Inositol- and Galactose-Binding Lectins of Chicken Brain Fractions Enriched with Glial Cells

Galactose- and inositol-binding proteins with lectin activity (GL-GAL and GL-I, respectively) were isolated from membranes enriched with cells of chicken brain fractions. Both lectins are glycoproteins of molecular mass 13.5 and 11.5 kDa, respectively; they show a high affinity to EDTA (GL-I) and EGTA (GL-GAL, GL-I), which indicates an important role of Ca⁺² in molecular organization of these lectins. In brain glial cells of chick embryos, unlike adult chickens, a soluble form of lectins has been revealed; it is easily extracted with 2 mM EDTA and shows sensitivity to L-lactose, D-galactose, and N-acetyl-D-galactosamine. It is suggested that in the course of embryonal and postembryonal development of the chicken brain, a transformation and qualitative changes of the lectin spectrum occur due to a change of function of glial cells.     

Im-trityl protection of histidine.

A rational attempt to prepare FmocHis(piTrt)OH regiospecifically gave in fact the well-known tau-trityl isomer, and experiments with model systems indicate that the prospects for access to pi-trityl histidine derivatives, which would be of great value for the racemization-free synthesis of histidine-containing peptides, are poor.     

Respiration rates of some greenhouse cultivated tropical and subtropical species

A comparative study of dark respiration and effects of high and low temperature on dark respiration in five greenhouse cultivated tropical and sub-tropical species was made. The respiration rates determined manometrically were low in all species. Respiration rates increased with increasing temperature. Low temperature treatment accelerated the rate of respiration at 25 °G except in two species. An attempt has been made to determine the critical and optimum temperature for these species. The respiratory behaviour of these species has been discussed with respect to their original habitats and prevailing environmental conditions.     

Leucostasis, an underestimated cause of death in leukaemia

Massive sludging of leukaemic cells in blood vessels is a frequent and often lethal complication of leukaemia. In a retrospective clinicopathological study on the causes of death in 52 patients with acute myeloid leukaemia and myeloproliferative disease, pulmonary leucostasis was found in 40% of the patients. In many of these patients the vessels of the heart, brain and testes were also involved. In search for signs and symptoms specific for leucostasis, the clinical records of the 21 patients with leucostasis (the study group) were compared to those of 20 patients without leucostasis (the control group). Dysfunction of the organs most affected by leucostasis, namely lungs, heart and brain, was found more often in the study group than in the controls, but the combination of unexplained fever with cardiopulmonary and/or central nervous system failure occurred almost exclusively and in half of the patients with leucostasis. Leucostasis occurs predominantly, but not exclusively, in patients with high leucocyte counts, and especially, but again not exclusively, when the leucocyte counts rise sharply.     

Primary structures of the mRNAs encoding the rat precursors for bradykinin and T-kinin. Structural relationship of kininogens with major acute phase protein and alpha 1-cysteine proteinase inhibitor

Three types of cloned cDNA sequences for rat low molecular weight prekininogens were isolated and determined by molecular cloning and sequence analysis. The deduced amino acid sequences indicated that one, termed K-prekininogen, represents the counterpart of the known low molecular weight prekininogen present in other mammals, while the other two, called T-prekininogens, contain a novel T-kinin sequence which was recently identified from rat plasma. Although T- and K-prekininogens are highly homologous with each other, both of the T-prekininogens contain methionine, instead of arginine or lysine, as an amino acid preceding T-kinin and exhibit two consecutive amino acid deletions in the preceding region of T-kinin as compared with K-prekininogen. The former finding accounts for the previous observation of strong resistance of T-kininogens to cleavage with trypsin or kallikreins, while the latter finding has been explained by the structural analysis of genomic clones in which T-kinin-coding exon is contracted at its intron junction. A partial nucleotide sequence reported recently for the rat major acute phase protein (alpha 1-MAP) mRNA was found to be extremely related to the corresponding portion of the rat T-prekininogen mRNA. Furthermore, consistent with the previous report of the structural identity of major acute phase protein and alpha 1-cysteine proteinase inhibitor, kininogen closely resembles not only the former but also the latter in the amino acid compositions. The interrelationship among the triad of these proteins has been discussed.