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Biomedical subjects

J Faller

Publications and source records attributed to J Faller.

At least 55 records · Page 3Linked to original sources

Echinococcus alveolaris treated by right trisegmentectomy.

A case of Echinococcus alveolaris of the liver treated by right trisegmentectomy is reported. The imaging procedures (sonography, CT, angiography) ensuring preoperative diagnosis were of help in performing of resections and they can also be used in the postoperative follow-up.

Echinococcosis, Hepatic↗

[Appendicitis in a personal 10-year patient sample].

862 patients underwent appendectomy for suspected acute appendicitis at the 3rd Surgical Department of the Semmelweis University, Budapest during the period from 1976-1985. In 111 cases neither the histologic examination nor the macroscopic finding at operation confirmed the inflammation. We considered these cases as "chronic appendicitis". The postoperative mortality rate was 0.8%. Surgical complications arose in altogether 10 patients. In the remaining 751 patients the mortality rate was 0.5% with 20 complications. The incidence of surgical complications was not significantly decreased in cases with "acute appendicitis" therefore we do not emphasize prophylactic appendectomy.

Appendectomy↗

Hyperuricemia in glycogen storage disease type I. Contributions by hypoglycemia and hyperglucagonemia to increased urate production.

Studies were performed to determine whether hypoglycemia or the glucagon response to hypoglycemia increases uric acid production in glycogen storage disease type I (glucose-6-phosphatase deficiency). Three adults with this disease had hyperuricemia (serum urate, 11.3-12.4 mg/dl) and reduced renal clearance of urate (renal urate clearance, 1.1-3.1 ml/min). These abnormalities were improved in one patient by intravenous glucose infusion for 1 mo, suggesting a role for hypoglycemia and its attendant effects on urate metabolism and excretion. A pharmacologic dose of glucagon caused a rise in serum urate from 11.4 to 13.0 mg/dl, a ninefold increase in urinary excretion of oxypurines, a 65% increase in urinary radioactivity derived from radioactively labeled adenine nucleotides, and a 90% increase in urinary uric acid excretion. These changes indicate that intravenous glucagon increases ATP breakdown to its degradation products and thereby stimulates uric acid production. To observe whether physiologic changes in serum glucagon modulate ATP degradation, uric acid production was compared during saline and somatostatin infusions. Serum urate, urinary oxypurine, radioactivity, and uric acid excretion increased during saline infusion as patients became hypoglycemic. Infusion of somatostatin suppressed these increases despite hypoglycemia and decreased the elevated plasma glucagon levels from a mean of 81.3 to 52.2 pg/ml. These data suggest that hypoglycemia can stimulate uric acid synthesis in glucose-6-phosphatase deficiency. Glucagon contributes to this response by activating ATP degradation to uric acid.

Adenosine Triphosphate↗

Ethanol induced alterations of uric acid metabolism.

Our observations have shown that chronic oral ethanol administration was associated with increased serum urate, urine uric acid excretion, urine uric acid clearance and oxypurine excretion. The daily rate of uric acid turnover was significantly increased. Intravenous ethanol administration was associated with increased uric acid excretion, increased uric acid clearance and significantly increased oxypurine excretion. Excretion of radioactivity derived from intravenously administered adenine increased significantly. We conclude that hyperuricemia related to ethanol consumption at lower blood ethanol levels (less than 150 mg/dl) results from increased production of uric acid probably secondary to accelerated degradation of adenine nucleotides.

Alcohol Drinking↗

Altered cell cycle distributions of cultured human lymphoblasts during cytotoxicity related to adenosine deaminase inhibition.

