Publications by authors named "ATSMON A"

This article analyzes the impact of the COVID-19 pandemic on the clinical practice of Drama Therapy, considering how a forced shift to the online setting impacted drama therapy's concepts and practice. Anchored in a qualitative analysis of 20 interviews with well-established drama therapy practitioners from 19 different countries, we put forward the notion of four positions of reaction to the online setting: . Our discussion of the four positions aims to reflect a composite exploration of practitioners' experiences during various phases of their online work.

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In latent hepatic porphyria normal porphyrins are frequently excreted, but porphyrinuria accompanies many clinical conditions not associated with porphyria. Therefore, the diagnosis of latent porphyria cannot be made by examining for urinary porphyrins alone. We use 16 laboratory methods, some of which which we developed, including sensitive HPLC separation procedures, for determining relevant enzymes, and porphyrins and their precursors in urine, feces and blood.

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This study demonstrates an experimental model of the biochemical pattern of the 'latent phase' of hepatic porphyria subject to 'acute attack', upon application of prophyrinogenic stimuli. The 'latent phase' was achieved by administering 3,5-diethoxycarbonyl-1, 4-dihydrocollidine [DDC], 70 mg kg-1 day, orally to non-fasted rats. A two- and threefold increase in coproporphyrin in urine and protoporphyrin in faeces, respectively, were observed.

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This investigation shows that the regulation of heme synthesis in the regenerating rat liver does not differ from the regulation in the normal liver. The heme saturation of tryptophan pyrrolase was found to be low, indicating a reduced concentration of heme in the regulatory heme pool of the regenerating rat liver. As expected, ALAS in the mitochondrial fraction was found to be elevated.

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L-Alanine: 4,5-dioxovalerate transaminase (ADT) was determined in liver homogenates of rats treated by either inducers of porphyrin synthesis or the repressor, hemin. ADT activity was not induced by the porphyrinogenic agents nor reduced by hemin, indicating that ADT probably has no regulatory role in the heme synthesis pathway. The same conclusion was drawn from similar experiments performed in monolayers of chick embryo liver cells.

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Four hepatic porphyria patients were treated with colchicine for abdominal pains. Colchicine administration during prodromal abdominal symptoms prevented the development of these abdominal crises. When colchicine was given after initiation of the crisis the duration and magnitude of the abdominal pains decreased.

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Attacks of acute hepatic porphyria have been previously reported to be frequently associated with transient hypercholesterolemia. This investigation was undertaken in order to establish whether the hypocholesterolemic effect of simvastatin (MK-733) is associated with inhibition of porphyrin metabolism. In two experimental models of acute hepatic porphyria--monolayers of chick embryo liver cells induced by DDC, and diethoxycarbonyl dihydrocollidine (DDC) injected rats--simvastatin was shown to increase porphyrin formation.

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The metabolism of heme is impaired in lymphocytes of patients with malignant lymphoproliferative disorders (MLPO). Two of the enzymes of the heme biosynthetic pathway, delta-aminolevulinic acid dehydrase (ALAD) (EC 4.2.

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Porphobilinogen deaminase (PBGD), one of the enzymes in the pathway of heme synthesis, was found to be elevated in peripheral mononuclear cells of 60% of patients with epithelial tumors and metastatic spread, but only in 14% of patients with tumor and no evidence of metastases. The combination of both high lactic dehydrogenase and high PBGD afforded a sensitivity of 40%, but a specificity of 96% in diagnosing metastatic spread.

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PBGD activity and growth rate were determined in cultures of rat embryo fibroblasts, nontransformed and MLV/MS transformed fibroblastic cell lines; NIH-3T3 cells, and in a mouse lymphosarcoma cell line [L-929]. The two parameters examined correlate positively (P less than 0.001).

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Macronodular liver cirrhosis and hepatocellular carcinoma were found in a 61-year-old male who had been exposed for 35 years to Trinitrotoluene (TNT). The question whether TNT had induced these pathological processes is raised.

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Enzymes of heme synthesis, porphyrins and heme content of regenerating rat livers were examined. During the first three days of regeneration the weights of livers of one-third and two-third hepatectomized rats increased 1.5-fold and 2.

