Page 1,483«..1020..1,4821,4831,4841,485..1,4901,500..»

SECOND OPINION | Your life is leaving genetic scars that might show up in your child’s genes – CBC.ca

Posted: August 19, 2017 at 5:42 pm

Hello and happy Saturday! Here's our summer roundup of eclectic and under-the-radar health and medical science news.

If you haven't subscribed yet, you can do that by clickinghere.

Scientists now know that the mere act of living leaves molecular scars on our genes.

But it was long assumed that those marks were wiped clean when the genes were passed on to the next generation.

Not so, according to research in the mysterious field of epigenetics. And a new paper shows some of the first evidence of how offspring are affected.

"It was assumed there was zero transmission of epigenetic information from one generation to another, McGill University pharmacology professor Moshe Szyf told us. "This paper adds to that body of evidence showing that assumption is not true."

Epigenetics is an emerging field of research proving once again that DNA is complicated. It won't work without a second layer of genetic activity called epigenetics, a series of biochemical processes that translate DNA's genetic information into cellular mechanisms in the human body.

And the way those epigenetic programs turn certain genes up or down, on or off can be affected by what we eat, and how we live, how much stress we experience, or what toxic exposures we have.

"The big question is how much the experiences we are going through, including trauma, diseaseor famine, etc.is passed to the next generation," said Szyf.

The studypublishedin Science shows evidence that fruit fly offspring inherit a specific epigenetic change critical to the embryo's development. But what do humans have in common with fruit flies? A lot.

"Evolution has taught us that principles that work in one organism usually work in many organisms. And if a basic process appears in a fruit fly, it usually also appears in humans," Szyf said.

The first clues to epigenetic heritability came from curiousobservationsfollowing a series of famine cycles in a northern province of Sweden in the early 1800s. Scientists linked changes in life expectancy to grandparents' exposure to feast or famine.

Otherobservationsmade after the Dutch famine during the Second World Warshowed persistent changes in DNA expression six decades later, adding to evidence that life experiences can leave permanent marks on our genes.

"We were under the illusion that if we know genetics we understand everything about life," Szyf said. "Epigenetic information is much more dynamic and responsive to the environment. And it raises the possibility that experience can be passed from one generation to the next. And that's the allure of this whole thing."

The irony of peer review is that the process itself is never peer reviewed. (Shutterstock)

Imagine having all of your colleagues and all of your competitors looking over your shoulder at everything you do. And now imagine them pointing out everything you did wrong and sending you back to do it all over again.

That's the basic premise of scientific peer review. Before a research paper is published in a scientific journal, several scientists examine the work to determine if the methods are sound and the conclusions are supported by the data. It's a much-heralded pillar of the scientific process.

But the irony of peer review is that the process itself is never peer reviewed. David Moher, a senior scientist at the Ottawa Hospital Research Institute, called for the "black box" of peer review to be opened, in a commentary he co-authored inScience.

"We have very little evidence that peer review works," Moher told us, pointing to the riseof predatory journals as evidence of the urgent need to improve peer review.

Predatory journals disguise themselves as legitimate scientific publications andmake money by charging scientists for publishing their papers. There isevidenceof these journals accepting scientificgibberishandappointingpeople who don't even exist to their editorial boards.(Readabout Dr. Fraud in our March 26 newsletter.)

"If journals do not get a handle on peer review, then they can't distinguish themselves from these predatory journals," Moher said.

Ivan Oransky and Adam Marcus arewatchdogswho track retractions of scientific papers on their blog Retraction Watch. Theycomparedthe current system of peer review to a toothless guard dog, incapable of spotting fraud or plagiarism, or keeping bad science from polluting the scientific record.

"There's a tremendous movement to open science," Moher said, calling on publishers to open their doors and allow scientists to study their peer review process. "I don't want to trash journals. I want to make them better."

As part of our summer Second Opinion series, we're featuring great Canadian moments in medical history. This week meetCharles BeerandRobert Noble.

Robert Noble and Charles Beer discovered a treatment for leukemia almost 60 years ago. (Canadian Medical Hall of Fame)

Together they discovered a chemotherapy drug in a Jamaican periwinkle plant that arrived in the mail.

It was an accidental discovery. They weren't looking for anti-cancer agents. Instead, the two researchers at the University of Western Ontario (now Western University) were searching for diabetes drugs. And they were curious what magic might be found in the periwinkle sample that had been mailed to Noble's brother.

"The disease of cancer was certainly far from our thoughts when we learned of a tea made from the leaves of a West Indian shrub that was supposedly useful in the control of diabetes mellitus," they wrote in their 1958 paper "Role of Chance Observations in Chemotherapy: Vinca Rosea."

Beer was an expert chemist, and he knew how to extract the plant's key compound. But whenthose extracts were fed to diabetic rabbits nothing happened. The blood sugar levels didn't change. But when they injected the extract into the rabbits' veins, the animals quickly died from a bacterial infection. "Apparently some natural barrier to infection was being depressed," they wrote.

They soon realized the periwinkle compound lowered the levels of white blood cells and depressed bone marrow. Could this be a possible treatment for leukemia, caused when white blood cells proliferate out of control?

They started growing the plant nearby so they could have a steady supply of the extract, even though in the Canadian climate the plants expressed much less of the active ingredient. Once they could reliably extract the compound they tested it on cancer patients at Princess Margaret Hospital in Toronto. That was almost 60 years ago.

Today vinblastine is on the World Health Organization'slistof essential medicines, used in combination with other drugs on lymphoma and other cancers.

Beerdiedin 2010 at age 95. Noble died in 1990 at age 80.

These fascinating stories of discovery were selected from the Canadian Medical Hall of Fame, a medical history organization that began in 1994. Every year, six Canadians are inducted. There is a small exhibit hall in London, Ont., but executive director Lissa Foster told us the real hall livesonline, with video features for the 125 laureates.

