MELBOURNE: Doctors may soon be able to draw new bone, skin and muscle on to patients, after scientists created a pen-like device that can apply human cells directly on to seriously injured people.

The device contains stem cells and growth factors and will give surgeons greater control over where the materials are deposited.

It will also reduce the time the patient is in surgery by delivering live cells and growth factors directly to the site of injury, accelerating the regeneration of functional bone and cartilage, scientists said.

The device developed at the University of Wollongong (UOW) will eliminate the need to harvest cartilage and grow it for weeks in a lab.

The Bio Pen works similar to 3D printing methods by delivering cell material inside a bio-polymer such as alginate, a seaweed extract, protected by a second, outer layer of gel material.

The two layers of gel are combined in the pen head as it is extruded onto the bone surface and the surgeon draws with the ink to fill in the damaged bone section.

A low powered ultra-violet light source is fixed to the device that solidifies the inks during dispensing, providing protection for the embedded cells while they are built up layer-by-layer to construct a 3D scaffold in the wound site.

Once the cells are drawn onto the surgery site they will multiply, become differentiated into nerve cells, muscle cells or bone cells and will eventually turn from individual cells into a thriving community of cells in the form of a functioning a tissue, such as nerves, or a muscle.

The device can also be seeded with growth factors or other drugs to assist regrowth and recovery, while the hand-held design allows for precision in theatre and ease of transportation.

The BioPen prototype was designed and built using the 3D printing equipment in the labs at Wollongong and was handed over to clinical partners at St Vincents Hospital Melbourne, led by Professor Peter Choong, who will work on optimising the cell material for use in clinical trials.

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Dr. Aidan R. Raney performs a checkup on heart attack patient Mark Athens, 52, on Tuesday, Dec. 17, at Scripps Green Hospital in La Jolla. Athens received a stem cell treatment to help his heart recover as part of a clinical trial to determine the treatments safety and effectiveness.

A new stem cell treatment may help heart attack patients do something once thought medically impossible regenerate dead heart muscle.

Scripps Health in La Jolla is one of three centers testing the therapy from Capricor, a Los Angeles biotech company. The cardiac stem cells are meant to boost the hearts natural ability to perform minor repairs. If it works, scars should shrink and functional heart muscle should grow.

Capricor gets the cells from donor hearts, grows them into the amount needed for treatment, then sends them to doctors taking part in what is called the Allstar trial. Doctors inject the cells into the coronary artery, where they are expected to migrate to the heart and encourage muscle regrowth.

The trial has successfully completed Phase 1, which mainly evaluates safety. On Dec. 17, Capricor said it had received permission to begin Phase 2, which will examine efficacy in about 300 patients who will get the treatment or a placebo. More information can be found at clinicaltrials.gov under the identifier NCT01458405.

The Allstar trial is funded with a $19.7 million disease team grant from the California Institute for Regenerative Medicine, or CIRM, the states stem cell agency.

This is a highly significant announcement for us at CIRM as its the first time weve funded a therapy into a Phase 2 clinical trial, Chairman Jonathan Thomas said in a Dec. 23 statement.

About 600,000 Americans die of heart disease annually, making it the leading cause of death, according to the Centers for Disease Control and Prevention in Atlanta. Even those surviving may be left permanently impaired, if the heart is severely damaged. These are the patients Capricor seeks to help.

Mark Athens received Capricors treatment on Sept. 25, about a month after having a moderate heart attack. The Encinitas resident was the last treated under Phase 1, said Scripps cardiologist Richard Schatz, who performed the procedure. It will take about six months to know whether the treatment worked, Schatz said.

Unlike many trials, Phase 1 was not placebo-controlled, so Athens knows he got the therapy. He appeared cheerful, smiling and bantering with his examining doctor during a Dec. 17 checkup at Scripps Green Hospital.

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Jacqu Lang of Ridgefield was co-chair of Swim Across America, which recently donated $460,000 to Stamford-based Alliance for Cancer Gene Therapy, the nations only nonprofit dedicated exclusively to cell and gene therapies for cancer.

Swim Across America is a national nonprofit dedicated to raising money and awareness for cancer research.

Jacqu Lang

Ms. Lang, who co-chaired the Greenwich/Stamford swim for the seventh time, has been involved with the organization for more than 20 years as a participant, board member and fund-raiser.

