[Mixed hepatoblastoma in an adult].
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Biomedical subjects
Publications and source records attributed to F Pozo.
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Integrated Friend murine leukemia virus copies were analyzed by the Southern blotting procedure in myeloblastic cell lines obtained after in vitro infection of long-term mouse bone marrow cultures. Several steps leading to the generation of malignant myeloblastic cells after a long latency period were observed in the evolution of infected cultures. Shortly after infection, a random distribution of integrated provirus copies was observed in the DNA of normally differentiating myeloid cells. In contrast, a distinct pattern of integrated Friend murine leukemia virus copies was evident in the first non-differentiating immature myeloblastic cells appearing in cultures, suggesting a monoclonal origin of these cells. For each cell line, characteristic hybridizing fragments were conserved during the 1-year culture period necessary for the acquisition of tumorigenic properties and were also observed in tumors grafted in vivo. We can conclude that monoclonality is effective very early in the myeloid transformation process, as soon as the precursor cells are blocked in their differentiation.
The effect of different stimuli applied in several parts of the digestive tract on blood pressure was studied in unconscious Wistar rats. Gastric distension and electrical and pinching stimuli produced a significant increase in both systolic and diastolic arterial blood pressure. When different gastric zones were stimulated by either electrical or pinching stimuli, the highest pressor response was found in the antropyloric zone. The stimuli applied to the small intestine, outside the duodenum, did not modify the blood pressure. The pinching of the abdominal peritoneum caused a pronounced (P less than 0.001) blood pressure decrease. These data suggest that the pressor response to gastric distension could be mediated by gastric mechanoreceptors. The pressor response observed after stimulation of the gastric antropyloric zone suggests that this area has a greater number of mechanoreceptors.
Three murine tumors induced by Moloney murine leukemia virus (M-MLV) which exhibited loss of some or all H-2 class I antigens at the cell surface were analyzed at the DNA and RNA level with molecular probes specific of H-2 heavy chains and beta 2-microglobulin sequences. No observable difference could be detected at the DNA level between the tumors and the parent animals. However, a decrease in H-2 mRNA was observed, especially in phenotypically H-2 negative tumor, BM5R, where H-2 transcripts were at least 30-fold less abundant. These results show that an H-2-negative character may result from a general alteration in the transcription of H-2 genes, which could reflect some kind of regulatory process.
A Friend virus induced erythroleukemia cell line (HFL/b cells) did not produce infectious MuLV and only expressed the defective SFFV component of Friend virus (SFFV (+), F-MuLV (-)). This line temporarily produced infectious F-MuLV following 5 azacytidine treatment. These results suggest that the F-MuLV expression is specifically repressed in these cells by a mechanism which does not affect the F-MuLV related SFFV genome.
The level of viremia and the appearance of leukemias were studied after inoculation wtih Moloney leukemia virus (M-MuLV) in different H-2 congenic strains of mice. The viremia was regularly measured on individual mice with a radioimmunoassay of the major internal virion component p30. Three genes within the major histocompatibility complex controlled the level of circulating virus. Two of them, called Rmv.1 and Rmv.2, appear to be located in the I region, respectively, in the IA, and the IC-S or G regions. The third gene, Rmv.3, was mapped to the D end of the complex in the D or T region. Crosses between resistant and sensitive strans demonstrated that the H-2 associated resistance was inherited as a dominant or semi-dominant Mendelian trait. Rmv.1, Rmv.2, and Rmv.3 were shown to complement for resistance in trans when the hybrids between sensitive strains were examined. A good correlation was found between viremia and the appearance of leukemias, the most viremic strains being also the most leukemic. Nevertheless, additional non-H-2 genes must control viremia and/or the appearance of leukemia since, despite high levels of viremia, some sensitive strains do not become leukemic.
The appearance of hematopoietic malignancies and the level of viremia were studied in mice of different inbred strains and their F1 or F2 hybrids inoculated with the Moloney leukemia virus (MLV). The viremia was regularly measured in individual mice by radioimmunoassay of the major internal virion component p30. A complex genetic control was found. (1) The level of circulating virus was controlled by at least two genes. An H-2 linked gene, tentatively called Rmv-1, displayed a dominant sensitivity. Alleles for resistance existed in H2b and H-2r haplotypes and alleles for sensitivity in H-2a, H-2d and H-2f. Another gene with dominant resistance mapped outside the H-2 complex and probably interacted with Rmv-1. (2) A good correlation existed between viremia and the appearance of leukemias, the most viremic strains being also the most leukemic. (3) Nevertheless, additional genes which were not involved in the viremia control could be determinant in the induction of malignancies. One of them with a resistant allele in DBA/2 mice seemed to inhibit the appearance of leukemia despite a high level of viremia. Another gene controlled the spleen involvement resulting in generalized leukemias in sensitive lines contrasting with mainly thymus-localized tumors in resistant animals.
The XC infectious center assay was used to study the nature of the lymphoid cells producing N-tropic C-type viruses in preleukemic AKR mice. Viral production by thymic cell suspensions was very low and was possibly due to contaminating cells. Production at least 100-fold higher was found in spleen cells and was probably due to non-T-cells. The significance of these results is discussed briefly, including the possibility that the N-tropic XC syncitia-inducing type C virus of young AKR mice is not the leukemogenic agent.
The use of our mink cell line maintained in vitro infected with the murine xenotropic AT 124 virus, and that of a (W/Fu x bn) f1 rat anti-124 serum allow us to define a new cell surface antigen specific of murine xenotropic type C viruses.
PGE1 increases cholesterolemia without lipemia modifications. In bile there are not modifications in cholesterol levels and total lipids appear diminished. PGE2 raise the lipemia and have no effect in cholesterolemia, moreover bile cholesterol and total lipids exhibit no changes. Both PGE1 and PGE2 decreased the bile volume.
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