Dr Saw Khay Yong Stem Cell Therapy for the Musculoskeletal System

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Dr Saw Khay Yong Stem Cell Therapy for the Musculoskeletal System - Video

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Nov 12, 2014 The HIV protein integrase (blue) can insert viral DNA (red) at different locations in the DNA of its human host (orange). But how the virus selects its insertion points has puzzled virologists for over 20 years. Now a team of KU Leuven researchers have discovered that the answer lies in two -- of the more than 200 -- amino acids that make up integrase's structure. Credit: Jonas Demeulemeester

The human immunodeficiency virus (HIV) can insert itself at different locations in the DNA of its human host - and this specific integration site determines how quickly the disease progresses, report researchers at KU Leuven's Laboratory for Molecular Virology and Gene Therapy. The study was published online today in the journal Cell Host & Microbe.

When HIV enters the bloodstream, virus particles bind to and invade human immune cells. HIV then reprogrammes the hijacked cell to make new HIV particles.

The HIV protein integrase plays a key role in this process: it recognises a short segment in the DNA of its host and catalyzes the process by which viral DNA is inserted in host DNA.

Integrase can insert viral DNA at various places in human DNA. But how the virus selects its insertion points has puzzled virologists for over 20 years.

Now a team of KU Leuven researchers has discovered that the answer lies in two amino acids. Doctoral researcher Jonas Demeulemeester, first author of the study, explains: "HIV integrase is made up of a chain of more than 200 amino acids folded into a structure. By modelling this structure, we found two positions in the protein that make direct contact with the DNA of the host. These two amino acids determine the integration site. This is not only the case for HIV but also for related animal-borne viruses."

In a second phase of the study, the researchers were able to manipulate the integration site choice of HIV, explains Professor Rik Gijsbers. "We changed the specific HIV integrase amino acids for those of animal-borne viruses and found that the viral DNA integrated in the host DNA at locations where the animal-borne virus normally would have done so."

"We also showed that HIV integrases can vary," says Professor Rik Gijsbers. "Sometimes different amino acids appeared in the two positions we identified. These variant viruses also integrate into the host DNA at a different site than the normal virus does."

Together with Dr. Thumbi Ndung'u (University of KwaZulu-Natal, Durban, South Africa), the team studied the impact of these viral variants on the progression towards AIDS in a cohort of African HIV patients, continues Professor Zeger Debyser: "To our surprise, we found that the disease progressed more quickly when the integration site was changed. In other words, the variant viruses broke down the immune system more rapidly. This insight both increases our knowledge of the disease and opens new perspectives. By retargeting the integration site to a 'safer' part of the host DNA, we hope to eventually develop new therapies."

Explore further: Redesigned protein opens door for safer gene therapy

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HIV virulence depends on where virus inserts itself in host DNA

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PUBLIC RELEASE DATE:

12-Nov-2014

Contact: Julia Evangelou Strait straitj@wustl.edu 314-286-0141 Washington University School of Medicine @WUSTLmed

Rare mutations that shut down a single gene are linked to lower cholesterol levels and a 50 percent reduction in the risk of heart attack, according to new research from Washington University School of Medicine in St. Louis, the Broad Institute at Massachusetts Institute of Technology and Harvard, and other institutions.

The gene, called NPC1L1, is of interest because it is the target of the drug ezetimibe, often prescribed to lower cholesterol.

The study appears Nov. 12 in The New England Journal of Medicine.

Everyone inherits two copies of most genes -- one copy from each parent. In the study, the researchers found that people with one inactive copy of NPC1L1 appeared to be protected against high LDL cholesterol --the so-called "bad" cholesterol -- and coronary heart disease, a narrowing of the heart's arteries that can lead to heart attacks.

"This analysis demonstrates that human genetics can guide us in terms of thinking about appropriate genes to target for clinical therapy," said first author Nathan O. Stitziel, MD, PhD, a cardiologist at Washington University School of Medicine. "When people have one copy of a gene not working, it's a little like taking a drug their entire lives that is inhibiting this gene."

