PUBLIC RELEASE DATE:

3-Feb-2014

Contact: Herb Booth hbooth@uta.edu 817-272-7075 University of Texas at Arlington

A UT Arlington bioengineer has received a four-year, $1.4 million National Institutes of Health grant to create a nanoparticle system to shore up arterial walls following angioplasty and stenting procedures to treat coronary arterial disease.

Kytai Nguyen, a UT Arlington associate professor of bioengineering, said the research looks to improve an established procedure like angioplasty, which opens arteries and blood vessels that are blocked.

"We have discovered a way to use nanoparticles to help the arteries heal themselves more effectively following one of the most common surgical procedures," said Nguyen, who joined UT Arlington in 2005. "This process promises to reduce complications that can occur in the arteries following surgery and may extend opportunities for patients to live longer, healthier lives."

The Centers for Disease Control and Prevention reported that nearly 1 million people in the United States have angioplasty or stent procedures done annually.

Khosrow Behbehani, dean of the College of Engineering, said Dr. Nguyen is specializing in developing innovative techniques for drug delivery which critical to advancing health care.

"Earning a National Institutes of Health grant puts Dr. Nguyen in very exclusive company," Behbehani said. The NIH reported that only 16.8 percent of its nearly 50,000 applications in 2013 were awarded grants. "Receiving this grant reflects the cutting-edge research that Dr. Nguyen is conducting. Her investigation will help improve the efficacy of stents in treating cardiovascular anomalies."

Following the angioplasty or stent, surgeons would insert the nanoparticles at the affected site, and the nanoparticles would attach themselves to the arterial wall. The nanoparticles would be programmed to recruit stem cells, which would regenerate the arterial wall's weakened cells naturally, Nguyen said.

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UT Arlington bioengineer to create new nanoparticle system to shore up arterial walls

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As one of the follically-challenged, any new breakthroughs in the area of hair regeneration will generally get my attention. When stem cells first started to gain widespread media attention I, no doubt like many others, thought a full head of hair was just around the corner. But despite numerous developments, years later my dome is still of the chrome variety. Providing the latest cause for cautious optimism, researchers have now developed a way to generate a large number number of hair-follicle-generating stem cells from adult cells.

In what they claim is a world first, researchers from the University of Pennsylvania (UPenn) and the New Jersey Institute of Technology have developed a technique to convert adult human stem cells into epithelial stem cells (EpSCs).

By adding three genes to human skin cells called dermal fibroblasts that live in the dermis layer of the skin and generate connective tissue, a team led by Xiaowei "George" Xu, MD, PhD, at the Perelman School of Medicine was able to convert them into induced pluripotent stem cells (iPSCs). The iPSCs, which have the ability to differentiate into any cell type, were then converted into epithelial stem cells (EpSCs) that are normally found at the bulge of hair follicles.

Through careful control of the timing of delivery of growth factors to the cells, the researchers say they were able to turn over 25 percent of the iPSCs into EpSCs in 18 days. When they then mixed these EpSCs with mouse follicular inductive dermal cells and grafted them onto the skin of immunodeficient mice, functional human epidermis and follicles similar to hair follicles were produced.

"This is the first time anyone has made scalable amounts of epithelial stem cells that are capable of generating the epithelial component of hair follicles, said Xu, who added that these cells have many potential applications, including wound healing, cosmetics, and hair regeneration.

But some hurdles still need to be jumped before I make my first trip to the hairdresser in a decade. Xu points out that when a person loses hair, they lose not only epithelial cells, but also a kind of adult stem cell called dermal papillae. "We have solved one major problem, the epithelial component of the hair follicle. We need to figure out a way to also make new dermal papillae cells, and no one has figured that part out yet."

On a positive note, researchers from the Tokyo University of Science have reported promising results in reconstructing hair follicle germs from adult epithelial stem cells and cultured dermal papilla cells, so even though we haven't rounded the corner yet,it definitely seems to be getting closer.

The teams research is published in the journal Nature Communications.

Source: University of Pennsylvania

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Stem cell-based treatment for baldness a step closer

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Emerging Medical Devices for Minimally Invasive Cell Therapy
Dr. Eoin O #39;Cearbhaill, a lecturer in biomedical engineering at the School of Mechanical and Materials Engineering, University of Dublin, in Dublin, Ireland, ...

