Category Archives: Genetics

Genetics

These 6 Simple Exercises Can Cut Body Weight, Even if You’re Predisposed to Obesity – ScienceAlert

We know that a range of factors influence weight, including those related to lifestyle and genetics, but researchers have now identified six specific exercises that seem to offer the best chance of keeping your weight down even if your genes don't want you to.

Based on an analysis of 18,424 Han Chinese adults in Taiwan, aged between 30 and 70 years old, the best ways of reducing body mass index (BMI) in individuals predisposed to obesity are: regular jogging, mountain climbing, walking, power walking, dancing (to an "international standard"), and lengthy yoga practices.

But interestingly, many popular exercise types weren't shown to do much good for those who's genetic risk score makes them more likely to be obese.

Specifically, exercises including cycling, stretching, swimming and legendary console game Dance Dance Revolution don't appear to be able to counteract genetic bias (though are beneficial in many other ways).

"Our findings show that the genetic effects on obesity measures can be decreased to various extents by performing different kinds of exercise," write the researchers in their paper published in PLOS Geneticsin August 2019.

"The benefits of regular physical exercise are more impactful in subjects who are more predisposed to obesity."

Besides BMI, the team also looked at four other obesity measures for a more complete picture: body fat percentage (BFP), waist circumference (WC), hip circumference (HC), and waist-to-hip ratio (WHR).

Regular jogging 30 minutes, three times a week turned out to be the most effective way of counteracting obesity genes across all of them.

The researchers also suggest, based on the information dug up in the Taiwan BioBank database, that the less effective forms of exercise typically don't use up as much energy, which is why they don't work quite so well.

The researchers specifically noted that activities in cold water, such as swimming, could make people hungrier and cause them to eat more.

The study was able to succeed in one of its main aims, which was to show that having a genetic disposition towards obesity doesn't mean that obesity is inevitable the right type of exercise, carried out regularly, can fight back against that built-in genetic coding.

"Obesity is caused by genetics, lifestyle factors, and the interplay between them," epidemiologist Wan-Yu Lin, from the National Taiwan University, told Newsweek. "While hereditary materials are inborn, lifestyle factors can be determined by oneself."

It's worth noting that not every type of exercise was popular enough within the sample population to be included: activities like weight training, table tennis, badminton or basketball may or may not be helpful, too. There wasn't enough data to assess.

But with obesity numbers rising sharply across the world and 13 percent of the global population now thought to quality as being obese it's clear that measures need to be taken to reverse the trend.

Being obese affects our physiological health in the way it increases the risk of cardiovascular disease, some cancers, and other issues; and there's evidencethat being seriously overweight can have a negative effect on our brains too.

Studies like this latest one can point towards ways of sticking at a healthy weight, even when the genetic cards are stacked against it. In some cases all it takes is a few minutes of exertion per day.

"Previous studies have found that performing regular physical exercise could blunt the genetic effects on BMI," conclude the researchers.

"However, few studies have investigated BFP or measures of central obesity. These obesity measures are even more relevant to health than BMI."

The research has been published in PLOS Genetics.

A version of this article was first published in August 2019.

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These 6 Simple Exercises Can Cut Body Weight, Even if You're Predisposed to Obesity - ScienceAlert

Genetics

How genetics and social games drive evolution of mating systems in mammals – Jill Lopez

Traditional explanations for why some animals are monogamous and others are promiscuous or polygamous have focused on how the distribution and defensibility of resources (such as food, nest sites, or mates) determine whether, for example, one male can attract and defend multiple females.

A new model for the evolution of mating systems focuses instead on social interactions driven by genetically determined behaviors, and how competition among different behavioral strategies plays out, regardless of external factors such as defensible resources. In this model, social interactions can drive evolutionary transitions from one mating system to another, and can even drive a population to split into two separate species with different mating systems.

The model is based on three fundamental behavioral strategies: aggression, cooperation, and deception. The conflict between competitive and cooperative social behaviors drives the evolution of the mating systems. In a paper published December 18 inAmerican Naturalist(online ahead of print publication in the February issue), researchers compared the predictions generated by this model with published data on the mating behavior of 288 species of rodents.

"By and large, everything in our predictions seems to be borne out in rodents," said first author Barry Sinervo, professor of ecology and evolutionary biology at the University of California, Santa Cruz. "Our model is a universal equation of sorts for mating systems."

The evolutionary story that emerges from the study goes something like this: An ancestral population of rodents is promiscuous in its mating behavior. Genetic variation within the population results in individuals with distinctive behaviors. Some males are highly aggressive, defend large territories, and mate with as many females as they can. Others are not territorial, but sneak onto the territories of other males for surreptitious mating opportunities. And some are monogamous and defend small territories, cooperating with neighboring males at territorial boundaries.

These three types can coexist, but any imbalance in the relative advantages of different strategies can lead to the elimination of some behaviors and an evolutionary transition to a species that is, for example, entirely monogamous or entirely polygamous. The cooperative behavior of monogamous males, for example, can include paternal care for the young and the ability recognize and affiliate with other cooperative males, making them stronger in the competition with other strategies.

"They are able to find each other and form colonies, and the bigger the colonies get the stronger they are against the barbarians at the gate. Then they split off from the rest of the population as a separate monogamous species," Sinervo said.

This may sound like little more than storytelling, but in fact it emerges from a set of mathematical equations based on game theory and population genetics, and it is supported by extensive research in animal behavior and genetics.

