Search PubMed⌕ Search

Biomedical subjects

R Cavallo

Publications and source records attributed to R Cavallo.

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

[Hyponatremia in neurosurgical patients].

Hyponatremia played an essential role in this case, determining the rapid transition from consciousness to a state of coma in female patient who had just come through the critical phase of intensive care. This circumstance underlines the importance of a correct water balance in patients undergoing neurosurgery, as well as a knowledge of the inappropriate antidiuretic hormone secretion (SIADH) syndrome responsible, either alone or in association, for the genesis of severe hyponatremia. In the differential diagnosis of hyponatremia, it is important to recall the role of an often mistaken syndrome (cerebral salt wasting syndrome) characterized by the secretion of a natriuretic factor that has still not been clearly identified.

Brain Injuries↗
PubMed1999

[Giromitra syndrome caused by false morel].

Three cases of mushrooms poisoning (by false morel) with associated gyromitra syndrome, due to a thermolabil toxin are reported. They showed a syndrome like to Amanita phalloides poisoning (gastroenteric symptomatology, diarrhoea) some hours after eating and then neurologic signs; they were hospitalized (without haemolytic signs) and were discharged from hospital a few days later in a good health.

Adult↗
PubMed1998

Interleukin-15 activates proinflammatory and antimicrobial functions in polymorphonuclear cells.

Interleukin-15 (IL-15) is a recently discovered cytokine produced by a wide range of different cell types including fibroblasts, keratinocytes, endothelial cells, and macrophages in response to lipopolysaccharide or microbial infection. This suggests that IL-15 may play a crucial role in the activation of phagocytic cells against pathogens. We studied polymorphonuclear leukocyte (PMN) activation by IL-15, evaluated as enhancement of PMN anti-Candida activity as well as IL-8 production, following stimulation with the cytokine. The PMN response to IL-15 depends on binding to the IL-15 receptor. Our experiments show that binding of a biotinylated human IL-15-immunoglobulin G2b IgG2b fusion protein was competed by the addition of human recombinant IL-15 (rIL-15) or of human rIL-2, suggesting that IL-15 binding to PMN might involve the IL-2Rbeta and IL-2Rgamma chains, which have been shown to be constitutively expressed by PMN. In addition, we show by reverse transcription-PCR and by flow cytometry with a specific anti-IL-15Ralpha chain monoclonal antibody that PMN express the IL-15Ralpha chain at the mRNA and protein levels. Incubation with IL-15 activated PMN to secrete the chemotactic factor IL-8, and the amount secreted was increased by costimulation with heat-inactivated Candida albicans. In addition, IL-15 primed the metabolic burst of PMN in response to formyl-methionyl-leucyl-phenylalanine but was not sufficient to trigger the respiratory burst or to increase the production of superoxide in PMN exposed to C. albicans. IL-15 also increased the ability of PMN to phagocytose heat-killed C. albicans organisms in a dose-dependent manner, without opsonization by antibodies or complement-derived products. In the same concentration range, IL-15 was as effective as gamma interferon (IFN-gamma) and IL-2 in increasing the C. albicans growth-inhibitory activity of PMN. Taken together, these results suggest that IL-15 is a potent stimulant of both proinflammatory and antifungal activities of PMN, activating several antimicrobial functions of PMN involved in the cellular response against C. albicans.

Candida albicans↗
PubMed1997

Armadillo coactivates transcription driven by the product of the Drosophila segment polarity gene dTCF.

The vertebrate transcription factors TCF (T cell factor) and LEF (lymphocyte enhancer binding factor) interact with beta-catenin and are hypothesized to mediate Wingless/Wnt signaling. We have cloned a maternally expressed Drosophila TCF family member, dTCF. dTCF binds a canonical TCF DNA motif and interacts with the beta-catenin homolog Armadillo. Previous studies have identified two regions in Armadillo required for Wingless signaling. One of these interacts with dTCF, while the other constitutes a transactivation domain. Mutations in dTCF and expression of a dominant-negative dTCF transgene cause a segment polarity phenotype and affect expression of the Wingless target genes engrailed and Ultrabithorax. Epistasis analysis positions dTCF downstream of armadillo. The Armadillo-dTCF complex mediates Wingless signaling as a bipartite transcription factor.

