Spark Therapeutics, which is developing gene therapy treatments for retinal dystrophies and hematologic disorders, announced terms for its IPO on Tuesday. The Philadelphia, PA-based company plans to raise $88 million by offering 5.5 million shares at a price range of $15 to $17. At the midpoint of the proposed range, Spark Therapeutics would command a fully diluted market value of $378 million.

Spark Therapeutics, which was founded in 2013, plans to list on the NASDAQ under the symbol ONCE. J.P. Morgan and Credit Suisse are the joint bookrunners on the deal. It is expected to price during the week of January 26, 2015.

Investment Disclosure: The information and opinions expressed herein were prepared by Renaissance Capital's research analysts and do not constitute an offer to buy or sell any security. Renaissance Capital, the Renaissance IPO ETF (symbol: IPO) or the Global IPO Fund (symbol: IPOSX) , may have investments in securities of companies mentioned.

The views and opinions expressed herein are the views and opinions of the author and do not necessarily reflect those of The NASDAQ OMX Group, Inc.

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Gene therapy biotech Spark Therapeutics sets terms for $88 million IPO

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Newswise PHILADELPHIA The University of Pennsylvania has announced an expanded relationship with Spark Therapeutics, a late-stage gene therapy company developing treatments for debilitating, genetic diseases. As part of the expanded relationship, which included both an exclusive license agreement to certain Penn-owned intellectual property rights and a clinical trial agreement, Penn will be one of the clinical sites for a clinical trial to evaluate the treatment of a rare genetic form of progressive blindness.

This expanded strategic relationship between the two organizations is representative of Penns strong commitment towards direct engagement with the private sector to advance promising technologies, said John Swartley, Associate Vice Provost for Research and Executive Director, Penn Center for Innovation (PCI). When Penn researchers on the cutting edge of their fields are able to partner effectively with innovators in the private sector it has the potential to accelerate the advancement of exciting new approaches for the treatment of disease. PCI serves as the University of Pennsylvanias commercialization center and actively works with the private sector to foster research and development collaborations leveraging Penn technology and research.

Spark today announced the start of Phase 1/2 clinical trial for patients with choroideremia (CHM), which will take place at The Childrens Hospital of Philadelphia and the University of Pennsylvania. CHM is a rare, genetic eye disorder that causes progressive vision loss, ultimately leading to complete blindness. CHM is characterized by deletions or mutations in the CHM gene. It is a degenerative eye disease which affects males that manifests in childhood as night blindness and a reduction in visual field, followed by progressive constriction of visual fields leading, ultimately, to blindness. There is currently no approved drug treatment for the disease.

The launch of this clinical trial is the latest facet of the ongoing partnership between Spark and Penn.Expanding upon an earlier collaboration around SPK-RPE65, in December of 2014, Spark and Penn, through PCI, entered into an exclusive license agreement to certain Penn-owned intellectual property rights, including assets related to the choroideremia program. As a part of the license agreement, Penn received equity shares in Spark and may receive additional milestone payments and royalties on net sales dependent on the success of the SPK-CHM program.

The new trial is designed to assess the safety and preliminary efficacy of sub-retinal administration of SPK-CHM. The investigators plan to enroll up to 10 patients afflicted with the CHM genetic mutation. In addition to evaluating safety, the trial will help define the dose required to achieve stable or improved visual function and identify appropriate endpoints for subsequent clinical trials. The trial will build on the work of the clinical trial teams that have conducted trials of Sparks therapy known as SPK-RPE65, which has been observed in clinical trials to improve vision in patients with rare blinding conditions due to mutations in the RPE65 gene.

I have a particular interest in choroideremia, says Jean Bennett, MD, PhD, the F.M. Kirby Professor of Ophthalmology and director of the Center for Retinal and Ocular Therapy (CAROT) at the Perelman School of Medicine at the University of Pennsylvania, and one of Sparks scientific co-founders. I am thrilled to now be able to test our gene therapy treatments with the potential to help the many men living with this disorder.

