StemCell Therapy

Sufferers of rare mitochondrial disease have new hope with a new method developed at the University of Sydney. The method provides a diagnosis within weeks instead of months or years through a simple blood sample.

Mitochondrial diseases are rare and hard to diagnose. They can affect any organ, at any age and are often 'hidden' in other diseases such as diabetes, blindness, liver and kidney failure and even Autism.

The new method has already led to two new disease gene discoveries where the patients suffered from lactate build-up and hyperglycemia (CYC1), and deafness and organ failure (MRPS7). The research published in the American Journal of Human Genetics and Human Molecular Genetics.

"One in 200 people will carry a mitochondrial genetic defect which means nearly 120,000 Australians are at risk of developing serious illness," says Minal. "And yet mitochondrial diseases are extremely difficult to diagnose. They are often referred to as the 'notorious masquerader'".

With the faster diagnosis, some people can be treated for what had previously been thought to be untreatable disease.

For others even if not treatment is available, the diagnosis gives them a cause for the illness and the possibility to enrol in clinical trials. This can result in enormous improvements in quality of life.

Families can also receive genetic counselling and many may choose to use IVF when building a family, with medical staff able to quantify the risk of the disease being passed on.

Explore further: New genetic analysis approach could improve diagnosis for mitochondrial disease

More information: Pauline Gaignard et al. Mutations in CYC1, Encoding Cytochrome c1 Subunit of Respiratory Chain Complex III, Cause Insulin-Responsive Hyperglycemia, The American Journal of Human Genetics (2013). DOI: 10.1016/j.ajhg.2013.06.015

Minal J. Menezes et al. Mutation in mitochondrial ribosomal protein S7 (MRPS7) causes congenital sensorineural deafness, progressive hepatic and renal failure and lactic acidemia, Human Molecular Genetics (2015). DOI: 10.1093/hmg/ddu747

Continued here:
Blood test uncovers hidden diseases - Medical Xpress

If youve ever gotten a nasty case of the flu even though you dutifully got a flu shot, you know that the vaccine is not 100 percent effective. Now, scientists believe that they have devised a new way of producing the vaccine that will offer better protection.

Part of the reason the vaccine is not fully effective is because the strains mutate. For decades, vaccine manufacturers have used chicken eggs to grow the flu virus strains used in the shot. Problems arise when the human strains mutate to adapt to their new environment, making the vaccine an imperfect match for the virus.

Researchers at Duke University have found a way to prevent the strains from mutating, which allows them to make a perfect match for the virus. Their findings have been published in the journal mBio.

We have solved a fundamental problem that scientists had accepted would be part of vaccine productionthat the virus is always going to mutate if it is grown in eggs, said senior study author Nicholas S. Heaton, Ph.D., assistant professor of molecular genetics and microbiology at Duke University School of Medicine. This research could lead to a significantly cheaper and more efficacious vaccine.

Getty Images | Tim Boyle

Despite the flu vaccines current efficacy rate, its probably still in your best interest to get one. According to theCDC Foundation,flu illness costs the U.S. more than $87 billion annually, which includes an estimated $10.4 billion in direct medical expenses.

And if its the needle thats preventing you from getting a flu shot, theres another new development in the world of the flu vaccine that might interest you. A version of a flu vaccine patch developed by Georgia Techs Laboratory for Drug Delivery showed promising results in its first human clinical trial, according to a study in The Lancet, which would make getting vaccinated as easy as slapping on a band-aid.

[h/t: Science Daily]

Originally posted here:
Scientists Have Pinpointed A Method To Make The Flu Vaccine More Effective - Simplemost

RUTHERFORD, N.J. and LOS ANGELES, Aug. 16, 2017 (GLOBE NEWSWIRE) -- Cancer Genetics, Inc. (Nasdaq:CGIX) (The Company and CGI), a leader in enabling precision medicine for oncology through molecular markers and diagnostics, announced todaythat it will host an investor and analyst call and webcast onTuesday,August 22, 2017at8:30 am Eastern. CGI willdiscuss the strategy and business rationale of the recent transformative and accretive acquisition ofvivoPharm.

CGIs acquisition ofvivoPharm, announced on August 14, 2017,will significantly strengthenthe Company's position as a leader for oncology discoveryand early phase clinical development and testing for biotechnology and pharmaceutical companies. With over a decade of experience in delivering a wide range of discovery and preclinical services to support drug development, target validation and biomarker analysis,vivoPharm has supported over 200 IND submissions for innovative therapies, with a significant focus on immuno-oncology.

Hosted by CGI's CEO and President, Mr. Panna Sharma, the call will introduceinvestors and analysts tonew members of the CGI team, including Dr. RalfBrandt, former CEO and Managing Director ofvivoPharm, who now serves as the President of Discovery & Early Development Services at CGI.

Mr. Sharma will also provide insight into both operational and customer synergies that will result from the integration ofvivoPharm, as well as the long-term strategy for growth. Additional details will also be provided onvivoPharms specialized tumor and disease models, toxicology and pharmacology services, biomarker analysis and animal imaging capabilitiesthat are expected toprovide CGInewopportunities to deepen its relationships with existing biopharma customers through additional discovery and downstream molecular work,while bolstering the Companys previously announced initiative aimed at early-phase drug repurposing and drug rescue programs.

The call details are noted in the table below.

ABOUT CANCER GENETICSCancer Genetics, Inc. is a leader in enabling precision medicine in oncology from bench to bedside through the use of oncology biomarkers and molecular testing. CGI is developing a global footprint with locations in the US, India and China. We have established strong clinical research collaborations with major cancer centers such as Memorial Sloan Kettering, The Cleveland Clinic, Mayo Clinic, Keck School of Medicine at USC and the National Cancer Institute.

The Company offers a comprehensive range of laboratory services that provide critical genomic and biomarker information. Its state-of-the-art reference labs are CLIA-certified and CAP-accredited in the US and have licensure from several states including New York State.

For more information, please visit or follow us:Internet:www.cancergenetics.comTwitter:@Cancer GeneticsFacebook:www.facebook.com/CancerGenetics

Forward Looking Statements:This press release may contain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements pertaining to future financial and/or operating results, future growth in revenues, margins, research, technology, clinical development and potential opportunities for Cancer Genetics, Inc. tests and services, along with other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements.

Any statements that are not historical fact (including, but not limited to, statements that contain words such as "will," "believes," "plans," "anticipates," "expects," "estimates") should also be considered to be forward-looking statements. Forward-looking statements involve risks and uncertainties, including, without limitation, risks inherent in the development and/or commercialization of potential products, risks of cancellation of customer contracts or discontinuance of trials, risks that anticipated benefits from acquisitions will not be realized, uncertainty in the results of clinical trials or regulatory approvals, need and ability to obtain future capital, maintenance of intellectual property rights and other risks discussed in the Cancer Genetics, Inc. Form 10-K for the year ended December 31, 2016 along with other filings with the Securities and Exchange Commission. These forward-looking statements speak only as of the date hereof. Cancer Genetics, Inc. disclaims any obligation to update these forward-looking statements.

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Cancer Genetics, Inc. to Host Conference Call to Discuss Strategic and Business Rationale of vivoPharm Acquisition - GlobeNewswire (press release)

Bow

Alex Locatelli Alfano, son of Paul and Debra Alfano of Bow, graduated from The Derryfield School in Manchester. While at Derryfield, Alex was a four-year member of both the basketball and baseball teams. He was also an active member of Key Club, the literary magazine, Excerpt, and the Current Events Club. He will be attending the University of New England in the fall.

Gabrielle Megan Brummett, daughter of Russ and Michelle Brummett of Bow, graduated from The Derryfield School in Manchester. She will be attending Duke University to play Division I soccer in the fall. While at Derryfield, Gabi maintained high honors throughout her Derryfield academic career and volunteered with Key Club as a youth soccer coach and with Samba International. Gabi played four years of varsity girls soccer and made her mark on the soccer community locally and nationally. A two-time Gatorade State Player of the Year, Gabi led the Derryfield Cougars to two state championships in four years.

Abigail Wadewas named to the honor roll for the spring semester at the University of Dallas in Irving, Texas. She is an art major.

Harry Gunn earned a bachelor of science degree, summa cum laude, in chemical engineering from Syracuse University in Syracuse, N.Y. He will be attending the University of Pennsylvania Law School this fall.

Kevin Hayes, son of Dan and Ellen Hayes, was named to the deans list for the spring semester at the University of Rochester in Rochester, N.Y. He is a junior majoring in molecular genetics.

Abigail Painchaud was named to the deans list for the spring semester at Trinity College in Hartford, Conn.

Tyler Hussey was named to the deans list for the spring semester at Nichols College in Dudley, Mass. He is a human resources major.

Maeghan Connor was named to the deans list for the spring semester at St. Lawrence University in Canton, N.Y. She is a senior conservation biology and global studies major.

Kyle Zollo-Venecek, son of Daniel Venecek and Linda Zollo of Concord, was named to the deans list for the spring semester at Bates College in Lewiston, Maine. He is a chemistry major.

Flannery Black-Ingersoll, daughter of Douglas Ingersoll and Rebecca Black of Concord, was named to the deans list for the spring semester at Bates College in Lewiston, Maine. She is a mathematics and arts and visual culture major.

Anastasia Toumpas earned a degree in biology and environmental studies from Wells College in Aurora, N.Y. She was also named to the deans list for the spring semester.

