Gene Therapy Research

Archive for the ‘Gene Therapy Research’ Category

Gene switch steers blood supply to the retina

April 9th, 2013

Apr. 8, 2013 Normal functioning of the eye depends on a proper supply of blood to the retina. Light entering the eye passes through the cornea, the lens, and the vitreous body before reaching the retina, where it stimulates the nerves. If the retina contains too few or too many blood vessels -- i.e., if it is under- or oversupplied with blood -- a number of severe, often blinding eye diseases can develop.

An international group of researchers led by Professor Alfred Nordheim at the University of Tbingen's Interfaculty Institute for Cell Biology has found, using experiments on mice, that genes for blood vessel growth in the retina are "switched on" by a known factor -- a protein called SRF. The scientists showed that by eliminating this factor, they could artificially induce a certain disease profile in newborn mice and a different one in adult mice. Their results, which are published now in The Journal of Clinical Investigation, offer important clues on the diseases afflicting human eyes and provide starting-points for the development of treatments for defective retinae and vitreous bodies.

Professor Alfred Nordheim's team has been examining the serum response factor (SRF) and its various functions for several years. SRF regulates the function of many genes in the genome of mice and men -- thereby setting in motion distinct growth processes for organs. Experimenting on mice in the laboratory, the Tbingen researchers have developed sophisticated mechanisms to influence the activity of SRF and its co-factors in distinct types of cells and at defined time points when the organism reaches a certain developmental stage.

In the current study, the researchers switched off SRF in the blood vessels of mouse embryos, as well as in newborn and adult mice. As a result, the blood vessels in the retinae of the newborns were not fully developed. Their eye problems were very similar to certain hereditary forms of a disease affecting the retina and vitreous body in the human eye (vitreoretinopathy and Norrie disease). Children affected by it often go blind at an early age. In mice of adult ages, however, switching off SRF had the opposite effect -- too many new blood vessels were formed in the retina, oversupplying it with blood. Doctors have made corresponding observations in elderly patients with a certain form of age-related macular degeneration (AMD), a disease which increasingly damages the retina and leads to vision loss. It is characterized by dilated blood vessels and the formation of excess blood vessels.

"I expected that SRF would play a role in the development of the vessel system, because it generally works to ensure the formation of cellular protrusions and new branched cellular structures in many organs, for instance in the nervous system and the vascular system," says Alfred Nordheim. But, he added, it was astonishing how closely the pathology of mice with switched-off SRF resembled that of human patients with particular eye diseases. "I think we have established a very good model with which we can investigate these diseases much more precisely," Nordheim says. It represents an important step for research into possible treatments, he adds.

The study was carried out in collaboration with researchers at the Max Planck Institute for Molecular Biomedicine in Mnster (Prof. Adams), the Institute for Ophthalmic Research Tbingen (Prof. Seeliger), the Pathology Department at the Tbingen University Hospital (Prof. Wolburg) and the University of Texas, Dallas, USA (Prof. Olson).

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Universitaet Tbingen.

Originally posted here:
Gene switch steers blood supply to the retina

Comments Closed|

Shedding light on a gene mutation that causes signs of premature aging

April 9th, 2013

Apr. 8, 2013 Research from Western University and Lawson Health Research Institute sheds new light on a gene called ATRX and its function in the brain and pituitary.

Children born with ATRX syndrome have cognitive defects and developmental abnormalities. ATRX mutations have also been linked to brain tumors. Dr. Nathalie Brub, PhD, and her colleagues found mice developed without the ATRX gene had problems in in the forebrain, the part of the brain associated with learning and memory, and in the anterior pituitary which has a direct effect on body growth and metabolism. The mice, unexpectedly, also displayed shortened lifespan, cataracts, heart enlargement, reduced bone density, hypoglycemia; in short, many of the symptoms associated with aging.

The research is published in the Journal of Clinical Investigation.

