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Biomedical subjects

L Rossi

Publications and source records attributed to L Rossi.

At least 379 records · Page 21Linked to original sources
PubMed1986

[Serum bile acids in cirrhosis: correlation with liver function parameters and with the severity of the disease].

The aim of this paper is to evaluate the relationships among the increase of serum bile acids (SBA) and other common liver function tests in subjects with liver cirrhosis. Our results show that SBA levels are well-correlated with the seriousness of the disease (classified according to Child's criteria), and with the presence of ascites, of oesophageal varices, of hepatic encephalopathy and with the gamma-globulin level. SBA also appear to be well-correlated with total bilirubinemia, and, at a lower extent, with cholesterolemia and albuminemia; no significant linear correlation was found among SBA and cholestasis (alkaline phosphatase, gamma-glutamyl-transpeptidase) or cytolysis (transaminases) indexes. In conclusion, the SBA increase in liver cirrhosis without evidence of cholestasis (as in our patients) seems to be related to liver cell reuptake disturbances and to the presence of porto-systemic shunts, with consequent alterations in entero-hepatic bile salt recirculation.

Adult↗
PubMed1986

[Clinico-epidemiological aspects of infectious endocarditis in a present-day Italian population].

This study has been carried out with the aim of assessing the incidence and other features of Infective Endocarditis in the region Veneto (Italy) in the years 1975-84, with particular regard to the patients admitted to the hospitals in Verona. Of the 692 patients admitted in hospitals of Veneto, 629 were resident in the region (an incidence equal to 1.6/100,000 inhabitants per year). The age range was from 8 to 72 (55 +/- 9). All social classes were affected, although retired, disabled and unemployed subjects were in the majority. The average stay in hospitals was 27.6 days. In 7.6% of the cases surgical therapy was required; the over-all mortality rate was 10%. Of the 80 patients admitted to the hospitals in Verona, 79% were suffering from pre-existing cardiopathy (40% rheumatic heart disease, 25% valvular prosthesis, 7.5% congenital heart disease, 5% prolapsing mitral valve, 1.2% obstructive hypertrophic cardiomyopathy); 54% of the cases had been exposed to bacteriological infections in the preceding months: bronchopulmonary, oropharyngeal, genitourinary or gall bladder infections processes or oral surgery or heart surgery or drug addiction. Only in 19% of these cases a correct antibiotic prophylaxis had been carried out. The responsible germ was identified in 50 patients (67% of the cases in which blood cultures had been performed): Streptococcus in 22%, Staphylococcus in 20%, Gram-negative in 12%, Corynebacterium in 4%, polymicrobial associations in 9% of the cases. These data stress the need for an improvement in antibiotic drug regimen (both in prophylaxis and treatment) and the diffusion of norms of hygiene aimed to the reduction of skin and mucous sources of bacteremia and interpersonal transmission of infections disease.

Adult↗
PubMed1986

[Late potentials, myocardial kinetics and ventricular vulnerability as markers of sudden death after myocardial infarct].

The 1st myocardial infarction requires the identification of patients who are at high risk of malignant ventricular arrhythmias. Our study group included 55 consecutive patients (age less than 70): all had non-invasive "signal averaging" recording and 24 hour dynamic electrocardiogram at the post-acute phase of their 1st myocardial infarction (MI) and 3 months later. Wall motion abnormalities were evaluated in each patient but two. 24 randomized patients (without documented sustained ventricular tachycardia) underwent right programmed ventricular stimulation at the 3rd month after MI and pathological repetitive responses were evaluated (Table III); they were hemodynamically stable and without persistent ischemia. Late potentials have been compared to spontaneous and induced ventricular arrhythmias, wall motion abnormalities (Table II) and two-year follow-up (Table VI), in order to identify predictive markers of sudden death or malignant arrhythmias. Ventricular late potentials were identified in 28 patients (51%) 4-8 days after MI: mean duration was equal to 75 +/- 33 msec; they did not show any relationship to the site (Table I) and to the extension of necrosis (Table II). Ventricular late potentials had no significant association with myocardial dyskinesia (Table II) while their association with complex ventricular arrhythmias, detected on Holter monitoring within 8 days after MI, and with the induction of repetitive ventricular responses (greater than or equal to 2 complexes) showed significant correlations (respectively p = 0.02; p = 0.01). In regard of the recognition of spontaneous ventricular tachycardia (greater than or equal to 3 complexes) in the follow-up, the detection of late potentials showed 75% sensibility with predictive value equal to 32% (Table V); the combination of late potentials and ventricular dyskinesia exhibited the highest specificity (88%) and predictive value (54%). By the end of follow-up there had been 6 cardiac deaths (2 sudden, 4 from left ventricular failure): late potentials longer than 75 msec were recorded in all patients who had cardiac death; in the post acute phase of MI repetitive ventricular arrhythmias were detected in only 1 of the 2 case of sudden cardiac death and in none of the patients who developed sustained ventricular tachycardia in the follow-up (Table VI). Myocardial dyskinesia was present in each patient who developed non sudden cardiac death (Table VI).(ABSTRACT TRUNCATED AT 400 WORDS)

