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Artículos de revistas sobre el tema "Stem cells ; Alpha 1-antitrypsin deficiency":
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Kaserman, Joseph E., Killian Hurley, Mark Dodge, Carlos Villacorta-Martin, Marall Vedaie, Jyh-Chang Jean, Derek C. Liberti et al. "A Highly Phenotyped Open Access Repository of Alpha-1 Antitrypsin Deficiency Pluripotent Stem Cells". Stem Cell Reports 15, n.º 1 (julio de 2020): 242–55. http://dx.doi.org/10.1016/j.stemcr.2020.06.006.
Kaserman, Joseph E. y Andrew A. Wilson. "Patient-Derived Induced Pluripotent Stem Cells for Alpha-1 Antitrypsin Deficiency Disease Modeling and Therapeutic Discovery". Chronic Obstructive Pulmonary Diseases: Journal of the COPD Foundation 5, n.º 4 (2018): 258–66. http://dx.doi.org/10.15326/jcopdf.5.4.2017.0179.
The future implementation of stem cell therapies to treat conditions thus far considered incurable has been envisioned as logical consequence of the fast-paced progress in stem cell research over the last few years. Still, many practical obstacles stand in the way to the routine application of these novel technologies in medicine. The conference “Stem Cell Therapies in Reparative Medicine,” held aboard the cruise vessel Majesty of the Seas (Miami, USA- Nassau, Bahamas, April 19–22, 2002), focused on the analysis of these problems from different perspectives, including developmental biology (cell proliferation, fate determination, and enrichment), immunology (allorejection and prevention of autoimmunity recurrence), and clinical therapy, emphasizing the impact of stem cell technologies on the emerging field of tissue engineering and the treatment of alpha-1 antitrypsin deficiency.
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Bari, Ferrarotti, Di Silvestre, Grisoli, Barzon, Balderacchi, Torre et al. "Adipose Mesenchymal Extracellular Vesicles as Alpha-1-Antitrypsin Physiological Delivery Systems for Lung Regeneration". Cells 8, n.º 9 (23 de agosto de 2019): 965. http://dx.doi.org/10.3390/cells8090965.
Accumulating evidence shows that Mesenchymal Stem/Stromal Cells (MSCs) exert their therapeutic effects by the release of secretome, made of both soluble proteins and nano/microstructured extracellular vesicles (EVs). In this work, for the first time, we proved by a proteomic investigation that adipose-derived (AD)-MSC-secretome contains alpha-1-antitrypsin (AAT), the main elastase inhibitor in the lung, 72 other proteins involved in protease/antiprotease balance, and 46 proteins involved in the response to bacteria. By secretome fractionation, we proved that AAT is present both in the soluble fraction of secretome and aggregated and/or adsorbed on the surface of EVs, that can act as natural carriers promoting AAT in vivo stability and activity. To modulate secretome composition, AD-MSCs were cultured in different stimulating conditions, such as serum starvation or chemicals (IL-1β and/or dexamethasone) and the expression of the gene encoding for AAT was increased. By testing in vitro the anti-elastase activity of MSC-secretome, a dose-dependent effect was observed; chemical stimulation of AD-MSCs did not increase their secretome anti-elastase activity. Finally, MSC-secretome showed anti-bacterial activity on Gram-negative bacteria, especially for Klebsiella pneumoniae. These preliminary results, in addition to the already demonstrated immunomodulation, pave the way for the use of MSC-secretome in the treatment of AAT-deficiency lung diseases.
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Hassan, Wassan Nori, Mazin A. A. Najm, Alaa Hussein Hasan y Khulood H. Oudah. "Immunological aspects of Alpha 1 Antitrypsin in COVID-19 infection among the Populace and Pregnant Women". AL-Kindy College Medical Journal 17, n.º 1 (30 de abril de 2021): 8–13. http://dx.doi.org/10.47723/kcmj.v17i1.242.
