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M Salio

Publications and source records attributed to M Salio.

30 records · Page 2Linked to original sources
PubMed1996

The angiogenesis induced by HIV-1 tat protein is mediated by the Flk-1/KDR receptor on vascular endothelial cells.

The HIV-1 Tat protein transactivates HIV, viral and some host cell genes. Tat can be released by infected cells and acts extracellularly in the microenvironment, regulating functions of immunocompetent and mesenchymal cells. One of the most striking effects of Tat is the induction of a functional program in vascular cells related to angiogenesis and inflammation (migration, proliferation and expression of plasminogen activator inhibitor-1 and E selectin). Tat induces growth of Kaposi's sarcoma (KS) spindle cells and is angiogenic in vivo and in transgenic mice10-12. We previously reported that Tat is a direct angiogenic factor and noted the Tat arginine- and lysine-rich sequence is similar to that of other potent angiogenic growth factors, such as vascular endothelial growth factor-A (VEGF-A). It is possible that Tat mimics one of these factors by interacting with its growth factor tyrosine kinase receptor. Here we demonstrate that Tat specifically binds and activates the Flk-1/kinase insert domain receptor (Flk-1/KDR), a VEGF-A tyrosine kinase receptor (for review see ref. 13), and that Tat-induced angiogenesis is blocked by agents blocking the Flk-1/KDR receptor. Endothelial cell stimulation by Tat occurs in the absence of activation of FLT-1, another VEGF-A tyrosine kinase receptor.

Animals↗
PubMed1995

Over-expression of CD3 epsilon transgenes blocks T lymphocyte development.

We have reported previously that mice carrying > 30 copies of the human CD3 epsilon transgene completely lose their T lymphocytes and NK cells (36). Here we demonstrate by immunohistology that in the most severely immunodeficient mouse, tg epsilon 26, the thymus is very small, has sizeable vacuoles and does not contain recognizable T lymphocytes except for a small percentage of Thy-1+ cells and B cells. Cell surface phenotyping and TCR alpha and -beta rearrangement studies confirm that the arrest in T lymphocyte development precedes the arrest in rag-1null, rag-2null and TCR beta nuli mice. Since the T cell progenitors in which the arrest occurred were absent in the transgenic mice, indirect approaches were taken to examine the causes of the block in T cell development. Analyses of 12 independently established mutant mouse lines, generated with five different transgenic constructs, revealed that the severity of the abrogation in T cell development was dependent on the number of copies of transgenes. Since the number of transgene copies generally correlated with the levels of expression of the transgenic CD3 epsilon proteins, we concluded that over-expression of the CD3 epsilon protein was the likely cause of the block in T lymphocyte development. The T cell immunodeficiency was caused by either the human or the murine CD3 epsilon protein. Since transgene coded mRNAs were found in significantly higher quantities than endogenous CD3 epsilon mRNAs in fetal thymi on days 13 and 14 of gestation, over-expression took place very early in development, probably prematurely. Over-expression of the CD3 epsilon transgene in thymocyte precursors may therefore affect T lymphocyte development in the absence of TCR and possibly in the absence of the other CD3 proteins. More importantly, over-expression of the CD3 epsilon protein in thymocytes of mice with a low copy number of transgenes had a significant effect on late thymic development. Over-expression of the CD3 epsilon protein in immature thymocytes mimicked the effects caused by exposure of CD4- CD8- thymocytes to anti-CD3 epsilon treatment: apoptosis and lack of TCR beta expression. We therefore speculate that in the homozygous tg epsilon 26 animals the arrest in T cell development was caused by excessive signal transduction events rather than by a toxic effect of the transgenic protein.

Amino Acid Sequence↗
PubMed1991

Chest wall involvement by lung cancer: computed tomographic detection and results of operation.

The aim of this prospective study was to evaluate: (1) the role of computed tomographic scanning in predicting chest wall invasion by peripheral lung cancer and (2) the results of operation according to the depth of chest wall involvement and other potential indicators of long-term survival. One hundred twelve patients with non-small cell lung cancer adjacent to the pleural surface who underwent computed tomographic scanning and subsequent thoracotomy were entered into this study. Tumor invasion was confined to the visceral pleura in 53 patients, to the parietal pleura in 18 patients, and to intercostal muscles in 25 patients; invasion extended beyond this layer in 16 patients. The computed tomographic criteria for chest wall invasion were (1) obliteration of the extrapleural fat plane, (2) the length of the tumor-pleura contact, (3) the ratio between the tumor-pleura contact and the tumor diameter, (4) the angle of the tumor with the pleura, (5) a mass involving the chest wall, and (6) rib destruction. The computed tomographic criteria 1 and 3 were significantly related to pathologic findings. Sensitivity was 85% for criterion 1 and 83% for criterion 3, specificity being 87% and 80%, respectively. Long-term survival of patients with T3 disease critically depended on the lymph node state and completeness of resection. The adenocarcinoma cell type and the T4 category were unfavorable prognostic factors. The depth of chest wall invasion did not affect survival, except for extensive rib and soft tissue infiltration. En bloc resection yielded better results than discontinuous resection.

Adenocarcinoma↗
PubMed1989

[Allergic bronchial asthma: an evaluation of immunofluorescence technics on bronchial biopsies].

