Enhanced Noradrenergic Neuronal Activity Increases Homovanillic Acid Levels in Cerebrospinal Fluid

Idazoxan, a highly specific and selective alpha 2-adrenoceptor antagonist, caused a dose-dependent increase in the concentration of homovanillic acid (HVA) a metabolite of 3,4-dihydroxyphenylethylamine, in cisternal CSF of freely moving rats. This increase in HVA level could be antagonized by the alpha 2-adrenoceptor agonist medetomidine. The increase was directly proportional to the concurrent elevation in level of 3-methoxy-4-hydroxyphenylglycol, a metabolite of noradrenaline, in the CSF of individual rats and followed a similar time course. It is suggested that the HVA level in CSF may be increased under conditions of enhanced noradrenergic activity and that, in such situations, it reflects noradrenergic rather than dopaminergic neuronal activity. Care should be taken, therefore, when changes in central dopaminergic activity are assessed by measurements of HVA level in CSF.     

Enzymatic O-glycosylation of kappa-caseinomacropeptide by ovine mammary Golgi membranes

The results of subcellular fractionation of sheep mammary gland membranes indicate that N-acetylgalactosaminyl polypeptide transferase and galactosyl-N-acetylgalactosaminyl transferase, which are involved in the assembly of disaccharide units of kappa-casein, are localized chiefly in Golgi membranes. The glycosyltransferase activities incorporating N-acetyl [1-14C] galactosamine and [U-14C] galactose from uridine diphosphate N-acetyl [1-14C] galactosamine and uridine diphosphate [U-14C] galactose, respectively, were measured after membrane solubilization with Triton X-100 either with unglycosylated caseinomacropeptide, or with this polypeptide containing the N-acetylgalactosamine side chain residues (desialylated and degalactosylated caseinomacropeptide). Radioactive N-acetylgalactosamine was incorporated in the unglycosylated acceptor peptide, and the glycosidic bonds in the product were alkali labile, suggesting that they were linked to the hydroxyamino acid residues. In addition radioactive N-acetylgalactosamine was released after alpha N-acetyl-D-galactosaminidase treatment of labelled caseinomacropeptide. [U-14C] galactose was incorporated in the desialylated and degalactosylated acceptor peptide. Reductive alkaline treatment of [U-14C] galactose peptide resulted in the release of a major product, the chromatographic properties of which in TLC were identical with authentic galactosyl (1 leads to 3) N-acetylgalactosaminitol. The structure of the labelled disacchariditol determined after periodate oxidation (two equivalents) by gas liquid chromatography-mass spectrometry revealed that the [U-14C] galactose was linked to position C-3 on the N-acetylgalactosaminyl-residue. The anomery of the galactose, as determined by a chemical method, indicates unambiguously a beta configuration.     

It’s a knockout: CCN3 suppresses neointimal thickening

The role of CCN proteins in vivo is only just becoming understood. A prototypical member of the CCN family, CCN3 suppresses proliferation. In a study in press, Shimoyama and colleagues show that mice lacking CCN3 have a hyperproliferative response to vascular injury. These data, along with other recent observations, suggest that CCN3 may represent a novel therapy for hyperproliferative diseases.     

Chemical and physical methods in dating human skeletal remains

Chemical and physical methods for dating skeletal remains were examined. Benzidine reaction, ultra-violet fluorescence, specific gravity and supersonic conductivity were carried out on 71 dated skeletal findings distributed over the span of the last 3,500 years. Results given by benzidine reaction and ultra-violet fluorescence basically coincide, and positive readings were obtained up to about 200–350 years. Values measured in specific gravity and supersonic conductivity testing show a parallel trend, pointing out a clear difference between samples of the three first centuries and the ones belonging to more ancient periods examined.