Since the COVID-19 pandemic alarm was made by the severe acute respiratory syndrome (SARS)-coronavirus (CoV) 2, several institutions and agencies have pursued to clarify the viral virulence and infectivity. The fast propagation of this virus leads to an unprecedented rise in the number of cases worldwide. COVID-19 virus is exceptionally contagious that spreads through droplets, respiratory secretions, and direct contact. The enveloped, single-stranded RNA virus has a specific envelop region called (S) region encoding (S protein) that specifically binds to the host cell receptor. Viral infection requires receptors' participation on the host cell membrane's surface, a key- step for the viral invasion of susceptible cells.
Recently, the Italian alpha 1 antitrypsin Registry results showed a close geographic distribution of positive cases like the one recorded for SARS -CoV-2 infection. AAT deficient patients presented with the highest infection rates. They were giving attention to alpha 1 antitrypsin AAT's role in COVID-19 infection. Alpha 1 antitrypsin deficiency (AATD) is undoubtedly the most common genetic condition in adults. AATD is characterized by decreased serum levels or impaired AAT action, raising the risk of developing many diseases, particularly pulmonary emphysema cirrhosis of the liver. This review will discuss the main immunological properties that AAT has as a protective agent against the infection and possible therapeutic application.
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Eggenschwiler, Reto, Komal Loya, Malte Sgodda, Francoise André y Tobias Cantz. "Hepatic Differentiation of Murine Disease-Specific Induced Pluripotent Stem Cells Allows Disease ModellingIn Vitro". Stem Cells International 2011 (2011): 1–11. http://dx.doi.org/10.4061/2011/924782.
Direct reprogramming of somatic cells into pluripotent cells by retrovirus-mediated expression of OCT4, SOX2, KLF4, and C-MYC is a promising approach to derive disease-specific induced pluripotent stem cells (iPSCs). In this study, we focused on three murine models for metabolic liver disorders: the copper storage disorder Wilson's disease (toxic-milk mice), tyrosinemia type 1 (fumarylacetoacetate-hydrolase deficiency, FAH−/−mice), and alpha1-antitrypsin deficiency (PiZ mice). Colonies of iPSCs emerged 2-3 weeks after transduction of fibroblasts, prepared from each mouse strain, and were maintained as individual iPSC lines. RT-PCR and immunofluorescence analyses demonstrated the expression of endogenous pluripotency markers. Hepatic precursor cells could be derived from these disease-specific iPSCs applying anin vitrodifferentiation protocol and could be visualized after transduction of a lentiviral albumin-GFP reporter construct. Functional characterization of these cells allowed the recapitulation of the disease phenotype for further studies of underlying molecular mechanisms of the respective disease.
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Wang, Wei, Christine Hale, Dave Goulding, Stuart M. Haslam, Bérangère Tissot, Christopher Lindsay, Stephen Michell et al. "Mannosidase 2, alpha 1 Deficiency Is Associated with Ricin Resistance in Embryonic Stem (ES) Cells". PLoS ONE 6, n.º 8 (23 de agosto de 2011): e22993. http://dx.doi.org/10.1371/journal.pone.0022993.
Rachinskaya, O. A., M. A. Vodyakova, E. V. Melnikova y V. A. Merkulov. "Treatment of Genetic Diseases: Current Trends in the Development of Biomedical Cell Products". BIOpreparations. Prevention, Diagnosis, Treatment 19, n.º 4 (11 de diciembre de 2019): 225–32. http://dx.doi.org/10.30895/2221-996x-2019-19-4-225-232.
