gluten/necrosis

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Epstein-Barr virus in primary gastrointestinal T cell lymphomas. Association with gluten-sensitive enteropathy, pathological features, and immunophenotype.

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Forty-three primary gastrointestinal T cell lymphomas were investigated for the presence of Epstein-Barr virus (EBV) by polymerase chain reaction, RNA in situ hybridization, and immunohistochemistry. In addition, the association between EBV and clinicopathological characteristics of these lymphomas

Serum soluble interleukin-2 receptor, interleukin-6, and tumor necrosis factor-alpha levels in children with celiac disease: response to treatment.

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OBJECTIVE T-cell mediated immune response to dietary gluten and cytokines release are important for the enteropathy seen in celiac disease. We investigated the serum levels of soluble interleukin-2 receptor, interleukin-6, and tumor necrosis factor-alpha in celiac children before and after gluten

[Bone mineral density in patients with gluten-sensitivity celiac disease].

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OBJECTIVE to determine the frequency of development of osteopenia/ostoporosis (OP) vitamin D deficiency, some population risk factors, and the effects of alpha-calcidol and calcitriol on bone mineral density (BMD) in patients with gluten-sensitivity celiac disease (GSCD). METHODS Densitometry of the

Altered osteoprotegerin/RANKL ratio and low bone mineral density in celiac patients on long-term treatment with gluten-free diet.

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Skeletal demineralization and mineral metabolism derangement are well-recognized features of untreated celiac disease (CD). Although treatment with a gluten-free diet appears to prevent bone loss while correcting skeletal demineralization in childhood, there is evidence that bone mineral density

Wheat gluten intake increases weight gain and adiposity associated with reduced thermogenesis and energy expenditure in an animal model of obesity.

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OBJECTIVE The association between gluten and body weight is inconsistent. Previously, we showed that a gluten-free diet reduces weight gain without changing food intake in mice fed high-fat diets. In the present study, we investigated the effects of gluten intake on fat metabolism, thermogenesis and

Effects of dietary gluten on the hepatotoxic action of galactosamine and/or endotoxin in rats.

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This study was done to clarify the effects of dietary wheat gluten on the hepatotoxic action of D-galactosamine (GalN) and endotoxin (Etx). Male Wistar rats fed a high casein or high gluten (supplemented with L-Lys and L-Thr) diet were injected with GalN or Etx, and the plasma glutamate oxaloacetate

Morphological and morphometric assessment of human duodenal biopsies maintained in organ culture. In vitro influences of gluten in coeliac disease.

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Duodenal biopsy specimens from 51 coeliac patients (children and young adults) and 13 non-coeliac controls were maintained in organ culture for 24 h. Morphometric determinants were compared after culture in the presence of different gluten fractions, after culture on gluten-free medium, and in

Gluten-free diet increases beta-cell volume and improves glucose tolerance in an animal model of type 2 diabetes.

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Gluten-free (GF) diet alleviates type 1 diabetes in animal models and possibly in humans. We recently showed that fatty acid-induced insulin secretion is enhanced by enzymatically digested gluten (gliadin) stimulation in INS-1E insulinoma cells. We therefore hypothesized that GF diet would induce

Gluten-induced nitric oxide and pro-inflammatory cytokine release by cultured coeliac small intestinal biopsies.

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OBJECTIVE To determine whether there was increased nitric oxide (NO) production from coeliac small intestinal biopsies cultured in vitro with gluten and whether the inhibition of NO production could prevent gluten-induced enterotoxicity. The relationship between NO production with the

The effects of reduced gluten barley diet on humoral and cell-mediated systemic immune responses of gluten-sensitive rhesus macaques.

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Celiac disease (CD) affects approximately 1% of the general population while an estimated additional 6% suffers from a recently characterized, rapidly emerging, similar disease, referred to as non-celiac gluten sensitivity (NCGS). The only effective treatment of CD and NCGS requires removal of

The role of soluble tumor necrosis factor like weak inducer of apoptosis and interleukin-17A in the etiopathogenesis of celiac disease: A cross-sectional study.

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Our aim in this study was to determine soluble tumor necrosis factor (TNF)-like weak inducer of apoptosis (sTWEAK) and interleukin-17A (IL-17A) levels in celiac disease, and their association with the gluten diet and autoantibodies. Eighty patients with celiac diagnosis and 80 healthy control

Elevated B cell-activating factor of the tumour necrosis factor family in coeliac disease.

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OBJECTIVE The B cell-activating factor of the tumour necrosis factor (TNF) family (BAFF) was recently described as a critical survival factor for B cells, and its expression is increased in several autoimmune diseases. Abnormal production of BAFF disturbs immune tolerance allowing the survival of

Gluten specific, HLA-DQ restricted T cells from coeliac mucosa produce cytokines with Th1 or Th0 profile dominated by interferon gamma.

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Coeliac disease is precipitated in susceptible subjects by ingestion of wheat gluten or gluten related prolamins from some other cereals. The disease is strongly associated with certain HLA-DQ heterodimers, for example, DQ2 (DQ alpha 1*0501, beta 1*0201) in most patients and apparently DQ8 (DQ alpha

Changes and relationships of IGFS and IGFBPS and cytokines in coeliac disease at diagnosis and on gluten-free diet.

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OBJECTIVE To evaluate changes and relationships of IGFs and IGFBPs, serum interleukin 6 (IL-6) and tumour necrosis factor (TNF)-alpha, and auxological parameters at diagnosis of coeliac disease (CD) and at 6 months and 12 months after starting a gluten-free diet (GFD), compared with a control

Combination of Gluten-Digesting Enzymes Improved Symptoms of Non-Celiac Gluten Sensitivity: A Randomized Single-blind, Placebo-controlled Crossover Study.

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BACKGROUND Recently, the population of individuals with non-celiac gluten sensitivity (NCGS) who do not have celiac disease but show improved symptoms with a gluten-free diet, has increased. Enzyme replacement therapy using digestive enzymes is expected to improve the symptoms of NCGS and be

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