| | | | | | | TE-RegenMed-StemCell feed | | | | | | | | | | | | | | | | Stem Cell Therapy in Stroke: Designing Clinical Trials. Neurochem Int. 2011 Mar 28; Authors: Kalladka D, Muir KW Stroke is a common and disabling condition that represents a potentially attractive target for regenerative therapy. Stem cells from a wide range of origins have been investigated in studies using animal models of stroke, with evidence that neural or mesenchymal cells migrate to the site of ischemic injury after intravascular or intraparenchymal delivery, and that a proportion of cells survive and differentiate into cells with characteristics of neurons or glia. In some studies there is evidence of electrical function of transplanted cells. Some studies report improvements in neurological function with cell implantation even when undertaken up to 30 days after the stroke is induced. Few clinical trials have been undertaken to date, with two studies of a teratocarcinoma-derived cell line delivered by direct brain injection, and two of bone-marrow derived mesenchymal stem cells delivered intravascularly. Ongoing trials of other cell lines are exploring safety. There are considerable difficulties in designing future efficacy trials, some being generic to the field of regenerative treatment in stroke, and some that are specific to stem cells or their mode of delivery. PMID: 21453739 [PubMed - as supplied by publisher] | | | | | | | | | | | | | | | | | | | | | The collapse of efforts to resolve California's financial crisis in June seems nearly certain to place the state's $3 billion stem cell research program perilously close to a serious cash crunch come next year.
The situation should come as no surprise to lame duck CIRM Chairman Robert Klein, who stunned the agency's governing board in 2009 with similar news. Additionally, in December of last | | | | | | | | | | | | | | | | | | | | | In case you missed it, The Sacramento Bee editorialized last week about the $3 billion California stem cell agency, deploring its much-criticized, dual-CEO structure and the possibility of a $400,000 salary for a new, part-time chairman.
The March 28 editorial also caught the eye of Wesley J. Smith, a bioethicist who doesn't have much truck with the state's stem cell research program. He wrote | | | | | | | | | | | | | | | | | | | | | In case you missed it, The Sacramento Bee editorialized last week about the $3 billion California stem cell agency, deploring its much-criticized, dual-CEO structure and the possibility of a $400,000 salary for a new, part-time chairman.
The March 28 editorial also caught the eye of Wesley J. Smith, a bioethicist who doesn't have much truck with the state's stem cell research program. He wrote | | | | | | | | | | | | | | | | | | | | | The California Stem Cell Report will resume postings later today from Bahia Ballena in Costa Rica. We have dropped the anchor for a few days and found an Internet connection, although it is a tad primitive. Look for an update on CIRM's looming financial problems and much more. | | | | | | | | | | | | | | | | | | | | | The California Stem Cell Report will resume postings later today from Bahia Ballena in Costa Rica. We have dropped the anchor for a few days and found an Internet connection, although it is a tad primitive. Look for an update on CIRM's looming financial problems and much more. | | | | | | | | | | | | | | | | | | | | | Ethical issues regarding the donation and source of cells for tissue engineering: A European focus group study. Tissue Eng Part B Rev. 2011 Apr 1; Authors: Oerlemans AJ, van den Berg PP, van Leeuwen E, Dekkers WJ This paper is part of the EuroSTEC project, which aims at developing tissue engineering-based treatments for structural disorders present at birth. EuroSTEC is positioned at the intersection of three areas with their own ethical issues: (1) regenerative medicine, (2) research with pregnant women and fetuses, and (3) research with neonates. Because of the link between these three areas in this project, one can expect to be confronted with new ethical challenges. To be able to respond adequately and timely to current and possible future ethical issues, a prospective and anticipatory ethical analysis is essential. To obtain a first impression of the ethical issues that might arise during the different phases of the project, a Delphi method was used. Based on the results of two previous rounds of questionnaires, two topics were selected for discussion in focus groups: ethical issues associated with (1) source of cells and (2) donation. The