Amino Acid Sequence↗
PubMed1997

Armadillo and dTCF: a marriage made in the nucleus.

Within the past year, Armadillo and beta-catenin's role in transducing the Wingless/Wnt signal has been substantially clarified. It is now clear that Armadillo and beta-catenin bind directly to members of the T-cell factor/lymphoid enhancer factor subfamily of HMG box DNA-binding proteins, forming bipartite transcription factors that regulate Wingless/Wnt responsive genes in both Drosophila and vertebrates. These partners not only play key roles in a variety of cell fate decisions during normal development but, when inappropriately activated, contribute to both colon cancer and melanoma.

Animals↗
PubMed1997

Phytosterol compounds having antiviral efficacy.

The present study is focused on the antiviral action patterns obtained in vitro with synthetic sterolester comprising compositions on virus-bearing host cell-lines. Appropriate cell-lines were infected with HIV-1, human Cytomegalovirus (HCMV) and Herpes simplex virus (HSV). There appears to exist a clear anti-infective efficacy for a selected number of such ester compounds, provided they are formulated into spontaneously dispersible concentrates, which in aqueous dilution engender ultramicro-emulsions having micelles in the lowest nanosize region. A significant protection against HIV-induced cytopathogenic effect was demonstrated employing a methyltetrazolium salt reduction assay on HIV-infected MT4 cells when they were incubated with such concentrates. A similar effect was evidenced with the same concentrates, when preincubating concentrated virus, but not the target cells. Antiviral activity appeared to be remarkable also on HCMV infections in vitro, where a blocking effect on immediate-early antigen expression in fibroblast monolayers could be observed. Similarly, HSV-associated glycoprotein antigen in VERO cells also suggests that virus-cell interaction and/or virus multiplication could have been blocked at a very early point of time. This would be quite different from antiviral action-patterns studied so far and imputed into the current models of explanation. Proper solubilization of the employed phytosterol compounds is essential for achieving the described activity modes. The often recommended liposome formulations would not be well suited for such compounds and such purpose, since after dilution they produce aqueous macro-emulsions, only. Furthermore, liposome formulations tend to coalesce and exhibit Marangoni effects.

Antiviral Agents↗
PubMed1996

The murine cytomegalovirus immediate-early 1 protein stimulates NF-kappa B activity by transactivating the NF-kappa B p105/p50 promoter.

The transcription of murine cytomegalovirus (MCMV) immediate-early (IE) genes is regulated by a large and complex enhancer containing several consensus binding sites for the ubiquitous transcription factor NF-kappa B. To verify whether MCMV, like the human CMV, can activate NF-kappa B-dependent transcription, we transfected murine embryo fibroblasts cells with a construct containing three copies of the NF-kappa B element in front of the homologous minimal MCMV IE1-3 promoter. Upon MCMV infection the reporter gene activity was transactivated to about three-fold above the basal level. The specificity of this transactivation was demonstrated by the lack of any significant effect on the activity of DNA constructs containing either a mutated NF-kappa B trimer or an ATF/CRE trimer. Gel shift assays with a NF-kappa B probe revealed that MCMV infection activated DNA binding proteins showing NF-kappa B characteristics. The DNA-binding activity remained elevated during the course of infection and was associated to an increase in the steady-state mRNA levels for the NF-kappa B subunit p105/p50. Since the promoter of the p105/p50 gene was transactivated by MCMV infection during the period in which the IE proteins are expressed, the role of the two major IE transcriptional regulatory proteins was examined. In cotransfection experiments, the IE1 protein transactivated the p105/p50 promoter, whereas the IE3 was ineffective in increasing the transcription of the reporter gene. Taken as a whole, these results demonstrate that MCMV, like its human counterpart, regulates the cellular NF-kappa B activity needed for the initial induction of the IE genes and the progression of the viral replicative cycle.

3T3 Cells↗
PubMed1996

[Epstein-Barr virus infection and lymphoproliferative disorders in patients after renal transplantation].