The new paper builds on Sinervo's decades-long research on mating behaviors in California's side-blotched lizards. He showed that three throat colors correspond with different behaviors in the male lizards: blue-throated monogamous males form partnerships and cooperate to protect their territories and their mates; orange-throated males are highly aggressive and usurp territories and mates from other lizards; and yellow-throated males sneak into the territories of other males to mate.

The competition between these strategies takes the form of a rock-paper-scissors game in which orange aggressors defeat blue cooperators, which defeat yellow sneakers, which defeat orange aggressors. Thus, no single type can dominate the population, and the abundance of each rises and falls in cycles. In 2007, Sinervo and his collaborators discovered the same dynamic in the distantly related European common lizard.

"That was when I started thinking that the same thing could be happening in mammals," Sinervo said.

In the new paper, Sinervo and two of his longtime collaborators--Alexis Chaine at the National Center for Scientific Research (CNRS) in Moulis, France, and Donald Miles at CNRS and Ohio University--generalized the rock-paper-scissors system and extended it to include additional behaviors such as paternal care for offspring (linked to monogamy). They focused on male strategies to simplify the analysis. Sinervo has documented corresponding female strategies in side-blotched lizards and is currently working to incorporate female strategies into the general model.

The three male behavioral strategies represented in the model are: - Polygyny, characterized by aggression to maintain large territories overlapping with several females, but without paternal care for the offspring, as seen in polygamous mating systems where one male mates with multiple females; - Monogamy, involving lower aggression and smaller territories, with cooperation at territorial boundaries and investment in paternal care; and - Sneak, a non-territorial strategy with no paternal care, resulting in sneaking behavior in otherwise territorial systems.

Using a computer to run a mathematical model of these strategies, the researchers simulated the evolution of mating systems over 1,000 generations, varying the strength of different parameters in each simulation. At the start of the simulations, the genes that determine the different strategies were assumed to be equally abundant in the population.

The results of the simulations revealed four evolutionarily stable outcomes determined by the interactions and payoffs (in terms of reproductive success) of the different behavioral strategies. Which stable outcome emerges depends on how much of an advantage each behavior provides.

One of the key factors influencing the effectiveness of a given strategy is a male's ability to recognize which behavioral group other males belong to and choose a neighborhood to settle in where his own strategy will have a competitive advantage. Cooperative, monogamous males need to recognize and affiliate with other cooperative males, whereas aggressive, polygynous males want to avoid other aggressive males and find cooperative males whose territories they can take over.

"It all depends on how good you are at finding the right neighborhood, or how good you are at cooperation and paternal care. By varying these parameters in the model, we were able to find the four different evolutionarily stable states," Sinervo said.

One stable outcome is the rock-paper-scissors dynamic documented in lizards, with the coexistence of all three male strategies. Another stable outcome is the coexistence of polygyny and sneak.

There are two stable outcomes in which only one strategy survives, either polygyny or monogamy. A mix of polygyny and monogamy is rare and unstable, eventually leading to a pure system of one or the other.

Turning to the empirical data, the researchers found evidence in studies of rodent behavior and territoriality of the mating systems and behavioral strategies described in the model. There is even a type of mole rat found in southern Africa that exhibits the rock-paper-scissors combo of all three male strategies that Sinervo discovered in lizards. He noted that, whereas mutual recognition of male strategies is based on throat colors in the lizards, in mammals it is more likely to be mediated by smells. "It's there, but we don't see it. We only saw it in lizards because of their bright colors," he said.

The researchers analyzed the phylogenetic tree of rodents (representing the evolutionary relationships among rodent species) and found the same patterns they had seen in the simulations. Species at the base of the phylogenetic tree, closer to the common ancestor of all rodents, tend to be promiscuous, with multiple mating strategies. Polygyny and monogamy very rarely occur together, but they frequently appear in sister species, suggesting they diverged from an ancestral population of mixed strategies.

The model showed that evolutionary transitions in mating systems are largely driven by increases in the benefits of monogamous behaviors. In rodents, monogamy is the most common evolutionary transition from a promiscuous ancestor, and more rodents are monogamous than polygynous. In the simulations, pure polygyny is a relatively uncommon outcome. "Polygyny is readily invaded by the sneak strategy," Sinervo explained.

Paternal care for the offspring is found in all monogamous species, supporting a key assumption linking paternal care to the evolution of monogamy.

"Promiscuity is very common, and can involve two or three different strategies. But the neat thing is that cooperation and monogamy are far more common than anyone realized," Sinervo said. "The frequency of monogamy in rodents is about 26 percent, much higher than for mammals in general and similar to primates."

The model assumes that these behavioral strategies are genetically based. Evidence in support of this includes research on the role of the hormone vasopressin (and the related hormone oxytocin) in complex social behaviors in numerous species, including rodents and humans. In the monogamous prairie voles, for example, vasopressin has been linked to pair bonding, mate guarding, and paternal care. In some rodent lineages, evolutionary transitions between monogamy and polygyny have been linked to a mutation in a vasopressin receptor gene.

The effects of the genes underlying monogamous behaviors may even drive the evolution of more advanced forms of sociality. Highly social species of rodents--such as mole rats, some of which live in colonies in which only one pair reproduces--originate from monogamous lineages.

Sinervo and his coauthors are not claiming that resources and other external ecological factors have no role in the evolution of mating systems. But the genetic model gives predictions that are consistent with the rodent data and can explain cases where a species' mating system does not match its resource ecology.

The authors also acknowledged that animal behavior can be very flexible and is not entirely determined by genetics. This is especially true in humans, whose behavior is so strongly influenced by cultural and environmental factors. In terms of mating systems, our species can be described as promiscuous, but with very high rates of monogamy. Sinervo said he sees a connection between monogamy and the deeply cooperative social behaviors that are at the core of the human condition.

