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C Baldi

Publications and source records attributed to C Baldi.

At least 55 records · Page 3Linked to original sources
PubMed1988

[Determination of serum neuron-specific enolase in bronchial tumors of neuroendocrine origin].

Neurone-specific enolase, a serum marker of neuroendocrine tumours has been determined in small-cell anaplastic bronchial carcinomas, in typical and atypical carcinoid. The marker presents good sensitivity in small-cell tumours and in atypical carcinoids, while blood levels are within normal limits in cases of typical carcinoid. The low serum levels of neurone-specific enolase found in typical carcinoid suggest a failure of the enzyme to express itself in the circulation owing to the poor or lack of cellular necrosis.

Biomarkers, Tumor↗
PubMed1988

[Exercise two-dimensional echocardiography in recent myocardial infarction. Is it useful in the detection of multivessel disease?].

Exercise two-dimensional echocardiography (2D-ECHO) can be used to detect coronary artery disease in patients (pts) by the development of stress-induced transient asynergy in areas without wall motion abnormalities when at rest. The aim of the study is to verify the accuracy of exercise 2D-ECHO in the identification of high risk pts with multivessel disease after the first acute myocardial infarction (AMI). Technically adequate 2D-ECHO examinations were obtained in 21 of 28 (75%) consecutive patients after acute myocardial infarction. 30-50 days after acute myocardial infarction, these 21 pts (19 males and 2 females, mean age +/- SD = 54.3 +/- 8.7) underwent 2D-ECHO during bicycle exercise in supine position. The marker of multivessel disease was the development, during the stress test, of new areas of asynergy not adjacent to the infarcted area (i.e. transient remote asynergy). Two months after acute myocardial infarction all pts underwent coronary angiography to verify the severity of coronary obstruction (reduction of luminal diameter greater than or equal to 75% in the non infarct related vessel).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1987

[Echographic identification of symptomatic gastric carcinoma and its lymph node metastases].

The diagnostic capability of ultrasound in symptomatic gastric cancer is stressed, on the basis of a prospective study of 64 neoplastic and 19 non-neoplastic patients. Aspecific signs are described which suggest the presence of five layers within the gastric wall as an index of absence of disease. The prospective importance of ultrasound investigation in 5 neoplastic patients with aspecific symptoms is emphasized.

Esophageal Neoplasms↗
PubMed1986

Cystamine induces toxicity in hepatocytes through the elevation of cytosolic Ca2+ and the stimulation of a nonlysosomal proteolytic system.

Infusion of cystamine into the isolated, perfused rat liver resulted in tissue damage preceded by the formation of cystamine-protein mixed disulfides which were mainly detected in the plasma membrane fraction. Hepatotoxicity was prevented when dithiothreitol was infused after cystamine or when the calcium antagonist, verapamil, was co-infused with the disulfide. In isolated hepatocytes, the formation of cystamine-protein mixed disulfides was associated with an inhibition of plasma membrane Ca2+-ATPase activity and a decreased rate of Ca2+ efflux from the cells. This resulted in intracellular Ca2+ accumulation which was followed by a stimulation of both phospholipid hydrolysis and proteolysis, as indicated by enhanced rates of release of radioactivity from hepatocytes prelabeled with [14C]arachidonate and [14C]valine, respectively. Preincubation of hepatocytes with the calmodulin inhibitor, calmidazolium, or with the phospholipase inhibitors, chlorpromazine and dibucaine, inhibited the stimulation of [14C]arachidonate release by cystamine. However, none of these agents prevented the onset of cystamine toxicity in hepatocytes. In contrast, pretreatment of the cells with antipain or leupeptin, two inhibitors of Ca2+-activated proteases, abolished the stimulation of proteolysis by cystamine and also protected the cells from cystamine toxicity. Our results suggest that the perturbation of intracellular Ca2+ homeostasis by cystamine is caused by the inhibition of Ca2+ efflux associated with the formation of cystamine-protein mixed disulfides in the plasma membrane and that subsequent cytotoxicity results from Ca2+-activation of a nonlysosomal proteolytic system.

Animals↗
PubMed1985

Glutathione S-conjugates stimulate ATP hydrolysis in the plasma membrane fraction of rat hepatocytes.