The investigators mined genetic data from large clinical trials to find individuals with naturally occurring mutations in the NPC1L1 gene that completely shut it down. They analyzed multiple existing studies, pooling data from about 113,000 people. Of these trial participants, only 82 were found to have a mutation that shut off one copy of the NPC1L1 gene. No one had two inactive copies of NPC1L1. Based on a subset of data in the analysis, the researchers estimate roughly 1 in 650 people carry one inactive version of the gene.

The investigators found that people with only one working copy of the gene had LDL cholesterol levels an average of 12 milligrams per deciliter lower than the wider population of people with two working copies of the gene. This approximately 10 percent reduction in LDL cholesterol is comparable to that seen in patients taking ezetimibe. But beyond simply lowering cholesterol, the 82 people with inactive copies also had about half the risk of coronary heart disease as people with two functional copies of the gene.

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Errors in single gene may protect against heart disease

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Health officials hit back at e-cig claims

Health professionals say more research is needed to prove using e-cigarettes is a good way to quit smoking.

According to new health figures, Australian women are far less likely to survive a heart attack than men.

Research says high factor sunscreen can't be relied on to protect against the deadliest skin cancer form.

A British study using skin electrodes has found men experience greater levels of emotion than women.

High protein diets may protect against stroke, especially if they contain a lot of fish, scientists say.

Driving too much is bad for your health, according to a study of 40-thousand middle-aged Australians.

Researchers say the financial crisis may have led to thousands of suicides in Europe and North America.

Biologists have devised a new weapon against malaria by genetically engineering mosquitoes.

Stomach-shrinking bariatric surgery beats other forms of treatment in bringing about remission of diabetes.

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Gene mutation linked to lower cholesterol

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Published November 13, 2014

Scientists have discovered gene mutations that give people naturally lower cholesterol levels and cut their risk of heart disease in half.

That discovery may have a big implication: A blockbuster drug that mimics these mutations has long been sold without evidence that it cuts the chance of heart disease. Results of a large study that looked for that evidence will be revealed on Monday.

The drug is Merck & Co.'s Zetia, also sold in combination with another medicine as Vytorin.

When Zetia was designed, scientists knew how it worked to lower LDL, or bad cholesterol, and it won federal approval based on its ability to do that. But the existence of gene mutations that could do the same thing was not known, nor was it known if lowering cholesterol this way would translate to a lower risk of heart problems.

The new research gives a biological basis to suggest the drug could help.

Researchers found that people with mutations in a gene called NPC1L1 had LDL that was 12 milligrams per deciliter lower on average than others without a mutation. That is similar to how much Zetia lowers LDL.

The bigger finding was that the gene mutations lowered the risk of heart disease by 53 percent.

"It's a stunner," said Dr. Eric Topol, director of the Scripps Translational Science Institute in La Jolla, California. "We're learning more and more about protective mutations," and the effect these had on heart disease risk was far greater than the degree to which they lowered cholesterol, he said.

Topol had no role in the study, which was led by researchers from the Washington University School of Medicine in St. Louis, the Broad Institute at the Massachusetts Institute of Technology and Harvard, and other institutions. Results were published online Wednesday by the New England Journal of Medicine.

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Gene mutation discovery boosts interest in heart drug

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Will Genetic Engineering And Organ Growing Bring Us The Dawn Of The Superman?
The Fortean Slip Daily Dose 2 The Chris 2.0 Episode. In this episode Chris wonders if research into genetic engineering and organ growing will bring us the d...

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13-Nov-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

New Rochelle, NY, November 13, 2014--The two U.S. FDA approved oligonucleotide-based drugs on the market both have a modified chemical backbone made of phosphorothioates. The therapeutic advantages of the phosphorothioate group and the new types of gene expression-regulation oligonucleotide drugs that it is enabling are detailed in a Review article in Nucleic Acid Therapeutics, a peer-reviewed journal from Mary Ann Liebert, Inc. publishers. The article is available free on the Nucleic Acid Therapeutics website until December 13, 2014.