Thanks for reading! You canemail usany time with your thoughts or ideas. And if you like what you read, consider forwarding this to a friend.

Go here to see the original:
SECOND OPINION | Your life is leaving genetic scars that might show up in your child's genes - CBC.ca

Posted in Epigenetics | Comments Off on SECOND OPINION | Your life is leaving genetic scars that might show up in your child’s genes – CBC.ca

Cambridge Epigenetix and NuGEN Technologies Sign Agreement … – Technology Networks

Posted: August 19, 2017 at 5:42 pm

Co-exclusive global licence covers manufacture and integration of CEGX TrueMethyl technology for oxidative bisulfite sequencing (oxBS-Seq) with Targeted Methylation and NuGEN Ovation Methyl-Seq systems.

Cambridge Epigenetix (CEGX) and NuGEN Technologies, leaders in innovative epigenetic technologies, have announced that they have entered into a partnership agreement to integrate the CEGX TrueMethyl technology for oxidative bisulfite sequencing (oxBS-Seq) with NuGENs innovative NGS library preparation kits. The signing of the agreement will enable CEGX to focus on its epigenetic biomarker discovery programmes, both in-house and in partnership with leading biopharma companies, and will further strengthen NuGENs epigenetics portfolio of whole genome Methyl-Seq, Reduced Representation Bisulfite Sequencing (RRBS), and patented SPET target enrichment systems.

The epigenetic DNA modifications 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) play very different roles in gene regulation. Cambridge Epigenetix enhanced the appreciation of 5hmC through the introduction of its TrueMethyl oxBS-Seq system. Their developments have enabled researchers to further elucidate the role of DNA methylation in disease occurrence and progression, highlighting the potential for such epigenetic marks in the development of improved diagnostic and prognostic assays. The integration of TrueMethyl oxBS and NuGENs patented library preparation technologies will broaden the scope of accessible samples for the detection of these emerging markers.

Jason Mellad, CEO at Cambridge Epigenetix, commented: This partnership will enable both CEGX and NuGEN to leverage our strengths to facilitate advances in the epigenetics field. CEGX is committed to realising the promise of epigenetics through the development of improved, minimally invasive diagnostic and prognostic tests for accurate and early detection of a range of diseases, including cancer. We are working with leading biopharma companies as well as progressing our own high-value internal programmes, applying our expertise and advanced proprietary technology for robust biomarker identification, particularly from liquid biopsy samples. NuGENs reach and reputation for delivering high-quality genomics solutions to the market makes them the ideal partner to further develop TrueMethyl technology to deliver a range of new products to enhance epigenetics research.

Nitin Sood, CEO at NuGEN Technologies, said: We are delighted to be working with CEGX to provide the tools to improve the understanding and appreciation of epigenetics in cellular function. The goal of all of our products has always been to maximize the information that our customers obtain from their nucleic acid samples. By combining the TrueMethyl oxBS technology with our NGS library preparation kits, we will provide our customers with whole genome and targeted methylation products to unlock the tremendous potential of epigenetics. The combination provides access to more detailed, higher resolution epigenetic information in an integrated, cost-effective solution. The technology complements our Methyl-Seq and Single Primer Enrichment Technology product lines, and we are delighted to provide researchers with the most comprehensive solution for epigenetics research.

New products resulting from this partnership are anticipated by the end of the year and will be available directly from NuGEN. TrueMethyl products should still be ordered through CEGX until further notice. For more information about TrueMethyl, including how to order, please visit https://www.cambridge-epigenetix.com/products.

Read more from the original source:
Cambridge Epigenetix and NuGEN Technologies Sign Agreement ... - Technology Networks

Posted in Epigenetics | Comments Off on Cambridge Epigenetix and NuGEN Technologies Sign Agreement … – Technology Networks

Bacteria May Rig Their DNA to Speed Up Evolution – WIRED

Posted: August 19, 2017 at 5:41 pm

In 1944, a Columbia University doctoral student in genetics named Evelyn Witkin made a fortuitous mistake. During her first experiment in a laboratory at Cold Spring Harbor, in New York, she accidentally irradiated millions of E. coli with a lethal dose of ultraviolet light. When she returned the following day to check on the samples, they were all deadexcept for one, in which four bacterial cells had survived and continued to grow. Somehow, those cells were resistant to UV radiation. To Witkin, it seemed like a remarkably lucky coincidence that any cells in the culture had emerged with precisely the mutation they needed to surviveso much so that she questioned whether it was a coincidence at all.

Original story reprinted with permission from Quanta Magazine, an editorially independent publication of the Simons Foundation whose mission is to enhance public understanding of science by covering research developments and trends in mathematics and the physical and life sciences.

For the next two decades, Witkin sought to understand how and why these mutants had emerged. Her research led her to what is now known as the SOS response, a DNA repair mechanism that bacteria employ when their genomes are damaged, during which dozens of genes become active and the rate of mutation goes up. Those extra mutations are more often detrimental than beneficial, but they enable adaptations, such as the development of resistance to UV or antibiotics.

The question that has tormented some evolutionary biologists ever since is whether nature favored this arrangement. Is the upsurge in mutations merely a secondary consequence of a repair process inherently prone to error? Or, as some researchers claim, is the increase in the mutation rate itself an evolved adaptation, one that helps bacteria evolve advantageous traits more quickly in stressful environments?

The scientific challenge has not just been to demonstrate convincingly that harsh environments cause nonrandom mutations. It has also been to find a plausible mechanism consistent with the rest of molecular biology that could make lucky mutations more likely. Waves of studies in bacteria and more complex organisms have sought those answers for decades.

