MEDevice Keynote: The Future of Personalized Medicine
Advances in device technology that are influencing personalized medicine Preparing for the impact of the pharmacogenomics revolution How will the availability of customized therapies...

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MEDevice Keynote: The Future of Personalized Medicine - Video

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The Postal Service- "Sleeping In"
Uploading a song a day for 30 days in September, raising money for the 2nd annual online fundraising event "Sing for Spinal Cord Injury". View all videos: http://www.facebook.com/singforspinalinj...

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The Postal Service- "Sleeping In" - Video

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"Cell Therapy" J. Dunja (Official Video)
Single from the debut album "Higher" Produced by C.J. Mitchel (Flawless Tracks) Mixed and Mastered at Grindhouze Studios Video Directed by Sargas Media.

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"Cell Therapy" J. Dunja (Official Video) - Video

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Stem Cell Therapy for Osteoarthritis
Ross Hauser, MD explains Stem Cell Prolotherapy using whole bone marrow. If you have osteoarthritis and are interested in how stem cell therapy may help you, we would love to see you in one...

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Stem Cell Therapy for Osteoarthritis - Video

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Spinal cord injury - Case Study- Stem cell therapy- Giostar
a brief introduction to Giostar and its Stem cell therapy Dr.Divyang Patel (MD) a spine surgeon at Giostar- INDIA, briefs about a case of cervical spine injury, which is also examined by a...

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United Therapeutics Advances to Second Cohort in Phase I Trial of PSTI #39;s PLX-PAD Cells
HAIFA, Israel, Sept. 8, 2014 (GLOBE NEWSWIRE) -- Pluristem Therapeutics Inc. (PSTI) (TASE:PLTR), a leading developer of placenta-based cell therapy products, announced today that its licensee,...

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United Therapeutics Advances to Second Cohort in Phase I Trial of PSTI's PLX-PAD Cells - Video

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Stacey Burling, Inquirer Staff Writer Posted: Sunday, September 14, 2014, 3:51 AM

It's getting harder to find the line between science and science fiction.

One of the hot research techniques these days, "optogenetics," uses gene therapy to deliver light-sensitive proteins to specific cells. Then researchers use light to control the cells. The field got its start in the brain, where scientists have demonstrated the technique by making contented mice fly into a rage - a remarkable, if slightly creepy, achievement.

Brian Chow, a University of Pennsylvania bioengineer, has bigger ambitions than that.

He wants to develop optogenetic tools that help scientists unlock the secrets of all kinds of cells by triggering discrete cellular activities on demand, say the expression of a gene or the activation of a protein.

Scientists have never had that kind of control over specific cell functions before. Drugs affect large numbers of different kinds of cells. Electricity can be used in a small region, but not just one cell type. Brain imaging studies have let scientists see which parts of the brain were active during certain activities, but they couldn't tell what role they played.

Optogenetics - the combination of optics and genetics - lets researchers see exactly what specific cells do, and control when they do it.

"It just fundamentally allows us to answer questions we have not been able to answer in the past," Chow said.

"The promise of it is demonstrating causality as opposed to correlation."

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Illuminating technology

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Newswise Kansas City, Mo. - If you never understood what ontogeny recapitulates phylogeny meant in high school, dont worry: biologists no longer think that an animals ontogeny, that is, its embryonic development, replays its entire evolutionary history. Instead, the new way to figure out how animals evolved is to compare regulatory networks that control gene expression patterns, particularly embryonic ones, across species. An elegant study published in the September 14, 2014 advance online issue of Nature from the Stowers Institute for Medical Research shows just how humbling and exhilarating that pursuit can be.

In the study, Investigator and Scientific Director Robb Krumlauf, Ph.D. and colleagues show that the sea lamprey Petromyzon marinus, a survivor of ancient jawless vertebrates, exhibits a pattern of gene expression that is reminiscent of its jawed cousins, who evolved much, much later. Those genes, called Hox genes, function like a molecular ruler, determining where along the anterior-posterior (AP) axis an animal will place a particular feature or appendage. The new study means that that the genetic program used by jawed vertebrates, including fish, mice, and us, was up and running ages before a vertebrate ever possessed a recognizable face.

Hox genes regulate a tissues character or shape, as in head or facial features. Our work in the past has addressed how factors make unique structures, for example, what makes an arm different from a leg, says Krumlauf. Now, we are excited by the common role that similar sets of genes play in creating a basic structural plan.

