Using natural prawn (Penaeus japonicus), a comparison study was conducted between super chilling (؊2˚C) and cool (5˚C) storage for the effectiveness of keeping fish meat fresh. Brightness of the tail color could be retained longer using super chilling storage compared to traditional refrigeration. In addition, a significant color difference in a values between the two methods was confirmed when a colorimeter was used. As a physical property of the meat, significant softening was observed after 2 days refrigeration. However, in super chilling storage, no softening was observed even after 3 days of storage. Light microscopy showed the lowering of intercellular connections in the softened meat. The rise in K-values was suppressed in super chilling storage. From these results, it can be expected that super chilling storage is able to maintain the color of prawns and the physical properties of the meat, and consequently offers potential as a new storage technique suitable for replacing refrigeration.

No abstract

OBJECTIVE To evaluate the cytotoxicity of various hand disinfectants and ozonated water to human keratinocytes using a cultured epidermal model. DESIGN Using a test protocol from the Organization for Economic Co-operation and Development, investigators applied hand disinfectants containing either 83% ethanol, 0.2% benzalkonium chloride, 0.5% povidone-iodine, 1% chlorhexidine, 1% chlorhexidine ethanol, or ozonated water to a cultured human epidermal model. Surface morphology and histologic changes were evaluated by scanning electron microscopy and hematoxylin-eosin staining. MAIN OUTCOME MEASURES Production of inflammatory cytokine interleukin 1α by keratinocytes and cell death rate. MAIN RESULTS Electron microscopic analysis revealed the creation of small holes on the stratum corneum, and hematoxylin-eosin staining revealed perinuclear vacuolation of keratinocytes and cells with a condensed nucleus. Interleukin 1α was detected in the culture supernatants. More than 80% of keratinocytes did not survive after a 15-minute application of disinfectants. However, no significant damage was detected with ozonated water. CONCLUSIONS Ozonated water did far less damage to keratinocytes than the tested disinfectants. Although the ability of ozonated water to disinfect hands of medical staff members requires further study, it might serve as an alternative with minimum cytotoxicity.

BackgroundIt has been reported that some single-nucleotide polymorphisms (SNPs) in lipid regulators such as apolipoproteins and cell surface molecules for hepatitis C virus (HCV) entry into hepatocytes are associated with HCV infection. However, it is unknown how HCV infection is affected by altered lipid metabolism resulting from the SNPs. We investigated the relationship between these SNPs and HCV infection status, and also analyzed the mechanism by which these SNPs mediate HCV infection via lipid metabolism alterations.MethodsSerum lipid and apolipoprotein profiles were tested in 158 HCV-positive and 220 HCV-negative subjects. We selected 22 SNPs in five lipid regulator genes which were related to HCV entry into hepatocytes and to lipid metabolism (APOA1, APOB, SR-B1, LDLR, and APOE), and their polymorphisms were analyzed using the PCR-sequence-specific oligonucleotide probe-Luminex method.ResultsAn APOB N4311S (g.41553a > g) SNP, rs1042034, was significantly associated with HCV positivity; the HCV positivity rate for the minor allele AA genotype was significantly higher than for genotype AG + GG (P = 0.016). Other SNPs except for APOB P2712L SNP rs676210, which is in linkage disequilibrium with rs1042034, showed no significant difference in genotype distribution. The serum level of low density lipoprotein-cholesterol (LDL-C) in the genotype AA group was significantly lower than in the genotype non-AA group (P = 0.032), whereas the triglyceride (TG) level was significantly higher (P = 0.007).ConclusionAn APOB SNP, rs1042034, is closely associated with HCV infection through lipid metabolism alteration. The minor allele AA genotype might contribute to facilitating serum LDL uptake into hepatocytes via LDLR by modifying their affinity and interaction and may have an influence on HCV infection by their entry to the liver through the LDLR.