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Biomedical subjects

S Ferrari

Publications and source records attributed to S Ferrari.

At least 109 records · Page 6Linked to original sources
PubMed1986

Tissue antigen distribution in hepatocellular carcinoma.

An immunohistochemical study on 63 hepatocellular carcinomas (HCC) was performed for the demonstration of alpha 1-antitrypsin (AAT), alpha-fetoprotein (AFP) and hepatitis B virus (HBV) antigens. AAT and AFP were also investigated in 54 cases of cirrhosis not associated with HCC. AAT was frequently expressed both in HCC (82.5%) and in cirrhosis (53.7%), whereas AFP was present in 41.2% of HCC and never detected in cirrhosis used as controls. These findings suggest that AFP is the more specific antigen for use as a marker of malignant cellular transformation. The HBsAg-positivity in 31.7% of HCC supports the hypothesis of a close link between virus B infection and the tumor.

Antigens↗
PubMed1986

Isolation of a cDNA clone for chick intestinal apolipoprotein AI (Apo-AI) and its use for detecting apo-AI mRNA expression in several chick tissues.

Three cDNA clones for chick apolipoprotein AI (Apo-AI), the major protein component of plasma high-density lipoproteins, have been isolated. The identity of the clones has been established first by screening a cDNA library in the pEX1 expression vector with anti-Apo-AI antibodies, second by Western blot analysis of the proteins expressed by positive clones. The use of the clone containing the largest, presumably full-size, cDNA insert (apo5C12) in molecular hybridization experiments confirms that apo-AI mRNA is expressed mainly in chick small intestine and liver. Furthermore, we provide evidence that brain, heart and skeletal muscle also synthesize significant amounts of apo-AI mRNA. The Southern-blot hybridization pattern of the restriction-enzyme-digested chick DNA with the apo5C12 DNA is consistent with there being a single copy of the apo-AI gene.

Animals↗
PubMed1986

Cellular levels of mRNA from c-myc, c-myb and c-fes onc-genes in normal myeloid and erythroid precursors of human bone marrow: an in situ hybridization study.

The expression of three onc-genes, c-myc, c-myb and c-fes, has been evaluated at the cellular level in myeloid and erythroid precursors of normal human bone marrow, by "in situ" hybridization with tritium-labelled probes. A relatively large amount of m-RNA from the three onc-genes was detected in myeloblasts and promyelocytes, but whereas the expression of c-myc and c-myb decreased in more advanced stage of maturation of the myeloid lineage, c-fes mRNA remained at a relatively high level until the granulocyte stage. c-myc and c-myb were expressed at a fairly high level in basophilic erythroblasts, which also showed low levels of c-fes mRNA. No expression of these onc-genes was detectable in more mature erythroblasts. Megakaryocytes showed high levels of m-RNA from all three onc-genes. Our results suggest that c-myc and c-myb expression is related in some way to the cellular proliferation of myeloid and erythroid precursors, whereas c-fes expression is more restricted to myeloid differentiation.

Bone Marrow Cells↗
PubMed1986

Coding sequence and growth regulation of the human vimentin gene.

We have established the complete coding sequence of the human vimentin gene. It had 91% homology to the coding sequence of the Syrian hamster vimentin gene (Quax et al., Cell 35:215-223, 1983) and partial homology to several other sequences coding for intermediate filament proteins. The most striking difference between the Syrian hamster and human vimentin genes was in the 3' untranslated region, which was considerably longer in the Syrian hamster. Using RNA blots and a human vimentin cDNA clone from an Okayama-Berg library, we have established that expression of the vimentin gene was growth regulated. The steady-state levels of cytoplasmic vimentin mRNA in 3T3 cells were increased by serum and platelet-derived growth factor, but not by epidermal growth factor, insulin, or platelet-poor plasma. The increase in expression of the vimentin gene that occurred when G0-phase cells were stimulated to proliferate was detected in six different cell types from four different species. The expression of the vimentin gene was also increased when HL60 cells were induced to differentiate by phorbol esters; it decreased when differentiation was induced by retinoic acid.

Amino Acid Sequence↗
PubMed1986

Expression of growth-regulated genes in human acute leukemias.