Although the immunofluorescence technique has mostly been applied to renal diseases, it may be of use in the examination of lung tissue. Immunofluorescence tests on bronchial bioptic samples can show: 1) presence of IgE, IgA, IgM, IgG and complement factors; 2) their location on the bronchial mucosa; 3) their relationships with epithelioid cells, mast cells and plasma cells. Patients with atopic asthma were examined. Bioptic samples were taken from the main bronchi and treated by immunofluorescence. Cellular positivity was found for IgE, IgA, IgM and complement components.

Asthma↗
PubMed1987

[Echography in the study of thoracic pathology. I--Indications and limitations].

The role of echography in the study of the thorax is evaluated: after reporting the technical limits due to the peculiar anatomy of this region, personal experience is presented. This method extremely precise to define the solid or liquid nature of tightly adherent to the chest wall lesions, but it is non specific to assess their benign or malignant behaviour. Ultrasounds have their on limits in drawing the extension of such lesions; these limits have been overcome by CT and MR. Finally the usefulness of the method in studying the diaphragm and its pathology is briefly described.

Evaluation Studies as Topic↗
PubMed1987

[Transthoracic needle aspiration in infectious pathology].

A study was conducted on 20 patients with isolated or multiple patches of doubtful significance in the framework of neoplastic or infectious pathologies or in the presence of probably infectious diffuse or localised pulmonary infiltrations in immunodepressed patients or those in whom broad spectrum antibiotic treatment had failed. Percutaneous needle aspiration and sterile brushing was performed for the purpose of bacteriological examination in all patients. The result showed the clear superiority of needle aspiration (75% positive) over sterile brushing (25%). The first method is therefore recommended for use in the diagnosis of so-called "difficult" lung pathologies.

Adult↗
PubMed1986

[Antibacterial and antifungal activity of isoflurane and common anesthetic gases].

An in vitro analysis was conducted to investigate the hypothetical antibacterial and antimycotic activity of the common anesthetic gases (halothane, enflurane, isoflurane, methoxyflurane) in view of the clinical absence of bronchopulmonary pathology after inhalation narcosis despite the many risk factors involved. For this purpose scalar dilutions of the four gases were prepared on cultures of Klebsiella pneumoniae and Candida albicans and the antibacterial action of the gases was tested in vitro. Even with the weaker concentrations used, halothane and methoxyflurane totally inhibited both microorganisms. Enflurane had less effect on Klebsiella p. and almost none on Candida. Isoflurane, a new halogen ether anesthetic was found to have an excellent inhibitory effect. In conclusion it is hypothesised that the anesthetic gases considered might have an in vivo antibacterial activity considering the experimental results obtained in vitro.

Anesthetics↗
PubMed1986

[Isolated endobronchial metastases].

Endobronchial metastases account for about 5% of autoptic findings in patients with multiple secondary locations. Five cases are reported of patients with malignant neoplasms in various organs with metastases to the trachea and the large bronchi without involvement of the pulmonary parenchyma and therefore with negative radiographic and CT scan findings.

Adenocarcinoma↗
PubMedDate not supplied

Aspirin does not interact with ACE inhibitors when both are given early after acute myocardial infarction: results of the GISSI-3 Trial.

Aspirin (ASA) and angiotensin-converting enzyme inhibitor (ACEi) therapy reduce mortality when administered early after the onset of myocardial infarction. ASA can antagonize some effects of ACEi therapy by inhibiting the synthesis of vasodilating prostaglandins; however, the evidence for this effect from large controlled trials is contradictory. The authors analyzed a database of 18,895 patients of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardio-3 (GISSI-3) Trial in which patients were allocated either to receive lisinopril or not to receive lisinopril within 24 hours of the onset of symptoms of myocardial infarction. The aim of the study was to verify the possible negative interaction between ASA and the ACEi lisinopril in the postacute phase of acute myocardial infarction. Of 18,895 analyzable patients, 15,841 received ASA at entry. Overall lisinopril reduced 42-day mortality from 7.1% to 6.3%. In patients receiving ASA, mortality was reduced by lisinopril from 6.0% to 5.4%, and from 13.0% to 10.8% in patients not receiving ASA. The difference in proportional reductions of mortality corresponds to the fact that a more marked lisinopril effect is seen in patients at higher baseline risk across all study subgroups, one of which coincides with the no-ASA group. The analysis of the inhospital incidence of major clinical events did not reveal a potentially negative interaction between ASA and lisinopril. The same findings were obtained from the analysis of reinfarction at 42 days. The interaction between ASA and lisinopril was also tested by multivariate analysis adjusted for confounding variables at entry, and the interaction tests were not statistically significant. Serum creatinine levels at 42 days were significantly higher in lisinopril group than in the control group. Systolic and diastolic blood pressures in lisinopril group were significantly lower than controls at 42 days. The effect of lisinopril on creatinine and blood pressure did not differ between the ASA and no-ASA groups. ASA does not decrease the mortality benefit of early lisinopril after myocardial infarction, nor does it increase the risk of major adverse events. Lisinopril is safe and effective when given early after the onset of myocardial infarction, regardless of a concomitant administration of ASA started early and continued over a 6-week period.

Aged↗