In the article "Phosphorothioates, Essential Components of Therapeutic Oligonucleotides," Fritz Eckstein, Max-Planck-Institut fr Experimentelle Medizin, Gttingen, Germany, describes how the chemical and biochemical properties of this significant nucleic acid modification have made DNA suitable for use as therapeutic agents. Initial applications focused on cleaving the mRNA product of genes to block protein production. Dr. Eckstein explores novel applications including microRNA and long non-coding RNA targets and the use of decoy oligonucleotides.

"We will advance the field of nucleic acid therapeutics by looking to key opinion leaders to educate and initiate the experienced and newcomers alike. In this review, Dr. Eckstein has produced a tour de force concerning the therapeutic application of phosphorothioates," says Executive Editor Graham C. Parker, PhD, The Carman and Ann Adams Department of Pediatrics, Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI.

###

Nucleic Acid Therapeutics is under the editorial leadership of Co-Editors-in-Chief Bruce A. Sullenger, PhD, Duke Translational Research Institute, Duke University Medical Center, Durham, NC, and C.A. Stein, MD, PhD, City of Hope National Medical Center, Duarte, CA; and Executive Editor Graham C. Parker, PhD.

About the Journal

Nucleic Acid Therapeutics is an authoritative, peer-reviewed journal published bimonthly in print and online that focuses on cutting-edge basic research, therapeutic applications, and drug development using nucleic acids or related compounds to alter gene expression. Nucleic Acid Therapeutics is the official journal of the Oligonucleotide Therapeutics Society. Complete tables of content and a sample issue may be viewed on the Nucleic Acid Therapeutics website.

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Modified DNA backbone enables success of existing and novel oligonucleotide therapeutics

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PUBLIC RELEASE DATE:

12-Nov-2014

Contact: David Ruth david@rice.edu 713-348-6327 Rice University @RiceUNews

The tree has been an effective model of evolution for 150 years, but a Rice University computer scientist believes it's far too simple to illustrate the breadth of current knowledge.

Rice researcher Luay Nakhleh and his group have developed PhyloNet, an open-source software package that accounts for horizontal as well as vertical inheritance of genetic material among genomes. His "maximum likelihood" method, detailed this month in the Proceedings of the National Academy of Sciences, allows PhyloNet to infer network models that better describe the evolution of certain groups of species than do tree models.

"Inferring" in this case means analyzing genes to determine their evolutionary history with the highest probability - the maximum likelihood - of connections between species. Nakhleh and Rice colleague Christopher Jermaine recently won a $1.1 million National Science Foundation grant to analyze evolutionary patterns using Bayesian inference, a statistics-based technique to estimate probabilities based on a data set.

To build networks that account for all of the genetic connections between species, the software infers the probability of variations that phylogenetic trees can't illustrate, such as horizontal gene transfers. These transfers circumvent simple parent-to-offspring evolution and allow genetic variations to move from one species to another by means other than reproduction.

Biologists want to know when and how these transfers happened, but tree structures conceal such information. "When horizontal transfer occurs, as with the hybridization of two species, the tree model becomes inadequate to describe the evolutionary history, and networks that incorporate horizontal gene transfer become the more appropriate model," Nakhleh said.

Nakhleh's Java-based software accounts for incomplete lineage sorting, in which clues to gene evolution that don't match the established lineage of species appear in the genetic record.

"We are the first group to develop a general model that will allow biologists to estimate hybridization while accounting for all these complexities in evolution," Nakhleh said.

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Rice University program models more detailed evolutionary networks from genetic data

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PUBLIC RELEASE DATE:

12-Nov-2014

Contact: Jane Finlayson jane.finlayson@uhn.ca 416-946-2846 University Health Network @UHN_News

(TORONTO, Canada - Nov. 13, 2014) - Prostate cancer researchers have developed a genetic test to identify which men are at highest risk for their prostate cancer to come back after localized treatment with surgery or radiotherapy.