"Editors note: The University of Pennsylvania has licensed technology involved in this research to Spark. Dr. Bennett is an inventor of this technology, and may benefit financially."

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Stem Cell Therapy | Recent Strides Quell Stem Cell Debate
Ethical concerns for stem cells for arthritis could be mute...maybe. Reports show that adult stem cells (Autologous) have been shown in recent studies to have significant effects on osteoarthritis...

By: Nathan Wei

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Published: January 19, 2015

Sharon Nordstrom feels ashamed for participating in a $38,000 multiple sclerosis stem cell treatment inIndia that was not all it was promoted to be. Submitted photo.

JONATHAN CHARLTON THE STARPHOENIX

Sharon Nordstrom feels ashamed for participating in a $38,000 multiple sclerosis stem cell treatment inIndia that was not all it was promoted to be.

Im going to be a real mouthpiece now for people who think theyre toosmartto fall for stuff like this, she said.

The WinnipegFreePress this week published aninvestigationinto Winnipeg-based Regenetek Research, finding that head researcher Doug Broeska fabricated his credentials, including his PhD, and overstated the effects of the stem-cell treatment.

The newspaper also discovered that the chairman of the medical ethics committee at the Inamdar Hospital in Pune,India, told Broeska his lack of credentials and followup violatedinternational ethical standards and ordered him to step down as principal investigator of the stem-cell study.

Broeska told theFreePress he was terminated only because it was decided to have a local principal investigator stationed inIndia.

TheFreePress further reported that the University of Winnipeg has cancelled a joint stem-cell treatment project involving Broeskas company.

Nordstrom says she last heard from Broeska on June 16, when he said in an email he would expel her from the trial after she questioned the absence of a followup care plan. For months, she kept her situation quiet.

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Saskatoon woman snared in alleged fraudulent MS trial held in India

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(MENAFN - The Peninsula) Japanese scientists say they are on their way to being able to create custom-made skin, bone and joints using a 3D printer.

Several groups of researchers around the world have developed small masses of tissue for implants, but now they are looking to take the next step and make them functional.

Tsuyoshi Takato, a professor at the University of Tokyo Hospital, said his team had been working to create "a next-generation bio 3D printer", which would build up thin layers of biomaterials to form custom-made parts.

His team combines stem cells - the proto-cells that are able to develop into any body part - and proteins that trigger growth, as well as synthetic substance similar to human collagen.

Using a 3D printer, they are working on "mimicking the structure of organs" - such as the hard surface and spongy inside for bones, Takato said.

In just a few hours, the printer crafts an implant using data from a Computer Tomography (CT) scan. These implants can fit neatly into place in the body, and can quickly become assimilated by real tissue and other organs in the patient, the plastic surgeon said.

"We usually take cartilage or bone from the patient's own body (for regular implants), but these custom-made implants will mean not having to remove source material," Takato said.

The technology could also offer hope for children born with bone or cartilage problems, for whom regular synthetic implants are no good because of the rate of their body's growth. The main hurdle was the heat generated by conventional 3D printers, which damages living cells and protein.

"We haven't fully worked out how to avoid heat denaturation but we already have some models and are exploring which offers the most efficient method," he said.

The artificial protein Takato and his team use was developed by Fujifilm, which has been studying collagen used in photographic films. Since it is modelled on human collagen and does not derive from animals, it can be easily assimilated in human bodies, reducing the risk of infections such as mad-cow disease.

