Biomedical subjects
Publications and source records attributed to L Rossi.
Histological examination showed acute haemorrhage of the bifurcating His bundle and of the left bundle branch in a 35 year old man who died after being given external cardiac massage for cardiac arrest. "Hammering" of the ventricular septum crest against the central fibrous skeleton of the heart by compression of the sternum was believed to have caused the haematoma of the junctional tissue.
A flow cytofluorimetric method was used to detect the immunoglobulin molecules present on human red blood cells. Normal human erythrocytes were separated into seven fractions of increasing mean age by density centrifugation on discontinuous gradients. Some biochemical and morphological properties of these cells were determined as well as their IgG content. The results obtained suggest that IgG binding during red cell aging is a cumulative process.
Cystic neoplasms of the pancreas are rare lesions. Following the Compagno-Oertel classification, we differentiated serous microcystic adenomas (SMA) from mucinous macrocystic adenomas/adenocarcinomas (MMA). The former are benign tumors with slow growth, composed by innumerable small and tiny cysts with central calcifications, resulting in a "honeycomb" pattern. They have a mixed US structure while CT densitometric values reflect a mixture of connective tissue and proteinaceous fluid. Postcontrast enhancement is frequently seen. MMA are potential (adenoma) or frankly (adenocarcinoma) malignant tumors. They appear as multilocular cystic masses containing septa and/or papillary bulges, with thickened walls. Both US and CT demonstrate their predominantly cystic character, and the eventual presence of excrescences. We report a series of 23 cases (6 SMA, 17 MMA) of cystic neoplasms of the pancreas studied during the past five years. A correct diagnosis of SMA was possible in all 6 cases, while MMA was correctly diagnosed in 17 out of 18 cases. There were no false negatives, and 1 false positive. All differential diagnoses are also discussed.
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3,5-Dimethyl-N-acetyl-p-benzoquinone imine (3,5-dimethyl-NAPQI) was cytotoxic to isolated hepatocytes from Sprague Dawley rats at levels between 200 and 300 microM. It rapidly oxidized intracellular glutathione within 10 sec, with the formation of oxidized glutathione. The cytotoxicity of 3,5-dimethyl-NAPQI could be prevented over a 3.5-hr period with the carboxylesterase inhibitor bis(p-nitrophenyl) phosphate, indicating that cytotoxicity involved N-deacetylation. The N-deacetylated product could be trapped with glutathione as 3-(glutathion-S-yl)-4-amino-2,6-dimethylphenol in 3,5-dimethyl-NAPQI-treated hepatocytes but not in hepatocytes pretreated with bis(p-nitrophenyl) phosphate, indicating that N-deacetylation activity had been inhibited. 3,5-Dimethyl-NAPQI was readily N-deacetylated by rat liver microsomes, in contrast to 3,5-dimethylacetaminophen. The latter was also not cytotoxic to hepatocytes at up to 2 mM. The N-deacetylated product 4-amino-2,6-dimethylphenol rapidly underwent autoxidation to form 2,6-dimethylbenzoquinone imine and was highly cytotoxic to hepatocytes at 200-300 microM. The latter reacted with glutathione to give the above conjugate and no glutathione oxidation occurred. Dithioerythritol (2 mM) added at 10, 20, and 30 min after 3,5-dimethyl-NAPQI delayed but did not prevent cytotoxicity. Dithioerythritol also resulted in the partial restoration of GSH, presumably as a result of reduction of protein mixed disulphides. The mechanism of cytotoxicity of 3,5-dimethyl-NAPQI therefore appears to be a result of a combination of oxidative stress and deacetylation resulting in arylation.
