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Grupo QI

Público·36 miembros
Thomas Richardson
Thomas Richardson

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hemizygous mice (haploinsufficient) are a widely used strain for immunological and metabolic studies, with many target proteins being deficient or expressed at reduced levels. mice harboring a mutation in the fas receptor gene (lpr) have been used extensively for the study of autoimmune diseases, but not for type i diabetes. this disorder, occurring in man, lacks an effective therapy. nod mice may be a suitable alternative for the study of autoimmune diabetes, although they are susceptible to virus infections. several approaches are available to induce diabetes in nod mice, including the administration of allergen, viral infection, and treatment with chemical compounds such as 12-0-tetradecanoylphorbol-13-acetate (tpa). genetic factors have been described for type i diabetes in the nod mouse model, including the major histocompatibility complex (mhc) and non-mhc loci. t-cell immunity has been associated with the development of insulitis and diabetes in the nod mouse. nod mice develop insulitis but not diabetes in the absence of inflammation. mice with the higher mhc haplotype (h2g7) develop diabetes even in the absence of insulitis. however, recent studies suggest that the mhc-a, h2g7, non-mhc genes such as zinc finger transcription factors and protein kinase c-beta may induce diabetes independent of insulin, including by inducing insulitis. this has led to the use of spontaneously diabetic nod mice to study the roles of immunological and non-immunological factors in the development of diabetes.

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understanding the biliary system and its pathophysiology is becoming increasingly important as h. pylori is increasingly seen as an emerging cause of chronic inflammatory disease states such as idiopathic inflammatory bowel disease (ibd).

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