Relevant bibliographies by topics / Stem cells – Research – Animal models

Academic literature on the topic 'Stem cells – Research – Animal models'

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Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Stem cells – Research – Animal models"

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Soria, Bernat, Francisco J. Bedoya, and Franz Martin. "Gastrointestinal Stem Cells I. Pancreatic stem cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 2 (August 2005): G177—G180. http://dx.doi.org/10.1152/ajpgi.00116.2005.

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The transplantation of islets isolated from donor pancreas has renewed the interest in cell therapy for the treatment of diabetes. In addition, the capacity that stem cells have to differentiate into a wide variety of cell types makes their use ideal to generate β-cells for transplantation therapies. Several studies have reported the generation of insulin-secreting cells from embryonic and adult stem cells that normalized blood glucose values when transplanted into diabetic animal models. Finally, although much work remains to be done, there is sufficient evidence to warrant continued efforts on stem cell research to cure diabetes.
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Villano, Jason S., Susan E. Vleck, Stephen A. Felt, Daniel D. Myers, and Patrick A. Lester. "Safety Considerations When Working with Humanized Animals." ILAR Journal 59, no. 2 (December 12, 2018): 150–60. http://dx.doi.org/10.1093/ilar/ily012.

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Abstract Research using laboratory animals has been revolutionized by the creation of humanized animal models, which are immunodeficient animals engrafted with human cells, tissues, or organs. These animal models provide the research community a unique and promising opportunity to mimic a wide variety of disease conditions in humans, from infectious disease to cancer. A vast majority of these models are humanized mice like those injected with human CD34+ hematopoietic stem cells and patient-derived xenografts. With this technology comes the need for the animal research enterprise to understand the inherent and potential risks, such as exposure to bloodborne pathogens, associated with the model development and research applications. Here, we review existing humanized animal models and provide recommendations for their safe use based on regulatory framework and literature. A risk assessment program—from handling the human material to its administration to animals and animal housing—is a necessary initial step in mitigating risks associated with the use of humanized animals in research. Ultimately, establishing institutional policies and guidelines to ensure personnel safety is a legal and ethical responsibility of the research institution as part of the occupational health and safety program and overall animal care and use program.
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Kim, Yoon-Young, Jin-Soo Kim, Jeong-Hwan Che, Seung-Yup Ku, Byeong-Cheol Kang, and Jun-Won Yun. "Comparison of Genetically Engineered Immunodeficient Animal Models for Nonclinical Testing of Stem Cell Therapies." Pharmaceutics 13, no. 2 (January 20, 2021): 130. http://dx.doi.org/10.3390/pharmaceutics13020130.

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For the recovery or replacement of dysfunctional cells and tissue—the goal of stem cell research—successful engraftment of transplanted cells and tissues are essential events. The event is largely dependent on the immune rejection of the recipient; therefore, the immunogenic evaluation of candidate cells or tissues in immunodeficient animals is important. Understanding the immunodeficient system can provide insights into the generation and use of immunodeficient animal models, presenting a unique system to explore the capabilities of the innate immune system. In this review, we summarize various immunodeficient animal model systems with different target genes as valuable tools for biomedical research. There have been numerous immunodeficient models developed by different gene defects, resulting in many different features in phenotype. More important, mice, rats, and other large animals exhibit very different immunological and physiological features in tissue and organs, including genetic background and a representation of human disease conditions. Therefore, the findings from this review may guide researchers to select the most appropriate immunodeficient strain, target gene, and animal species based on the research type, mutant gene effects, and similarity to human immunological features for stem cell research.
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Kordiyak, Olena J. "Periodontal Destruction and Regeneration in Experimental Models: Combined Research Approaches." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 5, no. 5 (October 24, 2020): 28–34. http://dx.doi.org/10.26693/jmbs05.05.028.

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Chronic periodontitis is a common dental disease, resulting in destruction of gingival tissue, periodontal ligament, cementum, alveolar bone and, consequently- teeth loss in the adult population. Experimental animal models have enabled the study of periodontal disease pathogenesis and are used to test new therapeutic approaches for treating the disease The purpose of this review study was to draw the evidence from animal models, required for future assessment of destructional and regenerative processes in periodontal tissues. Material and methods: a rat experimental periodontitis models of ligature, streptozotocin, and immune complexes induced periodontitis, periodontal defect, altered functional loading, stress exposures and surgically created chronic acid reflux esophagitis models. Histomorphomorphological/-metrical, immunohisto (-cyto)chemical and histopathological analysis, micro-computed tomography, scanning and transmission electron microscopy, polarizing light and confocal microscopy, spectrophotometry, radiographic and biomechanical analysis, descriptive histology and computer-assisted image analysis. Results and discussion. Scaling and root planing may not always be effective in preventing periodontal disease progression, and, moreover, with currently available therapies, full regeneration of lost periodontal tissues after periodontitis cannot be achieved. However, in 70.5% of the results of experimental studies reported, irrespective of the defect type and animal model used, beneficial outcome for periodontal regeneration after periodontal ligament stem cell implantation, including new bone, new cementum and new connective tissue formation, was recorded. Therefore, platelet-rich fibrin combined with rat periodontal ligament stem cells provides a useful instrument for periodontal tissue engineering. Conclusion. There is sufficient evidence from preclinical animal studies suggesting that periodontal tissue engineering would provide a valuable tool for periodontal regeneration. Further elaboration of the developed in preclinical studies experimental techniques should justify progress to clinical studies and subsequent medical application
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Norgren, Robert B. "Genetic modification of somatic cells for producing animal models and for cellular transplantation." Reproduction, Fertility and Development 18, no. 8 (2006): 811. http://dx.doi.org/10.1071/rd06074.

