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Biomedical subjects

M Russo

Publications and source records attributed to M Russo.

At least 37 records · Page 2Linked to original sources
PubMed1999

Significance of T-wave changes during early dobutamine stress echocardiography in patients with Q-wave acute myocardial infarction.

The relation between T-wave changes and regional contraction during dobutamine stress echocardiography at low (5 to 10 microg/kg/min) and high (20 to 40 microg/kg/min) doses in 43 consecutive patients, early (7+/-2 days) after first recent Q-wave acute myocardial infarction has been evaluated. T-wave changes detected in > or =2 infarct-related electrocardiographic leads during dobutamine infusion were defined as follow: (1) negative T waves becoming positive, (2) positive T waves becoming upright > or =2 mm, and (3) negative T waves becoming upright > or =2 mm from baseline. Wall motion score index (WMSI) was defined as the sum of the echocardiographic scores of 16 segments divided by total segments considered at baseline, and at low and peak doses of dobutamine. Patients were classified according to the absence or presence of dobutamine T-wave changes. Those without T-wave changes had a significantly higher WMSI at rest (1.68+/-0.23 vs 1.50+/-0.21; p <0.05) and at peak (1.77+/-0.34 vs 1.51+/-.30 p <0.05) of dobutamine stress testing, without higher incidence of viability, homozonal, and heterozonal ischemia and chest pain. The angiographic patterns were similar between groups. Regression analysis showed a significant correlation between WMSI and T-wave amplitude at baseline (R = 0.38, p = 0.01) and at peak dobutamine stress testing (R = 0.50, p = 0.0006). The sensitivity sensitivity, specificity, and accuracy of T-wave changes to detect myocardial viability were 0.27, 0.84, and 0.70, respectively. The sensitivity, specificity, and accuracy of T-wave changes to detect homozonal ischemia were 0.76, 0.27, and 0.46, respectively. In conclusion, dobutamine-induced T-wave changes are associated with a greater extent of wall motion abnormalities both at rest and at peak stress echocardiography, but they are of little value in predicting myocardial viability when analyzed early after myocardial infarction.

Adult↗
PubMed1999

Effect of cisplatin and paclitaxel on plasma free tryptophan levels. An in vitro study.

UNLABELLED: Emesis is a common side effect of some antineoplastic drugs. Cisplatin (CP) induces a biphasic pattern of emesis referred to as acute (AE) and delayed (DE) emesis. The serotonergic system plays a major role in the pathogenesis of CP-induced AE, as suggested by the therapeutic efficacy of 5HT3 receptor antagonists. The pathogenesis of CP-induced DE are not clear. To date, there are no pharmacological agents which satisfactorily control DE. We hypothesize that increased availability of tryptophan (TRP) for the synthesis of brain serotonin (5-HT) could, at least in part, contribute to CP-induced DE. In fact, within 2-4 hrs of administration, CP is largely bound to albumin (ALB) with consequent possible displacement of TRP which circulates in plasma mostly (90% of total plasma TRP) bound to its natural carrier, ALB. To test this hypothesis, we studied in vitro the effect of increasing doses of cisplatin on F-TRP in plasma obtained from healthy volunteers. We also tested the effects of therapeutic amounts of paclitaxel, an antineoplastc agent which does not cause emesis. RESULTS: F-TRP concentrations increased in a dose-dependent manner following incubation with cisplatin, in contrast to paclitaxel (PTX). CONCLUSIONS: The preliminary data obtained suggest that CP, but not PTX, at therapeutic doses, increases plasma F-TRP concentrations. This increase has likely negligible relevance in CP-induced AE, which is induced by the 5-HT released by the enterochromaffin cell system, while it might play a role in the pathogenesis of CP-induced DE. In fact, CP binding to ALB is stable for 4-5 days following administration, thus suggesting long-term TRP displacement from ALB and enhanced brain 5-HT synthesis and release. Whether increased TRP availability for 5-HT synthesis might be the pathogenic mechanism for CP-induced DE in vivo, is currently being tested.

Cisplatin↗
PubMed1999

C3 molecules internalize and enhance the growth of Lewis lung carcinoma cells.

