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Children being treated for blood cancer at Medical University Hospital will get a taste of hope Thursday.

A 5k run to raise awareness of the need for bone marrow donations is set for Saturday. The children are not strong enough to participate in that. So a Tot Run will be held on their hospital floor Thursday morning.

Several dozen children, their families and staff will run around the oncology floor as they are able from 11 a.m. to noon, said Ashley Collier, community representative for Be The Match, the state's bone marrow bank.

"It's a way the children to be involved," she said.

For every child that gets a bone marrow transplant, two more don't get one because a matching donor can't be found, Collier said.

The Match to Marrow 5K Run starts at 9 a.m. Saturday at Wannamaker County Park in North Charleston. The entry fee is $25. Representatives will also be on hand to explain how to donate blood from which stem cells for bone marrow are harvested.

Reach Dave Munday at 937-5553.

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Tot Run set for children with blood cancer

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Hilo native Daniel Kuramoto recently became one of about 540 registered bone marrow donors to help save a life.

Daniel doesnt want to talk about how hes a hero, but I will, said Roy Yonashiro, recruitment specialist for the Hawaii Bone Marrow Donor Registry.

According to the HBMR website, every year more than 12,000 patients in the United States are diagnosed with life-threatening diseases, such as leukemia or lymphoma. About 70 percent of patients in need of a transplant do not have a matching donor in their family and depend on the registry to find an unrelated donor.

Yonashiro said finding a match is difficult since bone marrow donors have to be compatible on a genetic level. This can be especially challenging for those in certain ethnic backgrounds, such as Hawaiians, who only make up .2 percent of the national registry.

Kuramoto said it took him 20 years to be a match. He joined in high school after his father, Dennis Kuramoto, died of leukemia. Before his death, Kuramoto said his aunt made an invaluable donation that gave him more time with his father.

After that, I knew if I ever got a chance, Im going to do it, he said.

That chance came on Feb. 27. After receiving word that he was a match, the registry flew him to Oahu to have tests done.

These guys make the experience very good. I really only had to just show up. Everything was taken care of, he said.

A couple weeks later he was in San Diego getting prepped for a peripheral stem cell donation.

According to the Be The Match website, operated by the National Marrow Donor Program, a PBSC donation is one of two methods of collecting blood-forming cells for bone marrow transplants.

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Hilo bone marrow donor matched up to save a life

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Newswise MADISON, Wis. Desperate patients are easy prey for unscrupulous clinics offering untested and risky stem cell treatments, says law and bioethics Professor Alta Charo of the University of Wisconsin-Madison, who is studying stem cell tourism.

Stem cells are cells that can form many types of cells in the body, and that makes them inherently promising and dangerous. Stem cell tourism refers to people traveling, both within the U.S. and abroad, in pursuit of advertised stem cell therapies to purportedly treat a variety of medical conditions.

The evidence for therapeutic use of stem cells is very limited, except for bone marrow stem cells, but patients all over the world are convinced stem cells will cure their disease, says Charo. While there are some very promising results in the early clinical trials for stem cell therapies using embryonic and other kinds of stem cells, the treatments being advertised by these clinics are dubious, mostly ineffective, and sometimes positively harmful.

Patients are being hoodwinked, but there are dilemmas about tackling (the treatments) at regulatory or political levels.

The outrage over failures in stem cell tourism is limited, Charo says. Patients may pay tens of thousands of dollars for procedures that may carry no promise of success or carry grievous risks of failure. Most people have no reason to pay attention, and those who are paying attention are sick, so they are focused on trying anything, Charo says. If it does not work, they are already in a bad position with plenty to think about.

During a search for stem cell therapies on the web, Charo found products that supposedly enhance the natural formation of stem cells in the skin alongside approved and unapproved treatments in the United States, and stem cell clinics outside the United States, like a stem cell treatment for spinal conditions that might be innocuous, but is probably useless.

Some American operators are trying to slip through Food and Drug Administration regulation, says Charo, who served as senior policy advisor in the Office of the Commissioner of the FDA between 2009 and 2011. The FDA regulates medical devices, tissue transplants and drugs, but not organ transplants or the way medicine is practiced.