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Great progress has been made in two technologies related to biomedical research: (1) manipulating the genomes of cells; and (2) inducing stem cells in culture to differentiate into potentially useful cell types. These technologies can be used to create animal models of human disease and to provide cells for transplantation to ameliorate human disease. Both embryonic stem cells and adult stem cells have been studied for these purposes. Genetically modified somatic cells provide another source of cells for creating animal models and for cellular transplantation.
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Struillou, Xavier, Hervé Boutigny, Assem Soueidan, and Pierre Layrolle. "Experimental Animal Models in Periodontology: A Review." Open Dentistry Journal 4, no. 1 (April 29, 2010): 37–47. http://dx.doi.org/10.2174/1874210601004010037.

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In periodontal research, animal studies are complementary to in vitro experiments prior to testing new treatments. Animal models should make possible the validation of hypotheses and prove the safety and efficacy of new regenerating approaches using biomaterials, growth factors or stem cells. A review of the literature was carried out by using electronic databases (PubMed, ISI Web of Science). Numerous animal models in different species such as rats, hamsters, rabbits, ferrets, canines and primates have been used for modeling human periodontal diseases and treatments. However, both the anatomy and physiopathology of animals are different from those of humans, making difficult the evaluation of new therapies. Experimental models have been developed in order to reproduce major periodontal diseases (gingivitis, periodontitis), their pathogenesis and to investigate new surgical techniques. The aim of this review is to define the most pertinent animal models for periodontal research depending on the hypothesis and expected results.
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Markoski, Melissa Medeiros. "Advances in the Use of Stem Cells in Veterinary Medicine: From Basic Research to Clinical Practice." Scientifica 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/4516920.

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Today, several veterinary diseases may be treated with the administration of stem cells. This is possible because these cells present a high therapeutic potential and may be injected as autologous or allogenic, freshly isolated, or previously cultured. The literature supports that the process is safe and brings considerable benefits to animal health. Knowledge about how adult stem cells modulate the molecular signals to activate cell homing has also been increasingly determined, evidencing the mechanisms which enable cells to repair and regenerate injured tissues. Preclinical studies were designed for many animal models and they have contributed to the translation to the human clinic. This review shows the most commonly used stem cell types, with emphasis on mesenchymal stem cells and their mechanistic potential to repair, as well as the experimental protocols, studied diseases, and species with the highest amount of studies and applications. The relationship between stem cell protocols utilized on clinics, molecular mechanisms, and the physiological responses may offer subsidies to new studies and therefore improve the therapeutic outcome for both humans and animals.
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Čamernik, Klemen, Ariana Barlič, Matej Drobnič, Janja Marc, Matjaž Jeras, and Janja Zupan. "Mesenchymal Stem Cells in the Musculoskeletal System: From Animal Models to Human Tissue Regeneration?" Stem Cell Reviews and Reports 14, no. 3 (March 20, 2018): 346–69. http://dx.doi.org/10.1007/s12015-018-9800-6.

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Gergi, Mansour, Sudarshana Sengupta, Prakash Sampath, and Sadhak Sengupta. "EXTH-44. TARGETING GLIOMA STEM CELLS WITH CAR-T IMMUNOTHERAPY IN XENOGRAFT ANIMAL MODELS." Neuro-Oncology 20, suppl_6 (November 2018): vi94. http://dx.doi.org/10.1093/neuonc/noy148.392.

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Kim, Sunil, Su-Jung Shin, Yunjung Song, and Euiseong Kim. "In VivoExperiments with Dental Pulp Stem Cells for Pulp-Dentin Complex Regeneration." Mediators of Inflammation 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/409347.

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In recent years, many studies have examined the pulp-dentin complex regeneration with DPSCs. While it is important to perform research on cells, scaffolds, and growth factors, it is also critical to develop animal models for preclinical trials. The development of a reproducible animal model of transplantation is essential for obtaining precise and accurate datain vivo.The efficacy of pulp regeneration should be assessed qualitatively and quantitatively using animal models. This review article sought to introducein vivoexperiments that have evaluated the potential of dental pulp stem cells for pulp-dentin complex regeneration. According to a review of various researches about DPSCs, the majority of studies have used subcutaneous mouse and dog teeth for animal models. There is no way to know which animal model will reproduce the clinical environment. If an animal model is developed which is easier to use and is useful in more situations than the currently popular models, it will be a substantial aid to studies examining pulp-dentin complex regeneration.
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Dissertations / Theses on the topic "Stem cells – Research – Animal models"

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Raut, Vivek P. "METHODS TO QUANTITATIVELY ASSESS THE PERFORMANCE OF CONNECTIVE TISSUE PROGENITOR CELLS IN RESPONSE TO SURFACE MODIFIED BIOMATERIALS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1372334668.