The latest and perhaps best answerfor explaining some kinds of mutations, anywayhas emerged from studies of yeast, as reported in June in PLOS Biology. A team led by Jonathan Houseley, a specialist in molecular biology and genetics at the Babraham Institute in Cambridge, proposed a mechanism that drives more mutation specifically in regions of the yeast genome where it could be most adaptive.

Its a totally new way that the environment can have an impact on the genome to allow adaptation in response to need. It is one of the most directed processes weve seen yet, said Philip Hastings, professor of molecular and human genetics at Baylor College of Medicine, who was not involved in the Houseley groups experiments. Other scientists contacted for this story also praised the work, though most cautioned that much about the controversial idea was still speculative and needed more support.

Rather than asking very broad questions like are mutations always random? I wanted to take a more mechanistic approach, Houseley said. He and his colleagues directed their attention to a specific kind of mutation called copy number variation. DNA often contains multiple copies of extended sequences of base pairs or even whole genes. The exact number can vary among individuals because, when cells are duplicating their DNA before cell division, certain mistakes can insert or delete copies of gene sequences. In humans, for instance, 5 to 10 percent of the genome shows copy number variation from person to personand some of these variations have been linked to cancer, diabetes, autism and a host of genetic disorders. Houseley suspected that in at least some cases, this variation in the number of gene copies might be a response to stresses or hazards in the environment.

Jonathan Houseley leads a team that studies genome change at the Babraham Institute in Cambridge. Based on their studies of yeast, they recently proposed a mechanism that would increase the odds for adaptive mutations in genes that are actively responding to environmental challenges.

Jon Houseley/QUANTA MAGAZINE

In 2015, Houseley and his colleagues described a mechanism by which yeast cells seemed to be driving extra copy number variation in genes associated with ribosomes, the parts of a cell that synthesize proteins. However, they did not prove that this increase was a purposefully adaptive response to a change or constraint in the cellular environment. Nevertheless, to them it seemed that the yeast was making more copies of the ribosomal genes when nutrients were abundant and the demand for making protein might be higher.

Houseley therefore decided to test whether similar mechanisms might act on genes more directly activated by hazardous changes in the environment. In their 2017 paper, he and his team focused on CUP1, a gene that helps yeast resist the toxic effects of environmental copper. They found that when yeast was exposed to copper, the variation in the number of copies of CUP1 in the cells increased. On average, most cells had fewer copies of the gene, but the yeast cells that gained more copiesabout 10 percent of the total population became more resistant to copper and flourished. The small number of cells that did the right thing, Houseley said, were at such an advantage that they were able to outcompete everything else.

But that change did not in itself mean much: If the environmental copper was causing mutations, then the change in CUP1 copy number variation might have been no more than a meaningless consequence of the higher mutation rate. To rule out that possibility, the researchers cleverly re-engineered the CUP1 gene so that it would respond to a harmless, nonmutagenic sugar, galactose, instead of copper. When these altered yeast cells were exposed to galactose, the variation in their number of copies of the gene changed, too.

The cells seemed to be directing greater variation to the exact place in their genome where it would be useful. After more work, the researchers identified elements of the biological mechanism behind this phenomenon. It was already known that when cells replicate their DNA, the replication mechanism sometimes stalls. Usually the mechanism can restart and pick up where it left off. When it cant, the cell can go back to the beginning of the replication process, but in doing so, it sometimes accidentally deletes a gene sequence or makes extra copies of it. That is what causes normal copy number variation. But Houseley and his team made the case that a combination of factors makes these copying errors especially likely to hit genes that are actively responding to environmental stresses, which means that they are more likely to show copy number variation.

The key point is that these effects center on genes responding to the environment, and that they could give natural selection extra opportunities to fine-tune which levels of gene expression might be optimal against certain challenges. The results seem to present experimental evidence that a challenging environment could galvanize cells into controlling those genetic changes that would best improve their fitness. They may also seem reminiscent of the outmoded, pre-Darwinian ideas of the French naturalist Jean-Baptiste Lamarck, who believed that organisms evolved by passing their environmentally acquired characteristics along to their offspring. Houseley maintains, however, that this similarity is only superficial.

What we have defined is a mechanism that has arisen entirely through Darwinian selection of random mutations to give a process that stimulates nonrandom mutations at useful sites, Houseley said. It is not Lamarckian adaptation. It just achieves some of the same ends without the problems involved with Lamarckian adaptation.

Ever since 1943, when the microbiologist Salvador Luria and the biophysicist Max Delbrck showed with Nobel prize-winning experiments that mutations in E. coli occur randomly, observations like the bacterial SOS response have made some biologists wonder whether there might be important loopholes to that rule. For example, in a controversial paper published in Nature in 1988, John Cairns of Harvard and his team found that when they placed bacteria that could not digest the milk sugar lactose in an environment where that sugar was the sole food source, the cells soon evolved the ability to convert the lactose into energy. Cairns argued that this result showed that cells had mechanisms to make certain mutations preferentially when they would be beneficial.

Budding yeast (S. cerevisiae) grow as colonies on this agar plate. If certain recent research is correct, a mechanism that helps to repair DNA damage in these cells may also promote more adaptive mutations, which could help the cells to evolve more quickly under harsh circumstances.

Jon Houseley/QUANTA MAGAZINE

Experimental support for that specific idea eventually proved lacking, but some biologists were inspired to become proponents of a broader theory that has come to be known as adaptive mutation. They believe that even if cells cant direct the precise mutation needed in a certain environment, they can adapt by elevating their mutation rate to promote genetic change.

The work of the Houseley team seems to bolster the case for that position. In the yeast mechanism theres not selection for a mechanism that actually says, This is the gene I should mutate to solve the problem, said Patricia Foster, a biologist at Indiana University. It shows that evolution can get speeded up.