Elizabeth Bailey was elected as secretary to the Board of Trustees of Leadership New Hampshire for the 2017-18 program year. She has been a member of the board since 2016.

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People for Aug. 12, 2017 - Concord Monitor

A new paper from Duke molecular genetics and microbiology shows how pathogenic Cryptococcus fungi evolved from having many sexes to just two through 50 million years of gene swapping. Credit: Kara Manke

Biologically speaking, nearly every species on Earth has two opposite sexes, male and female. But with some fungi and other microbes, sex can be a lot more complicated. Some members of Cryptococcus, a family of fungus linked to human disease, can have tens of thousands of different mating types.

In a study appearing early online Aug. 11 in PLOS Biology, Duke researchers have mapped the evolutionary turning point that transformed the pathogenic form of Cryptococcus from an organism of many sexes to one with only two. They found that during evolution, a reshuffling of DNA known as translocation brought together separate chunks of sex-determining genes onto a single chromosome, essentially mimicking the human X or Y chromosome.

Surprisingly, they've shown that these crucial translocations occurred at the centromeres, the twisty ties that hold together chromosomes at the center of an x-shaped pair. These regions of the chromosome are so dense that they were once thought to be removed from recombination.

"Recombination at the centromere doesn't have to happen frequently, it just has to happen often enough that it punctuates the evolution of the organism," said Joseph Heitman, MD, PhD, senior study author and professor and chair of molecular genetics and microbiology at Duke University School of Medicine. "With each translocation, the genome is altered again and again, until you have evolved an entirely new species."

Scientists have been studying the evolution of sex chromosomes for more than a century. In the 1960's, Japanese-American geneticist and evolutionary biologist Susumu Ohno proposed a theory in which the genes determining sex first arose at various spots scattered across the entire genome, but over time were "captured" on the sex chromosomes. In humans, those chromosomes go by the familiar X and Y; in birds, they are known as Z and W; in moss, they are called U and V.

Regardless of the name or species, Heitman contends that some universal principles could govern the evolution of all sex chromosomes. He and an international team of researchers focused on the last common ancestor of the human pathogen Cryptococcus neoformans and its nearest sibling species, a non-pathogen called Cryptococcus amylolentus.

In C. amylolentus, dozens of genes at two different locations on the chromosomes control what's called a tetrapolar, or four-part, mating system. At one location or locus known as P/R, genes encode pheromones and pheromone receptors that help the fungus recognize compatible mating types. At the other locus, called HD, genes govern the development of sexual structures and reproductive spores.

The researchers sequenced the entire genome of C. amylolentus, mapping the location of all the genes as well as the centromeres on each of the organism's 14 chromosomes.

They found that the genomes had undergone quite a bit of rearrangement since the two species shared a common ancestor, at least 50 million years ago. For example, chromosome 1 of C. neoformans contained pieces of four different chromosomes from C. amylolentus, providing evidence of multiple translocations, some within the centromere.

"That was very surprising. The dogma has been that recombination is repressed in centromeric regions," said Sheng Sun, PhD, lead study author and assistant research professor at Duke University School of Medicine.

In the 1980's, a seminal paper by Duke colleague Tom Petes demonstrated recombination could occur across the centromeres in Saccharomyces cerevisiae, but some attributed the finding to a quirk of the favored model organism with its tiny point centromeres. But since then, other studies have emerged suggesting that the phenomenon was wider spread.

In this study, the researchers showed that in Cryptococcus amylolentus, the ancestral state, the P/R locus resided on chromosome 10 and the HD locus on chromosome 11. But in Cryptococcus neoformans, the evolved state, those loci ended up in one place. According to their model, multiple translocations deposited the two sex determinants on the same chromosome, with a centromere in between. Subsequent rearrangements put P/R and HD next to each other. The result was an organism with a bipolar mating system, much like the male and female sexes that embody most species.

"In any kind of model like this, you are thinking about what could have been the organization in the last common ancestor, which is now extinct so you can't know definitively," said Heitman. "But in each of these lineages, there are multiple evolutionary events that have occurred, and you can use genomics to turn back the hands of time and deduce the trajectory."

Heitman says their study suggests that other researchers should actively look for translocations, both in the expected locations as well as within centromeres. These chromosomal rearrangements are a common cause of birth defects and cancer in humans.

He and his colleagues are currently investigating whether similar translocations occur in the evolution of sex chromosomes in other fungal families, such as Ustilago and Malassezia.

Explore further: Evolution of the Sexes: What a Fungus Can Tell Us

More information: "Fungal genome and mating system transitions facilitated by chromosomal translocations involving intercentromeric recombination," Sheng Sun, Vikas Yadav, R. Blake Billmyre, Christina A. Cuomo, Minou Nowrousian, Liuyang Wang, Jean-Luc Souciet, Teun Boekhout, Betina Porcel, Patrick Wincker, Joshua A. Granek, Kaustuv Sanyal and Joseph Heitman. PLOS Biology, Early online Aug. 11, 2017. DOI: 10.1371/journal.pbio.2002527

Journal reference: PLoS Biology

Provided by: Duke University

See the original post here:
Scientists map sex chromosome evolution in pathogenic fungi - Phys.Org

Product News Aug 11, 2017

Image Credit: Integrated DNA Technologies

Integrated DNA Technologies (IDT) will host a webinar titled "Increase on-target specificity of CRISPR genome editing using a novel, high-fidelity Cas9 nuclease on August 16, 2017. The webinar will be presented by Dr Chris Vakulskas, Staff Scientist, Molecular Genetics at IDT. Dr Vakulskas will present data from the development of the novel Alt-R S.p. HiFi Cas9 Nuclease 3NLS, as well as describe its benefits for improved specificity without compromising on-target activity.

Despite its revolutionary impact on life science research, the CRISPR/Cas9 genome editing system suffers from concerns related to target specificity, particularly for researchers considering therapeutic applications. Until now, modifications to guide RNAs and Cas9 proteins have been used to reduce off-target effects, but many of these have also reduced on-target editing. In this webinar, Dr Vakulskas will describe how his team developed the novel Alt-R S.p. HiFi Cas9 Nuclease 3NLS through an intensive screening and selection process. Webinar attendees will learn about the benefits and usefulness of this this novel nuclease as part of a ribonucleoprotein (RNP) complex to mitigate unwanted off-target gene editing.

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Stay On-Target With Novel, High-Fidelity Cas9 - Technology Networks

VANCOUVER, BC / ACCESSWIRE / August 11, 2017 / Friday Night Inc. (Friday Night) (CSE:TGIF) (1QF.F) (OTC PINK: VPGDF) is pleased to announce that the Company has appointed Dr. Anthony R. Torres, MD to its board of advisors and would also like to provide an update on the genetics breeding program at the Company's 91% owned subsidiary, Alternative Medicine Association, LC. (AMA).

NEW GENETIC STRAIN

Over the past several months, AMA has been cross breeding existing strains in hopes of creating an improved cannabis product. This time consuming and laborious process has resulted in a new product offering that only AMA will be able to provide.

One of AMA's favorite prototype plants from the genetics program is a strain they have created and named ''Naughty Cookies''. Over the last year and thousands of test plants later, AMA created the new strain by crossing the high-THC and popular 'Girl Scout Cookies' strain with the high-yielding 'Juggernaut' male. The buds are very frosty, aesthetically pleasing and dense with light purple coloration.

This week AMA received the test results for the first lot. The cannabinoid content was higher than any strain AMA had seen in the last 3 years, and the THC content came back as 34.9%. Most fortunately, AMA had the foresight to cultivate over 70 of these plants in anticipation of great results. These will be flowered during the next growing cycle and so far are yielding over 2 pounds per light of dried flower.

The creator of this strain and Director of Operations, Mr. Ben Horner said, ''This gives us a competitive edge in a market which we now control. When new cultivators come on board, we will be the only producer with this strain. I feel it will inevitably become a favorite in Las Vegas.''

NEW ADVISOR TO THE COMPANY

Anthony R. Torres, M.D. with training at the National Institutes of Health, Yale University School of Medicine and the University of Utah, has considerable experience in the separation sciences of biological molecules. Anthony is widely published and has made a career not only in university research, but also in the biotechnology field including protein enrichment and advance separation processes. He is an inventor and owns several patents in the field. He is not new to the world of start-up companies and continues to be a pioneer in biotechnology. He also brings a deep understanding of the cannabis plant and its molecular structure.

Dr. Torres commented, ''I am very interested in applying traditional laboratory processes to the rapidly developing field of molecular cannabis. I believe that there are many positive applications for the natural benefits of this plant in modern medicine and that it has the potential to help hundreds of thousands, perhaps even millions of people.''

About Friday Night Inc.

Friday Night Inc. is a Canadian public company, which owns and controls cannabis and hemp based assets in Las Vegas Nevada. The company owns 91% of Alternative Medicine Association, LC (AMA), a licensed medical and adult-use cannabis cultivation and production facility that produces its own line of unique cannabis-based products and manufactures other third-party brands. Infused MFG, also a 91% owned subsidiary, produces hemp-based, CBD products, thoughtfully crafted of high quality organic botanical ingredients. Friday Night Inc. is focused on strengthening and expanding these operations within and outside of the state.