Genetic diseases are often progressive in nature, and without proper treatment may result in disability or death. Difficulties with diagnosis of genetic diseases and lack of effective treatment are global public health challenges. Medical care for patients with genetic diseases is often confined to symptomatic and palliative care. Starting from the 2000s, great hopes have been placed on cell-based medicinal products (which are referred to as biomedical cell products in the Russian legislation) and gene therapy products. The aim of the study was to review current trends in the development of biomedical cell products for the treatment of genetic diseases. The paper focuses on cell-based products for the treatment of monogenic genetic diseases, such as severe combined immunodeficiency (SCID), recessive dystrophic epidermolysis bullosa (RDEB), beta-haemoglobinopathies, alpha-1-antitrypsin deficiency, haemophilia A, and Duchenne muscular dystrophy. Such drugs are being developed in many countries and are now entering preclinical and different stages of clinical trials. Products based on various types of viable cells, including differentiated cells, stem cells, induced pluripotent cells, as well as cells genetically modified ex vivo, may be developed for the treatment of one and the same disease. The main priority is the creation of such products that will obviate the need for replacement therapy or palliative care, and that will significantly increase life expectancy and quality of life.
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Mikhalkevich, Natallia y Michael W. Becker. "Alpha-Catenin Is Dispensable for Normal Hematopoietic Stem Cell Function." Blood 114, n.º 22 (20 de noviembre de 2009): 1438. http://dx.doi.org/10.1182/blood.v114.22.1438.1438.
Abstract Abstract 1438 Poster Board I-461 We previously demonstrated the loss of expression of alpha-E-Catenin, the product of the CTNNA1 gene, in primary leukemic stem cells isolated from patients with advanced Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML) associated with loss of all or part of the long arm of chromosome 5. To formally assess the impact of loss of Ctnna1 expression on hematopoiesis, we employed a murine model for the hematopoietic specific conditional loss of Ctnna1 expression. We demonstrate that Ctnna1 deficiency is associated with normal hematopoietic maturation and proliferation as assessed by peripheral blood examination and methycellulose colony assays. We assessed stem cell and early progenitor frequencies using both flow cytometry and functional assays. Ctnna1 deficiency was associated with equivalent frequencies of Sca1+C-Kit+CD135-Lineage- HSCs in both experimental animals and controls. Short term HSC and MPP frequencies were likewise unaltered. We assessed HSC function using transplantation studies. In competitive repopulation experiments, HSCs deficient for Ctnna1 maintained stable engraftment of recipient mice for up to 1 year. Limiting dilution analyses detected no significant difference in HSC frequency between wild type and Ctnna1 deficient mice. We examined the potential role of Ctnna1 deficient hematopoietic stem cells in two murine models for myeloid neoplasms 1.) exposure to mutagen ENU and 2.) a model for murine AML driven by the HoxA9-Nup98 fusion product. Following exposure of HSCs to ENU, loss of Ctnna1 was not associated with an increased risk of development of a myeloid neoplasm. Expression of the HoxA9-Nup98 fusion product by retroviral infection of Ctnna1 deficient and wild type Sca1+C-Kit+Lineage- cells resulted in no difference in time to development of the previously characterized myeloproliferative disorder or acute leukemia. Taken together, these data demonstrate that in the absence of specific genetic abnormalities, loss of Ctnna1 expression in primary murine HSCs is not associated with aberrant HSC function or the development of myeloid neoplasms. Further studies are necessary to define a role for of loss of Ctnna1 expression in human myeloid malignancies. Disclosures No relevant conflicts of interest to declare.
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Fässler, R., M. Pfaff, J. Murphy, A. A. Noegel, S. Johansson, R. Timpl y R. Albrecht. "Lack of beta 1 integrin gene in embryonic stem cells affects morphology, adhesion, and migration but not integration into the inner cell mass of blastocysts." Journal of Cell Biology 128, n.º 5 (1 de marzo de 1995): 979–88. http://dx.doi.org/10.1083/jcb.128.5.979.