Hastings at Baylor agreed, and praised the fact that Houseleys mechanism explains why the extra mutations dont happen throughout the genome. You need to be transcribing a gene for it to happen, he said.

Adaptive mutation theory, however, finds little acceptance among most biologists, and many of them view the original experiments by Cairns and the new ones by Houseley skeptically. They argue that even if higher mutation rates yield adaptations to environmental stress, proving that the higher mutation rates are themselves an adaptation to stress remains difficult to demonstrate convincingly. The interpretation is intuitively attractive, said John Roth, a geneticist and microbiologist at the University of California, Davis, but I dont think its right. I dont believe any of these examples of stress-induced mutagenesis are correct. There may be some other non-obvious explanation for the phenomenon.

I think [Houseleys work] is beautiful and relevant to the adaptive mutation debate, said Paul Sniegowski, a biologist at the University of Pennsylvania. But in the end, it still represents a hypothesis. To validate it more certainly, he added, theyd have to test it in the way an evolutionary biologist wouldby creating a theoretical model and determining whether this adaptive mutability could evolve within a reasonable period, and then by challenging populations of organisms in the lab to evolve a mechanism like this.

Notwithstanding the doubters, Houseley and his team are persevering with their research to understand its relevance to cancer and other biomedical problems. The emergence of chemotherapy-resistant cancers is commonplace and forms a major barrier to curing the disease, Houseley said. He thinks that chemotherapy drugs and other stresses on tumors may encourage malignant cells to mutate further, including mutations for resistance to the drugs. If that resistance is facilitated by the kind of mechanism he explored in his work on yeast, it could very well present a new drug target. Cancer patients might be treated both with normal courses of chemotherapy and with agents that would inhibit the biochemical modifications that make resistance mutations possible.

We are actively working on that, Houseley said, but its still in the early days.

Original story reprinted with permission from Quanta Magazine, an editorially independent publication of the Simons Foundation whose mission is to enhance public understanding of science by covering research developments and trends in mathematics and the physical and life sciences.

Link:
Bacteria May Rig Their DNA to Speed Up Evolution - WIRED

Posted in Human Genetics | Comments Off on Bacteria May Rig Their DNA to Speed Up Evolution – WIRED

Will Gene Editing Allow Us to Rid the World of Diseases? – Healthline

Posted: August 19, 2017 at 5:41 pm

Scientists recently used a gene-editing tool to fix a mutation in a human embryo. Around the world, researchers are chasing cures for other genetic diseases.

Now that the gene-editing genie is out of the bottle, what would you wish for first?

Babies with perfect eyes, over-the-top intelligence, and a touch of movie star charisma?

Or a world free of disease not just for your family, but for every family in the world?

Based on recent events, many scientists are working toward the latter.

Earlier this month, scientists from the Oregon Health & Science University used a gene editing tool to correct a disease-causing mutation in an embryo.

The technique, known as CRISPR-Cas9, fixed the mutation in the embryos nuclear DNA that causes hypertrophic cardiomyopathy, a common heart condition that can lead to heart failure or cardiac death.

This is the first time that this gene-editing tool has been tested on clinical-quality human eggs.

Had one of these embryos been implanted into a womans uterus and allowed to fully develop, the baby would have been free of the disease-causing variation of the gene.

This type of beneficial change would also have been passed down to future generations.

None of the embryos in this study were implanted or allowed to develop. But the success of the experiment offers a glimpse at the potential of CRISPR-Cas9.

Still, will we ever be able to gene-edit our world free of disease?

According to the Genetic Disease Foundation, there are more than 6,000 human genetic disorders.

Scientists could theoretically use CRISPR-Cas9 to correct any of these diseases in an embryo.

To do this, they would need an appropriate piece of RNA to target corresponding stretches of genetic material.

The Cas9 enzyme cuts DNA at that spot, which allows scientists to delete, repair, or replace a specific gene.

Some genetic diseases, though, may be easier to treat with this method than others.

Most people are focusing, at least initially, on diseases where there really is only one gene involved or a limited number of genes and theyre really well understood, Megan Hochstrasser, PhD, science communications manager at the Innovative Genomics Institute in California, told Healthline.

Diseases caused by a mutation in a single gene include sickle cell disease, cystic fibrosis, and Tay-Sachs disease. These affect millions of people worldwide.

These types of diseases, though, are far outnumbered by diseases like cardiovascular disease, diabetes, and cancer, which kill millions of people across the globe each year.

Genetics along with environmental factors also contribute to obesity, mental illness, and Alzheimers disease, although scientists are still working on understanding exactly how.

Right now, most CRISPR-Cas9 research focuses on simpler diseases.

There are a lot of things that have to be worked out with the technology for it to get to the place where we could ever apply it to one of those polygenic diseases, where multiple genes contribute or one gene has multiple effects, said Hochstrasser.

Although designer babies gain a lot of media attention, much CRISPR-Cas9 research is focused elsewhere.

Most people who are working on this are not working in human embryos, said Hochstrasser. Theyre trying to figure out how we can develop treatments for people that already have diseases.

These types of treatments would benefit children and adults who are already living with a genetic disease, as well as people who develop cancer.

This approach may also help the 25 million to 30 million Americans who have one of the more than 6,800 rare diseases.

Gene editing is a really powerful option for people with rare disease, said Hochstrasser. You could theoretically do a phase I clinical trial with all the people in the world that have a certain [rare] condition and cure them all if it worked.

Rare diseases affect fewer than 200,000 people in the United States at any given time, which means there is less incentive for pharmaceutical companies to develop treatments.

These less-common diseases include cystic fibrosis, Huntingtons disease, muscular dystrophies, and certain types of cancer.

Last year researchers at the University of California Berkeley made progress in developing an ex vivo therapy where you take cells out of a person, modify them, and put them back into the body.