Arrhythmias, Cardiac↗
PubMed1986

Comparison of effects of penicillin minimal inhibitory and sub-inhibitory concentration on Staphylococcus aureus and Streptococcus faecium does not support the view that antibiotic sub-inhibitory concentrations can specifically interfere with bacterial virulence.

The effect of minimal (MIC) and sub-minimal (sub-MIC) inhibitory concentrations of penicillin on Staphylococcus aureus and Streptococcus faecium were compared. It was found that similar alterations in both cell shape and ultrastructure were found in the presence of penicillin MIC and sub-MICs, the only difference being that while in the presence of penicillin MIC all individual cells were altered, in the presence of sub-MICs the damaged portion was smaller the lower the penicillin concentration and the longer the incubation time. By testing the effect of inoculum size on the penicillin MIC, it was found that penicillin concentrations, which were sub-MICs for rather dense population, turned out to be the MICs for lower density populations. These findings do not support the view that sub-MICs of antibiotics can cause specific damage to bacterial cells which, although not leading to growth inhibition, lowers their virulence. On the contrary, it is suggested that penicillin sub-MICs have no specific effect on Staphylococcus aureus and Streptococcus faecium cells, but simply differ from MIC in that they do not inhibit all cells.

Microbial Sensitivity Tests↗
PubMed1986

Embryotoxicity of benzo(a)pyrene and some of its synthetic derivatives in Swiss mice.

We have studied the teratogenicity of benzo(a)pyrene (BP), benzo(a)pyrene-4,5-oxide, and a racemic mixture of 7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene, a proximal metabolite and ultimate carcinogenic metabolite of BP, respectively, and of 6-methylbenzo(a)pyrene after direct injection into embryonal Swiss mice. The compounds were dissolved in acetone and trioctanoin (1:1) and injected at doses ranging from 0.4 to 16.0 nmol/embryo on days 10, 12, and 14 of development. The transplacental effects of BP given at the same gestational days and at comparable dose levels were also evaluated. The control groups received 0.5, 1.0, or 2.0 microliter/embryo of vehicle on days 10, 12, or 14 of pregnancy, respectively. The fetuses were examined when they were 18 days old. On the basis of gross external and internal malformations, 7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene appeared to be the most potent embryotoxic and teratogenic compound tested, causing 85% of embryolethality and 100% of malformed fetuses in the group treated on day 10 of intrauterine development. There were 61 and 27% of malformed fetuses following 7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene treatment on days 12 and 14 of gestation, respectively. The effects of this BP metabolite were very specific and malformations such as exencephaly, thoraco- and gastroschisis, phocomelia, and edema were found. The administration of BP (both transplacental and direct intraembryonal injection) and benzo(a)pyrene-4,5-oxide caused no significant increase of malformed fetuses in any of the developmental stages considered. 6-Methylbenzo(a)pyrene induced multiple malformations (among these a high percentage of protruding tongue) in 50, 46 and 31% of the fetuses treated on days 10, 12, and 14 of gestational age, respectively. These results combined with previous data concerning the induction of lung tumors by the tested compounds in 15-day-old Swiss mouse embryos, emphasize the requirement of a common metabolic derivative of BP to induce both teratogenesis and carcinogenesis in mice. Furthermore present data show that midgestation Swiss embryos are also highly sensitive to the 6-methyl derivative of BP.