"We can see analogues for human behavior in other animals, but there's really nothing else like humans," Sinervo said. "There are 'kneejerk' behavioral impulses in us that are not far from rodents, but our cultural and social complexity makes us very different from most mammals."

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How genetics and social games drive evolution of mating systems in mammals - Jill Lopez

Genetics

New Publication Demonstrates GeneSight Improved All Clinical Outcomes Using HAM-D6 Analysis in Large Prospective GUIDED Study – Associated Press

SALT LAKE CITY, Jan. 06, 2020 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (NASDAQ: MYGN, Myriad or the Company), a global leader in molecular diagnostics and precision medicine, announced that a new analysis of the GUIDED1 clinical trial using the 6-item Hamilton Depression Rating Scale (HAM-D6) was published online in BMC Psychiatry. The key finding is the HAM-D6 scale identified statistically significant improvements in all three clinical endpoints remission, response and symptoms between GeneSight-guided care and treatment-as-usual at Week 8 (Figure 1).

The HAM-D6 scale has been shown to be a better measure of core depressive symptoms than the HAM-D17 scale, said Boadie W. Dunlop, M.D., one of the study investigators and associate professor of Psychiatry and Behavioral Sciences at Emory University School of Medicine. This post hoc analysis provides further evidence that the GeneSight test led to significant and clinically meaningful improvements in clinical outcomes for patients with major depressive disorder relative to treatment-as-usual care.

To view Figure 1: GeneSight Test Significantly Improved Clinical Outcomes by Week 8 (HAM-D6), please visit the following link: https://www.globenewswire.com/NewsRoom/AttachmentNg/980daabb-fd8c-4bbb-b56e-48795fa16bdb

The GUIDED study was the largest prospective study to assess the benefit of pharmacogenomics-guided treatment for depression using the GeneSight Psychotropic test versus an active therapy control arm. All patients in the GUIDED study had the 17-item HAM-D17 questionnaire administered by blinded off-site raters as part of the study protocol. The 6-item HAM-D6 score represents a subset of HAM-D17 questions that have been shown to be more directly linked to depression. For example, questions such as have you had trouble sleeping which could be associated with conditions other than depression are excluded from the HAM-D6 score. Clinical studies have shown that the HAM-D6 score is superior to HAM-D17 at discriminating antidepressants from placebo.

About GeneSight PsychotropicGeneSight Psychotropic is a pharmacogenomic test that analyzes clinically important variations in DNA. The results of the test can inform doctors about genes that may impact how their patients metabolize or respond to depression medications.

About Myriad GeneticsMyriad Genetics Inc., is a leading precision medicine company dedicated to being a trusted advisor transforming patient lives worldwide with pioneering molecular diagnostics. Myriad discovers and commercializes molecular diagnostic tests that: determine the risk of developing disease, accurately diagnose disease, assess the risk of disease progression, and guide treatment decisions across six major medical specialties where molecular diagnostics can significantly improve patient care and lower healthcare costs. Myriad is focused on five critical success factors: building upon a solid hereditary cancer foundation, growing new product volume, expanding reimbursement coverage for new products, increasing RNA kit revenue internationally and improving profitability with Elevate 2020. For more information on how Myriad is making a difference, please visit the Companys website: http://www.myriad.com.

Myriad, the Myriad logo, BART, BRACAnalysis, Colaris, Colaris AP, myPath, myRisk, Myriad myRisk, myRisk Hereditary Cancer, myChoice, myPlan, BRACAnalysis CDx, Tumor BRACAnalysis CDx, myChoice CDx, EndoPredict, Vectra, GeneSight, riskScore, Prolaris, ForeSight and Prequel are trademarks or registered trademarks of Myriad Genetics, Inc. or its wholly owned subsidiaries in the United States and foreign countries. MYGN-F, MYGN-G.

Safe Harbor StatementThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements relating to a new analysis of the GUIDED clinical trial published online in BMC Psychiatry; and the Companys strategic directives under the caption About Myriad Genetics. These forward-looking statements are based on managements current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by forward-looking statements. These risks and uncertainties include, but are not limited to: the risk that sales and profit margins of our molecular diagnostic tests and pharmaceutical and clinical services may decline; risks related to our ability to transition from our existing product portfolio to our new tests, including unexpected costs and delays; risks related to decisions or changes in governmental or private insurers reimbursement levels for our tests or our ability to obtain reimbursement for our new tests at comparable levels to our existing tests; risks related to increased competition and the development of new competing tests and services; the risk that we may be unable to develop or achieve commercial success for additional molecular diagnostic tests and pharmaceutical and clinical services in a timely manner, or at all; the risk that we may not successfully develop new markets for our molecular diagnostic tests and pharmaceutical and clinical services, including our ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying our molecular diagnostic tests and pharmaceutical and clinical services and any future tests and services are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with operating our laboratory testing facilities and our healthcare clinic; risks related to public concern over genetic testing in general or our tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of the healthcare system or healthcare payment systems; risks related to our ability to obtain new corporate collaborations or licenses and acquire new technologies or businesses on satisfactory terms, if at all; risks related to our ability to successfully integrate and derive benefits from any technologies or businesses that we license or acquire; risks related to our projections about our business, results of operations and financial condition; risks related to the potential market opportunity for our products and services; the risk that we or our licensors may be unable to protect or that third parties will infringe the proprietary technologies underlying our tests; the risk of patent-infringement claims or challenges to the validity of our patents or other intellectual property; risks related to changes in intellectual property laws covering our molecular diagnostic tests and pharmaceutical and clinical services and patents or enforcement in the United States and foreign countries; risks of new, changing and competitive technologies and regulations in the United States and internationally; the risk that we may be unable to comply with financial operating covenants under our credit or lending agreements; the risk that we will be unable to pay, when due, amounts due under our credit or lending agreements; and other factors discussed under the heading Risk Factors contained in Item 1A of our most recent Annual Report on Form 10-K for the fiscal year ended June 30, 2019, which has been filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