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King, Marie A. "The Humanized Mouse Model: The Study of the Human Alloimmune Response: A Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/374.

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The transplantation of allogeneic cells and tissues for the treatment of human disease has been a life-saving procedure for many thousands of patients worldwide. However, to date, neither solid organ transplantation nor bone marrow transplantation have reached their full clinical potential. Significant limitations to the advancement of clinical transplantation stem from our current inability to prevent the rejection of allogeneic tissues by the immune system of the host. Similarly, in patients that receive allogeneic bone marrow transplants, we cannot permanently prevent the engrafted immune system from mounting a response against the patient. This problem, termed graft versus host disease is the most prevalent cause of morbidity and mortality in recipients of allogeneic bone marrow transplants. Clinically, we rely on lifelong immunosuppression to prolong survival of allogeneic tissues within the host. Our currently available therapeutics burden patients with side-effects that range from being unpleasant to life-threatening, while in most cases offering only a temporary solution to the problem of alloimmunity. Efforts are underway to develop protocols and therapeutics that more effectively prevent the pathology associated with alloimmunity. To minimize patient risk, extensive pre-clinical studies in laboratory animals are conducted to predict clinical responses. In the case of immunologic studies, many of these pre-clinical studies are carried out in murine models. Unfortunately, studies of murine immunity often do not predict outcomes in the clinic. One approach to overcome this limitation is the development of a small animal model of the human immune system. In this dissertation, we hypothesized that NOD-scid IL2rγnull mice engrafted with human peripheral blood mononuclear cells (PBMC), termed the hu-PBMC-NOD-scid IL2rγnull model, would provide a model that more accurately reflects human immunity in vivo than other models currently available. To investigate this possibility, we first investigated whether NOD-scid IL2rγnull mice were able to support the engraftment of human PBMC. We found that NOD-scid IL2rγnull mice engraft with human PBMC at much higher levels then the previous gold standard model, the NOD-scid mouse. We then investigated the kinetics of human cell engraftment, determined the optimal cell dose, and defined the influence of injection route on engraftment levels. Even at low PBMC input, NOD-scid IL2rγnullmice reproducibly support high levels of human PBMC engraftment. In contrast to previous stocks of immunodeficient mice, we observed low intra- and interdonor variability of engraftment. We next hypothesized that the human PBMC engrafted in NOD-scid IL2rγnull mice were functional and would reject transplanted allogeneic human tissues. To test this, human islets were transplanted into the spleen of chemically diabetic NOD-scid IL2rγnull mice with or without intravenous injection of HLA-mismatched human PBMC. In the absence of allogeneic PBMC, the human islets were able to restore and maintain normoglycemia. In contrast, human islet grafts were completely rejected following injection of HLA-mismatched human PBMC as evidenced by return to hyperglycemia and loss of human C-peptide in the circulation. Thus, PBMC engrafted NOD-scid IL2rγnull mice are able to provide an in vivomodel of a functional human immune system and of human islet allograft rejection. The enhanced ability of NOD-scid IL2rγnull mice to support human cell engraftment gave rise to the possibility of creating a model of graft versus host disease mediated by a human immune system. To investigate this possibility, human PBMC were injected via the tail vein into lightly irradiated NOD-scid IL2rγnull mice. We found that in contrast to previous models of GVHD using human PBMC-injected immunodeficient mice, these mice consistently (100%) developed GVHD following injection of as few as 5x106PBMC, regardless of the PBMC donor used. We then tested the contribution of host MHC in the development of GVHD in this model. As in the human disease, the development of GVHD was highly dependent on host expression of MHC class I and class II molecules. To begin to evaluate the extent to which the PBMC-engrafted NOD-scid IL2rγnull humanized mouse model of GVHD represents the clinical disease, we tested the ability of a therapeutic in clinical trials to modulate GVHD in these mice. In agreement with the clinical experience, we found that interrupting the TNFα signaling cascade with etanercept delayed the onset and severity of disease in this model. In summary, we conclude that humanized NOD-scid IL2rγnull mice represent an important surrogate for investigating in vivo mechanisms of both human islet allograft rejection and graft versus host disease.
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Fiumana, Emanuela <1975&gt. "Stem Cells as a therapy for myocardial infarction in animal models." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/643/.