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Characterization of mdx-iPS with DYS-HAC. (a) Morphology of mdx-MEF, mdx-iPS, and mdx-iPS (DYS-HAC) cells. Phase-contrast (left panel) and GFP-fluorescence (right panel) micrographs are shown. (b) Genomic PCR analyses for detecting DYS-HAC in mdx-iPS cells. (c) FISH analyses for mdx-iPS (DYS-HAC) cells. An arrow indicates the DYS-HAC and the inset shows an enlarged image of the DYS-HAC. (d) RT-PCR analyses of ES cellmarker genes, four exogenous transcription factors, and human dystrophin. EGFP and Nat1 were used as internal controls. Primers for DYS 6L/6R, 7L/7R, and 8L/8R detected the isoform of dystrophin expressed in ES and iPS cells. (e) Immunohistochemical analyses of dystrophin in muscle-like tissues of each teratoma. Immunodetection of mouse and human dystrophin (left panel), immunodetection of human-specific dystrophin (middle panel), and GFP micrography (right panel) are shown. The insets show enlarged images of immunohistochemistry. Nanog-iPS- and mdx-iPS-derived teratomas were used as positive and negative controls, respectively. CHO, Chinese hamster ovary; EGFP, enhanced green fluorescent protein; GFP, green fluorescent protein; HAC, human artificial chromosome; iPS, induced pluripotent stem cells; MEF, mouse embryonic fibroblast.

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Complete genetic correction of ips cells from Duchenne ...

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In a big step towards understanding the effects of a rare genetic disease, research by scientists at the RIKEN-Max Planck Joint Research Center in Japan implicates the enzyme ENGase as the factor responsible for deficient protein degradation that occurs in the absence of mouse Ngly1 gene expression.

Recently, a grassroots effort initiated by families and clinicians led to the discovery of a human genetic disorder with severe consequences that is linked to a mutation in the human NGLY1 gene. In a big step towards understanding the effects of this mutation, research by scientists at the RIKEN-Max Planck Joint Research Center in Japan implicates the enzyme ENGase as the factor responsible for deficient protein degradation that occurs in the absence of mouse Ngly1 gene expression. Published in Proceedings of the National Academy of Science, the paper details how lack of the Ngly1 protein results in the incomplete removal of the sugar portion of glycoproteins -- a process called deglycosylation. The result is that proteins that should be broken down in the cytosol are instead aggregated in the cells.

The ability of proteins to function and interact with other molecules properly often depends on their three-dimensional configuration, which can be changed through the addition or subtraction of sugar chains. When proteins are not made correctly, they are sent to be broken down in the cytosol. NGLY1 is a cytosolic enzyme that removes the sugar chains from specific types of glycoproteins, and ENGase is another cytosolic enzyme in animal cells that degrades the free sugars left behind. The big question is whether NGLY1 deficiency affects protein degradation, and if so, how.

The RIKEN researchers tackled this problem by first creating a model glycoprotein for examining this process in animal cells. Next, they expressed the model protein in cells derived from four types of mice -- wild-type, Ngly1 knockout, Engase knockout, and double knockout -- and measured how much of the model protein was degraded and how much of the undegraded portion still had attached sugar chains.

As expected, they found sugar chains were not removed from the model protein in the double knockout cells because they lacked both of the deglycosylation enzymes. Interestingly, Ngly1 knockout cells contained a normal proportion of de-sugared model protein. This indicated that ENGase might be responsible for the deglycosylation that occurred in the Ngly1 knockout cells.

Next, they inhibited protein synthesis in these four types of cells and found that normal protein degradation -- both sugared and de-sugared -- proceeded in the wild-type, Engase knockout, and double knockout cells. Critically, the amount of de-sugared protein remained high and undegraded in the Ngly1 knockout cells.

This indicated two key points. First, removal of sugar chains by ENGase appeared to have created a form of the protein that, in the absence of Ngly1 could not be degraded properly. To confirm this hypothesis, they used mass spectrometry and showed that when the model protein was de-sugared by ENGase, one sugar molecule remained attached to the protein. Second, normal protein degradation in the double knockout indicates that deglycosylation of the model protein by Ngly1 was not necessary as long as the incomplete removal of sugars by ENGase was prevented.

People with the NGLY1 mutation have many severe symptoms, from delayed development and epilepsy to abnormal liver function and the inability to make tears. The leader of the research effort, Tadashi Suzuki, notes that while "it is currently unclear how these symptoms correlate with reduced protein degradation caused by insoluble aggregates, if the abnormal aggregation of this type of glycoprotein is somehow related to them, it is tempting to speculate that inhibition of ENGase activity may serve as a therapeutic target for patients carrying mutations in the NGLY1 gene." He adds that as a proud advocate of curiosity-driven scientific research and the importance of glycoproteins in everyone's life, "I'm happy that there are still so many outstanding questions in my field that need to be explored."