C3 molecules from normal murine serum are mainly bound to Lewis lung carcinoma cells (3LL) that do not express CRs, mainly through covalent binding as determined by the appearance of bands stained with anti-C3 and larger than 190 kD in immunoblots of proteins in whole cell extracts. Methylamine-treated, or zymosan-treated normal mouse serum, heat inactivated, or EDTA-treated murine serum resulted in low C3 deposition on 3LL cells, as indicated by fluorescence tests and immunoblotting. Cytofluorimetric studies showed that C3 molecules bound to 3LL cells were internalized in a time- and temperature-dependent process. This was confirmed by electronmicroscopic studies. The conditions allowing C3 fixation to acceptor sites and subsequent internalization increased cell proliferation. This was also true, when serum from mice genetically deficient in C5 was used which stresses the role of C3 in contrast to effects of membrane attack complex formation.

Animals↗
PubMed1999

Bacterium-dependent induction of cytokines in mononuclear cells and their pathologic consequences in vivo.

Viridans streptococci are a heterogeneous group of gram-positive bacteria that are normal inhabitants of the mouth. These organisms are thought to contribute significantly to the etiology of infective endocarditis, although recently they have been implicated in serious infections in other settings. Another group of oral bacteria, gram-negative anaerobes, is associated with chronic dental infections, such as periodontal diseases or endodontic lesion formation. We evaluated the ability of the oral pathogens Streptococcus mutans and Porphyromonas endodontalis to induce a pathogenic response in vivo, with the goal of quantifying the inflammatory response in soft tissue by measuring leukocyte recruitment and hard tissues by measuring osteoclastogenesis. S. mutans induced a strong inflammatory response and was a potent inducer of osteoclast formation, while P. endodontalis was not. To further study the mechanisms by which P. endodontalis and S. mutans elicit significantly different levels of inflammatory responses in vivo, we tested the capacity of each to induce production of cytokines by mononuclear cells in vitro. S. mutans stimulated high levels of interleukin-12 (IL-12), gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha), all of which are associated with inflammation, enhanced monocyte function, and generation of a Th1 response. In contrast, P. endodontalis stimulated production of IL-10 but not of TNF-alpha, IL-12, or IFN-gamma. These results demonstrate that oral pathogens differ dramatically in their abilities to induce inflammatory and immunoregulatory cytokines. Moreover, there is a high degree of correlation between the cytokine profile induced by these bacteria in vitro and their pathogenic capacity in vivo.

Animals↗
PubMed1999

T cell reactivity to human insulinoma cell line (CM) antigens in patients with type 1 diabetes.

Autoimmune (type 1) diabetes mellitus results from a progressive destruction of insulin secreting beta cells operated by T lymphocytes in pancreatic islets. Circulating autoreactive T cells to specific beta cell antigens are detected in patients with type 1 diabetes. To date, several beta cell autoantigens have been identified in this disease (GAD, IA-2, 38kD secretory protein, insulin, ICA69 etc.), however, it is possible that also other unidentified self molecules contribute to trigger beta cell autoimmunity. In this study we used the human insulinoma cell line CM as source of beta cell antigens to detect reactive T lymphocytes in patients with type 1 diabetes mellitus. This cell line has been previously shown to express a number of recognized beta cell antigens. Since the expression of several beta cell antigens is affected by glucose stimulation we tested two preparations of CM cells cultured under different conditions containing low (0.8 mM) and high glucose concentration (11 mM). T cell proliferation was measured using cells from 32 patients with type 1 diabetes (19 of recent onset and 13 at 3 to 22 months from diagnosis) and 27 age-matched control subjects. A significant increase in T cell proliferation to CM cells grown in high glucose conditions (11 mM) (p < 0.05) was found in type 1 diabetic patients compared to controls. No significant differences were observed when using CM cells cultured at the low glucose concentration. Furthermore, the response to both extracts of CM cells was independent of disease duration (p = 0.6 for both CM cells cultured at 0.8 and 11 mM glucose). These data indicate that T cell reactivity to homogenates of CM cells is detectable in patients with type 1 diabetes and suggest that this human insulinoma cell line is an interesting potential source of beta cell material for immunological studies of autoimmune diabetes.

Adolescent↗
PubMed1999

Mycoplasma arginini enhances cytotoxicity of thioglycollate-elicited murine macrophages toward YAC-1 tumor cells through production of NO.

