A solvent partitioning procedure for the separation of chlorophylls from their degradation products and carotenoid pigments

A simple liquid/liquid partitioning procedure was developed which employed aqueous acetonitrile and hexane, for the isolation of chlorophyll and pheophytin. This procedure separated these pigments from other interfering pigmented compounds. The efficacy of this solvent separation method was evaluated using commercially available chlorophylla, b, pheophytina, b, carotenoids, and algal pigment extracts. The recovery efficiencies of this solvent partitioning process for chlorophyll a and pheophytina have been shown to be 95–98% and 93–96%, respectively, furthermore, the chlorophylla fraction was practically free of any contaminating pigments. It appears that a more accurate assessment of chlorophylla and pheophytina can be accomplished employing liquid/liquid partitioning than with the present standard method.     

TDAG51 Is Not Essential for Fas/CD95 Regulation and Apoptosis In Vivo

Fas/CD95 is a key regulator of apoptotic signaling, which is crucial for the maintenance of homeostasis in peripheral lymphoid organs. TDAG51 has been shown to play critical roles in the up-regulation of Fas gene expression and T-cell apoptosis in vitro. In order to identify the role of TDAG51 in vivo, we generated TDAG51-deficient (TDAG51-/-) mice. Northern blotting revealed no expression of TDAG51 in TDAG51-/- mice, indicating that the TDAG51 gene was successfully targeted. TDAG51-/- mice were healthy and showed no gross developmental abnormalities. While Fas-deficient mice display marked lymphadenopathy, splenomegaly, and lymphocytosis, TDAG51-/- mice had no apparent defects in secondary lymphoid organs. Although TDAG51 is required for up-regulation of Fas expression in T-cell hybridomas, TDAG51-/- mice expressed normal levels of Fas and had normal T-cell apoptosis. Therefore, we conclude that TDAG51 is not essential for Fas up-regulation and T-cell apoptosis in vivo. There are several known homologs of TDAG51, and these homologs may substitute for TDAG51 in TDAG51-/- mice.     

The leukoaraiosis is more prevalent in the large artery atherosclerosis stroke subtype among Korean patients with ischemic stroke

Background  

Several studies have suggested that the specific stroke subtype may influence the presence of leukoaraiosis in patients with ischemic stroke. We investigated the association between stroke subtype and leukoaraiosis in Korean patients with ischemic stroke by MRI.     

Induction of cellulose in Schizophyllum commune: thiocellobiose as a new inducer.

Several mono-, di, tetra-, and polysaccharides were screened for their ability to induced cellulase production by the tetrapolar hymenomycete Schizophyllum commune. Out of 21 carbohydrates screened, 4 (thiocellobiose, carboxymethylcellulose, cellobiose, and xylan) induced all three enzymes tested (carboxymethylcellulase, beta-glucosidase, and xylanase). The inducing effect increased with rising concentrations of the inducers up to a certain value, beyond which there was either a leveling off or a decrease of the enzymatic activities. The most powerful inducer, thiocellobiose, showed the highest activity at 0.5 mM. Cellobiose, carboxymethylcellulose, and xylan showed their highest activities at 1 mM and 1%, respectively. Surprisingly, sophorose did not enhance enzyme production. The enzymatic activities were monitored over a period of 24 h. Thiocelloboise elicited a response immediately after incubation, but with all other inducers there was a latency period before their effect could be measured. High-performance liquid chromatography showed no hydrolysis of thiocellobiose when incubated in the presence of S. commune extracellular enzymes.     

AML1, the target of chromosomal rearrangements in human leukemia, regulates the expression of human complement receptor type 1 (CR1) gene.

The human CR1 gene is expressed specifically in hematopoietic cells. It is suggested that some cell-type specific factors which involve in gene-specific activation or repression exist in cells according to the result that the gene expression varies differently depend on differentiation stage. Here, we demonstrate that the integrity of a polyomavirus enhancer core sequence, 5'-TGTGGT-3', is critical to the human CR1 promoter activity. AML1 is a site-specific DNA-binding protein that recognizes the enhancer core motif TGTGGT. We show that the AML1 binds specifically to this site and activates the human CR1 promoter. Furthermore, we demonstrate that the Ets binding site (GGAA) located 2 bp upstream of the AML1 site is also involved in the regulation of the human CR1 promoter activity. Point mutations of either the AML1 or the Ets binding site that abolish the binding of the respective factors result in significant decreases of the human CR1 promoter activity. These results suggest that AML1 and Ets proteins direct the expression of the human CR1 promoter.