The findings are published online today in Lancet Oncology. Study co-leads Dr. Robert Bristow, a clinician-scientist at Princess Margaret Cancer Centre, and Dr. Paul Boutros, an investigator at the Ontario Institute for Cancer Research, report that the gene test provides a much-needed quick and accurate tool to determine with greater precision the men who will do well with local treatment only (surgery or radiation), and those who will need extra treatment (chemotherapy and hormone therapy) to ensure the cancer is completely eradicated. Dr. Bristow talks about the research at http://youtu.be/7dZyVm_y5WU

"Our findings set the stage to tackle the ongoing clinical problem of under-treating men with aggressive disease that will recur in 30% to 50% of patients due to hidden, microscopic disease that is already outside the prostate gland during initial treatment," says Dr. Bristow.

"This genetic test could increase cure rates in intermediate- to high-risk men by preventing progression to this metastatic spread of prostate cancer." The next step will be testing the gene signature on many more patients worldwide for three to five years to turn the test into one that is readily available in the clinic to guide personalized prostate cancer treatments.

The predictive test analyses biopsy tissue taken before treatment even starts to identify abnormal genetic characteristics (abnormal DNA) of the prostate cancer and its oxygen content. Low oxygen, or hypoxia, is an already known factor in the spread of prostate cancer. Together, this information can predict with almost 80% accuracy - and in about three days - those prostate cancer patients who are at greatest risk of their disease returning, the study shows.

"The clinical potential is enormous for thousands of patients," says Dr. Bristow. "This is personalized cancer medicine to the hilt - the ability to provide more targeted treatment to patients based on their unique cancer genetic fingerprint plus what's going on in the cancer cell's surrounding environment. We hope to improve cure rates by reducing the chances of the cancer recurring and prevent the cells from spreading."

The researchers developed the genetic test with two groups of patients. In the first group, the team analyzed DNA from initial diagnostic biopsies of 126 men who were treated with image-guided radiotherapy (IGRT) and followed for an average 7.8 years. In the second group, the team used the test on 150 men whose tumours were removed surgically (radical prostatectomy). The genetic test produced similar results in both groups and therefore can be used in patients who choose radiotherapy or surgery as their initial treatment.

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Prostate cancer researchers develop personalized genetic test to predict recurrence risk

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CTVNews.ca Staff Published Wednesday, November 12, 2014 6:30PM EST Last Updated Wednesday, November 12, 2014 8:47PM EST

Canadian researchers have developed a new genetic test to identify prostate cancer patients who are at highest risk of recurrence after surgery or radiotherapy.

By analyzing DNA from diagnostic biopsies of men who underwent either surgery or image-guided radiotherapy to treat their prostate cancer, the researchers came up with a test that can determine with greater precision which men will need extra treatment, such as chemotherapy, to ensure that the cancer is eradicated.

The findings were published online Tuesday in the Lancet Oncology journal.

This genetic test could increase cure rates in intermediate- to high-risk men by preventing progression to this metastatic spread of prostate cancer, Dr. Robert Bristow, a clinician-scientist at Princess Margaret Cancer Centre in Toronto, said in a news release.

The test is currently still in research mode, Bristow told The Canadian Press. The hope is that the test will be validated, approved by Health Canada and ready for use in five years.

Bristow is the co-lead of the study, along with Dr. Paul Boutros, an investigator at the Ontario Institute for Cancer Research.

Hypoxia, or low oxygen, is a known factor is the spread of prostate cancer. The newly developed test can identify the cancers oxygen content, as well as the tumours abnormal genetic characteristics to determine which patients are at greatest risk of their prostate cancer returning, the study says.

The study showed that, among patients whose tumours had low levels of genetic changes and low hypoxia, the cancer recurrence rate was lower than seven per cent after five years.

Men with high levels of genetic changes and high hypoxia had much worse outcomes. More than 50 per cent of those patients had a recurrence of cancer.

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Genetic test predicts prostate cancer recurrence

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Newswise (TORONTO, Canada Nov. 13, 2014) Prostate cancer researchers have developed a genetic test to identify which men are at highest risk for their prostate cancer to come back after localized treatment with surgery or radiotherapy.