For further information please contact:Joe Bleackley, Corporate Communications604-674-4756Joe@FridayNightInc.com

Notice regarding Forward Looking Statements: This news release contains forward-looking statements. The use of any of the words ''anticipate,'' ''continue,'' ''estimate,'' ''expect,'' ''may,'' ''will,'' ''project,'' ''should,'' ''believe,'' and similar expressions are intended to identify forward-looking statements. Although the Company believes that the expectations and assumptions on which the forward-looking statements are based are reasonable, undue reliance should not be placed on the forward-looking statements because the Company can give no assurance that they will prove to be correct. This news release includes forward-looking statements with respect to the entering into a definitive agreement, the future exercise of the option regarding the vape lounge and the regulatory environment in Canada. Since forward-looking statements address future events and conditions, by their very nature they involve inherent risks and uncertainties. These statements speak only as of the date of this news release. Actual results could differ materially from those currently anticipated due to a number of factors and risks including failure to enter into a definitive agreement, inability to attract new customers in Nevada as a result of the license, the inability of the Company to take advantage of the license arrangement and various risk factors discussed in the Company's disclosure documents, which can be found under the Company's profile on http://www.sedar.com. Friday Night undertakes no obligation to update publicly or revise any forward-looking information, whether as a result of new information, future events or otherwise, except as required by law or the Canadian Securities Exchange.

Read More

SOURCE: Friday Night Inc.

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Friday Night Inc. Announces Dr. Torres Advisor and Genetics Update - Yahoo News

Some of you may remember back to the fun days when taking a pig to the fair was the highlight of summer. Early on I wrote about my sons exercising their pigs in the roadside ditch when the pigs started chasing cars. Of course, the more the pigs chased the car, the driver slowed down which of course egged the pigs on to run even faster alongside.

Now the 4-H swine business has become a much more serious project. Readers may remember that it wasnt only a couple years ago that all 4-H poultry projects in Ohio were banned from exhibition because of an epidemic of avian influenza a disease that might have easily caused an epidemic in humans.

It wasnt until the days of checking DNA and genomic testing did anyone realize the different strains of influenza. (I call it a strain even though a more appropriate term is genotype.) Influenza or flu as most people call it has a long history, even though most of us chalk it up as one of those diseases that might cause us to stay home from work or school for a couple of days.

The 1918 influenza outbreak caused a pandemic worldwide. In the spring of 1918 (and then a reappearance in the fall) this pandemic caused an estimated 50 million human deaths worldwide. So influenza isnt anything to trifle with, especially in this age of around-the-world travel. It is a virus that can jump back and forth between humans, pigs, poultry, and wild birds then back again.

You would need to live in a shoebox to not know about the influenza outbreak in pigs that occurred recently at the Clinton County Fair. What you may not know is that influenza in pigs at the Clinton Country Fair appears to actually contain some human DNA genetic code rather than just the normal flu virus found in pigs.

Here are some basic facts. From early in my career until recent years, influenza was primarily classified as H1N1. Now with molecular genetics and DNA analysis we know that the virus has been changing. It has mutated to several different new types. For instance just to name a few there are: H3N2, H7N8, H3N5 and then we could also discuss low-pathogen versus high pathogen influenza. You get the idea, as fast as the virus can modify itself to attack a vulnerable animal or a human, it will.

Formerly swine vaccines were primarily for H1N1. You can deduce that a vaccine for a specific genotype may be very effective. We cant vaccinate our way out of having either sick animals or sick humans if the latest infection is a different genotype.

The current strategy experts have espoused is biosecurity. This refers to use a common sense approach towards eliminating or minimizing exposure when evaluating the risk of contracting a disease in either humans or animals. Sick pigs, just like sick children, should have limited risk or no risk of exposing others. Dont send a sick pig with a fever to the fair just as you shouldnt send a sick child to school.

Someone took a sick pig with a fever to the Clinton County fair. Authorities know this because pigs started spiking fevers immediately upon arrival rather than the virus incubating several days before illness appeared. Fortunately the fair veterinarian recognized early on that too many pigs were getting sick and called for diagnostic expertise from the virologists at the State Animal Diagnostic Lab in Reynoldsburg. They responded immediately.

Nasal swabs confirmed a diagnosis of influenza H3N2. Over the next couple of days more pigs tested positive demonstrating that an epidemic had started. Approximately 68 pigs were confirmed ill of the slightly less than 300 pigs in the swine pavilion. Since then, the CDC in Atlanta has been doing further DNA sequencing to pinpoint its precise anatomy. A human DNA sequence has also been identified in the virus.

Dr. Tony Forshey, the state veterinarian, and his team quarantined the barn early in the course of the disease. The team made the decision to allow the youth to show their projects while in quarantine as the show arena was adjacent to the pig pens. Parents were allowed to attend to watch the 4-Hers show their animals, but other interested parties were excluded. At the conclusion of the show, the pigs were then sent to a packing plant for processing into meat a normal sequence of events after most county fair shows.

News outlets reported faster than the influenza could spread that the pigs were destroyed and the barn burned down. Talk about fake news! What a bunch of baloney, or perhaps I should say sausage, the pig kind. No pigs were destroyed at the fair and no barns burned. After the show the pigs were shipped to a packing company for processing into meat. With standard processing and inspection, all of the meat from chops to bacon was determined to be safe to consume. Contrary to what was reported by several other news outlets, the barn was not burned but cleaned and sanitized. Since those early reports news organizations did get their stories straight.

Some had several thousand dollars for their pigs. These exhibitors were angry because their plans were to ship these high dollar porkers from fair to fair and win as many prizes as possible. Perhaps they may have even planned on a climax at the State Fair. If their pig was a champion, it would bring a lot of recognition and money in the Sale of Champions.

These individuals would have chosen to ignore the health risks. Should these infected pigs be allowed to move to other show premises, a major epidemic was certain to occur at every exhibition the pigs appeared and likely start a human health crisis. Ohios commercial swine industry would also have been put to a serious health and economic risk. It is readily apparent that protecting all Ohioans and the commercial swine industry is critical. There are over two million commercial breeding and market swine in Ohio supplying high quality protein in the form of meat to consumers.

I grew up showing pigs, my sons showed pigs and my granddaughters are showing pigs next month. Today it is most important to protect the commercial swine industry rather than gunners going for the big prize. There is more to life than the big prize, the accompanying recognition and a big paycheck for a few individuals.

Dr. Forshey took a lot of heat for quarantining those Clinton County pigs, allowing them to show their pigs, then shutting down the swine exhibition and sending the pigs to slaughter. In view of the virus containing aberrant human DNA code, allowing the pigs to move onto other exhibitions may have started a human influenza epidemic. In my estimation he made a wise decision for the Ohio citizens and also the swine industry, but yet was compassionate to 4-Hers in Clinton County. Kudos to Dr. Forshey and his team!

The rest is here:
Learn how influenza topped fake news - Ohio's Country Journal and Ohio Ag Net

The humble kitchen sponge may not exactly be the cleanest thing around, but it's still your trusted tool for dealing with that sink of dirty dishes. So, it cant be that bad, right? Err Actually, those innocent-looking little sponges can be some of the most bacteria-packed things in your house.

Thats according to a recent study, published in the journal Scientific Reports, which analyzed the bacteria in sponges that people regularly used to clean their kitchens. For the study, researchers looked at the genetic information of microbes that live in the sponges and found 362 different species of bacteria in 14 sponges.

Granted, exposure to some bacteria can be good for you, and it takes a lot of the less-friendly types to actually make you sick. But in this study, five of the 10 most common species of bacteria in the sponges were kinds that can potentially cause infections, including three species in the Acinetobacter genus, for instance, which can cause pneumonia.

So, you should probably just clean your sponges more often, right? Not necessarily. The study also found that two of the most common bacteria found on the spongesChryseobacterium hominis and Moraxella osloensiswere more likely to be resistant to cleaning (including both conventional washing with hot, soapy water and microwaving). In fact, these bacteria actually thrived in sponges that were cleaned regularly. Fantastic.

The reason why cleaning the sponge doesn't solve the problem is a little confusing, but it comes down to simple math, Michael G. Schmidt, Ph.D., professor and vice chair of the department of microbiology and immunology at Medical University of South Carolina, tells SELF. The majority of disinfectants are designed to reduce the concentration of bacteria by 99.9 percent. Although we tend to assume that's "basically 100 percent," it's really not.

If there are 10 million bacteria associated with the sponge and the disinfectant did its job, a 99.9 percent reduction would still leave approximately 10,000 bacteria in the sponge, Schmidt explains. And those that escape the disinfectant end up with less competition and can, therefore, proliferate. Ultimately, its not that surprising that there were still microbes in the nooks and crannies of the sponge, he says.

It's also a good idea to pay attention to where you put your sponge. For most bacteria to grow and maintain that growth, they need moisture, Daniel Hassett, Ph.D., professor of molecular genetics at the University of Cincinnati College of Medicine, tells SELF. A lot of people let their sponges sit on top of the sink, and theres still moisture there, he points out. Ideally, you should put your sponge on an elevated, highly aerated area, he says, like a little soap dish with holes in the bottom so it won't just sit in moisture.

When it comes to the bacteria on your sponge, keep a few factors in mind before freaking out. The types of microbes you're dealing with, how concentrated they are, and their virulence factors (molecules that add to their ability to infect you) all affect the chances of you getting sick, Schmidt says. For the most part, your immune system will fight these bacteria off. But, occasionally, a nasty pathogen can slip through, he says. The chances of illness are always present, but if you eat well [and] get plenty of rest, your immune system and microbes will be able to resist the majority of the bugs in the sponge. If you have a compromised immune system for whatever reason, though, you may be more likely to get sick from these and other pathogens.

