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Biomedical subjects

D Catalano

Publications and source records attributed to D Catalano.

At least 19 recordsLinked to original sources

MitoNuc and MitoAln: two related databases of nuclear genes coding for mitochondrial proteins.

Mitochondria, besides their central role in energy metabolism, have recently been found to be involved in a number of basic processes of cell life and to contribute to the pathogenesis of many degenerative diseases. All functions of mitochondria depend on the interaction of nuclear and organellar genomes. Mitochondrial genomes have been extensively sequenced and analysed and the data collected in several specialised databases. In order to collect information on nuclear coded mitochondrial proteins we developed MitoNuc and MitoAln, two related databases containing, respectively, detailed information on sequenced nuclear genes coding for mitochondrial proteins in Metazoa and yeast, and the multiple alignments of the relevant homologous protein coding regions. MitoNuc and MitoAln retrieval through SRS at http://bio-www.ba.cnr.it:8000/srs6/ can easily allow the extraction of sequence data, subsequences defined by specific features and nucleotide or amino acid multiple alignments.

Databases, Factual↗

Update of KEYnet: a gene and protein names database for biosequences functional organisation.

KEYnet is a database where gene and protein names are hierarchically structured. Particular care has been devoted to the search and organisation of synonyms. The structuring is based on biological criteria in order to assist the user in data search and to minimise the risk of information loss. Links to the EMBL data library by the entry name and the accession number are implemented. KEYnet is available through the WWW at the following site: http://www.ba.cnr.it/keynet.html

Databases, Factual↗

[Hydatidiform mole with coexistent fetus. Cytogenetic features, diagnosis, and management].

Hydatidiform mole with coexistent fetus is an unusual entity caused by two distinct types of pregnancy: the first one is a partial hydatidiform mole, while the second is a twin pregnancy in which a mole coexists with a normal fetus. In these two separate genetic entities, the counseling and the mother-fetus prognosis are different. Two cases of mole with coexistent fetus are reported: a partial hydatidiform mole typically tripliod and a partial mole with unusual diploid karyotype. Prenatal diagnosis is remarkable for the evaluation of fetus development related with his karyotype. Triplody excludes all hope of a non-malformed surviving child and termination of pregnancy is desirable, while normal karyotype the possibility of a continuation of pregnancy may be considered.

Adolescent↗

[Hyperthyroidism, therapy with erythropoietin, malnutrition and systolic function in hemodialysis: echocardiography study].

Secondary hyperparathyroidism is a frequent condition of dialysis patients. Endocrine derangements, with disturbance of calcium metabolism are complex, involving bone, heart (left ventricular hypertrophy-dilatation), bone marrow (anemia and erythropoietin resistance), muscle (increase of body fat mass) and insulin resistance. Aim of the study was to assess how these conditions are inter-correlated in the same patients. 45 patients (m 20, f 25; years 61.8 +/- 11.6) in maintenance bicarbonate three-weekly hemodialysis since > 3 years were studied. Cardiac function was assessed by echocardiography (EF%: left ventricular ejection fraction), which showed an inverse correlation both with parathormone (iPTH vs EF%: r = -0.64; p < 0.001) and with erythropoietin (rHu-EPO vs EF%: r = -0.62; p < 0.001). This suggests the possibility of a multi-endocrine resistance in dialysis patients with chronic renal failure, secondary to the degree of malnutrition. Lower lean mass is correlated with hyperparathyroidism (iPTH vs fat mass%: r = 0.37; p < 0.01), with lower left ventricular systolic function (EF% vs fat mass%: r = -0.41; p < 0.005) and with rHu-EPO resistance. Moreover, patients with higher iPTH show a hypercatabolic disposition, assessed as protein catabolic rate (PCR/kg vs iPTH r = 0.54; p < 0.001). This pattern can be a consequence of chronic renal failure, but bio-compatibility of materials can be involved as well.

Body Mass Index↗

KEYnet: a keywords database for biosequences functional organization.