Media Contact: Ron Rogers Investor Contact: Scott Gleason (801) 584-3065 (801) 584-1143 rrogers@myriad.com sgleason@myriad.com

1 Greden JF, Parikh SV, Rothschild AJ, et al. Impact of pharmacogenomics on clinical outcomes in major depressive disorder in the GUIDED trial: A large, patient- and rater-blinded, randomized, controlled study. J Psychiatr Res. 2019; 111:59-67.

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New Publication Demonstrates GeneSight Improved All Clinical Outcomes Using HAM-D6 Analysis in Large Prospective GUIDED Study - Associated Press

Genetics

Epilepsy and Genes – Epilepsy Foundation

Is epilepsy genetic?

Advances in science and medicine over the last decade have led to a better understanding of the ways genetic factors contribute to epilepsy.

Not all epilepsies that are due to genetic causes are inherited.

The genetics of epilepsy is a new and emerging field. For some individuals, it is not yet possible to determine whether their seizures are due to genetic factors.

In general, if a person has a first-degree relative (mother, father, sibling) with epilepsy, the risk of developing epilepsy by the age of 40 is less than 1 in 20 (Peljto et al. 2014). The risk differs somewhat between focal and generalized epilepsy. There is an increased risk of developing epilepsy if the first-degree relative has a generalized epilepsy rather than focal epilepsy (Peljto et al. 2014; Helbig et al. 2016). These estimates come from population-based studies, meaning they are based on the average across a large group and may not apply for all individuals.

The likelihood of inheriting epilepsy may differ significantly if a person has a relative with a known genetic epilepsy diagnosis. In this case, the chance of developing epilepsy depends on the specific gene and inheritance pattern involved.

To fully appreciate this, we first need to review a few basic genetic terms.

Genes are sequences of DNA (deoxyribonucleic acid) that determine different proteins made in the body. These proteins have a variety of functions and ultimately determine how we develop, grow and function. There are about 20,000 genes in the human genome. With a few exceptions, humans have two copies of every gene: one inherited from each parent.

A genetic variant is a change in the DNA sequence, which can cause the gene not to work properly and ultimately can affect how the gene (protein) functions.

A de novo genetic variant arises for the first time in one individual. Usually, this is caused by a random change in the DNA of the egg or the sperm cell of the parent but is not otherwise present in either parent.

For some genetic conditions, not everyone with a disease-causing variant will develop the symptoms of the disease. This phenomenon is called incomplete penetrance.

Certain types of epilepsy are associated with specific genetic changes, including changes in an individual gene or changes in a chromosome.

Research is currently ongoing in many medical centers and laboratories around the world to help understand the role of genetics in the development of epilepsy. One long term goal of this research is precision medicine. This means individuals with genetic epilepsies would be treated with approaches specifically targeted to their genetic diagnosis.

Although there are many types of research studies, three main types relate to the field of epilepsy genetics:

Learn More

There are currently a limited number of clinical trials available to individuals and families with some forms of genetic epilepsies, but we anticipate the number of trials will continue to increase. The following links are a good place to start for information about currently available trials for genetic epilepsies:

Helbig I, Heinzen EL, Mefford HC, and Ilae Genetics Commission. Primer Part 1-The building blocks of epilepsy genetics. Epilepsia, 57 (2016): 861-8.

Peljto AL, Barker-Cummings, Vasoli VM, Leibson CL, Hauser WA, Buchhalter JR, and Ottman R. Familial risk of epilepsy: a population-based study. Brain, 137 (2014): 795-805.

National Library of Medicine (US). Adapted from Genetics Home Reference [Internet]: ghr.nlm.nih.gov. Bethesda (MD): The Library; 2013 Sep 16.

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Epilepsy and Genes - Epilepsy Foundation

Genetics

Gene editing breakthroughs that cured genetic diseases in 2019 – The Star Online

IN the summer of 2019, a mother in Nashville, Tennessee in the United States, with a seemingly incurable genetic disorder finally found an end to her suffering by editing her genome.

Victoria Grays recovery from sickle cell disease, which had caused her painful seizures, came in a year of breakthroughs in one of the hottest areas of medical research gene therapy.

I have hoped for a cure since I was about 11, the 34-year-old said.

Since I received the new cells, I have been able to enjoy more time with my family without worrying about pain or an out-of-the-blue emergency.

Over several weeks, Grays blood was drawn so that doctors could get to the cause of her illness stem cells from her bone marrow that were making deformed red blood cells.

The stem cells were sent to a Scottish laboratory, where their DNA was modified using Crispr/Cas9 pronounced Crisper a new tool informally known as a molecular scissors.

The genetically-edited cells were transfused back into Grays veins and bone marrow. A month later, she was producing normal blood cells.

Medics warn that caution is necessary, but theoretically, she has been cured.

This is one patient. This is early results. We need to see how it works out in other patients, said her doctor, Haydar Frangoul, at the Sarah Cannon Research Institute in Nashville.

But these results are really exciting.

In Germany, a 19-year-old woman was treated with a similar method for a different blood disease beta thalassemia.

