Auswahl der wissenschaftlichen Literatur zum Thema „Beta-cell protection“
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Zeitschriftenartikel zum Thema "Beta-cell protection"
MANDRUP-POULSEN, THOMAS. „Beta Cell Death and Protection“. Annals of the New York Academy of Sciences 1005, Nr. 1 (November 2003): 32–42. http://dx.doi.org/10.1196/annals.1288.005.
Der volle Inhalt der QuelleHosseini, Azar, Reza Shafiee-Nick und Ahmad Ghorbani. „Pancreatic beta cell protection/regeneration with phytotherapy“. Brazilian Journal of Pharmaceutical Sciences 51, Nr. 1 (März 2015): 1–16. http://dx.doi.org/10.1590/s1984-82502015000100001.
Der volle Inhalt der QuelleLjunggren, H. G., K. Sturmhöfel, E. Wolpert, G. J. Hämmerling und K. Kärre. „Transfection of beta 2-microglobulin restores IFN-mediated protection from natural killer cell lysis in YAC-1 lymphoma variants.“ Journal of Immunology 145, Nr. 1 (01.07.1990): 380–86. http://dx.doi.org/10.4049/jimmunol.145.1.380.
Der volle Inhalt der QuelleAsahara, Shun-ichiro, und Wataru Ogawa. „SGLT2 inhibitors and protection against pancreatic beta cell failure“. Diabetology International 10, Nr. 1 (17.09.2018): 1–2. http://dx.doi.org/10.1007/s13340-018-0374-y.
Der volle Inhalt der QuelleHong, Su Hee, Jee-In Heo, Jeong-Hyeon Kim, Sang-Oh Kwon, Kyung-Mok Yeo, Anna M. Bakowska-Barczak, Paul Kolodziejczyk et al. „Antidiabetic and Beta Cell-Protection Activities of Purple Corn Anthocyanins“. Biomolecules and Therapeutics 21, Nr. 4 (31.07.2013): 284–89. http://dx.doi.org/10.4062/biomolther.2013.016.
Der volle Inhalt der QuelleCostes, Safia, Gyslaine Bertrand und Magalie A. Ravier. „Mechanisms of Beta-Cell Apoptosis in Type 2 Diabetes-Prone Situations and Potential Protection by GLP-1-Based Therapies“. International Journal of Molecular Sciences 22, Nr. 10 (18.05.2021): 5303. http://dx.doi.org/10.3390/ijms22105303.
Der volle Inhalt der QuelleHashim, G. A., H. Offner, R. Y. Wang, K. Shukla, E. Carvalho, W. J. Morrison und A. A. Vandenbark. „Spontaneous development of protective anti-T cell receptor autoimmunity targeted against a natural EAE-regulatory idiotope located within the 39-59 region of the TCR-V beta 8.2 chain.“ Journal of Immunology 149, Nr. 8 (15.10.1992): 2803–9. http://dx.doi.org/10.4049/jimmunol.149.8.2803.
Der volle Inhalt der QuelleOffner, H., M. Vainiene, D. P. Gold, W. J. Morrison, R. Y. Wang, G. A. Hashim und A. A. Vandenbark. „Protection against experimental encephalomyelitis. Idiotypic autoregulation induced by a nonencephalitogenic T cell clone expressing a cross-reactive T cell receptor V gene.“ Journal of Immunology 146, Nr. 12 (15.06.1991): 4165–72. http://dx.doi.org/10.4049/jimmunol.146.12.4165.
Der volle Inhalt der QuelleChen, Qi, Zhida Shen, Yanjun Mao, Qinfeng Li, Yu Liu, Menghan Mei, Fuyu Qiu und Meihui Wang. „Inhibition of microRNA-34a mediates protection of thymosin beta 4 in endothelial progenitor cells against advanced glycation endproducts by targeting B-cell lymphoma 2“. Canadian Journal of Physiology and Pharmacology 97, Nr. 10 (Oktober 2019): 945–51. http://dx.doi.org/10.1139/cjpp-2018-0743.