The activity of fosfomycin trometamol (FOT) was compared with that of cotrimoxazole (COT) and norfloxacin (NOR) using urine as medium and 10(7) bacteria as inoculum, conditions as close as those found by the administration of the drugs in vivo during the course of a urinary tract infection. The minimum inhibitory concentrations (MIC) of all antibiotics against 100 strains isolated from urinary tract infections were found to be higher than the breakpoint. Concentrations of FOT corresponding to mean and maximal values found in urine after single dose administration within the 0-48 h interval killed the great majority of strains. COT and NOR, when tested under similar conditions, exhibited an antibacterial activity lower than and equal to that of FOT, respectively. In several strains belonging to different species the frequency of mutation to resistance to 2000 and 1000 micrograms/ml of FOT was very low (greater than 10(-7], whereas it was relatively high (1 x 10(-5) to 1 x 10(-7] for 150 micrograms/ml, the two former and the latter being the respective maximal, mean and minimal values found in urine after administration of a single dose.
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To investigate the sporadic occurrence of hemophilia A and to estimate the sex ratio of mutation rates directly, 17 families with isolated cases of the disorder were studied by RFLP analysis and by clotting assays. Three RFLPs, one intragenic and two with close linkage to hemophilia A, were used. In eight families the RFLP study excluded the carrier status of the maternal grandmothers. Since hemostatic studies showed that the eight mothers of these propositi were hemophilia carriers, the origin of the newly mutated genes was inferred from the RFLP patterns: six hemophilic genes derived from the normal maternal grandfathers and two, from maternal grandmothers. The data indicate a higher mutation rate in males than in females, as previously suggested by segregation analysis and coagulation studies. However the sex ratio indicated by the RFLP analysis is lower than previously reported and could explain previous conflicting estimates.
Hepatocyte cytotoxicity caused by substituted benzoquinones was associated with increased cytosolic Ca2+ concentration. p-Benzoquinone-induced hepatotoxicity was enhanced when the hepatocytes were loaded with Ca2+ by preincubation with ATP. A similar order of potency of the substituted benzoquinones in releasing Ca2+ from isolated mitochondria and inducing hepatocyte cytotoxicity was found; in decreasing order, this was 2-Br-, unsubstituted-, 2-CH3-, 2,6-(CH3O)2-, 2,6-(CH3)2-, 2,5-(CH3)2-, 2,3,5-(CH3)3-, and 2,3,5,6-(CH3)4-benzoquinones (duroquinone). The cellular products of quinone metabolism, hydroquinones and glutathione conjugates, did not cause mitochondrial Ca2+ release. Benzoquinone-induced mitochondrial Ca2+ release was preceded by GSH conjugate formation and NAD(P)H oxidation but followed by mitochondrial swelling. With duroquinone, a slow GSH and NADPH oxidation preceded Ca2+ release, but GSH oxidation did not occur with Se-deficient mitochondria lacking glutathione peroxidase activity. Cyanide-insensitive respiration was also observed with duroquinone but not with benzoquinone, suggesting that duroquinone undergoes redox cycling. GSH was depleted by both arylation and oxidation with 2,6-(CH3O)2-, 2,6-(CH3)2-, 2,5(CH3)2-, and 2,3,5-(CH3)3-benzoquinones. Benzoquinone concentrations that totally depleted GSH did not cause Ca2+ release until intramitochondrial NAD(P)H was oxidized. Ca2+ release was also prevented when NAD(P)H generation was stimulated by the presence of isocitrate or 3-hydroxybutyrate. This suggests that mitochondrial Ca2+ release is associated with NAD(P)H oxidation catalyzed by NADH dehydrogenase with benzoquinone or by the glutathione peroxidase-glutathione reductase system with duroquinone.
We confirmed the occurrence of IgG antibodies reacting with ox cardiac conducting tissue in the serum of some human subjects. These antibodies failed to react with all ox cardiac conducting tissue cells; they reacted only with the cells defined as Purkinje cells. Having checked 352 sera, we found that the prevalence of antibodies to Purkinje cells was 11% in normal subjects (no correlation with sex and age), 14% in systemic lupus erythematosus, 21% in rheumatoid arthritis, 18% in progressive systemic sclerosis, and 23% in Sjögren syndrome. In 50 patients with permanent pacemakers for chronic non-postinfarction atrioventricular (AV) block the prevalence was 30% (P = 0.008). In a selected set of 29 patients with clinically idiopathic AV block located at or below the level of the His bundle the prevalence was 34.5% (P = 0.006). The possible role of anti-Purkinje cell antibodies in autoimmune damage of cardiac conduction tissue is discussed.