By: Mayo Proceedings

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REGULATED INFORMATION FEBRUARY 4, 2014

TiGenix reaches major cell therapy milestone with 1000th implant of ChondroCelect

Leuven (BELGIUM) - February 4, 2014 - TiGenix (NYSE Euronext: TIG), a leader in the field of cell therapy, announced today that it reached a major milestone with the performance of the 1000th ChondroCelect implantation for cartilage repair in the knee. ChondroCelect is the first cell therapy that was granted approval by the European Medicines Agency (EMA) as an Advanced Therapy Medicinal Product (ATMP). Today it is routinely used in orthopedic centers of excellence across several European countries.

"A 1000 patients have already benefited from this innovative therapy, further supporting its efficacy and safety profile," said Eduardo Bravo, CEO of TiGenix. "A milestone such as today's is a clear demonstration of how far the cell therapy field has progressed over recent years, and I have no doubt that it is on its way to become a mainstay in clinical practice. We will continue to work towards turning our ChondroCelect franchise into a cash flow positive asset, and to push the clinical development of our pipeline of stem cell programs to a successful conclusion."

About ChondroCelect An innovative treatment, ChondroCelect has been shown to result in long-term durable clinical benefits in patients with recent cartilage lesions. Five-year follow-up data confirm that the therapeutic effect and the clinical benefit of ChondroCelect gained over baseline is maintained up to at least five years after the cartilage repair intervention. In addition, the data confirm that early treatment with ChondroCelect results in a superior clinical benefit over microfracture, and a lower failure rate.

Cartilage lesions of the knee are a frequent cause of disability in the active population. Caused by repetitive microtraumata, or due to sports or traffic accidents, cartilage lesions rarely heal spontaneously. When untreated, they predispose to osteoarthritis, which causes disability and represents a major socioeconomic burden. A treatment that allows symptom relief and functional recovery is key. To meet this important medical need, TiGenix developed ChondroCelect, the first cell therapy that was granted approval by the EMA as an ATMP.

ChondroCelect is administered to patients in an autologous chondrocyte implantation procedure known as Characterized Chondrocyte Implantation. TiGenix has designed a sophisticated manufacturing process to preserve the cells' characteristics and biological activity, and to maintain their ability to produce high quality cartilage. This process meets the highest quality standards and has been approved by the EMA.

For more information: Eduardo Bravo Chief Executive Officer eduardo.bravo@tigenix.com

Claudia D'Augusta Chief Financial Officer claudia.daugusta@tigenix.com

About TiGenix

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TiGenix : reaches major cell therapy milestone with 1000th.

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PHOENIX, Ariz. -

Stem cell research and therapy on humans has traveled a long and often politically troubled path.

Not so for pets, where stem cell treatment has been used for nearly 10 years and now it is so routine, and so successful, it can be done in a day.

Ava is a 90 pound, 2-year-old Akita, who is about to undergo stem cell surgery. A little IV, a little anesthesia and Ava is out.

"It is used for arthritis mostly," said Dr. Velvet Edwards.

Ava is just beginning her day at Pecan Grove Veterinary Hospital in Tempe. Dr. Edwards oversees the stem cell procedure.

"Stem cells are healing cells, so they seek out area of injury damage or destruction," explained Edwards. "They accelerate healing and help the animal, the patient, the pet just use their own natural abilities to get better."

Veterinary stem cells are harvested from the animal's own fat cells. They are separated and processed by machinery right inside the vet's office and then injected back into the dog's trouble spots.

Thanks to new technology developed by Meti Vet, the process is completed in just a day.

"The pet comes in the morning, it's anesthetized and I collect about two to four grams of fat usually behind the shoulder blade," said Edwards. "Then I hand that fat over to my technicians to run it through a series of steps.. basically to dissolve the fat and get down to a little stem cell pellet... Then we take that pellet and we reconstitute it and make it injectable. I will put it back into the animal's body wherever I need it later that day."

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Stem cell treatment: Controversial for humans, but not for pets

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PUBLIC RELEASE DATE:

4-Feb-2014

Contact: Jess C. Gomez jess.gomez@imail.org 801-718-8495 Intermountain Medical Center

SALT LAKE CITY A team of researchers, led by physicians and scientists at Intermountain Healthcare's Intermountain Medical Center and ARUP Laboratories, has made a medical breakthrough by discovering genetic mutations that cause a rare and deadly lung disease.