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Advances in stem cell biology have challenged the notion that infarcted myocardium is irreparable. The pluripotent ability of stem cells to differentiate into specialized cell lines began to garner intense interest within cardiology when it was shown in animal models that intramyocardial injection of bone marrow stem cells (MSCs), or the mobilization of bone marrow stem cells with spontaneous homing to myocardium, could improve cardiac function and survival after induced myocardial infarction (MI) [1, 2]. Furthermore, the existence of stem cells in myocardium has been identified in animal heart [3, 4], and intense research is under way in an attempt to clarify their potential clinical application for patients with myocardial infarction. To date, in order to identify the best one, different kinds of stem cells have been studied; these have been derived from embryo or adult tissues (i.e. bone marrow, heart, peripheral blood etc.). Currently, three different biologic therapies for cardiovascular diseases are under investigation: cell therapy, gene therapy and the more recent “tissue-engineering” therapy . During my Ph.D. course, first I focalised my study on the isolation and characterization of Cardiac Stem Cells (CSCs) in wild-type and transgenic mice and for this purpose I attended, for more than one year, the Cardiovascular Research Institute of the New York Medical College, in Valhalla (NY, USA) under the direction of Doctor Piero Anversa. During this period I learnt different Immunohistochemical and Biomolecular techniques, useful for investigating the regenerative potential of stem cells. Then, during the next two years, I studied the new approach of cardiac regenerative medicine based on “tissue-engineering” in order to investigate a new strategy to regenerate the infracted myocardium. Tissue-engineering is a promising approach that makes possible the creation of new functional tissue to replace lost or failing tissue. This new discipline combines isolated functioning cells and biodegradable 3-dimensional (3D) polymeric scaffolds. The scaffold temporarily provides the biomechanical support for the cells until they produce their own extracellular matrix. Because tissue-engineering constructs contain living cells, they may have the potential for growth and cellular self-repair and remodeling. In the present study, I examined whether the tissue-engineering strategy within hyaluron-based scaffolds would result in the formation of alternative cardiac tissue that could replace the scar and improve cardiac function after MI in syngeneic heterotopic rat hearts. Rat hearts were explanted, subjected to left coronary descending artery occlusion, and then grafted into the abdomen (aorta-aorta anastomosis) of receiving syngeneic rat. After 2 weeks, a pouch of 3 mm2 was made in the thickness of the ventricular wall at the level of the post-infarction scar. The hyaluronic scaffold, previously engineered for 3 weeks with rat MSCs, was introduced into the pouch and the myocardial edges sutured with few stitches. Two weeks later we evaluated the cardiac function by M-Mode echocardiography and the myocardial morphology by microscope analysis. We chose bone marrow-derived mensenchymal stem cells (MSCs) because they have shown great signaling and regenerative properties when delivered to heart tissue following a myocardial infarction (MI). However, while the object of cell transplantation is to improve ventricular function, cardiac cell transplantation has had limited success because of poor graft viability and low cell retention, that’s why we decided to combine MSCs with a biopolimeric scaffold. At the end of the experiments we observed that the hyaluronan fibres had not been substantially degraded 2 weeks after heart-transplantation. Most MSCs had migrated to the surrounding infarcted area where they were especially found close to small-sized vessels. Scar tissue was moderated in the engrafted region and the thickness of the corresponding ventricular wall was comparable to that of the non-infarcted remote area. Also, the left ventricular shortening fraction, evaluated by M-Mode echocardiography, was found a little bit increased when compared to that measured just before construct transplantation. Therefore, this study suggests that post-infarction myocardial remodelling can be favourably affected by the grafting of MSCs delivered through a hyaluron-based scaffold
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Zhao, Ming. "Neurorestorative strategies involving neurogenesis, neuronal precursors and stem cells in animal models of Parkinson's disease." Stockholm : Unit Injury and Repair in the Nervous System, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-649-1/.

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Luk, Sze-ue, and 陸施妤. "The potential effect of bioactive food supplements in targeting prostate cancer stem cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43223795.

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Seriola, Petit Anna. "Pluripotent stem cells as research models: the examples of trinucleotide repeat instability and X-chromosome inactivation." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/325148.

