[Tissue hypoxia due to stored blood].
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Biomedical subjects
Publications and source records attributed to R Ricci.
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A correlation between cimetidine and gastric cancer has been suggested. Nitrosation of cimetidine in the presence of nitrite and HCl and mutagenic activity as well as DNA damage in mammalian cells displayed by nitrosocimetidine, as these phenomena occur in vitro, were the supporting hypothesis. Previous studies have shown that liver DNA damage was a well correlated index of potential carcinogenic activity of N-nitroso compounds and that such a damage was found after long-term simultaneous oral administration of aminopyrine and nitrite in rats. In this work, liver DNA fragmentation was investigated by three different techniques: DNA alkaline elution, DNA alkaline denaturation followed by hydroxylapatite chromatography and a new viscometric method markedly more sensitive than the above mentioned ones in detecting DNA damage. Evidence of DNA damage was not gained in any of the groups of rats treated with high single or successive oral daily doses of cimetidine (250 mg/kg) along with nitrite (80 mg/kg) in approximately equimolar amounts. Cimetidine and nitrite given alone were also ineffective. The lowering of gastric pH, obtained with fasting and histamine administration before giving cimetidine and nitrite combination in a single dose, did not favor the induction of liver DNA fragmentation neither in the above condition nor even when the amount of cimetidine was lowered to 125 mg/kg in order to obtain an approximately 2-fold molar amount of nitrite.
In thirty-one patients (pts) with atrioventricular or intraventricular conduction disturbances, the Ajmaline test was used to evaluate the risk of evolution to complete atrioventricular block. Three groups of patients were identified: A = nine patients without history of syncope or dizziness; B = seventeen pts with history of syncope or dizziness but without evidence of complete atrioventricular block; C = five pts with recorded atrioventricular block and history of syncope or dizziness. All patients with symptoms (B-C groups) and with a positive Ajmaline test (i.e. HV greater than or equal to 90 msec.) were paced with regression of symptoms. All patients without symptoms (A group) and with a positive Ajmaline test (i.e. HV greater than or equal to 90 msec.) were not paced and did not progress to complete atrioventricular block in a follow-up period of two years. Our results confirm that the Ajmaline test is useful in demonstrating the cardiac origin of syncopal episodes, but an HV value of 90 msec, does not seem to be specific enough in identifying asymptomatic patients at risk of developing complete atrioventricular block.
The disaccharide 2-acetamido-2-deoxy-beta-D-glucopyranosyl-(1 goes to 3)-D-[1-3H]-galactitol, prepared from keratan sulfate, was rapidly hydrolyzed by the A and B isoenzymes of normal human liver hexosaminidase (EC 3.2.1.30), and by the B isoenzyme prepared from the liver of a patient who had died of Tay-Sachs disease. The disaccharide substrate was also hydrolyzed by extracts of normal, cultured-skin fibroblasts, and fibroblasts of patients with Tay-Sachs disease, whereas it was not hydrolyzed by fibroblast extracts of patients with Sandhoff disease. Thus, effective degradation of keratan sulfate, secondary to a defect of the beta subunits present in the A and B isoenzymes of hexosaminidase, may contribute to the appearance of skeletal lesions in patients affected by Sandhoff disease.
Type II fucosidosis in an autosomal recessive disease. The paper presents a case of a patient with alpha-L-fucosidase of whom a skin specimen was examined under the electron microscope. Storage material was observed mainly in endothelial cells of blood capillaries and Schwann cells surrounding small peripheral nerves of papillary dermis. Within both cells two different kinds of inclusions were revealed: (1) clear vacuoles and (2) dense bodies with an internal structure prevalently lamellar. All these ultrastructural alterations were observed long before the appearance of clinically defined angiokeratoma at cutaneous level. Hence, they present the same alteration found in the absence of angiokeratoma in type I fucosidosis.
The locomotor function of polymorphonuclear cells (cellular chemotaxis) and serum chemotactic activity (humoral chemotaxis) were studied in 51 patients with Crohn's disease using a method of migration under agarose gel. To study cellular chemotaxis patient's polymorphonuclear cells were challenged against normal Zymosan activated serum and humoral chemotaxis was evaluated testing the patient's Zymosan activated serum against normal polymorphonuclear cells. Cellular chemotaxis in the Crohn's disease group was normal (although 30% of the 51 patients had migration values out of the normal range), while humoral chemotaxis was significantly lower in Crohn's disease patients than in the control group. However, the value of humoral chemotaxis in the group of Crohn's disease patients treated with steroids was lower than that of patients not treated, thus accounting for the low mean value observed inthe Crohn's disease-group as a whole. The present results suggest that a defective chemotactic response may occur in some Crohn's disease patients, particularly during steroid treatment. These findings might be related either to a defective generation of complement derived chemotactic factors or to the presence of circulating inhibitors.
Circulating immune complexes (AgAb) were studied in 183 serum samples from 119 patients with Crohn's Disease. AgAb were studied by the solid phase C1q binding test in all sera and also by the conglutinin binding assay in 161 sera. A significantly higher prevalence of circulating AgAb was observed in Crohn's disease patients in comparison with the control population. About one half of the sera were AgAb positive when the results of both tests were combined whereas AgAb were found in about one third of the sera by each individual method. Complexes revealed by the C1q-SP appeared to be related to the disease activity and to the occurrence of complications. Such a correlation was not observed as far as conglutinin results are concerned. Data emerging from the present investigation indicate that circulating AgAb may be present in Crohn's disease and suggest that the AgAb material is heterogeneous. They also suggest the possibility that AgAb represent a secondary phenomenon.
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