KEYnet is a database where gene and protein names are hierarchically structured. Particular care has been devoted to the search and organisation of synonyms. The structuring is based on biological criteria in order to assist the user in the data search and to minimise the risk of loss of information. Links to the EMBL data library by the entry name and the accession number have been implemented. KEYnet is available through the World Wide Web at the following site: http://www.ba.cnr.it/keynet.html. Recently KEYnet has incorporated specific gene name classifications, which can be browsed starting from the above-mentioned KEYnet home page: the Mitochondrial Gene Names classification and the Rat Gene Names classification. KEYnet database has also been structured in a flatfile format and can be queried through SRS (http://bio-www.ba.cnr.t:8000/srs).

Animals↗

Inhibition of lipopolysaccharide-mediated NFkappaB activation by ethanol in human monocytes.

Alcohol use is typically associated with impaired immunity and increased host susceptibility to infection, partially due to decreased inflammatory response. Acute ethanol exposure has been shown to down-regulate monocyte production of inflammatory cytokines. Activation of the pluripotent transcription factor NFkappaB is a pivotal step in the induction of inflammatory cytokines, chemokines and growth factors. Therefore, we hypothesized that alcohol may alter NFkappaB activation, thus providing a mechanism for the decreased inflammatory cytokine production by monocytes after acute alcohol treatment. We show here for the first time that alcohol inhibits lipopolysaccharide (LPS)-induced NFkappaB activation in human monocytes by decreasing DNA binding of the p65/p50 heterodimer as seen in electrophoretic mobility shift and supershift assays. We also demonstrate that alcohol prevents LPS-induced nuclear translocation of p65 and to a lesser extent that of the p50 subunits. NFkappaB activation is regulated via phosphorylation and proteolytic degradation of IkappaB. Thus, we investigated the effect of acute ethanol treatment on IkappaB in human monocytes. Alcohol did not prevent LPS-induced IkappaBalpha degradation but decreased the levels of phospho-specific IkappaBalpha (Ser32). Finally, for the first time we show that de novo protein synthesis is necessary to bring about the ethanol-mediated inhibition of LPS-induced NFkappaB activation. Consequently, these results suggest that physiologically relevant concentrations of alcohol interfere with NFkappaB activation and thereby may affect the regulation of NFkappaB-controlled gene activation.

Adolescent↗

[Maternal-fetal transmission of HCV. Role of HIV as a risk factor].

BACKGROUND: The aim of this study is to determine the rate of vertical transmission of hepatitis C and to analyse the concomitant infection by HIV as a risk factor. METHODS: We have studied the perinatal transmission of HCV in 22 pregnancies: 14 in women HCV+/HIV-, 8 in women HCV+/HIV+. We have performed the following tests on sera: test RIBA II to search for Ab anti-HCV, alanine transaminase (ALT) evaluation and HCV-RNA research by PCR. These tests were performed on sera from infants at birth and, then, during one year every three months. RESULTS: Within one year Ab anti-HCV disappeared in 20 of 22 pregnancies: two infants positive by Ab anti-HCV were born to HIV+ mothers and they were the only two who showed abnormal ALT values and detectable levels of HCV-RNA. Finally 10 of 14 infants born to HCV+/HIV- mothers were breast-fed and none was infected. CONCLUSIONS: We conclude that HCV mother-to-child transmission is an uncommon event, breast-milking is safety, and the concomitant infection by HIV could represent a risk factor for vertical transmission of hepatitis C.

Female↗

Portal vein pulsatility ratio and heart failure.