The disease, pulmonary capillary hemangiomatosis or PCH, is a rare cause of pulmonary hypertension, which occurs predominantly in young adults. PCH affects less than one in a million people, and has been extremely difficult and expensive to diagnose, as well as challenging to treat.

This genetic discovery offers new hope.

"This is a significant finding. This discovery should advance our understanding of this rare pulmonary vascular disorder and other related disorders," said Greg Elliott, MD, MACP, senior investigator of the study and medical director of the Pulmonary Hypertension Center at Intermountain Medical Center in Murray, Utah, and professor of medicine at the University of Utah School of Medicine.

Results of the study will be published in the February issue of the journal CHEST, the official publication of the American College of Chest Physicians. The study is embargoed by CHEST until Feb 4 at 6am, EST.

Dr. Elliott and his team at Intermountain Medical Center and the University of Utah School of Medicine collaborated with researchers from Columbia University, Vanderbilt University and Mayo Clinic-Scottsdale.

To find the genetic mutation, the research team used a relatively new technology whole exome sequencing performed at ARUP Laboratories in Salt Lake City to test DNA samples. They discovered the genetic mutations in Eukaryotic Translation Initiation Factor 2 Alpha Kinase 4. EIF2AK4 is a protein responsible for down-regulating protein synthesis when cells are exposed to stress.

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New hope: Researchers discover genetic mutations that cause rare and deadly lung disease

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Newswise SALT LAKE CITY A team of researchers, led by physicians and scientists at Intermountain Medical Center and ARUP Laboratories in Salt Lake City, has made a medical breakthrough by discovering genetic mutations that cause a rare and deadly lung disease.

The disease, pulmonary capillary hemangiomatosis or PCH, is a rare cause of pulmonary hypertension, which occurs predominantly in young adults. PCH affects less than one in a million people, and has been extremely difficult and expensive to diagnose, as well as challenging to treat.

This genetic discovery offers new hope.

This is a significant finding. This discovery should advance our understanding of this rare pulmonary vascular disorder and other related disorders, said Greg Elliott, MD, MACP, senior investigator of the study and medical director of the Pulmonary Hypertension Center at Intermountain Medical Center in Murray, Utah, and professor of medicine at the University of Utah School of Medicine.

Results of the study will be published in the February issue of the journal CHEST, the official publication of the American College of Chest Physicians. The study is embargoed by CHEST until Feb 4 at 6am, EST.

Dr. Elliott and his team at Intermountain Medical Center and the University of Utah School of Medicine collaborated with researchers from Columbia University, Vanderbilt University and Mayo Clinic-Scottsdale.

To find the genetic mutation, the research team used a relatively new technology whole exome sequencing performed at ARUP Laboratories in Salt Lake City to test DNA samples. They discovered the genetic mutations in Eukaryotic Translation Initiation Factor 2 Alpha Kinase 4. EIF2AK4 is a protein responsible for down-regulating protein synthesis when cells are exposed to stress.

Researchers found that in patients with the genetic mutations, their bodies don't properly regulate blood vessels in the lung. As a result, the capillaries in the lungs proliferate and the patient develops pulmonary hypertension.

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New Hope As Researchers Discover Genetic Mutations That Cause Rare and Deadly Lung Disease

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Part 2 - Twins Raised Apart and other Unusual Pairings: Genetics, Personality and Social Relatedness
4/22/2013 Nancy Segal - California State University, Fullerton "Twins Raised Apart and other Unusual Pairings: Genetics, Personality and Social Relatedness" ...

By: UCLABEC

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Population Genetics. What is Disruptive Selection?
Disruptive selection, also called diversifying selection, describes changes in population genetics in which extreme values for a trait are favored over inter...

By: GeneticsLessons

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Population Genetics. What is Disruptive Selection? - Video

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GodBody Genetics Pop Faster Than T.G.A. Private Breeder Vs Commercial Breeder
I wont lie I #39;m happy they popped, but I #39;m not happy with the quality or the growth of T.G.A Seed as well as Epik Purple by So Cal Seed Company. While you hav...