The team at Stowers, collaborating with Marianne Bronner, Ph.D., professor of biology at Caltech, focused on the sea lamprey because the fossil record shows that its ancestors emerged from Cambrian silt approximately 500 million years ago, 100 million years before jawed fish ever swam onto the scene. The question was, could the hindbrain gene regulatory network that constructs the modern vertebrate head have originated in animals that lack those structures?

To answer it, the researchers created so-called reporter genes from stretches of regulatory DNA flanking a specific Hox gene in zebrafish or mice and linked them to fluorescent tags. When inserted into an experimental animal these types of reporters glow in tissues where the gene is activated, or expressed. The researchers chose this particular battery of Hox reporters because when inserted in embryos of a jawed fish they fluoresce in adjacent rainbow stripes up and down the embryonic hindbrain.

The papers startling finding came when they inserted the very same reporters into lamprey embryos using a technique developed by Hugo Parker, Ph.D., a postdoctoral fellow in the Krumlauf lab and the studys first author: the lamprey embryos displayed the same rainbow pattern of Hox reporters as did jawed fish, in exactly the same order along the AP axis of the hindbrain.

We were surprised to see any reporter expression in lamprey, much less a pattern that resembles the pattern in a mouse or fish, says Parker, who pioneered the lamprey reporter approach as a graduate student at Londons Queen Mary University. That means that the gene regulatory network that governs segmental patterning of the hindbrain likely evolved prior to divergence of jawed vertebrates.

Researchers knew that in mouse and zebrafish short stretches of DNA in one Hox reporter (Hoxb3) formed a landing pad recognized by a DNA-binding protein that flips on the gene. As you would expect, when inserted into zebrafish embryos, reporters mutant in those sequences were inactive (they didnt glow) in the hindbrain. Remarkably, the mutant reporter was inactive in lamprey embryos also, meaning that this control switch has been around for a very long time.

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How an Ancient Vertebrate Uses Familiar Tools to Build a Strange-Looking Head

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The disease starts with a feeling of increased clumsiness. Spilling a cup of coffee. Stumbling on the stairs. Having accidents that are easy to dismisseveryone trips now and then.

But it inevitably gets worse. Known as familial amyloid polyneuropathy, or FAP, it can go misdiagnosed for years as patients lose the ability to walk or perform delicate tasks with their hands. Most patients die within 10 to 15 years of the first symptoms.

There is no cure. The disease is caused by malformed proteins produced in the liver, so one treatment is a liver transplant. But few patients can get oneand it only slows the disease down.

Now, after years of false starts and disappointment, it looks like an audacious idea for helping these patients finally could work.

In 1998, researchers at the Carnegie Institution and the University of Massachusetts made a surprising discovery about how cells regulate which proteins they produce. They found that certain kinds of RNAwhich is what DNA makes to create proteinscan turn off specific genes. The finding, called RNA interference (RNAi), was exciting because it suggested a way to shut down the production of any protein in the body, including those connected with diseases that couldnt be touched with ordinary drugs. It was so promising that its discoverers won the Nobel Prize just eight years later.

The world went from believing RNAi would change everything to thinking it wouldnt work, to now thinking it will.

Inspired by the discovery, another group of researchersincluding the former thesis supervisor of one of the Nobel laureatesfounded Alnylam in Cambridge, Massachusetts, in 2002. Their goal: fight diseases like FAP by using RNAi to eliminate bad proteins (see The Prize of RNAi and Prescription RNA). Never mind that no one knew how to make a drug that could trigger RNAi. In fact, that challenge would bedevil the researchers for the better part of a decade. Along the way, the company lost the support of major drug companies that had signed on in a first wave of enthusiasm. At one point the idea of RNAi therapy was on the verge of being discredited.

But now Alnylam is testing a drug to treat FAP in advanced human trials. Its the last hurdle before the company will seek regulatory approval to put the drug on the market. Although its too early to tell how well the drug will alleviate symptoms, its doing what the researchers hoped it would: it can decrease the production of the protein that causes FAP by more than 80 percent.

