PubMed Health⌕ Search

Biomedical subjects

M A Rossi

Publications and source records attributed to M A Rossi.

At least 19 recordsLinked to original sources
PubMed1996

Purification and characterization of the vaccinia virus deoxyuridine triphosphatase expressed in Escherichia coli.

The deoxyuridine triphosphatase gene of vaccinia virus, encoded by the open reading frame F2L, was cloned into Escherichia coli and expressed under the control of a bacteriophage T7 promoter. After induction of T7 RNA polymerase by isopropyl beta-D-thiogalactopyranoside, a 16.5-kDa peptide accumulated to high levels. This 16.5-kDa protein was purified to homogeneity and characterized. Gel filtration of the purified protein revealed a trimeric native structure. Biochemical analysis revealed the enzyme to be a metalloenzyme; enzymatic activity is inhibited by EDTA. This inhibition was reversed by the addition of Mg2+, Mn2+, or Zn2+. While the enzyme activity was highly specific for dUTP with an apparent Km of 0.94 microM, inhibition studies show that 8-azido-ATP acted as a competitive inhibitor of dUTP with a Ki of approximately 173 microM. Also, protection studies demonstrated that nucleotide competitors inhibit photoincorporation of the photoaffinity analogues [gamma-32P]5-azido-dUTP and [gamma-32P]8-azido-ATP. This suggests that while catalytic activity is limited to dUTP, other nucleotides can bind the active site.

Adenosine Triphosphate↗
PubMed1996

Congenital coronary arteriovenous fistula: spontaneous rupture and cardiac tamponade.

Congenital coronary arteriovenous fistula is an unusual, but not rare, coronary anomaly. Management of asymptomatic fistulas is controversial because of great variability in natural history. We describe an 82-year-old female patient with spontaneous rupture of a previously undetected left main coronary artery-to-pulmonary artery coronary arteriovenous fistula, with resulting hemopericardium and cardiac tamponade. Emergent surgical exploration and repair provided successful treatment.

Aged↗
PubMed1996

Interactions between propofol and lipid mediator receptors: inhibition of lysophosphatidate signaling.

As a highly lipophilic drug, propofol may interact with lipophilic domains in addition to its likely primary site of action on the gamma-aminobutyrateA) (GABA(A)) receptor. Likely candidates for such interaction are the G protein-coupled membrane receptors for lipid intercellular mediators. The phospholipid lysophosphatidate (LP) has attracted attention as such a signaling molecule. It has a variety of biological actions, including vasoconstriction. We therefore studied the interaction between propofol and the LP receptor. Intracellular Ca2+ release in response to LP was assessed by measuring C1- flux through Ca(2+)-activated C1- channels in Xenopus oocytes. The average charge movement in response to LP 10(-7)M was 2.0 +/- 0.2 microCoulombs. Propofol in Intralipid (0.01%) dose-dependently inhibited LP signaling (50% inhibitory concentration [IC50] 5.38 microM). Propofol 28 microM inhibited LP signaling by 81%. Intralipid (0.01%) was without effect. To ascertain that intracellular signaling pathways and the Ca(2+)-activated C1- channel were not affected by propofol, we tested the effects of propofol (5.6 microM) on currents induced by methylcholine (10(-7)M) in oocytes expressing the m1 muscarinic acetylcholine receptor. No inhibition was observed. As both receptors share the same intracellular signaling pathway, we conclude that clinically relevant concentrations of propofol most likely inhibit the LP receptor or its G protein. Inhibition of LP signaling may explain some of propofol's vasodilating actions.

Anesthetics, Intravenous↗
PubMed1996

[Serum bactericidal rate. Methodological proposal to predict the efficacy of antimicrobial therapy].

Several in vitro techniques have been developed, which are able to quantify the bactericidal activity of a determined antibacterial drug against an infective agent. The Serum Bactericidal Rate (SBR) is proposed as a complementary technique for the determination of the "killing curve", the serum bactericidal test or the minimal bactericidal concentration. SBR takes into account the most advantageous features of both of them. SBR is based on quantifying at different times the survival of the bacterial inoculum exposed to the patient's serum. Thus, bactericide speed is evaluated in the first hours of contact with the microorganism (as in the "killing curve"), but taking into account drug concentrations which have been reached by the patient (as in the serum bactericidal test). Preliminary assays suggest that SBR may have greater capacity to discriminate an infectious agent in answer to different therapeutic schemes than other determinations, although prospective studies are required to evaluate its predictive value.

Drug Therapy, Combination↗
PubMed1996

Glucocorticoids: their role on gonadal function and LH secretion.

The aim of the study was to investigate gonadal function and LH reserve in patients on chronic therapy with supraphysiological doses of GC. We clinically evaluated 17 male subjects (aged 23-56 years-old) on chronic GC therapy. In four subjects (aged 23-39 years-old) randomly selected, three basal blood samples were drawn and pooled for measurement of SHBG, total, free and bioavailable testosterone. Following baseline samples, a GnRH stimulation test was performed. Starting with a priming of 5 micrograms, a bolus of 50 micrograms of GnRH was injected intravenously and samples obtained every 30 minutes for assessment of LH. Four healthy men (aged 24-28 years-old) were used as controls. Patients on steroids referred decreased libido (58%) and impotence (52%) and lower back pain (41%). Total, free and bioavailable serum testosterone were significantly lower than controls (p < 0.01, p < 0.05 and p < 0.05, respectively) while SHBG levels persisted unchanged. Baseline LH and its rise after GnRH was normal. This study shows that chronic GC administration involves gonadal function reducing sexual steroids without changes in baseline and stimulated LH secretion. In addition, the priming with physiological doses of GnRH optimizes the pituitary response to higher GnRH doses.

