Charcot-Marie-Tooth Disease – Wu Medical Center – A …

By adminJune 4, 2015Stem Cell Medical Center

Stem Cell Therapy for Charcot-Marie-Tooth DiseaseMay 26th, 2015

By Like Wu, Xiaojuan Wang, Sherry Xi, Bo Cheng, Susan Chu

Wu Medical Center

The patient is 34-year-old female. She was presented with involuntary movement of fingers and extremities prior weakness for the past 13 years without any apparent cause. The disease progressed gradually. She had nerve biopsy and gene analysis at a local hospital and was diagnosed with Charcot-Marie-Tooth disease (CMT). She took vitamins without any improvement. Her four limbs were weak. Her balance was bad. She always falls because of bad balance and lower limbs weakness. She had difficulty to hold objects. The distal ends of four limbs were depauperated, numbness and painful.

Physical examination: The general examination was normal. Her speech and spirit was good. The cranial nerves was normal. The distal ends of four limbs were depauperated. The proximal end muscle power of both upper limbs was at level 4, the distal ends muscle power of both upper limbs was at level 3, and the muscle power of all fingers was at level 3-. The proximal end muscle power of both lower limbs was at level 4. The distal ends muscle power of both lower limbs was at level 3. The muscle tension of four limbs was normal. The tendon reflex of four limbs disappeared, the pathology sign was negative. The deep and shallow sensation of her four limbs distal ends were not good.

Diagnosis: Charcot-Marie-Tooth disease (CMT)

Treatment target: Replace the heredodegeneration nerve cells with normal stem cells to repair the nerves, improve the nerve function, and also to improve equilibrium function and motor function.

Treatment procedure and results: We gave the patient 4 times neural stem cells (NSCs) and 4 times mesenchymal stem cells (MSCs) implantation treatment. The stem cells were activated in the patients body to repair the nerve damage. Together with nourishment of the neurons, improvement of circulation and regulating the immune, daily rehabilitation training was incorporated. During the treatment, the patient was happy, had a regular eating and sleeping pattern. With our doctors help, she was able to complete the treatment. After the treatment, the patient had significant improvement, her four limbs had less pain, numbness and weakness. Her exercise tolerance was better. The proximal end muscle power of both upper limbs was at level 5-. The distal ends muscle power of both upper limbs was at level 4, the muscle power of all fingers was at level 4-. The proximal end muscle power of both lower limbs was at level 5-. The distal ends muscle power of both lower limbs was at level 4-. Her balance and coordinate movement were better. Her life had been noticeably improved.

Charcot-Marie-Tooth disease (CMT) is also called Hereditary Motor and Sensory Neuropathy (HMSN), it has visible heredity. The main clinical characteristics: the distal ends of four limbs has progressive weakness, atrophia and sensory disturbance. CMT is one of the most common hereditary peripheral neuropathy (the incidence is around 1/2500). CMT is classified two types according to clinical and electrophysiological characteristics; CMT1 (demyelinating type) and CMT2 (axon type).

The patient had this disease when she was growing up, and the disease progressed slowly. She gradually had four limbs weakness, the distal ends of four limbs were depauperated, hypesthesia, tendon reflex of four limbs disappeared and balance disturbance. All the accessory examinations supported the diagnosis.

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Regenerative Medicine Symposium set for April 24 at GRU

By adminApril 14, 2015Stem Cell Medical Center

AUGUSTA, Ga. - Scientists and physicians from the region interested in regenerative and reparative medicine techniques, such as helping aging stem cells stay focused on making strong bone, will meet in Augusta April 24 to hear updates from leaders in the field and strategize on how to move more research advances to patients.

The daylong Regenerative Medicine and Cellular Therapy Research Symposium, sponsored by the Georgia Regents University Institute for Regenerative and Reparative Medicine, begins at 8 a.m. in Room EC 1210 of the GRU Health Sciences Building.

"We think this is a terrific opportunity for basic scientists and physicians to come together and pursue more opportunities to work together to get better prevention and treatment strategies to patients," said Dr. William D. Hill, stem cell researcher and symposium organizer.