This could be just the beginning for RNAi. Alnylam has more than 11 drugs, including ones for hemophilia, hepatitis B, and even high cholesterol, in its development pipeline, and has three in human trials progress that led the pharmaceutical company Sanofi to make a $700 million investment in the company last winter. Last month, the pharmaceutical giant Roche, an early Alnylam supporter that had given up on RNAi, reversed its opinion of the technology as well, announcing a $450 million deal to acquire the RNAi startup Santaris. All told, there are about 15 RNAi-based drugs in clinical trials from several research groups and companies.

The world went from believing RNAi would change everything to thinking it wouldnt work, to now thinking it will, says Robert Langer, a professor at MIT, and one of Alnylams advisors.

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Gene-Silencing Drugs Finally Show Promise

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Genetic Engineering. Stock Footage
This is a preview video. Download high quality footage at: http://www.pond5.com/stock-footage/12151081?ref=silverstepper More stock media here: http://www.po...

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Ending Osteoporosis
For Beyond 50 #39;s Natural Healing talks, listen to an interview with Dr. Sandy Bevacqua. Founder of the World Integrated Systems of Health, she has a background in Genetic Engineering,...

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Ending Osteoporosis - Video

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Citrus greening, the plague that could wipe out Florida's $9 billion orange industry, begins with the touch of a jumpy brown bug on a sun-kissed leaf.

From there, the bacterial disease incubates in the tree's roots, then moves back up the trunk in full force, causing nutrient flows to seize up. Leaves turn yellow, and the oranges, deprived of sugars from the leaves, remain green, sour, and hard. Many fall before harvest, brown necrotic flesh ringing failed stems.

For the past decade, Florida's oranges have been literally starving.

Since it first appeared in 2005, citrus greening, also known by its Chinese name, huanglongbing, has swept across Florida's groves like a flood. With no hills to block it, the Asian citrus psyllidthe invasive aphid relative that carries the diseasehas infected nearly every orchard in the state.

By one estimate, 80 percent of Florida's citrus trees are infected and declining.

The disease has spread beyond Florida to nearly every orange-growing region in the United States. Despite many generations of breeding by humanity, no citrus plant resists greening; it afflicts lemons, grapefruits, and other citrus species as well. Once a tree is infected, it will die. (See "Can Parasitic Wasps Help Save America's Citrus?")

Yet in a few select Floridian orchards, there are now trees that, thanks to innovative technology, can fight the greening tide. These trees have the potential to keep Florida orange juice on your breakfast tableprovided you are willing to drink the juice of oranges that have been genetically modified to contain genes from spinach. (Read "The Next Green Revolution" in National Geographic magazine.)

The trees are the work of Erik Mirkov, a plant pathologist at Texas A&M University who has spent his career applying the tools of biotechnology to citrus. Over the past few years, his research on genetically modified oranges has gone from an academic sideshow to one of the great hopes of the industry.

It's highly unlikely, researchers and growers agree, that oranges will remain in Florida unless new, modified strains like Mirkov's are widely growna view endorsed by the National Research Council several years ago.

Citrus greening incubates in the tree's roots, making it difficult to detect infection. A healthy citrus root system is shown at left, and an infected one at right.

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Can Genetic Engineering Save the Florida Orange?

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When Auburn alumni Michael and Sara Heatherly discovered their son Porter had a rare genetic disorder, they didn't know at first that their alma mater was leading the fight against it.

Researchers at Auburn's College of Veterinary Medicine have been researching how to treat the same genetic disorder in cats...and are now ready to move on to the human testing phase.

"When you get a diagnosis that your child might not live to be two, you kind of lose hope and that's the way we were for a few weeks, even months afterward,," Sara said. "Then when we find out something like this is happening down the road, it turned our life around. It gave us hope and made us realize that's Porter's purpose."

Porter has gangliosidosis, otherwise known as GM1, a genetic disorder that attacks the brain and spinal cord, similar to Alzheimer's. Only one in every 360,000 children will be affected and there is no cure or treatment. Life expectancy for those born with the disorder is just two years.

"The really cruel thing about this disease is that they appear to be normal for the first six to eight months of their life, and then they begin to miss certain milestones like sitting up or rolling over or maybe they acquire those acquire those milestones and then they lose them," said Dr. Doug Martin of the College of Veterinary Medicine.

Martin has been researching GM1 for nearly two decades. Porter's story has motivated him and his team in their research.

"Our group has always been really hard-working and motivated. But when we met Porter it took everything to a whole different level. The urgency we feel with the research now is just orders of magnitude above what it had been in the past because we have a great little kid right herein front of us who needs the research we're doing or needs the results of the research," Martin said.

