Category Archives: Connecticut Stem Cells

CROMWELL, Conn.--(BUSINESS WIRE)--Biological Industries USA (BI-USA), a division of Biological Industries Israel LTD, announced today a distribution agreement with Mill Creek Life Sciences LLC, a Rochester, Minnesota start-up that provides tools to support the development and application of cellular and biological therapeutics. The agreement provides for distribution of PLTMax Human Platelet Lysate, a product derived from human platelets and offers unparalleled cell growth and cytogenetic stability of adult stem cells over fetal bovine serum (FBS). PLTMax is available in research and clinical grades and has been used in more than 30 clinical trials worldwide, including several Phase III trials.

We are very pleased to announce our partnership with the team at Mill Creek Life Sciences, said Tanya Potcova, Chief Executive Officer of BI-USA. We have a great opportunity to expand our stem cell portfolio reach here in the US and beyond. We met with Mill Creek at the Cell & Gene Meeting on the Mesa in San Diego last October, where we discussed the potential use of PLTMax with our xeno-free NutriStem MSC Medium and EndoGo XF Medium. We found that we have a mutual interest in serving the needs of the stem cell industry through application development by pairing our leading technology together for use in both research and clinical development. We are excited about the potential for us to expand this collaboration.

Mill Creek Life Sciences is happy to announce this relationship withBiological Industries, said Bill Mirsch, Chief Executive Officer of Mill Creek Life Sciences. We tested their NutriStem MSC Medium and EndoGo XF Medium and found them to be very effective when paired with our PLTMax. We look forward to partnering with BI-USA to provide the best research and GMP grade media options for MSC and endothelial cell therapies.

About Biological Industries

Biological Industries (www.bioind.com) is one of the worlds leading and trusted suppliers to the life sciences industry, with over 35 years experience in cell culture media development and GMP manufacturing. BIs products range from classical cell culture media to supplements and reagents for stem cell research and potential cell therapy applications, to serum-free media and many other products for animal cell culture and molecular biology. BI is committed to a Culture of Excellence through advanced manufacturing and quality-control systems, regulatory expertise, in-depth market knowledge, and extensive technical customer-support, training, and R&D capabilities.

Biological Industries USA (BI-USA) is the US commercialization arm of BI, with facilities in Cromwell, Connecticut. Members of the BI-USA team share a history and expertise of innovation and success in the development of leading-edge technologies in stem cell research, cellular reprogramming, and regenerative medicine.

To receive ongoing BI communications, please join ouremail listor connect with the company onLinkedIn,Twitter, andFacebook.

About Mill Creek Life Sciences

Mill Creek Life Sciences (www.millcreekls.com) is the first company to commercialize human platelet lysate for cellular therapy. A spin-off out of the Human Cell Therapy Laboratory at the Mayo Clinic in Rochester, Minnesota, Mill Creek has been involved in clinical cellular therapies from the beginning. Mill Creek is dedicated to providing the highest quality products for the research and clinical community.

To find out more about Mill Creek Life Sciences, pleaseContact Usor connect with the company onLinkedIn,Twitter, andFacebook.

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Biological Industries USA Signs Agreement with Mill Creek Life ... - Business Wire (press release)

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Stormy Chamberlain - Faculty Directory UConn Health

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Talk Computational Neuroscience 2015 Brandeis University Neuroscience Journal Club - Responsible Research Conduct Talk Neuroscience Department 2015 Sparse, Strong and Large Area Targeting of Genetically Encoded Indicators Poster NIH Investigator Meeting 2015 Bethesda, MD Extrasynaptic receptors and dentritic spikes. See more at: https://royalsociety.org/events/2015/01/chemical-transmitters/ Talk The Royal Society, London 2015 London, UK Optical recordings of dendritic membrane potential and calcium transients. Talk Ministry of Science, Serbia 2014 Seventh Photonics Workshop 2014 (Kopaonik) Synapse discussion Other CT science festival neuroscience 2014 The Richard D. 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Faculty Directory UConn Health

Skip Article Header. Skip to: Start of Article. Neural progenitor cells derived from human urine cells. Image: Lihui Wang, Guangjin Pan and Duanqing Pei

By Liat Clark, Wired UK

Biologists in China have published a study detailing how they transformed common cells found in human urine into neural stem cells that can be used to create neurons and glial brain cells. The find holds huge potential for the rapid testing and development of new treatments for neurodegenerative disorders.

