StemCell Therapy

Puma Biotechnology, Inc. (NASDAQ:PBYI)market capitalization at present is $3.29B at the rate of $89.95 a share. The firms price-to-sales ratio was noted 0.00 in contrast with an overall industry average of 100.62. Most of the active traders and investors are keen to find ways to compare the value of stocks. The price-to-sales ratio offers a simple approach in this case. They just need to take the companys market capitalization and divide it by the companys total sales over the past 12 months. The lesser the ratio, the more attractive the investment. During the key period of last 5 years, Puma Biotechnology, Inc. (NASDAQ:PBYI) earnings per share growth remained at -44.40%.

How Company Returns Shareholders Value?

Dividends is a reward scheme, that a company presents to its shareholders. There can be various forms of dividends, such as cash payment, stocks or any other form. This payment is usually a part of the profit of the company. A companys dividend is mostly determined by its board of directors and it requires the shareholders approval.Puma Biotechnology, Inc. (NASDAQ:PBYI)for the trailing twelve months paying dividend with the payout ratio of 0.00% to its shareholders. Currently it is offering a dividend yield of 0.00% and a 5 year dividend growth rate of 0.00%. Over the last year Companys shares have been trading in the range of $28.35 and $98.85. However yesterday the stock remained in between $83.13 and $93.95. The stock is above its 52-week low with 217.28% and is in the wake of its 52-week high with -9.00%.

Performance & Technicalities

In the latest week Puma Biotechnology, Inc. (NASDAQ:PBYI) stock volatility was recorded 6.05% which for the previous full month was noted 4.93%. Meanwhile the stock weekly performance was subdued at -5.66%, which was upheld for the month at 2.92%. Likewise, the upbeat performance for the last quarter was 130.64% and for the full year it was 83.42%. Moreover the Companys Year To Date performance was 193.00%. Now a days one of the fundamental indicator used in the technical analysis is called Stochastic %D, Stochastic indicator was created by George Lane. The stochastic is a momentum indicator comparing the closing price of a security to the range of its prices over a fix period of time. The gauge is based on the assumption that if price surges, the closing price tends towards the values that belong to the upper part of the area of price movements in the preceding period. On the other hand if price drops, the contrary is right. For Puma Biotechnology, Inc. (NASDAQ:PBYI), Stochastic %D value stayed at 72.69% for the last 9 days. Considering more the value stands at 79.05% and 79.07% for 14 and 20 days, in that order.

Digital Realty Trust, Inc. (NYSE:DLR)closed at $117.59 a share in the latest session and the stock value rose almost 19.67% since the beginning of this year. The company has managed to keep price to sales ratio of 8.23 against an industry average of 10.53. The price to sales ratio is the ratio of the market value of equity to the sales. This ratio is internally not steady, since the market value of equity is divided by the total revenues of the firm. Its revenue stood at 15.10% a year on average in the period of last five years. Firms net income measured an average growth rate of 10.80%. Following last close companys stock, is 2.09% above their SMA 50 and -3.24% below the 52-week high. A simple moving average (SMA) is an mathematical moving average calculated by adding the closing price of the security for a number of time periods and then dividing this total by the number of time periods. Its most recent closing price has a distance of 4.77% from SMA20 and is 11.48% above than SMA200.

In-Depth Technical Study

Investors generally keep an extensive variety of technical indicators at their disposal for completing technical stock analysis. The average true range is a moving average, generally 14 days, of the true ranges.

The average true range (ATR) was fashioned to allow traders to more precisely evaluate the daily volatility of an asset by using straightforward calculations. However the indicator does not specify the price direction, rather it is used first and foremost to measure volatility caused by gaps and limit up or down moves. The ATR is fairly simple to calculate and only needs historical price data.

ATR is counted for different periods, like 9-day, 14-day, 20-day, 50-day and 100-day. At the moment, the 14-day ATR for Digital Realty Trust, Inc. (NYSE:DLR) is noted at 2.01.

Continue reading here:
Why Investors remained buoyant on: Puma Biotechnology, Inc. (PBYI), Digital Realty Trust, Inc. (DLR) - StockNewsJournal

HYDERABAD: Dr P M Bhargava, eminent scientist and founder-director of the city-based Centre for Cellular and Molecular Biology (CCMB), died here on Tuesday after a brief illness. He was 89 and is survived by two children.

Pushpa Mittra Bhargava was born on February 22, 1928. He was a pioneer in the field of biotechnology in India and among the first persons to use the term "genetic engineering". Bhargava was instrumental in the formation of the Department of Biotechnology in the '70s. He was also chairman of Medically Aware and Responsible Citizens of Hyderabad, Sambhavna Trust, Bhopal, and Basic Research, Education and Development Society (BREAD), New Delhi. He served as vice-chairman of the National Knowledge Commission between 2005 and 2007.