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The above story is based on materials provided by RIKEN. Note: Materials may be edited for content and length.

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Insights into a rare genetic disease

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The research group led by Professor Magnus Andersson at University of Helsinki has discovered a new inherited disease that causes ptosis, retarded growth, intellectual disability and mortality in Ayrshire calves. The disease proved to be associated with a mutation in UBE3B gene. Of the 129 tested Ayrshire AI bulls recently used in Finland, 17% carried the mutation. Moreover, UBE3B mutation may be connected to AH1 haplotype, which is associated with reduced fertility and has a carrier frequency of 26.1% in the North American Ayrshire population. The study was published in BMC Genomics journal on 12 October 2014.

An inherited disease that causes serious developmental disorder in Ayrshire breed has been studied at the Department of Production Animal Medicine, University of Helsinki. The phenotype has been defined as PIRM syndrome according to its typical features: ptosis, intellectual disability, retarded growth and mortality. The most easily noticeable symptom of affected calves is the ptosis. The exceptionally large upper eye lid gives a characteristic sleepy appearance of the affected animals. Some affected calves also suffered from feeding problems, minor structural changes of the head and muscular hypotonia. The disease is recessively inherited i.e. affected animals have inherited the mutation from both parents

Heredity research traced the disease to a mutation in UBE3B gene, which partially prevents the normal expression of the gene. Mutation screening of the 129 Ayrshire AI bulls that are in use or have recently been used in Finland indicated a high carrier frequency of 17.1%. "The results of this study can be utilized in bovine breeding programs. With the successful prevention of PIRM syndrome the animal welfare can be increased and at the same time the financial losses for farmers and breeding companies can be reduced" says PhD student Heli Venhoranta.

In humans, mutations in UBE3B gene are associated with Kaufman oculocerebrofacial syndrome with similar pathological findings as in PIRM syndrome. Furthermore, mice engineered to lack UBE3B expression were reported having increased lethality.

The mutation in UBE3B gene might be connected to the recently discovered Ayrshire haplotype 1 (AH1). The haplotype encompasses the mutation in UBE3B gene and of those tested 129 AI bulls, 29 had a known haplotype status for AH1. AH1 haplotype is associated with reduced fertility which could imply embryonic losses that agree with the findings of UBE3B deficiency in mice. The AH1 haplotype was perfectly associated with the UBE3B mutation in this study cohort. The estimated frequency of the AH1 haplotype was 26% in the North America Ayrshire herd. "The relationship between PIRM syndrome and AH1 haplotype needs to be clarified but our study does however provide an avenue for further investigation" concludes Venhoranta.

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The above story is based on materials provided by Helsingin yliopisto (University of Helsinki). Note: Materials may be edited for content and length.

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20.01.2015 - (idw) Universittsklinikum Heidelberg

A gene that influences the communication between nerve cells has a higher mutation rate in schizophrenia patients than in healthy individuals / Previously unknown gene mutations show a functional effect in nerve cells / Parallels between genetic alterations in patients with schizophrenia and autism / Scientists from Heidelberg publish in Molecular Psychiatry Researchers from Heidelberg University Hospital have identified 10 previously unknown genetic alterations (mutations) in schizophrenia patients. The affected gene defines the blueprint for a scaffolding protein, the SHANK2 protein, which plays a determinant role in the structures connecting nerve cells (neurons). These 10 gene variants represent risk factors for schizophrenia, said Prof. Dr. Gudrun Rappold, head of the Department of Molecular Human Genetics at Heidelberg University Hospital and senior author of the article. The alterations have only been found in schizophrenia patients and are not in any healthy individuals. Mutations that are not found in healthy people could have a direct effect on the disease says Dr. Slavil Peykov, researcher and first author of the study. The results have recently been published in the renowned scientific journal Molecular Psychiatry.