Incubation of a rat hepatocyte plasma membrane fraction with micromolar concentrations of either glutathione disulfide or various glutathione S-conjugates resulted in a several-fold increase in the rate of ATP hydrolysis. This stimulation was further enhanced when the plasma membrane fraction had been pretreated with agents that arylate or oxidize sulfhydryl groups, suggesting that this ATPase activity is modulated by the protein thiol status of the plasma membrane. It is proposed that this newly discovered ATPase may function in the cellular extrusion of both glutathione disulfide and glutathione S-conjugates.

Adenosine Triphosphatases↗
PubMed1985

Accumulation of Ca2+ induced by cytotoxic levels of menadione in the isolated, perfused rat liver.

Previous studies have indicated that the presence of cytotoxic levels of menadione (2-methyl-1,4-naphthoquinone) causes rapid changes in intracellular thiol and Ca2+ homeostasis in isolated rat hepatocytes. The present investigation was undertaken to examine these effects in the intact liver. Rat livers were therefore perfused with Krebs-Henseleit buffer containing 1.3 mM Ca2+ using a single-pass mode, and the perfusate Ca2+ level was monitored with an on-line Ca2+-selective electrode. Infusion of menadione elicited an increased O2 uptake by the liver, followed by a dose-dependent decrease in the perfusate level of Ca2+. Hepatic accumulation of Ca2+ was accompanied by stimulation of cytosolic phosphorylase a activity. Cessation of menadione infusion resulted in gradual recovery of perfusate Ca2+ to base levels. Ca2+ uptake was not accompanied by decreases in reduced pyridine nucleotide or ATP levels in the liver as evidenced by measurements either during maximal Ca2+ uptake or after recovery. However, Ca2+ uptake was correlated with decreased glutathione and increased glutathione disulfide levels in the liver, both of which reversed during recovery from Ca2+ uptake. Moreover, depletion of hepatic glutathione by pretreatment with diethylmaleate resulted in increased Ca2+ uptake during menadione infusion. The amount of protein-bound mixed disulfides showed a particularly striking relationship to Ca2+ uptake, reaching a maximal level during Ca2+ uptake and reversing toward normal value during recovery from Ca2+ accumulation. The present findings suggest that menadione-induced Ca2+ uptake is due to plasma membrane dysfunction as a result of loss of protein thiol groups critical for maintaining the plasma membrane Ca2+ extrusion mechanism. Our model offers a particularly useful opportunity to study mechanisms underlying toxic disturbances in Ca2+ homeostasis in the intact liver, since Ca2+ fluxes can be monitored under conditions in which cellular control mechanisms are not obliterated by excessive toxicity.

Animals↗
PubMed1985

Determination of total and hexavalent chromium in bile after intravenous administration of potassium dichromate in rats.

Total and hexavalent chromium were measured in bile samples obtained from cannulated bile ducts of male rats iv administered with potassium dichromate at various doses corresponding to 0.1, 0.5, and 1 mg of chromium. The evaluation of the hexavalent form was performed by separation with a liquid anion exchanger and electrothermal atomization-atomic absorption spectrophotometric determination. Within 2 hr 1.35-2.23% of the chromium injected was recovered in bile as total chromium, the hexavalent form accounting for less than 1% of the total chromium collected, which seems almost entirely excreted as trivalent chromium. Since Cr(VI) administered iv was quickly reduced to Cr(III) in blood, the possibility exists for chromium in trivalent form to penetrate into the liver cells and to be excreted in the bile, possibly by binding to a carrier such as the low-molecular-weight substance described by Yamamoto et al. (A. Yamamoto, O. Wada, and T. Ono, Toxicol. Appl. Pharmacol. 59, 515, 1981).

Animals↗
PubMed1985

[Echinococcal cyst of the right ventricle: diagnostic role of 2-dimensional echocardiography].

A case of cardiac echinococcosis in a 22 year-old woman is reported. Clinical findings and cardiac catheterization data offered only presumptive evidence of an intraventricular mass but failed to make a positive diagnosis of cardiac involvement by hydatid disease. Using Two-Dimensional Echocardiography (2-DE) we were able to identify a rounded structure with multiple loculation into the right ventricle, highly suggestive of a hydatid cyst. Surgery confirmed our findings. We confirm the ability of 2-DE to detect and characterise intracardiac masses and we suggest that 2-DE could be considered the procedure of choice in the diagnosis of cardiac hydatid disease.