Bhargava received over 100 national and international honours and awards. He was awarded the Padma Bhushan in 1986 but returned it in 2015 citing "matters of principle". He was honoured with the Legion d'honneur in 1998. He is popularly known as the architect of modern biology in India.

Read the rest here:
Dr Pushpa Mitra Bhargava, pioneer in biotechnology, passes away at 89 - Times of India

The August issue of the New Jersey State Bar Association's bi-monthly magazine, New Jersey Lawyer, focuses on the evolving topic of biotechnology, genetics and the law.

"Although a very specialized area, biotechnology law crosses many legal disciplines, including litigation, licensing, intellectual property, patents, agriculture, business, venture capitalism, antitrust, biosecurity and bioethics," said Angela Foster and David Opderbeck, who served as special editors for the issue.

"The use of biotechnology has raised a number of legal, ethical and social issues, including who owns genetically modified organisms (GMOs), whether genetically modified foods are safe to eat, and who controls a person's genetic information. This issue explores contemporary biotechnology issues impacting the legal community."

A dozen articles explore the topic in the award-winning magazine, beginning with a look at whether organs-on-chips are patentable in an article by Douglas Bucklin. Richard Catalina Jr.'s article on the Biologics Price Competition and Innovation Act follows.

Nancy Del Pizzo's article looks at the open source model in biotechnology, while Foster explores the truth and fiction behind genetically modified food. Jonathan Lourie reviews strategic licenses and collaborations.

Reproduction is the topic of two articles, one analyzing assisted reproductive technology, written by Alan Milstein, and one penned by Kimberly Mutcherson on regulating the right to procreate.

Opderbeck's contribution focuses on synthetic biology and biosecurity, while Anjana Patel and Patricia Wagner discuss biotech mergers, acquisitions and antitrust issues and Marina Sigareva and Ryan O'Donnell look at global strategies for protecting biotech inventions.

The edition closes with articles on the Patent Trial and Appeal Board's influence on the biotech and pharma industries, written by Nichole Valeyko and Maegan Fuller, and the privacy implications for biotechnology by Wagner.

The October edition of New Jersey Lawyer will explore pro bono issues.

Follow this link:
NJSBA magazine explores biotechnology and genetics - Yahoo News

Even though Richard Lopez is still in high school, he can already tell you a thing or two about the ureteric bud, the metanephric mesenchyme and the developing kidney.

More impressively, he was familiar with these terms before starting his summer internship in the lab of Andy McMahon, kidney researcher and director of the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC.

I knew I was going to come here, Lopez said. So from December on, I was just reading papers that were written by Dr. McMahons lab. And so I read about the development of the kidney, kidney organoids, experimental methods like in situ hybridization, immunohistochemistry, all that stuff. Im really glad I did all of that because now that Im here, I understand whats going on.

Lopez undertook this intense preparation as part of the Science Research Program at his Connecticut boarding school, Choate Rosemary Hall. In addition to familiarizing him with the McMahon labs research, the program provided experience with useful molecular biology techniques, ranging from gel electrophoresis to polymerase chain reaction.

Lopez didnt start his high school career at Choate. Growing up in Lennox near the Los Angeles International Airport, he attended local public schools until his sophomore year in high school. At that point, his exceptional scores on the California Standardized Test attracted the attention of the Young Eisner Scholar program, which empowers underserved students to fulfill their potential.

As an Eisner Scholar, he earned both admission and a full scholarship to attend Choate. But the decision to leave home wasnt easy.

I was terrified at first, leaving everything behind, he said. I talked to my mom about it, and at first she was hesitant because I was born and raised here, and Im the only child. But then she realized that this is an amazing opportunity, and I cant let it go by.

Lopez recalls that Choate was initially in a huge culture shock from the occasional Maserati to the international student body to the exceptional academic opportunities such as the Science Research Program that brought him to USC.

In the McMahon lab, Lopez has learned about the molecular signals that drive the branching development of the kidney, and he has practiced a wide range of lab techniques.

Im really excited about science because I know its potential.

Richard Lopez

Im really excited and passionate about science because I know its potential, he said. If you pair that with math, you have no boundaries. If you look at the lab where Im working right now creating kidney organoids, learning about kidney development, these kinds of things can solve really burdensome illnesses that are fatal to some people, like end-stage renal disease and polycystic kidney disease.

To get to the lab every day, Lopez bike commutes a total of 32 miles from his home in Lennox to USCs Health Sciences Campus. Hes run the Los Angeles Marathon once and the San Francisco Marathon twice. In November, hes planning to travel to Florida to celebrate his 18th birthday with his first Ironman Triathlon a 2.4-mile swim, 112-mile bike ride and 26.2-mile run.