Dr. Arnold I. Caplan, Director of the Skeletal Research Center at Case Western Reserve University and a pioneer in understanding mesenchymal stem cells, which give rise to bone, cartilage, muscle, and more, will give the keynote address at 8:45 a.m. Mesenchymal stem cell therapy is under study for a variety of conditions including multiple sclerosis, osteoarthritis, diabetes, emphysema, and stroke.

Other keynotes include:

The GRU Institute for Regenerative and Reparative Medicine has a focus on evidence-based approaches to healthy aging with an orthopaedic emphasis. "As you age, the bone is more fragile and likely to fracture," Hill said. "We want to protect bone integrity before you get a fracture as well as your bone's ability to constantly repair so, if you do get a fracture, you will repair it better yourself."

Bone health is a massive and growing problem with the aging population worldwide. "What people don't need is to fall and wind up in a nursing home," said Dr. Mark Hamrick, MCG bone biologist and Research Director of the GRU institute. "This is a societal problem, a clinical problem, and a potential money problem that is going to burden the health care system if we don't find better ways to intervene."

The researchers are exploring options such as scaffolding to support improved bone repair with age as well as nutrients that impact ongoing mesenchymal stem cell health, since these stem cells, which tend to decrease in number and efficiency with age, are essential to maintaining strong bones as well as full, speedy recovery.

Dr. Carlos Isales, endocrinologist and Clinical Director of the GRU institute, is looking at certain nutrients, particularly amino acids, and how some of their metabolites produce bone damage while others prevent or repair it. Isales is Principal Investigator on a major Program Project grant from the National Institutes of Health exploring a variety of ways to keep aging mesenchymal stem cells healthy and focused on making bone. "I think the drugs we have reduce fractures, but I think there are better ways of doing that," Isales said. "We are always thinking translationally," said Hill.

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Regenerative Medicine Symposium set for April 24 at GRU

U-M researchers find new gene involved in blood-forming stem cells

By adminApril 14, 2015Stem Cell Medical Center

ANN ARBOR--Research led by the University of Michigan Life Sciences Institute has identified a gene critical to controlling the body's ability to create blood cells and immune cells from blood-forming stem cells--known as hematopoietic stem cells.

The findings, scheduled for online publication in the Journal of Clinical Investigation April 13, provide new insights into the underlying mechanics of how the body creates and maintains a healthy blood supply and immune system, both in normal conditions and in situations of stress--like the body experiences following a bone marrow transplant.

Along with helping scientists better understand the body's basic processes, the discovery opens new lines of inquiry about the Ash1l gene's potential role in cancers known to involve other members of the same gene family, like leukemia, or those where Ash1l might be highly expressed or mutated.

"It's vital to understand how the basic, underlying mechanisms function in a healthy individual if we want to try to develop interventions for when things go wrong," said study senior author Ivan Maillard, an associate research professor at the Life Sciences Institute, where his lab is located, and an associate professor in the Division of Hematology-Oncology at the U-M Medical School.

"Leukemia is a cancer of the body's blood-forming tissues, so it's an obvious place that we plan to look at next. If we find that Ash1l plays a role, then that would open up avenues to try to block or slow down its activity pharmacologically," he said.

Graduate students Morgan Jones and Jennifer Chase were the study's first authors.

Dysfunction of blood-forming stem cells is well known in illnesses like leukemia and bone marrow failure disorders. Blood-forming stem cells can also be destroyed by high doses of chemotherapy and radiation used to treat cancer. The replacement of these cells through bone marrow transplantation is the only widely established therapy involving stem cells in human patients.

But even in the absence of disease, blood cells require constant replacement--most blood cells last anywhere from a few days to a few months, depending on their type.

Over more than five years, Maillard and his collaborators identified a previously unknown but fundamental role played by the Ash1l gene in regulating the maintenance and self-renewal potential of these hematopoietic stem cells.

The Ash1l (Absent, small or homeotic 1-like) gene is part of a family of genes that includes MLL1 (Mixed Lineage Leukemia 1), a gene that is frequently mutated in patients who develop leukemia. The research found that both genes contribute to blood renewal; mild defects were seen in mice missing one or the other, but lacking both led to catastrophic deficiencies.