Abnormalities, Drug-Induced↗
PubMed1986

Extranodal specialized sinoatrial cells.

To define the occurrence of specialized pacemaker and transitional (slender) cells beyond the anatomic limits of the sinoatrial node, cytomorphometric evaluations were carried out in specimens from ten human hearts. The morphometric analysis showed significant histocytologic peculiarities of the extranodal slender cells, which were 60% to 70% smaller than those of the ordinary atrial myocardium, and their location at a mean distance of 12 to 14 mm from the posterior sinoatrial nodal edge, beneath the crista terminalis. These data can help in understanding the substrates for subsidiary pacemaking in sinoatrial disease.

Female↗
PubMed1985

Valproate-induced hyperammonaemia in two epileptic identical twins.

The cases of two epileptic identical twins are described, one of whom had presented an episode of valproate (VPA)-induced stupor associated with very high blood ammonia (NH3) concentrations. Both twins showed a similar marked increase of venous NH3 concentrations after the administration of a single loading dose of VPA (800 mg).

Adult↗
PubMed1985

Auditory and somatosensory evoked potentials (AEPs and SEPs) and ballistic movements in Parkinson disease.

In five patients with initial idiopathic Parkinson disease AEPs (early and late components of auditory evoked potentials), SEPs (somatosensory evoked potentials) and arm ballistic movements (abduction of the humerus) were studied. Experimental sessions were conducted before starting treatment (L-Dopa plus Carbidopa) and at two and six month intervals. Before treatment evoked potential abnormalities were found in four out of five patients; EMG patterns underlying ballistic arm abduction movements were altered in all patients; corresponding prolonged duration of initial movements and low mean velocities were found. After treatment AEP and SEP showed a reduction of previously observed abnormalities and both EMG patterns and kinematic variables consistently improved. It is suggested that the electrophysiological investigations employed in this preliminary study may be a useful tool in clinical and pharmacological researches on Parkinson disease.

Aged↗
PubMed1985

Cardioneuropathy and extracardiac neural disease.

The pathology of cardiac innervation, both intrinsic and external to the heart (aortopulmonary glomera included), is scarcely known, yet it can be critical to life-threatening disorders in cardiac performance, or to reflexes discharging outside the heart, or both. Evidence has been supplied in cardiac neuroanatomy relevant to cardioneuropathy. The arrhythmogenic potential of imbalanced autonomic input in the heart has been corroborated by histopathologic findings in intrinsic plexuses. In turn, significant neurogenic substrates for cardiomyopathy have not been confirmed. Changes in the extrinsic sympathetic chain (left stellate ganglion) and in the prevailing vagal cardiac plexus were found in subjects with arrhythmias (with long QT interval and ventricular tachycardia/fibrillation, respectively). In myocardial infarction with sudden cardiac death, a complicating mediastinitis often presented and was seen to produce focal inflammation of mediastinal nerve plexus and paraganglia. This can worsen the imbalance in autonomic control of the performance of the heart and interfere with barochemoreflex regulation of the systemic or coronary circulation, or both. Such ill-understood sequelae of infarction as the shoulder-hand, chest pain and Dressler syndromes might also correlate with the newly described neuromediastinitis.

Arrhythmias, Cardiac↗
PubMed1985

B and T cell abnormalities in patients with primary IgA nephropathy.

The in vitro function of B and T cells was studied in 16 patients with primary IgA nephropathy (PIgA-N). The distribution of OKT3+ cells (total peripheral T cells) and of regulatory T cell subsets (helper OKT4+ and cytotoxic/suppressor OKT8+ cells) was evaluated and a testing for 47 HLA-A, B, C, DR, and DQ antigens was carried out in the 16. B lymphocyte IgA production, after stimulation by pokeweed mitogen in the presence of T cells from normal donors treated with mitomycin C, was significantly greater in patients than in controls. T lymphocytes from patients with PIgA-N were more efficient than T cells from controls in providing IgA specific helper activity for normal B cells. The analysis of the individual data showed that the overactivity of B cells and the T cell operational dysfunction was present in about 50% of the patients and did not correlate. No numerical imbalance between T lymphocyte subsets nor any association between lymphocyte behavior, HLA antigen distribution, and a number of clinical, laboratory, and immunohistological findings was observed. Our data, therefore, suggest that PIgA-N is an immunologically heterogeneous disease and that an IgA-specific B cell overactivity and/or overall IgA-specific T cell helper activity may be present in some patients.