And, according to Hassett, your odds of getting sick are virtually zero if you wash your hands well after using a sponge. Even if you use a tainted sponge to clean a plate, a lot of that bacteria will be killed as it dries.

For the vast majority of us, the go-to sanitization methods are still totally fine. The dishwasher is often considered the best way, since heat, soap, and water work quite well with each other to inactivate bacteria, Schmidt says.

And you can still microwave your (wet) sponge for a minute or two. Schmidt says the basic idea makes sense, but your results may vary based on the thickness of your sponge and concentration of the bacteria. "Steam needs to reach the microbeand effectively render the [bacteria] to an inactive state," he explains. Think about it like trying to make the perfect baked potato: Some microwaves can do it perfectly with a single presetting, while others require a little more fiddling. That's because both the power of the microwave and the thickness of the spud can vary. And, just like a microwaved potato, your sponge will be piping hot when it comes outso proceed with caution. Also, don't forget to wet the sponge before putting it in the microwave or you will set a small fire.

You can also make sure your sponge has a chance to fully dry out before you use it again. So remember to move it onto an elevated holder that allows it to drain.

Its also best to avoid using sponges to clean up meat and fish, since those foods are more likely to carry bacteria. Ideally, sponges are great for wiping up crumbs, Dr. Schmidt says. But, if you use them to decontaminate your counter or cutting board, be sure to spray a disinfectant on the dirty surface first, let it sit for a moment, and then use your sponge to wipe up the dead microbes.

And, of course, dont keep your sponge forever. The studys researchers recommend tossing them after a week. Yes, a week.

Related:

You May Also Like: 12 Healthy Foods You Should Always Keep in Your Pantry

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Your Sponge Holds a Disgusting Amount of Bacteria, BTW | SELF - SELF

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Helen McNeills work in developmental biology spans birth defects to cancer

Helen McNeill, PhD, has been named a BJC Investigator at Washington University School of Medicine in St. Louis. She is the first researcher named as part of the new BJC Investigators Program.

Helen McNeill, PhD, has been named a BJC Investigator at Washington University School of Medicine in St. Louis. She is the first researcher named as part of the new BJC Investigators Program, which aims to recruit scientists who bring innovative approaches to major biological quandaries and whose discoveries stand to inform new ways of understanding disease and developing treatments.

McNeill, the first of 10 expected BJC Investigators, is currently a professor in the Institute of Medical Science and the Department of Molecular Genetics, both at the University of Toronto. She is also a senior investigator at the Lunenfeld-Tanenbaum Research Institute, part of the Sinai Health System in Toronto. Her appointment as a BJC Investigator and a professor of developmental biology at Washington University begins Jan. 1, 2018.

We are excited to begin the BJC Investigators Program with the appointment of Dr. Helen McNeill, an international leader in the field of developmental biology, said David H. Perlmutter, MD, executive vice chancellor for medical affairs and dean of the School of Medicine. We sought candidates who had already indelibly changed their fields, whose discoveries will result in new and fundamental shifts in scientific thinking and whose laboratories will become a nidus for additional innovative work across Washington University. Helens scientific accomplishments, her high standards of excellence and ability to collaborate across disciplines make her a perfect fit.

The program is designed to specifically focus on basic science and is inspired by the Howard Hughes Medical Institutes philosophy of investing in people with exceptional creative talent. It plans to bring 10 renowned researchers to Washington University School of Medicine and the life sciences ecosystem of St. Louis.

We are very excited about the BJC Investigators Program at Washington University School of Medicine, said Steven H. Lipstein, CEO of BJC HealthCare. This program represents another joint effort between BJC and Washington University to help keep the schools biomedical research at the forefront of discovery. Pioneering research here in St. Louis offers our best hope for finding solutions to societys greatest medical challenges.

McNeills work is focused on understanding the processes that govern how cells make contact and work together to form the broader architecture of whole tissues, both during development and adulthood. Her work spanning studies of fruit flies, mice and human genetic data has relevance for understanding birth defects, cancer and diseases of specific organs, such as the kidney and lungs.

McNeill earned a bachelors degree in biology from the Ramapo College of New Jersey in 1985, followed by a doctorate in molecular and cellular physiology from Stanford University in 1993. She continued research at Stanford with a postdoctoral fellowship in fruit fly genetics. McNeill later led the Developmental Patterning Laboratory at the London Research Institute, a part of the Imperial Cancer Research Fund of the United Kingdom. She joined the faculty of the University of Toronto in 2005, where she has directed the Collaborative Program in Developmental Biology and earned numerous recognitions for her research, including the Petro-Canada Young Innovator Award and the Lloyd S.D. Fogler, QC, Award of Excellence for her research in cancer biology. Last year, she was awarded a Canada Tier 1 Research Chair, a position in which a scientist is recognized by peers as a world leader in his or her field.

I am delighted that Dr. McNeill will be joining us at Washington University, said Lilianna Solnica-Krezel, PhD, the Alan A. and Edith L. Wolff Professor of Developmental Biology and head of the Department of Developmental Biology. She is a leader in the field and among the most original and creative investigators of pathways that are vital for the regulation of tissue structure and growth. The pathways she studies are among the least understood cellular pathways, with implications for a variety of birth defects and other diseases, including cancer.

Specifically, McNeill studies molecules that govern how cells make contact and communicate with one another. Called giant cadherins for their large size, these molecules play important roles in controlling the size of organs and in orchestrating how cells assemble themselves into complex tissues at precise times and with specific patterns and orientations. Her work also has implicated these molecules in cellular metabolism and the function of mitochondria, molecular powerhouses that manufacture a cells fuel supply. According to McNeills research, disruption of the giant cadherins can interfere with early embryonic development leading to, for example, neural tube defects that cause spina bifida or defects in the development of the kidney and urinary tract. Her work has identified cadherins as a culprit in congenital kidney diseases such as cystic kidney disease.

I am excited and honored to be joining Washington University School of Medicine as a BJC Investigator, McNeill said. Supporting research in the basic sciences is so important in making new discoveries and pushing the boundaries of what is known about human health and development. I thank the School of Medicine and BJC HealthCare for their commitment to supporting basic biomedical science in my own lab and in the labs of my fellow investigators.

Washington University School of Medicines 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is one of the leading medical research, teaching and patient-care institutions in the nation, currently ranked seventh in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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First of 10 expected BJC Investigators named - Washington University School of Medicine in St. Louis

Reprinted with the kind permission of Cort Johnson and Health Rising.

By Cort Johnson

The Real Action - The Working Group

Davis has noticed that waiting for data to be validated in journal publications isn't exactly a pathway to quick results. Far better, he thinks, to give new data - recognizing that it's not been completely validated - the chance to inform and strengthen other researchers' work. (Suzanne Vernon did something similar with her Cold Spring Harbor meetings). The working session actually was planned before the Community Symposium; it's part of Davis' vision of a collaborative team of researchers working together to solve ME/CFS.

Drs. Bateman and Bell will provide clinical expertise to PhD's from a variety of fields. Some research names will be familiar (Naviaux, Younger, Hanson, Light, McGregor) but many others (Tompkins, Olivera, Xiao, Berg, Esfandyarpour, etc.) are experts from other fields whom Davis has enrolled in his fight to beat ME/CFS. Two Nobel Laureates (Paul Berg, Mario Capecchi) are attending, as well as several department heads/directors (Ron Tompkins, Michael Synder) and one person from industry (Integrative Bioinformatics). Stanford and Davis' Genome lab is widely represented.

That's a lot of brain power to assess the most recent findings in ME/CFS, suggest new directions, and produce new insights into ME/CFS.

The Symposium

The Community Symposium was conceived after the workshop, but it is a rare chance to hear from and interact with researchers doing some of the hottest work on ME/CFS.

You can either physically be there, view it live for free over a Livestream feed (how often does that happen?), or watch later via DVD's or YouTube downloads. The $75 participation fee for those who want to physically be there covers the costs of hosting the event and the breakfast and lunch provided. It's a chance to hear, ask questions and mingle with some of the top researchers in the field. We should hear some exciting early results from a number of researchers.

Speakers

Ron Davis, PhD - last seen using the Seahorse machine to determine if something in ME/CFS patients' blood is blocking their cells' energy production. He will be speaking on some early results from the Severe ME/CFS Big Data project.

Bob Naviaux, PhD - last seen publishing a successful pilot drug trial in autism and possibly about to gear up for one in ME/CFS.

Chris Armstrong, PhD - last seen doing a long term metabolomics study and attempting to rejuvenate metabolic functioning in ME/CFS patients.

Jonas Berquist, PhD - last seen doing metabolomics and proteomics studies on the cerebral spinal fluid of ME/CFS patients.

Mario Capecchi, PhD - last seen getting a Nobel Prize and exploring the interface between molecular genetics, the immune system and central nervous system diseases.

Mark Davis, PhD - last seen publishing (with Dr. Montoya) the biggest immune study ever in ME/CFS - which should go far to help legitimize ME/CFS. Ron Davis thinks Mark Davis' next project involving T-cells may be even more significant. NINDS director, Dr. Koroshetz, also singled out Mark Davis' findings in the recent NIH Teleconference call. Davis will talk on those findings in the Symposium.

Maureen Hanson, PhD - talk about an exciting project: last seen examining the effect exercise has on the immune system and metabolomics.

