[Seroprevalence of the hepatitis C virus in donors and in high and low risk groups in Salamanca].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Corral.
Explore the source record for details and available documents.
The presence of antibodies (Abs) against hepatitis C virus (HCV) was analyzed in 26 haemophiliac patients; a prevalence of 38% was found in the total series and 56% in the treated patients. There were no cases with a positive serology among the three patients who had only received pasteurized factor. The frequency of detection of anti-HCV was higher in the patients who had a positive serology for HIV (67%) and hepatitis B virus (56%) than in the seronegative patients (24 and 29%, respectively). The patients with HCV Abs showed a decrease in the helper (CD4+) lymphocytic population, mainly due to the decrease in the helper inducer (CD4+/Leu8-) cells, such alterations being more evident in the patients who also were HIV+ who showed as well an increase in the T-cell activated lymphocytes (CD3+/la+) and a decrease in CD16+ natural killer cells. These results suggest that the lymphocytic alterations found in the patients with anti-HCV Abs are not specific and would rather be related to the presence or not of HIV infection.
Since oxygen free radicals are believed to play an important role in cartilage degradation, we studied the effects of these radicals generated by the hypoxanthine xanthine oxidase system on rabbit articular chondrocytes in culture. Among the damages induced by these radicals, cell proliferation inhibition and G2 arrest were observed. To elucidate the mechanisms involved in this phenomenon, the expression of c-myc and c-Ha-ras genes whose products are associated with cell growth control was studied. Results showed that in chondrocytes, c-myc and c-Ha-ras expression was particularly important during the G1 phase of the cell cycle and that oxygen reactive species, especially H2O2, induced an important decrease of c-myc and c-Ha-ras mRNA levels. Chondrocytes cell cycle analysis revealed an accumulation of cells in G2 phase. It led us to suggest that the chondrocyte cell cycle perturbations observed after oxygen free radicals treatment could be associated with the decrease of c-myc and c-Ha-ras expression.
Using specific probes we show that sequences homologous to NADH dehydrogenase Subunit 6, and Cytochrome oxidase Subunits I, II, and III mitochondrial genes are present in nuclear DNA from various tissues. These mitochondrial-like sequences are also present in rat hepatoma nuclear DNA but with an abnormal organization and a higher copy number than in normal hepatocytes.
We have constructed a cDNA library prepared from an hepatoma cell line (HTC cells) and isolated a clone, pHT 13, which corresponds to mRNAs present at a much higher level in rat hepatomas than in normal hepatocytes. The sequence of the pHT 13 insert has been previously published (Nucleic Acids Res. 1988, 16,10935). This clone contains mitochondrial DNA sequences with an abnormal organization, since it includes part of the NADH dehydrogenase subunit 6 (ND6) and of the cytochrome oxidase subunit I (COI) genes separated by 230 bases instead of 9 kb in mitochondrial genome from normal hepatocytes. In this work we show (1) that RNAs homologous to this clone are present in hepatoma cells but not in normal hepatocytes, (2) that a 3 kb fragment of tumor mitochondrial DNA contains both the ND6 and the COI sequences. The abnormal structure of the DNA is confirmed by Southern blot analysis which shows that distinct types of mitochondrial DNAs are present in hepatoma cells.
We have constructed a cDNA library from a hepatoma cell line (HTC cells) and isolated the clones corresponding to mRNAs present at a much higher level in hepatomas than in normal hepatocytes. The characterization of one of these clones is described in this paper. This clone is homologous to part of the mitochondrial ND5 gene (a subunit of NADH-ubiquinone oxidoreductase). The level of this mRNA was found increased in HTC cells and in hepatocytes from diethylnitrosamine-treated rats long before the development of tumors and strongly increased in carcinoma nodules as compared to hepatocytes from nontreated rats. Southern blot analysis showed a mitochondrial DNA heterogeneity in hepatomas with an alteration of the structure of part of the molecules.
Explore the source record for details and available documents.
The activation of N-myc and c-myc genes has been implicated in the genesis of a variety of cancers. In order to determine whether this activation is related to the process of cell growth, we examined N-myc and c-myc expression in rat hepatocytes when growth was stimulated by partial hepatectomy and in rat liver during neoplastic growth induced by diethylnitrosamine. The levels of N-myc and c-myc mRNAs, which are very low in hepatocytes from normal rats, were increased at least 20-fold within 3 h after partial hepatectomy and decreased rapidly by 6 h. A second transient peak of c-myc and N-myc mRNAs occurred around 9 and 48 h, respectively. N-myc and c-myc expressions were also induced in carcinoma nodules by diethylnitrosamine. A high level of N-myc transcript was observed in hepatocytes as early as 1 month after the carcinogen administration, whereas c-myc transcript was detected at a high level only several months later in carcinoma nodules. Our results suggest that the transient expression of N-myc and c-myc oncogenes during the prereplicative stage of liver regeneration may be associated with the entry of hepatocytes into the cell cycle, and that N-myc expression is not limited to tumors of neural characteristics as has been previously shown but is also observed in cancer from epithelial origin.