To sell a product that can heal without claiming it is a drug, some clinics remove stem cells from a patient, grow them with minimal manipulation, and then reinsert the resulting cells back to the same patient. There has been a long-running battle over whether that is a tissue transplant akin to organ transplantation and thus the practice of medicine, or a tissue transplant that is acting like drug, Charo says. If the latter, then what you do is subject to FDA [regulation], so you have to prove that your product is safe and effective, which almost always requires expensive clinical trials.

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'Stem Cell Tourism' Takes Advantage of Patients, Says Law Professor

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PUBLIC RELEASE DATE:

21-Mar-2014

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

Preliminary basic research and clinical findings have demonstrated that electroacupuncture therapy exhibits positive effects in ameliorating depression. However, most studies of the underlying mechanism are at the single gene level; there are few reports regarding the mechanism at the whole-genome level. Using a rat genomic gene-chip, Dr. Dongmei Duan and co-workers from General PLA Hospital in China profiled hippocampal gene expression changes in rats after electroacupuncture therapy. Electroacupuncture therapy alleviated depression-related manifestations in the model rats. Using gene-chip analysis, electroacupuncture at Baihui (DU20) and Yintang (EX-HN3) regulates the expression of 21 genes. Real-time PCR showed that the genes Vgf, Igf2, Tmp32, Loc500373, Hif1a, Folr1, Nmb, and Rtn were upregulated or downregulated in depression and that their expression tended to normalize after electroacupuncture therapy. These results, published in the Neural Regeneration Research (Vol. 9, No. 1, 2014), indicate that electroacupuncture modulates depression by regulating the expression of particular genes.

###

Article: " Hippocampal gene expression in a rat model of depression after electroacupuncture at the Baihui and Yintang acupoints," by Dongmei Duan1, Xiuyan Yang2, Tu Ya3, Liping Chen1 (1 Department of Traditional Chinese Medicine of South Building, Chinese PLA General Hospital, Beijing 100853, China; 2 Institute of Health Maintenance, Beijing University of Chinese Medicine, Beijing 100029, China; 3 School of Acupuncture and Moxibustion, Beijing University of Chinese Medicine, Beijing 100037, China)

Duan DM, Yang XY, Ya T, Chen LP. Hippocampal gene expression in a rat model of depression after electroacupuncture at the Baihui and Yintang acupoints. Neural Regen Res. 2014;9(1):76-83.

Contact:

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

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Electroacupuncture effect on depression and variation of polygenes expression

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10 hours ago by Lynn Yarris With the new SIF-seq technique, mouse embryonic stem cells can be used to identify human embryonic stem cell enhancers even when the human enhancers are not present in the mouse genome. Credit: Axel Visel, Berkeley Lab

An international team led by researchers with the Lawrence Berkeley National Laboratory (Berkeley Lab) has developed a new technique for identifying gene enhancers - sequences of DNA that act to amplify the expression of a specific gene in the genomes of humans and other mammals. Called SIF-seq, for site-specific integration fluorescence-activated cell sorting followed by sequencing, this new technique complements existing genomic tools, such as ChIP-seq (chromatin immunoprecipitation followed by sequencing), and offers some additional benefits.

"While ChIP-seq is very powerful in that it can query an entire genome for characteristics associated with enhancer activity in a single experiment, it can fail to identify some enhancers and identify some sites as being enhancers when they really aren't," says Diane Dickel, a geneticist with Berkeley Lab's Genomics Division and member of the SIF-seq development team. "SIF-seq is currently capable of testing only hundreds to a few thousand sites for enhancer activity in a single experiment, but can determine enhancer activity more accurately than ChIP-seq and is therefore a very good validation assay for assessing ChIP-seq results."

Dickel is the lead author of a paper in Nature Methods describing this new technique. The paper is titled "Function-based identification of mammalian enhancers using site-specific integration." The corresponding authors are Axel Visel and Len Pennacchio, also geneticists with Berkeley Lab's Genomics Division. (See below for a complete list of authors.)

With the increasing awareness of the important role that gene enhancers play in normal cell development as well as in disease, there is strong scientific interest in identifying and characterizing these enhancers. This is a challenging task because an enhancer does not have to be located directly adjacent to the gene whose expression it regulates, but can instead be located hundreds of thousands of DNA base pairs away. The challenge is made even more difficult because the activity of many enhancers is restricted to specific tissues or cell types.