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To fight nasty digestive bugs, scientists set out to build a better gut — using stem cells

By adminApril 14, 2015Stem Cell Medical Center

New $6.4M federal grant support will fuel the development of 'guts in a dish' to study interaction between cells & microbes in both health and disease

IMAGE:These HIO structures, each about the size of a BB and grown from stem cells, allow scientists to study the interaction between the cells of the gut lining and microbes... view more

Credit: University of Michigan Medical School

ANN ARBOR, Mich. -- If you got hit with any of the 'intestinal bugs' that went around this winter, you've felt the effects of infectious microbes on your digestive system.

But scientists don't fully understand what's going on in gut infections like that - or in far more serious ones that can kill. Many mysteries remain in the complex interaction between our own cells, the helpful bacteria that live inside us, and tiny invaders.

Now, a team of University of Michigan scientists will tackle that issue in a new way. Using human stem cells, they'll grow tiny "guts in a dish" in the laboratory and study how disease-causing bacteria and viruses affect the microbial ecosystem in our guts. The approach could lead to new treatments, and aid research on a wide range of diseases.

This work was started as part of the U-M Medical School's self-funded Host Microbiome Initiative and Center for Organogenesis, and the U-M Center for Gastrointestinal Research, funded by the National Institutes of Health. It also received funding from the U-M's MCubed initiative for interdisciplinary work.

Now, the project has received a $6.4 million boost with a new five-year NIH grant.

It will allow the U-M team to expand their effort to grow human intestinal organoids, or HIOs - tiny hollow spheres of cells into which they can inject a mix of bacteria. They'll work with researchers at other institutions, as part of the Novel, Alternative Model Systems for Enteric Diseases, or NAMSED, initiative sponsored by the NIH's National Institute of Allergy and Infectious Diseases.

Balls of cells become mini-guts

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To fight nasty digestive bugs, scientists set out to build a better gut -- using stem cells

Researchers identify drug target for ATRA, the first precision cancer therapy

By adminApril 13, 2015Stem Cell Medical Center

Targeted cancer therapies work by blocking a single oncogenic pathway to halt tumor growth. But because cancerous tumors have the unique ability to activate alternative pathways, they are often able to evade these therapies -- and regrow. Moreover, tumors contain a small portion of cancer stem cells that are believed to be responsible for tumor initiation, metastasis and drug resistance. Thus, eradicating cancer stem cells may be critical for achieving long-lasting remission, but there are no drugs available that specifically attack cancer stem cells.

Now a research team led by investigators in the Cancer Research Institute at Beth Israel Deaconess Medical Center (BIDMC), has identified an inhibitor of the Pin1 enzyme that can address both of these challenges in acute promyelocytic leukemia (APL) and triple negative breast cancer.

Their surprising discovery demonstrates that the vitamin A derivative ATRA (all-trans retinoic acid), a treatment for APL that is considered to be the first example of modern targeted cancer therapy, can block multiple cancer-driving pathways and, at the same time, eliminate cancer stem cells by degrading the Pin1 enzyme. Reported online in Nature Medicine, these novel findings suggest a promising new way to fight cancer -- particularly cancers that are aggressive or drug resistant.

"Pin1 changes protein shape through proline-directed phosphorylation, which is a major control mechanism for disease," explains co-senior author Kun Ping Lu, MD, PhD, Director of Translational Therapeutics in the Cancer Research Institute at BIDMC and Professor of Medicine at Harvard Medical School who co-discovered the enzyme in 1996. "Pin1 is a common key regulator in many types of cancer, and as a result, can control over 50 oncogenes and tumor suppressors, many of which are known to also control cancer stem cells."

Until now, agents that inhibit Pin1 have been developed mainly through rational drug design. Although these inhibitors have proven to be active against Pin1 in the test tube, when they are tested in vitro in a cell model or in vivo in a living animal they are unable to efficiently enter cells to successfully inhibit Pin1 function.

In this new work, co-senior author Xiao Zhen Zhou, MD, an investigator in BIDMC's Division of Translational Therapeutics and Assistant Professor at Harvard Medical School, decided to take a different approach to identify Pin1 inhibitors: She developed a mechanism-based high throughput screen to identify compounds that were targeting active Pin1.

