glutamic acid decarboxylase/martwica

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Tumor necrosis factor microsatellite polymorphism influences the development of insulin dependency in adult-onset diabetes patients with the DRB11502-DQB10601 allele and anti-glutamic acid decarboxylase antibodies.

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Recently, several studies have demonstrated that tumor necrosis factor microsatellite polymorphism (TNFalpha) contributes to the susceptibility of type 1 diabetes. This study investigates the influence of TNFalpha on the predisposition to insulin dependency in adult-onset diabetic patients with type

CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer.

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Glutamic acid decarboxylase (GAD)65 is an early and important antigen in both human diabetes mellitus and the nonobese diabetic (NOD) mouse. However, the exact role of GAD65-specific T cells in diabetes pathogenesis is unclear. T cell responses to GAD65 occur early in diabetes pathogenesis, yet only

Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients.

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Several studies correlated genetic background and pancreatic islet-cell autoantibody status (type and number) in type 1A diabetes mellitus (T1AD), but there are no data evaluating the relationship among these markers with serum cytokines, regulatory T cells and β cell function. This characterization

Social behavior, neuroimmune markers and glutamic acid decarboxylase levels in a rat model of valproic acid-induced autism.

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Autism is a complex neurodevelopmental disorder characterized by impaired social communication and social interactions, and repetitive behaviors. The etiology of autism remains unknown and its molecular basis is not yet well understood. Pregnant Sprague-Dawley (SD) rats were administered 600 mg/kg

Acute inhibition of signalling phenotype of spinal GABAergic neurons by tumour necrosis factor-alpha.

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Spinal application of TNFα induces both allodynia and hyperalgesia, and at least part of the pronociceptive effects of TNFα have been suggested as due to the impaired function of spinal inhibitory neurons (disinhibition). The present study explores the effects of TNFα on the signalling phenotype of

Type I insulin-dependent diabetes mellitus: a model for autoimmune polygenic disorders.

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Insulin-dependent diabetes mellitus (IDD) affects between one in 250 and one in 500 Americans. The inheritance of IDD is non-Mendelian and polygenic. Genetic susceptibility predominantly results from specific alleles in the HLA complex and insulin gene region. Autoimmune destruction of pancreatic

[Endocrinology 1998-1999].

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In the cascade hormone--second messenger--cellular G-proteins (GTP binding proteins), impairment can occur also at the last step: Mutant G-proteins may amplify the response (e.g. hypophyseal and thyroid adenomas) or reduce it (pseudohypoparathyreosis, testitoxicosis). Other new group of diseases

A case of polyglandular autoimmune syndrome type III complicated with autoimmune hepatitis.

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A 58-year-old woman complaining of finger tremor was referred to our hospital. The diagnosis of Graves' disease was made based on increased free triiodothyronine (18.88 pg/ml) and free thyroxine (7.47 ng/dl), low TSH (<0.005 microIU/ml) and increased TSH receptor binding antibody activity (70.9%).

Comparative and correlative assessments of cytokine, complement and antibody patterns in paediatric type 1 diabetes.

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One of the most widespread and effective environmental factors is the infection with enteroviruses (EVs) which accelerate β cell destruction in type 1 diabetes (T1D). This study represented a comparison between diabetic EV+ and EV- children as well as correlation analysis between autoantibodies, T1D

Mapping genes located on human chromosomes 2 and 12 to porcine chromosomes 15 and 5.

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Informative microsatellites associated with two genes on HSA12 (lysozyme, LYZ; tumour necrosis factor receptor, TNFR) and one gene on HSA2 (glutamic acid decarboxylase 1, GAD1) were mapped in the US Meat Animal Research Center (MARC) swine reference population and the physical assignment of

High T-helper-1 cytokines but low T-helper-3 cytokines, inflammatory cytokines and chemokines in children with high risk of developing type 1 diabetes.