This treatment was for sickle cell disease. In this condition, a genetic mutation causes hemoglobin molecules to stick together, which deforms red blood cells. This can lead to blockages in the blood vessels, anemia, pain, and organ failure.

Researchers used CRISPR-Cas9 to genetically engineer stem cells to fix the sickle cell disease mutation. They then injected these cells into mice.

The stem cells migrated to the bone marrow and developed into healthy red blood cells. Four months later, these cells could still be found in the mices blood.

This is not a cure for the disease, because the body would continue to make red blood cells that have the sickle cell disease mutation.

But researchers think that if enough healthy stem cells take root in the bone marrow, it could reduce the severity of disease symptoms.

More work is needed before researchers can test this treatment in people.

A group of Chinese researchers used a similar technique last year to treat people with an aggressive form of lung cancer the first clinical trial of its kind.

In this trial, researchers modified patients immune cells to disable a gene that is involved in stopping the cells immune response.

Researchers hope that, once injected into the body, the genetically edited immune cells will mount a stronger attack against the cancer cells.

These types of therapies might also work for other blood diseases, cancers, or immune problems.

But certain diseases will be more challenging to treat this way.

If you have a disorder of the brain, for example, you cant remove someones brain, do gene editing and then put it back in, said Hochstrasser. So we have to figure out how to get these reagents to the places they need to be in the body.

Not every human disease is caused by mutations in our genome.

Vector-borne diseases like malaria, yellow fever, dengue fever, and sleeping sickness kill more than 1 million people worldwide each year.

Many of these diseases are transmitted by mosquitoes, but also by ticks, flies, fleas, and freshwater snails.

Scientists are working on ways to use gene editing to reduce the toll of these diseases on the health of people around the world.

We could potentially get rid of malaria by engineering mosquitoes that cant transmit the parasite that causes malaria, said Hochstrasser. We could do this using the CRISPR-Cas9 technique to push this trait through the entire mosquito population very quickly.

Researchers are also using CRISPR-Cas9 to create designer foods.

DuPont recently used gene editing to produce a new variety of waxy corn that contains higher amounts of starch, which has uses in food and industry.

Modified crops may also help reduce deaths due to malnutrition, which is responsible for nearly half of all deaths worldwide in children under 5.

Scientists could potentially use CRISPR-Cas9 to create new varieties of food that are pest-resistant, drought-resistant, or contain more micronutrients.

One benefit of CRISPR-Cas9, compared to traditional plant breeding methods, is that it allows scientists to insert a single gene from a related wild plant into a domesticated variety, without other unwanted traits.

Gene editing in agriculture may also move more quickly than research in people because there is no need for years of lab, animal, and human clinical trials.

Even though plants grow pretty slowly, said Hochstrasser, it really is quicker to get [genetically engineered plants] out into the world than doing a clinical trial in people.

Safety and ethical concerns

CRISPR-Cas9 is a powerful tool, but it also raises several concerns.

Theres a lot of discussion right now about how best to detect so-called off-target effects, said Hochstrasser. This is what happens when the [Cas9] protein cuts somewhere similar to where you want it to cut.

Off-target cuts could lead to unexpected genetic problems that cause an embryo to die. An edit in the wrong gene could also create an entirely new genetic disease that would be passed onto future generations.

Even using CRISPR-Cas9 to modify mosquitoes and other insects raises safety concerns like what happens when you make large-scale changes to an ecosystem or a trait in a population that gets out of control.

There are also many ethical issues that come with modifying human embryos.

So will CRISPR-Cas9 help rid the world of disease?

Theres no doubt that it will make a sizeable dent in many diseases, but its unlikely to cure all of them any time soon.

We already have tools for avoiding genetic diseases like early genetic screening of fetuses and embryos but these are not universally used.

We still dont avoid tons of genetic diseases, because a lot of people dont know that they harbor mutations that can be inherited, said Hochstrasser.

Some genetic mutations also happen spontaneously. This is the case with many cancers that result from environmental factors such as UV rays, tobacco smoke, and certain chemicals.

People also make choices that increase their risk of heart disease, stroke, obesity, and diabetes.

So unless scientists can use CRISPR-Cas9 to find treatments for these lifestyle diseases or genetically engineer people to stop smoking and start biking to work these diseases will linger in human society.

Things like that are always going to need to be treated, said Hochstrasser. I dont think its realistic to think we would ever prevent every disease from happening in a human.

Excerpt from:
Will Gene Editing Allow Us to Rid the World of Diseases? - Healthline

Posted in Human Genetics | Comments Off on Will Gene Editing Allow Us to Rid the World of Diseases? – Healthline

Older men with ‘low T’ can improve their sex lives with testosterone therapy, study says – Men’s Fitness

Posted: August 19, 2017 at 5:41 pm

We hate to say it, but low testosterone levels can have a slew of negative effects for older guys.

But even now there's a scientific tug-of-war over testosterone-replacement therapy. Sure, it sounds greatwhat guy doesn't want more of the "masculine hormone"?but risks of testosterone therapy can include the growth of pre-existing cancerous cells, testicular shrinkage, infertility, even heart attack or stroke, as one of our writers discovered.

The positives are just as extreme. Aside from increased strength and motivation, men can enjoy greater urinary health, better sexual function, and a higher quality of life, according to new research from Boston University Medical Center.

In the study, published in the Journal of Urology, researchersenrolled roughly 650 men in their 50s and 60s. Some of the men had unexplained testosterone deficiencies, while others suffered from genetic hypogonadism (when gonads fail to produce testosterone). About 360 men received testosterone therapy for eight years (the remaining didn't).