Adult↗
PubMed1984

Erythromycin estolate impairs the mitochondrial and microsomal calcium homeostasis: correlation with hepatotoxicity.

The effects of erythromycin estolate, a well known hepatotoxic macrolide antibiotic, on isolated rat hepatocyte viability and on subcellular Ca2+ transport have been investigated. Erythromycin estolate (0.5 mM), but not erythromycin base and erythromycin ethylsuccinate, induced 100% cell death after 60 min incubation, and caused maximal inhibition of mitochondrial and microsomal Ca2+ sequestration activities at 0.1 mM concentration. Sodium lauryl sulphate, which is the surfactant moiety of the erythromycin estolate molecule, caused effects similar to those exhibited by erythromycin estolate. Disorders of the intracellular calcium homeostasis seem to play a role in the lauryl sulphate-mediated hepatotoxic action of erythromycin estolate.

Animals↗
PubMed1984

Biological monitoring of occupational exposure to different chromium compounds at various valency states.

Chromium concentrations in the air were measured in seven different workroom environments, where exposure to water soluble hexavalent or trivalent compounds was expected. Urinary excretion of chromium was measured before and after the same arbitrarily chosen working day. End-of-shift urinary chromium and its increase above pre-exposure levels were closely related to the concentration of water soluble chromium (VI) in the air. The values corresponding to 50 micrograms m-3 in the air, which is the current threshold limit value in most countries, were 29.8 and 12.2 micrograms g-1 of creatinine, respectively. Urinary chromium in workers exposed to water insoluble chromates or to water soluble chromic (III) sulphate was definitely higher than that observed in subjects not occupationally exposed to chromium compounds, but it cannot be recommended as short-term exposure test for evaluation of the job-related hazard.

Absorption↗
PubMed1984

Blood levels of hexavalent chromium in rats. "In vitro" and "in vivo" experiments.

For the Cr(VI) selective separation from biological materials we have developed a highly rapid extraction-separation method with liquid anion exchanger as Amberlite LA-1 or LA-2. The analytical determination of Cr(VI) in organic phase was carried out using electrothermal atomic absorption spectroscopy (ETA-AAS). After i.v. administration of 0.5 and 2.5 mg/kg b.w. of K2Cr2O7 in male Wistar rats the biological samples, collected at different times, were immediately analyzed. Cr(VI) was not detected in whole blood one minute after administration of the lower dose. In blood of rats receiving higher dose an incomplete reduction of Cr(VI) was observed. Such data demonstrate a highly rapid but limited metabolic capacity of hematic compartment to reduce Cr(VI) to trivalent status. "In vitro" incubation of K2Cr2O7 (4 microM) with rat erythrocytes or plasma at 37 degrees C showed a rapid reduction of Cr(VI) in red cells while plasma samples demonstrated a limited reductive power. These results obtained with a new and specific analytical method, confirmed a trigger role of red cells in Cr(VI) metabolism.

Animals↗
PubMedDate not supplied

Corrected transposition of the great arteries with isolated aortic coarctation: In utero echocardiographic diagnosis.

Physiologically corrected transposition of the great arteries (cTGA), defined by discordant atrioventricular and ventriculoarterial connections, is an uncommon congenital cardiac malformation. It rarely exists without associated cardiac anomalies, the most common of which are ventricular septal defect, pulmonary outflow obstruction, tricuspid valve (systemic) deformity, and rhythm disturbances. Conversely, hypoplasia of the systemic ventricle and systemic inflow or outflow obstructions have seldom been reported, although their recognition may significantly influence surgical repair and the patient's prognosis. We report a case of cTGA with complete heart block, moderate hypoplasia of the systemic ventricle, and severe aortic coarctation that was echocardiographically diagnosed in utero at 30 weeks' gestation because of fetal growth retardation and persistent fetal bradycardia. After delivery the patient underwent epimyocardial pacemaker implantation and aortic coarctation repair at 2 weeks of age. Unfortunately, the patient died on the seventh postoperative day because of systemic ventricular hypertrophy. Although it is well known that fetal echocardiography may reliably diagnose uncommon congenital cardiac malformations, to the best of our knowledge, this paper represents the first reported case of antenatal diagnosis of this complex anomaly.

Adult↗