This weekend, Porter celebrated his 2nd birthday surrounded by loved ones and those working to find a treatment for future children born with GM1. The Heatherly's find hope in the fact that Porter's life will make an impact on the lives of future generations.

"Just because he can't do all the things that you dream about when you have a little boy of everything he could do as far as playing sports or going to hunt or fish or do those kind of things, his life still can have a huge impact on people," Michael Heatherly said. "I think that's extremely important for us because of all the things he can't do, there's so many things he can do, just in a totally different way."

ON THE WEB: To donate to GM1 research, visit the Auburn University College of Veterinary Medicine.

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East Alabama family fights rare genetic disorder

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Genetics of Wild Mice Behavior - Hopi Hoekstra
Sourcce - http://serious-science.org/videos/1549 Harvard Prof. Hopi Hoekstra on the extended phenotype, structure of mice burrows, and addiction encoded in g...

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Genetics of Wild Mice Behavior - Hopi Hoekstra - Video

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Lets Play The Sims 3 Perfect Genetics Part 10: All Done!
Watch as we finish teaching Stephan his skills and Adalyn ages up! My Sims 3 Page: http://mypage.thesims3.com/mypage/becky050890 Origin Account Name: GBabyCh...

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Lets Play The Sims 3 Perfect Genetics Part 10: All Done! - Video

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IT was a sale with an international flavour - visitors from Argentina, South Africa and Canada converged on Gracemere Saleyards for the National Braford Bull Sale last week.

However, it was the Canadians that made their presence felt early into the sale when global genetics company Semex Canada bid $20,000 for 32-month-old Carinya Onslow.

Global beef program manager Myles Immerkar made the bid, organised the paperwork and was back on a plane to Canada that afternoon.

"I have been here for 10 days looking at tropical breeds - Braford, Brangus, Droughtmaster and Brahmans," he said, before heading off to catch his flight.

"We don't have a source of these in our breeding program."

The company is set up to provide genetic and breeding solutions to more than 100 countries and exports 25 different beef breeds to global markets.

What was missing were the tropical breeds.

"We are certainly impressed with the quality of Brafords here."

Mr Immerkar bought a Braford bull at the Ascot sale last week and has organised to buy more bulls from different breeds at upcoming sales in central Queensland over the next three weeks.

"All the bulls we buy this month will go to the Victoria Livestock Genetics artificial insemination centre and we'll collect their genetics and take it to Canada and then export it to 110 countries."

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Canadians search for CQ genetics

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Sainik School Bijapur, Mahaling, Gene Therapy to Adjust Heartbeat,9 Sept 2014
Sainik School Bijapur, Mahaling, Gene Therapy to Adjust Heartbeat,9 Sept 2014.

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Brain inflammation can rapidly disrupt our ability to retrieve complex memories of similar but distinct experiences, according to UC Irvine neuroscientists Jennifer Czerniawski and John Guzowski.

Their study -- which appears today in The Journal of Neuroscience -- specifically identifies how immune system signaling molecules, called cytokines, impair communication among neurons in the hippocampus, an area of the brain critical for discrimination memory. The findings offer insight into why cognitive deficits occurs in people undergoing chemotherapy and those with autoimmune or neurodegenerative diseases.

Moreover, since cytokines are elevated in the brain in each of these conditions, the work suggests potential therapeutic targets to alleviate memory problems in these patients.

"Our research provides the first link among immune system activation, altered neural circuit function and impaired discrimination memory," said Guzowski, the James L. McGaugh Chair in the Neurobiology of Learning & Memory. "The implications may be beneficial for those who have chronic diseases, such as multiple sclerosis, in which memory loss occurs and even for cancer patients."

What he found interesting is that increased cytokine levels in the hippocampus only affected complex discrimination memory, the type that lets us differentiate among generally similar experiences -- what we did at work or ate at dinner, for example. A simpler form of memory processed by the hippocampus -- which would be akin to remembering where you work -- was not altered by brain inflammation.

In the study, Czerniawski, a UCI postdoctoral scholar, exposed rats to two similar but discernable environments over several days. They received a mild foot shock daily in one, making them apprehensive about entering that specific site. Once the rodents showed that they had learned the difference between the two environments, some were given a low dose of a bacterial agent to induce a neuroinflammatory response, leading to cytokine release in the brain. Those animals were then no longer able to distinguish between the two environments.