She had previously needed 16 blood transfusions per year. Nine months later, she is completely free of that burden.

For decades, the DNA of living organisms such as corn and salmon has been modified. But Crispr, invented in 2012, made gene editing more widely accessible.

It is much simpler than preceding technology, cheaper and easy to use in small labs.

The technique has given new impetus to the perennial debate over the wisdom of humanity manipulating life itself.

Its all developing very quickly, said French geneticist Emmanuelle Charpentier, one of Crisprs inventors and the co-founder of Crispr Therapeutics, the biotech company conducting the clinical trials involving Gray and the German patient.

Gene cures

Crispr was the latest breakthrough in a year of great strides in gene therapy, a medical adventure that started three decades ago, when the first TV telethons were raising money for children with muscular dystrophy.

Scientists practising the technique insert a normal gene into cells containing a defective gene.

It does the work the original could not, such as making normal red blood cells in Grays case or making tumour-killing super white blood cells for a cancer patient.

Crispr goes even further: instead of adding a gene, the tool edits the genome itself.

After decades of research and clinical trials on a genetic fix to genetic disorders, 2019 saw a historic milestone: approval to bring to market the first gene therapies for a neuromuscular disease in the US and a blood disease in the European Union.

They join several other gene therapies bringing the total to eight approved in recent years to treat certain cancers and an inherited blindness.

Serge Braun, the scientific director of the French Muscular Dystrophy Association, sees 2019 as a turning point that will lead to a medical revolution.

Twenty-five, 30 years, thats the time it had to take, he said. It took a generation for gene therapy to become a reality. Now, its only going to go faster.

Just outside Washington, at the US National Institutes of Health (NIH), researchers are also celebrating a breakthrough period.

We have hit an inflection point, said US NIHs associate director for science policy Carrie Wolinetz.

These therapies are exorbitantly expensive, however, costing up to US$2 million (RM8.18 million) meaning patients face grueling negotiations with their insurance companies.

They also involve a complex regimen of procedures that are only available in wealthy countries.

Gray spent months in hospital getting blood drawn, undergoing chemotherapy, having edited stem cells reintroduced via transfusion and fighting a general infection.

You cannot do this in a community hospital close to home, said her doctor.

However, the number of approved gene therapies will increase to about 40 by 2022, according to Massachusetts Institute of Technology (MIT) researchers.

They will mostly target cancers and diseases that affect muscles, the eyes and the nervous system.

In this Oct 10, 2018, photo, He speaks during an interview at his laboratory in Shenzhen, China. The scientist was recently sentenced to three years in prison for practicing medicine illegally and fined 3 million yuan (RM1.76 million). AP

Bioterrorism potential

Another problem with Crispr is that its relative simplicity has triggered the imaginations of rogue practitioners who dont necessarily share the medical ethics of Western medicine.

In 2018 in China, scientist He Jiankui triggered an international scandal and his excommunication from the scientific community when he used Crispr to create what he called the first gene-edited humans.

The biophysicist said he had altered the DNA (deoxyribonucleic acid) of human embryos that became twin girls Lulu and Nana.

His goal was to create a mutation that would prevent the girls from contracting HIV (human immunodeficiency virus), even though there was no specific reason to put them through the process.

That technology is not safe, said Kiran Musunuru, a genetics professor at the University of Pennsylvania, explaining that the Crispr scissors often cut next to the targeted gene, causing unexpected mutations.

Its very easy to do if you dont care about the consequences, he added.

Despite the ethical pitfalls, restraint seems mainly to have prevailed so far.

The community is keeping a close eye on Russia, where biologist Denis Rebrikov has said he wants to use Crispr to help deaf parents have children without the disability.

There is also the temptation to genetically edit entire animal species, e.g. malaria-causing mosquitoes in Burkina Faso or mice hosting ticks that carry Lyme disease in the US.

The researchers in charge of those projects are advancing carefully however, fully aware of the unpredictability of chain reactions on the ecosystem.

Charpentier doesnt believe in the more dystopian scenarios predicted for gene therapy, including American biohackers injecting themselves with Crispr technology bought online.

Not everyone is a biologist or scientist, she said.

And the possibility of military hijacking to create soldier-killing viruses or bacteria that would ravage enemies crops?

Charpentier thinks that technology generally tends to be used for the better.

Im a bacteriologist -- weve been talking about bioterrorism for years, she said. Nothing has ever happened. AFP Relaxnews

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Gene editing breakthroughs that cured genetic diseases in 2019 - The Star Online

Genetics

Finding the right mix of genetics balancing and costs – High Plains Journal

In challenging times, beef producers are looking for an edge and genetics, nutrition and production are all part of the equation.

Finding the balance is the key for producers, according to Frank Goedeken, was one of the speakers at the first Cattle U and Trade Show, a High Plains Journal event July 29 to 30, at the United Wireless Arena in Dodge City, Kansas.

Goedeken has been a consulting nutritionist in the High Plains since 1989, including 15 years at Purina Mills and as an owner of Integrated Beef Consultants LLC. Priorities of his practice have been gain, conversion, cost of gain and out weight.

The challenge for producers continues to be to bring these advances together without compromising cattle health, properly growing and developing the cattle are required to reverse the trend of increased death loss and medicine costs.

As he visits with clients one of his goals is to not only look at the facility where the calves are located but also to help them envision the final product so the consumer has an enjoyable eating experience. He noted it all starts with the calves and all phases, from the cow-calf producer, to the backgrounder to the feeder all need to be on the same page.