"For example, brain enhancers will not typically work in heart cells, which means that you must test your enhancer sequence in the correct cell type," Dickel says.

Currently, enhancers can be identified through chromatin-based assays, such as ChIP-seq, which predict enhancer elements indirectly based on the enhancer's association with specific epigenomic marks, such as transcription factors or molecular tags on DNA-associated histone proteins. Visel, Pennacchio, Dickel and their colleagues developed SIF-seq in response to the need for a higher-throughput functional enhancer assay that can be used in a wide variety of cell types and devel-opmental contexts.

"We've shown that SIF-seq can be used to identify enhancers active in cardiomyocytes, neural progenitor cells, and embryonic stem cells, and we think that it has the potential to be expanded for use in a much wider variety of cell types," Dickel says. "This means that many more types of enhancers could potentially be tested in vitro in cell culture."

In SIF-seq, hundreds or thousands of DNA fragments to be tested for enhancer activity are coupled to a reporter gene and targeted into a single, reproducible site in embryonic cell genomes. Every embryonic cell will have exactly one potential enhancer-reporter. Fluorescence-activated sorting is then used to identify and retrieve from this mix only those cells that display strong reporter gene expression, which represent the cells with the most active enhancers.

"Unlike previous enhancer assays for mammals, SIF-seq includes the integration of putative enhancers into a single genomic locus," says co-corresponding author Visel. "Therefore, the activity of enhancers is assessed in a reproducible chromosomal context rather than from a transiently expressed plasmid. Furthermore, by making use of embryonic stem cells and in vitro differentiation, SIF-seq can be used to assess enhancer activity in a wide variety of disease-relevant cell types."

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New technique for identifying gene-enhancers

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Genetic Engineering Infomercial
Bio Project 3rd Term AY 2013-2014 Sofia Suarez and Julia Saulog 8F -- Animation by Sofia (on Wideo.com) Voiceover and Final Editing by Julia -- ~more info~ M...

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GCSE Biology - Genetic Engineering Insulin
A quick tutorial, showing how we use restriction enzymes to cut out a desired gene from one organism, and insert it into the plasmid of a bacterium. This all...

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PUBLIC RELEASE DATE:

24-Mar-2014

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, March 24, 2014Marina Cavazzana, MD, PhD, Paris Descartes University, France and Adrian J. Thrasher, MD, PhD, University College London Institute of Child Health, UK, have been honored with the Pioneer Award for basic and clinical gene therapy for immunodeficiency disorders. Human Gene Therapy, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers, is commemorating its 25th anniversary by bestowing this honor on the leading 12 Pioneers in the field of cell and gene therapy selected by a blue ribbon panel* and publishing a Pioneer Perspective by the award recipients

Dr. Cavazzana has been at the forefront of advances in treating life-threatening inherited diseases of the immune system with gene therapy, using a patient's own modified stem cells. She describes the translation of this work to the clinic and its ongoing advances and novel applications in the article "Hematopoetic Stem Cell Gene Therapy: Progress on the Clinical Front." The article by Dr. Cavazzana is available free on the Human Gene Therapy website at http://online.liebertpub.com/doi/full/10.1089/hum.2014.2504.

A pioneer of gene therapy in the UK, Dr. Thrasher has been at the leading edge of basic science research on the function of therapeutic genes for inherited disorders and the development of viral vectors to deliver them to affected patients. He has collaborated on gene therapy clinical trials targeting immunodeficiency disorders with groups in Europe and the USA.

"Cell therapy and gene therapy are advancing together to improve patient care," says Dr. Cavazzana. "We can expect to be able to rebuild a new immune system not only in primary immunodeficiencies but also in severe acquired clinical conditions (such as those in HIV-1-infected patients)."

"I've seen some very exciting times in the field, from the first evidence that biochemical defects can be corrected in vitro, to some remarkable clinical successes in patients with devastating diseases. I look forward with huge enthusiasm to the exciting developments on the horizon, which are likely to impact on more patients with an even wider range of disorders," says Dr. Thrasher.

"These pioneers contributed to the first real clinical successes of gene therapy through their work in inherited immune deficiency disorders," says James M. Wilson, MD, PhD, Editor-in-Chief of Human Gene Therapy, and Director of the Gene Therapy Program, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia.