Hes participating in these events not only for fun and fitness, but also as a way to give back. Hes currently raising sponsorship money for the Partnership Scholars Program, which provides underserved junior high and high school students with educational and cultural experiences, ranging from theatergoing to restaurant outings to college tours. His goal is to raise $54,000 to fund three new scholars.

I was very lucky, he said. So I want to raise money for the scholarships that have helped me out along the way.

More stories about: Research, Stem Cells

Here is the original post:
High school student gets an early start in stem cell research at USC - USC News

SAN DIEGO, Aug. 1, 2017 /PRNewswire/ -- ViaCyte, Inc., a privately-held, leading regenerative medicine company, announced today that the first patients have been implanted with the PEC-Direct product candidate, a novel islet cell replacement therapy in development as a functional cure for patients with type 1 diabetes who are at high risk for acute life-threatening complications. The first implant procedures of the clinical trial took place at the University of Alberta Hospital in Edmonton, Alberta, and the UC San Diego School of Medicine's Altman Clinical Trials Research Institute. The goal of the open-label clinical trial is to evaluate the PEC-Direct product candidate for safety and definitive evidence of efficacy. In the coming months, the company expects to expand the trial to additional centers including the University of Minnesota and other sites in the US and Canada.

The first cohort of type 1 diabetes patients is receiving multiple small-format cell-filled devices called sentinels in order to evaluate safety and implant viability. These sentinel units will be removed at specific time points and examined histologically to provide early insight into the progression of engraftment and maturation into pancreatic islet cells including insulin-producing beta cells. A second cohort of up to 40 patients is expected to begin enrolling later this year to evaluate both safety and efficacy. The primary efficacy measurement in the trial will be the clinically relevant production of insulin, as measured by the insulin biomarker C-peptide, in a patient population that has little to no ability to produce endogenous insulin at the time of enrollment. Other important endpoints will be evaluated including injectable insulin usage and the incidence of hypoglycemic events. ViaCyte's goal is to demonstrate early evidence of efficacy in the first half of 2018 and definitive efficacy 6 to 12 months later.

"Islet transplants have been used to successfully treat patients with unstable, high-risk type 1 diabetes, but the procedure has limitations, including a very limited supply of donor organs and challenges in obtaining reliable and consistent islet preparations," said trial investigator James Shapiro, MD, PhD, FRCSC, Director of the Clinical Islet Transplant Program, University of Alberta. "An effective stem cell-derived islet replacement therapy would solve these issues and has the potential to help a greater number of people."

"Patients with high-risk type 1 diabetes complications, such as hypoglycemia unawareness, are at constant risk of life-threatening low blood glucose," said Jeremy Pettus, MD, investigator in the clinical trial and Assistant Professor of Medicine at UC San Diego. "The PEC-Direct islet cell replacement therapy is designed to help patients with the most urgent medical need."

The PEC-Direct product candidate is being developed for type 1 diabetes patients who have hypoglycemia unawareness, extreme glycemic lability, and/or severe hypoglycemic episodes. It is estimated that about 140,000 people in Canada and the US have such high-risk type 1 diabetes. In addition to providing an unlimited supply of cells for implantation, the PEC-Direct approach has other potential advantages relative to cadaver islet transplants such as delivering a more consistent product preparation under quality-controlled cGMP conditions, and a more straightforward and safe mode of delivery.

The clinical trial is being supported in part by JDRF, the leading global organization funding type 1 diabetes research. "JDRF remains dedicated to accelerating the delivery of beta cell replacement therapies to the T1D community, and we commend ViaCyte in its announcement of the first patients to be implanted with the PEC-Direct islet cell replacement therapy," said Derek Rapp, JDRF President and Chief Executive Officer. "JDRF is excited to support this clinical development given its potential to help those people with type 1 diabetes that need it the most those at high risk of life-threatening acute complications. JDRF and ViaCyte share a continuing commitment to realizing the potential of beta cell replacement strategies to deliver insulin independence without immune suppression for people living with type 1 diabetes, and ultimately, at JDRF we hope this will move us forward in fulfilling our vision of a world without type 1 diabetes."

"There are limited treatment options for patients with high-risk type 1 diabetes to manage life-threatening hypoglycemic episodes," said Paul Laikind, PhD, President and Chief Executive Officer of ViaCyte. "We believe that the PEC-Direct product candidate has the potential to transform the lives of these patients and we are excited to move closer to that goal with the initiation of clinical evaluation announced today. This also represents a step towards a broader application of the technology. We remain fully committed to developing a functional cure for all patients with insulin-requiring diabetes. To that end, we are hard at work on next-generation approaches as well, and expect the work with PEC-Direct to further advance our knowledge and drive progress."