Explore the source record for details and available documents.
Phorbol ester activates human lymphocyte proliferation as measured by [3H]thymidine incorporation and blast transformation. Phorbol ester and calcium ionophore A 23187 induce c-fos and c-myc expression in these cells as shown by the measure of the specific mRNA levels and of the c-fos nuclear protein amount. The combination of these two agents has a synergistic effect on c-fos but not on c-myc expression. Lymphocyte stimulation by phorbol ester for a short time induces c-fos and c-myc expression, but has no effect on [3H]thymidine incorporation. This result indicates that the induction of c-fos and c-myc expression is not sufficient to commit these cells to DNA synthesis.
The multimeric structure of von Willebrand factor (vWF) and its ristocetin-induced binding to platelets, using a simple and very sensitive radiomonoclonal antibody-labeled vWF method, was compared in normal plasma, single-donor cryoprecipitate (CP) and five different antihemophilic factor (AHF) concentrates. All the AHF showed a lack of larger vWF multimers, an abnormal 'triplet' pattern, and much lower vWF binding to platelets than that of plasma or CP, vWF being the lowest for those with a lesser proportion of larger vWF multimers. These results suggest that the combination of vWF multimeric analysis and the radiomonoclonal-labeled vWF method may be very useful in the assessment of AHF preparations.
The development of hypomania, mania and transient mood elevation within 2-3 days of antidepressant discontinuation, and lasting days to several weeks has been reported in unipolar depressed patients. Imipramine and desipramine are the antidepressants most frequently associated with the above phenomena. A reported case of transient mood elevation following abrupt reduction but not discontinuation of desipramine therapy in a woman with unipolar depression is described. The phenomenon was observed and documented on two separate occasions. Mood elevation occurred despite decreased plasma levels of the drug. Relapse followed despite maintenance of dose and similar drug plasma levels. Factors which could account for the transitory improvement of mood are examined. It is suggested that the patient's improvement in mood may have occurred due to a rebound paradoxical therapeutic effect. The features of the presented case history which appear to support this hypothesis are discussed. Also the clinical implications of this phenomenon are reviewed.
In order to characterize the genes overexpressed in an hepatoma cell line, the HTC cells, and in diethylnitrosamine induced solid hepatomas, we constructed a complementary DNA library from HTC cells and performed differential screening with probes from HTC cells, from malignant nodules obtained 70 weeks after the carcinogen treatment, and from hepatocytes from normal rat liver. Eight clones corresponding to messenger RNAs (mRNAs) much more expressed in hepatomas than in hepatocytes from normal liver were isolated. Three, clones pHT 71, pHT 13, and pHT 26, were further analyzed by the study of their corresponding transcripts in hepatocytes from regenerating liver and in the hepatocytes from the nontumorous parts of the liver. Clone pHT 71 corresponds to a single 2.3-kilobase mRNA which is present in high levels in carcinoma nodules in hepatoma cell lines, in the nontumorous parts of the liver, and in hepatocytes isolated from regenerating liver 30 h after partial hepatectomy. Clone pHT 13 hybridizes with three distinct transcripts 3.8, 2.6, and 1.6 kilobases long. High levels of the 3.8- and 1.6-kilobase mRNAs are present in carcinoma nodules, in hepatoma cell lines, and in the nontumorous parts of the liver. However, the levels of these RNAs are similar in hepatocytes from regenerating liver and in hepatocytes obtained from normal rat liver. Clone pHT 26 corresponds to a 0.6-kilobase mRNA which exists at a high level only in cancer nodules and in hepatoma cell lines. We were unable to observe any cross-hybridization between these clones and the oncogenes which have been found to be expressed in hepatomas (c-fos, c-Ha-ras, c-Ki-ras, N-ras, and c-myc). The mRNAs corresponding to the three clones have not been detected in various tissues from normal adult rats. Our study shows that a high level of these mRNAs might be associated with rat liver carcinogenesis.
After stimulation of human lymphocytes by 12-0 tetradecanoyl phorbol acetate (TPA) and by the calcium ionophore A23187 an early transient expression of proto-oncogene fos followed by an expression of c-myc is observed, as has been described in rodent fibroblast stimulated by growth factors. This observation suggests a direct role of protein Kinase C and of calcium flux an the induction of cellular oncogenes fos and myc that may be associated with the early steps of activation and proliferation of lymphocytes.
We have studied the expression of c-fos gene in rat hepatoma induced by DENA. An increase of c-fos mRNA concentration was observed after 8 days, but the maximal 5- to 6-fold increase was observed after 70 weeks. This increase was found in perinodular hepatocytes as well as in cancer nodules. c-fos expression was also enhanced during liver regeneration at a period corresponding to cell proliferation. In HTC cells the arrest of the cell cycle at early G1 phase by addition of sodium butyrate was accompanied by a strong increase of c-fos gene expression. However the c-fos mRNA rapidly decreased after removal of sodium butyrate during the progression of the cells in the cell cycle and increased transiently when the cells entered again in G1 phase.