[partner id=wireduk align=right]The team, from the Guangzhou Institute of Biomedicine and Health, had announced in 2011 that it had successfully reprogrammed skin-like cells from the kidneys, found in urine, into induced pluripotent stem (iPS) cells. These iPS cells can be tweaked to become pretty much any human cell in the body; however the traditional technique prompting this transformation inserting pluripotent genes into the blanket cells via a genetically engineered retrovirus has its flaws. It seems the presence of the retrovirus leads to a destabilisation of the genome, rendering it unpredictable, susceptible to mutations and thus a liability.

Stem cell biologist Duanqing Pei and his team opted for another route, that they claim presents a safer, faster alternative. Having extracted kidney epithelial cells from the urine of three donors aged 10, 25 and 37, the team used vectors a type of DNA molecule useful in transporting genetic information from cell to cell to transport the information without having to integrate the new genes into the chromosome of the kidney cell, something that is presumed to be partly to blame for the aforementioned mutations.

In one experiment the pluripotent stem cells formed in Petri dishes after 12 days, which is about half the time it normally takes for them to form. These cultured cells soon took on the shape of neural rosettes and were deemed to be neural progenitor cells a precursor to a fully blown neural cell. Eventually these neural progenitor cells were cultured to become neurons and astrocyte and oligodendrocyte glial cells

Though the team did not definitively prove that the cells would have less mutations in the long run, it did suggest the method could provide a good alternative to using embryonic stem cells to build new neurons. In a 2007 study, when the embryonic stem cells began their transformation into neurons and were transplanted into the brains of rats suffering from an equivalent to Parkinsons, they began to divide too quickly and tumours formed. This time around, however, when the neurons and astrocytes were transplanted into rat brains they appeared to still be thriving a month later, with no signs of abnormal cell division or tumour formation.

The technique is extremely promising for several reasons. For one, the material is readily available and no invasive extraction is necessary. We work on childhood disorders, commented University of Connecticut Health Centre geneticist Marc Lalande, not involved in the study, in Nature, and its easier to get a child to give a urine sample than to prick them for blood.

Its also far better to be able to develop a cell derived from an individuals own cells they are less likely to prompt an immune response and rejection, which could be the case when using embryonic or umbilical cord stem cells to make iPS cells. The fact that it bypasses the ethical questions of using embryonic cells, and appears to take half the time to develop also provides researchers with a faster, more efficient way to help combat neurological diseases such as Alzheimers and Parkinsons. And with millions suffering from these degenerative disorders worldwide, anything that can speed up research will be of huge benefit.

Source: Wired.co.uk

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Cells Harvested From Human Urine Used to Make Stem Cells

Reprod Biol Endocrinol. 2003; 1: 101.

1Department of Molecular and Cell Biology, Center for Regenerative Biology, University of Connecticut, 1392 Storrs Road Unit 4243, Storrs, CT 06269-4243, USA

Received 2003 Aug 20; Accepted 2003 Nov 13.

Satellite cells are myogenic stem cells responsible for the post-natal growth, repair and maintenance of skeletal muscle. This review focuses on the basic biology of the satellite cell with emphasis on its role in muscle repair and parallels between embryonic myogenesis and muscle regeneration. Recent advances have altered the long-standing view of the satellite cell as a committed myogenic stem cell derived directly from the fetal myoblast. The experimental basis for this evolving perspective will be highlighted as will the relationship between the satellite cell and other newly discovered muscle stem cell populations. Finally, advances and prospects for cell-based therapies for muscular dystrophies will be addressed.

