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Biomedical subjects

M Romano

Publications and source records attributed to M Romano.

At least 325 records · Page 18Linked to original sources
PubMed1989

Effect of cimetidine and ranitidine on drug induced damage to gastric epithelial cell monolayers in vitro.

The effect of the H2 blockers cimetidine and ranitidine on drug induced damage to gastric cell monolayers has been evaluated in conditions independent of systemic factors and their anti-acid properties. Monolayers of mucous cells from a human cell line MKN 28, obtained from a human gastric adenocarcinoma, have been studied. Cell damage has been assessed qualitatively by trypan blue dye exclusion test and quantitatively by 51Cr release assay. Cimetidine and ranitidine significantly protected cultured cells against damage induced by sodium taurocholate decreasing taurocholate induced 51Cr release by 36% (p less than 0.001) and 28% (p less than 0.01), respectively. Cimetidine was also protective in concentrations lower than ranitidine. This protection was not prevented by the prostaglandin synthesis inhibitor indomethacin nor by the sulph-hydryl blocker N-ethylmaleimide. Incubation with cimetidine and ranitidine did not increase the production of PGE2 by cultured cells nor did it affect the cellular level of sulph-hydryl compounds. Cimetidine and ranitidine did not afford protection against damage induced by indomethacin and ethanol. Cimetidine in a concentration of 10 4M increased ethanol induced damage significantly. In conclusion (1) cimetidine and ranitidine protect gastric cells against taurocholate induced damage in vitro, independently of their anti-acid effect; (2) this protection is not mediated by prostaglandin E2 or sulph-hydryl compounds; (3) cimetidine and ranitidine do not protect gastric cells against damage induced by indomethacin and ethanol.

Cell Line↗
PubMed1989

Mild pancreatic damage in acute viral hepatitis.

Whether and to what extent the pancreas is involved in acute viral hepatitis is still unclear. In order to address this issue we evaluated serum and urinary amylase and isoamylase levels in 92 patients with acute viral hepatitis of different etiology and in 60 healthy volunteers. Furthermore, pancreatic structure and volume were evaluated by ultrasound scanning. Significant increase in serum and urinary pancreatic isoamylases was found in 12 and 35% of patients, respectively, in the early stage of the disease. Increase in serum pancreatic isoamylases was found only in patients suffering from B and non-A, non-B hepatitis. Ultrasonographic evaluation did not show any change in pancreatic structure and volume. In conclusion, this study suggests that mild pancreatic damage may occur during viral hepatitis.

Adult↗
PubMed1989

Effect of ranitidine on taurocholate-, ethanol-, and indomethacin-induced damage to gastric epithelial cells in vitro.

We evaluated whether ranitidine protects gastric epithelial cells against damage induced by sodium taurocholate, ethanol or indomethacin, under conditions independent of its acid inhibitory effect as well as of systemic factors. We also studied the role of prostaglandins and sulfhydryls in any such protection. Ranitidine significantly reduced the amount of damage induced by taurocholate, but did not afford protection against ethanol- and indomethacin-induced damage. Incubation with ranitidine did not increase PGE2 production by cultured cells nor did it affect the cellular content of sulfhydryls. The protective effect of ranitidine against taurocholate was not prevented by indomethacin or by the sulfhydryl blocker, N-ethylmaleimide. In conclusion, this in vitro study confirms that H2 blockers such as ranitidine have a limited cytoprotective ability independent of acid secretion, which is not as extensive as agents such as prostaglandins and sulfhydryls. This may be because prostaglandins and sulfhydryls play no role in the protective effect of ranitidine.

Cell Line↗
PubMed1989

Protection of gastric epithelial cell monolayers from a human cell line by omeprazole in vitro.

Omeprazole has an anti-ulcerogenic effect and protects rat gastric mucosa against drug-induced damage in vivo. We have evaluated omeprazole protection against damage induced by sodium taurocholate to gastric epithelial cell monolayers, an experimental model that completely excludes the influence of systemic factors. Furthermore, since our model consists of mucus-producing cells, the acid inhibitory effect of the drug in any protection is negligible. The role of prostaglandin and sulfhydryls in any such protection has also been evaluated. Monolayers of gastric cells from a well-differentiated human cell line were studied. A chromium-51 release assay was used to assess cell damage. Sodium taurocholate damaged cells dose-dependently (r = 0.97, p less than 0.01). Pretreatment with omeprazole significantly reduced the amount of cell damage brought about by sodium taurocholate (p less than 0.001). Indomethacin did not prevent the protection afforded by omeprazole, nor did incubation with omeprazole increase the amount of prostaglandin E2 produced by cultured cells. Omeprazole did not increase the amount of sulfhydryl compounds in cultured cells. These results indicate that omeprazole protects gastric cells independently of systemic factors and of inhibition of gastric acid secretion. This protection is not related to stimulation of prostaglandin synthesis nor is it associated with an increase of endogenous sulfhydryl compounds.