What's more, the men who underwent testosterone therapy enjoyed a significant bump in their urinary and sexual function (lower instance of erectile dysfunction, higher sex drive), as well as better quality of life (sunnier mood, higher confidence).

Another interesting detail: Two men in the treatment group died from causes unrelated to cardiovascular failure, while 21 in the non-treatment group died (19 deaths were cardiovascular-related). Those mortality rates suggested that testosterone therapy isn't necessarily linked to a greater instance of heart attack or stroke, the researchers suggested.

"It is thought that testosterone treatment in men may increase prostate size and worsen lower urinary tract symptoms," study author Abdulmaged Traish, Ph.D., said in a press release. Researchers discovered somemenhad larger prostates post-testosterone therapy, but they experienced fewer instances of frequent urination, incomplete bladder emptying, and waking at night to urinate.

"[Testosterone therapy] is well-tolerated with progressive and sustained improvement in urinary and sexual function, and overall improvement in quality of life," Traish added.

Something to think about if your testosterone takes a hit one day and you want to fight manopause head-on.

Excerpt from:
Older men with 'low T' can improve their sex lives with testosterone therapy, study says - Men's Fitness

Posted in Testosterone Replacement Therapy | Comments Off on Older men with ‘low T’ can improve their sex lives with testosterone therapy, study says – Men’s Fitness

‘Bigfoot’ Silva responds to criticism of Rico Verhoeven fight, compares it to Mayweather vs. McGregor – MMA Fighting

Posted: August 19, 2017 at 5:41 pm

Glory heavyweight champion Rico Verhoeven will return to the ring in a non-title bout on Oct. 14 in Gangzhou, China, taking on former UFC fighter Antonio Silva, but fans didnt seem to approve the match-up.

Bigfoot" was knocked out seven times over the past four years, winning only one of his last 10 MMA bouts, and never competed in a kickboxing fight before. Verhoeven, on the other hand, holds a 51-10-1 kickboxing record with wins over the likes of Badr Hari, Peter Aerts, Gokhan Saki and Sergei Kharitonov.

"Critics will always exist and we have to know how to deal with them, Silva told MMA Fighting. "Sometimes they dont even mean to criticize you, but they are just jealous they wanted to be a professional fighter and dont have that talent. I was always a humble person, I came from a humble family in Paraba and competed around the world, and some people dont accept that.

"Its a heavyweight fight and anything can happen. I respect Rico, he's the champion, but when I step into the ring anything can happen."

The criticism is not of Silva taking a fight against the champion, but toward the promotion for booking someone who has been knocked out many times recently against the best heavyweight kickboxer on the planet.

Asked if someone in his team was against the match-up for health reasons, Silva said it was quite the opposite.

"As soon as we received the offer, everyone was in favor of it, "Bigfoot" said. "My manager, Alex Davis, said it was a good fight because he knows me and knows I can go there and put on a good fight. Everyone supported me because the impossible doesnt exist. If you go in there thinking that you cant do it, that hes the No. 1, or if you go there for the money, you already lost. I dont think like that. Im not going there for money or media, Im going there because I know I can put on a good fight."

"I went five rounds with Mark Hunt, and we stood and fought for 22 minutes. I knocked out (Alistair) Overeem, a K-1 champion, he continued. "Every athlete has to be versatile. I started in karate, but I always trained everything. Not having to worry about getting taken down or being pressed against the cage makes the camp and the actual fight easier."

Silva started his camp three weeks ago, as soon as he was offered the fight, and is excited about the challenge.

"Its a new experience for me, he said. "Im a professional athlete for years and I like to try new things, new challenges. I feel like an amateur going for his first fight, trying to show what he can do, and God willing everything will be alright.

The Brazilian heavyweight started in martial arts in karate, training for 12 years until he turned 17 and decided to add jiu-jitsu to his game. Now, he says, I train muay thai and boxing four times a week."

For his kickboxing debut, Bigfoot" will move his camp to his hometown Brasilia, Brazil, to train with UFC veteran Guto Inocente, a second-degree kickboxing black belt who holds a 34-8 kickboxing record, 5-1 under the Glory banner. Silva also invited Pedro Rizzo to join his camp in Brasilia.

"Rico is the champion, he deserves a lot of respect, Silva said. "Hes the best heavyweight kickboxer in the world. Im an amateur, its my first kickboxing fight, and I want to show what I can do. I have nothing to prove, I have no responsibility. Rico has the responsibility, hes the champion. The pressure is on him. Im cool."

The 37-year-old heavyweight compares his Glory debut to Conor McGregors upcoming clash with boxing legend Floyd Mayweather, when the UFC lightweight champion steps into the boxing ring for the first time against a 49-0 professional boxer in Las Vegas.

"Its a similar situation, Silva said. "McGregor never boxed and is going there to try to surprise. He has no pressure over himself because 99 percent of the people bet on Mayweather. Hes undefeated, 49-0, so most of the people think he will win. Its the same thing in this fight. But were two human beings stepping into a ring to fight. Anything can happen in a heavyweight fight, one hand can land and change the story."

"Im rooting for McGregor, he added. "He deserves respect. Hes a two-division champion in the UFC and is making history. Him as a person, he talks a lot, I dont consider him an idol, but he deserves respect. Anything can happen in this fight. Im rooting for him even though I think Mayweather will win because hes 49-0 and always trained that, so its complicated. But everything is possible."

According to Silva, hes getting paid "much more" in his recent fights compared to his previous bouts in the UFC, but thats not the only difference in this fight. The Brazilian heavyweight, who was only allowed to use testosterone replacement therapy once in the UFC against Mark Hunt, when he ended up testing positive for elevate testosterone levels restarted the treatment before his last MMA fight.