Afterward, the researchers explored the activity patterns of neurons -- the primary cell type for information processing -- in the rats' hippocampi using a gene-based cellular imaging method developed in the Guzowski lab. In the rodents that received the bacterial agent (and exhibited memory deterioration), the networks of neurons activated in the two environments were very similar, unlike those in the animals not given the agent (whose memories remained strong). This finding suggests that cytokines impaired recall by disrupting the function of these specific neuron circuits in the hippocampus.

"The cytokines caused the neural network to react as if no learning had taken place," said Guzowski, associate professor of neurobiology & behavior. "The neural circuit activity was back to the pattern seen before learning."

The work may also shed light on a chemotherapy-related mental phenomenon known as "chemo brain," in which cancer patients find it difficult to efficiently process information. UCI neuro-oncologists have found that chemotherapeutic agents destroy stem cells in the brain that would have become neurons for creating and storing memories.

Dr. Daniela Bota, who co-authored that study, is currently collaborating with Guzowski's research group to see if brain inflammation may be another of the underlying causes of "chemo brain" symptoms.

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Brain inflammation dramatically disrupts memory retrieval networks, study finds

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A small protein named GILZ appears to protect against the bone loss that often accompanies arthritis and its treatment, researchers report.

Arthritis as well as aging prompt the body to make more fat than bone, and the researchers have previously shown GILZ can restore a more youthful, healthy mix. It also tamps down inflammation, a major factor in arthritis.

Now they have early evidence that GILZ might one day be a better treatment option for arthritis patients than widely used synthetic glucocorticoids, which actually increase bone loss, said Dr. Xingming Shi, bone biologist at the Medical College of Georgia at Georgia Regents University.

Their research is being presented at The American Society for Bone and Mineral Research 2014 Annual Meeting Sept. 12-15 in Houston.

In addition to bone loss, glucocorticoids, such as prednisone, produce other side effects, including diabetes. While GILZ is induced by glucocorticoids, directly overexpressing the protein appears to better target sources of bone loss and inflammation and avoid these serious side effects. .

For this study, the focus was tumor necrosis factor alpha, a proinflammatory cytokine that helps regulate immune cells and is a major player in arthritis. Tumor necrosis factor alpha primarily works though promoting inflammation, which is great if the target is cancer. However, when tumor necrosis factor alpha becomes dysregulated, it can also cause diseases like arthritis and inflammatory bowel disease.

To look specifically at the impact on bone loss, the researchers crossed mice bred to overexpress tumor necrosis factor alpha throughout the body with mice that overexpressed GILZ in just their mesenchymal stem cells. These stem cells produce the osteoblasts, which make bone. They also make fat, and when the cells stop making as much bone, they tend to make more of it. Shi's lab has shown that GILZ can coax mesenchymal stem cells back to making more bone and less fat.

While the mice that overexpressed only tumor necrosis factor alpha quickly developed arthritis along with significant bone and weight loss, those that also overexpressed GILZ had significantly less bone loss, Shi said.

"Our previous studies have shown that the GILZ transgenic mouse can make more bone," said Dr. Nianlan Yang, MCG postdoctoral fellow. "We wanted to see if GILZ would still have a bone protective effect in an inflammatory environment similar to arthritis."

Next steps include developing an oral medication, a peptide specifically, that increases GILZ expression rather than the genetic alterations the researchers have used in animal models, said Yang. She just completed a National Arthritis Foundation fellowship, which helped support that effort. They also want to see if GILZ can prevent arthritis from developing in the face of inflammation.

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Protein appears to protect against bone loss in arthritis

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Scientists are celebrating a breakthrough in stem cell research.

A type of human stem cell has been replicated in a lab for the first time in history.

The cells, previously impossible to duplicate, have been recreated to the equivalent of those between seven and nine days old the same as found in an embryo before it implants in the womb.

The creation of the human pluripotent cells opens a door for specialised cells to be created in the future for use in regenerative medicine.

The Wellcome Trust - Medical Research Council Cambridge Stem Cell Institute led the research, which was carried out by both British and Japanese academics.

Professor Austin Smith, director, said: "Our findings suggest that it is possible to rewind the clock to achieve true ground state pluripotency in human cells.