The protein SHANK2 is already known to Professor Rappolds research department from another standpoint: in 2010, they identified several alterations in the SHANK2 gene in patients with autism disorders and intellectual disability. The recently identified mutations in schizophrenia patients reside in the same gene but their positions, and thus their detrimental effect, differ from those previously found in autism. Modifications in one gene can lead to very diverse neurobiological disorders, such as autism, intellectual disability or schizophrenia. Apparently the exact nature and position of the alteration influences the resulting neuropsychiatric disease and the gravity of the symptoms explains Prof. Rappold. In the study, experiments with neurons revealed that these mutations alter the connections between neurons (synapses) to varying degrees, in such a way that the communication between these cells is affected.

One percent of the worlds population suffers from schizophrenia

Worldwide, approximately 1% of the population is afflicted with schizophrenia. The disease most commonly develops in early adulthood. The affected patients can rarely lead normal, independent lives without treatment, ranging from needing help with everyday tasks to a complete loss of social and professional functioning. Schizophrenia is classified as a disorder of perception; typical symptoms are delusions and hallucinations, though symptoms and their severity vary from patient to patient. These individuals are also more likely to suffer from other disorders than the general population, such as speech deficits, addiction and depression. The exact causes and triggers of schizophrenia remain to date unknown.

In the most recently published study, the SHANK2 gene was investigated in DNA from 481 affected patients and 659 healthy controls, in collaboration with Professor Marcella Rietschel, Department of Genetic Epidemiology, Central Institute of Mental Health in Mannheim and Professor Markus Noethen, Institute of Human Genetics at the University of Bonn. Approximately twice as many genetic alterations were found in patients with schizophrenia compared to people with no psychiatric disorders. The onset of disease is likely prompted only when further factors are also present, for example, certain environmental risk factors, explains human geneticist Prof. Rappold.

Early diagnosis is paramount to a satisfactory quality of life for the patient; the earlier a patient is treated, both pharmacologically and socially, the less likely they are to relapse and develop further disorders. Therefore, our understanding of the genetic causes of this disorder could, in the future, help doctors distinguish individual patient groups suffering from similar disease courses, and consequently individualize treatment options explains Prof. Rappold. If scientists could find exactly which molecules in which molecular networks are faulty in the brain, precise therapies for that particular disease progression could be developed. For example, in the aforementioned 481 schizophrenia patients, 4 non-related patients were found to have an identical SHANK2 mutation. All four patients developed schizophrenia at similar time points and with similar symptoms. If one mutation could lead to a similar set of symptoms and one treatment could correct the consequences of that mutation, the genetic screening for this mutation in potential candidates could very much improve their treatment plan. The close relationship between geneticists, neurobiologists and clinicians should now lead to a better diagnosis and to the identification of knowledge based treatments.

Contact for journalists: Professor Dr. rer. nat. Gudrun A. Rappold Abteilung Molekulare Humangenetik Institut fr Humangenetik Universittsklinikum Heidelberg Tel.: 06221 / 56 50 59 E-Mail: Gudrun.Rappold@med.uni-heidelberg.de

Heidelberg University Hospital and Medical Faculty: Internationally recognized patient care, research, and teaching

Heidelberg University Hospital is one of the largest and most prestigious medical centers in Germany. The Medical Faculty of Heidelberg University belongs to the internationally most renowned biomedical research institutions in Europe. Both institutions have the common goal of developing new therapies and implementing them rapidly for patients. With about 12,600 employees, training and qualification is an important issue. Every year, around 66,000 patients are treated on a fully or partially inpatient basis and over 1,000,000 patients have been treated on an outpatient basis in more than 50 clinics and departments with 1,900 beds. Currently, about 3,500 future physicians are studying in Heidelberg; the reform Heidelberg Curriculum Medicinale (HeiCuMed) is one of the top medical training programs in Germany. Weitere Informationen:http://www.klinikum.uni-heidelberg.de/Abt-Molekulare-Humangenetik.6096.0.html Department of Molecular Human Genetics

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Schizophrenia: genetic alterations linked to functional changes in nerve cells

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OMD Genetic Engineering - Saturday Superstore
Here we have a very old and rare clip of Orchestral Manoeuvres in the Dark on the Saturday Superstore and they are doing Genetic Engineering.