We have studied EBV infection in renal transplant patients during the first year after transplantation. At trasplantation all patients were EBV seropositive and reactivation of EBV infection was demonstrated in 54% cases after one year. CMV active infection was also demonstrated in 42% of patients with EBV reactivation. No correlation was observed between EBV reactivation and age, sex, immunosuppressive treatment, degree of immunosuppression or donor/recipient HLA matching. A correlation between immunosuppressive treatment, EBV infection and lymphoproliferative disorders (LD) is described in literature, however none of our patients developed LD so far, probably due to the different immunosuppressive protocol employed.

Adult↗
PubMed1996

Aspecific adherence and cytotoxicity of Escherichia coli strains.

Two groups of Escherichia coli were assayed to evaluate hydrophobic characters and the secretion of enzymes and cytotoxic factors. Group 1 included strains isolated from the urine of patients with lower urinary tract infection (UTI) and group 2 included strains from the same sample of asymptomatic subjects. The bacterial hydrophobicity was similar in the two groups and related to their adhesion to plastic surfaces, while both cytotoxic factors (demonstrated using a microscopic and a spectrophotometric technique) and hydrolysing enymes were secreted more by the first group of E. coli. The superior production of these factors may be important in the pathogenesis and in the development of symptomatic UTI infections.

Adult↗
PubMed1995

Interferon-alpha inhibits the murine cytomegalovirus immediate-early gene expression by down-regulating NF-kappa B activity.

Transcription of murine cytomegalovirus (MCMV) immediate-early (IE) genes is regulated by the interaction of cellular transcription factors with a strong viral enhancer controlling promoters flanking both sides of the regulatory sequence. We have previously demonstrated that interferon-alpha (IFN-alpha) inhibits MCMV replication by impairing the transcription of IE genes. To define the cis-acting elements and trans-acting factors involved in this inhibition, permissive murine fibroblasts were transferred with DNA constructs containing the chloramphenicol acetyl transferase reporter gene and portions of the IE enhanced. The region spanning -1185 to -259 relative to the IE1-3 promoter was sufficient to allow IFN-alpha-induced inhibition. Since this segment contains several NF-kappa B sites, cells were transfected with a construct containing three copies of NF-kappa B element in front of the homologous minimal IE1-3 promoter. Upon IFN-alpha treatment the reporter gene activity was strongly reduced, indicating that NF-kappa B binding site is sufficient to confer inhibition. The specificity of this inhibition was demonstrated by the lack of a significant effect on the activity of DNA constructs containing either a mutated NF-kappa B trimer or an ATF/CRE trimer. Gel shift assays with NF-kappa B probes revealed that MCMV infection activated NF-kappa B proteins, whereas IFN-alpha treatment significantly reduced their ability to bind NF-kappa B sites. In cotransfection experiments using various NF-kappa B subunit expression vectors and a reporter driven by three copies of an NF-kappa B element, activation of NF-kappa B-dependent transcription was observed with expression of p65 or combinations of p50-p65. Taken as a whole, these results suggest that IFN-alpha inhibits MCMV IE gene enhancer activity by mechanisms that decrease the availability of virus-induced NF-kappa B transcriptionally active in the nuclei of infected cells.

3T3 Cells↗
PubMed1995

Modulation of HIV-LTR activity by ras oncogenes.

Cotransfection of NIH 3T3 cells with a mammalian expression vector containing a v-Ha-ras gene, together with a plasmid carrying the human immunodeficiency virus (HIV) long terminal repeat (LTR) linked to the chloramphenicol acetyl transferase (CAT) reporter gene, significantly stimulated CAT activity. High HIV LTR activation was also observed in cell lines carrying stably transfected ras oncogenes, activated by point mutation or amplification. By contrast an inactivated form of ras (Ha-ras Asn-17) did not stimulate the HIV-LTR but strongly inhibited its basal activity. Activation of the p21ras protein may thus be one of the signals that regulate LTR driven transcription during HIV infection.