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By RTT News, February 04, 2014, 06:24:00 PM EDT

(RTTNews.com) - Myriad Genetics Inc. ( MYGN ), the molecular diagnostic company, Tuesday reported a better-than-expected increase in second-quarter profit, led by a 37 percent jump in revenues.

Myriad also announced a deal to buy molecular diagnostic laboratory Crescendo Bioscience Inc. for $270 million, subject to adjustments including a reduction of $25 million for debt repayments. Myriad expects to close the deal before the end of its fiscal 2014.

Looking ahead, Myriad again lifted its outlook for fiscal year 2014, citing the Crescendo acquisition and growth in core markets. The news boosted investor sentiment, with Myriad shares surging about 14 percent in after-hours trade on the Nasdaq.

For the fourth quarter, the Salt Lake City, Utah-based company posted net income of $50 million or $0.66 per share, compared with $35 million or $0.42 per share last year.

On average, 19 Analysts polled by Thomson Reuters estimated earnings of $0.46 per share for the quarter. Analysts' estimates typically exclude special items.

Revenues for the second quarter climbed to $204 million from $149 million in the prior year. Analysts estimated revenues of $176 million for the quarter.

Among segments, Molecular diagnostic testing revenue jumped 39 percent year-over-year, on strong growth in oncology and women's health businesses.

For fiscal 2014, Myriad now projects earnings of $2.09 to $2.12 per share on revenues of $740 million to $750 million. The company earlier estimated earnings of $1.92 to $1.97 per share on revenues of $700 million to $715 million. Analysts currently expect earnings of $1.97 per share on revenues of $705.62 million.

CEO Peter Meldrum said, "We plan to continue to execute upon our strategic plan of transitioning our hereditary cancer market, expanding our business internationally, and diversifying our revenue base with new product launches."

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Myriad Genetics Profit Up, To Acquire Crescendo Bioscience; Stock Jumps 14%

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Gene Therapy May Treat Rare Form of Blindness1348

By: Amberly Swimm

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Gene Therapy May Treat Rare Form of Blindness1348 - Video

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Gene therapy defeats muscle disease in tests
Scientists studying myotubular myopathy, a devastating disorder, say a new therapy appears to rescue mice and dogs from the disease. The findings demonstrate...

By: UWMedicineHealth

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Gene therapy defeats muscle disease in tests - Video

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Researchers used blood platelets and bone marrow cells to deliver potentially curative gene therapy to mouse models of the human genetic disorder Hurler syndrome -- an often fatal condition that causes organ damage and other medical complications.

Scientists from Cincinnati Children's Hospital Medical Center and the National Institute of Neurological Disorders and Stroke (NINDS) report their unique strategy for treating the disease the week of Feb. 3-7 in Proceedings of the National Academy of Sciences (PNAS).

Researchers were able to genetically insert into the cells a gene that produces a critical lysosomal enzyme (called IDUA) and then inject the engineered cells into mice to treat the disorder. Follow up tests showed the treatment resulted in a complete metabolic correction of the disease, according to the authors.

"Our findings demonstrate a unique and somewhat surprising delivery pathway for lysosomal enzymes," said Dao Pan, PhD, corresponding author and researcher in the Division of Experimental Hematology and Cancer Biology at Cincinnati Children's. "We show proof of concept that platelets and megakaryocytes are capable of generating and storing fully functional lysosomal enzymes, which can lead to their targeted and efficient delivery to vital tissues where they are needed."

The mice tested in the study modeled human Hurler syndrome, a subset of disease known as mucopolysaccharidosis type I (MPS I), one of the most common types of lysosomal storage diseases. MPS I is a lysosomal storage disease in which people do not make an enzyme called lysosomal alpha-L-iduronidase (IDUA).

IDUA helps break down sugar molecules found throughout the body, often in mucus and fluids around joints, according to the National Library of Medicine/National Institutes of Health. Without IDUA, sugar molecules build up and cause organ damage. Depending on severity, the syndrome can also cause deafness, abnormal bone growth, heart valve problems, joint disease, intellectual disabilities and death.

Enzyme replacement therapy can be used to treat the disease, but it is only temporary and not curative. Bone marrow transplant using hematopoietic stem cells also has been tested on some patients with mixed results. The transplant procedure can carry severe risks and does not always work.

