Expression patterns of class I <Emphasis Type="Italic">KNOX</Emphasis> and <Emphasis Type="Italic">YABBY</Emphasis> genes in <Emphasis Type="Italic">Ruscus aculeatus</Emphasis> (Asparagaceae) with implications for phylloclade homology

STM (RaSTM) and YAB2 (RaYAB2) homologues were isolated from Ruscus aculeatus (Asparagaceae, monocots), and their expressions were analyzed by real-time polymerase chain reaction (PCR) to assess hypotheses on the evolutionary origin of the phylloclade in the Asparagaceae. In young shoot buds, RaSTM is expressed in the shoot apex, while RaYAB2 is expressed in the scale leaf subtending the shoot bud. This expression pattern is shared by other angiosperms, suggesting that the expression patterns of RaSTM and RaYAB2 are useful as molecular markers to identify the shoot and leaf, respectively. RaSTM and RaYAB2 are expressed concomitantly in phylloclade primordia. These results suggest that the phylloclade is not homologous to either the shoot or leaf, but that it has a double organ identity.     

Relationship between the redox change in yellow fluorescent protein of Vibrio fischeri strain Y1 and the reversible change in color of bioluminescence in vitro.

To elucidate the reversible change in the color of bioluminescence (BL) arising from Vibrio fischeri Y1, the relationship between the BL color and the redox state of endogenous yellow fluorescent protein (YFP), carrying riboflavin 5'-phosphate (FMN), has been investigated in vitro. YFP lost fluorescence with a maximum at 538 nm when reduced, and retrieved its original fluorescence upon reoxidation. Such a change in YFP fluorescence was analogous to that of free FMN. In the NADH/FMN oxidoreductase-coupled luciferase reaction with YFP, yellow BL peaking around 535 nm was largely depressed when sodium dithionite was added. This phenomenon can be attributed to the reduction of YFP; i.e., reduced YFP does not participate in the luciferase reaction as a secondary emitter. On admitting air into the reaction mixture, the yellow light characteristic of V. fischeri Y1 BL was regenerated. These results indicate that the reversible change in YFP fluorescence is caused by the redox change of YFP-bound FMN, and that the change in BL color between blue and yellow is associated with the redox state of YFP.     

Age-related changes of dietary intake and blood eicosapentaenoic acid, docosahexaenoic acid, and arachidonic acid levels in Japanese men and women

We studied the relationship between dietary intake and the blood compositions of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (ARA) in four study groups with different ages and sexes. One hundred and four subjects were recruited. Dietary records together with photographic records from 28 consecutive days were amassed and the fatty acid composition in erythrocyte membranes and plasma lipid fractions was analyzed. Fish intake in the elderly group was significantly higher than that in the young group in both men and women. The compositions of ARA in erythrocytes and plasma phospholipids in the elderly were lower than those in the young, but the ARA intake was nearly identical. In the elderly group, the percentage of dietary ARA consumed at the same time as EPA and DHA derived from fish was high. We considered that these fatty acids markedly inhibited the incorporation of dietary ARA into blood phospholipids.     

Metabolism of free oligosaccharides is facilitated in the och1Δ mutant of Saccharomyces cerevisiae

In eukaryotic cells, it is known that N-glycans play a pivotal role in quality control of carrier proteins. Although "free" forms of oligosaccharides (fOSs) are known to be accumulated in the cytosol, the precise mechanism of their formation, degradation and biological relevance remains poorly understood. It has been shown that, in budding yeast, almost all fOSs are formed from misfolded glycoproteins. Precise structural analysis of fOSs revealed that several yeast fOSs bear a yeast-specific modification by Golgi-resident α-1,6-mannosyltransferase, Och1. In this study, structural diversity of fOSs in och1Δ cells was analyzed. To our surprise, several fOSs in och1Δ cells have unusual α-1,3-linked mannose residues at their non-reducing termini. These mannose residues were not observed in wild-type cells, suggesting that the addition of these unique mannoses occurred as a compensation of Och1 defect. A significant increase in the amount of fOSs modified by Golgi-localized mannosyltransferases was also observed in och1Δ cells. Moreover, the amount of processed fOSs and intracellular α-mannosidase (Ams1) both increased in this mutant. Up-regulation of Ams1 activity was also apparent for cells treated with cell wall perturbation reagent. These results provide an insight into a possible link between catabolism of fOSs and cell wall stress.     

Thermal conversion of alkaline lignin and its structured derivatives to porous carbonized materials

Alkaline lignin was thermally converted to microporous carbon in ca. 50% yield by heating up from room temperature to 900 °C without activation process under flowing of an argon gas. The carbonized material prepared by heating up conditions of 1 °C min⁻¹ showed 530 m²/g of the Brunauer-Emmett-Teller (BET) specific surface area, which increased to 740 m²/g after washing with water. Furthermore, alkaline lignin derivatives were structured as micron scale particles by micelle formation and polymer gelation techniques. Carbonization of the structured lignins could afford high porous materials having BET surface areas above 1000 m²/g without surface activation processes.     