"These cells may represent the real starting point for formation of tissues in the human embryo. We hope that in time they will allow us to unlock the fundamental biology of early development, which is impossible to study directly in people."

The "reset" cells could be used as "raw material" for therapies, as well as diagnostic tools and drug screenings.

Scientists also hope that after further studying, the cells will help them learn more about how an embryo develops correctly, and how miscarriages and developmental disorders are caused.

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Significant milestone in stem cell research at The Wellcome Trust - Medical Research Council institute

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Surgeons implanted retinal tissue created after reverting the patient's own cells to a "pluripotent" state

Researchers were able to grow sheets of retinal tissue from induced pluripotent stem cells, and have now implanted them for the first time in a patient. Credit: RIKEN/Foundation for Biomedical Research and Innovation

A Japanese woman in her 70s is the world's first recipient of cells derived from induced pluripotent stem cells, a technology that has created great expectations since it could offer the same advantages as embryo-derived cells but without some of the controversial aspects and safety concerns.

In a two-hour procedure starting at 14:20 local time today, a team of three eye specialists lead by Yasuo Kurimoto of the Kobe City Medical Center General Hospital, transplanted a 1.3 by 3.0 millimeter sheet of retinal pigment epithelium cells into an eye of the Hyogo prefecture resident, who suffers from age-related macular degeneration.

The procedure took place at the Institute of Biomedical Research and Innovation Hospital, next to the RIKEN Center for Developmental Biology (CDB) where ophthalmologist Masayo Takahashi had developed and tested the epithelium sheets. She derived them from the patient's skin cells, after producing induced pluripotent stem (iPS) cells and then getting them to differentiate into retinal cells.

Afterwards, the patient experienced no effusive bleeding or other serious problems, RIKEN has reported.

The patient took on all the risk that go with the treatment as well as the surgery, Kurimoto said in a statement released by RIKEN. I have deep respect for bravery she showed in resolving to go through with it.

He hit a somber note in thankingYoshiki Sasai, a CDB researcher who recenty committed suicide. This project could not have existed without the late Yoshiki Sasais research, which led the way to differentiating retinal tissue from stem cells.

Kurimoto also thanked Shinya Yamanaka, a stem-cell scientist at Kyoto University without whose discovery of iPS cells, this clinical research would not be possible. Yamanaka shared the 2012 Nobel Prize in Physiology or Medicine for that work.

Kurimoto performed the procedure a mere four days after a health-ministry committee gave Takahashi clearance for the human trials (see 'Next-generation stem cells cleared for human trial').

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Next-Generation Stem Cells Transplanted in Human for the First Time

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## cell
# cell Sam gm cell therapy ...

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GIOSTAR- STEM CELL THERAPY DR ANAND SHRIVASTAVA
Global Institute of Stem cell Therapy and Research - GIOSTAR Introduction to Stem Cell Therapy, and Dr.Anand Shrivastava - Chairman Co-founder of GIOSTAR.

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GIOSTAR- STEM CELL THERAPY & DR ANAND SHRIVASTAVA - Video

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Two decades ago, Mary-Claire King made one of the most important contributions to modern healthcare when she discovered the first gene linked to breast cancer. Now, shes trying to one-up herself.

King, a genetics pioneer who won a major scientific award this week from the Albert and Mary Lasker Foundation, has issued a call to change how we think about gene testing in an approach she believes will prevent cancer, not just catch it early. (And if youve never met King, the fact that shes using her award to shed light on a serious public health need rather than to celebrate her own career tells you a little something about her character. You can read more about her inthis New York Times article.)

Most scientists would publish a proposal like this in Nature or Science, the two leading research journals. But King chose to publish in JAMA, one of the most respected medical journals, to get her message straight to physicians. And the message is this: Dont wait until someone has had breast cancer or shows risk factors before testing.Every woman age 30 and older, King says, should be screened for the genes linked to hereditary breast and ovarian cancer.

Make no mistake: Kings proposal is more than just a new approach to cancer screening. This is a watershed moment for all genetic testing, which is currently used in a highly targeted mannerusually for people at clear risk of a disease, or to confirm a diagnosis based on existing symptoms. For years, scientists have imagined a world in which genetic testing is done for everybody, possibly even at birth, so that diseases can be avoided rather than managed. But imagination and obvious clinical utility are very different things. Kings proposal is the first to focus on dramatically expanding the use of an existing and proven genetic test, making her plea far more likely to resonate with medical professionals and the patients they serve. (Whether the insurance companies who pay them will heed the call is another story entirely.)