In addition to JDRF, the California Institute for Regenerative Medicine (CIRM)'s Alpha Clinic, the Sanford Stem Cell Clinical Center, the JDRF Canadian Clinical Trials Network (CCTN), the Stem Cell Network, and Alberta Innovates Health Solutions (AIHS) are all providing support for the trial.

About the PEC-Direct Product Candidate The PEC-Direct product candidate delivers stem cell-derived pancreatic progenitor cells, called PEC-01 cells, in a device designed to allow direct vascularization of the cells in the device. After implantation, these cells are expected to become mature human islet tissue including well-regulated beta cells producing insulin on demand. The direct vascularization of the implanted cells is expected to allow for robust and consistent engraftment but will necessitate the use of maintenance immune suppression therapy.

About ViaCyte ViaCyte is a privately-held regenerative medicine company developing novel cell replacement therapies as potential long-term diabetes treatments to reduce the risk of hypoglycemia and diabetes-related complications. ViaCyte's product candidates are based on the derivation of pancreatic progenitor cells from stem cells, which are then implanted in a durable and retrievable cell delivery device. Once implanted and matured, these cells are designed to secrete insulin and other pancreatic hormones in response to blood glucose levels. ViaCyte has two products in clinical development. The PEC-Direct product candidate delivers the pancreatic progenitor cells in a non-immunoprotective device and is being developed for type 1 diabetes patients who have hypoglycemia unawareness, extreme glycemic lability, and/or recurrent severe hypoglycemic episodes. The PEC-Encap (also known as VC-01) product candidate delivers the same pancreatic progenitor cells in an immunoprotective device and is being developed for all patients with diabetes, type 1 and type 2, who use insulin. ViaCyte is headquartered in San Diego, California. The Company is funded in part by the California Institute for Regenerative Medicine (CIRM) and JDRF. For more information on ViaCyte, please visit http://www.viacyte.com and connect with ViaCyte on Twitter and Facebook.

View original content with multimedia:http://www.prnewswire.com/news-releases/viacyte-announces-first-patients-implanted-with-pec-direct-islet-cell-replacement-therapy-in-international-clinical-trial-300497290.html

SOURCE ViaCyte, Inc.

Original post:
ViaCyte Announces First Patients Implanted with PEC-Direct Islet Cell Replacement Therapy in International Clinical ... - Markets Insider

An estimated 30.3 million Americans have diabetes. The emotional and physical toil for those suffering from the disease is large, as are the associated medical bills: In 2012, the cost for caring for Americans with diabetes was $245 billion.

A new report from Blue Cross Blue Shield ranks the disease behind only mood disorders and hypertension as having the largest negative impact on commercially insured Americans health.

It also found that diabetes impact, which measures prevalence and severity of the condition as well as the risk of premature death, is growing at the fastest clip for millennials, defined as those between 18 to 34 years of age.

The worrying trend coincides with rising rates of obesity among the demographic. Nearly 90% of people diagnosed with diabetes are overweight or obese. Between 2001 and 2015, teenage rates of obesity rose over 30%, according to the CDC.

"Despite the impact of diabetes' continued growth across America, the good news is that this epidemic is preventable, Dr. Trent Haywood, senior vice president and chief medical officer for Blue Cross Blue Shield, said in a statement.

Type 2 diabetes was once thought to be largely irreversible, but today many doctors believe it can be managedin some cases, reversedthrough lifestyle changes and moderate weight loss. By losing as little as 5% of their body weight, participants in several studies were able to transition off medication to manage the condition.

A number of startups have launched to help people manage and/or reverse their diabetes by changing their diet and exercise routines. Virta Health, Glooko, and Omada Health have all raised venture capital to build technology platforms to this effect.

For millennials, a demographic endlessly lauded and derided for being the first generation to grow up with Internet, this could be encouraging news. Whereas many of their need to be taught to interact with a diabetes management app, theyre digital natives.

It remains to be seen, of course, whether a technology-based approach is enough to curb the tide. But as diabetes management goes digital, familiarity with a smartphone doesn't hurt.

Read the rest here:
Diabetes Impact Is Rising Fastest Among Millennials | Fortune.com - Fortune

By Mary Elizabeth Dallas

HealthDay Reporter

TUESDAY, Aug. 1, 2017 (HealthDay News) -- Women who gain weight after having a baby may be more likely to develop diabetes during their next pregnancy, a new study suggests.

Women's weight before conception and how much they gain during pregnancy are known risk factors for gestational diabetes, the study authors explained. Gestational diabetes is a form of high blood sugar diagnosed during pregnancy. It can cause complications for both mother and baby.