results could be divided into three clusters: Tissue, Donor and Scientist. Where the former two clusters roughly coincide with the results of the previous rounds, the third subject was entirely new but discussed by both groups: the role of the scientist in the tissue engineering process. PMID: 21453199 [PubMed - as supplied by publisher] | | | | | | | | | | | | | | | | | | | | | Human Epidermal Neural Crest Stem Cells (hEPI-NCSC)-Characterization and Directed Differentiation into Osteocytes and Melanocytes. Stem Cell Rev. 2011 Apr 1; Authors: Clewes O, Narytnyk A, Gillinder KR, Loughney AD, Murdoch AP, Sieber-Blum M Here we describe the isolation, characterisation and ex-vivo expansion of human epidermal neural crest stem cells (hEPI-NCSC) and we provide protocols for their directed differentiation into osteocytes and melanocytes. hEPI-NCSC are neural crest-derived multipotent stem cells that persist into adulthood in the bulge of hair follicles. Multipotency and self-renewal were determined by in vitro clonal analyses. hEPI-NCSC generate all major neural crest derivatives, including bone/cartilage cells, neurons, Schwann cells, myofibroblasts and melanocytes. Furthermore, hEPI-NCSC express additional neural crest stem cell markers and global stem cell genes. To variable degrees and in a donor-dependent manner, hEPI-NCSC express the six essential pluripotency genes C-MYC, KLF4, SOX2, LIN28, OCT-4/POU5F1 and NANOG. hEPI-NCSC can be expanded ex vivo into millions of stem cells that remain mulitpotent and continue to express stem cell genes. The novelty of hEPI-NCSC lies in the combination of their highly desirable traits. hEPI-NCSC are embryonic remnants in a postnatal location, the bulge of hair follicles. Therefore they are readily accessible in the hairy skin by minimal invasive procedure. hEPI-NCSC are multipotent somatic stem cells that can be isolated reproducibly and with high yield. By taking advantage of their migratory ability, hEPI-NCSC can be isolated as a highly pure population of stem cells. hEPI-NCSC can undergo robust ex vivo expansion and directed differentiation. As somatic stem cells, hEPI-NCSC are conducive to autologous transplantation, which avoids graft rejection. Together, these traits make hEPI-NCSC novel and attractive candidates for future cell-based therapies and regenerative medicine. PMID: 21455606 [PubMed - as supplied by publisher] | | | | | | | | | | | | | | | | | | | | | p14(Arf) acts as an antagonist of HMGA2 in senescence of mesenchymal stem cells-implications for benign tumorigenesis. Genes Chromosomes Cancer. 2011 Mar 31; Authors: Markowski DN, Winter N, Meyer F, von Ahsen I, Wenk H, Nolte I, Bullerdiek J HMGA2 is a major regulator of benign tumorigenesis from mesenchyme-derived tissues and stem-cell self-renewal. It has been postulated that HMGA2 mediates its critical function by decreasing p16(Ink4a) /p14(Arf) expression and cellular senescence. To repress the oncogenic activity of HMGA2, the lin-28-let-7 axis is thought to increasingly repress the expression of HMGA2 with age. To understand the HMGA2-p14(Arf) -relationship in benign tumorigenesis, we performed a series of experiments on mesenchymal stem-cells, i.e., the proposed cells of origin of lipomas and uterine leiomyomas. The expression of both genes was inversely correlated during senescence in vitro but contrary to the expectations in adipose tissue derived stem cells (ADSCs) stimulation of HMGA2 by FGF1 increased the expression of p14(Arf) . Based on the assumption that in ADSCs p14(Arf) is repressing HMGA2, siRNA silencing of p14(Arf) was performed resulting in a significant upregulation of HMGA2. To see if p14(Arf) can repress HMGA2 by a TP53-dependent mechanism, nutlin-3, a known MDM2 antagonist, was used which not only increased the activity of the senescence, associated markers p21 and beta-galactosidase, but also decreased the expression of HMGA2, suggesting that p14(Arf) indeed influences HMGA2 by a p53-dependent mechanism because nutlin-3 stabilizes p53. Accordingly, the HMGA2 response triggered by serum was reduced by treatment of ADSCs with nutlin-3. As to the interaction between HMGA2 and p14(Arf) in benign tumorigenesis, we propose a model where akin to MSC self-renewal during tissue repair the simultaneous increase of p14(Arf) with HMGA2 ensures genomic stability, whereas in turn p14(Arf) can repress HMGA2 via TP53. © 2011 Wiley-Liss, Inc. PMID: 21456046 [PubMed - as supplied by publisher] | | | | | | | | | | | | | |
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