Pan and her colleagues -- including Roscoe O. Brady, MD, a researcher at NINDS -- report that using platelets and megakaryocytes for gene therapy is effective and could reduce the risk of activating cancer-causing oncogenes in hematopoietic stem cells.

The authors said tests showed that human megakaryocytic cells were capable of overexpressing IDUA, revealing their capacity for potential therapeutic benefit. While engineering megakaryocytes and platelets for infusion into their mouse models of Hurler, the scientists report they were able to release IDUA directly into amply sized extracellular spaces or inside micro-particles as the cells matured or activated. The cells were able to produce and package large amounts of functional IDUA and retained the capacity to cross-correct patient cells.

After infusing mouse models of Hurler with the genetically modified cells, researchers said this led to long-term normalization of IDUA levels in the animal's blood with versatile delivery routes and on-target preferential distribution to the liver and spleen. The treatment led to a complete metabolic correction of MPS I in most peripheral organs of the mice.

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Gene therapy may be possible cure for Hurler syndrome: Mouse Study

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PUBLIC RELEASE DATE:

4-Feb-2014

Contact: Nick Miller nicholas.miller@cchmc.org 513-803-6035 Cincinnati Children's Hospital Medical Center

CINCINNATI Researchers used blood platelets and bone marrow cells to deliver potentially curative gene therapy to mouse models of the human genetic disorder Hurler syndrome an often fatal condition that causes organ damage and other medical complications.

Scientists from Cincinnati Children's Hospital Medical Center and the National Institute of Neurological Disorders and Stroke (NINDS) report their unique strategy for treating the disease the week of Feb. 3-7 in Proceedings of the National Academy of Sciences (PNAS).

Researchers were able to genetically insert into the cells a gene that produces a critical lysosomal enzyme (called IDUA) and then inject the engineered cells into mice to treat the disorder. Follow up tests showed the treatment resulted in a complete metabolic correction of the disease, according to the authors.

"Our findings demonstrate a unique and somewhat surprising delivery pathway for lysosomal enzymes," said Dao Pan, PhD, corresponding author and researcher in the Division of Experimental Hematology and Cancer Biology at Cincinnati Children's. "We show proof of concept that platelets and megakaryocytes are capable of generating and storing fully functional lysosomal enzymes, which can lead to their targeted and efficient delivery to vital tissues where they are needed."

The mice tested in the study modeled human Hurler syndrome, a subset of disease known as mucopolysaccharidosis type I (MPS I), one of the most common types of lysosomal storage diseases. MPS I is a lysosomal storage disease in which people do not make an enzyme called lysosomal alpha-L-iduronidase (IDUA).

IDUA helps break down sugar molecules found throughout the body, often in mucus and fluids around joints, according to the National Library of Medicine/National Institutes of Health. Without IDUA, sugar molecules build up and cause organ damage. Depending on severity, the syndrome can also cause deafness, abnormal bone growth, heart valve problems, joint disease, intellectual disabilities and death.

Enzyme replacement therapy can be used to treat the disease, but it is only temporary and not curative. Bone marrow transplant using hematopoietic stem cells also has been tested on some patients with mixed results. The transplant procedure can carry severe risks and does not always work.

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Mouse study shows gene therapy may be possible cure for Hurler syndrome

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Michal Schwartz -- Breaking The Wall Between Body and Mind @Falling Walls 2013
BREAKING THE WALL BETWEEN BODY AND MIND. How Neuroimmunology Develops New Strategies Against Brain Ageing and Degeneration Michal Schwartz The Maurice and Il...

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Miraculous Spinal Cord Injury Recovery - L1 Burst Fracture
6 months ago on the 9th of august 2013 I broke my back in four places (T10, T12, L1, S1) and burst fractured my L1 vertebra, leaving me paralyzed from my wai...

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Project Walk Claremont - Brandon R. Spinal Cord Injury Milestone
Brandon Rayburn, Level C-5, Incomplete injured in a snowboarding accident February 2, 2001. Thirteen years later, walking like a champ!

By: Project Walk

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Spinal Cord Injury, my friend!

By: Michelle Linnekin

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Scottsdale, AZ. (PRWEB) February 03, 2014

The team at Arizona Pain (arizonapain.com), has received approval to announce the much anticipated Phase II results of a potential medical breakthrough on the use of stem cells for chronic low back pain. The study, which first garnered international attention two years ago as one of the first trials of its kind in the U.S., has produced positive, promising results.