Led by Linn Sorbye of the University of Bergen in Norway, researchers investigated the diabetes risk among women who had been pregnant once or twice before.

The study involved about 24,200 women who gave birth between 2006 and 2014. The researchers considered the women's previous history of gestational diabetes and body mass index (BMI) when they got pregnant again. BMI is an estimate of body fat based on weight and height. A BMI of 30 is considered obese.

About 36 percent of the women gained more than 1 BMI unit of weight between the start of their first pregnancy and their second, the study found. These women were more likely than women whose weight was stable to develop diabetes during a second pregnancy.

Women who gained twice as much weight had double the risk for gestational diabetes. And the risk rose fivefold for women who had the greatest weight gain, the researchers found.

These risks were most striking among women whose weights were normal before their first pregnancy. The study showed, however, that overweight women who lost weight after delivery reduced their risk of diabetes during another pregnancy.

The study was published Aug. 1 in the journal PLOS Medicine.

WebMD News from HealthDay

SOURCE: PLOS, news release, Aug. 1, 2017.

See original here:
Weight Gain Between Babies Linked to Diabetes - WebMD

WNY's Great Kids: Wheatfield Boy Part of JDRF Childrens' Congress

Melissa Holmes, WGRZ 8:56 AM. EDT August 02, 2017

Mason Gfroerer, 11 of Wheatfield, doesn't let type 1 diabetes slow him down. His push for research and funding has earned him a spot as one of "WNY's Great Kids."

WHEATFIELD, NY- 11-year-old Mason Gfroerer's life revolves around soccer. The St. Christopher student plays in Northtown's travel league and is always out in his backyard practicing.

"I've been playing for 2 years now. I really enjoy it," said Mason.

But often he has to give himself a timeout in order to check his blood sugar, because Mason has type-1 diabetes.

"Sometimes I'll feel shaky, I get sweaty, my eye vision is a little blurry," said Mason. "I have to sit out until my blood sugar comes back up and then I can play again."

He was first diagnosed when he was 8-years-old, after his parents took him to the doctor for frequent and sudden urination. It turned out to be a diagnosis that affected the whole family. From the changing of his glucose monitor and insulin pump, to the constant worry and uncertainty.

"Every day is difficult," said Lauren Gfroerer, Mason's mother. "When his blood sugar is low, I give him what he needs. But sometimes I give him too much. And then his blood sugar is high, and he doesn't feel good either."

But this disease has given Mason a purpose - to be a voice for other kids just like him. He was recently selected from 1500 applicants to be part of theJDRFChildren's Congress. Only 10 children from New York State were selected.

Last week, Mason went to Washington, DC, and met with Sen. Chuck Schumer and Rep. Tom Reed and our other elected officials to help secure continued funding for important type 1 diabetes research.

"I was nervous because I didn't want to mess up and I want funding to keep going," said Mason.

His mother couldn't be more proud.

"What he does with diabetes, his strength, what he has to endure. He perseveres. He doesn't let it hold him back," she said.

Mason imagines a day when there's better treatment or even a cure, so diabetes won't keep him on the soccer sidelines.

"Someday I won't have to live with type-1 diabetes anymore," he said.

If you know of a boy or girl or group of kids who should be featured on Daybreak's "WNY's Great Kids," call 716-849-2216 or email melissa.holmes@wgrz.com .

2017 WGRZ-TV

The rest is here:
WNY's Great Kids: Wheatfield Boy Goes to Washington to Fight for Diabetes Research - WGRZ-TV

American Diabetes Association and Oakmont present Diabetes 101

By Signal Staff

Last update:5 hours ago

Diabetes strikes nearly 30 million Americans. Thats 1 in 10 SCV residents.

To help us learn more about diabetes and adopting healthy habits, the American Diabetes Association presents an informative diabetes discussion about the importance of knowing the risk and available Type 2 diabetes prevention programs.

It will be held on Tuesday, August 1 from 4-5:30 p.m. at Oakmont of Santa Clarita, 28650 Newhall Ranch Road, Santa Clarita.

The Association will provide free health screenings, cooking demonstrations, exercise demonstrations, diabetes workshops, giveaways, and more.

The discussion will be given by the Prevent T2 program, a 12-month lifestyle change program for helping people with the little things that reduce the risk of developing Type 2 diabetes.

To attend, RSVP by July 28, 2017. You can register at Oakmont of Santa Clarita; 661-295-2025. The event is free.

For more information, contact the American Diabetes Association at 1.800.DIABETES or 323.966.2890, or visit http://www.diabetes.org.

Diabetes strikes nearly 30 million Americans. Thats 1 in 10 SCV residents.