The findings are published online today in Lancet Oncology. Study co-leads Dr. Robert Bristow, a clinician-scientist at Princess Margaret Cancer Centre, and Dr. Paul Boutros, an investigator at the Ontario Institute for Cancer Research, report that the gene test provides a much-needed quick and accurate tool to determine with greater precision the men who will do well with local treatment only (surgery or radiation), and those who will need extra treatment (chemotherapy and hormone therapy) to ensure the cancer is completely eradicated. Dr. Bristow talks about the research at http://youtu.be/7dZyVm_y5WU

Our findings set the stage to tackle the ongoing clinical problem of under-treating men with aggressive disease that will recur in 30% to 50% of patients due to hidden, microscopic disease that is already outside the prostate gland during initial treatment, says Dr. Bristow.

This genetic test could increase cure rates in intermediate- to high-risk men by preventing progression to this metastatic spread of prostate cancer. The next step will be testing the gene signature on many more patients worldwide for three to five years to turn the test into one that is readily available in the clinic to guide personalized prostate cancer treatments.

The predictive test analyses biopsy tissue taken before treatment even starts to identify abnormal genetic characteristics (abnormal DNA) of the prostate cancer and its oxygen content. Low oxygen, or hypoxia, is an already known factor in the spread of prostate cancer. Together, this information can predict with almost 80% accuracy and in about three days those prostate cancer patients who are at greatest risk of their disease returning, the study shows.

The clinical potential is enormous for thousands of patients, says Dr. Bristow. This is personalized cancer medicine to the hilt the ability to provide more targeted treatment to patients based on their unique cancer genetic fingerprint plus whats going on in the cancer cells surrounding environment. We hope to improve cure rates by reducing the chances of the cancer recurring and prevent the cells from spreading.

The researchers developed the genetic test with two groups of patients. In the first group, the team analyzed DNA from initial diagnostic biopsies of 126 men who were treated with image-guided radiotherapy (IGRT) and followed for an average 7.8 years. In the second group, the team used the test on 150 men whose tumours were removed surgically (radical prostatectomy). The genetic test produced similar results in both groups and therefore can be used in patients who choose radiotherapy or surgery as their initial treatment.

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Prostate Cancer Researchers Develop Personalized Genetic Test to Accurately Predict Recurrence Risk

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TORONTO - Canadian researchers have developed a genetic test to identify which men are at highest risk for recurrence of prostate cancer following localized treatment with surgery or radiation therapy.

The genetic test provides a quick and highly accurate tool to determine which men with prostate cancer would do well with only surgery or radiation, and those who would need additional treatment chemotherapy and hormone therapy, say the researchers, whose findings are described in Wednesday's online edition of the journal Lancet Oncology.

"Our findings set the stage to tackle the ongoing clinical problem of under-treating men with aggressive disease that will recur in 30 per cent to 50 per cent of patients due to hidden, microscopic disease that is already outside the prostate gland during initial treatment," said Dr. Robert Bristow, a clinician-scientist at Princess Margaret Cancer Centre in Toronto.

"This genetic test could increase cure rates in intermediate- to high-risk men by preventing progression to this metastatic spread of prostate cancer," said Bristow, who co-led the study with Dr. Paul Boutros, a scientist at the Ontario Institute for Cancer Research.

The predictive test analyzes biopsy tissue taken before treatment even starts to identify abnormal genetic characteristics in the tumour and its oxygen content. Low oxygen, known as hypoxia, makes prostate cancer cells "leaner and meaner," giving them the ability to invade blood vessels and spread throughout the body.

Together, this information can predict with almost 80 per cent accuracy which men with prostate cancer are at greatest risk of their disease returning in the form of secondary tumours outside the prostate, the study shows.

"The clinical potential is enormous for thousands of patients," said Bristow. "This is personalized cancer medicine to the hilt the ability to provide more targeted treatment to patients based on their unique cancer genetic fingerprint plus what's going on in the cancer cell's surrounding environment. We hope to improve cure rates by reducing the chances of the cancer recurring and prevent the cells from spreading."

An estimated 23,600 Canadian men will be diagnosed this year with prostate cancer, the most common cancer diagnosed in men and the third leading cause of death from cancer. About 4,000 Canadians will die from the disease this year, according to Canadian Cancer Society statistics.

The researchers developed the genetic test with two groups of patients. In the first group, they analyzed DNA in biopsied cancer cells from 126 men who were treated with image-guided radiotherapy, monitoring them for an average of eight years. The test was also used in a second group of 150 men whose tumours were removed surgically.