Adult↗
PubMed1995

Sudden cardiac death in the indeterminate phase of Chagas' disease associated with acute infarction of the right carotid body.

We recently came across a case of a patient in the indeterminate phase of Chagas' disease who died suddenly with cardiac arrhythmia associated with acute infarction of the right carotid body due to occlusive thrombosis in the glomic artery. Although the available data in this case do not offer definite evidence to support a cause-and-effect relationship between carotid body infarction and patient's sudden cardiac arrest, it is very likely that the acute infarction of the carotid body could be the distinct morphological counterpart of the functional disturbance. The infarction would affect the vagal-sympathetic interactions augmenting sympathetic action.

Carotid Body↗
PubMed1995

The challenge of chagasic cardiomyopathy. The pathologic roles of autonomic abnormalities, autoimmune mechanisms and microvascular changes, and therapeutic implications.

The evidence provided by both human and animal studies on chronic Chagas' heart disease suggests that the cardiomyopathy occurs as a consequence of several physiopathological processes occurring after infection interacting with unidentified host factors. The development of the chronic fibrosing myocarditis is related to progressive and additive focal cellular necrosis, and associated inflammatory lymphomononuclear infiltrate and reactive and reparative myocardial fibrosis and surrounding myocyte hypertrophy. These processes may be initiated and perpetuated by alterations in the myocardial microcirculation and by autoimmune factors. The autonomic impairment and/or the chronic fibrosing myocarditis and the left ventricular dysfunction could act as factors predisposing one to an increased risk of sudden cardiac death.

Animals↗
PubMed1995

Evidences of 4-hydroxynonenal involvement in modulation of phagocyte activities.

The peroxidative breakdown of membrane polyunsaturated fatty acids leads to the production of various carbonylic compounds: among these, 4-hydroxynonenal (HNE) displays many biological properties related to neutrophil functions. It stimulates rat and human polymorphonuclear (PMN) cell migration and has been detected during inflammation. The aim of this study was to elucidate and well characterize the mechanism of action of HNE. We observed that micromolar HNE concentrations that influence migration do not stimulate differently from many other chemoattractants the human PMN chemiluminescence (CL) induced by opsonized zymosan or phorbol 12-myristate 13-acetate (PMA). Higher HNE concentrations inhibit the light emission of stimulated PMN. Addition of 0.5 mM L-arginine (L-arg), the substrate of nitric oxide synthase, into the incubation medium had the effect of modifying human CL. In fact, HNE at 10-6 M, a concentration which is ineffective in absence of L-Arg, at 10-5 M reduces CL emission of PMA-stimulated human PMN. These observations have been confirmed by electron-spin resonance (ESR) analysis. HNE, according to other stimuli, induced PMN phosphoinositide-specific phospholipase C (PL-C). All these results considered together suggest the conclusion that HNE represents an interesting endogenous molecule that plays a role as an inflammatory mediator involved a) in the recruitment of phagocytic cells at the inflamed area, and b) in the modulation of respiratory burst and of nitric oxide (NO) production.

Aldehydes↗
PubMed1994

Activation of phosphoinositide-specific phospholipase C of rat neutrophils by the chemotactic aldehydes 4-hydroxy-2,3-trans-nonenal and 4-hydroxy-2,3-trans-octenal.

A comparison has been made between the effects of 4-hydroxy-2,3-trans-nonenal (HNE) and 4-hydroxy-2,3-trans-octenal (HOE), two lipid peroxidation products, on the basal and GTPgammaS-stimulated activities of phosphoinositide-specific phospholipase C (PL-C) of rat polymorphonuclear leukocytes. PL-C activity was determined in vitro by measuring the hydrolysis of [3H] phosphatidylinositol-4,5-bis- phosphate (PtdIns-P2) added as exogenous substrate to neutrophil plasma membranes. PL-C was activated by concentrations of HNE ranging from 10(-8) to 10(-6) M both in the presence and in the absence of 2 x 10(-5) M GTPgammaS; HOE stimulated the enzymatic activity between 10(-11) and 10(-8) M; maximal stimulation was given by 10(-11) M HOE plus GTPgammaS. The aldehyde concentrations able to accelerate PtdIns-P2 breakdown displayed a good correspondence with those which have been reported to stimulate the oriented migration of rat neutrophils. Pretreatment of neutrophils with pertussis toxin prevented the stimulation of PL-C by 10(-11) M HOE and by HOE plus GTPgammaS. Our results suggest that the chemotactic action of HNE and HOE might depend on the activation of PL-C; furthermore a regulatory G protein appears to be involved in the acceleration of PtdIns-P2 turnover by HOE.

Aldehydes↗
PubMed1994

Focal cerebral ischemia and patent cardiac foramen ovale.

By means of transthoracic contrast echocardiography, the prevalence of a patent foramen ovale (PFO) was studied, in a continuous series of 48 patients aged less than 50 years with a recent episode of acute cerebral ischemia. A PFO was found in 11 subjects (23%). In the subgroup of younger patients (aged less than 30 years), the prevalence was much higher than in those aged 30 or more (58% against 11%, p = 0.0022). In the 19 patients with clear evidence of extracardiac causal factors of cerebral ischemia, there was no PFO; of the remaining 29 subjects, a PFO was present in 11 (38%) (p = 0.0015). In conclusion, the possible presence of a PFO must be carefully investigated in subjects with cerebral ischemia aged less than 30, as well as in subjects aged between 30 and 50 in whom there is no acceptable explanation for their cerebral ischemic episode.

Adult↗