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Biomedical subjects

M Romano

Publications and source records attributed to M Romano.

At least 343 records · Page 19Linked to original sources
PubMed1988

Liver DNA alkylation after a single carcinogenic dose of dimethylnitrosamine to newborn and adult CFW Swiss mice.

N-nitrosodimethylamine N-demethylase activity, DNA alkylation, capacity for O6-methylguanine repair and cell proliferation were measured in livers of newborn and adult CFW mice after a single carcinogenic dose of DMNA. DNA alkylation was found in newborn and adult mouse livers but it was significantly higher in the newborn. 6- and 7-methyl substitutions of guanine were identified by HPLC analysis in newborn and in adult mouse livers. Metabolic 14C incorporation into adenine and guanine was observed only in liver DNA of newborns. O6-methylguanine levels were higher in newborn than adult mice after a single i.p. dose of [14C]DNMA. Liver DNA repair capacity measured as O6-meG-DNA methyltransferase was higher in adults than in newborns. De novo liver DNA synthesis was more inhibited by DMNA pretreatment in newborn than in adult mice. The relationship between these parameters and the greater neonatal liver tumor susceptibility is discussed.

Alkylation↗
PubMed1988

Effect of ACTH4-10 on nerve fiber regeneration after sciatic nerve crush in rabbits: an electrophysiological and morphological study.

Crush of sciatic nerve in rabbits supported by morphologic and electrophysiologic data was used to evaluate the effects of ACTH4-10 on nerve fiber regeneration. Treated animals showed a statistically significant higher regeneration rate than did control rabbits. Fiber density and mean diameters of myelinated nerve fibers were measured in semithin nerve sections at 1 and 3 cm distal from the crushed point at three different time points. Nerve fiber density results were higher in ACTH4-10-than in vehicle-treated rabbits. This difference showed an unequivocal trend and attained a statistically significant level in the sections 3 cm distal from the crush. ACTH4-10 seemed therefore to have a beneficial effect on nerve fiber regeneration.

Adrenocorticotropic Hormone↗
PubMed1988

Effect of aspartame on seizures in various models of experimental epilepsy.

We investigated in rats whether aspartame intake affected the susceptibility to seizures induced chemically (metrazol, quinolinic acid) or electrically (electroshock). Aspartame (0.75-1.0 g/kg), given orally as a single bolus to 16-hr fasted animals 60 min before metrazol, significantly increased the number of animals showing clonic-tonic seizures. At 1.0 g/kg the ED50 for clonic-tonic convulsions was lowered by 23%. A similar increase in seizure susceptibility was observed with 0.25-0.5 g/kg of the aspartame's metabolite phenylalanine. When aspartame was administered to fasted rats in three divided doses (0.33 g/kg) over 120 min or to fed animals after a meal, or overnight with the diet, no significant changes in the incidence of animals showing seizures was observed. One gram per kilogram aspartame and 0.5 g/kg phenylalanine did not modify the CC50 (mA) for tonic hindlimb extension induced by electroshock and the electroencephalographic seizures caused by intrahippocampal injection of 120 nmol quinolinic acid. Plasma and brain levels of phenylalanine and tyrosine significantly raised after both 1 g/kg aspartame as a single bolus (plasma: Phe 285%, Tyr 288%; brain: Phe 146%, Tyr 192%; above controls) or in three divided doses (plasma: Phe 207%, Tyr 315%; brain Phe 103%, Tyr 211%; above controls) and 0.5 g/kg phenylalanine (plasma: Phe 339%, Tyr 410%; brain: Phe 219%, Tyr 192%; above controls), but the ratio Phe/Tyr was not modified. Our data indicate that aspartame cannot be regarded as a general proconvulsant agent. The mechanisms of potentiation of seizures induced by metrazol after the administration of the sweetner in a single rapid intake will be discussed.

Animals↗
PubMed1988

Rupture of the right ventricular free wall. An unusual complication of mediastinitis after cardiac surgery.

