Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inbred non-obese diabetic (NOD) mouse is a spontaneous model for insulin-dependent diabetes mellitus (IDDM). As in man and BB rats, IDDM in the NOD mouse has an autoimmune aetiology. The disease is controlled by several genes, one of which, Idd-1, has been mapped to the major histocompatibility complex (MHC) on chromosome 17. However, Idd-1 has not yet been identified. To facilitate the identification of Idd-1 we have further analysed the MHC region for restriction fragment length polymorphisms and we find that the NOD mouse has a distinct haplotype: H-2K1nod Kd A beta nod A alpha d E beta nod TNF-alpha beta. In addition, the NOD mouse shows some similarities with the H-2b haplotype in the Q region, in that either the Q7 or the Q9 gene seems to be like that in the b-haplotype and that the Qa2 antigen is expressed, while other parts of this region are distinct from the b- as well as the d- haplotype. In contrast, the sister strain, the non-obese normal (NON) mouse, derived from the same cataract-prone line of mice as the NOD mouse, has an MHC Class I region indistinguishable from the b-haplotype, but the MHC Class II region is distinct from the NOD mouse as well as the b-, d- and k-haplotype.
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PMID:Restriction fragment length polymorphisms in the major histocompatibility complex of the non-obese diabetic mouse. 197 42

It has been suggested that one of the recessive genes controlling diabetes in non-obese diabetic mice is linked to the major histocompatibility complex. We, therefore, performed restriction fragment length polymorphism studies of major histocompatibility complex genes (class I, II, and III) in non-obese diabetic mice in comparison with those of their non-diabetic sister strains, non-obese non-diabetic, cataract, and ILI mice which were derived from the same Jcl-ICR mice as the non-obese diabetic mouse was. When class II and III probes and a minimum of four restriction enzymes were used, class II and III genes of non-obese diabetic mice were indistinguishable from those of cataract and ILI mice but totally different from those of non-obese non-diabetic mice. The studies also indicated that A beta, E beta, and C4-Slp genes of non-obese diabetic, cataract, and ILI mice, and A alpha, A beta, E beta and C4-Slp genes of non-obese non-diabetic mice are different from those of BALB/c and C57BL/6 mice, respectively. While non-obese non-diabetic mice expressed the E alpha gene, non-obese diabetic, cataract, and ILI mice appeared to carry a deletion in the 5' end of the E alpha gene resulting in failure to transcribe the E alpha gene. When class I probe was used, cataract mice showed very different band patterns from those of the other ICR-derived mice. It is suggested that non-obese diabetic, non-obese non-diabetic, and ILI mice contain only a single class I D region gene.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Restriction fragment length polymorphism analysis of major histocompatibility complex genes in the non-obese diabetic mouse strain and its non-diabetic sister strains. 256 47

We have studied with a series of monoclonal antibodies and restriction fragment analysis the K, D, and class II region of the major histocompatibility complex of the non-obese diabetic mouse in comparison with its sister strains, the non-obese non-diabetic and cataract Shionogi mouse. (1) K region: Monoclonal antibody 31-3-4S (anti-Kd) reacted with splenocytes from non-obese diabetic mice while other anti-K (Kb, Kk, Kq) monoclonals did not react. Splenocytes from non-obese non-diabetic mice reacted with both anti-Kb and Kk monoclonals while splenocytes from cataract Shionogi mice reacted with anti-Kd and Kk monoclonals. Both sister strains, therefore, differ from the non-obese diabetic and other known mice strains by monoclonal analysis of H-2K. (2) D region: Splenocytes from both non-obese diabetic and non-obese non-diabetic mice reacted with monoclonal antibody 28-14-8S (anti-Db) while splenocytes from cataract Shionogi mice did not react with any anti-D monoclonal antibody tested. (3a) Class II region (non-obese diabetic and non-obese non-diabetic mice): Three of 11 monoclonal antibodies to class II molecules reacted with splenocytes of the non-obese diabetic mouse. The 3 reacting monoclonals have I-Ak primary specificities though additional anti-I-Ak monoclonal antibodies were negative. Among these monoclonals, 39B and 40A reacted with the non-obese diabetic mouse but not with the non-obese non-diabetic mouse, while 10-2-16 reacted with non-obese diabetic, non-obese non-diabetic and cataract Shionogi mice. Monoclonal MKD6 (anti-I-Ad) reacted with non-obese non-diabetic but not non-obese diabetic mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cataract Shionogi mouse, a sister strain of the non-obese diabetic mouse: similar class II but different class I gene products. 313 69