Adolescent↗
PubMed1985

Benzo[a]pyrene-induced DNA damage in mouse fetal tissues.

We have studied the occurrence and persistence of DNA damage in the hepatic and pulmonary tissues of fetal, newborn and adult CD1 mice exposed to selected doses of benzo[a]pyrene (BP) by utilizing the alkaline elution technique. Firstly 12-, 15- and 18-day pregnant and 1-, 7- and 82 to 85-day-old mice were treated i.p. with 10 mg/kg BP and the DNA fragmentation evaluated 4 h later. This approach indicated that, among the ages considered, 15-day-old fetuses were the most sensitive to BP genotoxicity. Therefore we concentrated on this intrauterine stage and evaluated the role of the maternal and fetal environment on the induction and the kinetics of disappearance of DNA damage by BP. BP at the dose levels of 0, 2 and 10 mg/kg was injected i.p. into pregnant females or directly into single fetuses and the fetal livers and lungs recovered 2, 4, 24 and 48 h later. According to the above protocol other 12-day-pregnant mice were treated i.p. with 500 mg/kg arochlor and their 15-day-old fetuses directly injected with the same doses of BP. The results showed that the maximum DNA damage is present at 4 h following BP treatment and it almost disappeared at 48 h irrespective of the route of BP administration. However, the decrease was not uniform and while at 48 h the lesion reached the control level in the liver, it remained slightly higher in the lung. The effects where markedly magnified in the arochlor-induced groups where the intrafetal injection of BP caused an average 2-fold increase and an earlier appearance of DNA damage in both liver and lung compared with uninduced animals. The amplified BP activity induced by arochlor was particularly evident in the lung where at 48 h there was still a significant amount of DNA damage. Since the lung is a preferential site of transplacental carcinogenic effects in CD1 mice, our results favor the conclusion that a correlation exists between DNA damage and tumor induction in the fetuses of this mouse strain.

Animals↗
PubMed1985

Electrophysiologic and histopathologic correlations in a case of permanent form of reciprocating tachycardia.

A case of permanent junctional reciprocating tachycardia with post-mortem documentation of an accessory atrioventricular pathway as the substrate of the arrhythmia is reported. Tachycardia had lasted for 15 years and showed a retrograde P wave (P') and R-P' longer than P'-R interval. The tachycardia circuit utilized a concealed posterior septal accessory pathway as the retrograde limb. Because the arrhythmia was disabling and unresponsive to pharmacological treatment, the patient underwent closed chest ablation of the His bundle. After the procedure, no anterograde or retrograde conduction over the normal conduction system was observed; anterograde conduction over the anomalous pathway showed decremental properties. Because of previous myocardial infarction, the patient developed a ventricular aneurysm and died suddenly 5 months after His bundle ablation. Histological examination of the heart revealed a group of tiny fibromuscular bundles joining the lower rim of the coronary sinus outlet to the summit of the interventricular septums; the anomalous atrioventricular connection pursued a sinuous, tortuous path. The geometrical disposition of the accessory pathway may have been responsible for the decremental properties of conduction observed during life.

Atrioventricular Node↗
PubMed1985

Kainic acid differentially affects the synaptosomal release of endogenous and exogenous amino acidic neurotransmitters.