PURPOSE: Heart diseases can alter liver volume, morphology, and circulation. The Doppler pulsatility of the portal vein and its pulsatility ratio (PR) have been reported as being closely associated with the right atrial pressure and with the New York Heart Association (NYHA) class. We examined the relationships between measurements of liver and spleen dimensions and blood flow in portal and hepatic veins, assessed noninvasively by Doppler sonography, and compared them with echocardiographic data. METHODS: The study group comprised 87 inpatients with heart failure. The mean age was 64+/-12 years. Patients underwent duplex Doppler sonography of the heart and portal and hepatic veins. RESULTS: Patients with more severe left ventricular failure (NYHA class III-IV) showed more dilatation of the left ventricle and atrium, reduced systolic function, and reduced portal vein mean velocity compared with patients with milder heart failure (NYHA class I-II); in addition, the hepatic vein diameter was increased and portal vein PR was reduced. Considering all patients, significant positive correlations were found between portal vein PR and left ventricular shortening fraction (r= 0.34, p < 0.01) and ejection fraction (r= 0.38, p < 0.001). Significant negative correlations were found between PR and hepatic vein diameter (r= -0.44, p < 0.001), right ventricle diameter (r = -0.38, p < 0.001), left ventricular end-diastolic volume (r = -0.31, p < 0.01), and left atrium diameter (r = -0.33, p < 0.01). Patients with hepatic vein dilatation had increased left ventricular volumes, reduced systolic function indices, and portal vein alterations (increased diameter, reduced mean velocity, and reduced PR). In patients with an ejection fraction of no more than 50%, only PR was significantly reduced, while other sonographic liver measurements were not significantly different. CONCLUSIONS: The effects of cardiac failure on portal blood flow, which declines progressively with worsening cardiac function, is shown better by the pulsatility pattern of the portal vein than by morphologic caval and hepatic vein measurements. PR can be used as a reliable adjunctive sign of heart failure.

Echocardiography, Doppler↗

Regulation of monocyte IL-12 production: augmentation by lymphocyte contact and acute ethanol treatment, inhibition by elevated intracellular cAMP.

IL-12, a monocyte-derived cytokine, is pivotal in activation of cellular immune response and inflammation. Both inflammatory response and cellular immunity are impaired by acute ethanol consumption. Here, we found that in vitro acute ethanol treatment (25-100 mM) results in a dose-dependent and significant increase of IL-12 in IFN-gamma (100 U/ml) plus Staphylococcal enterotoxin B (SEB; 1 microg/ml) stimulated monocytes and mononuclear cells but not in unstimulated cells from non-alcoholic blood donors. There was significantly greater IL-12 production in the MNC population compared to isolated Mphi (P < 0.001). Prevention of monocyte surface contact with either purified T lymphocytes or monocyte-depleted MNC resulted in a significant, 65+/-20%, decrease in IL-12 production regardless of IFN-gamma, SEB or ethanol stimulation suggesting that Mphi T-cell surface contact provides an additional signal for IL-12 production. In addition to cell surface contact, soluble mediators, particularly IL-10 and PGE2 may regulate IL-12 production. The cyclooxygenase inhibitor, Indomethacin (10(-6)M), augmented both IL-12 and IL-10 levels in isolated monocytes and mononuclear cells whether induced by medium, SEB or SEB plus 25 mM ethanol suggesting that regulation of IL-12 production via the cyclooxygenase pathway is independent of IL-10. Finally, elevation of intracellular cAMP levels by dbcAMP treatment consistently inhibited IL-12 as well as IL-10 production in monocytes induced by IFN-gamma or IFN-gamma plus 25 mM ethanol. These data suggest that augmentation of monocyte IL-12 by acute ethanol is not mediated via the cAMP pathway.

Adult↗

Regulation of monocyte interleukin-12 production by acute alcohol: a role for inhibition by interleukin-10.

Acute ethanol treatment results in decreased antigen presentation capacity (Th1-type immunity) and elevated interleukin IL-10 (Th2 cytokine) production in human monocytes. Monocytes can contribute to both Th1 (IL-12) and Th2 (IL-10) immune responses via production of IL-12 and IL-10, respectively. Thus, we tested the hypothesis that acute alcohol treatment might affect Th1/Th2 immune balance by altering monocyte production of IL-12 and IL-10. Neither acute ethanol treatment alone (25 to 100 mM) nor its combination with a bacterial challenge Staphylococcal enterotoxin B (SEB) induced IL-12 production in isolated blood monocytes. In contrast, the same physiological alcohol concentrations increased monocyte IL-10 levels, suggesting that ethanol can induce a dysbalance of monocyte-derived mediator production at the expense of Th1 cytokines. However, we found that monocyte activation with interferon-gamma (IFN-gamma) can prevent the preferential IL-10 induction by ethanol. IFN-gamma (100 units/ml) inhibited monocyte IL-10 production whether induced by 1 microg/ml of lipopolysaccharide (p < 0.01), 1 microg/ml of SEB (p < 0.02), or a combination of bacterial stimulation + ethanol (lipopolysaccharide: p < 0.01). Furthermore, decreased IL-10 was concomitant to an increase in IL-12 production in IFN-gamma-treated monocytes. Moreover, acute ethanol treatment augmented IL-12 production in IFN-gamma-treated monocytes in response to SEB stimulation (25 mM ethanol, p < 0.01; 100 mM ethanol, p < 0.01). Experiments with anti-IL-10 neutralizing antibody show that ethanol may prevent monocyte IL-12 induction via IL-10. These results suggest that inhibition of ethanol-induced IL-10 production by IFN-gamma treatment is permissive for IL-12 induction by alcohol stimulation in monocytes. Thus, our results imply that the presence or absence of IFN-gamma is critical in determining the effect of acute ethanol treatment on monocyte IL-12 versus IL-10 induction.