"We are pleased to report that a clinical study has indicated that a single injection of adult, donor marrow stem cells into degenerating intervertebral discs has reduced low back pain and improved function in trial participants for at least 12 months, says Dr. Paul Lynch, M.D., Arizona Pain Co-Founder and double-board certified Pain Management physician. The results of this study, if confirmed, could change the way we treat low back pain.

Arizona Pain was the first clinic in the U.S. to have been selected for an FDA-cleared study on this advanced treatment. Since then, 100 qualified patients were offered an opportunity to participate in a controlled, double-blind study that monitored any changes in the patients degenerative lumbar discs throughout the trial. The stem cells were taken from the bone marrow of a young healthy adult donor, were culture expanded and were administered through a minimally invasive, single injection. Trial participants remained unaware of whether or not they received injections with stem cells or one of the control treatments.

Key findings at 12 months in the trial were reported as follows: improvement in chronic low back pain with reduction in mean pain score; increased proportion of patients achieving 50% reduction in pain score; increased proportion of patients achieving minimal residual back pain; reduced opioid use for pain relief; and reduced need for additional surgical and non-surgical interventions for persistent pain.

Arizona Pain is incredibly proud to have partnered with the trial sponsor Mesoblast, a world leader in regenerative medicine (http://www.mesoblast.com) on this sentinel research study, says Dr. Lynch. The results are promising and we are hopeful that these findings will be confirmed in a Phase III trial beginning this year."

On January 29, 2014, Mesoblast announced positive 12 month outcome results from the 100-patient Phase II clinical trial of its proprietary allogeneic, or off-the-shelf, Mesenchymal Precursor Cells (MPCs) in patients with chronic moderate to severe discogenic low back pain. The results showed that a single injection of MPCs into degenerating intervertebral discs reduced low back pain and improved function for at least 12 months. When compared with controls, MPC-treated patients used less opioids for pain relief, had greater radiographically-determined disc stability, and underwent less additional surgical and non-surgical treatment interventions. MPC treatments also appeared to be well tolerated during the study.

Mesoblast Chief Executive Silviu Itescu said, On the basis of these positive results, Mesoblast plans to meet shortly with regulatory authorities in major jurisdictions, including the United States Food and Drug Administration, to discuss product registration trials for the potential treatment of disc degeneration."

More than 6 million patients in the United States alone are currently dealing with chronic back pain that has persisted for at least three months, with around 3.5 million people affected by moderate or severe degenerative intervertebral disc disease. The United States Centers for Disease Control and Preventions National Center for Health Statistics reported in 2010 that low back pain was the leading cause of pain, affecting 28% of American adults, and the second most common cause of disability in American adults.

This study shows we are progressing toward major advances in pain medicine, says Dr. Tory McJunkin, M.D., co-founder of Arizona Pain and PainDoctor.com. Stem cell therapy focuses on addressing the source of the pain, rather than just the symptoms. We truly hope this will unlock a vital solution for people suffering from debilitating low back pain, says Dr. McJunkin.

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Arizona Pain Announces Positive Results in Revolutionary Stem Cell Study on Chronic Low Back Pain

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Editors note: What follows is a guest post. Michael Zhang is an MD-PhD student studying at the University of Louisville School of Medicine. He is one of my go-to experts on matters of cell biology and stem cells. (His bio is below.)

As you may have heard, this week brought striking news in the field of stem cell biology. Researchers from Boston and Japan published two papers in the prestigious journal Nature in which they describe new and easy ways to transform mouse cells back into stem cells. (NPR coverage here.) Make no mistake, this is not mundane science news. This is big.

I follow cell biology because I believe it is the branch of science that will bring the next major advance in modern medicine. Rather than implant a pacemaker, future doctors may inject a solution of sinus node stem cells, and voila, the heart beats normally. Rather than watch a patient with a scarred heart die of heart failure or suffer from medication side effects, future doctors may inject stem cells that replace the non-contracting scar. And the same could happen for kidneys, pancreas, spinal nerves, etc.

When I heard the news, I emailed Michael the link with the following subject line: This is pretty cool, right? He wrote back. What he taught me is worth sharing.