Ashley Watson, a PhD candidate working in the Brub lab and the first author on the paper, discovered the loss of ATRX caused DNA damage especially at the ends of chromosomes which are called telomeres. She investigated further and discovered the damage is due to problems during DNA replication, which is required before the onset of cell division. Basically, the ATRX protein was needed to help replicate the telomere.

Working with Frank Beier of the Department of Physiology and Pharmacology at Western's Schulich School of Medicine & Dentistry, the researchers made another discovery. "Mice that developed without ATRX were small at birth and failed to thrive, and when we looked at the skeleton of these mice, we found very low bone mineralization. This is another feature found in mouse models of premature aging," says Brub, an associate professor in the Departments of Biochemistry and Paediatrics at Schulich Medicine & Dentistry, and a scientist in the Molecular Genetics Program at the Children's Health Research Institute within Lawson. "We found the loss of ATRX increases DNA damage locally in the forebrain and anterior pituitary, resulting in systemic defects similar to those seen in aging."

The researchers say the lack of ATRX in the anterior pituitary caused problems with the thyroid, resulting in low levels of a hormone called insulin-like growth factor-one (IGF-1) in the blood. There are theories that low IGF-1 can deplete stores of stem cells in the body, and Brub says that's one of the explanations for the premature aging. This research was funded by the Canadian Institutes of Health Research.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Western Ontario.

Here is the original post:
Shedding light on a gene mutation that causes signs of premature aging

Comments Closed|

Mutant gene cancer link probed

April 9th, 2013

A faulty gene normally associated with breast cancer can lead to aggressive and deadly prostate cancer in men, research has shown.

Prostate cancer spreads more quickly and is more likely to be fatal in men with a defective BRCA2 gene, a study found.

The researchers argue that men with the gene who are diagnosed with the disease should be given more radical treatment than non-carriers. They need immediate surgery or radiotherapy, it is claimed.

Currently many men with early-stage prostate cancer are advised to wait and see if the disease starts to progress.

This "active surveillance" approach suits men with slow-growing, non aggressive tumours, but not those with the BRCA2 mutant, say the scientists.

The new study, published in the Journal of Clinical Oncology, involved analysing the medical records of 61 BRCA2 mutation carriers, 18 carriers of a sister faulty gene, BRCA1, and 1,940 non-carriers.

Men with either of the defective genes were more likely to be diagnosed with advanced stage prostate cancers, or tumours that had already spread.

Those with BRCA2 mutations were also significantly less likely to survive. They lived an average of 6.5 years after diagnosis compared with 12.9 years for non-carriers.

Study co-leader Professor Ros Eeles, from the Institute of Cancer Research in London, said: "It is clear from our study that prostate cancers linked to inheritance of the BRCA2 cancer gene are more deadly than other types.

"It must make sense to start offering affected men immediate surgery or radiotherapy, even for early-stage cases that would otherwise be classified as low-risk. We won't be able to tell for certain that earlier treatment can benefit men with inherited cancer genes until we've tested it in a clinical trial, but the hope is that our study will ultimately save lives by directing treatment at those who most need it."

Read the original here:
Mutant gene cancer link probed

Comments Closed|

'Deadly' prostate cancer gene find

April 9th, 2013

8 April 2013 Last updated at 20:31 ET By Michelle Roberts Health editor, BBC News online

Men with prostate cancer and an inherited gene mutation have the worst form of the disease, research reveals.

The BRCA2 gene is linked to hereditary breast cancer, as well as prostate and ovarian cancer.

Now scientists say that as well as being more likely to get prostate cancer, men with BRCA2 are also more likely to develop aggressive tumours and have the poorest survival rates.

They say these men should be treated quickly to save lives.

This study shows that doctors need to consider treating men with prostate cancer and a faulty BRCA2 gene much sooner than they currently do, rather than waiting to see how the disease develops

Around one in every 100 men with prostate cancer will have the BRCA2 mutation.