By: Neil Taylor

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OMD Genetic Engineering - Saturday Superstore - Video

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22 hours ago by Vicky Just The technique can edit DNA at the point of fertilisation, speeding up the process of genetic research

Scientists from our Department of Biology & Biochemistry have developed a new technique that will streamline biomedical research and could in the future prevent genetic diseases before the moment of conception.

In a study published in the Nature Group journal Scientific Reports, the scientists used 'molecular scissors' that can edit the DNA of either the egg or sperm of mice during fertilisation.

The researchers used the enzyme Cas9 to cut a precise point in the genome, enabling them accurately to inactivate a specific gene. This allows scientists to study specified gene function in mice by creating a 'knock-out' in closer to one month rather than the six required using conventional techniques.

This powerful tool should accelerate biomedical research and promises to reduce the number of animals used in experiments to answer fundamental medical questions.

Dr Tony Perry, the study's senior author at the University's Laboratory of Mammalian Molecular Embryology, explained: "We're really excited about this research. Previously, this technique had been demonstrated with established embryos but we've shown that we can accurately edit genes in the sperm or egg around the time of fertilisation, just as the embryo is starting to develop.

"Cas9 works by cutting the DNA at a precise point in the genome. The cell repairs this cut but chews the frayed ends before rejoining them, destroying the function of the gene.

"The technique has many exciting potential applications. It could help to provide disease resistance to livestock or perhaps provide a method for preventing serious genetic conditions in humans at the point of conception - for example by allowing carriers of life-threatening genetic conditions such as cystic fibrosis to conceive healthy babies without the risk of passing on the disease."

Researchers anticipate that the method could also be used to enable the transplant of organs of some large animals into humans without the problem of rejection, by making the organs immunologically invisible.

Dr Perry added: "This is a dream for transplant surgeons and patients awaiting immunologically matched organs. It means that one day it may be possible to transplant these engineered organs - even if only until a suitable human one is found - and save lives."

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'Molecular scissors' could prevent genetic diseases before conception

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Annunaki, Elohim and Human Genetics: Basis, Bias, or BS? Please Share!
This video covers the HARD SCIENCE behind the properties observed in DNA and various aspects of the Origins of Life. We will cover various concepts of geneti...

By: Cullen Smith Lifting The Veil

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Annunaki, Elohim and Human Genetics: Basis, Bias, or BS? Please Share! - Video

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Update: psygen genetics
Ak47 x covelo sour diesel got one male hope the other is a female.

By: (RMC)rockymountaincultivators

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Update: psygen genetics - Video

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Perfect Genetics - C-A-S Option 3
Correction she is the 3rd choice - the 4th and final choice will be out soon* Leaving a like on this video really helps guys, thanks Leave a comment below...

By: xSimSugar

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Perfect Genetics - C-A-S Option 3 - Video

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Gene Therapy: Hope For The Blind?
In medicine, doctors often talk about treatments, but rarely about cures. Now, gene therapy is offering the potential to actually cure certain diseases and an experimental breakthrough could...

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Gene Therapy: Hope For The Blind? - Video

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UAMS -- We AR the People
At UAMS, we AR dedicated to your health from the start, specializing in you with personalized medicine. We are shaping the future with promising new breakthroughs, focused on treatments you...

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UAMS -- We AR the People - Video

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#DoefStrong
The 67 #39;s held a ceremony in honour of Neil Doef, a Smiths Falls Bears player who suffered a serious spinal cord injury. Doef #39;s teammates and family were on hand to participate in the pre-game...

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#DoefStrong - Video

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NAMS Symposium on Personalized Medicine- Dr J N Pande
Dr J N Pande delivered key note address on Personalized Medicine at the 54th Annual Conference of National Academy of Medical Sciences (India) held at AIIMS,...