###

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Pioneer Award recipients Marina Cavazzana and Adrian Thrasher recognized for advancing gene therapy to the clinic for ...

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Genetics Lesson 1, Part 4: Complex patterns of inheritance
This video screencast was created with Doceri on an iPad. Doceri is free in the iTunes app store. Learn more at http://www.doceri.com.

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Genetics Lesson 1, Part 5: Complex Patterns of Inheritance continued...
This video screencast was created with Doceri on an iPad. Doceri is free in the iTunes app store. Learn more at http://www.doceri.com.

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Sun Exposure, Genetics, and Melanoma: A Worldwide Health Challenge
Sohail Tavazoie, Debra Black, Jennifer Stein, Marc Tessier-Lavigne: The Women Science and Parents Science initiatives were pleased to present their Winte...

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Attack of the B Team E9 - Advanced Genetics and the Cartographer from OpenBlocks
Welcome to my Attack of the B Team modded Minecraft lets play series. In this episode we enhance our genetic structure and try to make a map using the cartog...

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Can #39;t Hide- Genetics Final
WARNING: This video has been identified by Epilepsy Action to potentially trigger seizures for people with photosensitive epilepsy. For educational purposes ...

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Can't Hide- Genetics Final - Video

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Can #39;t Hide - Genetics (all platforms of watching)
WARNING: This video has been identified by Epilepsy Action to potentially trigger seizures for people with photosensitive epilepsy. For educational purposes ...

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One in a thousand children in the United States is deaf, and one in three adults will experience significant hearing loss after the age of 65. Whether the result of genetic or environmental factors, hearing loss costs billions of dollars in healthcare expenses every year, making the search for a cure critical.

Now a team of researchers led by Karen B. Avraham of the Department of Human Molecular Genetics and Biochemistry at Tel Aviv University's Sackler Faculty of Medicine and Yehoash Raphael of the Department of Otolaryngology-Head and Neck Surgery at University of Michigan's Kresge Hearing Research Institute have discovered that using DNA as a drug -- commonly called gene therapy -- in laboratory mice may protect the inner ear nerve cells of humans suffering from certain types of progressive hearing loss.

In the study, doctoral student Shaked Shivatzki created a mouse population possessing the gene that produces the most prevalent form of hearing loss in humans: the mutated connexin 26 gene. Some 30 percent of American children born deaf have this form of the gene. Because of its prevalence and the inexpensive tests available to identify it, there is a great desire to find a cure or therapy to treat it.

"Regenerating" neurons

Prof. Avraham's team set out to prove that gene therapy could be used to preserve the inner ear nerve cells of the mice. Mice with the mutated connexin 26 gene exhibit deterioration of the nerve cells that send a sound signal to the brain. The researchers found that a protein growth factor used to protect and maintain neurons, otherwise known as brain-derived neurotrophic factor (BDNF), could be used to block this degeneration. They then engineered a virus that could be tolerated by the body without causing disease, and inserted the growth factor into the virus. Finally, they surgically injected the virus into the ears of the mice. This factor was able to "rescue" the neurons in the inner ear by blocking their degeneration.

"A wide spectrum of people are affected by hearing loss, and the way each person deals with it is highly variable," said Prof. Avraham. "That said, there is an almost unanimous interest in finding the genes responsible for hearing loss. We tried to figure out why the mouse was losing cells that enable it to hear. Why did it lose its hearing? The collaborative work allowed us to provide gene therapy to reverse the loss of nerve cells in the ears of these deaf mice."

Although this approach is short of improving hearing in these mice, it has important implications for the enhancement of sound perception with a cochlear implant, used by many people whose connexin 26 mutation has led to impaired hearing.

Embryonic hearing?

Inner ear nerve cells facilitate the optimal functioning of cochlear implants. Prof. Avraham's research suggests a possible new strategy for improving implant function, particularly in people whose hearing loss gets progressively worse with time, such as those with profound hearing loss as well as those with the connexin gene mutation. Combining gene therapy with the implant could help to protect vital nerve cells, thus preserving and improving the performance of the implant.