I swam growing up, and this organization provided a wonderful way to take my love of swimming and do great things with it, she said.

Her sister, Janel Jorgensen McArdle, who also grew up in Ridgefield, has been the national executive director of Swim Across America since 2005 she was also a 1988 U.S. Olympic silver medalist.

She asked if I would mind helping out to launch a new swim, and here we are going into our eighth annual event having raised over $2 million for the Alliance for Cancer Gene Therapy.

Nationally, Swim Across America raised more than $5 million in 2013.

The next Greenwich-Stamford swim is Saturday, June 21. See http://www.swimacrossamerica.org for details.

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Research into axon degeneration hits a nerve

University of Queensland (UQ) researchers have made a significant discovery that could one day halt a number of neurodegenerative diseases.

Scientists at the Queensland Brain Institute (QBI) have identified a gene that protects against spontaneous, adult-onset progressive nerve degeneration.

Dr Massimo Hilliard said that the discovery of gene mec-17 causing axon (nerve fibre) degeneration could open the door to better understand the mechanisms of neuronal injury and neurodegenerative diseases characterised by axonal pathology, such as motor neuron disease, Parkinsons, Alzheimers and Huntingtons diseases.

This is an important step to fully understand how axonal degeneration occurs, and thus facilitates development of therapies to prevent or halt this damaging biological event, Dr Hilliard said.

Dr Hilliard runs a laboratory at QBI specialising in neuronal development, and focuses on how nerves both degenerate and regenerate.

The team found that mec-17 protects the neuron by stabilising its cytoskeletal structure, allowing proper transport of essential molecules and organelles, including mitochondria, throughout the axon.

This discovery has also the potential to accelerate the identification of human neurodegenerative conditions caused by mutations in genes similar to mec-17.

Its our hope that this could one day lead to more effective treatments for patients suffering from conditions causing neuronal degeneration, Dr Hilliard said.

This discovery highlights the axon as a major focal point for the health of the neuron.

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A fast-growing Detroit fertility laboratory that became a world leader in the business of screening embryos for birth defects has left the city for Plymouth.

Genesis Genetics Institute moved its headquarters and 32 employees from the Samaritan Center on Detroits east side to an office complex on South Main Street in Plymouth. The company this week announced the relocation, which happened in October.

The company was founded in Detroit in 2003 by its CEO, Dr. Mark Hughes, a former professor at the Wayne State University School of Medicine and pioneer in a type of genetic diagnosis, which involves the screening of embryos for potential birth defects or disease prior to an in vitro fertilization procedure.

In an interview Thursday, Genesis Genetics Managing Director Tony Gordon said the company outgrew its Detroit lab and offices and now has twice the space. The Plymouth site also is closer to Detroit Metro Airport and Ann Arbor and is an easier location for recruiting employees, he said.

Detroits a great city and it was a great location, but it was getting a little bit difficult to attract staff and things like that where we were, Gordon said in phone call from London, where Genesis Genetics has one of its eight branch laboratories.

In the news release announcing the move, Gordon said Genesis Genetics sought a location that would be inspirational for its workforce. The company did not receive any tax breaks or relocation incentives for the Plymouth move.

Our mission is to help couples build healthy families, he said. Plymouth is a quintessential American family town with concerts in the park, a multitude of family festivals, events and parades, and a bustling downtown replete with couples with young families. It just made sense.

Gordon said the company outgrew its lab space in the Samaritan Center and cited security concerns as another issue. The company considered other locations in Detroit, but did not find a suitable one.

Genesis Genetics is considered a world leader in pre-implantation genetic diagnosis and provides services to about 3,000 to 4,000 families a year.

It employs more than 100 researchers and staff in Michigan, Arizona, Argentina, Brazil, Jordan, South Africa, Taiwan and the United Kingdom.

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Washington, Dec 27 : Researchers evaluated a patient with a genetic skin disorder known as epidermolysis bullosa (EB) nearly seven years after he had undergone a gene therapy procedure as part of a clinical trial.

They found that a small number of skin stem cells transplanted into the patient's legs were sufficient to restore normal skin function, without causing any adverse side effects.

To evaluate stem cell-based gene therapy as a potential treatment, Senior study author Michele De Luca of the University of Modena and Reggio Emilia, and his colleagues previously launched a phase I/II clinical trial at the University of Modena and recruited an EB patient named Claudio.