Serial-flow cytometric analysis of DNA content of T lymphoblasts (MOLT-4) and B lymphoblasts (MGL-8) was performed to correlate the cytotoxic properties of adenosine deaminase inhibition with alterations of DNA synthesis and disruptions of the cell cycle. The addition of deoxyadenosine up to 50 mumol/L potently decreased the growth of T lymphoblasts, and these changes were enhanced with the addition of 100 mumol/L homocysteine thiolactone. These conditions caused a virtual absence of cells from S and G2M phases after 24 hours. The DNA distribution was similar in cells cultured for 24 hours in 50 mumol/L deoxyguanosine or 2.5 mumol/L hydroxyurea. These observations suggested accumulation of cells in the G1 phase. T lymphoblasts cultured with up to 50 mumol/L adenosine had a substantial decrease in growth, which was not modified by the addition of homocysteine thiolactone. Cell cycle distributions of T lymphoblasts cultured for 24 to 48 hours under these conditions showed mild decreases in the G2M population. The addition of adenosine up to 50 mumol/L decreased the growth of B lymphoblasts, and these changes were enhanced by the addition of 100 mumol/L homocysteine thiolactone. These conditions induced mild decreases in the S-phase population in B lymphoblasts. The addition of deoxyadenosine, even with homocysteine thiolactone, did not modify growth in B lymphoblasts and the cell-cycle distributions were indistinguishable from distributions of control populations after 24 and 48 hours. The observations provide independent support for a reduction of DNA synthesis associated with cytotoxicity during adenosine-deaminase inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Deaminase Inhibitors↗

Ethanol-induced hyperuricemia: evidence for increased urate production by activation of adenine nucleotide turnover.

Consumption of alcoholic beverages is associated with hyperuricemia and gout. To determine the contributions to this process of increased production and decreased excretion of uric acid, we gave oral ethanol (1.8 g per kilogram of body weight every 24 hours) for eight days or intravenous ethanol (0.25 to 0.35 g per kilogram per hour) for two hours to six patients with gout. During the long-term oral study we observed the following: serum urate levels increased from 8.4 +/- 0.4 (mean +/- S.E.) to 10.1 +/- 0.9 mg per deciliter; whole blood lactate reached a peak of 3.1 +/- 0.7 mM from a base line of 1.3 +/- 0.3 mM; and urinary oxypurines increased to 641 +/- 397 per cent of the base-line value. Urate clearance increased to 145 +/- 25 per cent of the base-line value. Daily uric acid turnover increased from 1010 mg per deciliter to 170 +/- 17 per cent of the base-line value. During short-term intravenous ethanol administration, serum urate levels, urate clearance, and urinary uric acid excretion were not substantially altered from the base-line period. Urinary oxypurine levels increased to 341 to 415 per cent of base-line values. Urinary radioactivity, originating from the adenine nucleotide pool labeled by [8-(14)C]adenine, increased to 127 to 149 per cent of base-line values. These data indicate that ethanol increases urate synthesis by enhancing the turnover of adenine nucleotides.

Adenine Nucleotides↗

Ultrastructure of the liver after 24-hour preservation with various solutions.

The effect of 24-hour preservation with 5% dextrane solution, Collins C3 solution and 5% human albumin solution, as well as of pretreatment with phenoxybenzamine on the ultrastructure of the rat liver has been studied. It was found that 1. the moment of the irreversible damage of the liver cannot be assessed from the electron microscopic picture; 2. though the ultrastructure offers no clue to the exact length of the effectiveness of a preservation procedure, the different methods can be compared among each other; 3. of the investigated solutions the 5% solution of human albumin appeared to be the most favourable, as with this solution the ultrastructural changes appeared late and in the least pronounced form; 4. phenoxybenzamine pretreatment might be of importance in warm ischaemia as it seems to delay the consequences.

Albumins↗

Enzyme histochemical studies of the preserved rat liver.

The effect of depersolone, of the oxygenation of the perfusing solution and of phenoxybenzamine pretreatment has been studied in the isolated rat liver intermittently perfused with a solution containing low molecular weight dextran at 4 degrees C. The use in liver preservation of Collins' C3-solution and of a special albumin-containing solution was tested. The behaviour of acid and alkaline phosphatase, esterase, lactate dehydrogenase and adenosine triphosphatase in the preserved liver was followed by means of histochemical methods allowing semi-quantitative evaluation. Pretreatment with phenoxybenzamine and perfusion by an albumin-containing solution reduced the lesion of the liver, while prednisolone and oxygenation of the perfusion solution improved preserving effect only moderately.

Acid Phosphatase↗