The exotoxin of Bacillus thuringiensis: a new C-mitotic agent

Thuringiensin A, an exotoxin from Bacillus thuringiensis, a constituent of the microbial insectide thuricide has been found to inhibit mitotic spindle, condense and scatter chromosomes. It may therefore be a promizing tool in future cell biological studies.     

Secretion by parafollicular cells beginning at birth: ultrastructural evidence from developing canine thyroid

The ultrastructure of developing canine parafollicular cells has been examined. The hypothesis that secretion is relatively inactive prior to birth but very active at and following birth was tested. Parafollicular cells develop and accumulate characteristic secretory granules prior to birth. However, there is little or no evidence of exocytosis at this time. At birth and during the neonatal period, but not in adult thyroids, signs of exocytosis of granular contents by parafollicular cells are abundant. Just prior to the expected date of birth and before evidence of exocytosis appears, parafollicular cells accumulate intracisternal granules within rough endoplasmic reticulum. These observations are consistent with the view that parafollicular cells first become actively secretory around the time of birth and are more active at this time than in early fetal or later adult life.     

Click‐ligation of coumarin to polyether polyols for polyurethane foams

A simple strategy for the synthesis and functionalization of polyurethanes is described. Anionic ring‐opening polymerization was combined with ‘click’ chemistry to synthesize polyols with fluorescent properties. This route allows the incorporation of a wide range of functionalities in the polyols with an easy, clean and highly selective process compatible with several types of functional groups. The proposed strategy opens the way to the production, in a cost‐effective way, of ‘smart’ polyurethanes with non‐conventional properties like fire retardancy, antimite properties, antibacterial properties, etc. Alkynyl groups were introduced into the polyol chains by the controlled addition of glycidyl propargyl ether as co‐monomer during a conventional anionic ring‐opening copolymerization with propylene oxide. Subsequently 4‐azidomethyl‐7‐methoxycoumarin molecules were introduced onto the alkynyl‐polyether polyols by copper‐catalysed cycloaddition reactions to produce end‐functionalized polyols. The chemical structure of the novel polyols was characterized using infrared spectroscopy, nuclear magnetic resonance spectroscopy, gel permeation chromatography with triple detection and matrix‐assisted laser desorption/ionization time‐of‐flight mass spectroscopy. These characterization techniques confirmed the presence of a considerable amount of functional groups in the structure of the polyols. Finally, various fluorescent rigid foams, based on the functionalized polyols, were synthesized. Copyright © 2012 Society of Chemical Industry     

Marked decrease of neuropeptide Y Y2 receptor binding sites in the hippocampus in murine prion disease

Using autoradiographic binding methodology with monoiodinated peptide YY together with the agonists neuropeptide Y (NPY) and NPY (13-36), as well as in situ hybridization with oligonucleotide probes complementary to the NPY Y2 receptor (Y2-R) mRNA, we have studied whether or not intracerebral prion inoculation affects Y2-Rs in male CD-1 mice. Monoiodinated peptide YY binding, mainly representing Y2-Rs, was down-regulated by 85% in the CA1 strata oriens and radiatum and by 50-65% in the CA3 stratum oriens 110-140 days postinoculation. In the CA3 stratum radiatum, where the mossy fibers from the dentate granule cells project, there was a significant decrease in PYY binding at 110-120 days. Y2-R mRNA, moderately expressed both in the CA1 and CA3 pyramidal cell layers and the granule cell layer in the dentate gyrus, showed a slight, but not significant, decrease in CA3 neurons 130 days postinoculation. The results indicate that the accumulation of the scrapie prion protein in the CA1-3 region strongly inhibits NPY binding at the Y2-Rs, which, however, is only marginally due to reduced Y2-R mRNA expression. The loss of the ability of NPY to bind to inhibitory Y2-Rs may cause dysfunction of hippocampal circuits and may contribute to the clinical symptoms in mouse scrapie.