid loss. The researchers proved this defect could be reversed by treating cells lacking PTPN2 with recombinant -; or synthetic -; matriptase.


A team of researchers led by a biomedical scientist at the University of California, Riverside, has identified a novel mechanism by which loss-of-function mutations in the gene PTPN2, found in many patients with inflammatory bowel disease, or IBD, affect how intestinal epithelial cells maintain a barrier.

The intestinal epithelium, a single layer of cells, plays a critical role in human health by providing a barrier while also allowing nutrient and water absorption. Intestinal epithelial cells are needed for regulating immune function, communicating with the intestinal microbiota, and protecting the gut from pathogen infection -; all of which critically depend on an intact epithelial barrier.

Affecting roughly 3 million Americans, IBD is a set of chronic intestinal diseases in which the lining of the gut becomes inflamed and leaky. Increased gut leakiness has recently been confirmed to increase the risk of developing IBD.

Cats have many superior genetic mutations like night vision even immunity to the current pandemic. If we can find the key to their immunity we could find a way to have near super human immunity.


“Getting a better understanding of the cat’s biology and genetic makeup will help us better understand the biology of humans, too,” says Leslie Lyons. (Credit: Lottie/Flickr)

The findings, published in Trends in Genetics, come after decades of genome DNA sequencing by Leslie Lyons, professor of comparative medicine in the University of Missouri College of Veterinary Medicine. Their cat genome assembly is nearly 100% complete.

The late 21st century belongs to Superhumans. Technological progress in the field of medicine through gene editing tools like CRISPR is going to revolutionize what it means to be human. The age of Superhumans is portrayed in many science fiction movies, but for the first time in our species history, radically altering our genome is going to be possible through the methods and tools of science.

The gene-editing tool CRISPR, short for clustered regularly interspaced short palindromic repeats, could help us to reprogram life. It gives scientists more power and precision than they have ever had to alter human DNA.

Genetic engineering holds great promise for the future of humanity. A growing number of scientists including David Sinclair believe that we will soon be able to engineer and change our genes in a way that will help us live longer and healthier lives.

But how much should we really tinker with our own nature? What is the moral responsibility of scientists and humans towards future generations?

Circa 2015 Clues of the genetic material in vultures could give rise to humans that have immunity to nearly all bacteria and viruses.


WASHINGTON WASHINGTON (Reuters) — A diet of putrid rotting flesh may not be your cup of tea, but to the cinereous vulture, found across southern Europe and Asia, it is positively delightful. This tough bird, it turns out, is genetically wired to thrive on the stuff.

Researchers on Tuesday said they have sequenced the genome of this big scavenger, also called the Eurasian black vulture, identifying genetic traits that account for a stalwart stomach and powerful immune system that let it carry on eating carrion.

They pinpointed genetic features related to gastric acid secretion that help explain this vulture’s ability to digest carcasses and other features linked to its immune system defense against microbial and viral infections from decomposing flesh.

Why not eradicate disease for everyone?


Zolgensma – which treats spinal muscular atrophy, a rare genetic disease that damages nerve cells, leading to muscle decay – is currently the most expensive drug in the world. A one-time treatment of the life-saving drug for a young child costs US$2.1 million.

While Zolgensma’s exorbitant price is an outlier today, by the end of the decade there’ll be dozens of cell and gene therapies, costing hundreds of thousands to millions of dollars for a single dose. The Food and Drug Administration predicts that by2025it will be approving 10 to 20 cell and gene therapies every year.

I’m a biotechnology and policy expert focused on improving access to cell and gene therapies. While these forthcoming treatments have the potential to save many lives and ease much suffering, health care systems around the world aren’t equipped to handle them. Creative new payment systems will be necessary to ensure everyone has equal access to these therapies.

We think of DNA as the vitally important molecules that carry genetic instructions for most living things, including ourselves. But not all DNA actually codes proteins; now, we’re finding more and more functions involving the non-coding DNA scientists used to think of as ‘junk’.

A new study suggests that satellite DNA – a type of non-coding DNA arranged in long, repetitive, apparently nonsensical strings of genetic material – may be the reason why different species can’t successfully breed with each other.

It appears that satellite DNA plays an essential role in keeping all of a cell’s individual chromosomes together in a single nucleus, through the work of cellular proteins.

Mitochondrial DNA diseases are common neurological conditions caused by mutations in the mitochondrial genome or nuclear genes responsible for its maintenance. Current treatments for these disorders are focused on the management of the symptoms, rather than the correction of biochemical defects caused by the mutation. Now, scientists at Kyoto University’s Institute for Integrated Cell-Material Science (iCeMS) in Japan report a new approach where mutant DNA sequences inside cellular mitochondria can be eliminated using a bespoke chemical compound. The approach may lead to better treatments for mitochondrial diseases.

Their findings are published in the journal Cell Chemical Biology in a paper titled, “Targeted elimination of mutated mitochondrial DNA by a multi-functional conjugate capable of sequence-specific adenine alkylation.”

“Mutations in mitochondrial DNA (mtDNA) cause mitochondrial diseases, characterized by abnormal mitochondrial function,” the researchers wrote. “Although eliminating mutated mtDNA has potential to cure mitochondrial diseases, no chemical-based drugs in clinical trials are capable of selective modulation of mtDNA mutations. Here, we construct a class of compounds encompassing pyrrole-imidazole polyamides (PIPs), mitochondria-penetrating peptide, and chlorambucil, an adenine-specific DNA-alkylating reagent.”

As work in real and model embryos movesforward, scientists are keen to know how similar the two really are. Finding out how models differ in their molecular details, and how their cells behave, is the main reason researchers wish to push beyond 14 days in real embryos. “We can learn a lot from a model,” says Jesse Veenvliet, a developmental biologist at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany. “But it’s important to know where it goes wrong.”


Researchers are now permitted to grow human embryos in the lab for longer than 14 days. Here’s what they could learn.