Alan Light, PhD - last seen demonstrating how the receptors that react to exercise by-products go bonkers in ME/CFS and FM.

Neil McGregor, PhD - last seen promoting the use of metabolomics to study ME/CFS.

Baldomero Olivera, PhD - last seen developing ion channel drugs to relieve pain.

Wenzhong Xiao, PhD - last seen analyzing the Severe ME/CFS Big Data project results.

Rules of the Game

Ron Davis is easy to talk to and has a great sense of humor - you'd never know you were talking to one of the great figures in biology. Davis has won some of the highest prizes in medical research, has been mentioned as a Nobel Prize candidate, and created some of the building blocks that made the human genome project possible.

He's a different sort of researcher than we've come to expect. Running a major lab at Stanford, Davis inhabits a different world than we're used to with ME/CFS. Plus, he's 76 years old, has nothing to prove, and wants to save his son's life. Given that context, one might think that Davis would be out tooting his own horn and ginning everyone up constantly. What Davis really wants to talk about, though, is not the latest breakthrough, but how to do good science and just how difficult and rare that is.

He's just relentless on the subject. Whether it's doing good studies, the grant awarding process, publication procedures, or study methodology, this theme crops up again and again. Davis has had a life-time of solving complex problems. Now, it's solving ME/CFS. It's a game he really wants to win. He's won games like this before - and he dearly wants to communicate how to win this game.

Rules of the Game (Note - I came up with these rules after listening to Davis)

Davis has dealt with staggeringly complex problems throughout his career (his "former life" he says) - he loves the really knotty stuff - but that legacy has left him with a real appreciation for just how incredibly complicated the human body is. He knows the curve balls the body often brings. He never underestimates its ability to fool us. So one of the rules is to be humble and expect surprises.

Expect Surprises

One of the rules of being successful at the game of solving ME/CFS (or any biological mystery) is recognizing that surprises - false leads and unexpected breakthroughs - are inevitable. That's a humbling thing - we all want quick answers - but once you recognize that surprises are inevitable, you don't get too carried away at any one finding. You stop discarding things that don't, at first blush, make sense. Instead, you investigate them fully. You try and poke holes in your breakthroughs. Above all you try to avoid wasting precious time and resources on something you should have discarded long ago.

Davis said his team is following many preliminary leads, but I got the feeling that it's the results they didn't expect (they are getting some surprising data) that he finds the most interesting. Some of those unanticipated results, he said, will turn out to be fortuitous, but others could change everything.

That kind of thinking is rare. We tend to go where we know to go. After all, humanity almost destroyed the ozone layer because researchers' computer programs automatically discarded the "aberrant" reading that they thought must be wrong.

It takes some daring to think outside the box. Davis wondered how many ME/CFS patients with lymphoma it took before two doctors recognized that Rituximab was helping with ME/CFS. No one at that time would put a chemotherapy drug and ME/CFS in the same sentence - and that kind of closed thinking had consequences; it probably took us much longer than necessary to glom onto Rituximab than it could have.

Davis clearly does not want that to happen with ME/CFS. Investigating everything is part of the process. That seems slow, but it really isn't in a disease where not that much is known. Unless you look at EVERYTHING, you might - in fact you almost certainly will - miss anything which is out of the ordinary - hence the Open Medicine Foundation's Severe ME/CFS Big Data project and the NIH's Intramural study.

Collaboration is Key

Davis has many times said he can't solve chronic fatigue syndrome on his own - the disease is simply too complex. He needs to collaborate, and that means enrolling researchers who have successfully worked on complex projects before, who are experts in the fields he is not expert in, and people with a high intellect to arrogance ratio.

Davis said his PhD advisor had the highest intellect to arrogance ratio of anyone he's ever known. That mentor basically provided a template for effectiveness and collegiality that Davis has followed ever since. If you're arrogant (unless you're an out and out genius - it is a ratio, after all 🙂 ) you probably won't be welcome at Davis' table. Davis wants people who work well with others.

Luckily, arrogance is not normally a problem: biology, Davis, said, has a way of humbling one - the really smart people know enough to know that there's too much that they don't know for them to be arrogant about the little they do know.

Davis didn't say so, but the underlying message for me was that it's going to take time. We are getting some good results, but my guess is that the process - bringing good people in, getting them to collaborate, getting them thinking more and more about ME/CFS - is the most important thing right now.

If the field follows that kind of process, if it focuses on doing the best work, on collaborating, if it's fiercely critical and remains curious and creative - ME/CFS will yield its secrets and fold.

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OMF Symposium to Provide First Look at Metabolomic / Immune Results in ME/CFS - ProHealth

Myriad Genetics (NASDAQ: MYGN) and HTG Molecular Diagnostics (NASDAQ:HTGM) are both small-cap medical companies, but which is the better investment? We will contrast the two businesses based on the strength of their profitabiliy, analyst recommendations, earnings, valuation, institutional ownership, risk and dividends.

Valuation and Earnings

This table compares Myriad Genetics and HTG Molecular Diagnostics revenue, earnings per share (EPS) and valuation.

Myriad Genetics has higher revenue and earnings than HTG Molecular Diagnostics. HTG Molecular Diagnostics is trading at a lower price-to-earnings ratio than Myriad Genetics, indicating that it is currently the more affordable of the two stocks.

Profitability

This table compares Myriad Genetics and HTG Molecular Diagnostics net margins, return on equity and return on assets.

Institutional & Insider Ownership

28.0% of HTG Molecular Diagnostics shares are held by institutional investors. 6.2% of Myriad Genetics shares are held by insiders. Comparatively, 7.6% of HTG Molecular Diagnostics shares are held by insiders. Strong institutional ownership is an indication that endowments, hedge funds and large money managers believe a stock will outperform the market over the long term.

Analyst Ratings

This is a summary of current recommendations and price targets for Myriad Genetics and HTG Molecular Diagnostics, as provided by MarketBeat.

Myriad Genetics presently has a consensus target price of $21.55, suggesting a potential downside of 13.44%. HTG Molecular Diagnostics has a consensus target price of $6.17, suggesting a potential upside of 175.30%. Given HTG Molecular Diagnostics stronger consensus rating and higher probable upside, analysts clearly believe HTG Molecular Diagnostics is more favorable than Myriad Genetics.

Volatility and Risk

Myriad Genetics has a beta of 0.31, suggesting that its share price is 69% less volatile than the S&P 500. Comparatively, HTG Molecular Diagnostics has a beta of 0.55, suggesting that its share price is 45% less volatile than the S&P 500.

Summary

HTG Molecular Diagnostics beats Myriad Genetics on 7 of the 13 factors compared between the two stocks.

Myriad Genetics Company Profile

Myriad Genetics, Inc. is a molecular diagnostic company. The Company is engaged in the discovery, development and marketing of transformative molecular diagnostic tests. The Company operates through two segments: diagnostics and other. The diagnostics segment provides testing and collaborative development of testing that is designed to assess an individuals risk for developing disease later in life, identify a patients likelihood of responding to drug therapy and guide a patients dosing to enable optimal treatment, or assess a patients risk of disease progression and disease recurrence. The other segment provides testing products and services to the pharmaceutical, biotechnology and medical research industries, research and development, and clinical services for patients, and also includes corporate services, such as finance, human resources, legal and information technology. Its molecular diagnostic tests include myRisk Hereditary Cancer, BRACAnalysis CDx and COLARIS.

HTG Molecular Diagnostics Company Profile

HTG Molecular Diagnostics, Inc. is a commercial-stage company that develops and markets a technology platform to facilitate the routine use of complex molecular profiling. The Companys HTG Edge and HTG EdgeSeq platforms, consisting of instrumentation, consumables and software analytics, are used in sample profiling applications, including tumor profiling, molecular diagnostic testing and biomarker development. The Companys HTG Edge and HTG EdgeSeq platforms automate the molecular profiling of genes and gene activity using its nuclease protection chemistry on a range of biological samples. The Companys HTG EdgeSeq chemistry, together with its HTG Edge or HTG EdgeSeq instrumentation and software, automates and adapts its nuclease protection chemistry to enable analysis using next generation sequencing (NGS) instrumentation. The HTG EdgeSeq system utilizes substantially the same sample preparation reagents as its original chemistry, but allows for read out on an NGS instrument.

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Analyzing Myriad Genetics (NASDAQ:MYGN) and HTG Molecular Diagnostics (HTGM) - BNB Daily (blog)

BETHESDA, Md., Aug. 4, 2017 /PRNewswire-USNewswire/ --Madhuri Hegde, PhD, FACMG of PerkinElmer, Inc. in Waltham, MA has been elected to the ACMG Foundation for Genetic and Genomic Medicine Board of Directors, the supporting educational foundation of the American College of Medical Genetics and Genomics. The ACMG Foundation is a national nonprofit foundation dedicated to facilitating the integration of genetics and genomics into medical practice. The board members are active participants in serving as advocates for the Foundation and for advancing its policies and programs. Dr. Hegde has been elected to a 2-year renewable term starting immediately.

Dr. Hegde joined PerkinElmer in 2016 as Vice President and Chief Scientific Officer, Global Genetics Laboratory Services. She also is an Adjunct Professor of Human Genetics in the Department of Human Genetics at Emory University. Previously, Dr. Hegde was Executive Director and Chief Scientific Officer at Emory Genetics Laboratory in Atlanta, GA and Professor of Human Genetics and Pediatrics at Emory University and Assistant Professor, Department of Human Genetics and Senior Director at Baylor College of Medicine in Houston, TX.

