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Biomedical subjects

N D'Urso

Publications and source records attributed to N D'Urso.

13 recordsLinked to original sources
PubMed1991

Hepatitis C virus-related chronic liver disease with autoantibodies to liver-kidney microsomes (LKM). Clinical characterization from idiopathic LKM-positive disorders.

This study was carried out on 33 patients who were sero-positive for liver-kidney microsomal antibodies (LKM) in order to examine clinical features and the presence of underlying hepatitis C virus infection. Twenty-four sera were positive for antibodies against HCV (anti-HCV) as detected by enzyme immunoassay and confirmed by recombinant immunoblot assay. These patients had chronic liver disease and the majority of those treated with interferon responded favourably. Three of the nine anti-HCV-negative patients had idiopathic chronic hepatitis and two responded favourably to steroids. Two patients were diagnosed as having toxic hepatitis and the other four had various extrahepatic disorders without evidence of liver involvement. The immunoblotting analysis showed reactivity with a 50 kDa microsomal protein which presumably corresponded to cytochrome P-450 db1 both in anti-HCV-positive and -negative sera. In addition a few anti-HCV-positive sera also reacted with a 35 kDa microsomal antigen. Autoimmune markers different from LKM were absent in both groups. The high prevalence of antibodies to the hepatitis C virus among LKM-positive sera confirms that this infection plays a role in forms of chronic hepatitis that had previously been labelled autoimmune. In patients with LKM the presence of anti-HCV may help to forecast a therapeutic response to interferon, while its absence may forecast response to steroid therapy.

Adolescent↗
PubMed1991

Chronic active hepatitis B. Interferon-activated natural killer-like cells against a hepatoma cell line transfected with the hepatitis B virus nucleic acid.

In a rapid 51Cr release assay, peripheral blood mononuclear cells from 12 healthy donors did not lyse the hepatitis B virus deoxyribonucleic-acid-transfected human hepatoma cell line 2.2.15, but under the same experimental conditions they did lyse K562 cells. Peripheral blood mononuclear cells from 10 out of 16 patients with chronic active hepatitis B exhibited cytotoxic activity against 2.2.15 cells in the presence of a relatively reduced natural killer cell activity to the K562 cell target. Enhancement of the cytotoxic activity to 2.2.15 cells was statistically significant in the group of patients being treated with leukocyte alpha-interferon. The activity was not influenced by the degree of human leukocyte antigen type matching between effector and target, and was enhanced by depletion of T-cells and by in vitro interferon treatment. These results therefore support the concept of a natural killer-like cell activated by clinical administration of interferon in chronic active hepatitis B patients. This cell effector was lytic for the virus B negative HEP-G2 cells also. However, T-cells purified from a few patients failed to lyse the HEP-G2 while lysing the 2.2.15 target, thus indicating that a preferential recognition of the virus-infected target may be exerted by certain T-lymphocyte subsets. The use of the human leukocyte antigen type defined, highly differentiated, hepatitis B virus releasing 2.2.15 cell line as target for fresh lymphocytes in this cytolytic assay did not disclose cytolytic T-cells in an obvious way. Further manipulation of this system perhaps using T-cell clones may be the next step to exploit the investigative possibilities offered by the availability of the 2.2.15 cell target.

Adult↗
PubMed1988

Vanadate-treated baby hamster kidney fibroblasts show cytoskeleton and adhesion patterns similar to their Rous sarcoma virus-transformed counterparts.

