PubMed Health⌕ Search

Biomedical subjects

F Negro

Publications and source records attributed to F Negro.

At least 145 records · Page 8Linked to original sources

Behaviour of cyclic nucleotides and Ca2+ levels in liver tissue of rats poisoned by white phosphorus and trichlorobromomethane.

The content of hepatic cyclic AMP was increased soon after intoxication by white phosphorus. Its level reached a maximum 4 h after poisoning, but in subsequent phases tended to return to normal. In contrast, the cyclic GMP concentration was altered only 24 and 36 h after treatment with the same hepatotoxin. Similar modifications of cAMP and cGMP content were also detected after poisoning by trichlorobromomethane (CBrCl3). As a consequence, an altered cGMP/cAMP ratio was found in both experimental conditions. Further, the modification of cAMP content after white phosphorus was detected prior to liver damage (steatosis and necrosis), while the highest concentration of the cyclic nucleotide in CBrCl3-poisoned rats was found when fatty liver was already evident. In addition, in phosphorus-poisoned rats, the hepatic content of Ca2+ was found to be unmodified during all phases of the intoxication, while after CBrCl3 a phasic increase of the Ca2+ level was observed at 4, 24 and 36 h.

Animals↗

Hepatitis B virus DNA (HBV-DNA) in anti-HBe positive sera.

HBV-DNA measured by the spot hybridization technique, was found in the sera of 28 of 106 (26.4%) anti-HBe positive carriers of HBsAg. Dane particle-associated HBeAg, HBcAg and HBV-specific DNA-polymerase activity were found in the sera of nine (8.5%), five (4.7%) and two (1.9%) of these patients, respectively. All carriers with serum HBV-DNA had chronic liver disease and 18 had intrahepatic delta-Ag and serum anti-delta at titers higher than 1/5000. Intrahepatic HBcAg was detected in the nuclei of 90% of delta negative individuals; 50% of them also had cytoplasmic fluorescence. Only two of the 18 patients with intrahepatic delta-Ag (11%) had HBcAg in the liver. Viral nucleic acid was not found in the sera of 15 other patients with chronic hepatitis, seven of whom had intrahepatic delta-Ag. Serum HBV-DNA was also negative in the remaining 63 symptomless carriers of HBsAg lacking markers of delta infection. Interestingly, although DNA-polymerase negative, some sera gave autoradiographic spots of high optical density. HBV-DNA was detected in them at concentrations typical of sera which are usually both DNA-polymerase and HBeAg positive. Detection of HBV-DNA in serum represents the most direct and sensitive in vitro assay for assessing HBV infectivity and characterizes HBsAg carriers with HBV-related liver damage and ongoing HBV replication independently from the state of HBeAg/anti-HBe system. In the Mediterranean area, the majority of anti-HBe positive carriers with serum HBV-DNA have chronic liver disease and delta infection.

Carrier State↗

Microsomal autoantibodies in chronic infection with the HBsAg associated delta (delta) agent.

A cytoplasmic autoantibody is described which gives a distinct immunofluorescence pattern in tissues of man and of varied animal species. Fluorescence is maximal in human substrates; it is strong in human hepatocytes and nephron cells and weak in thyroid adrenal and pancreatic cells. Complement fixation and fluorescence absorption studies have shown that the homologous antigen is localized in the microsomal membranes of human liver. The autoantibody was found in 13% of 81 carriers of HBsAg with chronic delta infection. It was not detected in patients with acute delta infection or in HBsAg positive and HBsAg negative patients without delta infection. The apparently exclusive occurrence of this antibody in chronic delta infection suggests that its expression is induced by persistence of the viral event.

Adult↗

[Preliminary data on the influence of 4-hydroxyalkenals on the phagocytic activity polymorphonuclear leukocytes in the rat].

The effect of low concentrations of 4-hydroxy-2-trans-pentenal, 4-hydroxy-2-trans-nonenal and 4-hydroxy-2-trans-tetradecenal (4-hydroxyalkenals produced during lipid peroxidation) was evaluated on the phagocytic activity of polymorphonuclear cells obtained from rat peritoneum. Our results show that the above compounds can influence, at different degrees, the endocytic powers, as measured "in vitro", of leukocytes through an inhibition that appears, to some extent, dose-related. Since lipoperoxidative processes can take place at the inflammed area, aldehydes originating from the peroxidative derangement of fatty acids may play a role in interfering with the cellular reactions at the inflammatory site.

Aldehydes↗

[Chemotaxis and chemokinesis of rat polymorphonuclear leukocytes in response to 4-hydroxy-2-tetradecenal and 4-hydroxy-2-nonenal].

Since a number of experimental evidences suggests that some lipoperoxidation products can affect leukocyte migration "in vitro", we have investigated the chemotactic and chemokinetic properties of two of these products (4-hydroxy-2,3-trans-tetradecenal and 4-hydroxy-2,3-trans-nonenal) using rat neutrophils. The cells were obtained from the pleural cavity after injection of 1.0 ml isologous serum. The granulocytes were suspended in Hanks' plus BSA 2% and the motility determined by means of a modified Boyden chamber. For evaluating the chemotactic properties, the aldehyde were added into the lower compartment, while for detecting the chemokinetic power, the compounds were placed in both the compartments. Our results show that both the chemicals (in a range between nano- and micromolar concentrations) are able to exert -at different degree- a chemotactic activity. In this connection, the more active aldehyde appeared to be the tetradecenal. On the contrary, the same compounds seem uneffective in stimulating the random migration of polymorphonuclear cells.

Aldehydes↗

[Influence of thyroid states on PGE2 biosynthesis].