Dr. Hegde has served on a number of Scientific Advisory Boards for patient advocacy groups including Parent Project Muscular Dystrophy, Congenital Muscular Dystrophy and Neuromuscular Disease Foundation. She was a Board member of the Association for Molecular Pathology and received the Outstanding Faculty Award from MD Anderson Cancer Center. She earned her PhD in Applied Biology from the University of Auckland in Auckland, New Zealand and completed her Postdoctoral Fellowship in Molecular Genetics at Baylor College of Medicine in Houston, TX. She also holds a Master of Science in Microbiology from the University of Mumbai in India. She has authored more than 100 peer-reviewed publications and has given more than 100 keynote and invited presentations at major national and internal conferences.

"We are delighted that Dr. Hegde has been elected to the ACMG Foundation Board of Directors. She has vast experience in genetic and genomic testing and is a longtime member of the College and supporter of both the College and the Foundation," said Bruce R. Korf, MD, PhD, FACMG, president of the ACMG Foundation.

The complete list of the ACMG Foundation board of directors is at http://www.acmgfoundation.org.

About the ACMG Foundation for Genetic and Genomic Medicine

The ACMG Foundation for Genetic and Genomic Medicine, a 501(c)(3) nonprofit organization, is a community of supporters and contributors who understand the importance of medical genetics and genomics in healthcare. Established in 1992, the ACMG Foundation for Genetic and Genomic Medicine supports the American College of Medical Genetics and Genomics' mission to "translate genes into health" by raising funds to help train the next generation of medical geneticists, to sponsor the development of practice guidelines, to promote information about medical genetics, and much more.

To learn more about the important mission and projects of the ACMG Foundation for Genetic and Genomic Medicine and how you too can support the work of the Foundation, please visit http://www.acmgfoundation.org or contact us at rel="nofollow">acmgf@acmgfoundation.org or 301-718-2014.

Contact Kathy Beal, MBA ACMG Media Relations, rel="nofollow">kbeal@acmg.net

View original content with multimedia:http://www.prnewswire.com/news-releases/madhuri-hegde-phd-is-elected-to-the-board-of-the-acmg-foundation-for-genetic-and-genomic-medicine-300499860.html

SOURCE American College of Medical Genetics and Genomics

Read more from the original source:
Madhuri Hegde, PhD is Elected to the Board of the ACMG Foundation for Genetic and Genomic Medicine - Markets Insider

by Brandon Voss 4h ago

Baby, were you born this way?

AsapSCIENCE duo Mitchell Moffit and Gregory Brown explore the genetics of being gay in their latest myth-busting YouTube video.

Ultimately, a specific gay gene has not been found, but scientific evidence does suggest that human sexual orientation is strongly linked to genetics and tightly regulated at the molecular level, the guys say.

While unpacking their many findings, you may be surprised to learn that gay men have more gay relatives than straight men do. Gay people are also more likely to have gay siblings who share similar linkages on their chromosomes.

But gay people dont reproduce as much as straight people, so shouldnt they die out? A controversial UCLA study using twins proposed that everyone has the gay gene, even if its not triggered. And according to the Gay Uncle Hypothesis, gay members of a family that dont reproduce still increase the prevalence of their familys genes in future generations by helping to provide resources for offspring that theyre related to.

Putting genetic manipulation into more of a social context, Moffit and Brown also made a companion video in which they address the LGBT communitys fears about this type of research, pointing out that the Nazis tried to understand the biology behind homosexuality in order to eliminate it.

Could genetic research be used against gay people in the future? In theory, absolutely. There may not be a gay gene, but from a biological perspective, yes, being gay is likely highly controlled by genetics, Brown says.

Moffit, however, believes that the community will benefit from research that proves being gay is not a choice. The more we can understand the genetic background of homosexuality, the more we can mitigate the types of punishments that gay people are receiving around the world, he says.

Moffit and Brown came out to their followers as gay and a couple in 2014.

Geek out over gay genetics below.

Celebrity interviewer. Foodie and Broadway buff in Manhattan. Hates writing bios.

The rest is here:
Is There Really A Gay GeneAnd Can You Get Rid Of It? - NewNowNext

Many of us have been curious as to why some of us are straight or gay; "Why are some of us attracted to the opposite sex?" "Why are some men attracted to men?" "Why are some women attracted to women?" Currently, we don't know why we vary in sexual orientation, but science suggests being gay at least is partly genetic, rather than a lifestyle choice.

In AsapSCIENCE's latest video, "Does Everybody Have A Gay Gene," Mitchell Moffit and Gregory Brown explain genetics and epigenetic factors the study of how the environment can chemically modify our genes can be used to prove that being gay is not a choice.

Read More: Study Finds Same Sex Couples Make Better Parents

A 2016 study, published in the Archives of Sexual Behavior, found linkages in a specific region of the X chromosome labelled Xq28 and in another region of chromosome 8, known as 8q12, in over 400 gay siblings. Traits like hair color, height and intelligence varied between each brothers in a pair and between all groups of brothers. In other words, any single nucleotide polymorphisms (SNPs) differences on a single letter in the genetic code found in the same genetic locations across the group would likely be associated with sexual orientation.

The region on the X chromosome, Xq28, was previously identified in 1993 by Dean Hamer of the US National Institutes of Health in Bethesda, Maryland. However, there needs to be more work done to determine the specific genes involved and how they work, including if there are equivalent genes in women. The study provides researchers with the potential to narrow down fewer genes linked to sexual preference.

The belief that homosexuality is genetic can create a paradox. For example, homosexuals have 80 percent fewerchildren than heterosexuals, which suggests the genes would not be passed down and would eventually die out.

Enter epigenetics.

A 2015 study published in Science used epigenetics to propose that everyone has a gay gene, but it's contingent on whether the attachment of a methyl group to specific regions of DNA is triggered and turned on. Upon analyzing gay and straight male twins, researchers found a specific methylation pattern was closely linked to sexual orientation. The model was able to predict the sexuality of men with 70 percent accuracy.

However, a caveat of the study is its small sample size, which means there is not too much power to make such a claim. Evidently, there were certain correlations, but a predicting model may not yet be an actual reality. Larger studies are needed to replicate these findings if valid.

A specific gay gene has not been found, but there's scientific data that suggests sexual orientation is linked to genetics on a molecular level. Previous research has found giving birth to a son increases the odds of homosexuality in the next son by 33 percent. Scientists believe a woman's body adjusts the androgen level in her womb as she has more sons, and the androgens interactwith genes to produce homosexuality.

Read More: Kids Of Same-Sex Parents Have Same Emotional, Physical Health As Those With A Mom And Dad

The scientific community still has a long way to go when it comes to studying the causes of homosexuality. Currently, most research only focuses on gay men and neglect other groups, like lesbians. Further research on the genetic and epigenetic factors of homosexuality could help reduce homophobic laws around the world by proving it's not a lifestyle choice.

Science is working on proving the biology of homosexuality, but it also raises the question, does it matter if someone is straight or gay?

See Also:

Why Discrimination Against Gays Is A Global Health Hazard

Heterosexual Providers Found To Hold Bias On Sexual Orientation

The rest is here:
Homosexuality Partly Rooted In Genetics Rather Than Lifestyle Choice, Says Science - Medical Daily

Those images of a robust Star Trek Captain James T. Kirk beaming around the solar system at maximum warp, or an irreverent Han Solo with his sidekick Chewbacca bustling through space on a quest to save Princess Leia, are sadly, an illusion.

The truth of the matter is that humans or any other living thing be it a plant or a fruit fly from planet Earth are not meant for space travel. Traveling in space is very hard on creatures, producing physiological effects similar to premature aging.

Thats one of the reasons the Stein Institute on Aging at UC San Diego brought NASA affiliate Brinda K. Rana, Ph.D., to speak to a packed audience of mostly older adults at the Garren Auditorium of the UCSD School of Medicine, last week.

Rana, who has been the Principle Investigator (PI) on three NASA studies, spoke at length about the effects of space travel on all aspects of the human body everything from vision to genetics.

Everything I say has to be approved by NASA. I have to be very careful about the data I reveal, Rana wryly explained. Her chief NASA project was a comprehensive medical study of twin brother astronauts Scott and Mark Kelly who spent different lengths of time in space.

Since the brothers are genetically identical, researchers thought they could ferret out the effects of time in space on their bodies. Mark had 54 days in space, while Scott spent 365 days living on the space station.

Rana headed up a team of scientists from UCSD, one of 10 university-based teams from around the world chosen by NASA to study the astronauts. It was a difficult assignment requiring a great deal of cooperation. For instance, all 10 teams had to share just one vial of blood among themselves from each of the two astronauts.

Rana explained that space travel impairs blood and lymph circulation, especially to the lower parts of the body: Your face gets puffy and your legs get weak. Space travel is like hanging upside down for a long time! she said.

Thats why astronauts have to be helped out of their space capsule when they return to Earth. They cant stand up on their own because their legs are so weak due to poor circulation.

NASA knows that space travel, specifically spending time in zero gravity, is hard. But since the plan is to send men and women up to Mars, which is a six-month flight one way, it is trying hard to develop ways to counteract the debilitating aspects of space travel so the astronauts can function when they get to the red planet. Luckily, the gravity on Mars is less than it is on Earth, so they should be able to stand up and carry out their activities.