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Selfless strangers who donate their stem cells are like gold-dust, according to a young husband fighting to find a bone marrow match.

Father of two Jaso Manokaran, fell ill last October, experiencing severe pain in his bones and a fever-like temperature.

After being rushed to A&E again and again, doctors ordered a bone biopsy which revealed the 29-year-old had Acute Lymphoblastic Leukaemia.

He said: I thought it was a viral infection, I didnt expect it to be cancer at all. When my consultant said I had leukaemia, I was crying like a river. I couldnt really hear what he was saying, I was so worried.

While undergoing chemotherapy, Jaso was told that he needed a bone marrow transplant but he has no siblings who could be a match and is a Sri Lankan Tamil, which means he has a 20.5 per cent chance of finding a match on the Anthony Nolan bone marrow register.

He added: It felt like a double dose of bad news. I had no idea what a transplant was, I had so many questions: How will I get it? Where will I get it? How will I find a match? I was so worried.

Now its not in my hands, I cant run around and get it myself - I need a stranger to save my life. Anyone who signs up to the register is priceless, not only to me but to everyone waiting for a transplant. These people are so selfless and special, theyre like gold-dust.

Wife Jasmini has now decided to kick start the Help Save Jaso campaign in order to recruit more people to the register - especially people from Tamil and Sri Lankan communities in the hope of finding a match for her husband.

She said: Its been a scary time for all of us but I was so inspired to get going for Jaso. I have found that many people from my community dont know how to sign up to the register and many myths around donating have come up.

Some people think its a big operation or involves lengthy surgery because of the word bone but this is not true - now the process is usually just like giving blood.

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Young Dad searching for gold-dust' bone marrow match

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Shin splints/muscle atrophy three months after stem cell therapy by Harry Adelson, N.D.
Angela is a life-long triathlete. Ten years ago she developed severe shin splints in her left leg that resulted in atrophy of her lower leg muscles. Here, sh...

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Shin splints/muscle atrophy three months after stem cell therapy by Harry Adelson, N.D. - Video

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Pet Stems Cell Therapy for Pets Prolong the life of your pet
http://petstems.com Pet Stems is cutting edge orally administered cell therapy designed for pets. No other company in the world offers this kind of nutritional cell therapy for pets. We love...

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Overview of Stem Cell Therapy at New Jersey Pain Management Clinics
http://nj-pain.com/treatments/stem-cell-procedure/ Stem Cell Therapy falls under regenerative medicine, and it is now a reality in musculoskeletal medicine. This includes stem cells being...

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A Winnipeg-based company that has touted its ability to improve the lives of Multiple Sclerosis patients through stem cell therapy is now under the microscope after allegations of fraud from a client.

The CEO of Regenetek Research Inc. has been collecting thousands of dollars from Canadian patients looking for help. Some of the patients are now questioning the research and credentials of the man they know as Dr. Doug.

One of them is Lee Chuckry, 47. He has been living with MS for nearly two decades.

MS just keeps progressing, thats what it does. Hopefully I could stop it. That was my ultimate goal, Chuckry said in an interview with CTV News.

His efforts led him to Regenetek, and its CEO: Doug Broeska.

In testimonials, MS patients attributed miraculous medical improvement to experimental stem cell therapy. For $35,000, Regenetek patients were flown to India for the procedure.

Chuckry was one of the participants. But when he returned home, he says his symptoms worsened.

When he started digging deeper, he said, he found the doctor hed put his faith in wasnt what he claimed to be.

Im going to call Doug a con artist, Chuckry said. You are preying on people who are desperate. They are looking for hope of any sort.

Chuckry and at least one other patient have gone to the RCMP. They allege Broeska, who claims to hold a PhD and a Bachelor of Science, is a fraud who is operating as a medical researcher without proper credentials.