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Els models de malalties són una eina bàsica per la comprensió de les malalties humanes. Actualment, la majoria de la informació de la que disposem de malalties humanes es basa en models animals. Tot i això, els models animals difereixen molecular i fenotípicament dels humans, i no sempre reprodueixen fidelment la malaltia humana. En les últimes dècades, les cèl·lules mare humanes s’han establert com una opció molt interessant en el camp de la modelització cel·lular. En aquest treball hem volgut caracteritzar les cèl·lules mare embrionàries com a models per a l’estudi de la inestabilitat de la repetició de trinucleotids a la distròfia miotonica tipus 1 (DM1) i la malaltia de Huntington (HD). Així mateix, hem volgut estudiar la inactivació del cromosoma X amb la intenció de fer servir linees cel·lulars com a models per l’estudi del desenvolupament embrionàri humà. A la primera part d’aquest treball, hem observant una inestabilitat de repeticions de trinucleotids significativa al locus de la malaltia DM1 de les cèl·lules mare estudiades. La diferenciació d’aquestes cèl·lules va estabilitzar el número de repeticions. L’estabilització de les repeticions va ser concomitant amb la regulació a la baixa de l’expressió de gens involucrats en els mecanismes de reparació cel·lular. Posteriorment a la publicació del nostre article, altres grups varen reproduir els nostres resultats, però en aquest cas utilitzant cèl·lules mare induïdes. Els estudis recolzen la reproductibilitat dels nostres resultats, suggerint que poden ser extrapol·lats a altres linees de cèl·lules mare arreu del mon. Referent a la mutació de HD, varem trobar que era estable en totes les condicions estudiades, en cèl·lules indiferenciades, diferenciades a progenitors d’os, teratomes i progenitors neurals. Aquests resultats estan en concordancia amb els resultats obtinguts per altres grups que descriuen un baix nombre de repeticions al locus de HD. Per altra banda, varis grups han descrit la presencia de inestabilitat de les repeticions en cèl·lules diferenciades a la linea neural. La discrepància entre els nostres resultats i aquests últims podria ser deguda a la obtenció de cèl·lules neurals menys madures en el moment del nostre estudi. A la segona part d’aquesta tesis hem estudiat la inactivació del cromosoma X en 23 línies femenines de cèl·lules mare pluripotents. Vàrem observar una ràpida progressió de les cèl·lules de dependència de XIST en la inactivació del cromosoma X cap a un estat d’adaptació al cultiu que es caracteritza per un estadi de inactivació independent de l’expressió de XIST i amb una erosió de la metilació. També describim un patró d’inactivació esbiaixat en la majoria de les línies estudiades, contrari al patró aleatori observat en cèl·lules femenines adultes. A més a més, aquest patró és independent de XIST, de l’origen del cromosoma X i d’aberracions cromosòmiques. Aquests resultats suggereixen que el patró esbiaixat observant esta dirigit provablement per l’activació o repressió d’al·lels específics que es troben en el cromosoma X i que li confereixen a la cèl·lula un avantatge respecte a les altres cèl·lules. En conclusió, les cèl·lules mare pluripotents semblen ser un bon model in vitro per a l’estudi d’ambdues malalties, DM1 i HD, ja que presenten el mateix patró d’inestabilitat de la repetició del trinucleotid que s’observa in vivo. Cal remarcar també la depencia Overall, hPSC appear to be a good in vitro model for the study of both DM1 and HD TNR instability, as the repeat follows in vitro the same patterns as found in vivo, including its dependency of the MMR machinery, particularly in the case of DM1. However, our results on the study of the X chromosome inactivation (XCI) state suggest caution when using hPSC as early human developmental research models. The eroded state of XCI found in many of the hPSC lines, and the frequency of skewed XCI patterns suggests that these cells are not a good proxy to early embryonic cells, at least what XCI is concerned. Conversely, they may still provide an interesting model to study gene function and mechanisms implicated.
Disease modelling is an essential tool for the understanding of human disease. Currently, much of the information we have on human diseases is based on animal models. However, animal models differ molecularly and phenotypically from humans, and are not always suitable to reproduce with fidelity human diseases. In the past decades, human pluripotent stem cells (hPSC) have emerged as an interesting option in the field of cellular modelling, this development recently having taken up much momentum. In this work, we aimed at characterizing hPSC as models for the study of Myotonic dystrophy type 1 (DM1) and Huntington’s disease (HD) trinucleotide repeat (TNR) instability and to investigate the status of the X-chromosome inactivation with an eye on using these cells as models for early human development. In the first part of our work, we observed a significant TNR instability for the DM1 locus in hESC, and that differentiation resulted in a stabilization of the repeat. This stabilization was concommitant with a downregulation of the mismatch repair (MMR). Our results were later replicated in hiPSC by other researchers, showing their reproducibility and suggesting they may be extrapolated to other hPSC lines worldwide. Regarding the HD repeat, we found it was very stable in all conditions studied, both in undifferentiated hESC and cells differentiated into osteogenic progenitor-like cells, teratoma cells and neural progenitors. This is in line with other studies showing that hESC show very limited TNR in the HD locus. On the other hand, some groups have now reported some instability of this locus in cells differentiated into the neuronal lineage. The instability seen in neuronal lineage in later studies, not in our study, is probably explained by the use of hPSC derived neurons more similar to the cells showing in vivo instability than the ones we were able to generate at the time of the study. In the second part of the thesis we studied the X-chromosome inactivation in 23 female hPSC lines. We found that hPSC rapidly progress from a XIST-dependent XCI state to a culture-adapted, XIST-independent XCI state with loss of repressive histone modifications and erosion of methylation. We also report a remarkably high incidence of non-random XCI patterns, and that this skewing of the methylation patterns is independent from the transition to the XIST-independent XCI state, the origin of the X chromosome or chromosomal aberrations. These results suggest that XCI skewing is possibly driven by the activation or repression of a specific allele on the X chromosome, conferring a growth or survival advantage to the cells. Overall, hPSC appear to be a good in vitro model for the study of both DM1 and HD TNR instability, as the repeat follows in vitro the same patterns as found in vivo, including its dependency of the MMR machinery, particularly in the case of DM1. However, our results on the study of the X chromosome inactivation (XCI) state suggest caution when using hPSC as early human developmental research models. The eroded state of XCI found in many of the hPSC lines, and the frequency of skewed XCI patterns suggests that these cells are not a good proxy to early embryonic cells, at least what XCI is concerned. Conversely, they may still provide an interesting model to study gene function and mechanisms implicated.
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Patel, Nirmal Praful School of Medicine UNSW. "Olfactory progenitor cell transplantation into the mammalian inner ear." Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/26180.