"My case is not for muscular gain or to enhance performance, but for health issues, said Silva, who lost his last fight to former Bellator heavyweight champion Vitaly Minakov in Russia. "I really need this in my life to be physically and mentally well. Ive fought in the UFC when my testosterone levels were at 77 three weeks before the fight. That's the level of a 90-year-old man. My levels were always low, 300, when someone at my age would be 800. I have doctors following me, making sure my levels are always at the normal range.

Continued here:
'Bigfoot' Silva responds to criticism of Rico Verhoeven fight, compares it to Mayweather vs. McGregor - MMA Fighting

Posted in Testosterone Replacement Therapy | Comments Off on ‘Bigfoot’ Silva responds to criticism of Rico Verhoeven fight, compares it to Mayweather vs. McGregor – MMA Fighting

Low T Center returning to sponsor Sorenson – ESPN

Posted: August 19, 2017 at 5:41 pm

Mooresville, NC (August 17, 2017) - 'Low T Center' is continuing their partnership with Reed Sorenson and Premium Motorsports as the team heads to Bristol Motor Speedway for this weekend's battle under the lights in the Monster Energy NASCARS Cup Series, 'Bass Pro Shops NRA Night Race'. Sorenson will be back in his familiar No.15 Chevrolet SS.

'Low T Center' is the leader of physician-led diagnosis and treatment of low testosterone with 50 locations nationwide and growing. Studies indicate testosterone deficiency has been linked to diabetes, metabolic syndrome, obesity, and high blood pressure. 'Low T Center' was designed so men can walk in, take a simple blood test, and know within 45 minutes if they are a candidate for Testosterone Replacement Therapy. Experience shows testosterone injections may lead to improved energy, strength, and libido, as well as decreases in body fat, irritability and depression. Most health insurance is accepted for treatment. Now with new locations in downtown Chicago,IL and Murfreesboro,TN.

To find your closest center and to learn more, go to https://lowtcenter.com.

--- Premium Motorsports ---

View post:
Low T Center returning to sponsor Sorenson - ESPN

Posted in Testosterone Replacement Therapy | Comments Off on Low T Center returning to sponsor Sorenson – ESPN

SpaceX Dragon Delivers Supplies (and Science) to Space Station – Space.com

Posted: August 19, 2017 at 5:40 pm

A SpaceX Dragon cargo ship arrived at the International Space Station early Wednesday (Aug. 16), delivering 3 tons of supplies, experiments and even some ice cream for the orbiting lab's crew.

The uncrewed Dragon spacecraft was captured by astronauts using the station's robotic arm at 6:52 a.m. EDT (1052 GMT) as the two spacecraft were flying over the Pacific Ocean, just north of New Zealand.

"Congratulations on a job well done," astronaut Andreas Morgenson of the European Space Agency radioed the station's crew from NASA's Mission Control in Houston. "You've just earned yourself some food." [Watch SpaceX Launch Dragon, then Land a Rocket]

The Dragon cargo ship is filled with more than 6,400 lbs. (2,900 kilograms) of supplies, science experiments and food - and yes, ice cream - for the space station's Expedition 52 crew. SpaceX launched delivery mission Monday (Aug. 14) on a Falcon 9 rocket, which then returned its first stage to Earth in a smooth landing.

Called SpaceX-12 or CRS-12, this flight is SpaceX's 12th cargo flight for NASA under the Commercial Resupply Service program. NASA initially agreed to buy 12 delivery flights from SpaceX, but has extended the agreement to include 20 flights. SpaceX did lose one mission in 2015 when a Falcon 9 rocket failed during liftoff, but the rest have been a success.

"Today has special significance because SpaceX-12 is the last flight on the original cargo resupply contract," NASA astronaut Jack Fischer said from the station. "And this, the 36th flight of a Dragon, stands as a testament to a burgeoning commercial industry that has become a pillar of support to NASA's and really all of humanity's quest to explore the universe."

SpaceX's Dragon cargo ship flies over Italy (the country's boot shape can be seen upside in the background) while delivering vital NASA supplies to the International Space Station on Aug. 16, 2017.

Fischer and ESA astronaut Paolo Nespoli captured the Dragon using the station's robotic arm. At one point, cameras on the space station captured Dragon as it soared high over Italy, Nespoli's home country.

Most of the cargo riding on Dragon is science gear, a massive haul that includes a protein crystal experiment to research a new treatment for Parkinson's disease, an experiment to grow lung tissue from stem cells and 20 live mice to help scientists study the effects of long space missions. The U.S. Department of Defense also has a small microsatellite prototype on board, and the Cosmic Ray Energetics and Mass for the International Space Station (which has the tasty acronym ISS-CREAM) will study cosmic rays.

The Dragon spacecraft will stay docked to the space station for about a month, after which it will be filled with science experiment results and other items for the return to Earth.

NASA has used SpaceX and another spaceflight company, the Virginia-based Orbital ATK, to make commercial resupply flights the space station since 2012. The space agency has since picked SpaceX, Orbital ATK and a third company Sierra Nevada Corp. to make future deliveries under a new agreement.

In addition to cargo delivery flights, SpaceX will fly NASA astronauts to the space station on a crewed version of the Dragon spacecraft. (NASA has also picked Boeing for astronaut trips to space using that company's CST-100 Starliner spacecraft.)

The first crewed flights on Dragon and the Starliner are expected in mid-2018, NASA has said.

Email Tariq Malik at tmalik@space.com or follow him@tariqjmalikandGoogle+.Follow us@Spacedotcom,FacebookorGoogle+. Original story onSpace.com.