***

Michael Zhang MD-PhD candidate Univ of Louisville

By Michael Zhang:

Japanese and American cell biologists have recently reported dramatic new findings that are likely to upend biological dogma.

For much of the past century, the prevailing consensus held that once animal cells move past the earliest embryonic stages, they are irreversibly committed to specialized roles in the adult brain cells, heart cells, lung cells etc. In the past decade, two Nobel-winning biologists each separately demonstrated that committed specialist cells (aka differentiated cells) could be reprogrammed back to a primordial, embryonic state (aka pluripotent stem cell) that could then morph into any new type of specialized cell.

Now, Professor Obokata and her colleagues describe new methods to induce this reprogramming of specialized cells to (pluripotent) stem cells. Whereas previous methods involved draconian procedures the transfer of entire nuclei between cells, or the transfer of multiple genes Obokatas group found that simply squeezing a terminally differentiated cell, or immersing it in an acidic solution, could induce reprogramming to an embryonic stem cell state.

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Progress in stem cell biology: This could change everything about the practice of medicine

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stem cell therapy treatment for traumatic brain injury by dr alok sharma, mumbai, india
improvement seen in just 5 days after stem cell therapy treatment for traumatic brain injury by dr alok sharma, mumbai, india. Stem Cell Therapy done date 7 ...

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Newswise When it comes to finding cures for heart disease, scientists at Icahn School of Medicine at Mount Sinai are working to their own beat. They may have developed a tissue model for the human heart that can bridge the gap between animal models and human clinical trial patients.

Mount Sinai researchers generated their engineered cardiac tissue from human embryonic stem cells with the resulting muscle having remarkable similarities to native heart muscle, including the ability to beat and contract like the human heart. This research breakthrough study was highlighted as the cover story of the February 2014 issue of The FASEB Journal.

"We hope that our human engineered cardiac tissues will serve as a platform for developing reliable models of the human heart for routine laboratory use," said lead researcher Kevin D. Costa, PhD, Associate Professor of Cardiology and Director of the Cardiovascular Cell and Tissue Engineering Laboratory at the Cardiovascular Research Center of Icahn School of Medicine at Mount Sinai.

"This could help accelerate and revolutionize cardiology research by improving the ability to efficiently discover, design, develop, and deliver new therapies for the treatment of heart disease, and by providing more efficient screening tools to identify and prevent cardiac side effects, ultimately leading to safer and more effective treatments for patients suffering from heart disease," says Dr. Costa.

The international team of researchers led by Mount Sinai created human engineered cardiac tissue, known as hECTs, within a custom bioreactor device designed to exercise the tissue and measure its contractile force throughout the culture process. Within 7-10 days, the human cardiac cells self-assembled into a three-dimensional tissue strip that beats spontaneously like natural heart muscle, and can survive a month or more for long-term experimental testing. These hECTs displayed contractile activity in a rhythmic pattern of 70 beats per minute on average, similar to the human heart.

In addition, research results show the heart tissue model responds to electrical stimulation and is able to incorporate new genetic information delivered by adenovirus gene therapy. During functional analysis, some of the responses known to occur in the natural adult human heart were also elicited in hECTs through electrical, mechanical, and pharmacological interventions, while some responses of hECTs more closely mimicked the immature or newborn human heart.

"We've come a long way in our understanding of the human heart," said Gerald Weissmann, MD, Editor-in-Chief of The FASEB Journal, "but we still lack an adequate tissue model which can be used to test promising therapies and model deadly diseases. This advance, if it proves successful over time, will beat anything that's currently available."

About the Mount Sinai Health System The Mount Sinai Health System is an integrated health system committed to providing distinguished care, conducting transformative research, and advancing biomedical education. Structured around seven member hospital campuses and a single medical school, the Health System has an extensive ambulatory network and a range of inpatient and outpatient servicesfrom community-based facilities to tertiary and quaternary care.

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Engineered Cardiac Tissue Developed to Study the Human Heart

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PUBLIC RELEASE DATE:

3-Feb-2014

Contact: Kim Newman sciencenews@einstein.yu.edu 718-430-3101 Albert Einstein College of Medicine

February 3, 2014 (Bronx, NY) Researchers at Albert Einstein College of Medicine of Yeshiva University and Montefiore Medical Center have found a chemical "signature" in blood-forming stem cells that predicts whether patients with acute myeloid leukemia (AML) will respond to chemotherapy.