"We had previously identified Pin1 substrate-mimicking peptide inhibitors," explains Zhou. "We therefore used these as a probe in a competition binding assay and screened approximately 8,200 chemical compounds, including both approved drugs and other known bioactive compounds." To increase screening success, Zhou chose a probe that specifically binds to the Pin1 enzyme active site very tightly, an approach that is not commonly used for this kind of screen.

"Initially, it appeared that the screening results had no positive hits, so we had to manually sift through them looking for the one that would bind to Pin1. We eventually spotted cis retinoic acid, which has the same chemical formula as all-trans retinoic acid [ATRA], but with a different chemical structure." It turned out, Zhou explains, that Pin1 prefers binding to ATRA and cis retinoic acid needs to convert ATRA in order to bind Pin1.

ATRA was first discovered for the treatment of acute promyelocytic leukemia (APL) in 1987. "Before tamoxifen or other targeted drugs, there was ATRA," says Lu. It was originally thought that ATRA was successfully treating APL by inducing cell differentiation, causing cancer cells to change into normal cells by activating the cellular retinoic acid receptors. But as these new findings reveal, although this differentiation activity is obvious, it is not the mechanism that is actually behind ATRA's successful outcomes in treating APL.

"While it has been previously shown that ATRA's ability to degrade the leukemia-causing fusion oncogene PML-RAR causes ATRA to stop the leukemia stem cells that drive APL, the underlying mechanism has remained elusive," says Lu. "Our new high throughput drug screening has revealed the ATRA drug target, unexpectedly showing that ATRA directly binds, inhibits and ultimately degrades active Pin1 selectively in cancer cells. The Pin1-ATRA complex structure suggests that ATRA is trapped in the Pin1 active site by mimicking an unreleasable enzyme substrate. Importantly, ATRA-induced Pin1 ablation degrades the fusion oncogene PML-RAR and treats APL in cell and animal models as well as in human patients.

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Researchers identify drug target for ATRA, the first precision cancer therapy

Stem Cells, Fecal Transplants Show Promise for Crohn's Disease

By adminApril 11, 2015Stem Cell Medical Center

By Amy Norton HealthDay Reporter

FRIDAY, April 10, 2015 (HealthDay News) -- Two experimental therapies might help manage the inflammatory bowel disorder Crohn's disease, if this early research pans out.

In one study, researchers found that a fecal transplant -- stool samples taken from a healthy donor -- seemed to send Crohn's symptoms into remission in seven of nine children treated.

In another, a separate research team showed that stem cells can have lasting benefits for a serious Crohn's complication called fistula.

According to the Crohn's & Colitis Foundation, up to 700,000 Americans have Crohn's -- a chronic inflammatory disease that causes abdominal cramps, diarrhea, constipation and rectal bleeding. It arises when the immune system mistakenly attacks the lining of the digestive tract.

A number of drugs are available to treat Crohn's, including drugs called biologics, which block certain immune-system proteins.

But fecal transplants take a different approach, explained Dr. David Suskind, a gastroenterologist at Seattle Children's Hospital who led the new study.

Instead of suppressing the immune system, he said, the transplants alter the environment that the immune system is reacting against: the "microbiome," which refers to the trillions of bacteria that dwell in the gut.

Like the name implies, a fecal transplant involves transferring stool from a donor into a Crohn's patient's digestive tract. The idea is to change the bacterial composition of the gut, and hopefully quiet the inflammation that causes symptoms.

And for most kids in the new study, it seemed to work. Within two weeks, seven of nine children were showing few to no Crohn's symptoms. Five were still in remission after 12 weeks, with no additional therapy, the researchers reported in a recent issue of the journal Inflammatory Bowel Diseases.

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iPSC model helps to better understand genetic lung/liver disease

By adminApril 4, 2015Stem Cell Medical Center

Using patient-derived stem cells known as induced pluripotent stem cells (iPSC) to study the genetic lung/liver disease called alpha-1 antitrypsin (AAT) deficiency, researchers have for the first time created a disease signature that may help explain how abnormal protein leads to liver disease.