More research remains. "Safety is the main question. And what about timing? Although over 80 percent of human and mouse genes are similar, which makes mice the perfect lab model for human hearing, there's still a big difference. Humans start hearing as embryos, but mice don't start to hear until two weeks after birth. So we wondered, do we need to start the corrective process in utero, in infants, or later in life?" said Prof. Avraham.

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From mouse ears to human's? Gene therapy to address progressive hearing loss

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PUBLIC RELEASE DATE:

24-Mar-2014

Contact: George Hunka ghunka@aftau.org 212-742-9070 American Friends of Tel Aviv University

One in a thousand children in the United States is deaf, and one in three adults will experience significant hearing loss after the age of 65. Whether the result of genetic or environmental factors, hearing loss costs billions of dollars in healthcare expenses every year, making the search for a cure critical.

Now a team of researchers led by Karen B. Avraham of the Department of Human Molecular Genetics and Biochemistry at Tel Aviv University's Sackler Faculty of Medicine and Yehoash Raphael of the Department of OtolaryngologyHead and Neck Surgery at University of Michigan's Kresge Hearing Research Institute have discovered that using DNA as a drug commonly called gene therapy in laboratory mice may protect the inner ear nerve cells of humans suffering from certain types of progressive hearing loss.

In the study recently published in the journal Hearing Research, doctoral student Shaked Shivatzki created a mouse population possessing the gene that produces the most prevalent form of hearing loss in humans: the mutated connexin 26 gene. Some 30 percent of American children born deaf have this form of the gene. Because of its prevalence and the inexpensive tests available to identify it, there is a great desire to find a cure or therapy to treat it.

"Regenerating" neurons

Prof. Avraham's team set out to prove that gene therapy could be used to preserve the inner ear nerve cells of the mice. Mice with the mutated connexin 26 gene exhibit deterioration of the nerve cells that send a sound signal to the brain. The researchers found that a protein growth factor used to protect and maintain neurons, otherwise known as brain-derived neurotrophic factor (BDNF), could be used to block this degeneration. They then engineered a virus that could be tolerated by the body without causing disease, and inserted the growth factor into the virus. Finally, they surgically injected the virus into the ears of the mice. This factor was able to "rescue" the neurons in the inner ear by blocking their degeneration.

"A wide spectrum of people are affected by hearing loss, and the way each person deals with it is highly variable," said Prof. Avraham. "That said, there is an almost unanimous interest in finding the genes responsible for hearing loss. We tried to figure out why the mouse was losing cells that enable it to hear. Why did it lose its hearing? The collaborative work allowed us to provide gene therapy to reverse the loss of nerve cells in the ears of these deaf mice."

Although this approach is short of improving hearing in these mice, it has important implications for the enhancement of sound perception with a cochlear implant, used by many people whose connexin 26 mutation has led to impaired hearing.

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From mouse ears to man's?

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PUBLIC RELEASE DATE:

24-Mar-2014

Contact: Jen Gundersen jeg2034@med.cornell.edu 646-317-7402 Weill Cornell Medical College

NEW YORK (March 24, 2014) Scientists from Weill Cornell Medical College and Houston Methodist have found that a gene previously unassociated with breast cancer plays a pivotal role in the growth and progression of the triple negative form of the disease, a particularly deadly strain that often has few treatment options. Their research, published in this week's Nature, suggests that targeting the gene may be a new approach to treating the disease.

About 42,000 new cases of triple negative breast cancer (TNBC) are diagnosed in the United States each year, about 20 percent of all breast cancer diagnoses. Patients typically relapse within one to three years of being treated.

Senior author Dr. Laurie H. Glimcher, the Stephen and Suzanne Weiss Dean of Weill Cornell Medical College, wanted to know whether the gene already understood from her prior work to be a critical regulator of immune and metabolic functions was important to cancer's ability to adapt and thrive in the oxygen- and nutrient-deprived environments inside of tumors. Using cells taken from patients' tumors and transplanted into mice, Dr. Glimcher's team found that the gene, XBP1, is especially active in triple negative breast cancer, particularly in the progression of malignant cells and their resurgence after treatment.

"Patients with the triple negative form of breast cancer are those who most desperately need new approaches to treat their disease," said Dr. Glimcher, who is also a professor of medicine at Weill Cornell. "This pathway was activated in about two-thirds of patients with this type of breast cancer. Now that we better understand how this gene helps tumors proliferate and then return after a patient's initial treatment, we believe we can develop more effective therapies to shrink their growth and delay relapse."