If you talk to most feedyards and say, Youre going to bring in 100 calves that are being weaned on the truck? Hes not going to be very happy, Goedeken said. Why is that? Health is going to be an issue. So youre trying to improve the health of the cattle with good nutrition and good management.

At the same time producers need to keep tabs on feed costs and commodity prices, he said.

A cow-calf producer also needs to study the genetics of his herd and how the calves perform beyond the boundaries of the ranch, Goedeken said.

From his observations, Goedeken has noticed the comfort level of cattle is not always tied to feed. Good questions producers need to ask include do the cattle have the right pens and configurations? Should the producer do something different?

Sometimes the right environment for the cattle can make a big difference, too.

Have you ever noticed that cattle do not like to lay on bare dirt? You go out in your pasture, wheat stubble or whatever, he said. Very seldom would you see him or her lay on bare dirt. If you put some hay down or some straw out there theyd all be laying down. So thats kind of what we start with. Providing a comfortable environment is important.

Paying attention to nutrition is essential because of the life stages and physiological needs of the animal changes as they grow and mature and wrong decisions can even cause death to a young animal, he said.

Managing stress for the calf is also important, the consulting nutritionist said. A new environment can be a factor others may seem trite but are important, too, such as the water may taste different or the calfs mother is no longer with her calf. Goedeken said sometimes with all the stress, it can be wrongly assumed that all the calves are under stress. Then we run through, shoot, tag them and vaccinate.

He said, on the surface, it sounds like the right approach but it does not mean the situation was managed best for the cattle.

The more we stress the cattle the less likely they are to respond to challenges to their immune system, he said. They are less likely to respond to vaccines and the less likely they are to be healthy their entire life.

He also noted that timing of vaccines can make a difference and working with veterinarians is essential.

Nutritional stress occurs while trying to get those animals quickly up to speed to meet delivery needs but he says energy has to be balanced with health of the animals. In making a point he says distillers grain is an example in which feeders thought was a magic bullet but he says studies show the key remains balance in feeding nutrients.

A healthy animal means he is less likely to be stressed as a more stressed animal means more medication is needed, Goedeken said. Also, immune functions might become compromised and that can lead to unexpected death.

In looking at nutritional matters, he said striving to get to the right level of energy, protein and other nutrients in the diet does pay. Supplementing the diet with zinc can help producers because zinc is tied to muscle development and immune functions.

Stress negatively affects health and performance. As an industry, we need to pay more attention to that. When I grew up in the business I thought, Man, lets get all that stress over with, lets process them and lets get them into their pens? But it may not have been the right time to process those cattle based on what we talked about.

Healthier cattle perform better, he said, and that dynamic has not changed and much more information is available with studies to back it up.

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Finding the right mix of genetics balancing and costs - High Plains Journal

Genetics

‘Counting On’: Amy Duggar Just Started A Debate About Genetics On Her Instagram Page and It’s Hilarious – Showbiz Cheat Sheet

Well, its official, AmyDuggar doesnt want to be associated with the Duggar family any longer. Fanshave long suspected that cousin Amy has been slowly removing herself from theinner workings of the Duggar clan ever since MaryDuggar, the famed grandmother of 20 children, passed away unexpectedly inJune 2019. Now, Amy wants to make sure people know that her son, DaxtonRyan, isnt a Duggar, and its created quite the debate on Instagram.

Amy recently took to Instagram to share a photo of her youngson. The themed photo was all about ringing in the New Year, but followersseemed to want to discuss genetics and the Duggar name. One commentercomplimented Amy, claiming her son was beautiful because he was a Duggar. Apparently,Amy couldnt let that one go and reminded the commenter that while sheappreciated the sentiment her son, Daxton, was a King.

Amy married DillonKing in September 2015. Amy promptly changed her name to her husbands lastname. Their first child, Daxton Ryan, was born on Oct. 9, according to People.Since his birth, Amy has been postingalmost nonstop snapshots of the chubby baby, and while fans are absolutelyloving her pictures, they all seem to insist hes a Duggar. Amy wants everyoneto know he is not. Her most recent reminder kicked off a debate about geneticsand lineage.

The second Amy suggested her son was not a Duggar, thefamilys most prominent supporters came crawling out to comment. While manyinsist that he is a Duggar because Amy is a Duggar, their understanding of geneticsseems a little elementary. Yes, technically, Daxton is 25% Duggar because hismother, Amy, is 50% Duggar. Remember, Amy has a father, too. Daxton also shareshalf of his genetics with his father, Dillion. That means this child is not justa Duggar and not only a King.

While fans might be correct that he has Duggar blood, he carrieshis fathers surname, which appears to be what Amy was really trying to pointout. While several fans took it as a sign of disrespect, when you think about it,Duggar fans are actually the ones being disrespectful. Since Amy and Dillon havechosen to give their child the King name, fans should probably respect him aspart of that family.

Amy might be related to the Duggar clan through her mother,Deanna Duggar, but that doesnt mean she wants to be associated with their values.It has been clear, for years, that Amy was raised markedly different from her19 cousins. She was allowed to date, didnt need a chaperone, and while still aChristian, isnt a part of the ultra-conservative Christian ministry the Duggarfamily belongs to. She also was not homeschooled.

While Amy remains friendly with some of her cousins, shedoesnt seem to be particularly interested in being a part of the largerfamily. Back in November 2019, Amyinsisted she knew nothing about the rumored raids on the Duggar property,stating that she had no idea why people would think her aunt and uncle would tellher anything. Fans took the statement to mean that Amy isnt particularly closeto the supersized family.