The study, which appears in Stem Cell Reports, also found that liver cells derived from AAT deficient iPSCs are more sensitive to drugs that cause liver toxicity than liver cells derived from normal iPSCs. This finding may ultimately lead to new treatments for the condition.

IPSC's are derived from the donated skin or blood cells of adults and, with the reactivation of four genes, are reprogrammed back to an embryonic stem cell-like state. Like embryonic stem cells, iPSC can be differentiated toward any cell type in the body, but they do not require the use of embryos. Alpha-1 antitrypsin deficiency is a common genetic cause of both liver and lung disease affecting an estimated 3.4 million people worldwide.

Researchers from the Center for Regenerative Medicine (CReM) at Boston University and Boston Medical Center (BMC) worked for several years in collaboration with Dr. Paul Gadue and his group from Children's Hospital of Philadelphia to create iPSC from patients with and without AAT deficiency. They then exposed these cells to certain growth factors in-vitro to cause them to turn into liver-like cells, in a process that mimics embryonic development. Then the researchers studied these "iPSC-hepatic cells" and found the diseased cells secrete AAT protein more slowly than normal cells. This finding demonstrated that the iPSC model recapitulates a critical aspect of the disease as it occurs in patients. AAT deficiency is caused by a mutation of a single DNA base. Correcting this single base back to the normal sequence fixed the abnormal secretion.

"We found that these corrected cells had a normal secretion kinetic when compared with their diseased, parental cells that are otherwise genetically identical except for this single DNA base," explained lead author Andrew A. Wilson, MD, assistant professor of medicine at Boston University School of Medicine and Director of the Alpha-1 Center at Bu and BMC.

They also found the diseased (AAT deficient) iPSC-liver cells were more sensitive to certain drugs (experience increased toxicity) than those from normal individuals. "This is important because it suggests that the livers of actual patients with this disease might be more sensitive in the same way," said Wilson, who is also a physician in pulmonary, critical care and allergy medicine at BMC.

According to Wilson, while some patients are often advised by their physicians to avoid these types of drugs, these recommendations are not based on solid scientific evidence. "This approach might now be used to generate that sort of evidence to guide clinical decisions," he added.

The researchers believe that studies using patient-derived stem cells will allow them to better understand how patients with AAT deficiency develop liver disease. "We hope that the insights we gain from these studies will result in the discovery of new potential treatments for affected patients in the near future," said Wilson.

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

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iPSC model helps to better understand genetic lung/liver disease

Key Mechanism Identified in Pediatric Bone Cancers That Allows Proliferation of Tumor-Forming Stem Cells

By adminApril 2, 2015Stem Cell Medical Center

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Newswise A particular molecular pathway permits stem cells in pediatric bone cancers to grow rapidly and aggressively, according to researchers at NYU Langone Medical Center and its Laura and Isaac Perlmutter Cancer Center.

In normal cell growth, the Hippo pathway, which controls organ size in animals, works as a dam, regulating cell proliferation. What the researchers found is that the transcription factor of a DNA binding protein called sex determining region Y box 2, or Sox2 for short, which normally maintains cell self-renewal, actually releases the floodgates in the Hippo pathway in osteosarcomas and other cancers, permitting the growth of highly aggressive, tumor-forming stem cells.

Results from the study are to be published in the journal Nature Communications online April 2.

This study is one of the first to identify the mechanisms that underlie how an osteosarcoma cancer stem cell maintains its tumor-initiating properties, says senior study investigator Claudio Basilico, MD, the Jan T. Vilcek Professor of Molecular Pathogenesis at NYU Langone and a member of its Perlmutter Cancer Center.

In the study, the investigators used human and mouse osteosarcomas to pinpoint the molecular mechanisms that inhibit the tumor-suppressive Hippo pathway. The researchers concluded that Sox2 represses the functioning of the Hippo pathway, which, in turn, leads to an increase of the potent growth stimulator Yes Associated Protein, known as YAP, permitting cancer cell proliferation.