The researchers took skin stem cells from Claudio's palm, corrected the genetic defect in these cells, and then transplanted them into Claudio's upper legs.

In the new study, De Luca and his team found that this treatment resulted in long-term restoration of normal skin function. Nearly seven years later, Claudio's upper legs looked normal and did not show signs of blisters, and there was no evidence of tumour development. Remarkably, a small number of transplanted stem cells was sufficient for long-lasting skin regeneration. Even though Claudio's skin had undergone about 80 cycles of renewal during this time period, the transplanted stem cells still retained molecular features of palm skin cells and did not adopt features of leg skin cells.

The study is published in journal Stem Cell Reports.

--ANI (Posted on 27-12-2013)

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ATLANTA, Ga. -

One family is exemplifying the spirit of the holidays. A 13-year-old girl has twice donated bone marrow to her little brothers who suffer from a rare blood disorder.

At 13, Julia Jenkins doesn't always see eye-to-eye with her three little brothers. They can be rowdy and more than a little competitive. But the Jenkins kids share a connection that runs deep.

Julia Jenkins watched one brother get sick and then another and then another. Then she learned that she was the one person who might be able to help save them.

It started in 2008 when Will, then 2, developed a swollen lymph node in his neck. The diagnosis: Burkitt's lymphoma, a rare cancer of the lymphatic system.

"I had asked the Lord, Please don't let it be cancer.' But then when it turned to be cancerous, I had to change my perspective and say, Thank you that's it's curable. If you get it in time, it's curable, you can fight it,'" said Christy Jenkins.

Will started chemotherapy, but then John, who was 6, began having severe stomach problems.

"They diagnosed John with Burkitt's lymphoma two years to the exact day later," said Christy Jenkins.

Doctors at the Aflac Cancer Center at Children's Healthcare of Atlanta started looking for answers. Burkitt's doesn't usually run in families, but a specialist remembered hearing about a rare, genetic immune disorder called XLP carried by boys that could cause very similar symptoms. Blood tests showed both Will and John had XLP, as did 2-year-old Matthew.

"Here I was approached with the plate of, 'All three boys need a bone marrow transplant to possibly survive,'" said Christy Jenkins.

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The breakthrough could also provide the key to skin generation for burn victims and skin cancer sufferers, according to a team at the University of Southern California

Bald men could have a full head of hair after the discovery of the gene that promotes hair growth.

The breakthrough could also provide the key to skin generation for burn victims and skin cancer sufferers.

A team at the University of Southern California investigated stem cells found in follicles which can regenerate hair and skin.

Stem cell specialist Dr Krzysztof Kobielak said: Collectively, these new discoveries advance basic science and, more importantly, might translate into novel therapeutics for various human diseases.

Since BMP signaling has a key regulatory role in maintaining the stability of different types of adult stem cell populations, the implication for future therapies might be potentially much broader than baldness - and could include skin regeneration for burn patients and skin cancer.

The papers were published in the journals Stem Cells and the Proceedings of the National Academy of Sciences (PNAS).

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Revolutionary Skin Cell Therapy
My First Project.

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Dec. 26 (UPI) -- Neanderthals may have passed down a gene variant to Latin Americans, putting them at a high risk of developing type-2 diabetes.

The largest genome-wide association study involving more than 8,000 Mexicans and other Latin Americans studied many genes in individuals and tried to find links to certain traits.

The high risk gene called SLC16A11 has been found in around half of those with recent Native American ancestry, including Latin Americans. The variant was also found in 20 percent of East Asians, but was rare in Europe and Africa.

"To date, genetic studies have largely used samples from people of European or Asian ancestry, which makes it possible to miss culprit genes that are altered at different frequencies in other populations," said co-author Jose Florez, associate professor of medicine at Harvard Medical School in Massachusetts.

According to Florez, by expanding the scope of research to look at Latin American samples they have found the strongest genetic risk factor discovered to date, which accounts for 20 percent of that population's increased prevalence of type 2 diabetes.

Earlier research has shown that Neanderthals interbred with modern humans nearly 60,000 to 70,000 years ago, and researchers believe this is how SLC16A11 was introduced.

Altering the levels of SLC16A11 protein can change the amount of a fat that has been involved in the risk of diabetes. The study, published in the journal Nature, suggests that the SLC16A11 could be involved in the transport of an unknown metabolite the affects the fat level in cells.