Space travel also produces bodily changes you cannot see, affecting the chemistry and physiology of the body. It also affects DNA and RNA. Rana found that while in space, astronaut Scott Kelly had 200,000 differences or mutations in RNA actions, which returned to normal when he came back to Earth. This just shows that genes are not static, but very sensitive to the environment around us, Rana said.

Space travel also changes the intestinal flora or probiotics in the gut, which aid digestion. There are also cardiovascular changes, muscular atrophy, arteriosclerosis, glaucoma and bone loss. It looks just like the signs of aging!

Space travelers also experience increased cranial pressure. There are changes to the eyes and vision problems develop. This syndrome is known as VIIP or Visual Impaired Intracranial Pressure syndrome.

Rana is an associate professor in the Department of Psychiatry at UCSD and has a lab at the Stein Institute of Aging. She is an alumna of UCSD with a B.A. in math from Revelle College. She also has an M.S. in math from the University of Illinois Urbana-Champaign and a Ph.D. from the University of Texas in molecular genetics. At the Stein Institute, her chief duty is to look for the genes that seem to keep some older adults from getting age-related disorders.

Ranas NASA studies are relevant because the results have an application to understanding aging on Earth and in helping people in similar situations to space travel, like those who are bedridden for long periods of time. In one experiment, Ranas lab studied people who were confined to bed with their body inclined downward toward the head at a 15-degree angle, mimicking the effects of space flight.

Karen Ocorr, Ph.D., was at the lecture because she is also working with NASA. Ocorr is a professor in the Development, Aging and Regeneration Program at the Sanford Burham Prebys Medical Discovery Institute on North Torrey Pines Road.

Ocorr studies the ion channels responsible for the relaxation of the human heart, which she says is similar in fruit flies. She just got back a batch of fruit flies that were flown to the space station on the SpaceX CRS-11 mission. She is looking at the effects of zero gravity on their heart function, which can provide models to help understand the human heart. The fruit flies arent doing too well after their space flight, she confided.

Einstein once predicted that if we start to travel faster in space and get closer to the speed of light, which is about as fast as we could ever go, time will slow down. Thus we would age slower (happy thought!) in terms of chronology. But if we are in zero gravity at light-speed our bodies will age faster (unhappy thought!). Professor Rana says not to worry. NASA will figure it out!

Original post:
Astronaut twins study shows space travel causes premature aging - La Jolla Light

In collaboration with scientists from the U.K., Europe, Japan and the United States, researchers at the Human Genome Sequencing Center at Baylor College of Medicine have discovered a whole genome duplication during the evolution of spiders and scorpions. The study appears in BMC Biology.

Researchers have long been studying spiders and scorpions for both applied reasons, such as studying venom components for pharmaceuticals and silks for materials science, and for basic questions such as the reasons for the evolution and to understand the development and ecological success of this diverse group of carnivorous organisms.

As part of a pilot project for the i5K, a project to study the genomes of 5,000 arthropod species, the Human Genome Sequencing Center analyzed the genome of the house spider Parasteatoda tepidariorum - a model species studied in laboratories - and the Arizona bark scorpion Centruroides sculpturatus, - the most venomous scorpion in North America.

Analysis of these genomes revealed that spiders and scorpions evolved from a shared ancestor more than 400 million years ago, which made new copies of all of the genes in its genome, a process called whole genome duplication. Such an event is one of the largest evolutionary changes that can happen to a genome and is relatively rare during animal evolution.

Dr. Stephen Richards, associate professor in the Human Genome Sequencing Center, who led the genome sequencing at Baylor, said, "It is tremendously exciting to see rapid progress in our molecular understanding of a species that we coexist with on planet earth. Spider genome analysis is particularly tricky, and we believe this is one of the highest quality spider genomes to date."

Similarly, there also have been two whole genome duplications at the origin of vertebrates, fuelling long-standing debate as to whether the duplicated genes enabled new biological complexity in the evolution of the vertebrate lineage leading to mammals. The new finding of a whole genome duplication in spiders and scorpions therefore provides a valuable comparison to the events in vertebrates and could help reveal genes and processes that have been important to our own evolution.

"While most of the new genetic material generated by whole genome duplication is subsequently lost, some of the new gene copies can evolve new functions and may contribute to the diversification of shape, size, physiology and behavior of animals," said Dr. Alistair McGregor, professor of evolutionary developmental biology at Oxford Brookes University and lead author of the research. "Comparing the whole genome duplication in spiders and scorpions with the independent events in vertebrates reveals a striking similarity. In both cases, duplicated clusters of Hox genes have been retained. These are very important genes that regulate development of body structures in all animals, and therefore can cause evolutionary changes in animal body plans."

The study also found that the copies of spider Hox genes show differences in when and where they are expressed, suggesting they have evolved new functions.

McGregor explains that these changes may help clarify the evolutionary innovations in spiders and scorpions including specialized limbs and how they breathe, as well as the production of different types of venom and silk, which spiders use to capture and kill their prey.

"Many people fear spiders and scorpions, but this research shows what a beautiful part of the evolutionary tree they represent," said Dr. Richard Gibbs, director of the Human Genome Sequencing Center and the Wofford Cain Chair and professor of molecular and human genetics at Baylor.

"Costs have now dropped rapidly enough from tens of millions of dollars to merely a few thousand dollars for this genomic analyses to now be performed on any species," Richards said. "There is still so much more to learn about the life on earth around us, and I believe this result is just the beginning of understanding the molecular make up of spiders."

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Genome Sequencing Shows Spiders, Scorpions Share Ancestor - R & D Magazine

Pink areas are bone and blue areas are cartilage in this head skeleton of a larval fish. Craig Albertson of UMass Amherst and a colleague report on experiments that looked at how a gaping behavior, a factor in the fish larvae's developmental environment that precedes bone formation, influences later development of cranio-facial bones. Credit: UMass Amherst

An unspoken frustration for evolutionary biologists over the past 100 years, says Craig Albertson at the University of Massachusetts Amherst, is that genetics can only account for a small percentage of variation in the physical traits of organisms. Now he reports experimental results on how another factor, a "bizarre behavior" that is part of early cichlid fish larvae's developmental environment, influences later variation in their craniofacial bones.

Albertson has studied African cichlid fish for 20 years as a model system for exploring how biodiversity originates and is maintained, with a focus on genetic contributions to species differences. In a new series of experiments with former Ph.D. student Yinan Hu, now a postdoctoral fellow at Boston College, they examined a "vigorous gaping" behavior in larval fish that starts immediately after the cartilaginous lower jaw forms and before bone deposition begins. Results appear in the current early online issue of Proceedings of the Royal Society B.

As Albertson explains, "We predicted that the baby fish are exercising their jaw muscles, which should impose forces on the bones they attach to, forces that might stimulate bone formation." Albertson and Hu observed that gaping frequency, which could reach as high as 200 per minute, varied by species "in a way that foreshadows differences in bone deposition around processes critical for the action of jaw opening."

Albertson, an evolutionary geneticist, says, "For over a hundred years, we've been taught that the ability of a system to evolve depends largely on the amount of genetic variation that exists for a trait. What is ignored, or not noted for most traits, is that less than 50 percent of genetic variation can typically be accounted for by genetics." He adds, "Variation in skull shape is highly heritable, so why can we only find genetic variability that accounts for such a small amount of variability in bone development? In my lab we have shifted from elaborating our genetic models to looking more closely at the interaction between genetics and the environment."

How the environment influences development is known as epigenetics in its original and broadest meaning, Albertson points out. Coined in the 1940s to mean anything not encoded in the nucleotide sequence, it has narrowed to refer to how the 3D structure of the DNA molecule is modified, he notes. "That meaning is true, but it isn't the only one. We're returning to the original definition."

In this sense, gaping is part of "a very dynamic developmental environment," Albertson notes. "Bones are not forming in static lumps of tissue. Rather, they are developing as part of, and perhaps in response to, a highly complex and dynamic system." The fact that species differ in gaping rate led the researchers to test the idea that differences in bone development could be accounted for by variation in this behavior. "We performed experiments to see if we could slow the rate in fast-gaping species and speed it up in slow-gaping species, and to see if this behavioral manipulation could influence bone development in predictable ways."

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Not only did these experiments work, but the magnitude of difference in skeletal morphology induced by these simple shifts in behavior was similar to those predicted to be caused by genetic factors. Albertson says, "What I find really exciting is that in 15 years of manipulating the genetics of craniofacial bone development we can account for up to 20 percent of the variability, so it's modest. When we manipulate gaping behavior, we can influence developmental variability by about 15 percent, which is comparable, almost equal to the genetic response."

The geneticist adds, "When I give talks, this is what surprises colleagues the most, that the environmental effect is on par with the genetic effect, and that it is not systemic but highly specific to important bones involved in fish feeding."

Alberston says this behavior makes sense because "Nature is all about efficiency. Fine-tuning an adaptive response to a particular niche increases the chances of survival. Sometimes longer bones are better, and one way to get there is to kick-start the bone developmental program. This gaping behavior precedes bone formation, so it may represent a way to increase efficiency by setting an animal on the trajectory toward an adaptive phenotype earlier."

He adds, "This is just the beginning. Our field has been entrenched in a gene-centered view of evolution for nearly a century. My hope is that this study adds to a growing body of literature that shows there are other important sources of variation. I hope we can expand the paradigm to consider the environmental context where development takes place, because the effects are likely greater and more widespread than we'd predict."