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A practical consideration in the development of cellular therapy technology for the inner ear is the development of an in vitro model for assessing the optimal conditions for successful application of cells. The first part of this thesis describes the adaptation of the cochleovestibular structure harvested from P1 mouse pups for analysis of factors critical for the optimal implantation of stem cells in the inner ear. Results of these studies establish that the c17.2 neural stem cell line can be introduced into the cochleovestibular structure in vitro. Using this model, c17.2 cells demonstrated survival predominantly within the vestibule and basal spiral ganglion regions. Furthermore, the addition of the ototoxin, cisplatin and the neurotrophin, Brain Derived Neurotrophic Growth Factor (BDNF) enhanced the survival and migration/dispersion of c17.2 cells within the cochleovestibular explant. The second part of this thesis examines the hypothesis that olfactory neurosphere (ONS) and progenitor cells harvested from the olfactory epithelium represent a viable source of graft material for potential therapeutic applications in the inner ear. Olfactory epithelium represents a unique source of pluripotent cells that may serve as either homografts or autografts. The feasibility of ONSs to survive and integrate into a mammalian cochlea in vivo was assessed. The ONSs were isolated as a crude fraction from the olfactory epithelium of P1 to P3 day old swiss webster mouse pups, ubiquitously expressing the Green Fluorescent Protein (GFP) marker. The ONSs were microinjected into the cochleae of adult CD1 male mice. Four weeks following their implantation, ONS cells expressing the GFP marker and stained by Nestin were identified in all areas of the cochlea and vestibule, including the spiral ganglion. Robust survival and growth of the implanted ONS and ONS derived cells in the cochlea also included the development of ???tumor-like??? clusters, a phenomenon not observed in control animals implanted with c17.2 neural stem cells. Collectively, the results of this thesis illustrate the potential of olfactory neurosphere and progenitor cells to survive in the inner ear and expose a potential harmful effect of their transplantation.
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Lin, Kaili. "Neural stem cells as therapeutic agents for treatments of Parkinson's disease in rat model." HKBU Institutional Repository, 2019. https://repository.hkbu.edu.hk/etd_oa/692.

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Parkinson's disease (PD) is the second most common neurodegenerative disease. With the rapid global increase in population aging, neurodegenerative diseases are considered a primary threat to human health. As dopaminergic neuronal cell death and dysfunction are the main pathogenic mechanisms of PD, neural stem cell (NSC) replacement therapy has been identified as a potentially effective and indeed ideal therapeutic strategy. However, current in vitro stem cell culture methods, which require various chemical growth factors (GFs), are unsafe and relatively inefficient. To solve this problem, we developed two strategies for enhancing the proliferation and differentiation of NSCs in vitro based on extracellular nanomatrices and natural active ingredients. First, we developed novel nanomatrices comprising biomaterials used for promoting NSCs proliferation and differentiation without requiring additional GFs. We developed two types of inorganic sculptured extracellular nanomatrices comprising SiO2 (iSECnMs) which deposited by glancing angle deposition (GLAD). The physiological properties of nanomatrices mediate the activation of multiple bio-signaling pathways. Accordingly, iSECnMs, especially those sculptured in zigzag forms, can significantly promote the proliferation and specific neuronal phenotypic differentiation of NSCs without requiring additional GFs. The differentiated neurons survived well in vivo and achieved outstanding therapeutic effects in a rat model of 6-OHDA-induced parkinsonism. Second, 20(S)-protopanaxadiol (PPD) and oleanolic acid (OA), two crucial active ingredients derived from ginseng, significantly enhanced the proliferation and neuronal differentiation of NSCs through activating Wnt/GSK-3β/β-catenin pathway. This research is expected to promote significant developments in the induction of NSCs and provide insights into stem cell therapies for PD without undesirable prognoses
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Citro, Lucas Abraham. "High-field Cardiac Magnetic Resonance Imaging in Small Animal Models of Cardiovascular Disease." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1365082830.

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Wu, Gang, and 吳剛. "Telomerase expression in the adult rodent central nervours system and telomeric characteristics of neural stem cells from adult brain." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41633635.

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Books on the topic "Stem cells – Research – Animal models"

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Animal models for stem cell therapy. [New York]: Humana Press, 2014.

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Media, Springer Science+Business, ed. Stem cells and tissue repair: Methods and protocols. New York: Humana Press, 2014.

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Brakebusch, Cord. Mouse as a Model Organism: From Animals to Cells. Dordrecht: Springer Science+Business Media B.V., 2011.

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S, Koka Prasad, ed. Leading-edge stem cell research. New York: Nova Science Publishers, 2008.