[BBC] [Nature]

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December 26, 2013

redOrbit Staff & Wire Reports Your Universe Online

A previously undetected genetic risk factor could help explain why there is an elevated risk of type 2 diabetes among Mexican and other Latin American populations, according to a new study published online Wednesday in the journal Nature.

In the study, an international team of researchers known as the SIGMA (Slim Initiative in Genomic Medicine for the Americas) Type 2 Diabetes Consortium performed the largest genetic study to date in people of Mexican and Mexican-American descent. They discovered that people who had the higher-risk version of the gene SLC16A11 could be 25 percent more likely to have diabetes than those lacking said gene.

Furthermore, individuals who inherit copies from both patents are 50 percent more likely to have diabetes. The higher-risk version has been found in up to half of people with recent Native American ancestry (including Latin Americans) as well as 20 percent of East Asians, and elevated frequency of SLC16A11 in Latin American could account for up to one-fifth of the populations increased prevalence of diabetes, the authors explained.

To date, genetic studies have largely used samples from people of European or Asian ancestry, which makes it possible to miss culprit genes that are altered at different frequencies in other populations, said co-corresponding author Jos Florez, an assistant physician in the Massachusetts General Hospital Diabetes Unit. By expanding our search to include samples from Mexico and Latin America, weve found one of the strongest genetic risk factors discovered to date, which could illuminate new pathways to target with drugs and a deeper understanding of the disease.

In addition to validating the relevance to Mexico of already known genetic risk factors, we discovered a major new risk factor that is much more common in Latin American populations than in other populations around the world, added Teresa Tusie-Luna, principal investigator at the National University of Mexicos Biomedical Research Institute. We are already using this information to design new studies that aim to understand how this variant influences metabolism and disease, with the hope of eventually developing improved risk assessment and possibly therapy.

According to BBC News Science Editor Paul Rincon, the SLC16A11 sequence discovered by the SIGMA team was found in a recently sequenced Neanderthal genome originating from Denisova cave in Siberia. That would suggest, he explained, that the gene variant might have been inherited by the ancient, now-extinct species of early human.

This marks the first time that SLC16A11, which belongs to a family of genes that code for proteins that transport metabolites, has been identified as factoring into a human disease. As such, the researchers said that little information was previously available about its function. The study authors report that SLC16A11 is expressed in the endoplasmic reticulum, a cellular structure located within the liver.

Furthermore, the SIGMA investigators went on to demonstrate that altering levels of the protein could change the amount of a type of fat that had previously been implicated in the risk of diabetes. That discovery led the team to hypothesize that SLC16A11 could be involved in the transport of an unknown metabolite a metabolite which affects fat levels in cells, resulting in an increased risk of type 2 diabetes.

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Which rule to use in order to solve a genetics probability problem?
Probability Basics Probabilities are mathematical measures of likelihood. The empirical probability of an event is calculated by dividing the number of times...

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DNA Genetics Seeds @ Cannafest 2013 Prague / Praha
Herbies Seeds Interview with Don of DNA Genetics Seeds @ Cannafest 2013 in Prague / Praha Czech Republic Buy DNA Genetics Seeds http://www.herbiesheadshop.co...

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Minecraft FTB - Big Bee Project - Part 11 - Eldritch Bee Genetics, getting ready for next species
We are going to set up one of the biggest bee projects known to minecraft! watch and enjoy!! watch, enjoy, subscribe, like and await the rest 😉 Add me on twitter @ http://www.twitter.com/weirdhans...

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DNA Genetics / Big Buddha / True Canna Genetics Seminar PART 1 Cannabis Cup 2013 Amsterdam
http://andrew.pyrah.net Thanks for watching! COMMENT and LIKE if you enjoyed the video and SUBSCRIBE to see my new videos as they are released. This video is...

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Interpreting Technical Material Genetics

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Neurotrophin Gene Therapy for Repair of the Injured Spinal Cord
George M. Smith, PhD | Shriners Hospitals Pediatric Research Center and Temple University 2013 Rare Neuro-Immunologic Disorders Symposium Repair and Recovery, Today and in the Future | October...

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Stem Cell Therapy for Feline Kidney Disease
Stem cells show promising results for a number of diseases conditions in humans. Can they do the same for our animal friends?

