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Notes: 1. Heavy alcohol consumption has been known as a risk factor for hypertension, although the mechanism by which alcohol intake causes hypertension remains elusive.2. We tested the hypothesis that brief exposure to ethanol augments vascular contractility through the stress response in human chorionic plate arteries.3. Human chorionic plate arteries were mounted in organ baths and exposed to 5% ethanol for 15, 30 or 45 min.4. Brief exposure for 45 min, but not 15 min, not only augmented contractility to KCl and 5-hydroxytryptamine 5 h after the end of exposure, but also increased the expression of heat shock protein (HSP) 70 in the tissues.5. Reverse transcription–polymerase chain reaction showed gradual increases of hsp70 mRNA expression, but not heat shock cognate 70 (hsc70), hsp90α or glucose regulatory protein 78 (grp78) mRNA expression, in an exposure time-dependent manner 3 h after the end of exposure.6. These results indicate that ethanol augments vascular contractility through the stress response.

Notes: Mixed vegetable juice was acidified to a pH below 4 and subjected to pasteurization regimes between 80 and 100 °C. Hunter colour scale values (L, a and b) of the pasteurized samples were analysed to determine the kinetics of green and total colour degradation. The ‘a’ value was chosen as the physical parameter for green colour while ‘Lab’ represented the total colour. A concept, based on fractional conversion, was used for the determination of kinetic parameters. The results revealed that degradation of green and total colour of the acidified vegetable juice followed first-order kinetics. Temperature dependency of the rate constants for both the green and the total colour could be described by the Arrhenius relationship. The activation energies of green and total colour degradation were 49.19 and 29.00 kJ mol−1, respectively.

Notes: Background  A keloid results from excessive collagen deposition, the cause of which remains elusive. A thorough understanding of the pathophysiology of keloid tissue can help determine the most appropriate treatment strategy.Objectives  To assess the differences in gene expression between keloids and adjacent normal skin in order to define the genes involved in keloid formation.Methods  Three Korean patients with keloids underwent excision of the keloid and adjacent normal skin, which was used as the control. We investigated expression patterns of genes in the keloids and the normal skin using cDNA microarray and in situ hybridization techniques.Results  Nine genes in the keloid tissue were consistently upregulated over the 2·0 ratio compared with the normal control from the cDNA microarray composed of 3063 clones: collagen type I α1 (〈accessionId ref="info:ddbj-embl-genbank/NM_000088"〉NM_000088), DNA segment on chromosome 21 (unique) 2056 expressed sequence (D21S2056E, NNP-1, 〈accessionId ref="info:ddbj-embl-genbank/NM_003683"〉NM_003683), suppressor of Ty 5 homologue (〈accessionId ref="info:ddbj-embl-genbank/NM_003169"〉NM_003169), phosphoglycerate dehydrogenase (〈accessionId ref="info:ddbj-embl-genbank/NM_032692"〉NM_032692), adenosine triphosphate synthase β (〈accessionId ref="info:ddbj-embl-genbank/NM_001686"〉NM_001686), serine (or cysteine) proteinase inhibitor, clade H (heat shock protein 47, 〈accessionId ref="info:ddbj-embl-genbank/NM_001235"〉NM_001235), LIV-1 protein, oestrogen regulated (LIV-1, 〈accessionId ref="info:ddbj-embl-genbank/NM_012319"〉NM_012319), interleukin-11 receptor α (IL11RA, 〈accessionId ref="info:ddbj-embl-genbank/NM_004512"〉NM_004512) and carbonyl reductase 3 (CBR3, 〈accessionId ref="info:ddbj-embl-genbank/NM_001236"〉NM_001236). From the in situ hybridization study, the staining signals in the keloid tissue hybridized with anti sense probes of NNP-1 mRNA were stronger than signals in normal controls. Further, endothelial epithelium, but not the epidermis, expressed the signal equally in both keloid and normal control tissue.Conclusions  We identified nine upregulated genes in keloid tissue using cDNA microarray. Of the nine, the NNP-1 gene was confirmed by topological information using the in situ hybridization technique. We conclude that these nine genes, especially NNP-1, probably contribute either directly or indirectly to keloid formation.