April 9th, 2013

Public release date: 8-Apr-2013 [ | E-mail | Share ]

Contact: Bill Ferguson bferguson@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, April 8, 2013New Space (http://www.liebertpub.com/space), the groundbreaking, peer-reviewed Journal published by Mary Ann Liebert, Inc., publishers (http://www.liebertpub.com), launched its inaugural issue (http://online.liebertpub.com/toc/space/1/1) at the 29th National Space Symposium being held April 8-11 at the Broadmoor Hotel in Colorado Springs, CO. Spearheaded by Editor-in-Chief Professor Scott Hubbard from the Department of Aeronautics and Astronautics at Stanford University, the Journal facilitates the emerging multidisciplinary and entrepreneurial opportunities for space-based collaborations of industry, academia, and government. New Space (http://www.liebertpub.com/space) is published quarterly online with Open Access (http://www.liebertpub.com/openaccess/new-space/610/) options and in print.

The inaugural issue includes premium content from leading experts in the field, including an editorial by Scott Hubbard, a cogent opinion statement by Space Foundation CEO Elliot Holokauahi Pulham, and a roundtable discussion titled "Growing the Future of Commercial Space" hosted by Dr. Hubbard with timely, valuable perspectives from participants Ken Davidian, Steve Isakowitz, John Logsdon, James R. (Russ) McMurry, George Nield, and Marcia Smith. Additionally, the issue includes new peer-reviewed original articles "Industry Structural Analysis of the Commercial Suborbital Research Market" by Ken Davidian and Cindy Conrad; "The State of Space Economical Analyses: Real Questions, Questionable Answers" by Henry R. Hertzfeld; "Commercial On-Orbit Satellite Servicing" by Alanna Krolikowski and Emmanuelle David; "The B612 Foundation Sentinel Space Telescope" by Edward T. Lu, Harold Reitsema, John Troeltzsch, and Scott Hubbard; and "Certification Versus Licensing for Human Spaceflight in Commercial Space Transportation" by George C. Nield, Mahamane Toure', John Sloan, and David Gerlach.

"This new Journal provides a much-needed forum for the rapidly advancing knowledge, engineering, and technological developments in this important fieldwith great potential for benefit to humanity and our world," says Editor-in-Chief Hubbard.

In addition to peer-reviewed manuscripts, New Space publishes interviews with leading innovators, roundtable discussions with experts in a variety of fields, point-counterpoint discussions, and briefs describing lab demonstrations and field trials.

###

About the Journal

New Space (http://www.liebertpub.com/space) facilitates and supports the efforts of researchers, engineers, analysts, investors, business leaders, and policymakers to capitalize on the opportunities of commercial space ventures. Spanning a broad array of topics including technological advancements, global policies, and innovative applications, the journal will bring the new space community together to address the challenges and discover new breakthroughs and trends in this epoch of private and public/private space discovery. The Journal is published quarterly online with Open Access options (http://www.liebertpub.com/openaccess/new-space/610/) and in print. Complete table of contents are available on the New Space (http://www.liebertpub.com/space) website.

About the Publisher

The rest is here:
Premier issue of New Space journal launched at 29th National Space Symposium in Colorado Springs

Comments Closed|

The Pros of Genetic Engineering: Why â€˜Playing Godâ€™ Could Help The Human Race

April 9th, 2013

April 8, 2013

Brett Smith for redOrbit.com Your Universe Online

Despite the frequently encountered that scientists are playing God with nature, the pros of genetic engineering are numerous and significant.

When discussing genetically modified organisms (GMO), it is important to note that the FDA and the World Health Organization have both deemed that the food products created with the technology are considered safe.

GMO produce has several genetically altered advantages over non-GMO fruits and vegetables, including increased resistance to pests, disease and drought.

These benefits of genetic engineering translate directly into cheaper prices. A recent Iowa State University study found that prices would be at least 10 percent higher for soybeans and 6 percent higher for corn worldwide without biotechnical modifications.