Der volle Inhalt der QuelleFu, Y. X., C. E. Roark, K. Kelly, D. Drevets, P. Campbell, R. O'Brien und W. Born. „Immune protection and control of inflammatory tissue necrosis by gamma delta T cells.“ Journal of Immunology 153, Nr. 7 (01.10.1994): 3101–15. http://dx.doi.org/10.4049/jimmunol.153.7.3101.
Der volle Inhalt der QuelleDissertationen zum Thema "Beta-cell protection"
Chellan, Nireshni. „The effect of Cyclopia maculata extract on β-cell function, protection against oxidative stress and cell survival“. Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/95861.
Der volle Inhalt der QuelleENGLISH ABSTRACT: Insights into the role of oxidative stress and pancreatic β-cell dysfunction in the pathogenesis of type 2 diabetes (T2D) reveals an opportunity for the development of novel therapeutics that directly protect and preserve β-cells. The protective role of dietary antioxidants, such as plant polyphenols, against oxidative stress induced diseases, including T2D, is increasingly under scrutiny. Polyphenol-rich extracts of Cyclopia spp, containing mangiferin, may provide novel therapeutics. An aqueous extract of unfermented Cyclopia maculata, containing more than 6 % mangiferin, was assessed for its protective effect in pancreatic β-cells in vitro, ex vivo and in vivo under conditions characteristic of T2D. The effect of mangiferin was also evaluated in vitro and ex vivo, with N-acetyl cysteine (NAC) as an antioxidant control. In this study, we established in vitro toxicity models in RIN-5F insulinoma cells based on conditions β-cells are exposed to in T2D; i.e. lipotoxicity, inflammation and oxidative stress conditions. To achieve this, cells were exposed to the following stressors: palmitic acid (PA), a pro-inflammatory cytokine combination and streptozotocin (STZ), respectively. Thereafter, the ability of the C. maculata extract, mangiferin and NAC to protect RIN-5F cells from the effects of these stressors was assessed by measuring β-cell viability, function and oxidative stress. Cell viability was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, adenosine triphosphate and annexin-V and propidium iodide assays. Cell function was evaluated by measuring glucose stimulated insulin secretion, cell proliferation and cellular calcium. To assess oxidative stress in the RIN-5F cells, diaminofluorescein-FM and dihydroethidium fluorescence, and superoxide dismutase enzyme activity were measured. The in vitro findings were then verified in isolated pancreatic rat islets using methods and models established in the RIN-5F experiments. The protective effect of the extract, NAC and metformin was assessed in STZ induced diabetic Wistar rats, using two treatment regimes, i.e. by treating rats with established diabetes and by pretreating rats prior to induction of diabetes by STZ. Glucose metabolism, oxidative stress and pancreatic morphology were assessed by performing an oral glucose tolerance test, measuring serum insulin, triglycerides, nitrites, catalase and glutathione. Hepatic thiobarbituric acid reactive substances and nitrotyrosine were also assessed. Immunohistochemical labelling of pancreata with insulin, glucagon and MIB-5 was used for morphological assessment. The extract improved β-cell viability, function and attenuated oxidative stress, most apparently in STZ and PA induced toxicity models comparable with NAC both in vitro and in isolated islets. Mangiferin was not as effective, showing only marginal improvement in RIN-5F cell and islet function, and oxidative stress. Pretreatment of STZ induced diabetic Wistar rats with extract was as effective as, if not better than, metformin in improving glucose tolerance, hypertriglyceridaemia and pancreatic islet morphology related to improved β-cell function. This study demonstrated that the aqueous extract of unfermented C. maculata was able to protect pancreatic β-cells from STZ and PA induced toxicity in vitro and ex vivo. In vivo, pretreatment with the extract improved glucose metabolism and pancreatic islet morphology in STZ induced diabetic Wistar rats.