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Kursad, Turksen, ed. Embryonic stem cell protocols. 2nd ed. Totowa, N.J: Humana Press, 2006.

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Turksen, Kursad. Embryonic Stem Cell Protocols: Volume II: Differentiation Models (Methods in Molecular Biology). 2nd ed. Humana Press, 2006.

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Embryonic stem cell protocols: Volume 1: isolation and characterization. 2nd ed. Totowa, NJ: Humana Press, 2006.

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Turksen, Kursad. Embryonic Stem Cell Protocols: Volume I: Isolation and Characterization (Methods in Molecular Biology). 2nd ed. Humana Press, 2006.

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Drapeau, Elodie, Hala Harony-Nicolas, and Jacqueline N. Crawley. Animal and Cellular Models of Pediatric Psychiatric Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0061.

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The study of childhood psychiatric disorders is especially challenging, not only because of the difficulties in obtaining relevant human samples but also because of ethical considerations regarding the ability of children to provide informed consent. Models that can be experimentally manipulated are therefore indispensable to study those disorders. Traditionally, biological psychiatry research has extensively employed animal models and characterizations of rodent behavior. More recently, induced pluripotent stem cells (iPSCs), and induced differentiation of iPSCs into different types of brain cells have offered new alternative strategies to elucidate mechanisms underlying cellular processes. Regardless of how they are created, optimal models should demonstrate face validity, construct validity, and predictive validity to be considered most relevant. This chapter highlights the major animal and cellular models currently used in the research of childhood-onset psychiatric disorders.
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Schatt, Stephan. An animal model for in utero HSC transplantation and the role of cytokine secretion by T- and NK cells in pregnancy /von Stephan Schatt. Schatt, 2000.

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Book chapters on the topic "Stem cells – Research – Animal models"

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Houbracken, Isabelle, Iris Mathijs, and Luc Bouwens. "Lineage Tracing of Pancreatic Stem Cells and Beta Cell Regeneration." In Animal Models in Diabetes Research, 303–15. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-068-7_20.

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Young, Michael J., and Jea Young Park. "Cell and Animal Models used for Retinal Stem Cell Research." In Regenerative Medicine and Stem Cell Therapy for the Eye, 87–122. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-98080-5_4.

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Bubak, Andrew N., John D. Elsworth, and John R. Sladek. "Animal models in regenerative medicine." In Stem Cells in Regenerative Medicine, 301–16. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118846193.ch16.

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Pavlović, Mirjana, and Ksenija Radotić. "Nanotechnology in Stem Cell Research." In Animal and Plant Stem Cells, 133–35. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47763-3_15.

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Brevini, Tiziana A. L., and Fulvio Gandolfi. "Use of Large Animal Models for Regenerative Medicine." In SpringerBriefs in Stem Cells, 29–42. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4899-8053-3_3.

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Kron, Michelle M., and Jack M. Parent. "Neural Stem Cells in Experimental Mesial Temporal Lobe Epilepsy." In Animal Models of Epilepsy, 251–64. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-263-6_14.

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Pavlović, Mirjana, and Ksenija Radotić. "Topic Novelties in Animal Stem Cell Research." In Animal and Plant Stem Cells, 163–64. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47763-3_18.

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Pavlović, Mirjana, and Ksenija Radotić. "Current Status and Perspectives in Stem Cell Research: The Concept of Normal Stem (NSC) and Cancer Stem Cell (CSC)." In Animal and Plant Stem Cells, 7–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47763-3_2.

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Rojas, Mauricio, Smita Iyer, Carter Co, and Kenneth L. Brigham. "Animal Models of Lung Injury: Role for Mesenchymal Stem Cells." In Stem Cells in the Respiratory System, 141–58. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-775-4_8.

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Nauta, Allison C., Geoffrey C. Gurtner, and Michael T. Longaker. "Adult Stem Cells in Small Animal Wound Healing Models." In Methods in Molecular Biology, 81–98. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-505-7_5.

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Conference papers on the topic "Stem cells – Research – Animal models"

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Peterson, Sherket B., Zannatul Ferdous, Magnus Höök, and K. Jane Grande-Allen. "Decorin Deficient Cells Demonstrate Increased Proliferation and Altered Phenotypic Properties." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176043.