Skeletal muscle is subject to constant injury resulting from weight bearing, exercise, and trauma, thereby requiring an ever-available, renewable source of cells for muscle repair and regeneration. Since its identification, the satellite cell has been a popular candidate for the adult skeletal muscle "stem cell" [1]. Residing dormant beneath the basal lamina of mature skeletal muscle fibers, this cell is ideally located for timely repair of degenerating muscle fibers. Additionally, these quiescent cells are activated to proliferate upon muscle injury, a necessary step towards generating sufficient numbers of myoblasts for muscle differentiation and myotube formation. However, the identification of multiple stem cell populations resident in skeletal muscle has added further complexity to understanding the process of muscle regeneration. In this mini-review, we will briefly examine the molecular and morphological characteristics of the satellite cell, its role in muscle regeneration, and discuss outstanding questions regarding its origin, developmental potential, and uses in myoblast therapy.

Although the developmental origin of satellite cells remains unknown, in vertebrates, the majority of skeletal muscle progenitors arise in the somites. Somites are transient epithelial spheres that pinch off of the paraxial mesoderm lining both sides of the neural tube. Myogenic precursors are first identified in the dermomyotome, an epithelial layer located in the dorsal compartment of the somite. These precursors are characterized by their expression of the paired box transcription factors Pax-3 and Pax-7; in response to signals such as Wnts and Sonic hedgehog from surrounding embryonic structures, the myogenic determination genes Myf-5 and MyoD are activated [3]. Coinciding with the down-regulation of Pax gene expression, muscle precursor cells committed to the skeletal muscle lineage (myoblasts) translocate to the subjacent myotome, where the muscle regulatory factors Myogenin and MRF4 direct differentiation and fusion into multi-nucleated myofibers.Satellite cells are first apparent towards the end of embryogenesis, and function as a primary source for the myogenic cells required for post-natal muscle growth [2].

In adult muscles, dormant, Pax-7-expressing satellite cells reside between the plasmalemma and basal lamina at frequencies that vary with age, muscle fiber type, and species [4]. The activation of satellite cells in vivo can be induced by muscle fiber injury brought on by acute injury [5-7], exercise [8-10], and denervation [11]. Upon injury, satellite cells are stimulated to re-enter the cell cycle to generate a pool of proliferating myogenic precursors analogous to the embryonic myoblasts, while the inflammatory response mounted by the immune system clears affected myofibers [2]. Recently, certain Wnt-family members were found to be up-regulated in muscle following injury, suggesting a parallel to myogenic signaling pathways in the embryo [12]. Additionally, up-regulation of Myf-5 and MyoD occurs at the injury site in proliferating satellite cells indicating cell commitment [13-17]. Pax-7 expression declines with the up-regulation of MRF-4 and Myogenin, and differentiated myocytes fuse to new and existing fibers as part of the repair process. One of the hallmarks of regenerating myofibers is the centrally located position of the myonuclei; upon maturing, muscle fiber nuclei are located along the cell periphery [4]. Notably, repeated cycles of injury and regeneration do not appear to deplete satellite cell numbers, suggesting that these cells have the ability to self-renew [2].

Satellite cells were initially identified in frog leg muscles by electron microscopy [1], and subsequently have been identified in all higher vertebrates. In humans and mice, these quiescent [18], non-fibrillar, mononuclear cells are most plentiful at birth (estimated at 32% of sublaminar nuclei) [19]. The frequency declines post-natally, stabilizing to between 1 to 5% of skeletal muscle nuclei in adult mice [2]. Satellite cell frequency varies in different muscles, likely as a function of variation in fiber type composition (i.e. slow oxidative, fast oxidative, or fast glycolytic fibers). For example, the mouse soleus muscle, which is predominantly made up of slow oxidative fibers, has a higher number of satellite cells than the extensor digitorum longus (EDL) muscle, which primarily contains fast glycolytic fibers. Additionally, the absolute numbers of satellite cells increases in the soleus but not the EDL between 1 and 12 months of age, although the proportion of satellite cells decreases in both muscle types with increasing age [20]. In humans, the proportion of satellite cells in skeletal muscles also decreases with age, which may explain the decreased efficiency of muscle regeneration in older subjects [21]. Satellite cells from aged muscle also display reduced proliferative and fusion capacity, as well as a tendency to accumulate fat, all of which likely contribute to deteriorating regeneration capability [22,23]. That endurance training can offset the decline in satellite cell number with age suggests that poorer regeneration is not simply a result of limited replicative potential of older satellite cells [24].