The group, which included investigators from nine institutions, examined several types of breast cancer cell lines. They found that XBP1 was particularly active in basal-like breast cancer cells cultivated in the lab and in triple negative breast cancer cells from patients. When they suppressed the activity of the gene in laboratory cell cultures and animal models, however, the researchers were able to dramatically reduce the size of tumors and the likelihood of relapse, especially when these approaches were used in conjunction with the chemotherapy drugs doxorubicin or paclitexel. The finding suggests that XBP1 controls behaviors associated with tumor-initiating cells that have been implicated as the originators of tumors in a number of cancers, including that of the breast, supporting the hypothesis that combination therapy could be an effective treatment for triple negative breast cancer.

The scientists also found that interactions between XBP1 and another transcriptional regulator, HIF1-alpha, spurs the cancer-driving proteins. Silencing XBP1 in the TNBC cell lines reduced the tumor cells' growth and other behaviors typical of metastasis.

"This starts to demonstrate how cancer cells co-opt the endoplasmic reticulum stress response pathway to allow tumors to grow and survive when they are deprived of nutrients and oxygen," said lead author Dr. Xi Chen, a postdoctoral associate at Weill Cornell, referring to the process by which healthy cells maintain their function. "It shows the interaction between two critical pathways to make the cells better able to deal with a hostile microenvironment, and in that way offers new strategies to target triple negative breast cancer."

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Gene implicated in progression and relapse of deadly breast cancer finding points to potential Achilles' heel in ...

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Embryonic Stem Cell Therapy
Short fun video about Stemaid #39;s Embryonic Stem Cells Visit http://www.stemaid.com.

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Lead researcher Dr Peter Taylor, from the University of Cardiff's School of Medicine, said: "If other studies confirm our finding then there may be benefit in carrying out a genetic test for this gene variant in addition to the standard neonatal thyroid screening, which would identify children most at risk of developing low IQ.

Around 4 per cent of the population have the gene variant coupled with a lower than normal thyroid hormone levels.

The finding could mean that up to 2.5 million people in Britain could be suffering from the effects of low IQ which might have been treatable.

The new research focused on an enzyme called deiodonase-2 which is involved in processing thyroid hormones within cells.

A mutation in the gene coding for the enzyme had already been associated with other health problems including diabetes and high blood pressure.

In the new study, scientists from the universities of Cardiff and Bristol looked at genetic data on 3,123 children under the age of seven who also had their IQ tested.

Those with thyroid hormone levels at the bottom of the normal range who also possessed the deiodonase-2 variant were four times more likely to have an IQ under 85.

Children with lower thyroid hormone levels alone were not at greater risk of low IQ.

The findings were presented at the Society for Endocrinology's British Endocrine Societies (BES) conference in Liverpool.

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Genetic test could show which babies will have low IQ

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TGA Subcool Genetics, Dr. Who, 9 Pound Hammer, Galactic Jack, and Dairy Queen Veg
A little look at the next run as it finally shows me whats a boy and whats a girl. should be another nice run of TGA genetics. This time all the TGA bases ar...

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Attack of The B-team Ep.2 Advanced Genetics
Join me as I dive into all the mods in Attack of the B-team! Server Address:abteam.bluestoneservers.com.

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Could Genetics Be To Blame For Weight Gain From Fried Foods?
Harvard researchers say the more pro-obesity genes a person has, the worse off his or her waistline will be from eating fried foods. Follow Elizabeth Hagedor...

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Vatican considers the canonization of Jrme Lejeune, the Dr. of #39;modern genetics #39;
The Dr. discovered the gene that causes Down Syndrome and publicly spoke out against abortion at the United Nations.

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Vatican considers the canonization of Jrme Lejeune, the Dr. of 'modern genetics' - Video

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Sims 3 genetics (prettacy) - day 279 - 032114
I talk about sims 3 and how you can work with genetics and heredity in the game to do certain challenges. We also come up with a couple of our own.

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BIOLOGY I: Applied Genetics Infomercial
F9B Lizzie Jaehn Aja Ellett twinniez.

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