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Winnipeg company offering stem cell therapy is fraudulent, MS sufferer alleges

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Volume 9, Issue 2 Summary

In patients with type 1 diabetes, pancreatic beta cells self-destruct, leaving the body bereft of insulin. Yasuhiro Ikeda, D.V.M., Ph.D., is working to create a customizable gene and stem cell therapy system that will arrest the loss of these beta cells possibly permanently eliminating the need for insulin injections.

Yasuhiro Ikeda, D.V.M., Ph.D., is spearheading stem cell research in the Mayo Clinic Center for Regenerative Medicine.

Nearly everyone knows someone with diabetes it's hard not to. In the United States, 1 in 3 adults and 1 in 6 children have high blood sugar, according to the National Institutes of Health.

After you eat, glucose is absorbed into your bloodstream and carried throughout your body. Insulin a hormone made by beta cells in your pancreas then signals your cells to take up glucose, helping your body turn the food into energy.

With diabetes, this process can go wrong in two basic ways:Type 1 diabetes results from the body's failure to produce insulin;type 2 diabetes occurs when there's plenty of insulin but the cells lose their ability to perceive its signal. In both cases, cells starve.

Living well with diabetes requires a lifelong commitment to monitoring blood sugar, eating properly, exercising regularly and maintaining a healthy weight. People with type 1 diabetes must also rely on insulin replacement therapy, usually through insulin injections. People with type 2 diabetes might need oral medication.

Still, every year, diabetes kills about 70,000 people in the United States and is a contributing cause in another 160,000 deaths each year, according to the Centers for Disease Control and Prevention.

Yasuhiro Ikeda, D.V.M., Ph.D., a molecular biologist at Mayo Clinic in Rochester, Minn., wants to change that.

After beginning his career as a veterinary feline specialist, Dr. Ikeda had to change course when he developed an allergy to his four-legged patients that made it impossible to be in a room with them. He turned his attention toward research and discovered that his interest in molecular virology had human as well as feline applications.

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Gene therapy and regenerative medicine lend hope to ...

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A world authority on the brains natural ability to form new neuronal connections will speak at New Zealands first Neuroplasticity Symposium in Auckland soon.

The symposium, at the University of Aucklands Grafton campus on Wednesday 4 February, will feature Emeritus Professor Michael Merzenich from the University of California, the leading pioneer in brain plasticity research.

Keynote speakers include Professor Tony Hannan, an expert on gene-environment interactions and experience dependent plasticity, from the University of Melbourne; and leading neuroplasticity researchers from the University of Aucklands Centre for Brain Research (CBR), including Melanie Cheung, Greg Finucane, Johanna Montgomery, Cathie Stinear, and Karen Waldie. (The CBR is sponsoring the symposium).

The speakers will present the most recent developments on how neuroplasticity can be harnessed in novel and imaginative treatments for brain diseases, environmental enrichment for brain plasticity, the science behind neuroplasticity, and the clinical applications of these treatments.

The day will conclude with a panel discussion on neuroplasticity.

Professor Merzenichs visit to New Zealand includes a public lecture at the University of Aucklands Grafton campus on Tuesday 3 February (from 5.30pm to 7pm), titled "Brain Plasticity based therapeutics".

He will also talk to audiologists on the clinical applications of auditory plasticity, particularly in relation to auditory rehabilitation.

Professor Merzenich is a leading pioneer in brain plasticity research who led a research team that conducted extensive, original research that is the basis for the development and application of multiple-channel cochlear implants.

More recently he has dedicated his time to delivering brain plasticity-based training programmes from bench to bedside at minimal cost. Using these therapies, he and his team have helped more than five million children overcome their learning disabilities.

In 2002 he co-founded Posit Science, which produces and delivers computer-based programmes to help aging, psychiatrically impaired, and brain-injured populations. He has published more than 150 articles in leading peer-reviewed journals (including both Science and Nature), been granted nearly 100 patents for his work, and received numerous awards and prizes such as the Russ Prize, Ipsen Prize, Zlch Prize, Thomas Alva Edison Patent Award and the Purkinje Medal.

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Brain plasticity symposium for Auckland

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