Adult↗

[Essential thrombocythemia in pregnancy. A case report and general considerations].

Essential thrombocythemia is a rare disease of unknown etiology characterized by an abnormal increase in the platelet count which cannot be explained by other identifiable causes such as malignancy, infection, chronic inflammatory diseases or other myeloproliferative disorders. It rarely affects people less than 50 years of age and may be associated with hemorrhagic or thrombotic tendencies. A care of pregnancy complicated by essential thrombocythemia treated with aspirin, antiaggregating agent, throughout pregnancy and with hydroxyurea, a platelet lowering drug is reported. Also examine are some pathogenetic and therapeutic aspects of the thrombotic tendency secondary to elevated platelet count in pregnancy.

Adult↗

[The role of transvaginal ultrasonography in the screening of ovarian tumors].

BACKGROUND: From January 1992 to March 1996, 1987 women underwent vaginal sonography screening, at the Department of Obstetrics and Gynaecology of the II Faculty of Medicine and Surgery "Federico II" in Naples. This mass screening aimed at early diagnosis of ovarian cancer. METHODS: Patients included in this investigations were all asymptomatic and had no pelvic abnormalities. Each ovary was measured in three planes and ovarian volume was calculated using the prolate ellipsoid formula. In premenopausal women, ovaries were normal if their volume was of > or = 18 cm3 and if they were hypoechogenic or anechogenic. In postmenopausal women a normal ovary was defined as having a volume of > or = 8 cm3 and a uniformly hypogenic internal structure. RESULTS AND CONCLUSIONS: In thirty-five premenopausal women was detected an abnormal volume of the ovaries. Forty-six postmenopausal women had abnormal vaginal sonograms. In this investigations vaginal sonography has permitted the detection of about 4.88% ovarian tumors in asymptomatic women, so that, it can be considered a more accurate and direment screening method for ovarian cancer than abdominal sonography.

Adult↗

Alcohol-induced regulation of nuclear regulatory factor-kappa beta in human monocytes.

Acute ethanol exposure has the capacity to modulate immune functions, particularly, to down regulate monocyte production of inflammatory cytokines. However, the intracellular mechanisms for these effects of ethanol are yet to be understood. Considering that nuclear regulatory factor-kappa beta (NF-kappa B)/Rel is a common regulatory element of the promoter region of the inflammatory cytokine genes, herein, we tested the hypothesis that acute ethanol affects NF-kappa B activation in human monocytes. Adherence-isolated monocytes showed constitutive DNA binding activity of NF-kappa B. A clinically relevant dose (25 mM) of acute ethanol treatment in vitro increased NF-kappa B binding activity in monocytes with a preferential induction of the inhibitory, p50/p50, NF-kappa B/Rel homodimer, and resulted in no induction of the p65/p50 heterodimer. In contrast, lipopolysaccharide stimulation primarily induced the p65/p50 heterodimer that has been shown to result in gene activation. Thus, such unique activation of the inhibitory p50/p50 homodimer by acute ethanol treatment may result in inhibition rather than activation of NF-kappa B-regulated inflammatory cytokine genes. Consequently, these results suggest that physiologically relevant concentrations of ethanol may affect production of inflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 by disrupting NF-kappa B signaling in monocytes.

Adolescent↗