Association of HLA and post-schistosomal hepatic disorder: a systematic review and meta-analysis

Several human genetic variants, HLA antigens and alleles are reportedly linked to post-schistosomal hepatic disorder (PSHD), but the results from these reports are highly inconclusive. In order to estimate overall associations between human genetic variants, HLA antigens, HLA alleles and PSHD, we systematically reviewed and performed a meta-analysis of relevant studies in both post-schistosomal hepatic disorder and post-schistosomal non-hepatic disorder patients. PubMed, Scopus, Google Scholar, The HuGE Published Literature database, Cochrane Library, and manual search of reference lists of articles published before July 2009 were used to retrieve relevant studies. Two reviewers independently selected articles and extracted data on study characteristics and data regarding the association between genetic variants, HLA antigens, HLA alleles and PSHD in the form of 2×2 tables. A meta-analysis using fixed-effects or random-effects models to pooled odds ratios (OR) with corresponding 95% confidence intervals were calculated only if more than one study had investigated particular variation. We found 17 articles that met our eligibility criteria. Schistosoma mansoni and Schistosoma japonicum were reported as the species causing PSHD. Since human genetic variants were only investigated in one study, these markers were not assessed by meta-analysis. Thus, only HLA-genes (a total of 66 HLA markers) were conducted in the meta-analysis. Our meta-analysis showed that human leucocyte antigens HLA-DQB1*0201 (OR=2.64, P=0.018), DQB1*0303 (OR=1.93, P=0.008), and DRB1*0901 (OR=2.14, P=0.002) alleles and HLA-A1 (OR=5.10, P=0.001), A2 (OR=2.17, P=0.005), B5 (OR=4.63, P=0.001), B8 (OR=2.99, P=0.02), and B12 (OR=5.49, P=0.005) serotypes enhanced susceptibility to PSHD, whereas HLA-DQA1*0501 (OR=0.29, P≤0.001) and DQB1*0301 (OR=0.58, P=0.007) were protective factors against the disease. We further suggested that the DRB1*0901-DQB1*0201, DRB1*0901-DQB1*0303 and A1-B8 haplotypes enhanced susceptibility to PSHD, whereas DQA1*0501-DQB1*0301 linkage decreased the risk of PSHD. The result improved our understanding of the association between the HLA loci and PSHD with regard to pathogenic or protective T-cells and provided novel evidence that HLA alleles may influence disease severity.     

Morphological analysis of ghrelin and its receptor distribution in the rat pancreas

Ghrelin, a novel peptide isolated from stomach tissue of rats and humans, has been identified as the endogenous ligand for the growth hormone secretagogue receptor (GHS-R). In addition to its secretion from the stomach, ghrelin is also expressed in the hypothalamic arcuate nucleus, intestine, kidney, placenta, and pancreas. GHS-R mRNA, on the other hand, is expressed in the hypothalamus, pituitary, heart, lung, liver, pancreas, stomach, intestine, and adipose tissue. Ghrelin is considered to have important roles in feeding regulation and energy metabolism as well as in the release of growth hormone (GH). Recent physiological experiments on the pancreas have shown that ghrelin regulates insulin secretion. However, sites of action of ghrelin in the pancreas are yet to be identified. In this study, to gain insight into the role of ghrelin in rat pancreatic islets, we used immunohistochemistry to determine the localization of ghrelin and GHS-R in islet cells. Double fluorescence immunohistochemistry revealed that weak GHS-R-like immunoreactivity was found in B cells containing insulin. GHS-R immunoreactivity overlapped that of glucagon-like immunoreactive cells. Moreover, both ghrelin and GHS-R-like immunoreactivities were detected mostly in the same cells in the periphery of the islets of Langerhans. These observations suggest that ghrelin is synthesized and secreted from A cells, and acts back on A cells in an autocrine and/or paracrine manner. In addition, ghrelin may act on B cells via GHS-R to regulate insulin secretion.     

Luteolin inhibits endothelin-1 secretion in cultured endothelial cells

We discovered that luteolin, a typical flavonoid contained in various kinds of plants, inhibits the secretion and gene expression of endothelin-1 (ET-1), a potent vasoconstrictor regulating blood pressure, in porcine aortic endothelial cells. Its ED50 was about 10 microM. In addition, the inhibition of ET-1 by a glycoside compound of luteolin (luteolin-6-C-glucoside) was weak.     

Evaluation of adriamycin nephropathy by an in vivo electron paramagnetic resonance

A rat model for human minimal change nephropathy was obtained by the intravenous injection of adriamycin (ADR) at 5 mg/kg. By using an in vivo electron paramagnetic resonance (EPR) spectrometer operating at 700 MHz, the temporal changes in signal intensities of a nitroxide radical, 4-hydroxyl-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL), in the kidneys of rats with ADR nephropathy were investigated. The decay rate of the EPR signal intensity obtained in the kidney is indicative of the renal reducing ability. It was found that the reducing ability in the kidney declined on the 7th day after ADR administration and recovered after the 14th day. Impairment of the reducing ability occurred before the appearance of continuous urinary protein. The in vitro EPR study showed that this impairment of in vivo renal reducing ability is related to impairment of the reducing ability in the mitochondria.