Likely, shes not, to be honest. Her values dont jive withthe Duggars, and her husband recently investedin a whiskey lounge, a business that is undoubtedly not Duggar approved.Amy is also a business owner herself, meaning she works outside the home,another decision that is verboten in the Duggars social circle. Likely, Amyhas quietly been distancing herself from the large family for years, but a bombshellreason for the rift probably doesnt exist.

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'Counting On': Amy Duggar Just Started A Debate About Genetics On Her Instagram Page and It's Hilarious - Showbiz Cheat Sheet

Genetics

The supercells’ that cured an infants genetic illness – Jamaica Observer

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MCLEAN, United States (AFP) When a person's immune system is impaired by a genetic disease a bone marrow transplant can be a powerful therapeutic tool, but with a major downside during the first few months the recipient's defences against viruses are severely weakened. The slightest infection can lead to a hospital trip.

A still-experimental type of treatment known as T-cell therapy aims to assist during this vulnerable period the months during which the body is rebuilding its natural defences. After two decades of clinical trials, the technology has been refined and is being used to treat more and more patients, many of them children.

A boy named Johan is one of them.

Today he is a mischievous, smiling toddler, with a thick shock of light-brown hair, who never tires, playfully tormenting the family's puppy, Henry.

There is no sign of the three-year-long medical and emotional roller coaster ride he and his family, who live in an affluent Washington suburb, have been on.

The first traumatic surprise came with the results of a pregnancy test Johan was not planned.

That was a huge shock. I cried, said his mother, 39-year-old Maren Chamorro.

Risky procedure

She had known since childhood that she carried a gene that can be fatal in a child's first 10 years, chronic granulomatous disease (CGD).

Her brother died of it at the age of seven. The inexorable laws of genetics meant that Maren had a one in four chance of transmitting it to her child.

For their first children, she and her husband Ricardo had chosen invitro fertilisation, allowing the embryos to be genetically tested before implantation.

Their twins Thomas and Joanna were born both disease-free seven and a half years ago.

But in Johan's case, a post-birth genetic test quickly confirmed the worst: He had CGD.

After conferring with experts at Children's National Hospital in Washington, the couple took one of the most important decisions of their lives, Johan would receive a bone marrow transplant a risky procedure but one that would give him a chance of a cure.

Obviously, the fact that Maren had lost a sibling at a young age from the disease played a big role, Ricardo confided.

Bone marrow, the spongy tissue inside bones, serves as the body's factory for the production of blood cells both red and white.

His brother's immune system

Johan's white blood cells were incapable of fighting off bacteria and fungal infections. A simple bacterial infection, of negligible concern in a healthy child, could spread out of control in his young body.

Luckily, Johan's brother Thomas, six years old at the time, was a perfect match. In April 2018, doctors first cleansed Johan's marrow using chemotherapy. They then took a small amount of marrow from Thomas's hip bones using a long, thin needle.

From that sample they extracted supercells, as Thomas calls them stem cells, which they reinjected into Johan's veins. Those cells would eventually settle in his bone marrow and begin producing normal white blood cells.

The second step was preventive cell therapy, under an experimental programme led by immunologist Michael Keller at Children's National Hospital.

The part of the immune system that protects against bacteria can be rebuilt in only a matter of weeks; but for viruses, the natural process takes at least three months.

Hurdles remain

From Thomas's blood, doctors extracted specialised white blood cells T-cells that had already encountered six viruses.

Keller grew them for 10 days in an incubator, creating an army of hundreds of millions of those specialised T-cells. The result: A fluffy white substance contained in a small glass vial.

Those T-cells were then injected into Johan's veins, immediately conferring protection against the six viruses.

He has his brother's immune system, said Keller, an assistant professor at Children's National.

Johan's mother confirmed as much: Today, when Thomas and Johan catch a cold they have the same symptoms, and for nearly the same amount of time.

I think it's pretty cool to have immunity from your big brother, Maren Chamorro said.

This therapeutic approach boosting the body's immune system using cells from a donor or one's own genetically modified cells is known as immunotherapy.

Its main use so far has been against cancer, but Keller hopes it will soon become available against viruses for patients, like Johan, who suffer from depressed immune systems.

The chief obstacles to that happening are the complexity of the process and the costs, which can run to many thousands of dollars. These factors currently restrict the procedure to some 30 medical centres in the United States.

For Johan, a year and a half after his bone marrow transplant, everything points to a complete success.

It's neat to see him processing things, and especially play outside in the mud, his mother said.

You know, what a gift!

Her only concern now is the same as any mother would have that when her son does fall ill, others in the family might catch the same bug.

Now you can read the Jamaica Observer ePaper anytime, anywhere. The Jamaica Observer ePaper is available to you at home or at work, and is the same edition as the printed copy available at http://bit.ly/epaperlive

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The supercells' that cured an infants genetic illness - Jamaica Observer

Genetics

The Face of Science – Clemson World magazine

That next day, Drake preferred sleeping over eating. But then, thats common with newborns. Tarah and Eric would wake him for feeding, careful to make sure he got plenty of nourishment.

By Saturday, these experienced parents became uneasy. Drake was just too lethargic. It was harder to wake him for feedings. The OSullivans called Drakes doctor and were assured there was nothing to be concerned about; Drake had been healthy when he left the hospital two days ago. And, the doctors office assured them, they would be checking him again on Monday at a scheduled office visit.

But the OSullivans disquiet grew by the hour. By Sunday evening, Drake would not open his eyes or respond to them. He was growing limp and struggling to breathe. The OSullivans rushed Drake to the hospital where the staff flew into emergency mode. Too sick for care at the local hospital, Drake was stabilized for transport to the pediatric intensive care unit (PICU) at Greenville Memorial Hospital. Just 72 hours after birth, Drake lapsed into a coma. And no one knew why.