Bacterial products stimulate macrophage tumoricidal activity through release of tumor necrosis factor (TNF) and nitric oxide (NO). We show here that thioglycollate-elicited macrophages acquire cytotoxic activity when cocultured with Mycoplasma arginini-infected YAC-1 tumor cells and release TNF and NO. Fixed mycoplasma-infected cells, supernatants from infected-cell cultures, or purified heat-killed mycoplasma obtained from cell-free cultures were all able to induce TNF and NO production. Thus, the mycoplasma per se and not a product of infected cells induce the release of these molecules. Addition of prostaglandin E2 (PGE2) to the cocultures, which reduced TNF release, or antibodies to TNF, did not affect macrophage cytotoxicity nor NO release. Inhibition of NO production by L-NAME or aminoguanidine reduced the cytotoxicity, and treatment with a NO donor was toxic to YAC-1 cells. These results indicate that M. arginini activates thioglycollate-elicited murine macrophages for NO and TNF release increasing their cytotoxic activity toward YAC-1 cells and that this activity is dependent on NO but not TNF release.

Animals↗
PubMed1999

A study on bronchial responsiveness to methacholine in subjects with untreated autoimmune hyperthyroidism.

Because hyperthyroidism can mimic respiratory disorders with dyspnoea, this study was carried out in order to determine whether bronchial hyperresponsiveness is more frequent in hyperthyroid patients versus controls. Eighteen nonatopic subjects with newly-diagnosed untreated Graves' disease and 18 control subjects entered the study. All subjects underwent an aspecific bronchial provocation test with methacholine. Bronchial hyperresponsiveness was diagnosed in seven patients with hyperthyroidism and in two controls, with no statistically significant difference between the groups (Fisher's exact test; p = 0.1212). In conclusion, these results suggest that hyperthyroidism is not associated with a higher frequency of bronchial hyper-responsiveness to methacholine with respect to euthyroid subjects.

Adolescent↗
PubMed1998

Membrane targeting sequences in tombusvirus infections.

Infection of Nicotiana benthamiana cells with cymbidium ringspot (CymRSV) and carnation Italian ringspot (CIRV) viruses results in the formation of conspicuous membranous bodies [multivesicular bodies (MVBs)], which develop from modified peroxisomes or mitochondria, respectively. The organelle targeting signal is located in the proteins of 33 kDa (CymRSV) or 36 kDa (CIRV) encoded by ORF 1, which contain an N-terminal hydrophilic portion followed by two predicted hydrophobic transmembrane segments. Biochemical analysis showed that the 33- and 36-kDa proteins are integral membrane proteins. By exchanging small portions of the ORF 1 sequence between the infectious full-length clones of the two viruses, hybrid constructs were obtained of which the in vitro synthesized RNA was inoculated to N. benthamiana plants and protoplasts. The structure of infectious clones suggested that both the N-terminal hydrophilic region and the transmembrane segments of the ORF 1-encoded proteins specify which organelle is involved in the synthesis of MVBs. Mutational analysis of the CIRV 36-kDa protein also suggested the presence of an internal mitochondrial targeting sequence similar to that found in several normal host proteins that are synthesized in the cytoplasm and transported to mitochondria. The CymRSV 33-kDa protein did not contain the obvious consensus signals thought to be characteristic of proteins targeted to peroxisomes, and an mitochondrial targeting sequence motif was not evident.

Amino Acid Sequence↗
PubMed1998

Lipid mediators, tumor necrosis factor and nitric oxide and their interactions in immune-complex-induced lung injury.

We investigated the contribution of eicosanoids, platelet-activating factor, tumor necrosis factor and nitric oxide to the neutrophil influx and development of pulmonary haemorrhagic lesions following immune-complex-induced pneumonitis in rats and possible interactions between these mediators. Increased levels of leukotriene B4 and tumor necrosis factor, measured by enzyme immunoassay and L-929 cytotoxicity assay, were found in the bronchoalveolar lavage 1 and 4 h after induction of the reaction, respectively, and their release was dependent on the previous generation of platelet activating factor. Antagonism of leukotriene B4 receptors by RO-0254094 (2-[(5-carboxypentyl])oxy]-6-[6-[3,4-dihydro-4-oxo-8-propyl-2H-1-benzopy ran-7-yl)oxy]hexyl] benzenepropanoic acid), inhibition of nitric oxide synthesis by L-NAME (Nw-nitro-L-arginine methyl ester) and antagonism of PAF-receptors by WEB-2170 (5-(2-chlorphenyl)-3-4-dihydro-10-methyl-3-((4-morpholinyl)carbony l)-2 H,7H-cyclopenta (4,5)thieno(3,2-f)(1,2,4)-triazolo-4,3,a)91,4)diazepine), significantly inhibited the intensity of haemorrhage, evaluated by the increased levels of extravascular hemoglobin in homogenates of lung tissues. Little evidence support the role of tumor necrosis factor in these lesions. The infiltration of neutrophils, evaluated by measuring myeloperoxidase in homogenates of lungs, was reduced by compounds L-663,536 (3-[1-(4 chlorobenzyl)-3-t-butyl thio-5-isopropylindol-2-yl]-2-2-dimethylpropanoic acid), WEB-2170 and L-NAME. These results indicate that neutrophil infiltration and haemorrhagic lesions in immune-complex-induced lung inflammation are mediated by platelet activating factor, leukotriene B4 and nitric oxide and point out to interesting interactions between these mediators.