To help us learn more about diabetes and adopting healthy habits, the American Diabetes Association presents an informative diabetes discussion about the importance of knowing the risk and available Type 2 diabetes prevention programs.

It will be held on Tuesday, August 1 from 4-5:30 p.m. at Oakmont of Santa Clarita, 28650 Newhall Ranch Road, Santa Clarita.

The Association will provide free health screenings, cooking demonstrations, exercise demonstrations, diabetes workshops, giveaways, and more.

The discussion will be given by the Prevent T2 program, a 12-month lifestyle change program for helping people with the little things that reduce the risk of developing Type 2 diabetes.

To attend, RSVP by July 28, 2017. You can register at Oakmont of Santa Clarita; 661-295-2025. The event is free.

For more information, contact the American Diabetes Association at 1.800.DIABETES or 323.966.2890, or visit http://www.diabetes.org.

View post:
American Diabetes Association and Oakmont present Diabetes 101 - Santa Clarita Valley Signal

That glass of wine or pint of beer you enjoy with dinner every night might come with an added benefit -- a lower risk of type 2 diabetes, a new Danish study contends.

The researchers found that men who had 14 drinks each week and women who had nine drinks a week appeared to have the lowest risk of type 2 diabetes, compared to nondrinkers or people who drank more heavily, said senior researcher Janne Tolstrup.

People received the most benefit if they spread those drinks out during the week, rather than downing them all in one or two binges, Tolstrup added.

"Drinking pattern seemed to play a role for the risk of diabetes," Tolstrup said. "Drinking frequency was important, as those who were drinking three to four times per week had lower risk as compared to those drinking only once per week -- regardless of the total weekly amount."

The potential protective effect of alcohol also appeared to be limited to wine and beer, Tolstrup said. Hard liquor provided no benefit to men, and could actually increase a woman's risk of diabetes, the findings showed.

"There seemed to be little beneficial effects from spirits," Tolstrup said.

She's a professor of epidemiology with the University of Southern Denmark's National Institute of Public Health in Copenhagen.

But at least one diabetes expert suggested that if you're thinking of drinking just to prevent type 2 diabetes, you might want to put the corkscrew down.

"I wouldn't recommend increasing alcohol consumption on the basis of this study," said Dr. Adrian Vella, an endocrinologist and internist with the Mayo Clinic in Rochester, Minn.

Also, the study only found an association between alcohol consumption and diabetes risk, not a cause-and-effect connection.

The new research included data from the Danish Health Examination Survey. The survey of more than 70,000 people was done in 2007-2008. The participants provided details of their alcohol consumption, lifestyle and overall health. These people were followed through 2012, with an average follow-up of about five years.

The study revealed that men who had 14 drinks per week had a 43 percent lower risk of type 2 diabetes compared to non-drinkers, and women who had nine drinks per week had a 58 percent lower risk compared to non-drinkers.

The risk of type 2 diabetes was lower when people spread their drinking over three or four days a week, rather than drinking once per week. The researchers found a 27 percent lower risk in men and a 32 percent lower risk in women who drank on about half the days of a typical week.

Wine appeared to provide the most protective benefit, as men and women who drank seven or more glasses per week had up to a 30 percent lower risk of type 2 diabetes compared with those having less than one glass per week.

Women didn't benefit at all from drinking beer, but men who drank one to six beers a week had a 21 percent lower risk of diabetes, the investigators found.

Hard liquor provided no benefit to men. Women who had seven or more shots per week had an 83 percent increased risk of diabetes, the study reports.

Researchers can't say why alcohol might protect against diabetes, since this was an observational study rather than an experiment or clinical trial, Tolstrup said.

"Alcohol has been suggested to increase insulin sensitivity and lower fasting insulin resistance, which might play an important role in the progression of diabetes," Tolstrup said.

"But again, due to limited knowledge about mechanisms between alcohol and [blood sugar] control, the mechanism explaining our results is not clear," she added.

Mayo Clinic's Vella pointed out that studies that depend on people's self-reported food and alcohol consumption can be flawed, since participants may have a hard time remembering what they ate and drank in the past.

It's also tough to accurately capture through a questionnaire other things that might lower type 2 diabetes risk, such as daily exercise and a family history of diabetes.

In addition, it's not likely that a lot of people would develop type 2 diabetes during the relatively short follow-up time of five years used in this study, according to Vella.

The new study was published July 27 in the journalDiabetologia.

See the article here:
Could a little alcohol lower your diabetes risk? - CBS News

Agilis Biotherapeutics has formed a joint venture with Japans Gene Therapy Research Institution (GTRI). The alliance gives Agilis a base in Japan and a partnership with a fellow CNS specialist to support its development of adeno-associated virus (AAV) vectors and gene therapies.