AFRIKAANSE OPSOMMING: Insigte oor die rol wat oksidatiewe stres en pankreas β-sel disfunksie in die patogenese van tipe 2-diabetes (T2D) speel, bied 'n geleentheid vir die ontwikkeling van nuwe terapeutiese middels wat β-selle direk daarteen beskerm. Die beskermende rol van antioksidante in die dieët soos plantaardige polifenole teen oksidatiewe stres geinduseerde siektes soos T2D, is toenemend onder die soeklig. Polifenolryk ekstrakte van Cyclopia spp wat mangiferin bevat mag nuwe terapeutiese middels lewer. ‘n Waterekstrak van ongefermenteerde Cyclopia maculata wat meer as 6% mangiferin bevat, is ondersoek vir sy beskermende effek op pankreas ß-selle in vitro, ex vivo en in vivo teen kondisies kenmerkend aan T2D. Die effek van mangiferin is ook in vitro en ex vivo geëvalueer, met N-asetielsistien (NAC) as 'n antioksidant kontrole. In hierdie studie is in vitro toksisiteitsmodelle in RIN-5F insulinoomselle gevestig. Die modelle is gebaseer op toestande waaraan β-selle blootgestel word tydens T2D; d.w.s. lipotoksisiteit, inflammasie en oksidatiewe stres. Hiervoor is die selle aan die volgende stressors blootgestel: palmitiensuur (PA), ‘n pro-inflammatoriese sitokien mengsel en streptozotosien (STZ). Vervolgens is die vermoë van die C. maculata ekstrak, mangiferin en NAC om die RIN-5Fselle teen hierdie stressors te beskerm, beoordeel deur die meting van β-sellewensvatbaarheid, funksie en oksidatiewe stres. Sellewensvatbaarheid is bepaal met 3-(4,5-dimetielthiazol-2-yl)-2,5-difenieltetrazolium bromied, adenosientrifosfaat en anneksien-V and propidium jodied toetse. Selfunksie is geëvalueer d.m.v. glukose gestimuleerde insuliensekresie, selproliferasie en sellulêre kalsium bepaling. Oksidatiewe stres in die RIN-5Fselle is geëvalueer d.m.v. diaminofluorescein-FM en dihidroethidium fluoressensie bepalings, asook meting van superoksied dismutase ensiemaktiwiteit. Die in vitro bevindings is daarna in geїsoleerde rot pankreaseilande bevestig deur die metodes en modelle wat in die RIN-5F eksperimente gebruik is. Die antidiabetiese effekte van die ekstrak, NAC en metformien in STZ-geїnduseerde diabetiese Wistar rotte is bepaal d.m.v. twee behandlingsregimes, d.w.s. die behandeling van rotte met gevestigde diabetes of deur die behandeling voor die induksie van diabetes te begin. Glukose metabolisme, oksidatiewe stres en veranderinge in die pankreasmorfologie is ondersoek d.m.v. orale glukose toleransie toetse en die bepaling van serum insulien, trigliseriedes, nitriete, katalase en glutationien. Hepatiese tiobarbituursuur reaktiewe stowwe en nitrotirosien is ook geëvalueer. Immunohistochemiese kleuring van pankreas snitte is gebruik vir morfologiese assessering van insulien, glukagon en MIB-5. Die ekstrak het mees opvallend β-sel lewensvatbaarheid en funksie verbeter, terwyl oksidatiewe stres verminder is in die STZ- en PA-geїnduseerde toksisiteitmodelle. Bogenoemde effekte van die ekstrak in vitro en in die geїsoleerde eilande was vergelykbaar met die van NAC. Mangiferin was minder effektief, met slegs ‘n marginale verbetering in die funksie van RIN-5Fselle en eilande, asook t.o.v. oksidatiewe stres. Behandeling van die Wistar rotte met die ekstrak voor induksie van diabetes met STZ was net so effektief, of selfs beter as metformien in terme van verbeterde glukosetoleransie, trigliseriedvlakke en die morfologie van pankreas eilande wat verband gehou het met β-sel funksie. Hierdie studie het getoon dat die waterekstrak van ongefermenteerde C. maculata pankreas β-selle teen veral STZ- en PA-geїnduseerde toksisiteit in vitro en ex vivo beskerm het. In vivo het behandeling met die ekstrak voor en na induksie van diabetes, glukosemetabolisme en die morfologie van pankreas eilande in STZ-geїnduseerde diabetiese Wistar rotte verbeter.