Continued here:
SpaceX Dragon Delivers Supplies (and Science) to Space Station - Space.com

Posted in Virginia Stem Cells | Comments Off on SpaceX Dragon Delivers Supplies (and Science) to Space Station – Space.com

Scientists Discover New Hair Growth Technique Using Stem Cells – TrendinTech

Posted: August 18, 2017 at 10:45 am

Those suffering from hair loss problems could soon be worry free thanks to a bunch of researchers at UCLA. The team found that by activating the stem cells in the hair follicles they could make it grow. This type of research couldnt come soon enough for some. We may have finally found a cure for patients suffering from alopecia or baldness.

Hair loss is often caused by the hair follicle stem cells inability to activate and induce a new hair growth cycle. In doing the study, researchers Heather Christofk and William Lowry, of Eli Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCLA discovered that the metabolism of hair follicle stem cells is far different to any other cell found within the skin. They found that as hair follicle stem cells absorb the glucose from the bloodstream they use it to produce a metabolite called pyruvate. The pyruvate is then either sent to the cells mitochondria to be converted back into energy or is converted into another metabolite called lactate.

Christofk is an associate professor of biological chemistry and molecular and medical pharmacology and he says, Our observations about hair follicle stem cell metabolism prompted us to examine whether genetically diminishing the entry of pyruvate into the mitochondria would force hair follicle stem cells to make more lactate and if that would activate the cells and grow hair more quickly. First, the team demonstrated how blocking the lactate production in mice prevented the hair follicle stem cells from activating. Then, with the help of colleagues at the Rutter lab at the University of Utah, they increased the lactate production in the mice and as a result saw an accelerated hair follicle stem cell activation and therefore an increase in the hair cycle.

Once we saw how altering lactate production in the mice influenced hair growth, it led us to look for potential drugs that could be applied to the skin and have the same effect, confirms Lowry, a professor of molecular, cell and developmental biology. During the study, the team found two drugs in particular that influenced hair follicle stem cells to promote lactate production when applied to the skin of mice. The first is called RCGD423. This drug is responsible for allowing the transmission of information from outside the cell right to the heart of it in the nucleus by activating the cellular signaling pathway called JAK-Stat. The results from the study did, in fact, prove that JAK-Stat activation will lead to an increased production of lactate which will enhance hair growth. UK5099 was the second drug in question, and its role was to block the pyruvate from entering the mitochondria, forcing the production of lactate and accelerating hair growth as a result.

The study brings with it some very promising results. To be able to solve a problem that affects millions of people worldwide by using drugs to stimulate hair growth is brilliant. At the moment there is a provisional patent application thats been filed in respect of using RCGD423 in the promotion of hair growth and a separate provisional patent in place for the use of UK5099 for the same purpose. The drugs have not yet been tested in humans or approved by the Food and Drug Administration as fit for human consumption.

More News to Read

comments

Read this article:
Scientists Discover New Hair Growth Technique Using Stem Cells - TrendinTech

Posted in Utah Stem Cells | Comments Off on Scientists Discover New Hair Growth Technique Using Stem Cells – TrendinTech

Stem cell researchers discover promising lead in quest for hair regrowth – PhillyVoice.com

Posted: August 18, 2017 at 10:45 am

The ever-elusive cure for thinning hair, a concern that plagues both men and women, may have taken a taken a tentative step forward with the results of a new research study that focuses specifically on the role of follicle stem cells.

In new findings published in Nature Cell Biology, UCLA researchers revealed the discovery of a new way to activate hair regrowth by focusing on the unique metabolism of "quiescent" hair follicle stem cells. Although long-lived, these stem cells are normally inactive until the start of a new hair cycle, when they quickly spur regrowth in the anagen phase.

The UCLA study authors explain how the metabolism of hair follicle stem cells the way they divide, produce energy and respond to their environment differs from other cells of the skin:

Converting pyruvate into lactate could be the key to promoting more active follicles.

Our observations about hair follicle stem cell metabolism prompted us to examine whether genetically diminishing the entry of pyruvate into the mitochondria would force hair follicle stem cells to make more lactate, and if that would activate the cells and grow hair more quickly, said Heather Christofk, an associate professor of biological chemistry and molecular and medical pharmacology.

In one test on mice, the researchers found that when they genetically blocked lactate production, hair follicle stem cell activation was prevented. A second test, completed in collaboration with the Rutter Lab at the University of Utah, found that genetically increasing lactate production in mice accelerated hair follicle stem cell activation and increased the overall hair cycle.

Before this, no one knew that increasing or decreasing the lactate would have an effect on hair follicle stem cells, said Lowry, a professor of molecular, cell and developmental biology. Once we saw how altering lactate production in the mice influenced hair growth, it led us to look for potential drugs that could be applied to the skin and have the same effect.

The research team identified two drugs, RCGD423 and UK5099, that each promoted lactate production when applied to the skin of mice. The first drug works by activating a cellular signaling pathway called JAK-stat, increasing lactate production and in turn the activation of hair follicle stem cells to stimulate hair growth. The second drug blocks pyruvate from entering the mitochondria, forcing the production of lactate in the hair follicle stem cells and accelerating hair growth in mice.

Both experimental drugs are covered by provisional patent applications filed by the UCLA Technology Development Group on behalf of UC Regents. They have been used in preclinical tests only and have not been tested in humans or approved by the Food & Drug Administration.

Through this study, we gained a lot of interesting insight into new ways to activate stem cells, said Aimee Flores, a predoctoral trainee in Lowrys lab and first author of the study. The idea of using drugs to stimulate hair growth through hair follicle stem cells is very promising given how many millions of people, both men and women, deal with hair loss. I think weve only just begun to understand the critical role metabolism plays in hair growth and stem cells in general.

Continue reading here:
Stem cell researchers discover promising lead in quest for hair regrowth - PhillyVoice.com

Posted in Utah Stem Cells | Comments Off on Stem cell researchers discover promising lead in quest for hair regrowth – PhillyVoice.com

Page 1,483«..1020..1,4821,4831,4841,485..1,4901,500..»