Amino acid sequence of a four-iron-four-sulphur ferredoxin isolated from Bacillus stearothermophilus

A novel method of RNA fractionation based on a gradual release of the RNA molecules from ribonucleoprotein complexes has been used for the analysis of ribosomal and non-ribosomal complexes of rat liver cytoplasm. Adsorption of native ribonucleoproteins on a Celite column (occuring through only the protein moiety) followed by a consequent dissociation of RNP complexes brought about by various agents results in RNA fractionation in accordance with the tightness of the RNA-protein bonds. The cytoplasmic ribosomal and rapidly labelled non-ribosomal RNA species are separated into several fractions identified as 18S and 28S rRNA's, mRNA and messenger-like RNA. A relatively small fraction (about 10% of the total) of rRNA tenaciously bound to protein has been also revealed.     

Analysis of linkage between beta-lactoglobulin and J blood group system loci in cattle

Linkage between loci controlling variants of beta-lactoglobulin and blood groups of the J system in cattle was studied by means of stochastic genetic methods reported earlier. The studies were conducted on a herd of Black Pied cattle improved with Holstein sires; population genetic data were analyzed. A plot for lod score was constructed, and point (r - 0.28) and interval estimations of the coefficient of recombination were obtained. The results are in good agreement with earlier reported data on other subjects.     

Short-term effects of thyroid hormones on the Na/H antiport in L-6 myoblasts: high molecular specificity for 3,3',5-triiodo-L-thyronine

The thyroid hormones L-T3 and L-T4 were shown to activate the Na/H antiport in L-6 cells from rat skeletal muscle by a rapid, nongenomic mechanism. Under pH equilibrium conditions, a significant rise in the intracellular pH, measured by the fluorescent pH indicator 2',7'-bis-(carboxyethyl)-5(6)-carboxyfluorescein was observed after the addition of physiological concentrations (10(-10) M) of either L-T3 or L-T4, but with different time courses. L-T3 at all concentrations increased the pH after a delay of 2 min, whereas L-T4 showed a concentration-dependent lag time, going from 11 min at 10(-11) M down to 5 min for a hormone concentration of 10(-6) M. The effect of L-T4 was blocked in the presence of the 5'-deiodinase inhibitor 6-n-propyl-2-thiouracil, suggesting that the difference in lag time between L-T3 and L-T4 was due to the 5'-deiodination process that transforms L-T4 into the bioactive L-T3. In short term studies (<5 min), a high molecular specificity for L-T3 was found, as L-T4, rT3, the D-isomer of T3, and the deaminated analogues were ineffective at physiological concentrations. In analogy with the results found at equilibrium, intracellular pH recovery from an acid load and set-point were increased after 2 min for L-T3 (10(-9) M) and after 10 min for L-T4 (10(-9) M). The effect of the hormones on the intracellular pH was completely blocked by the specific antiport inhibitor 5-(ethyl-N-isopropyl)amiloride. These findings suggest that thyroid hormones may play an active role in the recovery from muscular acidosis through direct stimulation of the Na/H antiport.     

Artificial neural networks in cancer research

Current therapy does not cure the majority of patients with B cell non-Hodgkin's lymphoma (NHL) and further intensification does not benefit the patient. Therefore, new approaches are necessary. Immunotherapy has become again a major interest as a new treatment modality for B cell lymphoma since the discovery that the lymphoma specific Id can be presented to antigen-specific T cells. Vaccination of the tumour-bearing host is one of the major strategies to induce a T cell mediated anti-tumour immunity in vivo. For B cell lymphomas the lymphoma specific Id can be used as a tumour-specific antigen to stimulate T cells. Alternatively, the malignant B cells can be modified to become efficient antigen presenting cells (APCs) and present peptides from their own tumour-specific antigens to the autologous T cells. Currently explored and future vaccination strategies for B cell lymphoma will be discussed here.     

Human Myt1 is a cell cycle-regulated kinase that inhibits Cdc2 but not Cdk2 activity

Activation of the Cdc2.cyclin B kinase is a pivotal step of mitotic initiation. This step is mediated principally by the dephosphorylation of residues threonine 14 (Thr14) and tyrosine 15 (Tyr15) on the Cdc2 catalytic subunit. In several organisms homologs of the Wee1 kinase have been shown to be the major activity responsible for phosphorylating the Tyr15 inhibitory site. A membrane-bound kinase capable of phosphorylating residue Thr14, the Myt1 kinase, has been identified in the frog Xenopus laevis and more recently in human. In this study, we have examined the substrate specificity and cell cycle regulation of the human Myt1 kinase. We find that human Myt1 phosphorylates and inactivates Cdc2-containing cyclin complexes but not complexes containing Cdk2 or Cdk4. Analysis of endogenous Myt1 demonstrates that it remains membrane-bound throughout the cell cycle, but its kinase activity decreased during M phase arrest, when Myt1 became hyperphosphorylated. Further, Cdc2. cyclin B1 was capable of phosphorylating Myt1 in vitro, but this phosphorylation did not affect Myt1 kinase activity. These findings suggest that human Myt1 is negatively regulated by an M phase-activated kinase and that Myt1 inhibits mitosis due to its specificity for Cdc2.cyclin complexes.