Ngamjariyawat, Anongnad, Kyril Turpaev, Svitlana Vasylovska, Elena N. Kozlova und Nils Welsh. „Co-Culture of Neural Crest Stem Cells (NCSC) and Insulin Producing Beta-TC6 Cells Results in Cadherin Junctions and Protection against Cytokine-Induced Beta-Cell Death“. Uppsala universitet, Neuroanatomi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-198839.
Der volle Inhalt der QuelleDaziano, Guillaume. „Rôle du propeptide de la sortiline et de ses dérivés dans les mécanismes de survie de la cellule bêta pancréatique“. Electronic Thesis or Diss., Université Côte d'Azur, 2021. http://www.theses.fr/2021COAZ6025.
Der volle Inhalt der QuelleIn 2019, the International Diabetes Federation revealed that nearly 500 million people have diabetes worldwide. It is estimated that this incidence will reach 700 million people by 2045. In addition to the financial aspect of treatment, diabetes is a real public health issue. Indeed, the deleterious hyperglycemic environment associated with diabetes is could induce serious complications, leading to a functional alteration of many organs such as the heart, the brain or the kidney. Insulin resistance associated with the deterioration of insulin secretion and the loss of pancreatic beta cell mass are the main characteristics of type 2 diabetes. Thus, in order to improve the management of diabetic patients, the identification of a controlled therapeutic approach to protect beta cell mass and promote insulin secretion only in response to glucose and without side effects, appears ideal.The laboratory has identified the endogenous PE and its synthetic derivatives Spadin and Mini-Spadin as selective inhibitors of TREK-1 potassium channels. By this mechanism, the peptides showed also a strong antidepressant potential by modulating serotonin secretion, neuronal proliferation and survival. At the peripheral level, Spadin has been described in vitro and in vivo as a peptide with an incretin effect comparable to that of exendin-4, an antidiabetic commonly used in the clinic. Thus, following this study and by analogy to the protective effects observed on the neuron, we hypothesized that PE and its derivatives may have a beneficial role in the survival mechanisms in the pancreatic beta-cell.In this thesis, we demonstrate that endogenous PE and its derivatives protect beta cells from apoptosis induced by the chronic presence of the pro-inflammatory and diabetogenic interleukin IL-1β, as well as from an acute toxic shock induced by staurosporine. Furthermore, analysis of intracellular mechanisms reveals that these peptides cause an increase in intracellular calcium concentration, activate the ERK and Akt proliferative and survival pathways, and maintain CREB transcriptional factor activity in a deleterious environment via a calmodulin kinase-dependent pathway.Thus, this work shows that PE and its synthetic derivatives protect the pancreatic beta-cell and initiate virtuous cellular processes through an original PKA-independent signaling pathway, where membrane potential and calcium play a crucial role. This suggests the sortilin-derived peptides as a new class of pancreatic beta-cell protective molecules
Hägerkvist, Robert. „Anti-Diabetic and Beta-Cell Protective Actions of Imatinib Mesylate“. Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7078.
Der volle Inhalt der QuelleType 1 diabetes is a disease resulting from the progressive immune-mediated destruction of insulin producing β-cells. In order to understand more about diabetes we need to understand the mechanisms governing β-cell death.
The leukemia drug Gleevec is a tyrosine kinase inhibitor that targets c-Abl. Surprisingly, Gleevec also counteracts Type 2 diabetes and acts as a cell death inhibiting agent, via inhibition c-Abl. Since both Type 1 and Type 2 diabetes are characterized by an increased β-cell death, and the role of c-Abl is unknown in β-cells, we wanted to investigate the following:
1.Does Gleevec act via inhibition of c-Abl in β-cells?
2.Can Gleevec treatment prevent beta-cell death and diabetes?
3.Which downstream signaling pathways are affected by Gleevec?
In paper I, in order to determine whether Gleevec acts by inhibiting c-Abl, we used RNA-interference. Interestingly, siRNA against c-Abl produced by recombinant Dicer mediate almost complete and non-toxic silencing of c-Abl mRNA in dispersed islet cells and conferred protection from streptozotocin and cytokines.
In paper II we show that Gleevec protects β-cells from nitric oxide, pro-inflammatory cytokines and streptozotocin in vitro and that Gleevec can prevent diabetes development in the NOD mouse and the streptozotocin-injected mouse. We also present the hypothesis that Gleevec induces a state resembling ischemic preconditioning.