Several signals and growth factors have been implicated in promotion of satellite cell activation and proliferation (Figure ). For example, the Notch signaling pathway, which is activated upon muscle injury, regulates satellite cell transition from quiescence to proliferation in single fiber cultures, thereby expanding the myoblast population in injured muscle [25]. Basic fibroblast growth factor (bFGF) stimulates satellite cell proliferation while inhibiting differentiation [2]. bFGF also promotes muscle regeneration in mdx mice [26], which undergo repeated cycles of degeneration and regeneration resulting from a mutation in the dystrophin gene; in humans, deficiency of dystrophin causes Duchenne muscular dystrophy [27,28]. In addition to expressing all known FGF receptors [29,30], satellite cells also express the tyrosine kinase receptor c-met [16,31]. The c-met ligand, hepatocyte growth factor/scatter factor (HGF/SF), is also a known activator of satellite cells [29,32].

Model for the development, activation, and maintenance of the satellite cell. Upon skeletal muscle injury, quiescent satellite cells expressing Pax-7 and Foxk1 are activated to proliferate, up-regulating the myogenic determination factors, MyoD and Myf-5 ...

Targeted deletion of the gene encoding the Forkhead/winged helix transcription factor Foxk1 [previously known as myocyte nuclear factor (MNF)], which is expressed in quiescent satellite cells, causes a severely runted phenotype, and cardiotoxin-induced muscle regeneration is delayed and accompanied by prominent accumulation of adipose cells, suggesting a defect in skeletal muscle commitment [33]. Interestingly, the myopathy associated with the Foxk1 mutant is rescued when bred into a p21-null background. p21 is up-regulated in Foxk1-null muscles, and while mice lacking this cyclin-dependent kinase inhibitor show a defect in satellite cell differentiation, double mutants exhibit normal muscle growth and regeneration, suggesting that p21 is a downstream target of Foxk1 [34,35].

The muscle determination gene MyoD is also required for normal muscle regeneration [36]. Regenerating muscles in MyoD-null animals accumulate high numbers of mononuclear cells and have few differentiated myotubes; this phenotype is exacerbated in an mdx background, with MyoD-/-; mdx muscles exhibiting severely reduced cross-sectional area and mass. MyoD-null animals exhibit increased numbers of satellite cells, suggesting that the cells fail to progress through the differentiation program and instead participate in self-renewal [36]. The abnormal proliferation observed with MyoD-null adult myoblasts and failure to up-regulate the muscle differentiation factors MRF-4 or Myogenin under differentiation conditions support this hypothesis [37,38]. In addition, MyoD-null satellite cells express increased levels of Myf-5 [37,38]. In embryos lacking MyoD, myogenesis is dependent on Myf-5 and vice versa: while single mutant embryos have normal muscles at birth, MyoD-/-; Myf-5-/- double mutant embryos fail to develop myoblasts or myotubes [39-41]. Given the defects in muscle regeneration observed in adult MyoD mutants, it is evident that the functional redundancy between MyoD and Myf-5 that ultimately rescues embryonic muscle development is not sufficient to rescue myogenesis in injured muscle.

Interestingly, while traditionally thought to be committed to the skeletal muscle fate, it is now evident that muscle stem cells, including satellite cells, are multipotent. For example, bone morphogenetic protein (BMP) treatment activates osteogenic markers while down-regulating MyoD in C2C12 myoblasts, an immortalized cell line derived from mouse limb muscle [42,43]. Additionally, treatment with thiazolidinediones and fatty acids converts C2C12 cells to the adipogenic cell fate [44]. Primary myoblast cultures from adult muscles respond similarly to C2C12 cells in the presence of strong osteogenic and adipogenic inducers; interestingly, satellite cells derived from intact single fiber cultures (and thought to be more representative of true myogenic stem cells) spontaneously form adipocytes and osteocytes when cultured on Matrigel, a soluble basement membrane matrix lacking strong osteogenic or adipogenic signals [45]. The finding that undifferentiated cells in adult myoblast cultures co-express MyoD, Runx2, and PPAR, key regulators for myogenesis, osteogenesis, and adipogenesis, respectively, supports the hypothesis that satellite cells have a multipotential predisposition [46].

