Administration of low doses of tumor necrosis factor-alpha protects rat liver from ischaemic damage and reperfusion injury.

Liver ischaemia and reperfusion (IR) injury is a significant clinical problem. The aim of our study was to investigate the protective effect of tumor necrosis factor-alpha (TNF-alpha) on rat liver ischaemia-reperfusion injury. A TNF-alpha dose of 3 microg/kg body weight was injected into rats that had undergone partial (70%) ischaemia and reperfusion. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), total blood antioxidant level (using the FRAP test), and the concentrations of TNF-alpha, myeloperoxidase (MPO) and malondialdehyde (MDA) in liver homogenates after 1, 6, and 72 hours of reperfusion were measured. It was demonstrated that, rats subjected to IR, the administration of small doses of TNF-alpha significantly reduced ALT and AST activities after 60- minute liver ischaemia and 1 or 6 hour of reperfusion. The strongest reductions in ALT and AST activities were seen after 1 hour of reperfusion (30% and 35%, respectively). Exogenous TNF-alpha reduced the release of this cytokine in all observed periods, with the greatest reduction observed after 1 hour of reperfusion. Decreases in MPO concentration (by 40-45% in all periods of observation), as a marker of hepatic neutrophil infiltration, and in MDA concentration, the end-product of lipid peroxidation (by 55-60% at all time points), accompanied the reduction of TNF-alpha release. The administration of TNF-alpha to the rats after IR did not alter total plasma antioxidant potential, as assayed by the FRAP test, after 1 hour of reperfusion; however, at the later times a marked increase (approximately 40-50%) occurred. We demonstrated that intraperitoneal injections of small doses of TNF-alpha protect rat livers from IR injury. The mechanism of this protection is related to reductions in the release of TNF-alpha during IR after injection of this cytokine, resulting in reductions in oxidative stress and inflammation during the later phase of reperfusion.

[Neurological picture and selected diagnostic indices of vitamin b12 malabsorption syndrome]. / Obraz neurologiczny oraz niektóre wskazniki diagnostyczne w zespole uposledzonego wchlaniania witaminy B12.

Funicular myelosis is considered to be the main neurological syndrome in vitamin B12 deficiency. However, many authors tend to think that sensory neuropathy is the most common neurological manifestation of vitamin B12 deficiency. The aim of this paper was to assess neurological condition of patients with vitamin B12 malabsorption. The absorption of vitamin B-12 was assessed by Schilling's test. Patients with abnormal results of this test underwent neurological and medical examinations as well as series of accessory investigations. 16 cases of deficient vitamin B12 absorption accompanied by neurological symptoms were presented. The results of the investigation showed that the most common clinical manifestation of vitamin B12 deficiency was sensory neuropathy. In over 93% of described cases pathologic changes in gastric mucous membrane were found.

[Chronic hepatic encephalopathy--clinical features and diagnosis]. / Przewlekla encefalopatia watrobowa--objawy i rozpoznanie.

Neuropsychiatric abnormalities affecting patients with chronic liver disease are termed chronic hepatic encephalopathy. The spectrum of hepatic encephalopathy varies from mild intellectual impairment to deep coma. The diagnosis is based on clinical findings, and psychometric and electroencephalographic testing.

[Ischaemic heart disease and chronic helicobacter pylori infection--present views]. / Choroba niedokrwienna serca a przewlekle zakazenie Helicobacter pylori--aktualne poglady.

In connexion with the high prevalence of coronary heart disease its additional reasons are searched, which could lead to the occurrence and development of the disease. Chronic infections have been lately recognized as an additional reason. In the article we presented opinions regarding the influence of long-lasting Helicobacter pylori infection on the development of inflammation process, atheromatous changes, initiation and development of ischaemic heart disease.

Influence of chronic cadmium exposure during pregnancy on DNA synthesis in different organs of rat offspring.

Though partly bound by placental metallothionein, cadmium easily enters fetal circulation and exerts toxic effects in offspring tissues and organs. The synthesis of DNA in different organs of rat offspring, whose dams were exposed to cadmium during pregnancy was examined in this study. Scintillation technique was applied for quantification of tritiated thymidine incorporation. In most studied organs a significant increase of DNA synthesis was noted, pronounced especially in small intestine and bone marrow (over 2-fold increase in comparison with controls). In view of known carcinogenic effects of cadmium in animals, our data suggest alteration of cell cycle in selected organs, which may correspond to increase of proliferation rate typical of neoplastic conditions. Further studies are necessary for correlating these findings with proliferation indices and expression of protooncogenes in situ.

Brain protein synthesis in rats with portacaval shunts.

Effects of portacaval shunts on the brain protein synthesis were studied in rats 7, 10 and 13 weeks after the surgery. We evaluated the incorporation of [3H]-glycine with the usage of liquid scintillation. In comparison to the controls, the labelled amino acid was incorporated less effectively in all the examined brain regions throughout the experimental period. The lowest values were observed 10 weeks after the portacaval shunt and the drop was most distinct in the cerebellum (47%). The least profound changes occurred within 7 weeks after the surgery and the results were statistically significant only in the frontal cortex and the brain stem. Thirteen weeks after the shunting the incorporation of [3H]-glycine was moderately decreased (the drop ranged between 12% and 18%) but all the differences were statistically significant. It seems that the inhibition of the brain protein synthesis may contribute to the pathogenesis of the portal-systemic encephalopathy.

[Effect of sulfuric acid vapors on the respiratory system]. / Wplyw par kwasu siarkowego na uklad oddechowy.

The influence of a mixture of sulphuric acid vapour and SO2 mist upon the respiratory tract of animals was investigated during on exposure lasting 8 and 12 hours. Marked inflammatory changes in the upper respiratory tract, bronchioli and lung parenchyma were found. These changes were manifested by inflammatory infiltrations and abundant production of mucous in the bronchial tree. A significant increase in the number of dust cells in the lumen of bronchioli was also observed. A decrease of mitotic index was found in the epithelium of oral cavity after inhalator intoxication with sulphuric acid. This may lead to disturbances in the repair of epithelium. The authors emphasize the intensity of changes in proportion to H2SO4 dosage.