3T3 Cells↗
PubMed1995

Interferon alpha treatment of relapsing-remitting multiple sclerosis: long-term study of the correlations between clinical and magnetic resonance imaging results and effects on the immune function.

Interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) are proinflammatory cytokines which may be involved in the pathogenesis of MS. IFN-alpha counteracts many of the proinflammatory actions of IFN-gamma and TNF-alpha. We treated 20 patients with relapsing-remitting (RR) MS with 9 MIU of recombinant IFN-alpha-2a (rIFN-alpha) (n = 12) or placebo (n = 8) intramuscularly every other day for 6 months. Clinical exacerbations or new or enlarging lesions at serial MRI occurred in 2/12 rIFN-alpha-treated and in 7/8 placebo-treated patients (P < 0.005). Only one new MRI lesion was detected in the rIFN-alpha group, while 27 new or enlarging lesions were detected in placebo group (P < 0.01). Baseline lymphocyte IFN-gamma (19.10 +/- 7.12 U ml-1) and TNF-alpha (18.05 +/- 5.34 pg ml-1) production significantly decreased to 3.03 +/- 0.66 (P < 0.04) (for IFN-gamma) and to 5.78 +/- 0.90 (P < 0.04) (for TNF-alpha) after rIFN-alpha treatment. IFN-gamma and TNF-alpha production was unchanged in the placebo group. rIFN-alpha was tolerated without drop-outs or serious side-effects, but fever, malaise, fatigue (interfering with daily activities in two patients) and leukopenia frequently occurred. High-dose chronic systemic rIFN-alpha might reduce clinical and MRI signs of disease activity in RRMS. The changes in cytokine production suggest that the effect is probably mediated by a down-regulation of proinflammatory cytokine.

Adolescent↗
PubMed1994

Characterization of nuclear factors involved in 202 gene induction by interferon-alpha in murine leukemia cells.

The 5' terminal flanking region of the interferon-inducible gene, 202, contains an interferon-stimulable response element (ISRE), called a GA box, that confers inducibility by interferon(IFN)-alpha, but not by IFN-gamma, on a reporter gene, such as the chloramphenicol acetyltransferase (CAT). Nuclear extracts from L1210 murine leukemia cells, stimulated for various periods of time with IFN-alpha, were mixed with 32P-labeled GA box and analyzed for the presence of retarded complexes in electrophoretic-mobility-shift assays. In addition to a few constitutive retarded complexes, an inducible GA box-binding activity (GAbf-1) appeared after 5 min, peaked at about 2 h, and was still abundant 12 h after IFN-alpha treatment. In the cytoplasmic fraction GAbf-1 was not detectable before 30 min, continued to increase up to 2 h, but had disappeared within 12 h. GAbf-1 activity was not observed in nuclear extracts treated with IFN-gamma, and was not inhibited by prior treatment with the protein-synthesis inhibitor cycloheximide. When the binding properties of GAbf-1 were compared with those of ISGF-3, the primary transcriptional activator for IFN-alpha-induced genes, a different pattern of retarded complexes was observed. Moreover, as observed by immunoblotting analysis, nuclear extracts from IFN-alpha-treated L1210 cells did not contain the p91/84 subunit of the ISGF3, the best characterized nuclear complex activated by IFN-alpha. Altogether these results indicate that GAbf-1 may be a novel transcription factor exploited by IFN-alpha to activate the 202 inducible gene in murine pre-B leukemia cells.

Animals↗
PubMed1994

Effect of ceftriaxone on the phagocytosis and intracellular killing of Staphylococcus aureus by human macrophages.

The efficacy of an antimicrobial agent in the treatment of infections depends upon the interactions of bacteria, antibiotic and phagocytes. The influence of ceftriaxone on the phagocytic and bactericidal activity of human macrophages in vitro and ex vivo was investigated. At concentrations one-half the minimum inhibitory concentration (1/2 x MIC) the antibiotic caused in vitro a significant enhancement of phagocytosis and a reduction in the survival of intracellular Staphylococcus aureus. The distinction between any effect of ceftriaxone on the staphylococci and the macrophages was made by exposure of each of them to the antibiotic before they were incubated together. The results suggest that ceftriaxone may have a direct positive action on macrophages, possibly by interfering with the cellular membrane functions and hence enhancing engulfment of bacteria. The ex vivo data seem to corroborate this hypothesis.