The plasticity of muscle stem cells has also been demonstrated using ex vivo approaches. Muscle stem cells isolated via serial preplating enrich for a population of cells which, in addition to contributing to regenerating myofibers when injected directly into dystrophic muscle, are detected in differentiated vascular and nerve cells [47,48]. Furthermore, these cells, which express the myoblast markers desmin and MyoD, are sufficient to completely heal skull defects in vivo when engineered to express BMP [49]. These muscle-derived stem cells are also capable of reconstituting bone marrow in lethally irradiated mice [50].

Another muscle-based stem cell with hematopoietic potential is the muscle side population (SP) cell, which can be isolated based on its specific exclusion of the vital dye Hoechst 33342 [51]. Initially sorted from bone marrow derived (BMD) stem cells by FACS analysis and observed to possess the majority of hematopoietic stem cell activity in bone marrow [52], SP cells have since been identified in a variety of tissues, including skeletal muscle, brain, heart, spleen, kidney and lung, although they are notably absent in peripheral blood [53]. It is important to note that the relationship between these different SP populations, and whether or not they derive from a common precursor, remains to be determined. Muscle SP cells reconstitute bone marrow in lethally irradiated mdx mice, although less efficiently than BMD SP cells. Interestingly, donor-derived nuclei also appear in regenerating muscle fibers after bone marrow reconstitution, indicating a contribution by the hematopoietic system in muscle repair [51,54]. The heterogeneity of muscle stem cells is underscored by the observation that SP cells within normal, uninjured skeletal muscle can be distinguished as positive for the hematopoietic marker CD45 (and poorly myogenic) or CD45-negative (a population that readily differentiates along the myogenic pathway) [55]. The CD45-positive subpopulation of cells has also been shown to contribute to neo-vascularization in regenerating muscle, whereas the CD45-negative population does not [56]. Interestingly, Wnts 5a, 5b, 7a and 7b, which are up-regulated in myoblasts and myofibers of regenerating muscle, convert the normally resistant CD45-positive muscle SP fraction to the myogenic program; this property to induce a switch in fate could contribute to the recruitment of much-needed progenitors upon injury [12].

A recent study of the Pax-7-null mouse revealed that this paired box transcription factor is essential for satellite cell formation. In addition to exhibiting severe muscle deficiency at birth and premature lethality, Pax-7 mutants are completely devoid of satellite cells [57]. However, while this observation demonstrates the requirement for Pax-7 in satellite cell formation, it remains to be seen whether the satellite cell arises from a pre-determined myoblast in the dermomyotome, a fetal myoblast, or from a non-somitic progenitor. Satellite cells may originate from specified Pax-7-positive cells prior to the activation of Myf-5 and MyoD, and thus represent a true precursor to the myogenic lineage. Alternatively, satellite cells may arise from determined myoblasts which, instead of differentiating, continue to proliferate until withdrawing from the cell cycle and taking up residence beneath the basal lamina of myofibers. While relatively little is known about the cis regulation of the Pax-7 gene, the extensive characterization of Myf-5 and MyoD regulatory elements [3,58] can be used to determine if satellite cells originate from a Myf-5 or MyoD-positive population by in vivo cell tracing. Interestingly, while Pax-7-null animals lack satellite cells, the muscle SP population remains intact, although exhibiting increased hematopoietic potential; Pax-7 may direct specification of pluripotent SP cells to satellite cells [57,59].

The observation that various non-muscle stem cells can participate in skeletal muscle regeneration has expanded the candidate pool for the satellite cell precursor. For example, myogenic potential has been demonstrated in vivo by mesoangioblasts, which are vessel-associated stem cells [60-62], neural stem cells [63], and, as mentioned previously, bone marrow cells [64,65].