Cell Line↗
PubMed1989

Development of an information reporting system on illicit drug use in Mexico.

In Mexico, drug abuse is considered a public health problem that is growing rapidly, especially among minors, who constitute about one half of the total population of the country. To facilitate an estimation of the drug problem and its trends in the country, the Information Reporting System on Drugs (IRSD) was established in 1986 by the Mexican Institute of Psychiatry at the request of the National Council against Addictions. IRSD is an "event-reporting" type of information system based on two month-long cross-sectional evaluations that are made each year in June and November. Data for IRSD are gathered via a questionnaire called the individual report on drug abuse, which is completed by illicit drug users upon admission to health and criminal justice facilities and institutions at Mexico City during the evaluation periods. This article describes the objectives of IRSD, its development and its functioning, as well as some of its findings.

Adolescent↗
PubMed1988

Impairment of in vitro natural antibacterial activity in HIV-infected patients.

Circulating PBMC of healthy subjects possess an in vitro natural antibacterial (NA) against enteropathogenic bacteria, including Salmonella species. The effector cell of NA activity is a CD: 4+, 8-, Leu-8/TQ-1+ T lymphocyte acting against bacteria via cytophylic IgA in a mechanism similar to antibody-dependent cellular activity. Because AIDS is a profound immunodeficiency caused by HIV involving primarily CD4 lymphocytes and in particular the Leu-8/TQ-1 subset, it was of interest to assess NA activity of HIV+ subjects at various stages of the disease. Results indicate that NA activity against Salmonella typhi and Salmonella paratyphi C is significantly decreased in AIDS as well as in lymphadenopathy syndrome patients. Furthermore, sera containing IgA against salmonellae were not able to arm PBMC from HIV+ patients. The humoral response against S. typhi-LPS was also greatly decreased after HIV infection, in contrast to the known hypergammaglobulinemia seen in these subjects. Defective NA activity might contribute to the increased incidence of salmonellosis observed in AIDS.

AIDS-Related Complex↗
PubMed1988

Dissecting human T cell responses against Bordetella species.

To identify the minimal structures that may be important for the creation of a synthetic and/or recombinant vaccine against whooping cough, human T cell clones were obtained against Bordetella antigens. Cloned peripheral blood T lymphocytes from an immune donor were grown in IL-2 and tested for proliferation in response to inactivated Bordetella species (B. pertussis, B. parapertussis, and B. bronchiseptica) and mutants deficient for the expression of virulence-associated antigens. All the T cell clones obtained were CD4+8- and recognized specifically the Bordetella antigens when presented by autologous B cells. On the basis of the responsiveness to the whole inactivated bacteria, it was possible to cluster the 12 clones obtained into four groups with the following specificity: (1) filamentous hemagglutinin (FHA); (2) B. pertussis-specific antigens; (3) virulence-associated Bordetella-specific antigens; and (4) nonvirulence-associated Bordetella-specific antigens. Using two new B. pertussis deletion mutants, clone 6 (representative of cluster 1) was found to recognize the COOH terminus of FHA. Furthermore, three out of four clones of cluster 3 were specifically stimulated by the soluble 69-kD protein from the outer membrane of B. pertussis. Surprisingly, none of the twelve clones obtained by stimulation in vitro with whole inactivated bacteria recognized pertussis toxin (PT), which is believed to be the most important protein to be included in an acellular vaccine. However, when a new generation of clones was obtained using soluble PT as the in vitro stimulus, it was observed that 11 clones of this group recognized this antigen. Thus, PT does not seem to be the most representative antigen on the whole inactivated bacteria, although T cell memory against PT exists in a donor who had the disease several years ago.

Adult↗
PubMed1988

Polyamine oxidase activity in serum of cancer patients and healthy subjects.

Polyamine oxidase (PAO) activity was determined in the serum of cancer patients and healthy subjects. However, the data obtained showed that PAO activity was extremely low or undetectable in the serum of cancer patients and healthy subjects. The difference in PAO activity observed between the sera of cancer patients and healthy subjects was statistically insignificant. Thus, the measurement of PAO activity in serum has no value as a cancer marker.