Hyperthyroid and hypothyroid states were induced in the rat by daily injection of 3,3',5-triiodothyronine (T3; 33 microgram/100 g b. wt., ip for 6 days) or by thyroparathyroidectomy, respectively. Control animals underwent only a sham operation or received the T3 vehicle. In these experimental conditions the biosynthesis of PGE2-like substance was determined "in vitro" in the fraction obtained after centrifugation at 80,000xg for 60 min of pooled spleens (5). Assays of PGE2 activity were carried out on rat stomach strip preparations according to Vane (8). In a series of additional experiments the influence of thyroid states on the inhibitory activity exerted by Indomethacin, Oxametacine and Phenylbutazone on PGE2 biosynthesis was also evaluated. The results obtained indicate that the hyperthyroidism induces a significant increase of PGE2 production "in vitro" from added arachidonic acid (100% enhancement above the control values) while thyroparathyroidectomy is unable to interfere with such biosynthetic activity. In addition, the inhibitory effect of Indomethacin, Oxametacine and Phenylbutazone on PGE2 production is not affected by hyperthyroid state whereas hypothyroidism significantly limits the action of the mentioned non-steroid anti-inflammatory agents.

Animals↗

[Lipid peroxidation in the rat liver after acute inflammation induced by carrageenan. I. Influence of non-steroidal anti-inflammatory agents].

Oral administration of Indomethacin (3 mg/Kg) and Phenylbutazone (200 mg/Kg) induces an increase of TBA reacting substances (TBArs) by total liver homogenates, while treatment with Ibuprofen(200 mg/Kg, os) does not affect the susceptibility of liver tissue to lipid peroxidation. The former compounds do not influence the pro-oxidant action of CCl4 (1,0 ml/Kg, os) as evaluated "in vitro", whereas Ibuprofen appears to limit the extension of the TBArs production induced by the halomethane. The acute inflammatory state determined by carrageenan injection in the rat hind paw does not interfere with the peroxidative derangement found "in vitro" neither in the presence or in the absence of the all mentioned chemicals. Carbon tetrachloride (1,0 ml/Kg, os) is able in depressing significantly the rat paw oedema provoked by carrageenan, but does not potentiates the anti-inflammatory action of non-steroid agents.

Animals↗

[Susceptibility of the liver to lipid peroxidation after treatment with paracetamol].

Intoxication of rats with paracetamol (2.0 g/kg, b. wt.,os) is not followed by peroxidative decomposition of liver microsomal lipids "in vivo" but seems to interfere with ATPase and 5'-Nucleotidase activity in isolated plasmamembranes. Treatment with reduced glutathione, cys=teine and 2. mercaptopropionylglycine results in partial protection against liver injury provoked by the toxin. However, these sulphydryl compounds are not able to prevent the fall of liver GSH content occurring after paracetamol.

Acetaminophen↗

[Removal of foreign bodies from the upper airways and the bronchial tree of small children].

Food remnants are the foreign bodies most frequently aspirated by young children. Larger foreign objects are nearly always rejected spontaneously. In many cases, however, aspiration of foreign bodies lead to death by suffocation. From March 1975 to August 1979, 27 endoscopies removing 22 foreign bodies have been carried out by us. All children were less than 7 years old. The foreign bodies most commonly found were peanuts. Endoscopy was not only carried out when diagnosis was clear, but also if there was suspicion of foreign body aspiration. It is nowadays a treatment without risk when the following conditions are met: 1. Careful medical preparation leading to bronchial dilatation. 2. Effective collaboration with a paediatric anaesthetist. 3. Exact knowledge of the bronchial tree of children.

Bronchi↗

[Interference of antioxidants E/O of some free radical "scavengers" with the activity of glucose-6-phosphatase after administration of carbon tetrachloride].

G-6-Pase activity was investigated in the microsomal fraction from rat liver in the presence of carbon tetrachloride and/or propyl gallate (PG), reduced glutathione (GSH) and superoxide dismutase. Results obtained "in vitro" demonstrated that CCl4 induced a 60% inhibition of the microsomal enzyme activity. Moreover, a marked inhibition of G-6-Pase activity was found also when propyl gallate and reduced glutathione were added, at different concentrations, to incubation mixture. In addition, these drugs were unable to interfere with the dangerous effect exerted on the enzymatic activity by the haloalkane. Additional experiments carried out "in vivo" with propyl gallate produced evidence that intraperitoneal administration of the antioxidant was followed by a significant inhibition of G-6-Pase activity, while the damaging action of CCl4 was unaffected. Some possible explanations of these results are reported.

Animals↗

Serial passage of hepatitis delta virus in chronic hepatitis B virus carrier chimpanzees.

Five consecutive passages of hepatitis delta virus in hepatitis B virus carrier chimpanzees were performed in order to further characterize the infectious and pathogenic nature of this naturally occurring defective virus. Three animals received identical inocula at fourth passage in order to assess individual animal variation as a factor in the course of infection and disease. Acute hepatitis delta virus infection occurred in all hepatitis B virus carrier chimpanzees as demonstrated by coincident intrahepatic hepatitis delta antigen, serum hepatitis delta antigen and serum hepatitis delta virus RNA followed by seroconversion to antibody to hepatitis delta antigen. In all animals, acute hepatitis was temporally associated with hepatitis delta virus infection and was self-limited. The incubation period to hepatitis shortened with passage, whereas biochemical and histologic evidence of liver diseases increased. The marked increase in liver disease with passage was not associated with increasing markers of hepatitis delta virus replication or expression, thus indicating that adaptation to the chimpanzee by serial passage resulted in increased hepatitis delta virus virulence. The duration of hepatitis due to hepatitis delta virus infection in three chimpanzees which received the same inoculum varied from 1 to 8 months. The observations of passage adaptation and individual host variation in this experimental model of hepatitis delta virus disease parallel known pathogenic variations in human hepatitis delta virus infection.

Animals↗