Cambridge, Massachusetts-based Agilis set up the joint venture using a grant from the Japanese government. The agreement will establish an AAV manufacturing facility in Japan, from where Agilis and GTRI will work on vectors using Sf9 baculovirus and HEK293 mammalian cell systems. Agilis and GTRI plan to develop and manufacture AAV gene therapy vectors through the joint venture.

Agilis and GTRI also plan is to collaborate on the development and commercialization of certain CNS gene therapies.

GTRIs background suggests it is well-equipped to contribute to the project. The Japanese company grew out of the work of Shin-ichi Muramatsu, M.D., a scientist who sequenced AAV3 in the 1990s before going on to create AAVs designed to cross the blood-brain barrier. GTRI is working on gene therapies against diseases including Alzheimers, amyotrophic lateral sclerosis and Parkinsons that build on this research into AAVs.

Both biotechs are developing gene therapies to treat aromatic l-amino acid decarboxylase (AADC) deficiency. GTRI aims to get its candidate into the clinic in 2019. Agilispicked up its candidate from a university in Taiwan, which enrolled 18 patients in two clinical trials of the gene therapy. Those trials have taken the candidate toward a pivotal trial.

These programs may benefit from the joint venture. Working out of the Life Science Innovation Center of Kawasaki City, the joint venture intends to develop and produce AAVs for use in gene therapies against AADC deficiency and Parkinson's.

The joint venture marks the second time Agilis has looked outside of its walls for help with AAV vectors. Late in 2013, Agilis struck a deal with Intrexon that gave it access to the latters vector platform. Agilis is using the vectors to develop a treatment for Friedreichs ataxia.

Follow this link:
Agilis forms joint venture to advance gene therapy vectors - FierceBiotech

Dive Brief:

Even as gene therapies are being touted as the next wave of innovation that could offer cures for certain genetic conditions, it remains to be seen whether these products are actually commercially viable. There has yet to be a gene therapy approved in the U.S. (although Spark Therapeutics' application is pending), but two of the transformative drugs have been on the market in Europe.

Yet neither of those commercially available gene therapies have found much success. GlaxoSmithKline plc. said just last week it is looking to move away from its rare disease portfolio, including the gene therapy Strimvelis. Meanwhile, uniQureannounced back in April it would not renew the marketing authorization application in Europe for its already-approved gene therapy Glybera.

This latest move by Chiesifurther exemplifies the challenges gene therapy producers face. The announcement ends a deal which has been in place since 2013. Chiesisaid in a statement that the decision was "driven by recent changes in our strategic priorities."

uniQuretried to put brave face on the news, but partnership exits are rarely good news for a biotech.

"By regaining unencumbered, global rights to a late-stage program that has demonstrated significant clinical benefit for patients with hemophilia B, we believe uniQure is better positioned to accelerate the global clinical development plan, maximize shareholder return on our pipeline and take advantage of new potential opportunities related to the program," said CEO Matthew Kapusta.

The company recently announced positive developments in a Phase 1/2 trial of AMT-060, which supported further expansion of the eligibility of the adeno-associated virus 5 (AAV5) gene therapy to nearly all patients with hemophilia B. Meanwhile, investors are paying close attention to Spark's gene therapy for hemophilia B, which is also in early-to mid-stage development.

View post:
Chiesi hands back gene therapy to uniQure | BioPharma Dive - BioPharma Dive

Researchers at the University of Missouri have developed a new method to efficiently deliver the correct form of dystrophin gene to muscles as a way to correct the faulty gene that characterizes Duchenne muscular dystrophy (DMD), a mouse study shows.

Their study, A Five-Repeat Micro-Dystrophin Gene Ameliorated Dystrophic Phenotype in the Severe DBA/2J-mdx Model of Duchenne Muscular Dystrophy, appearedin the journal Molecular TherapyMethods & Clinical Development.

DMD is caused by a modification of the gene that encodes the dystrophin protein, which is essential for normal muscle activity. Such mutations interfere withproduction of the functional protein, severely affecting muscle fiber structure and strength.

Correcting the faulty gene could potentially treatthis disease. Several attempts atgene therapyhave been tried, but all have failed to efficiently reverse all DMD symptoms.

Gene therapy commonly uses vectors basedviral genetic sequences to achieve the desired gene transfer capacity. The therapeutic potential of these techniques rely not only on the delivery system, but also on the sequence of the gene of interest that is used. In this case, smaller versions of dystrophin known asmicrodystrophinmust be used, since its natural form is just too big to be useful in gene therapy.

There have been other gene-transfer vectors attempted in the past (such as adenoviral vector, herpes simplex virus and plasmid), but they have largely been unsuccessful due to the complexity of the disease, challenges associated with delivery, and the large size of the native dystrophin gene, the studys senior author, Dongsheng Duan, said in a news release.