Animals↗
PubMed1994

Chronic systemic high-dose recombinant interferon alfa-2a reduces exacerbation rate, MRI signs of disease activity, and lymphocyte interferon gamma production in relapsing-remitting multiple sclerosis.

We report a randomized, double-blind, placebo-controlled pilot trial of systemic high-dose recombinant interferon alfa-2a (rIFNA) in 20 patients with relapsing-remitting (RR) multiple sclerosis (MS). Patients received 9 million IU rIFNA (n = 12) or placebo (n = 8) intramuscularly every other day for 6 months. Clinical exacerbations or new or enlarging lesions on serial MRI occurred in two of 12 rIFNA-treated and in seven of eight placebo-treated patients (p < 0.005). There was only one enlarging MRI lesion in the rIFNA group, whereas 27 new or enlarging lesions were present in the placebo group (p < 0.01). Baseline lymphocyte interferon gamma production of 19.10 +/- 7.12 IU/ml significantly decreased to 3.03 +/- 0.66 IU/ml (p < 0.04) in the rIFNA group, whereas production was unchanged in the placebo group. The rIFNA was tolerated without dropouts or serious side effects, but fever, malaise, fatigue (interfering with daily activities in two patients), and leukopenia occurred frequently. Neuropsychological tests excluded neurotoxicity. High-dose systemic rIFNA might reduce clinical and MRI signs of disease activity in RR MS and should be investigated in larger trials.

Adolescent↗
PubMed1994

Presence of murine retroviral sequences in human cell line transplanted in immunosuppressed SCID-mice.

The SCID-hu mouse, a severe combined immunodeficient mouse transplanted with human hematopoietic cells, has been proposed as an experimental model for HIV-1 infection. However, like other animal models for infectious diseases, the SCID-hu mouse should provide the replication of the experimental agent without conferring any alteration during growth in the host. In this study using Southern blot hybridization, in situ hybridization and PCR analysis we demonstrate the presence of specific murine retroviral sequences in human cells recovered from the in vivo passages in SCID mice. Since the acquisition of endogenous retrovirus by human cells was demonstrated after their growth in nude mice, the data reported here extend this observation to the SCID model.

Animals↗
PubMed1993

Interferons inhibit onset of murine cytomegalovirus immediate-early gene transcription.

Treatment of NIH 3T3 fibroblasts with interferon-alpha or interferon-gamma (IFN-alpha or IFN-gamma) significantly reduced murine cytomegalovirus (MCMV) replication. Determination of viral DNA in the nuclei of the infected cells before onset of DNA replication demonstrated that virus uptake, transport to the nucleus, and DNA stability were not decreased. Analysis of the virus specified mRNAs soon after infection revealed that in the cells exposed to IFNs expression of the immediate early (IE) genes was strongly reduced. Nuclear run-off transcription analysis showed that this inhibition is due to significant reduction of IE gene transcription rates following IFN treatment. Since transcription of the MCMV IE region is regulated by a strong enhancer element, a construct containing the chloramphenicol acetyltransferase (CAT) reporter gene, driven by an 1.2 kb segment spanning the enhancer and IE1/3 promoter region of the IE transcription unit, was transfected into NIH 3T3 cells. Treatment with IFN-alpha or IFN-gamma after transfection strongly reduced CAT activity compared to untreated controls. In an attempt to define a negative IFN-responsive element in the IE enhancer, a series of deletion mutants driving the CAT reporter gene were transfected into NIH 3T3 cells that were then treated with IFN-alpha. With the sole exception of the construct containing the minimal MCMV IE1/3 promoter (-102 to the cap site), all other deletion mutants were strongly down-regulated by IFN-alpha-treatment. Taken as a whole, these results suggest that IFNs inhibit MCMV replication by impairing the transcription of the IE transcription units, and that this negative regulation is carried out by sequences scattered throughout the IE enhancer region.

3T3 Cells↗