Bone marrow cells have long been known to have myogenic potential [66,67]. Direct injection of -galactosidase-positive bone marrow cells into cardiotoxin-injured muscle gives rise to labeled myofibers, although at a lower frequency than injected satellite cells [64]. Interestingly, bone marrow cells contribute directly to regenerating myofibers in lethally irradiated mdx bone marrow transplant recipients [68]. Surprisingly, in the absence of myogenic induction, a subset of bone marrow cells in mdx mice are positive for both early and late myogenic markers including Pax3, MyoD, and myosin heavy chain, suggesting that muscle commitment and differentiation are underway [69]. Also intriguing is the finding that GFP-labeled BMD cells take up residence beneath the basal lamina of skeletal muscle fibers in irradiated transplant recipients following injury (in this case, an exercise model), with subsequent injury provoking an increased contribution of BMD cells to regenerated muscle fibers [65]. This suggests that satellite cells are maintained in regenerating fibers through self-renewal as well as replenishment from the bone marrow. It remains to be seen what proportion of satellite cells arise anew with each round of injury, and whether multiple rounds of injury results in a complete turnover of host satellite cells with donor bone marrow cells.

The use of muscle stem cells for therapeutic purposes holds much promise for treatment of diseases affecting skeletal muscle, including muscular dystrophy [70]. Dystrophic muscles that receive myoblast transplants exhibit some dystrophin-positive myofibers, and persistence of donor fibers in regenerated muscles is observed [71-73]. However, certain roadblocks hinder the efficacy of this therapy, including the limited migration of donor cells into dystrophic muscle and problems with poor donor cell survival and inefficient myogenic contribution. Advances have been made in identifying chemotactic factors and cell surface molecules that enhance the migration of transplanted cells [74-76]. In addition, careful selection of donor cells has been shown to enhance efficiency of rescue and cell survival in transplant hosts. In particular, Huard and colleagues have found that their serial preplated muscle stem cell cultures display enhanced proliferative capabilities and readily contribute to regenerating muscle while failing to trigger a strong immune response [47,77]. Furthermore, CD45-positive muscle SP cells also contribute to regenerating muscle with high efficiency [54,59].

The use of bone marrow transplants for treating muscular dystrophy has been contemplated as an alternative therapy to myoblast injection and, as mentioned previously, BMD cells do contribute to regenerating muscle. In fact, bone marrow derived nuclei have been identified in muscle biopsies from a 15-year-old patient who received a bone marrow transplant at age 1, and was diagnosed with a mild case of Duchenne muscular dystrophy at age 12 [78]. While this demonstrates the longevity of transplanted cells in muscle, it remains to be seen whether the contribution of these cells to regenerating muscle is responsible for the mild form of the patient's disease. Intriguingly, intra-arterial injection of wild-type mesoangioblasts into mice suffering from limb girdle muscle dystrophy results in complete functional recovery of all affected muscles [62]. This presents a promising solution to difficulties encountered with myoblast transplantation therapy, and makes all muscles accessible for treatment. This is especially important for the treatment of essential muscles such as the diaphragm, impairment of which results in severe respiratory problems.

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Nearly 500 scientists, business leaders, and students met April 27 in Hartford for StemConn2015. Held every two years, StemConn is Connecticuts premier conference on Stem Cell and Regenerative Medicine research.

The enthusiastic audience, the largest ever for a StemConn conference, was welcomed by Connecticut officials, including Governor Dannel P. Malloy, U.S. Senator Chris Murphy, U.S. Congresswoman Rosa DeLauro, Connecticut State Representative Lonnie Reed, and Hartford Mayor Pedro E. Segarra.StemConn2015 marked the anniversary of Connecticuts bold decision 10 years ago to encourage stem cell research via $100 million in state funding, giving Connecticut researchers a jump start in a critical biomedical area. Today Connecticut is a world-leader in stem cell research, and UConn, Wesleyan, and Yale each have significant programs in place.

The expansion of research towards clinical developments in this area has been remarkable, said UConns Dr. Caroline Dealy, organizing chair of the conference. We heard from researchers who are using stem cells to restore vision, to build bio-scaffolds, and to one day treat diseases like spinal injury, lung disease, and bone defects.