Presynaptic actions of kainic acid have been tested on uptake and release mechanisms in synaptosome-enriched preparations from rat hippocampus and goldfish brain. Kainic acid increased in a Ca2+-dependent way the basal release of endogenous glutamate and aspartate from both synaptosomal preparations, with the maximum effect (40-80%) being reached at the highest concentration tested (1 mM). In addition, kainic acid potentiated, in an additive or synergic way, the release of excitatory amino acids stimulated by high K+ concentrations. Kainic acid at 1 mM showed a completely opposite effect on the release of exogenously accumulated D-[3H]aspartate. The drug, in fact, caused a marked inhibition of both the basal and the high K+-stimulated release. Kainic acid at 0.1 mM had no clear-cut effect, whereas at 0.01 mM it caused a small stimulation of the basal release. The present results suggest that kainic acid differentially affects two neurotransmitter pools that are not readily miscible in the synaptic terminals. The release from an endogenous, possibly vesiculate, pool of excitatory amino acids is stimulated, whereas the release from an exogenously accumulated, possibly cytoplasmic and carrier-mediated, pool is inhibited or slightly stimulated, depending on the external concentration of kainic acid. Kainic acid, in addition, strongly inhibits the high-affinity uptake of L-glutamate and D-aspartate in synaptic terminals. All these effects appear specific for excitatory amino acids, making it likely that they are mediated through specific recognition sites present on the membranes of glutamatergic and aspartatergic terminals. The relevance of the present findings to the mechanism of excitotoxicity of kainic acid is discussed.

Animals↗
PubMed1985

Regulation of penicillin-binding protein activity: description of a methicillin-inducible penicillin-binding protein in Staphylococcus aureus.

The penicillin-binding proteins (PBPs) of two methicillin-resistant strains of Staphylococcus aureus (R2 and R1) were analyzed in cells grown in the absence and in the presence of methicillin. Under the former condition, strain R2 showed the typical PBP pattern of beta-lactam-susceptible strains, while strain R1 showed a markedly increased amount of PBP-3. Under the latter condition, on the other hand, a novel PBP (PBP-2a) located between PBP-2 and -3 was detected in strain R2, while strain R1 appeared to synthesize an even greater amount of PBP-3, in respect to untreated cells. Both R2 PBP-2a and R1 PBP-3 showed a very low affinity for methicillin, which was consistent with the MICs for the respective strains.

Bacterial Proteins↗
PubMed1985

Transition from resistance to hypersusceptibility to beta-lactam antibiotics associated with loss of a low-affinity penicillin-binding protein in a Streptococcus faecium mutant highly resistant to penicillin.

Penicillin-binding protein (PBP) 5 of Streptococcus faecium has been shown to have a very low affinity for penicillin, and this PBP was suggested to be responsible for both the natural low susceptibility and high resistance to the antibiotic in this species (R. Fontana, R. Cerini, P. Longoni, A. Grossato, and P. Canepari, J. Bacteriol. 155:1343-1350, 1983). In this study, an S. faecium mutant (Rev 14) hypersusceptible to penicillin was derived from the highly resistant S. faecium R40 treated with novobiocin, and its properties were compared with those of the parent and S. faecium PS, a relatively susceptible strain from which R40 was isolated. The hypersusceptible strain did not synthesize PBP 5, but it did resemble the parent in cell morphology, growth rate, and autolytic activity. In addition, it was highly susceptible to other beta-lactams but remained as susceptible as R40 and PS to antibiotics of a different mechanisms of action. The affinity of individual PBPs for the beta-lactams tested was the same in all the strains. This finding suggested that Rev 14 hypersusceptibility was due to the lack of PBP 5 and strongly supported the role of this protein in the mechanism of both natural low susceptibility and high-level resistance to beta-lactams in S. faecium.

Anti-Bacterial Agents↗
PubMed1985

Biochemical mechanism of oxidative damage by redox-cycling drugs.

Biochemical mechanisms of production of redox intermediates of redox-cycling drugs include: photochemical events, either photoionization process or electron transfer from photoexcited states; electron exchange of reduced form of a drug with the oxy state of oxygen-binding hemoproteins; oxidation by catalytic metal centers (oxidases, peroxidases, oxygenases) of the reduced forms of drugs; or electron transfer to the oxidized form of a drug from activated intracellular electron transfer chain (mitochondria, microsomes, etc.). Further reaction of these drug free radicals can lead to oxidative damage by either direct attack of biological macromolecules or via oxygen reduction, giving O2-, H2O2, and OH. The reaction pathway depends on the presence of metal ions, natural scavengers, enzymes that control relative concentrations of reactive species, and availability of oxygen in the environment.

Animals↗