Animals↗
PubMed1998

Dose variation at bone/titanium interfaces using titanium hollow screw osseointegrating reconstruction plates.

PURPOSE: To evaluate dose variations at bone/titanium interfaces in an experimental model designed to simulate postoperative radiotherapy in patients with mandibular reconstructions using a titanium hollow-screw osseointegrating reconstruction plate (THORP) system. MATERIALS AND METHODS: The model consisted of a 25 x 25 x 10 mm3 block of fresh bovine femoral diaphysis, to the surface of which a segment of THORP system reconstruction plate was fixed by means of a solid titanium screw 4 mm in diameter and 10 mm in length. Using specially designed thermoluminescent dosimeters (TLD) 2 mm in diameter and 0.13 mm in thickness, dose measurements were carried out at four distances from the screw axis (0.1, 0.3, 0.6, and 1 mm). 60Co and 6-MV photon beams were used at incidences both perpendicular and parallel ("axial") to the screw axis. RESULTS: For 6-MV X-ray beams incident perpendicular to the screw axis, the maximum dose enhancement (due to backscatter) and the maximum dose reduction (due to attenuation) at the bone/titanium interface were 5% (+/- 2%) and 6% (+/- 2%), respectively. The corresponding values for 60Co beams were 6% (+/- 5%) and 10% (+/- 5%). For the axial incidences, a maximum dose enhancement of 5-7% was noted for both 6-MV X-rays and 60Co for beams incident on the surface containing the THORP plate segment, whereas beams incident on the opposite surface induced only a very small dose enhancement (2-3%). CONCLUSION: Using a new experimental model, TLD measurements showed only marginally significant dose variations at bone/titanium interfaces around THORP screws, all measured values being very close to the uncertainty limits (+/- 5%) associated with the method. For both 60Co and 6-MV beams, dose variations appeared smaller for axial than for perpendicular incidences. Because photon beams used in head and neck cancer treatment are most often directed parallel to the screw axes, these results suggest that failures of prosthetic osseointegration are unlikely to be explained by an overdosage at the bone/titanium interface.

Animals↗
PubMed1998

Molecular cloning and complete nucleotide sequence of galinsoga mosaic virus genomic RNA.

The complete genomic sequence of galinsoga mosaic virus (GaMV) was determined. The genome consists of 3,803 nucleotides and has five open reading frames (ORFs). The 5' ORF (ORF 1) encodes a protein with predicted molecular mass of 23 kDa and readthrough of its amber stop codon probably yields a 82 kDa protein (ORF 2). ORFs 3 and 4 encode two polypeptides with molecular masses of 8 and 7 kDa, respectively. ORF 5 encodes the 36 kDa capsid protein. Amino acid sequence comparisons revealed that the nonstructural proteins encoded by ORFs 1, 3, and 4 were more similar to the corresponding gene products of tobacco necrosis virus, strain A, than to those of carmoviruses. Conversely, the coat protein was more similar to that of tombusviruses. The readthrough region of the viral replicase (ORF 2) had high sequence homology with that of carmo-, tombus-, and necroviruses. Computer analysis of the protein encoded by ORF 1 as well as of the corresponding product of turnip crinkle (TCV) and melon necrotic spot (MNSV) carmoviruses revealed the presence of a sequence with local hydrophobicity and hydrophobic moment characteristic of mitochondrial targeting sequence which may explain the origin of the carmovirus-induced multivesicular bodies from mitochondria.

Amino Acid Sequence↗