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Decorin (DCN), a class I member of the small leucine-rich proteoglycan (SLRP) family, is composed of a protein core of approximately 40kDa [1, 2] substituted with a single glycosaminoglycan (GAG) chain of chondroiton/dermatan sulfate on the N-terminal site [3]. DCN has been reported to interact with collagen [4,5] via its core protein, influence collagen fibrillogenesis [6], and inhibit the growth rates of various cell types when added exogenously to cell cultures [5,6]. There has recently been growing interest and studies in DCN related research using the knockout (KO) mice model which provides an excellent example of inherited disorders that stem from deficiencies in decorin expression [7]. Skin and tendon tissues from DCN KO mice have been characterized as being extremely fragile with significantly reduced strength and stiffness [8, 9]. The DCN KO tissues also show potential functional biglycan compensation [9] and at the microscopic level collagen fibrils with highly irregular diameters, abnormal lateral fusion, and loose packing [6] in contrast to wild type (WT) mice. Despite the intensive investigation of the DCN KO mice, the complexity of the animal model makes it difficult to assess the actual influence of decorin. In an attempt to take a more simplistic approach 2D cell phenotypic characterization studies were performed in addition to studying cell growth, contraction, and matrix organization in 3-D models to show the very distinct biochemical responses to type I collagen when compared to WT control cells.
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Ha, Soo Jung, Marisol Herrera-Perez, Jiri Adamec, R. Timothy Bentley, Jenna L. Rickus, and Kari L. Clase. "Abstract B23: Characterization of canine glioma cancer stem cells for human glioblastoma models." In Abstracts: AACR Special Conference: Advances in Brain Cancer Research; May 27-30, 2015; Washington, DC. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.brain15-b23.

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Parada, Luis F. "Abstract IA27: Glioma stem cells: What are they?" In Abstracts: AACR Special Conference: Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; November 9-12, 2015; Fort Lauderdale, Florida. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.pedca15-ia27.

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Agarwal, Saurabh, Zaowen Chen, Sanjeev Vasudevan, and Jason M. Shohet. "Abstract A15: Epigenetic regulators maintain neuroblastoma cancer stem cells: Model to treatment." In Abstracts: AACR Special Conference: Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; November 9-12, 2015; Fort Lauderdale, Florida. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.pedca15-a15.

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Lenna, S., C. Bellotti, S. Duchi, M. Ballestri, E. Martella, B. Dozza, M. Columbaro, A. Guerrini, G. Varchi, and DM Donati. "PO-435 Photoactivation of nanoparticles delivered by mesenchymal stem cells induces osteosarcoma cell death inin vitro3D co-culture models." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.459.

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Alcantara Llaguno, Sheila R., Jian Chen, Chang‐Hyuk Kwon, Erica Jackson, Yanjiao Li, Jingsheng Yan, Yang Xie, et al. "Abstract C10: Neural stem cells and lineage‐restricted progenitors can initiate malignant astrocytoma formation in somatic tumor suppressor mouse models." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-c10.

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Alamsyah, F., AG Fadhlurrahman, JI Pello, N. Firdausi, S. Evi, FN Karima, R. Pratiwi, L. Fitria, L. Nurhidayat, and WP Taruno. "PO-111 Non-contact electric fields inhibit the growth of breast cancer cells in animal models and induce local immune reaction." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.636.

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Kim, Gyu-Sik, and Kyung-Chul Choi. "Abstract B13: A growth of human choriocarcinoma cells was selectively inhibited by therapeutic neural stem cells expressing cytosine deaminase and interferon-β in cellular and xenograft models." In Abstracts: AACR International Conference: New Frontiers in Cancer Research; January 18-22, 2017; Cape Town, South Africa. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.newfront17-b13.

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Roberts, Stephen S., Yudelca Ogando, Irina Ostrovnaya, Faranak Fattahi, Irene Cheung, Nai-Kong V. Cheung, Lorenz Studer, and Mark Tomishima. "Abstract A08: Using directed differentiation of human pluripotent stem cells and gene expression profiling to characterize the cell of origin of neuroblastoma." In Abstracts: AACR Special Conference: Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; November 9-12, 2015; Fort Lauderdale, Florida. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.pedca15-a08.

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Singh, Ankur, Shalu Suri, Ted T. Lee, Jamie M. Chilton, Steve L. Stice, Hang Lu, Todd C. McDevitt, and Andrés J. Garcia. "Adhesive Signature-Based, Label-Free Isolation of Human Pluripotent Stem Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80044.

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Generation of human induced pluripotent stem cells (hiPSCs) from fibroblasts and other somatic cells represents a highly promising strategy to produce auto- and allo-genic cell sources for therapeutic approaches as well as novel models of human development and disease1. Reprogramming protocols involve transduction of the Yamanaka factors Oct3/4, Sox2, Klf4, and c-Myc into the parental somatic cells, followed by culturing the transduced cells on mouse embryonic fibroblast (MEF) or human fibroblast feeder layers, and subsequent mechanical dissociation of pluripotent cell-like colonies for propagation on feeder layers1, 2. The presence of residual parental and feeder-layer cells introduces experimental variability, pathogenic contamination, and promotes immunogenicity3. Similar to human embryonic stem cells (hESCs), reprogrammed hiPSCs suffer from the unavoidable problem of spontaneous differentiation due to sub-optimal feeder cultures4, growth factors5, and the feeder-free substrate6. Spontaneously differentiated (SD)-hiPSCs display reduced pluripotency and often contaminate hiPSC cultures, resulting in overgrowth of cultures and compromising the quality of residual pluripotent stem cells5. Therefore, the ability to rapidly and efficiently isolate undifferentiated hiPSCs from the parental somatic cells, feeder-layer cells, and spontaneously differentiated cells is a crucial step that remains a bottleneck in all human pluripotent stem cell research.
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