The findings are based on data from nearly 700 AML patients. If validated in clinical trials, the signature would help physicians better identify which AML patients would benefit from chemotherapy and which patients have a prognosis so grave that they may be candidates for more aggressive treatments such as bone-marrow transplantation. The paper was published today in the online edition of the Journal of Clinical Investigation.

Sparing Patients from Debilitating Side Effects

According to the American Cancer Society, AML accounts for nearly one-third of all new leukemia cases each year. In 2013, more than 10,000 patients died of AML.

"AML is a disease in which fewer than 30 percent of patients are cured," said co-senior author Ulrich Steidl, M.D., Ph.D., associate professor of cell biology and of medicine and the Diane and Arthur B. Belfer Faculty Scholar in Cancer Research at Einstein and associate chair for translational research in oncology at Montefiore. "Ideally, we would like to increase that cure rate. But in the meantime, it would help if we could identify who won't benefit from standard treatment, so we can spare them the debilitating effects of chemotherapy and get them into clinical trials for experimental therapies that might be more effective."

Analyzing Methylation Patterns

The Einstein study focused on so-called epigenetic "marks" chemical changes in DNA that turn genes on or off. The researchers focused on one common epigenetic process known as methylation, in which methyl (CH3) groups attach in various patterns to the genes of human cells. Researchers have known that aberrations in the methylation of hematopoietic, or blood-forming, stem cells (HSCs) can prevent them from differentiating into mature blood cells, leading to AML.

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Chemical stem cell signature predicts treatment response for acute myeloid leukemia

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5 hours ago by Dan Krotz One protein complex, two very different shapes and functions: In the top image, the scientists created an Mre11-Rad50 mutation that speeds up hydrolysis, yielding an open state that favors a high-fidelity way to repair DNA. In the bottom image, the scientists slowed down hydrolysis, resulting in a closed ATP-bound state that favors low-fidelity DNA repair. Credit: Tainer lab

(Phys.org) Maybe you've seen the movies or played with toy Transformers, those shape-shifting machines that morph in response to whatever challenge they face. It turns out that DNA-repair machines in your cells use a similar approach to fight cancer and other diseases, according to research led by scientists from the U.S. Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab).

As reported in a pair of new studies, the scientists gained new insights into how a protein complex called Mre11-Rad50 reshapes itself to take on different DNA-repair tasks.

Their research sheds light on how this molecular restructuring leads to different outcomes in a cell. It could also guide the development of better cancer-fighting therapies and more effective gene therapies.

re11-Rad50's job is the same in your cells, your pet's cells, or any organism's. It detects and helps fix the gravest kind of DNA breaks in which both strands of a DNA double helix are cut. The protein complex binds to the broken DNA ends, sends out a signal that stops the cell from dividing, and uses its shape-shifting ability to choose which DNA repair process is launched to fix the broken DNA. If unrepaired, double strand breaks are lethal to the cell. In addition, a repair job gone wrong can lead to the proliferation of cancer cells.

Little is known about how the protein's Transformer-like capabilities relate to its DNA-repair functions, however.

To learn more, the scientists modified the protein complex in ways that were designed to affect just one of the many activities it undertakes. They then used structural biology, biochemistry, and genomic tools to study the impacts of these modifications.

"By targeting a single activity, we can make the protein complex go down a different pathway and learn how its dynamic structure changes," says John Tainer of Berkeley Lab's Life Sciences Division. He conducted the research with fellow Berkeley Lab scientist Gareth Williams and scientists from several other institutions.

Adds Williams, "In some cases, we sped up or slowed down the protein complex's movements, and by doing so we changed its biological outcomes."

Much of the research was conducted at the Advanced Light Source (ALS), a synchrotron located at Berkeley Lab that generates intense X-rays to probe the fundamental properties of substances. They used an ALS beamline called SYBILS, which combines X-ray scattering with X-ray diffraction capabilities. It yields atomic-resolution images of the crystal structures of proteins. It can also watch the transformation of the protein as it undergoes conformational changes.

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How a shape-shifting DNA-repair machine fights cancer

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