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WASHINGTON Every year, the editors of Science huddle together and pick an outstanding scientific achievement as the Breakthrough of the Year. This year's winner is:

CANCER IMMUNOTHERAPY: harnessing the immune system to battle tumors.

Scientists have thought for decades that such an approach to cancer therapy should be possible, but it has been incredibly difficult to make it work. Now many oncologists say we have turned a corner, because two different techniques are helping a subset of patients. One involves antibodies that release a brake on T cells, giving them the power to tackle tumors. Another involves genetically modifying an individual's T cells outside the body so that they are better able to target cancer, and then re-infusing them so they can do just that.

We are still at the beginning of this story and have a long way to go. Only a very small proportion of cancer patients have received these therapies, and many are not helped by them. Doctors and scientists still have a lot to learn about why the treatments do and do not work. But the results have been repeated at different centers and in different tumor types, giving doctors hope that immunotherapy for cancer may benefit more and more people in the future

The editors also singled out nine runners-up for special praise:

GENETIC MICROSURGERY

A year-old gene-editing technique called CRISPR touched off an explosion of research in 2013. It's short for "clustered regularly interspaced short palindromic repeats": repetitive stretches of DNA that bacteria have evolved to combat predatory viruses by slicing up the viral genomes. The "knife" is a protein called Cas9; in 2012, researchers showed they could use it as a scalpel to perform microsurgery on genes. This year the new technology became red hot, as more than a dozen teams wielded it to manipulate specific genes in mice, rats, bacteria, yeast, zebrafish, nematodes, fruit flies, plants and human cells, paving the way for understanding how these genes function and possibly harnessing them to improve health.

CLARITY BRAIN IMAGING

This year, researchers invented a new way of imaging the brain which many say will fundamentally change the way labs study the intricate organ. CLARITY, a method of rendering brain tissue transparent, removes the biggest obstacle to traditional brain imaging: the fatty, light-scattering molecules, called lipids, which form cellular membranes. By replacing lipids with single molecules of a clear gel, the technique renders brain tissue transparent while leaving all neurons, other brain cells and their organelles intact. This allows researchers to infiltrate the brain with labels for specific cell types, neurotransmitters, or proteins, wash them out, and image the brain again with different labels - a process they say could speed up by a hundredfold tasks such as counting all the neurons in a given brain region.

CLONING HUMAN STEM CELLS

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PUBLIC RELEASE DATE:

25-Dec-2013

Contact: Nicole Davis ndavis@broadinstitute.org 617-714-7152 Broad Institute of MIT and Harvard

Cambridge and Boston, MA; Los Angeles, CA; Mexico City, Mexico. Wed. December 25, 2013 An international team of researchers in Mexico and the United States has uncovered a new genetic clue that contributes to an increased risk of developing type 2 diabetes, particularly the elevated risk among Mexican and other Latin American populations.

The team, known as the SIGMA (Slim Initiative in Genomic Medicine for the Americas) Type 2 Diabetes Consortium, performed the largest genetic study to date in Mexican and Mexican American populations, discovering a risk gene for type 2 diabetes that had gone undetected in previous efforts. People who carry the higher risk version of the gene are 25 percent more likely to have diabetes than those who do not, and people who inherited copies from both parents are 50 percent more likely to have diabetes. The higher risk form of the gene has been found in up to half of people who have recent Native American ancestry, including Latin Americans. The variant is found in about 20 percent of East Asians and is rare in populations from Europe and Africa.

The elevated frequency of this risk gene in Latin Americans could account for as much as 20 percent of the populations' increased prevalence of type 2 diabetes the origins of which are not well understood.

"To date, genetic studies have largely used samples from people of European or Asian ancestry, which makes it possible to miss culprit genes that are altered at different frequencies in other populations," said co-corresponding author Jos Florez, a Broad associate member, an associate professor of medicine at Harvard Medical School and an Assistant Physician in the Diabetes Unit and the Center for Human Genetic Research at the Massachusetts General Hospital. "By expanding our search to include samples from Mexico and Latin America, we've found one of the strongest genetic risk factors discovered to date, which could illuminate new pathways to target with drugs and a deeper understanding of the disease."

A description of the discovery of the newly implicated gene named SLC16A11 and the consortium's efforts to characterize it, appear online in Nature December 25.