Researchers are also understanding how the bodys own stem cells may be stimulated to heal tissue damage. Much of the research in Regenerative Medicine is aimed at using adult stem cells now, Dealy said.More than 100 college and high school students participated in the StemConn2015 event as part of an education and public outreach initiative. Graduate students and fellows presented an extensive poster session, and students had the opportunity to meet with the invited speakers over lunch. Our students had a fantastic time at the Conference, said Tom Vrabel, a teacher at the Trumbull Agriscience Biotechnology High School. Exposures such as this can change their life paths.

This years event featured a special Commercialization and Translation session highlighting Connecticuts entrepreneurial activities in bioscience. Dr. Susan Froshauer, president and CEO of CURE, the states bioscience cluster, points out that that the states original $100 million has proved a fertile investment. We have tripled that, in terms of the amount of money that these researchers have brought into Connecticut, Froshauer says.

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StemCONN

Overview To be part of our organization, every employee should understand and share in the YNHHS Vision, support our Mission, and live our Values. These values-integrity, patient-centered, respect, accountability, and compassion-must guide what we do, as individuals and professionals, every day.

Under the direction of the Laboratory Manager, Stem Cell Specialist, and Assistant Chief Technologists, demonstrates ability to perform a wide variety of routine and some special technical procedures in the Stem Cell Laboratory. Demonstrates good time management and organizational skills. Interprets data based on knowledge and experience. Evaluates, troubleshoots and solves routine problems. Participates in quality control, quality assurance, and equipment maintenance programs in the laboratory.

EEO/AA Minority/Female/Disability/Veteran

Responsibilities

Qualifications EDUCATION

Education: BS Degree in a Biological Science or equivalent required.

EXPERIENCE

One to two years of relevant clinical or research laboratory experience required. Previous laboratory experience in the cell therapy field preferred.

SPECIAL SKILLS

Knowledge of stem cell regulation and accreditation requirements preferred. Familiarity with personal computer (Excel, Word) desired. Excellent interpersonal, verbal and written communication skills to interact with clinical trial sponsors and other hospital staff required. Must have excellent organizational skills.

Company Description:

Yale-New Haven Hospital is a destination hospital for patients from around the corner, around the country, and around the world. As a Magnet-recognized*, tertiary medical center, with 1,500+ beds, we are the 4th largest hospital in the country, with two acute care campuses and three emergency departments, including a Level I trauma center. We're ranked as one of "America's Best Hospitals" by U.S. News & World Report, which is a testament to the unrivaled expertise, compassion and character of our staff, and as the primary teaching facility for Yale Schools of Medicine and Nursing, we are nationally recognized for our commitment to teaching and clinical research.

Located on the Connecticut shoreline, Yale-New Haven Hospital includes Smilow Cancer Hospital at Yale-New Haven, Yale-New Haven Children's Hospital and Yale-New Haven Psychiatric Hospital.

*Yale-New Haven Hospital's York Street campus and associated ambulatory sites are Magnet-designated by the ANCC.

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STEM CELL TECHNOLOGIST with Yale-New Haven Hospital | 31281935

Eight years ago, Dr. Diane Krause was one of only two scientists at the Yale School of Medicine whose work was specifically focused on stem cells.

Today, more than 70 Yale faculty members are involved in some form of stem cell research, which since 2007 has been supported at Yale by more than $230 million in state and federal grants and funding foundations. Yale stem cell researchers have published 472 papers exploring a host of medical and scientific questions, from the origins of leukemia to the molecular basis of hair growth.

This field has grown more quickly than any of us could have envisioned, said Krause, professor of laboratory medicine, cell biology, and pathology, and since 2006 associate director of the Yale Stem Cell Center.

On Wednesday April 3, Krause will join more than 430 registrants and Governor Dannel Malloy in celebrating Connecticuts successful discoveries at the 2013 StemConn scientific symposium at the Omni Hotel in New Haven. Held every other year, the gathering will be the largest since the conference began in 2007 an outgrowth of the establishment in 2005 of the Connecticut Stem Cell Research program by the state legislature.