That unforgettable night was the beginning of a long journey of test after test and a diagnosis by elimination.

Drake continued to decline as each negative test pushed aside another horrible possibility. You would think that eliminating terrible diseases would be a good thing, says Eric. But that just meant we were looking at something very rare.

Finally, blood tests revealed an ever-elevating level of glycine in Drakes blood, a symptom of an extremely rare, genetic metabolic disease called nonketotic hyperglycinemia or NKH.

The words nonketotic hyperglycinemia meant nothing to Tarah and Eric. But the next words were clear: Drake had a less than 10 percent chance of survival.

The diagnosis was like a starters pistol for the OSullivans. From that moment, everything would be a race against time to save Drake.

After 28 days of tests, monitors, tubes and wires, Drake was released to go home. There, as Tarah explains, Our house became a sort of lab. There were blood tests, feedings, medications and monitoring day and night, 24/7. Glycine became the OSullivans obsession as they tried desperately through medication and diet to moderate Drakes levels. They began to search for information, research, treatment, medical advice anything to save his life.

The OSullivans contacted anyone who might know about NKH, have a related research project or could tell them more. They learned that NKH affects fewer than 500 people worldwide and has no cure. There was no research underway, and no funding for research. And because there is no medically recognized cure for NKH, all treatments are considered experimental and not covered by medical insurance. Period.

So Tarah became a lay scientist. She read everything, called and emailed medical researchers and established the Drake Rayden Foundation to raise awareness for NKH, fight for better treatment and support research. She entered a world of genetics and vectors, glycine and metabolic pathways. Tarah had quit college just shy of completing her business degree. Now she desperately needed the scientific expertise that would help her understand the disease and find the cure.

Tarah decided to return to college.

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The Face of Science - Clemson World magazine

Genetics

A Note On Genetics Generation Advancement Corp.s (GTSM:4160) ROE and Debt To Equity – Simply Wall St

While some investors are already well versed in financial metrics (hat tip), this article is for those who would like to learn about Return On Equity (ROE) and why it is important. Well use ROE to examine Genetics Generation Advancement Corp. (GTSM:4160), by way of a worked example.

Our data shows Genetics Generation Advancement has a return on equity of 5.7% for the last year. One way to conceptualize this, is that for each NT$1 of shareholders equity it has, the company made NT$0.06 in profit.

Check out our latest analysis for Genetics Generation Advancement

The formula for return on equity is:

Return on Equity = Net Profit (from continuing operations) Shareholders Equity

Or for Genetics Generation Advancement:

5.7% = NT$20m NT$352m (Based on the trailing twelve months to September 2019.)

Its easy to understand the net profit part of that equation, but shareholders equity requires further explanation. It is all earnings retained by the company, plus any capital paid in by shareholders. You can calculate shareholders equity by subtracting the companys total liabilities from its total assets.

ROE looks at the amount a company earns relative to the money it has kept within the business. The return is the profit over the last twelve months. That means that the higher the ROE, the more profitable the company is. So, all else being equal, a high ROE is better than a low one. Clearly, then, one can use ROE to compare different companies.

One simple way to determine if a company has a good return on equity is to compare it to the average for its industry. Importantly, this is far from a perfect measure, because companies differ significantly within the same industry classification. The image below shows that Genetics Generation Advancement has an ROE that is roughly in line with the Biotechs industry average (5.7%).

That isnt amazing, but it is respectable. ROE doesnt tell us if the share price is low, but it can inform us to the nature of the business. For those looking for a bargain, other factors may be more important. If you like to buy stocks alongside management, then you might just love this free list of companies. (Hint: insiders have been buying them).

Companies usually need to invest money to grow their profits. The cash for investment can come from prior year profits (retained earnings), issuing new shares, or borrowing. In the first two cases, the ROE will capture this use of capital to grow. In the latter case, the use of debt will improve the returns, but will not change the equity. Thus the use of debt can improve ROE, albeit along with extra risk in the case of stormy weather, metaphorically speaking.

Shareholders will be pleased to learn that Genetics Generation Advancement has not one iota of net debt! So although its ROE isnt that impressive, we shouldnt judge it harshly on that metric, because it didnt use debt. After all, with cash on the balance sheet, a company has a lot more optionality in good times and bad.

Return on equity is one way we can compare the business quality of different companies. In my book the highest quality companies have high return on equity, despite low debt. If two companies have around the same level of debt to equity, and one has a higher ROE, Id generally prefer the one with higher ROE.

But ROE is just one piece of a bigger puzzle, since high quality businesses often trade on high multiples of earnings. Profit growth rates, versus the expectations reflected in the price of the stock, are a particularly important to consider. Check the past profit growth by Genetics Generation Advancement by looking at this visualization of past earnings, revenue and cash flow.

Of course Genetics Generation Advancement may not be the best stock to buy. So you may wish to see this free collection of other companies that have high ROE and low debt.

If you spot an error that warrants correction, please contact the editor at editorial-team@simplywallst.com. This article by Simply Wall St is general in nature. It does not constitute a recommendation to buy or sell any stock, and does not take account of your objectives, or your financial situation. Simply Wall St has no position in the stocks mentioned.

We aim to bring you long-term focused research analysis driven by fundamental data. Note that our analysis may not factor in the latest price-sensitive company announcements or qualitative material. Thank you for reading.

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A Note On Genetics Generation Advancement Corp.s (GTSM:4160) ROE and Debt To Equity - Simply Wall St