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Patients with malignant lymphoproliferative diseases, ie, chronic lymphocytic leukemia and lymphoma, were found to have higher porphobilinogen deaminase (PBGD) activity in their peripheral lymphocytes than normal control subjects, patients with other malignant neoplasms, and patients with various infectious diseases. The specificity and sensitivity of the test were 99% and 87%, respectively. The sensitivity of the test was 100% in patients with chronic lymphocytic leukemia and 82% in patients with lymphoma.

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The activity of lymphocyte uroporphyrinogen synthase (URO-S) was examined in 51 non-Hodgkin's lymphoma (NHL) patients at various follow-up periods. Mean +/- SD activity (pmol porphyrin/mg protein/hr) at diagnosis (n = 24), on relapse (n = 14) and during active disease (n = 14) were 31.7 +/- 19.

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Carbamazepine, a drug which is widely used in neurological diseases, has a porphyrogenic effect in chick embryo liver cells in culture. It increased the concentration of cellular porphyrins by 80-fold and delta-aminolevulinate synthase activity by 4-fold. The increase in the accumulation of porphyrins preceded that of ALAS activity.

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Treatment of monolayers of chick embryo hepatocytes with the calcium channel blocking drugs nifedipine and verapamil resulted in a decrease in the activity of uroporphyrinogen decarboxylase, an increase in the activity of delta-aminolaevulinate synthase and accumulation of porphyrins with uroporphyrin and heptacarboxylic porphyrin predominating. Diltiazem, another calcium channel blocking drug, did not affect uroporphyrinogen decarboxylase activity and had a slight effect only on the accumulation of porphyrins. Experiments with nifedipine and verapamil in the presence of various concentrations of calcium indicate that the porphyrogenic effect is apparently not related to blocking of calcium channels.

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This study was undertaken in a system of chick embryo liver cells incubated in Earle's Basal Salt Solution with hormones. Impairment of induction of delta-aminolevulinic acid synthase (ALAS) by allyl-isopropylacetamide (AIA) was observed in the presence of glucose. Fructose and various gluconeogenic substances including gluconeogenic amino acids had a similar effect.

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Colchicine at the concentrations of 5 X 10(-7) - 5 X 10(-6) M decreased significantly both delta-aminolevulinic acid synthase activity and accumulation of porphyrins in monolayers of chick embryo liver cells induced by allyl-isopropylacetamide, by 3,5-diethoxycarbonyl-1,4-dihydrocollidine or by phenobarbitone. No effect was noted in non-induced cells. In rats, colchicine 0.

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High doses of propranolol administered to rats during pregnancy and lactation cause inhibition of growth of the neonatal rats. Growth remains inhibited if drug treatment is continued after weaning. Cessation of drug administration after weaning leads to a nearly normal growth rate but a relatively long period elapses before normal weight is attained.

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Patients with active lymphoproliferative diseases (LPD) were shown to have high activity of lymphocyte uroporphyrinogen synthase (L-UROS), the enzyme which converts porphobilinogen to uroporphyrinogen. The mean L-UROS activity of 64 first-degree relatives of patients with LPD was significantly higher than that of a control group and 45% of these relatives had pathological values of L-UROS. L-UROS activity was also determined in the spouses of 2 patients and was pathologically elevated in both.

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The effect of various metals, porphyrins and metalloporphyrins on the activity of delta-aminolevulinate synthase (ALAS) was measured in monolayers of chick embryo liver cells in order to determine whether the metal moiety of heme or heme itself is the regulator of ALAS activity. Iron, magnesium, zinc, copper, manganese and nickel did not decrease ALAS activity in non-induced and in cells induced by allyl-isopropylacetamide (AIA). Cobalt decreased both non-induced and induced activity.

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It is known that fasting may provoke an acute attack in patients with latent hepatic porphyrias. We examined the influence of fasting on some aspects of heme synthesis in rats. Urinary excretion of both uroporphyrin and coproporphyrin, as well as fecal elimination of protoporphyrin and coproporphyrin, were increased on fasting.

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Patients with active lymphoproliferative diseases were shown to have high activity of erythrocyte uroporphyrinogen synthetase (URO-S), the enzyme which converts porphobilinogen to uroporphyrinogen. In a few patients examined the lymphocyte URO-S was markedly increased. No correlation was found between the high URO-S activity and the degree of anemia, reticulocytosis, or the presence of hemolysis.

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