The diabetogenic major histocompatibility complex (MHC) (H2(g7)) of NOD mice comprises contributions from several class II loci collectively designated as Idd1. Introduction of the H2(gx) haplotype from the related but diabetes-resistant cataract Shionogi (CTS) strain demonstrated an additional MHC-linked locus designated Idd16. The NOD-related alloxan resistant (ALR)/Lt strain is also characterized by the H2(gx) haplotype, which does not differ from H2(g7) from the class I H2-K(d) gene distally through the class II and into the class III region. Polymorphisms distal to the heat shock protein 70 locus (Hspa1b) include a rare H2-D(dx) rather than the H2(g7) encoded D(b) allele. Two differential-length NOD.ALR-H2(gx) congenic stocks (D.R1 and D.R2), both containing H2-D(dx), significantly suppressed diabetogenesis. This protection was lost when ALR alleles between the class III region and H2-D were removed in a shorter interval congenic (D.R3). Because no differences were observed in the ALR-derived interval extending 0.41 mB proximal to H2-K in any of these congenic stocks, a component of what was originally designated "Idd16" was sited to an interval shorter than 7.33 mB, distinguishing D.R2 from D.R3. Evidence supporting the candidacy of the ALR/CTS-shared H2-D(dx) MHC class I variant present in both diabetes-resistant stocks, but not the susceptible stock, is discussed.
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PMID:Major histocompatibility complex-linked diabetes susceptibility in NOD/Lt mice: subcongenic analysis localizes a component of Idd16 at the H2-D end of the diabetogenic H2(g7) complex. 1585 53

Diabetes Mellitus (DM) is a serious medical problem that causes long-term systemic complications and considerable associated morbidity. DM can cause retinopathy (DRP), maculopathy, cataract, optic neuropathy, defects of eye muscles. DM is a risk factor for acute infectious conjunctivitis, bacterial keratitis, herpes virus infections and endophtalmitis. Elevated blood glucose induces structural, physiological and hormonal changes which affect retinal capillaries. DRP is recognized by loss of pericyte function and capillary occlusions together leading to breakdown of blood-retinal barrier, edematous changes and proliferation of vessels and fibrous tissue. Depending on stage of DRP, there are different preferable therapeutic approaches applied. In the case of ETDRS, in the area of leakage focal treatment should be performed, while panretinal photocoagulation is applied towards ischemic areas or beginning proliferations. Vitreal haemorrhage followed by fibroproliferative changes or tractional retinal detachment is treated by vitrectomy alone or in combination with ILM peeling. In pathogenesis of DRP, Insulin Growth Factor (IGF-1) can play an important role in production of VEGF (Vascular Endothelial Growth Factor). Hypoxia can up-regulate VEGF expression levels leading to pathologic ocular neovascularisation. An application of intravitreal corticosteroid treatment modulates vascular permeability by suppressing the production of VEGF, reducing both extracellular matrix metalloproteinase activity and basic fibroblast growth factor, decreasing major histocompatibility complex 2 Ag expression levels, and inhibiting activity of inflammatory cells. Clinical effects of treatment using intravitreal corticosteroids are evaluated by reduction of macular thickness and visual improvement. Intravitreal use of Anti-VEGF drugs, Pegaptanib, Ranibizumab and Bevacizumab can modify vasoproliferation, trigger macular edema, and, therefore, influence a prognosis for visual loss.
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PMID:Eye disorders in diabetes: potential drug targets. 1853 2