Rous sarcoma virus-transformed baby hamster kidney fibroblasts (RSV/B4-BHK) adhere to a fibronectin-coated substratum by means of dot-like adhesion sites called podosomes in view of their shape and function as cellular feet (Tarone et al.: Exp Cell Res 159:141, 1985). Podosomes concentrate tyrosine-phosphorylated proteins, including pp60v-src, and appear in many cells transformed by oncogenes coding for tyrosine kinases. In this paper we used orthovanadate, an inhibitor of phosphotyrosine phosphatases, in order to increase the cellular concentration of phosphotyrosine and to study whether this treatment induced the cytoskeleton remodeling leading to the formation of podosomes. Indeed, orthovanadate (10-100 microM) induced in a time- and dose-dependent manner the redistribution of F-actin and the formation of podosomes in BHK cells. Cytoskeleton remodeling occurred along with a marked increase of tyrosine phosphorylated proteins. The vanadate effect on the cytoskeletal phenotype was enhanced by the simultaneous treatment of cells with a phorbol ester. Under the latter conditions almost all BHK cells showed podosomes. The vanadate effect was reversible insofar as podosomes and tyrosine-phosphorylated proteins disappeared. Then, vanadate treatment of normal cells induced the cascade of events leading to the cytoskeletal changes typical of transformation and suggested that the transformed cytoskeletal phenotype may be primarily induced by the tyrosine phosphorylation of unknown target(s) operated by endogenous kinases.

Actin Cytoskeleton↗
PubMed1988

Vinculin, talin, and integrins are localized at specific adhesion sites of malignant B lymphocytes.

The microanatomy of the dot-shaped, close-contact sites called podosomes and the mechanism of their formation have been investigated in vitro in the malignant lymphocytes of B chronic lymphocytic leukemia (B-CLL). In this paper the authors demonstrate that in B-CLL podosomes: (1) vinculin, talin, and beta 2 integrin (CD18) rings surround an F-actin core; (2) the beta 1 integrin is localized within the F-actin core; (3) the beta 3 integrin is not present. This distribution and organization of adhesion-related molecules appears to be unique to B-CLL lymphocytes, since it has not been observed in normal B cells. B-CLL adhesion and podosome formation are inhibited by the synthetic peptide GRGDSP that contains the Arg-Gly-Asp (RGD) sequence.

Amino Acid Sequence↗
PubMed1987

Human endothelial cells are target for platelet-activating factor. I. Platelet-activating factor induces changes in cytoskeleton structures.

Platelet-activating factor (PAF), but not its deacetylated and biologically inactive metabolite lyso-PAF, in a dose dependent-manner (0.1 to 10 nM), induces human endothelial cells (EC) in culture to change their shape. EC retract and tend to lose reciprocal contact, whereas the distribution of stress fibers is changed and the cells tend to assume a migratory phenotype. The normal localization of vinculin at streaks corresponding to adhesion plaques and located at stress fiber endings is mostly lost and replaced by diffuse distribution of this protein related to the cell-substratum adhesion complex. The effects of PAF are appreciable after 10 min, become maximal after 30 min, and are fully reversible. The disappearance of F-actin in stimulated EC was analyzed by measuring the fluorescence of the cells after staining with fluorosceinated phalloidin, PAF, but not lyso-PAF and the enantiomer of PAF ([S] form), decreases in a time- and concentration-dependent fashion the fluorescence of the cells stained with fluoresceinated phalloidin. EC grown on fibronectin-coated polycarbonate filters restrict the diffusion of 125I-albumin; PAF promotes 125I-albumin diffusion with a concentration dependency similar to that for the PAF-induced cytoskeleton changes. Four different PAF-receptor antagonists belonging to four different series, CV-3988 (PAF-related framework), BN52021 (a natural terpenoid), BN53013 (a natural lignan) and 48740 RP (a synthetic antagonist) prevent the alteration induced by PAF. These findings, coupled to the lack of effect of the enantiomer of PAF ([S] form), support the existence of a specific mechanism of PAF-mediated activation of EC, most probably mediated by a putative receptor. These results explain part of the PAF mechanism of action in inducing the increase of vascular permeability in vivo.

Actin Cytoskeleton↗
PubMed1978

Plasma and semen androgens in normospermic and dysspermic subjects.

The seminal and plasmatic concentrations have been examined of testosterone, 5 alpha-dihydrotestosterone, and delta 4-androstenedione in normospermic and dysspermic subjects. The results obtained did not provide evidence of significant differences of androgen levels in fertile, hypofertile and sterile men.

Adult↗