The study showed that the men with the best outcomes those who had a less than seven per cent recurrence of prostate cancer at five years had low levels of genetic changes and little hypoxia. For men with high levels of genetic changes and high hypoxia, outcomes were worse more than half had their cancer come back.

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Personalized genetic test could predict prostate cancer recurrence

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Newswise INDIANAPOLIS -- People with a newly identified genetic variant perform better on certain types of memory tests, a discovery that may point the way to new treatments for the memory impairments caused by Alzheimer's disease or other age-associated conditions.

In what the international research team is calling the largest study to date of human memory, an analysis of genomic data and memory test results from more than 14,000 older adults identified a location in the genome that was associated with better memory performance. The researchers noted that the gene has not been associated with cognition in the past.

The research team, led by IU School of Medicine post-doctoral researcher and medical student Vijay K. Ramanan, Ph.D., and Andrew J. Saykin, Psy.D., director of the Indiana Alzheimer Disease Center and the IU Center for Neuroimaging, reported its results in the journal Molecular Psychiatry.

The genome-wide study found that better performance on tests of episodic memory was associated with a change in the DNA on chromosome 2 -- a G instead of the more common A nucleotide in a gene known as FASTKD2. The genetic variant -- known as a single nucleotide polymorphism, or SNP -- was also associated with a larger hippocampus and more dense gray matter in the brain on magnetic resonance imaging scans. The hippocampus is a brain structure involved in storing and retrieving memory. The inability to recall a recent current event, a newspaper article or what one had for dinner is one of the earliest symptoms of Alzheimer's disease and is also related to hippocampal atrophy.

The FASTKD2 gene is responsible for the production of a protein involved in apoptosis, a process of programmed cell death. The researchers also examined cerebrospinal fluid samples from 82 participants and found lower levels of proteins associated with cell death in the participants with the memory-protective G variant.

More research will be needed to determine whether drugs targeting the FASTKD2 gene could be used to protect against memory loss and related issues in Alzheimer's disease, Dr. Saykin said.

"There is likely no single 'memory gene'; we expect that memory is driven by a combination of multiple genes along with environment and lifestyle," Dr. Saykin said. "Although the influence of FASTKD2 was modest, there are parallels to research in diabetes, cancer and hypertension that uncovered genetic variants with similar effects that turned out to be targets for drugs that are now commonly used."

Other researchers contributing to the work were Kwangsik Nho, Ph.D., Li Shen, Ph.D., Shannon L. Risacher, Ph.D., Sungeun Kim, Ph.D., Brenna C. McDonald, Psy.D., Martin R. Farlow, M.D., Tatiana M. Foroud, Ph.D., and Sujuan Gao, Ph.D., of the IU School of Medicine; on behalf of the AddNeuroMed Consortium: Hilkka Soininen, M.D., Ph.D. University of Eastern Finland; Iwona Koszewska, M.D., Ph.D., Medical University of Lodz, Poland; Patrizia Mecocci, M.D., Ph.D., University of Perugia, Italy; Magda Tsolaki, M.D., Ph.D., Aristotle University, Greece; Bruno Vellas, M.D., Ph.D., University of Toulouse, France and Simon Lovestone, Ph.D., MRCPsych, University of Oxford, U.K.; Paul S. Aisen, M.D., University of California, San Diego; Ronald C. Petersen, M.D., and Clifford R. Jack, Jr., M.D., Mayo Clinic Minnesota; Leslie M. Shaw, Ph.D., and John Q. Trojanowski, Ph.D., University of Pennsylvania School of Medicine; Michael W. Weiner, M.D., University of California, San Francisco; Robert C. Green, M.D., M.P.H., and Philip L. De Jager, M.D., Ph.D., Harvard Medical School; Arthur W. Toga, Ph.D., University of Southern California; Lei Yu, Ph.D., and David A. Bennett, M.D., Rush University Medical Center, Chicago.

