Behaviour in biotin-deficient rats of thymic peptides controlling DNA transcription

Biotin-deficient rats show a slowing down of the growth and an involution of the thymus. The amount of the thymic peptides controlling DNA template, if referred to the thymus weight is higher in deficient than in control rats; no significant difference is noticed among the contents of the active peptides when evaluated per rat. The inhibiting activity on RNA synthesis is the same for the peptides extracted from normal and from biotin-deficient rat thymus.     

Effect of biotin on DNA and histone phosphorylation in the rat liver

The results offer further evidence for biotin activity in the phosphorylation mechanism. The decreased 32p incorporation into DNA and histones found in the biotin deficient rat liver is indicative of the importance of the vitamin in the DNA and histones synthesis and in the interactions between histone proteins and DNA, and consequently on the RNA and proteins synthesis.     

Fusicoccin Binding to its Plasma Membrane Receptor and the Activation of the Plasma Membrane H+-ATPase. II. Stimulation of the H+-ATPase in a Plasma Membrane Fraction Purified by Phase-partitioning

The effect of fusicoccin (FC) on the activity of the PM H⁺-ATPase was investigated in a plasma membrane (PM) fraction from radish seedlings purified by the phase-partitioning procedure. FC stimulated the PM H⁺-ATPase activity by up to 100 %; the effect was essentially on V_max with only a slight decrease of the apparent K_M of the enzyme for ATP. FC-induced stimulation of the PM H⁺-ATPase was evident within the first minute and maximal within five minutes of membrane treatment with the toxin indicating that transmission of the signal from the activated receptor to the PM H⁺-ATPase is very rapid. Both FC-induced stimulation of the PM H⁺-ATPase and FC binding to its receptor decreased dramatically upon incubation of the membranes in ATPase assay medium at 33 °C in the absence of FC, due to the lability of the free FC receptor. FC-induced stimulation of the PM H⁺-ATPase was strongly pH dependent: absolute increase of activity was maximal at pH 7, while percent stimulation increased with the increase of pH up to pH 7.5; FC binding was scarcely influenced by pH in the pH range investigated. Taken as a whole, these results indicate that FC binding is a condition necessary, but not sufficient, for FC-induced stimulation of the PM H⁺-ATPase.     

Expression of p53 gene in B-CLL peripheral lymphocytes.

The p53 tumor suppressor gene expression has been studied in 23 B-CLL cases at different clinical stages. The analysis failed to show a direct correlation with each stage, but the significantly lower frequency of a BglII RFLP in the pathologic population suggests a role of this gene in B-CLL. Northern Blot analysis showed the expression of p53 mRNA in all the B-CLL cases. A protocol for the RT-PCR methods was set up to study a very small amount of materials which should be better used for sequence analysis.     

KARYOTYPIC DATA ON NORTH AND CENTRAL AMERICAN ZAMIACEAE (CYCADALES) AND THEIR PHYLOGENETIC IMPLICATIONS

Chromosome numbers and karyotypes of species from four American Zamiaceae (Cycadales) are reported. Zamia shows interspecific and intraspecific chromosome variation, whereas Microcycas, Ceratozamia, and Dioon have constant karyotypes within each genus. In Zamia, all karyotypes have the same number of submetacentric and acrocentric chromosomes, but they differ in the number of metacentric and telocentric chromosomes. Centric fission of metacentric chromosomes is proposed to explain the karyotypic variation in this genus. Zamia shows karyological relationships with Microcycas and Ceratozamia, whereas Dioon appears very distinct from the other American cycad genera. Affinity among Zamia, Ceratozamia, and Microcycas karyotypes and distinctiveness of Dioon karyotypes are supported by comparative analysis of phenotypic characters in the four genera.     

The epoxide hydrolase catalyzed hydrolysis of trans-3-bromo-1,2-epoxycyclohexane. A direct proof for a general base catalyzed mechanism of the enzymatic hydration

The hydrolysis of (±)-$\text{trans}$-3-bromo-1,2-epoxycyclohexane in the presence of rabbit liver microsomes was investigated, and found to yield, beside $\text{c}$-3-bromocyclohexane-$\text{r}$-1,$\text{t}$-2-diol, 2,3-epoxycyclohexanol. It was demonstrated that the latter compound was the only product of the enzymatic reaction, whereas the diol resulted from a non enzymatic hydration in the reaction medium. These data provide the first direct proof for a general base catalysis in the enzymatic epoxide hydration, previously hypothesized on the basis of several lines of indirect evidence, and disprove alternative mechanisms involving protonation of the oxirane oxygen.     

Role of growth factors, steroid and peptide hormones in the regulation of human prostatic tumor growth

Previous work carried out in the authors' laboratory has shown that LHRH agonists directly inhibit the proliferation of hormone-responsive and hormone-independent human prostatic cancer cell lines (respectively LNCaP and DU145). In addition, the hormone-dependent LNCaP cells respond to a challenge with testosterone with an increase in growth rate. The following experiments have been performed to investigate whether the LHRH agonists might act by interfering with the stimulatory actions of either the EGF/TGF system or androgens. The results obtained in LNCaP and DU145 cells show that LHRH agonists counteract the mitogenic action of the EGF/TGF system. This effect is mediated by a decrease in the concentration of EGF receptors. In addition, in the hormone-dependent LNCaP cells, the treatment with LHRH agonists antagonizes the proliferation promoting effect of testosterone, which in turn appears to be mediated by the activation of the locally expressed EGF/TGF system. Finally, the results suggest the presence in LNCaP cells of a soluble peptidase able to degrade LHRH. In conclusion, the present data suggest an intimate interplay among the actions of LHRH agonists, of androgens and of growth factors, thus, supporting the hypothesis that LHRH agonists may interfere with the EGF/TGF stimulatory loop and with androgens in the control of the proliferation of human prostatic tumors.