Our research is an important step forward in developing novel targeted therapies for these highly aggressive cancers, says study co-investigator Alka Mansukhani, PhD, an associate professor at NYU Langone and also a member of the Perlmutter Cancer Center. One possibility is to develop a small molecule that could knock out the Sox2 transcription factor and free the Hippo pathway to re-exert tumor suppression.

Mansukhani adds that the research suggests that drugs such as verteporfin, which interfere with cancer-promoting YAP function, might prove useful in Sox2-dependent tumors.

The study expands on previous work in Basilicos and Mansukhanis molecular oncology laboratories at NYU Langone and on earlier work by Upal Basu Roy, PhD, MPH, the lead study investigator, who found that Sox2 was an essential transcription factor for the maintenance of osteosarcoma stem cells.

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Key Mechanism Identified in Pediatric Bone Cancers That Allows Proliferation of Tumor-Forming Stem Cells

Researchers produce iPSC model to better understand genetic lung/liver disease

By adminApril 2, 2015Stem Cell Medical Center

(Boston)--Using patient-derived stem cells known as induced pluripotent stem cells (iPSC) to study the genetic lung/liver disease called alpha-1 antitrypsin (AAT) deficiency, researchers have for the first time created a disease signature that may help explain how abnormal protein leads to liver disease.

The study, which appears in Stem Cell Reports, also found that liver cells derived from AAT deficient iPSCs are more sensitive to drugs that cause liver toxicity than liver cells derived from normal iPSCs. This finding may ultimately lead to new treatments for the condition.

IPSC's are derived from the donated skin or blood cells of adults and, with the reactivation of four genes, are reprogrammed back to an embryonic stem cell-like state. Like embryonic stem cells, iPSC can be differentiated toward any cell type in the body, but they do not require the use of embryos. Alpha-1 antitrypsin deficiency is a common genetic cause of both liver and lung disease affecting an estimated 3.4 million people worldwide.

Researchers from the Center for Regenerative Medicine (CReM) at Boston University and Boston Medical Center (BMC) worked for several years in collaboration with Dr. Paul Gadue and his group from Children's Hospital of Philadelphia to create iPSC from patients with and without AAT deficiency. They then exposed these cells to certain growth factors in-vitro to cause them to turn into liver-like cells, in a process that mimics embryonic development. Then the researchers studied these "iPSC-hepatic cells" and found the diseased cells secrete AAT protein more slowly than normal cells. This finding demonstrated that the iPSC model recapitulates a critical aspect of the disease as it occurs in patients. AAT deficiency is caused by a mutation of a single DNA base. Correcting this single base back to the normal sequence fixed the abnormal secretion.

"We found that these corrected cells had a normal secretion kinetic when compared with their diseased, parental cells that are otherwise genetically identical except for this single DNA base," explained lead author Andrew A. Wilson, MD, assistant professor of medicine at Boston University School of Medicine and Director of the Alpha-1 Center at Bu and BMC.

They also found the diseased (AAT deficient) iPSC-liver cells were more sensitive to certain drugs (experience increased toxicity) than those from normal individuals. "This is important because it suggests that the livers of actual patients with this disease might be more sensitive in the same way," said Wilson, who is also a physician in pulmonary, critical care and allergy medicine at BMC.

According to Wilson, while some patients are often advised by their physicians to avoid these types of drugs, these recommendations are not based on solid scientific evidence. "This approach might now be used to generate that sort of evidence to guide clinical decisions," he added.

The researchers believe that studies using patient-derived stem cells will allow them to better understand how patients with AAT deficiency develop liver disease. "We hope that the insights we gain from these studies will result in the discovery of new potential treatments for affected patients in the near future," said Wilson.

###

Funding was provided by an ARRA stimulus grant (1RC2HL101535-01) awarded by the National Institutes of Health (NIH) to Boston University School of Medicine, Boston Medical Center and the Children's Hospital of Philadelphia. Additional funding was provided by K08 HL103771, FAMRI 062572_YCSA, an Alpha-1 Foundation Research Grant and a Boston University Department of Medicine Career Investment Award. Additional grants from NIH 1R01HL095993 and 1R01HL108678 and an ARC award from the Evans Center for Interdisciplinary Research at Boston University supported this work.