The success of stem cell research at Yale, as well as the University of Connecticut and Wesleyan University, is directly attributable to the programs $100 million in grants promised to state researchers over 10 years.

The states contribution has been critical to this growth and continues to be, Krause said. Every dollar the state has contributed has led to $4 more dollars in additional research funding.

The existence of the fund was a major factor in the recruitment internationally renowned stem cell biologist Haifan Lin to head the Yale Stem Cell Center. Members of the center have submitted over 130 patent applications and 26 intellectual property licenses.

The research funding program, created in response to a ban on federal funding for research using embryonic stem cells by President George W. Bush, has taken on even more importance now that scientists have discovered how to create pluripotent stem cells from an individuals own cells, notes Krause. The breakthrough holds the promised of individualized patient-specific therapy for a host of diseases.

The funding has also helped to recruit and jumpstart the careers of young scientists at Yale such as Jun Lu, whose work on how blood cells regenerate promises to help patients to better tolerate chemotherapy, and Valerie Horsley, whose work with skin stem cells has applications for wound healing and even hair growth. Scientists at Yale are researching the use of stem cells for treating diabetes and Parkinsons disease; repairing spinal cord injuries; building blood vessels to treat congenital heart defects; creating living, growing blood vessels from scratch; and even rebuilding a heart.

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Stem cell research blooms at Yale and in Connecticut

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Bridgeport CT Stem Cell Research is a complex and beneficial science using stem cells in a lab environment to better understand how normal human development works, and also to look for and develop new treatments for a wide range of human ailments. Bridgeport Connecticut Stem Cell Research involves two types of stem cells, classified as either embryonic stem cells or adult stem cells, which are used according to the type of Bridgeport CT Stem Cell Research that is desired.

Embryonic stem cells are derived from pre-embryos, called blstocysts, approximately three to five days old. They are created specifically for fertilization treatments in the Bridgeport Connecticut Stem Cell Research lab, will not be used to start a pregnancy, and will be discarded if not used for research. Doctors use in-vitro fertilization to create an embryo in a culture dish, which after three to five days becomes a blstocysts. Bridgeport CT Stem Cell Research lab technicians then extract the inner cell mass from the blstocysts, which is used to derive embryonic stem cells in the Bridgeport Connecticut Stem Cell Research facility.Embryonic stem cells are classified as pluripotent.

This means they can develop into any type of cell in a fully developed human body. It should be noted that embryonic stem cells cant develop into placenta or umbilical cord tissues, but they do appear to be able to develop into any other type of cell in a human body. What is so important about embryonic Bridgeport CT Stem Cell Research is that it enables very flexible research, as the stem cells can be grown into any type of cell needing to be researched, at any time, at the Bridgeport Connecticut Stem Cell Research facility. This makes for more efficient and more productive stem call research, promising a faster path to cures for ailments that devastate humanity. Bridgeport CT Stem Cell Research cannot use adult stem cells to generate just any desired tissues since they are already programmed. They are quite useful nonetheless, and Bridgeport Connecticut Stem Cell Research doctors have identified caches of adult stem cells in several tissues of the human body.

Bridgeport CT Stem Cell Research in general has been able to make some wonderful advancement and create excellent treatments using adult stem cells. But there are limitations to doing Bridgeport Connecticut Stem Cell Research using "only" adult stem cells. Adult stem cells are able to give rise to related kinds of cells in their home tissues, but for example Kidney stem cells cannot generate heart cells, and liver stem cells cannot generate brain cells.

A great deal of Bridgeport CT Stem Cell Research remains to be done, and at this point Bridgeport Connecticut Stem Cell Research doctors have developed a technique for getting an adult stem cell to behave similar to an embryonic stem cell. This specialized Bridgeport CT Stem Cell Research technique creates what are called induced pluripotent stem cells (iPS). They can be produced from adult cells in skin, fatty tissue, and other sources. With this, Bridgeport Connecticut Stem Cell Research remains a promising field. There is of course a great deal more work to do, but Bridgeport CT Stem Cell Research promises to benefit mankind in many profound ways.

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