"We conducted the largest and most comprehensive genomic study of type 2 diabetes in Mexican populations to date. In addition to validating the relevance to Mexico of already known genetic risk factors, we discovered a major new risk factor that is much more common in Latin American populations than in other populations around the world. We are already using this information to design new studies that aim to understand how this variant influences metabolism and disease, with the hope of eventually developing improved risk assessment and possibly therapy," said Teresa Tusie-Luna, project leader at the Instituto Nacional de Ciencias Mdicas y Nutricin Salvador Zubirn and principal investigator at the Biomedical Research Institute, National University of Mexico.

This work was conducted as part of the Slim Initiative for Genomic Medicine for the Americas (SIGMA), a joint U.S.-Mexico project funded by the Carlos Slim Foundation through the Carlos Slim Health Institute. SIGMA focuses on several key diseases with particular relevance to public health in Mexico and Latin America, including type 2 diabetes and cancer. The current paper is the team's first report on type 2 diabetes.

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Stem Cell Therapy: Knee Pain, Regenerative Therapy Options
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Stem Cell Therapy: Knee Pain, Failed Knee Surgery
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Stem Cell Therapy: Achilles Tendonitis
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PUBLIC RELEASE DATE:

23-Dec-2013

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research

In a recent study published in the Neural Regeneration Research (Vol. 8, No. 33, 2013), Prof. Feng Li and team from Zhongshan School of Medicine, Sun Yat-sen University in China, synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein (A) production, and introduced it into the pSilenCircle vector to construct a short hairpin (shRNA) expression plasmid against the BACE1 gene. Researhcers transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing A protein production. This technique combining cell transplantation and gene therapy will open up novel therapeutic avenues for Alzheimer's disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.

###

Article: " Targeting -secretase with RNAi in neural stem cells for Alzheimer's disease therapy " by Zhonghua Liu, Shengliang Li, Zibin Liang, Yan Zhao, Yulin Zhang, Yaqi Yang, Minjuan Wang, Feng Li (Department of Neurobiology and Anatomy, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China)

Liu ZH, Li SL, Liang ZB, Zhao Y, Zhang YL, Yang YQ, Wang MJ, Li F. Targeting -secretase with RNAi in neural stem cells for Alzheimer's disease therapy. Neural Regen Res. 2013;8(33):3095-3106.

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research http://www.nrronline.org/

Full text: http://www.sjzsyj.org/CN/article/downloadArticleFile.do?attachType=PDF&id=783

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December 24, 2013

redOrbit Staff & Wire Reports Your Universe Online

The same gene that influences bonding between mothers and their infant children, as well as the attachment between partners in a monogamous relationship, could also be involved in the ability to remember faces.

The gene in question is the oxytocin receptor, a member of the G-protein coupled receptor family which receives chemical signals from the hormone and neurotransmitter oxytocin. The receptors modulate a variety of behaviors, including stress, anxiety, bonding, maternal behavior, social memory and recognition.

In a study scheduled to appear in an online Early Edition of Proceedings of the National Academy of Sciences, researchers report that the discovery could help diagnose and treat autism spectrum disorder and other conditions in which a persons ability to process social information is adversely affected.

In addition, the authors report that the findings could also help experts develop new methods of improving social cognition skills in patients suffering from serious psychiatric disorders. Researchers from Emory University, University College London and the University of Tampere in Finland were involved in the research.

According to author Dr. Larry Young of the Emory University School of Medicine and Center for Translational Social Neuroscience (CTSN), this is the first paper to demonstrate that variation in the oxytocin receptor gene has an impact on an individuals facial recognition skill.

He and his colleagues stated that while oxytocin plays an important role in promoting our ability to recognize one another about one-third of the population possesses only the genetic variant that negatively impacts that ability, the university said in a statement. They say this finding may help explain why a few people remember almost everyone they have met while others have difficulty recognizing members of their own family.

Dr. Youngs team analyzed 198 families with one autistic child, as those families had previously been found to demonstrate a wide range of variability when it came to the ability to recognize faces. Approximately 66 percent of the families hailed from the UK, while the rest of them resided in Finland, the university said.

Previously, researchers from Emory University discovered that the oxytocin receptor played a vital role in olfactory-based social recognition in rodents. While attempting to discern whether or not the same gene played a similar role in people, they looked at how subtle differences in the structure of the receptor gene impacted facial memory skills in parents, autistic children and their non-autistic brothers and sisters.

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