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BACKGROUND Type 1 diabetes (T1D) is suggested to be of T-helper (Th)1-like origin. However, recent reports indicate a diminished interferon (IFN)-gamma secretion at the onset of the disease. We hypothesize that there is a discrepancy in subsets of Th-cells between children with a high risk of

Anti-inflammatory Approach With Early Double Cytokine Blockade (IL-1β and TNF-α) Is Safe and Facilitates Engraftment in Islet Allotransplantation.

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The approach to reducing nonspecific inflammation after islet allotransplantation has been designed to improve engraftment, typically using 1 agent. We report results with the use of combination inflammatory blockade consisting of anti-interleukin (IL)-1β and tumor necrosis factor

[Effect of mechanical stretch preconditioning on pathological stretch-induced activation of γ-aminobutyric acid signaling pathway in human type II alveolar epithelial cells].

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To evaluate the effect of mechanical stretch preconditioning on pathological stretch-induced activation of γ-aminobutyric acid (GABA) signaling pathway in human type II alveolar epithelial cells (AEC II). AEC II cell line (A549 cells) cultured in vitro were divided into control group (group C),

Accumulation of GABAergic neurons, causing a focal ambient GABA gradient, and downregulation of KCC2 are induced during microgyrus formation in a mouse model of polymicrogyria.

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Although focal cortical malformations are considered neuronal migration disorders, their formation mechanisms remain unknown. We addressed how the γ-aminobutyric acid (GABA)ergic system affects the GABAergic and glutamatergic neuronal migration underlying such malformations. A focal freeze-lesion

Switch from a dominant Th1-associated immune profile during the pre-diabetic phase in favour of a temporary increase of a Th3-associated and inflammatory immune profile at the onset of type 1 diabetes.

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BACKGROUND Type 1 diabetes (T1D) is an autoimmune disease dominated by loss of self-tolerance resulting in depletion of the beta-cells. This study aims to confirm previous observations of a dominant T-helper (Th)1-like profile during the period close to onset of disease. Further, to follow the

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glutamic acid decarboxylase/martwica

Tumor necrosis factor microsatellite polymorphism influences the development of insulin dependency in adult-onset diabetes patients with the DRB1*1502-DQB1*0601 allele and anti-glutamic acid decarboxylase antibodies.

CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer.

Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients.

Social behavior, neuroimmune markers and glutamic acid decarboxylase levels in a rat model of valproic acid-induced autism.

Acute inhibition of signalling phenotype of spinal GABAergic neurons by tumour necrosis factor-alpha.

Type I insulin-dependent diabetes mellitus: a model for autoimmune polygenic disorders.

[Endocrinology 1998-1999].

A case of polyglandular autoimmune syndrome type III complicated with autoimmune hepatitis.

Comparative and correlative assessments of cytokine, complement and antibody patterns in paediatric type 1 diabetes.

Mapping genes located on human chromosomes 2 and 12 to porcine chromosomes 15 and 5.

High T-helper-1 cytokines but low T-helper-3 cytokines, inflammatory cytokines and chemokines in children with high risk of developing type 1 diabetes.

Anti-inflammatory Approach With Early Double Cytokine Blockade (IL-1β and TNF-α) Is Safe and Facilitates Engraftment in Islet Allotransplantation.

[Effect of mechanical stretch preconditioning on pathological stretch-induced activation of γ-aminobutyric acid signaling pathway in human type II alveolar epithelial cells].

Accumulation of GABAergic neurons, causing a focal ambient GABA gradient, and downregulation of KCC2 are induced during microgyrus formation in a mouse model of polymicrogyria.

Switch from a dominant Th1-associated immune profile during the pre-diabetic phase in favour of a temporary increase of a Th3-associated and inflammatory immune profile at the onset of type 1 diabetes.

Najbardziej kompletna baza danych ziół leczniczych poparta naukowo

Tumor necrosis factor microsatellite polymorphism influences the development of insulin dependency in adult-onset diabetes patients with the DRB11502-DQB10601 allele and anti-glutamic acid decarboxylase antibodies.