We have investigated the expression of six growth-regulated genes (c-myc, c-myb, p53, 4F1, 2F1, and ornithine decarboxylase) and the S-phase-specific histone H3 gene in acute myeloid and lymphoid leukemic cells. We have purposely chosen three growth-regulated protooncogenes that share similar biological features and three gene sequences that have in common the cell cycle dependence of their expression in cells of different tissue and in different species. The level of expression was determined by measuring the amounts of specific RNA by Northern blot analysis. Levels of expression of the six growth-regulated genes were compared to the level of expression of the S-phase-specific H3 gene and among themselves. This method distinguishes the increased expression of a growth-regulated gene due to a true altered activation from over-expression which simply reflects an increase in the fraction of cycling cells. We have found that six of 14 patients with acute leukemias have markedly high ratios of c-myc/H3, c-myc/p53, and c-myc/c-myb expression. Two patients with altered c-myc expression have also a high ratio p53/H3. Within the group of cell cycle-dependent genes the ratios of expression seem in the overall much more regular with the clear exception of a patient with acute myelogenous leukemia in which the ratios 4F1/H3 and 2F1/H3 are significantly increased. A possible interpretation of these findings is that the fraction of noncycling leukemic cells that often constitute the majority of the entire leukemic population is in some cases in a true resting state, whereas in other cases heterogeneous degrees of growth arrest might occur. The altered expression of c-myc seems the feature most commonly associated with this putative growth arrest of leukemic cells suggesting that this gene may contribute to the impairment of proliferative control that is associated with the leukemic phenotype.

Acute Disease↗
PubMed1985

Induction of a 70,000 dalton protein in hypertrophic rat heart.

Two-dimensional gel electrophoresis analysis of the product of in vitro translation of polyadenylated RNAs extracted from rat heart rendered hypertrophic by aortic constriction, shows a new protein species not present in the map of control hearts. The same is also obtained when hypertrophy is induced by treatment with thyroxine.

Animals↗
PubMed1985

The effect of cycloheximide on the expression of cell cycle dependent genes.

We have investigated the inducibility of several cell cycle-dependent genes (plus control sequences, not expressed in a cell cycle-dependent manner) in the presence of cycloheximide, an inhibitor of protein synthesis. The genes studied include: 1) five cDNA clones that are preferentially expressed in the G1 phase of the cell cycle: KC-1, JE-3, 2F1, 4F1 and 2A9; 2) one gene preferentially expressed in late G1/S phase: histone H3; and 3) the cell cycle-dependent oncogene p53. All the genes studied are induced by serum even in the presence of cycloheximide. Previous results in the literature have shown that 2 other oncogenes, c-myc and c-fos, can be induced by growth factors in the presence of cycloheximide. Together with our results, these findings indicate that protein synthesis is not required for the induction of at least nine cell cycle genes by growth factors.

Animals↗
PubMed1985

Distinct structural requirements of Ca2+/phospholipid-dependent protein kinase (protein kinase C) and cAMP-dependent protein kinase as evidenced by synthetic peptide substrates.

Protein kinase C, purified to near homogeneity from the brain, has been tested toward a variety of synthetic peptide substrates including different phosphorylatable residues. While it proved totally inactive toward the tyrosyl peptide Asp-Ala-Glu-Tyr-Ala-Ala-Arg-Arg-Arg-Gly, as well as toward several more or less acidic seryl peptides, it phosphorylates with a Ca2+/phospholipid-dependent mechanism, at seryl and/or threonyl residues, many basic peptides, some of which are also good substrates for cAMP-dependent protein kinase (A-kinase). Among the peptides tested, however, the best substrate for protein kinase C, with kinetic constants comparable to those of histones, is the nonapeptide Gly-Ser-Arg6-Tyr, which is not a substrate for A-kinase. Moreover, although the peptide Pro-Arg5-Ser-Ser-Arg-Pro-Val-Arg is a good substrate for both kinases, its derivative with ornitines replacing arginines is phosphorylated only by protein kinase C. Some typical substrates of A-kinase on the other hand, like the peptides Phe-Arg2-Leu-Ser-Ile-Ser-Thr-Glu-Ser and Arg2-Ala-Ser-Val-Ala, are phosphorylated by protein kinase C rather slowly and with unfavourable kinetic constants. It is concluded that, while both protein kinase C and A-kinase need basic groups close to the phosphorylatable residues, their primary structure determinants are quite distinct.

Animals↗
PubMed1985

Characterization of the sites phosphorylated on tyrosine hydroxylase by Ca2+ and phospholipid-dependent protein kinase, calmodulin-dependent multiprotein kinase and cyclic AMP-dependent protein kinase.

Tyrosine hydroxylase purified from rat pheochromocytoma is phosphorylated rapidly by the Ca2+- and phospholipid-dependent protein kinase (protein kinase C) purified from rat or sheep brain. Phosphorylation was stimulated 14-fold by Ca2+ and phosphatidylserine and occurred at a rate comparable with that of the phosphorylation of histone Hl. The phospholipid-dependent protein kinase phosphorylates a single site which is identical to that phosphorylated by cyclic AMP-dependent protein kinase and to the secondary site of phosphorylation by the calmodulin-dependent multiprotein kinase. The implications of these results with respect to the regulation of catecholamine biosynthesis in adrenal medulla are discussed.

Animals↗
PubMed1985

Study of the levels of expression of two oncogenes, c-myc and c-myb, in acute and chronic leukemias of both lymphoid and myeloid lineage.