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IU-Led Research Team Identifies Genetic Variant Linked to Better Memory Performance

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Let #39;s Try Apex Genetics
Apex Genetics, it is a small game created by 6 university students for their capstone project. The game is set on a Sci-Fi world, where you control a cat like creature and use stealth to reach...

By: Ythmevge

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Let's Try Apex Genetics - Video

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S2E2 - We Talk Genetics - The Adam Dunn Show
Mitch Crunchy are joined by Max Montrose to talk about the true history of the Bruce Banner strains w their creator Jason of Darkhorse Genetics, and have a conversation about genetics, genotype...

By: The Adam Dunn Show

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S2E2 - We Talk Genetics - The Adam Dunn Show - Video

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Biol 100FA14 Meiosis-genetics 2
Made with Explain Everything.

By: Maurie Beck

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Biol 100FA14 Meiosis-genetics 2 - Video

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Cancer Gene Therapy by Deirdre Creegan group 9
Description.

By: Deirdre Creegan

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Cancer Gene Therapy by Deirdre Creegan group 9 - Video

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PUBLIC RELEASE DATE:

13-Nov-2014

Contact: Service de presse AFM-Tlthon gmonfort@afm-telethon.fr AFM-Tlthon @AfmPresse

Duchenne muscular dystrophy is the most common neuromuscular disease of children (affecting 1 boy in 3500-5000 births). It is caused by a genetic defect in the DMD gene residing on the X chromosome, which results in the absence of the dystrophin protein essential to the proper functioning of muscles.

The treatment being developed by researchers at Atlantic Gene Therapies, Gnthon and the Institute of Myology, is based on the use of an AAV vector (Adeno Associated Virus) carrying a transgene for the skipping of a specific exon which allows functional dystrophin production in the muscle of the patient.

Safety, efficacy and stability of the treatment in dogs

In GRMD (Golden Retriever Muscular Dystrophy) dogs the treatment aimed at skipping exons 6, 7 and 8 of the dystrophin gene. The product was given by loco-regional administration in the forelegs of 18 dogs who were followed for 3.5 months after injection. It was well tolerated by all treated dogs; no immune response against the synthesized dystrophin was observed. Exon skipping resulted in high levels of expression of dystrophin in the treated muscles. The results of this treatment also indicate that, once injected into the muscle tissue a prolonged and stable effect is produced over the observation time of the study and, unlike antisense oligonucleotides already used clinically for exon skipping, it does not need to be re- administered regularly. The synthesis of "new" dystrophin is dependent on the dose of vector injected: the higher the dose, the greater the exon skipping is effective. Muscle strength also increases with dose. 80% of muscle fibers expressed the "new" dystrophin at the highest dose. This is a very encouraging result because a minimum of 40% of dystrophin in muscle fibers is believed to be necessary for the muscle force to be significantly improved.

A phase I/II clinical trial phase

These results open the way for a phase I / II clinical trial by loco-regional administration in the upper limb of non-ambulatory Duchenne muscular dystrophy patients which are amenable to treatment by the specific skipping of exon 53. The regulatory toxicology and biodistribution studies have just ended and the filing of an application with regulatory authorities is planned for 2015.

###

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Effectiveness of innovative gene therapy treatment demonstrated in canine model of DMD

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update

Linda Carroll TODAY contributor

5 hours ago

The parents of Eliza ONeill, the little girl with an incurable and deadly brain disorder, are making one final desperate push to raise funds for the clinical trial that will test a gene therapy for the diseaseand perhaps offer hope for Eliza.

Courtesy of Glenn ONeill

The ONeills have already raised $1.3 million through a viral video and hope that by Elizas fifth birthday on Sunday theyll hit their $1.8 million goal.

While there is no guarantee that Eliza will be among those chosen to participate in the trial, which could start sometime in the middle of 2015, its organizers say that at this point there is no reason that she wouldnt qualify.

Over the past year, the ONeills have tried to focus on aspects of life over which they have some control, such as helping to make the trial a reality and keeping their daughter as healthy as possible. Sometimes, they even allow themselves to think about what life might be like if Eliza was helped by the experimental medication.

Our hopes are for Eliza to have a life, and a good life, said her dad, Glenn ONeill. I sometimes let my mind go to places of future birthdays and her dating and getting married.