Adult↗
PubMed1988

Human erythrocyte glucose-6-phosphate dehydrogenase. Identification of a reactive lysyl residue labelled with pyridoxal 5'-phosphate.

Human erythrocyte glucose-6-phosphate dehydrogenase contains a reactive lysyl residue, which can be labelled with pyridoxal 5'-phosphate. The binding of one mole of pyridoxal 5'-phosphate per mole of enzyme subunit produces substantial inactivation. The substrate glucose-6-phosphate prevents the loss of activity, suggesting that the reaction site is close to the substrate-binding site. A tryptic peptide containing the pyridoxal-5'-phosphate-binding lysyl residue has been isolated and characterised. The reactive lysyl residue has been identified in the glucose-6-phosphate dehydrogenase amino acid sequence. Comparison with glucose-6-phosphate dehydrogenase from other sources shows a high homology with a peptide containing a reactive lysyl residue, isolated from the enzyme from Saccharomyces cerevisiae; glucose-6-phosphate dehydrogenase from Leuconostoc mesenteroides also contains a region highly homologous with the sequence around the reactive lysyl residue in the human enzyme. The results of this communication provide the first direct evidence for the association of an essential catalytic function with a specific region of the molecule of human erythrocyte glucose-6-phosphate dehydrogenase.

Affinity Labels↗
PubMed1988

Heart rate, PR, and QT intervals in normal children: a 24-hour Holter monitoring study.

A dynamic electrocardiographic Holter monitoring study was performed in 32 healthy children (20 males and 12 females, age range 6-11 years old), without heart disease, according to clinical and noninvasive instrumental examination. We evaluated atrioventricular conduction time (PR), heart rate (HR), and QT interval patterns defining the range of normality of these electrocardiographic parameters. The PR interval ranged from 154 +/- 10 ms (mean +/- SD) for HR less than or equal to 60 to 102 +/- 12 ms for HR greater than or equal to 120 (range 85-180). The absolute mean HR was 87 +/- 10 beats/min (range 72-104), the minimum observed HR being 61 +/- 10 (range 51-79), the maximum 160 +/- 20 beats/min (range 129-186). Daytime mean HR gave a mean value of 93 +/- 10 (range 71-148), while during night hours it was 74 +/- 11 (range 54-98). The minimum QT interval averaged 261 +/- 10 ms for HR greater than 120 and the maximum 389 +/- 9 ms for HR less than or equal to 60; the corresponding mean value of QTc (i.e., QT corrected for HR) ranged from 388 +/- 8 for HR less than or equal to 60 beats/min to 403 +/- 14 ms for HR greater than 120 beats/min. The results of the present study provide data of normal children which can be readily compared against those of subjects in whom cardiac abnormalities are suspect or patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1988

Characterization of a partial deletion of the factor VIII gene in a haemophiliac with inhibitor.

Genomic DNA from 49 Italian patients affected with severe haemophilia A was analysed by Southern blotting technique using a cDNA probe corresponding to exons 14-26 of coagulation factor VIII. No TaqI site mutation was observed in this sample. A partial deletion, eliminating exons 15-18 and spanning about 13kb, was identified and characterized in one patient with anti-factor VIII antibodies.

Antibodies↗
PubMed1988

Somatostatin stimulates prostaglandin production by rat gastric epithelial cells in vitro, but is not cytoprotective.

Whether somatostatin stimulates prostaglandin synthesis by gastric cells is controversial. Also, it is unknown whether somatostatin protects gastric cells against exogenous injury in conditions independent of systemic factors and of inhibition of gastric acid secretion. The present study was undertaken (1) to evaluate the effect of somatostatin on prostaglandin production by rat gastric epithelial cells in monolayer culture and (2) to assess whether somatostatin protects gastric cells against taurocholate- and indomethacin-induced damage in vitro. Somatostatin at concentrations of 10(-5) M and 10(-4) M significantly stimulated PGE2 and 6-keto-PGF1 alpha production by rat gastric epithelial cells but was not able to prevent damage induced by sodium taurocholate and indomethacin to rat gastric cells in monolayer culture. These results suggest that: (1) somatostatin stimulates prostaglandin synthesis by cultured rat gastric epithelial cells, but (2) is not directly protective to rat gastric epithelial cell monolayers against drug-induced damage in vitro.

6-Ketoprostaglandin F1 alpha↗