Notes: R-curve behavior of Si3N4–BN composites and monolithic Si3N4 for comparison was investigated. Si3N4–BN composites showed a slowly rising R-curve behavior in contrast with a steep R-curve of monolithic Si3N4. BN platelets in the composites seem to decrease the crack bridging effects of rod-shaped Si3N4 grains for small cracks, but enhanced the toughness for long cracks as they increased the crack bridging scale. Therefore, fracture toughness of the composites was relatively low for the small cracks, but it increased significantly to ∼8 MPa·m1/2 when the crack grew longer than 700 μm, becoming even higher than that of the monolithic Si3N4.

Notes: Background.  Helicobacter pylori is a causative agent of gastritis, and H. pylori infection is thought to be correlated with iron-deficiency anemia (IDA) at puberty. The H. pylori feoB gene product, a high-affinity ferrous iron transporter, plays a central role in iron acquisition and virulence. This study was undertaken to analyze H. pylori feoB status according to clinical data, including antral gastritis with or without IDA.Methods.  Fourteen H. pylori-positive patients aged from 10 to 18 years were categorized into subgroups based on the presence or absence of IDA. Eight patients were diagnosed as having IDA; the other six showed normal hematological findings. Genomic DNA was isolated from H. pylori cultured from each gastric biopsy specimen. Five sets of primers were used for the PCR amplification of the feoB gene. Linking and sequencing of PCR products generated the feoB region, which was 1.93 kb in size. The feoB gene sequences of H. pylori J99 and 26695 were compared with the clinical strains, and the sequences of feoB regions in the IDA (+) and (–) groups were compared.Results.  Sequence analysis of the complete coding region of the feoB gene revealed 16 sites of polymorphism or mutation. Among these, three polymorphisms (E/T254A, I263V, and K511Q) were indigenous to the Korean clinical strains. Although statistically significant differences were observed at four sites (K127T, A273S/P, I438V and I441T) between IDA (+) and (–), the number of specimens was too low to assess the significance of the differences.Conclusion.  The four polymorphisms of the feoB gene observed appear to be related to the clinical phenotype of IDA, but the relation is unclear because of the small number of strains studied. Further studies are required to confirm a correlation between IDA and H. pylori infection.

Notes: Vibrio vulnificus causes fatal septicemia in human hosts, which is the consequence of raw shellfish consumption. The mortality following septicemia is dependent on the in vivo production of inflammatory mediators, including tumor necrosis factor-alpha (TNFα). The present study was set up to investigate the association of quorum sensing in V. vulnificus with the host immune response. The effect of quorum sensing on cytotoxicity and the production of proinflammatory mediators was examined using the murine macrophage cell-line RAW264.7. Cytotoxicity was determined by measuring lactate dehydrogenase release in the culture medium. Extracellular products from luxS- and smcR-deficient mutants exhibited weak cytotoxic effects on RAW264.7 cells. The production of the proinflammatory cytokines TNFα, IL-1β and IL-6 was measured with real-time PCR and ELISA, and production was measured with Griess reagents. Mutation of both luxS and smcR delayed the transcription of TNFα, IL-1β and IL-6 genes. Also, levels of both TNFα and nitric oxide induced by luxS- and smcR-deficient mutants were significantly lower than those induced by parent strains. These results suggest that quorum sensing could be involved in the modulation of TNFα and nitric oxide produced from host cells by regulating virulence factors, and that V. vulnificus facilitates its host's mortality and bacterial survival by enhancing virulence on host cells.

Notes: Investigation of γ -channel widening behavior in a nickel-base single crystal superalloy during uniaxial tensile creep tests was carried out. Scanning electron microscopy (SEM) was adopted to reveal the microstructural evolution of γ -channel and the dimension of γ -channel. It was found that different tests condition such as temperature, time and stress in tensile creep tests all influenced the γ -channel widening behavior, and a parabolic rate law governs the mean increase value of γ -channel width. The stress and temperature enhanced the γ -channel widening. The γ -channel widening was the result of directionally diffusion of multiatom

Notes: In order to quantitatively analyze the critical strain for the initiation of dynamicrecrystallization in Ni-Fe-based Alloy 718, a series of uniaxial compression tests was conducted in the temperature range 927°C - 1066°C and the strain rate range 5 x 10〈sup〉-4〈/sup〉 s〈sup〉-1〈/sup〉 - 5 s〈sup〉-1〈/sup〉 with varying initialgrain size. The critical strains were graphically determined based on one parameter approach and microscopically confirmed. The effect of γ'' (matrix-hardening phase) and δ (grain boundary phase)on the critical strain was simply discussed. The constitutive model for the critical strain of Alloy 718 was constructed using the experimental data obtained from the higher strain rate and the temperaturerange between 940°C and 1040°C