1,721,548 research outputs found

    From iron accumulation to organ damage

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    Iron is an important metal in the complex biochemistry in human beings. However there are primary or secondary diseases that lead to an accumulation of iron in parenchymal organs and induce progressive and serious systemic harm. This review aims to define the fundamental steps of cell biology and physiology of iron and the pathophysiological mechanisms responsible for its accumulation in the parenchyma. In addition, we analyze the main primitive (hemochromatosis) and secondary (inflammation, liver diseases and hematological) diseases, responsible for the damage caused by iron, and we analyze the clinical consequences of iron overload. Furthermore, we pass under review a particular classification of general mechanisms and kinetics of iron overload responsible for its clinical phenotypes, dividing them into systemic, cellular and subcellular overload mechanisms. Finally we describe the main pathologic stages resulting from iron overload, with particular reference to liver damage and progression to hepatocellular carcinoma

    Effect of arginine thiazolidinecarboxylate (ATCA)* * SULFILE is the trade name for arginine thiazolidinecarboxylate (200 mg vials) manufactured by Poli-Industria Chimica, Italy. on some clinical and functional parameters in cirrhotic patients

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    Forty patients with chronic active hepatopathy- or hepatic cirrhosis were randomly treated with arginine thiazolidinecarboxlyate (ATCA) or placebo, administered by intravenous infusion through phleboclysis. Tests for revealing the effects of the drug on liver function or liver damage were carried out. Comparison of the values of transaminases, alkaline phosphatase, total bilirubinaemia and aromatic amino acids at the end of treatment, showed significantly lower levels in the ATCA-treated patients than the placebo group. No local or general intolerance reactions, ascribable to the ATCA were observed. © 1981

    Apoptosis and gastrointestinal tract.

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    The gastrointestinal tract is characterized by a rapid proliferation of stem cells that differentiate to become terminal mature cells and ultimately die through a genetically programmed form of cell death, termed apoptosis, which is responsible for maintaining of tissue size. Apoptosis has also been shown to play an important role in the pathophysiology of several gastrointestinal diseases. The development of many infectious and immune-mediated diseases, such as gastritis, coeliac disease, inflammatory bowel diseases, may be triggered by the prevalence of pro-apoptotic signals, whereas prolonged cell survival, due to apoptosis inhibition, may give rise to neoplastic clones. Elucidation of the biochemical pathways and of specific proteins regulating apoptosis may provide a remarkable opportunity to manipulate the life and death decisions of the gastrointestinal cells and to develop new therapeutic strategies. This review will deal with the mechanisms potentially involved in apoptosis and with the clinical relevance of this phenomenon in gastrointestinal diseases

    Celiac disease associated with autoimmune myocarditis.

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    BACKGROUND: Both celiac disease (CD) and myocarditis can be associated with systemic autoimmune disorders; however, the coexistence of the 2 entities has never been investigated, although its identification may have a clinical impact. METHODS AND RESULTS: We screened the serum of 187 consecutive patients with myocarditis (118 males and 69 females, mean age 41.7+/-14.3 years) for the presence of cardiac autoantibodies, anti-tissue transglutaminase (IgA-tTG), and anti-endomysial antibodies (AEAs). IgA-tTG-positive and AEA-positive patients underwent duodenal endoscopy and biopsy and HLA analysis. Thirteen of the 187 patients were positive for IgA-tTG, and 9 (4.4%) of them were positive for AEA. These 9 patients had iron-deficient anemia and exhibited duodenal endoscopic and histological evidence of CD. CD was observed in 1 (0.3%) of 306 normal controls (P<0.003). In CD patients, myocarditis was associated with heart failure in 5 patients and with ventricular arrhythmias (Lown class III-IVa) in 4 patients. From histological examination, a lymphocytic infiltrate was determined to be present in 8 patients, and giant cell myocarditis was found in 1 patient; circulating cardiac autoantibodies were positive and myocardial viral genomes were negative in all patients. HLA of the patients with CD and myocarditis was DQ2-DR3 in 8 patients and DQ2-DR5(11)/DR7 in 1 patient. The 5 patients with myocarditis and heart failure received immunosuppression and a gluten-free diet, which elicited recovery of cardiac volumes and function. The 4 patients with arrhythmia, after being put on a gluten-free diet alone, showed improvement in the arrhythmia (Lown class I). CONCLUSIONS: A common autoimmune process toward antigenic components of the myocardium and small bowel can be found in >4% of the patients with myocarditis. In these patients, immunosuppression and a gluten-free diet can be effective therapeutic options

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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