Stacey Quattlebaum

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A birthday wish: 'Saving Eliza' gets final push for medical trial

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Capt Robert #39;s Recovery
After Spinal Cord Injury, you don #39;t have to accept your "generic" prognosis that you will likely never walk again. You can stay as healthy as possible through activity based therapy programs....

By: Sheila Tramontana

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Capt Robert's Recovery - Video

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Run In The Dark - Dublin 2014
Unbroken by blindness in 1998, Mark Pollock suffered a catastrophic spinal cord injury in 2010 that left him paralysed. As Mark strives to walk again, his most complex journey is ahead of him - to fin.

By: Silesian Sailor

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Run In The Dark - Dublin 2014 - Video

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Innovation (Re)Generation: Exploring Regenerative Medicine
Over recent years, considerable interest has been developing in regard to therapies that have become and may become available based on what is known as #39;regenerative medicine #39; (RM). Currently,...

By: Mason Institute

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Innovation (Re)Generation: Exploring Regenerative Medicine - Video

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Science Documentary: Stem Cells,Regenerative Medicine,Artificial Heart,a future medicine documentary
Science Documentary: Stem Cells,Regenerative Medicine,Artificial Heart,a future medicine documentary In each and every one of our organs and tissue, we have ...

By: ScienceRound

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Science Documentary: Stem Cells,Regenerative Medicine,Artificial Heart,a future medicine documentary - Video

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Kids get arthritis
http://www.anthonynolan.org/8-ways-you-could-save-life/donate-your-stem-cells/apply-join-our-register for people who might want to join the register to help adults and children like Alex.

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Kids get arthritis - Video

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By C. Rajan, contributing writer

Researchers at Lund University in Sweden have made a major breakthrough in Parkinson's disease treatment by developing stem cell-derived brain cells that can replace the cells lost due to the disease, thus paving the way for the first stem cell transplant treatment for Parkinsons patients.

Parkinson's disease, which affects about 10 million people worldwide, is a degenerative nervous system condition which causes tremors, muscle weakness, stiffness, and loss in mobility. Parkinson's is caused by loss of dopamine-producing neurons in the brain. Dopamine is an essential neurotransmitter that is required for regulating movement and emotions.

In this study, for the first time ever, the researchers were able to convert human embryonic stem cells into dopamine producing neurons, which behaved like native dopamine cells lost in the disease.

The study was led by Malin Parmar, associate professor in Lund's Department of Medicine, and conducted at both Lund University and at MIRCen in Paris as part of the EU networks NeuroStemCell and NeuroStemcellRepair.

According to Medical News Today, the researchers produced rat models of Parkinson's disease by destroying the dopamine cells in one part of the rat's brain, and then they transplanted the new dopamine producing stem cell neurons. These next generation dopamine neurons were found to survive long term, restore the lost dopamine, and form long distance connections to the correct parts of the brain when transplanted into rats. Most excitingly, these transplanted stem cells reversed the damage from the disease.

As the new dopamine neurons have the same properties and functions of native cells lost in Parkinson's disease and can be produced in unlimited quantities from stem cell lines, this treatment shows promise in moving into clinical applications as stem cell transplants for Parkinsons.

"This study shows that we can now produce fully functioning dopamine neurons from stem cells. These cells have the same ability as the brains normal dopamine cells to not only reach but also to connect to their target area over longer distances. This has been our goal for some time, and the next step is to produce the same cells under the necessary regulations for human use. Our hope is that they are ready for clinical studies in about three years", says Malin Parmar.

Human embryonic stem cells (ESC) are powerful treatment options due to their ability to change into any cell type in the body. However, it is difficult to get them to change into the desired cell types, and research efforts are also hampered due to the ethical concerns associated with embryonic stem cells.

The study is published in the journal,Cell Stem Cell, titled Human ESC-Derived Dopamine Neurons Show Similar Preclinical Efficacy and Potency to Fetal Neurons when Grafted in a Rat Model of Parkinsons Disease.

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Researchers Discover Breakthrough Stem Cell Treatment For Parkinson's Disease

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