“
“Six kinds of

Bifidobacterium bifidum microcapsules were prepared by extrusion methods, emulsion methods and coacervation methods. Effects of preparation methods on the survival of encapsulated B. bifidum were examined. Results showed that microcapsules prepared by emulsion method with PXD101 order alginate and chitosan exhibited the best protection for B. bifidum. The diameter was 10-20 mu m, encapsulation efficiency was 90.36% and the live cell amount was 3.01 x 10(9) cfu/g after freeze-drying. Encapsulated cells exhibited significantly higher resistance to artificial gastrointestinal juice and the cell numbers were above 10(9) cfu/g after exposure to simulated gastric (pH 1.2) and bile salt (1%, w/v). Cell numbers of microencapsulated B. bifidum was 8.61 x 10(8) cfu/g after storage at High Content Screening 37 degrees C, relative humidity 60%-65% for 3 months. Results indicated microcapsules prepared with alginate

and chitosan by emulsion method could successfully protect B. bifidum against adverse conditions and it might be useful in the delivery of probiotic cultures as a functional food.”
“Phytochemical investigation of the stem bark and leaves of Hymenostegia afzelii resulted in the isolation of three new flavonoids, named afzelin A-C (1-3), together with five known compounds: 7,6-(2 ”,2 ”-dimethylpyrano)-3,5,4′-trihydroxyflavone, apigenin, 3-O-alpha-L-rhamnopyranosylcincholic acid, 3-O-beta-D-glucopyranosylcincholic acid, and dodecanoic acid 1,1′-[(1S)-1-(hydroxymethyl)-1,2-ethanediyl] ester. The

structures of 1-3 were determined by means of spectroscopic buy QNZ methods. Compounds 1-3 were tested in vitro for their preliminary cytotoxicity using the Artemia salina assay. (C) 2011 Phytochemical Society of Europe. Published by Elsevier B.V. All rights reserved.”
“Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurological disorder caused by the expansion of a polyglutamine tract in the mutant protein ataxin-1. The cerebellar Purkinje cells (PCs) are the major targets of mutant ataxin-1. The mechanism of PC death in SCA1 is not known; however, previous work indicates that downregulation of specific proteins involved in calcium homeostasis and signaling by mutant ataxin-1 is the probable cause of PC degeneration in SCA1. In this study, we explored if targeted deprivation of PC specific calcium-binding protein calbindin-D28k (CaB) exacerbates ataxin-1 mediated toxicity in SCA1 transgenic (Tg) mice. Using behavioral tests, we found that though both SCA1/+ and SCA1/+: CaB null (-/+) double mutants exhibited progressive impaired performance on the rotating rod, a simultaneous enhancement of exploratory activity, and absence of deficits in coordination, the double mutants were more severely impaired than SCA1/+ mice.