Of 2171 patients who underwent open heart surgery between 1981 and 1986, 41 (1.8%) developed postoperative mediastinitis and were treated by closed irrigation drainage or open chest therapy. Six patients, (mean age 59 years) developed rupture of the right ventricular free wall. The primary procedures were: resection of akinetic fibrous plaque (2), mitral valve replacement (1), coronary bypass grafting (1), removal of a left atrial myxoma (1) and repair of post-infarction rupture of the left ventricle (1). In 2 patients, rupture occurred in the operating theatre during revision of the irrigation drainage. Both patients died after repair. In 4 patients, rupture occurred during coughing. One died before surgery. In the 3 other cases, the defects were repaired either by direct suture (2 patients) or with a pericardial patch (1 patient) with the aid of normothermic extracorporeal circulation. Three days later, a muscular flap (pectoral or dorso-lumbar) was mobilized to protect the mediastinal viscera. All 3 patients are alive and well. When bleeding occurs during treatment of mediastinitis, an immediate exploration with extracorporeal circulation to close the defect should be considered.

Aged↗
PubMed1988

Treatment of ruptured or elongated anterior mitral valve chordae by partial transposition of the posterior leaflet: experience with 29 patients.

We report a series of 29 patients, 5 to 75 years of age (mean age, 31.8 +/- 21.4 [SD] years), with pure mitral regurgitation caused by ruptured or elongated chordae of the anterior mitral leaflet. These patients underwent mitral valve repair by segmental transposition of the posterior leaflet with its attached chordae sutured to the free edge of the flail anterior leaflet. There were 2 hospital deaths. Follow-up ranged from 1 to 35 months (mean follow-up, 14.9 +/- 8.5 months). One patient is lost to follow-up. Two patients are in New York Heart Association Functional Class II; all others are in Class I. In 17 patients there is no detectable murmur; in 5 patients a mild to moderate systolic murmur can be detected, while 4 have a marked systolic murmur. The adequacy of the repair could be confirmed by Doppler echocardiography, which has shown no evidence of prolapse in 22 patients. A mild regurgitation jet is present in 4 patients, and a marked jet, in 3. Postoperative cardiac catheterization performed in 5 patients has confirmed the Doppler echocardiographic findings. Although longer follow-up is necessary, this technique appears adequate for repairing a major prolapse of the anterior leaflet caused by multiple ruptured or elongated chordae, therefore obviating the need for a prosthetic valve substitute.

Adolescent↗
PubMed1988

Platelet 3H-imipramine binding and response to minaprine in patients with major depression.

Platelet 3H-imipramine binding was studied in 37 patients fulfilling Research Diagnostic Criteria for major depressive disorder, examined before and after four weeks of treatment with minaprine 200 mg/day, and in 19 healthy controls. Mean baseline Bmax values of depressed patients were found to be significantly lower than those of controls, while no significant difference between the two groups was observed with respect to mean Kd. Treatment with minaprine did not significantly affect Bmax or Kd in depressed patients. When patients who responded to treatment (n = 18) were compared with nonresponders (n = 19), mean baseline Bmax values were found to be significantly lower in the former group, whereas mean Kd values did not differ. It is hypothesized that reduced 3H-imipramine binding may represent a predictor of a favorable response to antidepressant drugs which potentiate serotonergic transmission.

Adult↗
PubMed1988

Acetaminophen directly protects human gastric epithelial cell monolayers against damage induced by sodium taurocholate.

The present study evaluated whether acetaminophen can reduce sodium-taurocholate-induced damage to human gastric epithelial cells grown in monolayer culture (a preparation which excludes systemic factors). Further, the role of endogenous prostaglandin production by gastric cells in any such protection has been assessed. Results showed that (1) acetaminophen significantly protects human gastric epithelial cells against taurocholate-induced damage in vitro, in conditions independent of systemic factors, (2) protection of gastric cells by acetaminophen in vitro appears unrelated to stimulation of prostaglandin synthesis, and (3) a direct protective effect on gastric epithelial cells may play a role in protection of gastric mucosa by acetaminophen in vivo.

Acetaminophen↗
PubMed1988

Human cell line for study of damage to gastric epithelial cells in vitro.

UNLABELLED: We evaluated whether monolayers from a well-differentiated human gastric epithelial cell line (MKN 28) are suitable for studying the effect of drugs on gastric mucosa. MKN 28 monolayers and monolayers of human gastric epithelial cells from surgical specimens were studied morphologically and functionally. The protective effect of acetaminophen against taurocholate-induced damage was evaluated as was its effect on prostaglandin production. Both types of cultures showed similar morphologic and histochemical characteristics. Indomethacin inhibited and arachidonic acid stimulated prostaglandin production by both types of monolayers similarly. Both monolayers responded similarly to drug-induced damage. Acetaminophen decreased taurocholate-induced damage by 33% and 40% in MKN 28 cells and in primary human gastric cell culture, respectively. Indomethacin did not prevent acetaminophen protection nor did the amount of prostaglandin produced by cells increase after incubation with acetaminophen. IN CONCLUSION: (1) in the MKN 28 cell line model acetaminophen protected against taurocholate-induced damage; the percentage of protection was similar to that in primary cultures of human gastric epithelial cells; (2) acetaminophen protection in both models was not related to increased prostaglandin production; (3) the MKN 28 cell line is a suitable model to study damage to and protection of gastric epithelial cells in vitro.