Duans team used an engineered form of the adeno-associated virus (AAV) vector to replace the damaged gene specifically in the muscles.

Researchers alsoused a version of the dystrophin gene that can potentiallyminimize the toxicity signs commonly associated with such methods, such as inadequate blood supply and fatigue during muscle contraction. This AAV viral vector has also been used in the past, but this is the first time researchers have combined it with such a version of dystrophin.

This strategy boostedlevels of dystrophin protein in the muscles of mice models of DMD, and significantly reduced some disease symptoms. Yet researchers could not accurately measure the impact of this new potential therapy to correct DMD-associated effects on the hearts of the animals.

Human studies have shown that one-time intramuscular injection of an AAV vector can result in the expression of a therapeutic protein for many years. For example, a study showed Factor IX expression for 10 years in a hemophilia patient, Duan said. In preclinical studies in murine and canine models, we have also observed persistent multiyear microdystrophin expression from AAV vectors. In the case of mice, a single injection can lead to microdystrophin expression throughout the lifespan.

Original post:
DMD Gene Therapy to Fix Dystrophin Deficiency in Mice Shows ... - Muscular Dystrophy News

With its lead gene therapy under FDA review, Spark Therapeutics $ONCE is now unveiling the first encouraging responses on the hemophilia A front.

Jeffrey Marrazzo

With analysts looking for a 12%-plus Factor VIII response, the company says that investigators tracked an 11% and 14% stabilized rise in Factor VIII activity in the first two patients who were given the therapy in the dose-escalation study.

Key to this part of the process, researchers say they have seen no Factor VIII inhibitors appear, no thrombotic events, no spontaneous bleeds and no need to use corticosteroids on the patients, who have been tracked for 23 and 12 weeks.

As a result, the biotech says that it has now doubled the dose and treated the third patient in the proof-of-concept study. States the company: While the results for this third participant are early, his factor activity level is tracking proportionally higher, consistent with the dose escalation.

Spark shares surged 15% this morning as the biotech updated the data as well as its Q2 results.

Noted Jefferies Michael Yee recently: First data from Phase I/II of Hemophilia A gene therapy SPK-8011 in July/Aug could establish early proof-of-concept and be a (+) catalyst. Given small no. of pts to start, key is demonstrating potential to get to 12%+ Factor VIII.

Spark Therapeutics is the most advanced biotech in the US gene therapy field, with a good chance to win the first ever FDA approval for a once-and-done treatment. As a result, analysts are watching every step CEO Jeff Marrazzo makes. The biotech has been making steady progress with a gene therapy for hemophilia B after getting over some early safety jitters. And just days ago Spark was handed a priority review of its lead program forRPE65-mediated inherited retinal disease, putting it first in line for a US approval.

To be sure, Spark isnt alone in hemophilia A. Sangamo has a program underway. But the leader in this field is BioMarin $BMRN, which has produced some stellar though also puzzling results. Now ready to go into Phase III, early-stage studies demonstrateda wide variability in Factor VIII expression needed to keep hemophilia in check. Joseph Schwartz at Leerink has noted that investors will look closely to see if regulators are concerned by the much-higher-than-normal levels of Factor VIII in some patients before approving the Phase III design. In the meantime, look for some careful examination of stability versus high but variable impact.

Once over the finish line, gene therapies will present payers with a thorny issue. How do you cover therapies that have the promise of being used just once, without any guarantees that they can last a lifetime? Prices are expected to be sky high, which has held back the two gene therapies that have been approved in Europe, though only rarely used.

Katherine High

The encouraging start of our SPK-8011 clinical trial reinforces the strength of our gene therapy platform, delivers human proof-of-concept in a second liver-mediated disease a significant achievement in the gene therapy field and positions us well to potentially transform the current treatment approach for this life-altering disease with a one-time intervention, said Katherine High, president and chief scientific officer of Spark Therapeutics. We are excited about the progress we are making to achieve our goals of our investigational hemophilia A and B programs: to safely achieve predictable, consistent and sustained activity levels that prevent spontaneous bleeding.

Continued here:
Spark Therapeutics offers a glimpse of efficacy in first two hemophilia A gene therapy patients - Endpoints News

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

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

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."

The video will load shortly

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

More:
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.

_____________________

Read more:

UAE researcher in breakthrough that could reduce problems associated with older women conceiving

_____________________

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.

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

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."

Originally posted here:
Genome Sequencing Shows Spiders, Scorpions Share Ancestor - R & D Magazine

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.

Read more from the original source:
Hunger-controlling brain cells may offer path for new obesity drugs - The Rockefeller University Newswire