Total cellular RNA from a series of leukemic cell populations, both myeloid and lymphoid, as well as from normal circulating lymphocytes was analysed for the expression of two cellular oncogenes, c-myc and c-myb, by Northern blot hybridization assay. Expression of c-myc but not of c-myb was observed in unstimulated normal lymphocytes. Stimulation by PHA was shown to activate the expression of both genes. Remarkably different levels of expression of c-myc were observed in ALL, whereas in CLL the expression of c-myc was uniformly low or absent. Differential expression of c-myc was detected in AML as well as in CML, c-myb was differentially expressed in AML and ALL, and absent in CLL and CML. Other single cases of hemopoietic disorders were studied, but the expression of the two oncogenes was low or absent. Neither evident genome amplification nor genome rearrangements were detected in the cell DNAs digested with restriction endonucleases.

DNA, Neoplasm↗
PubMed1985

Expression of human c-fes onc-gene occurs at detectable levels in myeloid but not in lymphoid cell populations.

Total cellular RNA from a variety of myeloid and lymphoid cell populations, normal and leukaemic, was analysed for the expression of a human cellular onc-gene, c-fes, by northern blot hybridization assays. The probe used was a molecularly cloned human DNA sequence homologous to the 5' terminal sequence of v-fes. All the myeloid cellular populations expressed the c-fes gene. In some cell populations at an advanced stage of differentiation (circulating leucocytes from Chronic myeloid leukaemia (CML), HL60 cells induced to differentiate by retinoic acid) the level of expression was even higher than in early stages of the myeloid lineage (blast cells from AML, uninduced HL60 cells). No transcript of the c-fes gene was detected in the different lymphoid populations studied. The occurrence of an RNA complementary to the c-fes sequence appears sufficiently characteristic of a myeloid population to distinguish it from a lymphoid population, normal and leukaemic.

Cell Differentiation↗
PubMed1985

Activation of c-myb expression by phytohemagglutinin stimulation in normal human T lymphocytes.

The expression of c-myb in normal human T lymphocytes directly derived from a normal subject and not adapted to continuous growth in culture was found to be markedly increased after phytohemagglutinin stimulation. In the same cells, the expression of c-myc mRNA is a much earlier event compared with the appearance of c-myb mRNA, which takes place soon after that of histone H3 mRNA. The increase in c-myb expression was not due to a particular T-lymphocyte subset, as shown by in situ hybridization assays.

Cells, Cultured↗
PubMed1985

Hypothalamic-pituitary-adrenal function in children with atopic dermatitis treated with clobetasone butyrate and its clinical evaluation.

Twenty-nine patients with symmetrical eczematous lesions were treated with 0.05% clobetasone butyrate cream. Clinical conditions and cortisol and ACTH concentrations were evaluated at the beginning and after 1 week in 12 children and after 2 weeks of treatment in 17 patients respectively. The lesions and symptoms improved steadily and no significant change in cortisol and ACTH plasma levels was observed throughout the study in all children. This steroid offers clinically effective topical antiinflammatory activity with a wide margin of safety.

Adolescent↗
PubMed1979

Kinetics of hybridization to human DNA of heterogeneous nuclear RNA isolated from normal human lymphoblasts and acute leukemia blast cells.

Heterogeneous nuclear RNA was extracted from normal PHA-stimulated human lymphocytes and acute myeloid leukemia blast cells. Experiments were performed to determine the hybridization kinetics of these RNA's to human DNA. The best least squares solutions indicate in the hybridization reaction of both normal and leukemic RNA two main components. For leukemic cell RNA the rate constants of both components were significantly different from that of normal cell RNA. In particular, the difference between the rate constants of the second lower component suggests that the slowly hybridizing sequences in leukemic cell RNA have a degree of repetition higher than of the corresponding sequences of normal cell RNA.

Base Sequence↗
PubMed1979

Reassociation kinetics of the DNA of human acute leukemia cells.

Human DNA isolated from normal phytohaemagglutinin-stimulated human lymphocytes and from acute leukemia blast cells have been studied by renaturation techniques using hydroxyapatite binding and DNA hyperchromism. In the leukemic genome, the unique sequences account for 62% of the genome of leukemic DNA. Repetitive sequences may be subdivided into at least three fractions: (a) foldback sequences, which represent 5% of the genome; (b) sequences with high repetition frequency (3. 10(4) times on the average), which represent 12% of the genome; (c) sequences with low repetition frequency (10 times on the average), which represent 16% of the genome. The average length of the repetitive sequences is evaluated to be between 200 and 500 nucleotides. There are at least two patterns of interspersion of repetitive sequences with unique sequences of different length: short (about 2000 nucleotides on average) and long (not defined). The results of our experiments on DNA from normal phytohaemagglutinin-stimulated human lymphocytes are in close agreement with those reported by other authors studying different types of human cells. The human leukemic DNA, as far as the parameters that have been studied, does not significantly differ from normal human DNA.

Acute Disease↗