Acetaminophen↗
PubMed1988

Atenolol and/or nifedipine in effort angina: which is the treatment of choice for exercise coronary protection?

The authors performed a long-term, double-blind, crossover, randomized study on the effects of two drugs (atenolol, 100 mg/day, or nifedipine, 10 mg t.i.d.) when administered alone or in combination on the exercise tolerance in 10 patients with stable angina on effort (mean age 52 +/- 4 years, 8 males and 2 females) and documented significant (greater than or equal to 70%) obstructive coronary lesions at angiography. None of the drug treatments improved exercise duration or maximal sustained work load. Atenolol decreased significantly ST segment depression to -1 +/- 0.8 from -1.91 +/- 0.7, baseline and -2.05 +/- 0.5, placebo. Nifedipine was not better than placebo. The atenolol plus nifedipine treatment was better than placebo (p less than 0.001) or nifedipine alone (p less than 0.05) but was not more significantly efficacious than atenolol alone. Long-term management of exertional angina can be usefully performed using atenolol. The use of nifedipine at the present dose of 10 mg, although well tolerated, did not improve the ST signs of ischemia.

Adult↗
PubMed1988

Effect of calcium channel blocker diltiazem on cytoprotection and prostaglandin and sulfhydryl production by rat gastric epithelial cells.

The calcium channel blockers verapamil and diltiazem protect gastric mucosa against exogenous injury in vivo. Whether this protection is mediated by systemic factors, such as blood flow, is due to inhibition of gastric acid secretion, or is associated with stimulation of endogenous protective agents such as prostaglandins or sulfhydryls, is unknown. We have evaluated whether diltiazem protects rat gastric epithelial cells in tissue culture (a model which excludes the influence of systemic factors) against damage induced by sodium taurocholate, indomethacin, or ethanol. Further we have assessed the effect of diltiazem on prostaglandin and sulfhydryl production. 51Chromium release assay and phase contrast microscopy have been used to assess cell damage. Sodium taurocholate, indomethacin, and ethanol-damaged cultured cells in a dose-dependent manner. Pretreatment with diltiazem did not prevent the drug-induced damage. Diltiazem did not increase PGE2 and 6-keto PGF1a production by cultured cells nor did it affect the cellular level of endogenous sulfhydryls. In conclusion, the calcium channel blocker diltiazem is not directly protective to rat gastric mucosal cells in vitro. Diltiazem does not stimulate prostaglandin production by gastric cells nor does it increase the cellular level of protective sulfhydryls.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Combined use of DNA probes in first-trimester prenatal diagnosis of hemophilia A.

First-trimester prenatal diagnoses of hemophilia A were heretofore obtained by using either intragenic factor VIII markers or linked extragenic polymorphic markers. Postulating that the combined use of all the available intragenic and extragenic markers can render such diagnoses more frequently feasible and more reliable, we carried out ten first-trimester prenatal diagnoses in male fetuses at risk for hemophilia A by DNA analysis of chorionic villus employing in combination the intragenic Bcl I polymorphism and the St 14 (DXS 52) or DX 13 (DXS 15) extragenic probes. A diagnosis of hemophilia was obtained in three fetuses, with a diagnosis of normal fetus obtained in the remaining seven. Seven diagnoses are confirmed by factor VIII assays carried out at the time of abortion, in the mid-trimester or at birth. A factor VIII probe recognizing Bcl I polymorphism was useful in 4 of 6 diagnoses; St 14, in 5 of 6; and DX 13 in 3 of 5. In two cases, St 14 was the only useful probe for diagnosis. Even though no recombination between extragenic probes and factor VIII gene was detected in this study, when only extragenic markers were informative we advised diagnostic confirmation on fetal plasma obtained by fetoscopy. Hence, first-trimester prenatal diagnosis of hemophilia A is feasible for the great majority of fetuses at risk through combined use of all the available intragenic and extragenic probes, providing key family members are available.

Adult↗