Paper III presents an additional mechanism by which Gleevec might improve β-cell survival, i.e. via the inhibition of the downstream stress-activated protein kinase c-Jun N-terminal kinase (JNK), the activity of which has been implicated in β-cell death signaling pathways.
In paper IV we explore the interactions between the adaptor protein Shb and c-Abl. We presently show an association between Shb-c-Abl and that Shb is a substrate for the c-Abl kinase that might regulate stress-induced c-Abl activity.
Hägerkvist, Robert. „Anti-diabetic and beta-cell protective actions of imatinib mesylate /“. Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7078.
Der volle Inhalt der QuelleGonçalves, Patricia de Almeida Machado. „Ação citotóxica e antioxidante da beta lapachona em células endoteliais“. Universidade Federal de Goiás, 2017. http://repositorio.bc.ufg.br/tede/handle/tede/8138.
Der volle Inhalt der QuelleApproved for entry into archive by Luciana Ferreira (lucgeral@gmail.com) on 2018-01-31T14:31:11Z (GMT) No. of bitstreams: 2 Dissertação - Patricia de Almeida Machado Gonçalves - 2017.pdf: 2160802 bytes, checksum: 939d23474b7308d62b12f4b66224829d (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5)
Made available in DSpace on 2018-01-31T14:31:11Z (GMT). No. of bitstreams: 2 Dissertação - Patricia de Almeida Machado Gonçalves - 2017.pdf: 2160802 bytes, checksum: 939d23474b7308d62b12f4b66224829d (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Previous issue date: 2017-12-18
Conselho Nacional de Pesquisa e Desenvolvimento Científico e Tecnológico - CNPq
Oxidative stress is the overproduction of reactive oxygen species that cause cell damage and even the death. It is a mechanism related to ischemia and reperfusion, a process that affects several organs and is involved in neurodegenerative diseases, cardiac and/or renal insufficiencies, hepatic dysfunction, among others. The discovery of new antioxidant substances derived from natural sources, is important for the prevention and treatment of these diseases. Beta lapachone is a substance with antioxidant action obtained from sawdust of Ipe wood, a symbolic tree from the Brazilian cerrado. This study aimed to analyze the cytotoxic and antioxidant action of beta lapachone in endothelial cells, in vitro. EA.hy 926 lineage cells were subcultured, treated with different concentrations of beta lapachone and subjected to ischemia and reperfusion. Cytotoxicity and antioxidant action were assessed through the cellular viability analysis by the tetrazolium reduction method. The averages were verified by the Tukey test (5% of significance) and by variance analysis. There was a dose-dependent progression of cytotoxicity in the non-ischemia/reperfusion (control) group and cell viability increase in the ischemia/reperfusion group. However, there was no statistical difference between the concentrations and between groups. Considering the settings of this experiment, Beta lapachone did not present cytotoxic or antioxidant action on endothelial cells.
O estresse oxidativo é o excesso de produção de espécies reativas de oxigênio que causam danos e até a morte das células. É um mecanismo que pode se originar da isquemia e reperfusão, um processo que acomete diversos órgãos e que está envolvido em doenças neurodegenerativas, cardíacas, insuficiências renais, disfunção hepática, entre outras. A necessidade da descoberta de novas substâncias antioxidantes, derivadas de fontes naturais, é importante para a prevenção e tratamento dessas doenças. A beta lapachona é uma substância com ação antioxidante, obtida da serragem da madeira do ipê, vegetação símbolo do cerrado brasileiro. Neste estudo objetivou-se analisar a ação citotóxica e antioxidante da beta lapachona em células endoteliais, in vitro. Células da linhagem EA.hy 926 foram subcultivadas, tratadas com a β lapachona em diferentes concentrações e submetidas à isquemia e reperfusão. A citotoxidade e a ação antioxidante foram obtidas por meio da análise da viabilidade celular pelo método de redução do tetrazólio. As médias foram averiguadas pelo teste de Tukey (5% de significância) e pela análise de variância. Houve progressão dose dependente da citotoxidade no grupo sem isquemia/reperfusão e da viabilidade celular no grupo com isquemia/reperfusão. No entanto, não houve diferença estatística entre as concentrações e entre os grupos. A beta lapachona, nas condições desse experimento, não apresentou ação citotóxica ou antioxidante nas células endoteliais.