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Researchers produce iPSC model to better understand genetic lung/liver disease

Cellular Dynamics Webinar Spotlights Diabetic Cardiomyopathy-in-a-dish Model that May Elucidate Mechanisms for Repair …

By adminMarch 31, 2015Stem Cell Medical Center

Yorba Linda, CA (PRWEB) March 30, 2015

Developing new treatments for Diabetes Type 2 complications is challenging due to the use of cellular models that recapitulate only some subset of the specific features, but not the entirety of the disease.

A company that specializes in developing and manufacturing fully functioning human cells to precise specifications has created iPSC-derived cardiomyocytes (heart muscle cells), which have been used to develop environmentally and genetically driven in vitro models of Diabetes Type 2. The development process involves mimicking diabetic clinical chemistry to induce a phenotypic surrogate of diabetic cardiomyopathy, observing structural and functional disarray.

Cellular Dynamics International (CDI) is sponsoring a new educational webinar, Diabetic Cardiomyopathy Modeling & Screening with iPSC-derived Cardiomyocytes, to present the first patient-specific iPSC model of a complex metabolic condition, demonstrating the power of this model for discovery and testing of new therapeutic strategies. The webinar concludes with the presentation of a new approach using chemical biology to ultimately elucidate novel mechanisms activating the repair and regeneration of cardiomyocytes. Webinar speakers are Roberto Iacone, PhD and Brad Swanson, PhD.

Dr. Iacone, Senior Principal Scientist at Roche, pharma and research development (pRED), Basel, Switzerland, established the Stem Cell Group in the Cardiovascular and Metabolic Discovery at the company. Research in his group has focused on understanding the pathophysiological mechanisms and development complications in the heart using patient-specific iPSCs: the patient in a dish paradigm. The group is establishing in vitro disease modeling to identify new drugs for the retina remodeling linked to age-related macular degeneration. His research interest includes the identification and characterization of genes that regulate tissue repair and regeneration, aiming to develop regenerative medicines activating endogenous tissue progenitors.

Dr. Swanson is Senior Director of Cell Biology Research and Development, Cellular Dynamics International, Madison, Wisconsin, where he led the effort to develop the first commercially available human iPSC-derived cell product, iCell Cardiomyocytes, and several other iPSC models. Previously, he was a Senior Scientist at Roche NimbleGen, where he established the industrys first sequence capture product for targeted next generation sequencing workflows. Swanson received his PhD in Cellular and Molecular Biology (cardiac differentiation) from UW-Madison, undertook postdoctoral research in T cell behavior at the National Jewish Medical Center-HHMI in Denver, Colorado, and joined Columbus Childrens Research Institute/Ohio State University Center for Vaccines and Immunity as an Assistant Professor.

The free webinar, hosted by LabRoots, will be presented on April 7, 2015, at 8:30 am PST/11:30 am EST/5:30 pm CET.

For full details and free registration, click here.

About Cellular Dynamics International, Inc. Cellular Dynamics International, Inc. is a leading developer and producer of fully functioning human cells in industrial quantities to precise specifications. CDI's proprietary products include true human cells in multiple cell types (iCell products), human induced pluripotent stem cells (iPSCs) and custom iPSCs and iCell products (MyCell Products). CDI's products provide standardized, easy-to-use, cost-effective access to the human cell, the smallest fully functioning operating unit of human biology. Customers use our products, among other purposes, for drug discovery and screening; to test the safety and efficacy of their small molecule and biologic drug candidates; for stem cell banking; and in the research and development of cellular therapeutics. CDI was founded in 2004 by Dr. James Thomson, a pioneer in human pluripotent stem cell research at the University of Wisconsin-Madison. CDI's facilities are located in Madison, Wisconsin, with a second facility in Novato, California. See http://www.cellulardynamics.com.

About LabRoots: LabRoots is the leading scientific social networking website and producer of online educational events and webinars. And we are a powerful advocate in amplifying global networks and communities, and contributing to the advancement of science through content sharing capabilities and encouraging group interactions.

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Cellular Dynamics Webinar Spotlights Diabetic Cardiomyopathy-in-a-dish Model that May Elucidate Mechanisms for Repair ...