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Anti-glutamic acid decarboxylase

The exact mechanisms of tacrolimus-induced diabetes are unknown. In one renal transplant patient with genetic susceptibility, tacrolimus was associated with insulin-dependent diabetes mellitus and the simultaneous occurrence of anti-glutamic acid decarboxylase antibody (1096). Within 2 months after conversion from tacrolimus to ciclosporin, the antibody was no longer detected and the patient s insulin requirements fell dramatically. Tacrolimus-induced direct beta cell toxicity, with... [Pg.649]

Yoshioka K, Sato T, Okada N, Ishii T, Imanishi M, Tanaka S, Kim T, Sugimoto T, Fujii S. Post-transplant diabetes with anti-glutamic acid decarboxylase antibody during tacrolimus therapy. Diabetes Res Clin Pract 1998 42(2) 85-9. [Pg.688]

Langer P, Tajtakova M, Guretzki HJ, Kocan A, Petrik J, Chovancova J, Drobna B, Jursa S, Pavuk M, Tmovec T, Sebokova E, Klimes I (2002) High prevalence of anti-glutamic acid decarboxylase (anti-GAD) antibodies in employees at a polychlorinated biphenyl production factory. Arch Environ Health, 57(5) 412-415. [Pg.290]

Cao, C., and Sim, SJ. (2007) Signal enhancement of surface plasmon resonance immunoassay using enzyme precipitation functionalized gold nanoparticles a femto molar level measurement of anti glutamic acid decarboxylase antibody. Biosensors and Bioelectronics, 22, 1874 1880. [Pg.377]

An assay for diagnosing type I diabetes mellitus based on the detection of anti-glutamic acid decarboxylase (GAD) antibodies in buffer by a Biacore 2000, is presented in [47,48]. Biotinylated GAD was immobihzed on a streptavidin-coated surface. The effect of mixed SAM composition (differing in ratios of hydroxyl- and carboxyl-terminated alkanethiols) on the sensitivity of the sensor was investigated. On SPR sensor chips prepared with the optimized SAM composition (10 1 ratio of 3-mercaptopropanol to 11-mercaptoundecanoic acid), a concentration of anti-GAD as low as... [Pg.238]

Type I diabetes mellitus and thyroid disease reportedly develop in 0.08-2.6% and 10-15% of patients treated with combined interferon alfa- -ribavirin for chronic hepatitis C but rarely coexist however, both conditions have been reported in a 33-year-old woman [50 ]. In another case, a 55-year-old woman developed type 1 diabetes and had a recurrence of Graves disease during treatment with peginterferon alfa -I- ribavirin for chronic hepatitis C [51 ]. There were serum anti-glutamic acid decarboxylase antibodies and the authors suggested that she had autoimmune polyglandular syndrome type III. [Pg.454]

The most definitive laboratory test to distinguish type 1 from type 2 diabetes is the C-peptide assay, which is a measure of endogenous insulin production. With type 2 diabetes, proinsulin can be split into insulin and C-peptide lack of C-peptide indicates type 1 diabetes. The presence of anti-islet antibodies (to glutamic acid decarboxylase, insulinoma associated peptide-2 or insulin) or absence of insulin resistance (determined by a glucose tolerance test) is also suggestive of type 1. [Pg.48]

Fig. 9. Aspartate aminotransferase immunoreactivity in glutamic acid decarboxylase (GAD)-immunoreactive neuronal processes in the cerebral cortex. sAAT but not mAAT is colocalized with GAD in fine, probably axonal processes (arrows). Rat sections were double-immunostained by incubation with a mixture of anti-sAAT or mAAT rabbit serum and anti-GAD sheep serum, then with biotinylated anti-rabbit IgG donkey antibody, and finally with Texas Red-conjugated avidin and fluorescein-labeled anti-sheep IgG donkey antibody. The photographs in each row were taken at the same site under different excitations. Asterisks in (a) and (o ) indicate the unlabeled cell body of a pyramidal neuron. Fig. 9. Aspartate aminotransferase immunoreactivity in glutamic acid decarboxylase (GAD)-immunoreactive neuronal processes in the cerebral cortex. sAAT but not mAAT is colocalized with GAD in fine, probably axonal processes (arrows). Rat sections were double-immunostained by incubation with a mixture of anti-sAAT or mAAT rabbit serum and anti-GAD sheep serum, then with biotinylated anti-rabbit IgG donkey antibody, and finally with Texas Red-conjugated avidin and fluorescein-labeled anti-sheep IgG donkey antibody. The photographs in each row were taken at the same site under different excitations. Asterisks in (a) and (o ) indicate the unlabeled cell body of a pyramidal neuron.
As mentioned, GABA is an important neural transmitter and deficiencies in GABA are associated with diseases that exhibit neuromuscular dysfunction such as epilepsy, Huntington s disease and Parkinson s disease. S-Aminopentanoic acid (S-aminovaleric acid, DAVA) is also a neurotransmitter and used for treatment of neuromuscular disease. In at least one study, 3-alkyl-4-aminobutanoic acid derivatives were shown to be in vitro activators of f glutamic acid decarboxylase and they showed anti-convulsant activity. ... [Pg.190]


See other pages where Anti-glutamic acid decarboxylase is mentioned: [Pg.270]    [Pg.95]    [Pg.247]    [Pg.247]    [Pg.63]    [Pg.270]    [Pg.95]    [Pg.247]    [Pg.247]    [Pg.63]    [Pg.856]    [Pg.512]    [Pg.17]    [Pg.16]    [Pg.180]    [Pg.258]   
See also in sourсe #XX -- [ Pg.247 ]

See also in sourсe #XX -- [ Pg.247 ]

See also in sourсe #XX -- [ Pg.247 ]




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