Mangone, Flavia Regina Rotea. „"Determinação do perfil de expressão dos RNAs mensageiros da família das Smads e dos componentes do complexo AP-1 em carcinoma de célula escamosa de cabeça e pescoço"“. Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-10082005-153351/.
Der volle Inhalt der QuelleSmad and AP1 messenger RNA expression may underlie disruptions affecting TGFb signaling in head and neck squamous cell carcinoma (HNSCC). Analysis of Smads1-8 mRNA expression by RPA has shown Smad expression is globally increased in tumor as compared to adjacent normal tissue. Kaplan Meier survival curves and multivariate analysis revealed that Smad6 positivity in tumor was an independent good prognostic factor in HNSCC. In relation to AP-1, as measured by Northern blot, only Fra-1 was overexpressed in tumor and directly related to the presence of lymph node involvement. Our data suggest that Smad6 may be a marker of good prognosis in HNSCC
Elavummoottil, Ouseph Chacko. „Mecanismes de l'adaptation au lactose de souches de vinca minor l. Et de datura innoxia mill. Cultivee in vitro : etude de la beta -galactosidase et autres enzymes impliquees dans cette adaptation“. Paris 6, 1987. http://www.theses.fr/1987PA066356.
Der volle Inhalt der QuelleWolf, Horrell Erin M. „Regulation of UV-Protective Pathways Downstream of the Melanocortin 1 Receptor in Melanocytes“. UKnowledge, 2016. http://uknowledge.uky.edu/physiology_etds/29.
Der volle Inhalt der QuelleWang, Ting-Hsuan, und 王廷軒. „Beta-cell protective effects of lotus seedpod extracts against oxidative injury in vitro and in vivo“. Thesis, 2015. http://ndltd.ncl.edu.tw/handle/926953.
Der volle Inhalt der QuelleBuchteile zum Thema "Beta-cell protection"
Han, Seung Jin, Sung-E. Choi, Hae Jin Kim, Kwan Woo Lee und Yup Kang. „β-Cell Protective Effect of 2-Aminobicyclo[2.2.1]heptan-2-Carboxylic Acid (BCH) as Glutamate Dehydrogenase (GDH) Activator indb/dbMice“. In BASIC/TRANSLATIONAL - Beta Cell Biology, P2–475—P2–475. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p5.p2-475.
Der volle Inhalt der QuelleBhopal, Raj S. „A causal synthesis and models“. In Epidemic of Cardiovascular Disease and Diabetes, 198–220. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.003.0009.
Der volle Inhalt der QuelleErhabor, Osaro, Teddy Charles Adias, Tosan Erhabor, Osaro Mgbere, Sadiya Usman und Bibiana Nonye Egenti. „Role of Sociodemographic and Economic Variables in Predisposition to Vaso-Occlusive Crisis and Mortality in Patients with SCD: Case Study of Sub-Saharan Africa“. In Sickle Cell Disease [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105685.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Beta-cell protection"
Okuno, A., Y. Harada und T. Ando. „Development of Plasma Sprayed Corrosion Protection Coatings for Sodium Sulfur Battery Cell Containers“. In ITSC2004, herausgegeben von Basil R. Marple und Christian Moreau. ASM International, 2004. http://dx.doi.org/10.31399/asm.cp.itsc2004p0070.
Der volle Inhalt der QuelleO'Konek, Jessica J., Petr Illarionov, Deborah Stewart Khursigara, Elena Ambrosino, Bernard F. Castillo, Ravinder Raju, Maryam Khalili et al. „Abstract 5613: Beta-mannosylceramide: a novel NKT cell agonist which synergizes with alpha-galactocylceramide to induce protection against tumors“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5613.
Der volle Inhalt der QuelleBerichte der Organisationen zum Thema "Beta-cell protection"
Elmann, Anat, Orly Lazarov, Joel Kashman und Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, März 2015. http://dx.doi.org/10.32747/2015.7597913.bard.
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