Kings scientific path could be described as a sleeper hit of a career. Starting in the 70s, she toiled away,largely unnoticed, for nearly 20 years on a quest to find a gene linked to increased risk of breast cancer. At the time, the vast majority of scientists believed there was no such thing as genetic cancer risk, and that people like King were tilting at windmills. When she finally did locate the gene she named BRCA1a feat that made her a household name among geneticistsit was almost immediately snapped up in the whirlwind of corporate gene patenting that took place during the early days of the Human Genome Project. BRCA1 was essentially off-limits to all but the patent holders from the late 90s until last year, when a Supreme Court ruling declared that genes could not be patented. At last, the gene King had dedicated most of her career to was accessible for testing by any clinical lab, for any patient.

If ever there was a time for a prominent scientist to make such a proposal, this is it. The genes (BRCA1 and its companion, BRCA2) are available for testing with the best DNA analysis tools yet. Last years announcement by Angelina Jolie that she had a prophylactic double mastectomy based on her gene test results has sparked what medical geneticists are calling the Angelina Effect: anecdotal evidence suggests that labs are seeing double or even quadruple the number of women interested in breast cancer gene testing now than they did a year ago. At the same time, the preventive value of mammograms has increasingly been called into question, leading women to seek alternatives.

King has gone from contrarian scientist to a highly respected researcher who has been honored by her peers, the prestigious Lasker Foundation, and even Hollywood (Helen Hunt played King inthis indie filmreleased last year). If youd like to show her some gratitude, here are two things you can do:

1. Tell your doctor you want to have the BRCA1 and BRCA2 gene test to determine your risk of hereditary breast and ovarian cancer. If youre a dude, encourage your wife/sister/daughter to do so.

2. When you ask for the test, pronounce BRCA1 the way King intended it: spelled out, letter by letter, rather than the brah-kuh pronunciation that has caught on instead.

Article originally published atTechonomy.com.

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Our Era of Preventive Genetic Screening: Brought to You in Part by Mary-Claire King

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(PRWEB) September 13, 2014

The Cell Culture Market by Equipment (Bioreactor, Incubator, Centrifuge), by Reagent (Media, Sera, Growth Factors, Serum Free Media), by Application (Cancer Research, Gene Therapy, Drug Development, Vaccine Production, Toxicity Testing) - Global Forecast to 2018 report provides a detailed overview of the major drivers, restraints, challenges, opportunities, current market trends, and strategies impacting the global cell culture market along with the estimates and forecasts of the revenue and market share analysis.

Browse 91 market data tables and 19 figures spread through 209 Pages and in-depth TOC on"Cell Culture Market" http://www.marketsandmarkets.com/Market-Reports/cell-culture-market-media-sera-reagents-559.html

Early buyers will receive 10% customization on this report.

The global cell culture market was valued at an estimated $14,772 million in 2013. This market is expected to grow at a CAGR of 10.71% between 2013 and 2018, to reach $24,574 million in 2018.

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Cell culture has its applications in a large number of fields including biopharmaceutical production, drug screening and development, gene therapy, toxicity testing, and life science research. It is one of the most widely used techniques for biopharmaceutical and vaccine production. According to IMS Health, biologics (which includes biopharmaceuticals and vaccines) are expected to grow at a CAGR of about 18% by 2017. The rapid growth in biopharmaceutical and vaccine production will be the primary driver for the cell culture market between 2013 and 2018. Furthermore, increase in the healthcare spending and increased R&D activities will aid the growth of this market.

Cell culture is the most widely used techniques for biopharmaceutical production and has its applications in drug screening and development, gene therapy, toxicity testing, and cancer research. Rapid growth in the biopharmaceutical market, increase in the healthcare spending, and increased R&D activities will drive the growth of the global cell culture market.

The global cell culture market is a highly evolved market. There is a high degree of consolidation in this market. An analysis of the market developments between 2011 and 2014 reveals that new product launches was the most important growth strategy employed by market leaders in this period. This strategy was adopted by all players in this market, except Lonza (Switzerland). Lonza was the only company among all the market leaders that did not launch any new products between 2011 and 2014.

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Cell Culture Market by Equipment, Reagent, Application worth $24,574 million by 2018 - New Research Report by ...

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