The new approach to computer processing of exercise electrocardiography has been made easier by the development of microcomputers. Studies are necessary to validate analyzed electrocardiographic data for the diagnosis of ischemia. We describe and assess in this paper a new program for the analysis "on line" of 12 leads during effort. The program detects "normal QRS" and ectopic beats. Amplitude of R wave, length of QRS, ST level after a programmable delay from J point, ST maximal slope and amplitude of T wave are calculated and recorded every 15 sec in the 12 leads. In 200 exercise stress tests quantitative data provided by the processor were compared with visual analysis and with clinical data. ST level less than or equal to -0.8 mm and ST slope less than or equal to 1.2 mV/sec or ST level greater than or equal to +2.0 mm and ST slope less than or equal to 0.6 mV/sec were the best analyzed criteria for ischemia. Using these criteria, sensitivity increased from 86.6% by visual reading to 92% by computer analysis, without change in specificity (94%).
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We present clinical, electrophysiologic and morphologic correlations of a patient with a permanent form of junctional reciprocating tachycardia, who died from a lung tumor. At electrophysiologic study, the tachycardia circuit was suspected to involve an atrio-Hisian accessory pathway antegradely and the AV node retrogradely; a ventriculo-atrial accessory pathway was excluded. Pathologic examination revealed a right-sided atrio-Hisian accessory pathway and an area of abnormal dispersion in the distal His bundle fibers. This case is consistently different from another previously reported case in which a concealed, serpiginous, septal atrioventricular accessory pathway was demonstrated by anatomic examination. Thus, different substrates seem to be responsible for the permanent form of junctional reciprocating tachycardia.
Glomerular size-selective properties in animals made nephrotic by adriamycin (ADR) injection and fed standard (20% protein) or high-protein (35% protein) diets were investigated using dextran fractional clearances. To interpret filtration and dextran-sieving data, a theoretical approach previously developed for analysis of experimental data in healthy and nephrotic humans was used. Four types of hypothetical pore-radius distributions were compared in order to establish the best tool for describing membrane pore structure in normal and nephrotic rats. This analysis revealed that a spread distribution of pores, the lognormal probability distribution, is the most adequate in representing membrane intrinsic characteristics. ADR animals on standard diet developed massive proteinuria and a lower glomerular filtration rate (GFR) than control animals. High-protein feeding in ADR rats induced a further increase in urinary protein excretion and in GFR. Dextran fractional clearance was more elevated for larger dextran fractions (greater than 46 A) in ADR animals on the standard diet than in control rats. No differences were observed in dextran-sieving curves between ADR rats on the standard and high-protein diet. Theoretical analysis of filtration and fractional clearance data revealed comparable changes in the intrinsic parameters of glomerular size selectivity in the two groups of nephrotic animals. These observations indicate that increased traffic of plasma proteins through the glomerular capillary wall does not imply, in our experimental condition, a further loss of glomerular size-selective properties. The greater urinary protein excretion of ADR animals on high-protein diet than ADR animals on a standard diet cannot be explained by further impairment of glomerular size selectivity but more likely reflects hemodynamic changes.
A cDNA for coagulation factor XII has been used to investigate the presence of gene lesions and restriction fragment length polymorphisms in two brothers with Hageman trait and their family. A TaqI polymorphic fragment has been found in the two propositi and in 11 members of the paternal lineage. This polymorphism, absent in the normal population, is correlated with the reduction of factor XII activity and enables the identification of heterozygous factor XII deficiency. Factor XII gene deletion as the cause of Hageman trait in this family has been excluded. A restriction map has been constructed, and the TaqI polymorphic site has been localized within the 5' portion of the gene. The mutation in the polymorphic site is probably the cause of the factor XII deficiency. Data suggest the presence of one factor XII gene per haploid genome.
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