A gene trap-type targeting vector was designed to inactivate the beta 1 integrin gene in embryonic stem (ES) cells. Using this vector more than 50% of the ES cell clones acquired a disruption in the beta 1 integrin gene and a single clone was mutated in both alleles. The homozygous mutant did not produce beta 1 integrin mRNA or protein, while alpha 3, alpha 5, and alpha 6 integrin subunits were transcribed but not detectable on the cell surface. Heterozygous mutants showed reduced beta 1 expression and surface localization of alpha/beta 1 heterodimers. The alpha V subunit expression was not impaired on any of the mutants. Homozygous ES cell mutants lacked adhesiveness for laminin and fibronectin but not for vitronectin and showed a reduced association with a fibroblast feeder layer. Furthermore, they did not migrate towards chemoattractants in fibroblast medium. None of these functions were impaired in heterozygous mutants. Scanning electron microscopy revealed that homozygous cells showed fewer cell-cell junctions and had many microvilli not usually found on wild type and heterozygous cells. This profound change in cell shape is not associated with gross alterations in the expression and distribution of cytoskeletal components. Unexpectedly, microinjection into blastocysts demonstrated full integration of homozygous and heterozygous mutants into the inner cell mass. This will allow studies of the consequences of beta 1 integrin deficiency in several in vivo situations.
También puede estar interesado en las bibliografías ampliadas sobre el tema "Stem cells ; Alpha 1-antitrypsin deficiency" para tipos de fuentes particulares:
Tesis sobre el tema "Stem cells ; Alpha 1-antitrypsin deficiency":
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Rashid, Sheikh Tamir. "Human induced pluripotent stem cells for in vitro modeling and cell based therapy of α-1 antitrypsin deficiency". Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610175.
Segeritz, Charis-Patricia. "Investigating the pathophysiology of [alpha]-1-antitrypsin deficiency using human induced pluripotent stem cells". Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708860.
Witek, Rafal Piotr. "Novel application of gene therapy and somatic stem cells in treating metabolic liver disorders". [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0009820.
Thesis (Ph.D.)--University of Florida, 2005. Typescript. Title from title page of source document. Document formatted into pages; contains 127 pages. Includes Vita. Includes bibliographical references.
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Geiger-Schredelseker, Sabine [Verfasser] y Peter [Akademischer Betreuer] Nelson. "Mesenchymal stem/stromal cells engineered to express the protease inhibitor alpha-1 antitrypsin for the treatment of inflammatory lung diseases / Sabine Geiger-Schredelseker ; Betreuer: Peter Nelson". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1144177839/34.
Capítulos de libros sobre el tema "Stem cells ; Alpha 1-antitrypsin deficiency":
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"Alpha 1-Antitrypsin Gene Expression in Neutrophils and Other Cells". En Alpha 1 - Antitrypsin Deficiency, 157–70. CRC Press, 2014. http://dx.doi.org/10.1201/9781498710534-17.
Actas de conferencias sobre el tema "Stem cells ; Alpha 1-antitrypsin deficiency":
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Hurley, Killian, Anjali Jacob, Dylan Thomas, Finn Hawkins, Andrew Wilson y Darrell Kotton. "Deriving type II alveolar cells from pluripotent stem cells to produce a novel model of alpha-1 antitrypsin deficiency pathogenesis". En ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa4659.
Mikosz, A., D. Cao, A. A. Wilson, D. N. Kotton, I. Petrache y K. A. Serban. "Functional Characterization of Alveolar Macrophages (AM) Derived from Alpha-1 Antitrypsin (AAT) Deficient (AATD) Human Induced Pluripotent Stem Cells". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7426.
Escribano, Amparo, Sara Pastor, Ana Reula, Silvia Castillo, Shirley Camacho, Francisco Sanz, Pilar Codoñer-Franch y Francisco Dasi. "Telomere attrition in peripheral blood mononuclear cells of children with alpha-1 antitrypsin deficiency". En Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1255.
Hurley, K. J., A. Jacob, J. Kaserman, F. J. Hawkins, A. A. Wilson y D. N. Kotton. "Misfolded Alpha-1 Antitrypsin Protein Produced by Alveolar Epithelial Cells Generated from Patient-Derived Induced Pluripotent Stem Cells Is Absent After CRISPR/Cas9 Gene Editing". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3776.