The next step for his lab will be to figure out how environmental stimuli influence development, Albertson explains. "We now need to understand how bone cells sense and respond to their mechanical environment. What are the molecules that enable this mechano-sensing?"

To this end, the researchers demonstrated that mechanical-load-induced shifts in skeletal development are associated with differences in expression of the ptch1 gene, implicated previously in mediating between-species skeletal shap differences. "That the same molecule is involved in mechano-sensing within species and genetic divergence between species is very cool as it's consistent with evolutionary theory," Albertson says.

The idea is that when an animal population is exposed to a new environment, certain molecules will enable them to respond by conforming their bodies to meet new challenges. If the new environment is stable, natural selection should favor genetic mutations in these molecules that fix the original, transient response. This theory establishes a framework for the initial steps in species divergence. "We think that we now have a molecular foothold into this process," Albertson explains. "These are exciting times."

Explore further: A mechanism of how biodiversity arises

More information: Baby fish working out: An epigenetic source of adaptive variation in the cichlid jaw, Proceedings of the Royal Society B, rspb.royalsocietypublishing.or .1098/rspb.2017.1018

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Evolutionary biologists identify non-genetic source of species variability - Phys.Org

Few areas of science are advancing as rapidly as molecular biology.It is 64 years since James Watson and the late Francis Crick published their famous double-helix model for the structure of DNA, the genetic material, and since then progress has happened at an ever-faster pace.The practical results of this have been seen in everything from genetically engineered crops to more effective treatments for disease.A study by Dr Youssef Idaghdour, an assistant professor of biology at New York University Abu Dhabi, could offer further advances by suggesting pointers that could help develop cancer drugs. It could also help clinicians to understand why some patients respond better than others to treatment.The focus is on a molecule closely related to DNA called ribonucleic acid (RNA) and, in particular, a form called transfer RNA (tRNA).Published in the journal Genome Medicine and written with Dr Alan Hodgkinson, from the Department of Medical and Molecular Genetics at Kings College London, the work is focused on tRNA within mitochondria, which are organelles involved in energy production within cells. Mitochondria have their own genetic material separate to that of cell nuclei.The researchers looked at the extent to which tRNA has methyl groups, which consist of one carbon atom and three hydrogen atoms, attached to it.The methylation of DNA or RNA has become a major area of focus for molecular biologists. It is part of the field of epigenetics, which looks at how characteristics develop and can be transmitted based upon how genes are expressed, instead of simply what the sequence of DNA is.Interest in epigenetics in relation to cancer is huge, said Professor Stephan Beck, a German-trained researcher who is professor of medical genomics at University College London.Its well established and the expectation is that this field will become much, much bigger than it currently is, he said.Cancer is the consequence of genetic and epigenetic changes - thats what cancer is. Thats why so much research goes on.Transfer RNA is involved in the events required for a gene to produce a protein. The double-stranded DNA opens up and is initially transcribed into a strand of messenger RNA (mRNA).Translation comes next, involving a tRNA molecule with an amino acid attached to it bonding temporarily to a strand of mRNA with a complementary chemical sequence. This allows the amino acid to link itself to the growing protein molecule for which the gene codes.

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In the recently published research, a genetic analysis was carried out on mitochondrial tRNA data generated from 1,226 samples of normal human tissue or tumour tissue by The Cancer Genome Atlas (TGCA) project. These samples, taken from a database, were paired, so that for any given sample of normal tissue there was a cancerous sample from the same individual.Dr Idaghdour and Dr Hodgkinson found that tumour samples tended to have higher methylation levels than normal samples, a pattern seen across multiple cancer types.For a patient, if the methylation of their mitochondrial tRNA [in normal tissue] tends to be low, the moment they have cancer, they tend to have significantly higher levels. The question is, What is it doing? said Dr Idaghdour, a Moroccan scientist who studied for his PhD in the United States before undertaking post-doctoral research in Canada.Dr Idaghdour and Dr Hodgkinson think methylation patterns may affect translation and in doing so cause mitochondria to produce more energy. This, in turn, allows cells to divide faster and helps the tumour to grow.You can think about developing drugs that would block the cancer cell from making this modification [to the methylation levels]; thats how you would make the link to potential therapeutics. The methylation would stay the same as a normal cell, said Dr Idaghdour.In a further key finding, a genetic analysis by the researchers found that 18 positions on the nuclear DNA of individuals influenced the degree to which their mitochondrial tRNA became methylated. This means that individuals with particular genotypes were liable to see the methylation of their mitochondrial tRNA increase very rapidly when they developed cancer, while individuals with other genotypes saw much less of a change. In some cases those patients with less of a change in methylation were more likely to survive cancer. This suggests a way in which measuring the extent of methylation could be useful to clinicians.You could use the rate of methylation as a biomarker. [If the] individual has high methylation, the clinician can be more aggressive in terms of treatment, said Dr Idaghdour.Any potential use in a clinical setting of Dr Idaghdours research would be many years away and it is not clear yet whether it could be turned into improved methods to treat particular forms of cancer.But the potential for this to happen is there, since there have been other cases where methylation has been used in the development of cancer treatments.Professor Robert Brown, head of the cancer division at Imperial College London, said that, until now, most research has been on DNA methylation, rather than RNA methylation, which this latest study looks at.Demethylating agents, which can prevent aberrant patterns of gene expression associated with cancer, are being used to combat some forms of cancer.Looking at DNA methylation and other epigenetic changes has tended to lag behind the classical genomic analysis but theres a lot of really good technologies coming through that allow one to look at DNA methylation, he said.He described RNA methylation as a very emerging area.Theres good evidence emerging about the biological significance of [RNA methylation]. The clinical relevance of it in terms of cancer is still to be evaluated, he said.Although the ultimate significance of Dr Idaghdour and Dr Hodgkinsons findings is yet to be determined, they are operating at the cutting edge of a field that could in years to come offer important benefits to patients.

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Molecular biology study by Abu Dhabi researcher has cancer breakthrough potential - The National

Is the solution to the obesity epidemic all in our heads? A study by researchers at The Rockefeller University suggests that it might be.

We have identified two new populations of cells in the brain that potently regulate appetite, says Alexander Nectow, first author of the paper, published in Cell last week. The two types of cells, located in a part of the brainstem called the dorsal raphe nucleus, are potential targets for new drugs to treat obesity by controlling the hunger signals that drive the search for and consumption of food.

The new findings are the latest evidence that eating is a complex biological behavior mediated by multiple sites in the brain. They also offer a possible solution to a problem that has dogged previous efforts to address obesity at the neuronal level.

Different brain regions are activated in mice that are well fed (left) and hungry (right).

In 1994, Jeffrey M. Friedman, Marilyn M. Simpson Professor and head of Rockefellers Laboratory of Molecular Genetics, launched a new era in obesity research by discovering a hormone called leptin, which acts on neurons in the brains hypothalamus region to suppress hunger. Injections of the hormone have been shown to promote dramatic weight loss in patients with a rare leptin deficiency, however many obese people dont respond to this therapy.

Obesity is generally associated with leptin resistance, says Friedman, whose lab produced the new study. And our recent data suggest that modulation of the activity of specific neurons with drugs could bypass leptin resistance and provide a new means for reducing body weight.

The cells that trigger eating

Nectow and his colleagues zeroed in on the dorsal raphe nucleus, or DRN, when whole-brain imaging made with iDISCO, an advanced technique developed at Rockefeller, revealed that this part of the brain becomes activated in hungry mice. Subsequent imaging of other mice that were fed more than their normal amount of food, until they were full, revealed a different pattern of DRN activity.

These results indicated quite clearly that neurons in that part of the brain played a role in feeding behavior.

The next step, explains Nectow, now an associate research scholar at Princeton University who did the research while a Ph.D. student and visiting fellow in Friedmans lab, was to determine which of the several types of neurons that make up the DRN were involved. Genetic analysis of the activated cells in the two groups of mice showed that the neurons triggered by a full belly released glutamate, a chemical that nerve cells use to signal one another, while the neurons triggered by hunger released a different neurotransmitter, known as GABA.

There are two possibilities when you see something like that, Nectow says. One is that the cells are just along for the ridethey are getting activated by hunger but theyre not actually driving the food intake process. The other possibility is that they are in fact part of the sense and respond mechanism to hungerand in this case, we suspected the latter.

Manipulating the system

Armed with two proven methods for activating targeted neurons at willone optical, one chemicalthe researchers were able to turn on the glutamate-releasing cells in obese mice. This suppressed the animals food intake and made them lose weight. And it confirmed that the DRN neurons turned on by hunger did indeed drive food intake.

Similarly, flipping on the GABA-releasing neurons in the same part of the brain had the opposite effect and increased food intake. Notably, turning on the hunger neurons automatically turned off the satiety neurons, maximizing the effect.

The researchers also studied the effect of switching off hunger neurons in obese mice. We were excited to see that prolonged inhibition of these neurons could dramatically reduce body weight, says postdoctoral fellow Marc Schneeberger Pane, a co-first author of the paper.

The findings open up new avenues of research into exactly how the brain controls eating, and suggest that drugs designed to activate or inhibit neurons in the DRN could be effective in treating obesity and preventing its related disorders, such as diabetes and hypertension.

And it offers fresh hope to hundreds of millions of obese people around the world. As it turns out, the brainstem, the oldest part of the brain in evolutionary terms, is the new frontier.

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Hunger-controlling brain cells may offer path for new obesity drugs - The Rockefeller University Newswire