Some GMOs have even been found to taste better than their conventional counterparts. In a study published in the journal Nature Biotechnology, researchers found that as many as 60 percent of the people they surveyed actually preferred the taste of a genetically modified tomato.

The study focused on a particular modified tomato that had the genetically engineered advantage of a rose-scented compound that was coded into the tomato genome. The researchers said their study proves that food products can not only be made more resilient through biotechnology, but that they can also be made more flavorful.

The pros of genetic engineering can also be seen in fields besides agriculture. Scientists at the Department of Energy revealed that they have created a modified virus capable of generating electrochemical energy. Using the genetically modified viruses, they were able to create a device that is powered simply by applying pressure.

Cancer researchers and patients are also constantly reaping the benefits of genetic engineering. Many experimental treatments use genetically modified viruses to target and destroy cancer cells. A recent study showed that oncologists from Memorial Sloan-Kettering Cancer Center in New York were able to effectively treat a specific form of acute leukemia using genetically engineered viruses.

Here is the original post:
The Pros of Genetic Engineering: Why â€˜Playing Godâ€™ Could Help The Human Race

Comments Closed|

Silver but buy buy – Video

April 9th, 2013

Silver but buy buy

By: PastorDowell

Researcher finds genetic link to couch potato-itis in rats, maybe humans

April 9th, 2013

COLUMBIA, Mo. A Mizzou researcher has found genes that may predispose laziness in rats. The findings may translate to humans.

Frank Booth, professor with the College of Veterinary Medicine, said, We have shown that it is possible to be genetically predisposed to being lazy, Booth said. This could be an important step in identifying additional causes for obesity in humans, especially considering dramatic increases in childhood obesity in the United States."

Booth's team was able to breed rats that exhibited traits of either extreme activity or extreme laziness. They wrote in an academic paper that these rats indicate that genetics could play a role in exercise motivation, even in humans.

"It would be very useful to know if a person is genetically predisposed to having a lack of motivation to exercise, because that could potentially make them more likely to grow obese, Booth said.

Studies show 80 to 97 percent of American adults get less than 30 minutes of exercise a day, which is the minimum recommended by federal guidelines.

Roberts' team put rats in cages with running wheels and measured how much each rat willingly ran on its wheel over six days. They then bred the top 26 runners with each other and bred the 26 rats that ran the least with each other.

They repeated this process through 10 generations and found that the line of running rats chose to run 10 times more than the line of lazy rats.

Once the researchers created their super runner and couch potato rats, they studied the levels ofmitochondriamitochondria in muscle cells, compared body composition and conducted genetic evaluations.

While we found minor differences in the body composition and levels of mitocondriain muscle cells of the rats, the most important thing we identified were the genetic differences between the two lines of rats, Roberts said. Out of more than 17,000 different genes in one part of the brain, we identified 36 genes that may play a role in predisposition to physical activity motivation.

The study is in the April 3 edition of the American Journal of Physiology: Regulatory, Integrative and Comparative Physiology.

Excerpt from:
Researcher finds genetic link to couch potato-itis in rats, maybe humans

Comments Closed|

Genetic link to laziness found in rats

April 9th, 2013

09 April 2013| last updated at 10:52AM

"We have shown that it is possible to be genetically predisposed to being lazy," China's Xinhua news agency quoted study author Frank Booth, a professor from the Department of Physiology, School of Medicine, as saying.

"This could be an important step in identifying additional causes forobesity in humans," Booth said.

Booth and his fellow Michael Roberts were able to selectively breed rats that exhibited traits of either extreme activity or extreme laziness.

These rats indicate that genetics could play a role in exercise motivation, even in humans, according to the study published in the American Journal of Physiology: Regulatory, Integrative and Comparative Physiology.

"It would be very useful to know if a person is genetically predisposedto having a lack of motivation to exercise, because that could potentially makethem more likely to grow obese," said Booth.

Booth put rats in cages with running wheels and measured how much each rat willingly ran on their wheels during a six-day period.