日本人男性集団では肥満の体格測定指標の方がCTによる指標よりも頸動脈中膜内膜肥厚とより強く関係していた

Journal of atherosclerosis and thrombosis. 2019 Dec 1;26(12):1102-1114滋賀医科大学令和元年

Platinum group elements in the precipitation of the dry region of Xinjiang and factors affecting their deposition to land: the case of Changii City, China

AbstractPlatinum group elements and their compounds are a class of incident allergens and some platinum group element compounds also have carcinogenic effects. They accumulate in city environment as a result of emissions from catalysts used for vehicle exhausts. In this study, sixteen precipitation samples were collected on the north campus of Changji University located in the center of Changji. They were analyzed for palladium (Pd), platinum (Pt), and rhodium (Rh) by inductively coupled plasma–mass spectrometry. The average concentrations of Pd, Pt, and Rh were found to be 26.73ng L-1 (range: 3.18–84.25ng L-1), 1.71ng L-1 (range: below the detection limit to 6.38ng L-1), and 1.49ng L-1 (range: below the detection limit to 3.53ng L-1), respectively. Pd deposition was most pronounced for single precipitation events, reaching 35.47ng m-2 (range: 1.27–101.10ng m-2), followed by Rh (max. 4.96ng m-2, range: 0–14.85ng m-2) and Pt (max. 1.38ng m-2, range: 0-7.66ng m-2). Both Pd and Pt were higher in winter than in other seasons in terms of their wet deposition amounts and their concentrations in precipitation, whereas Rh was lower in winter. Moreover, the results indicated that discharge from coal combustion in winter, the amount of precipitation, and the number of dry days before rainfall events all significantly affected the wet deposition amount and precipitation concentration of platinum group elements. Pd deposition flux was highest (reaching 5.47×103 ng m-2) corresponding to 18 and 16 times the Rh and Pt fluxes, respectively. Finally, vehicle exhaust catalyst emissions from motor vehicles were not the only source of atmospheric platinum group metals in the city environment; in fact, combustion of coal in winter was found to be the dominant contributor of Pt and Pd in the atmosphere

Fermentation of tomato juice improves \u3cem\u3ein vitro\u3c/em\u3e bioaccessibility of lycopene

The impact of fermentation (Saccharomyces cerevisiae ATCC 9763) on the bioaccessibility of lycopene in a model tomato juice was examined. The physicochemical and structural properties of the tomato tissue were determined after fermentation and the bioaccessibility of lycopene was monitored using a simulated gastrointestinal tract. A lycopene concentration of 45.1 mg/100 g was obtained under optimal fermentation conditions. The cell walls of the tomato cells were hydrolyzed and disrupted by fermentation. Cell disruption decreased the pectin content and reduced the tissue fragment size, thereby reducing gravitational separation and facilitating lycopene release. The lycopene bioaccessibility in the tomato juices increased in the following order: unfermented (8.5%) \u3c fermented (11.4%) \u3c unfermented-emulsified (13.6%) \u3c fermented-emulsified (22.7%). These effects were attributed to a combination of greater tomato tissue disruption and enhanced mixed micelle formation. Our results may be useful for the development of functional foods and beverages with improved health benefits

CI431, an Aqueous Compound from Ciona intestinalis L., Induces Apoptosis through a Mitochondria-Mediated Pathway in Human Hepatocellular Carcinoma Cells

In the present studies, a novel compound with potent anti-tumor activity from Ciona intestinalis L. was purified by acetone fractionation, ultrafiltration, gel chromatography and High Performance Liquid Chromatography. The molecular weight of the highly purified compound, designated CI431, was 431Da as determined by HPLC-MS analysis. CI431 exhibited significant cytotoxicity to several cancer cell types. However, only a slight inhibitory effect was found when treating the benign human liver cell line BEL-7702 with the compound. To explore its mechanism against hepatocellular carcinoma, BEL-7402 cells were treated with CI431 in vitro. We found that CI431 induced apoptotic death in BEL-7402 cells in a dose- and time-dependent manner. Cell cycle analysis demonstrated that CI431 caused cell cycle arrest at the G2/M phase, and a sub-G1 peak appeared after 24 h. The mitochondrial-mediated pathway was implicated in this CI431-induced apoptosis as evidenced by the disruption of mitochondrial membrane potential. The results suggest that the CI431 induces apoptosis in BEL-7402 human hepatoma cells by intrinsic mitochondrial pathway

Dynamic Interplay between the Co-Opted Fis1 Mitochondrial Fission Protein and Membrane Contact Site Proteins in Supporting Tombusvirus Replication

Plus-stranded RNA viruses have limited coding capacity and have to co-opt numerous pro-viral host factors to support their replication. Many of the co-opted host factors support the biogenesis of the viral replication compartments and the formation of viral replicase complexes on subverted subcellular membrane surfaces. Tomato bushy stunt virus (TBSV) exploits peroxisomal membranes, whereas the closely-related carnation Italian ringspot virus (CIRV) hijacks the outer membranes of mitochondria. How these organellar membranes can be recruited into pro-viral roles is not completely understood. Here, we show that the highly conserved Fis1 mitochondrial fission protein is co-opted by both TBSV and CIRV via direct interactions with the p33/p36 replication proteins. Deletion of FIS1 in yeast or knockdown of the homologous Fis1 in plants inhibits tombusvirus replication. Instead of the canonical function in mitochondrial fission and peroxisome division, the tethering function of Fis1 is exploited by tombusviruses to facilitate the subversion of membrane contact site (MCS) proteins and peroxisomal/mitochondrial membranes for the biogenesis of the replication compartment. We propose that the dynamic interactions of Fis1 with MCS proteins, such as the ER resident VAP tethering proteins, Sac1 PI4P phosphatase and the cytosolic OSBP-like oxysterol-binding proteins, promote the formation and facilitate the stabilization of virus-induced vMCSs, which enrich sterols within the replication compartment. We show that this novel function of Fis1 is exploited by tombusviruses to build nuclease-insensitive viral replication compartment

Role of MicroRNA-26b in Glioma Development and Its Mediated Regulation on EphA2

BACKGROUND: MicroRNAs (miRNAs) are short, non-coding RNAs that regulate the expression of multiple target genes. Deregulation of miRNAs is common in human tumorigenesis. Low level expression of miR-26b has been found in glioma cells. However, its underlying mechanism of action has not been determined. METHODOLOGY/PRINCIPAL FINDINGS: Real-time PCR was employed to measure the expression level of miR-26b in glioma patients and cells. The level of miR-26b was inversely correlated with the grade of glioma. Ectopic expression of miR-26b inhibited the proliferation, migration and invasion of human glioma cells. A binding site for miR-26b was identified in the 3'UTR of EphA2. Over-expression of miR-26b in glioma cells repressed the endogenous level of EphA2 protein. Vasculogenic mimicry (VM) experiments were performed to further confirm the effects of miR-26b on the regulation of EphA2, and the results showed that miR-26b inhibited the VM processes which regulated by EphA2. SIGNIFICANCE: This study demonstrated that miR-26b may act as a tumor suppressor in glioma and it directly regulates EphA2 expression. EphA2 is a direct target of miR-26b, and the down-regulation of EphA2 mediated by miR-26b is dependent on the binding of miR-26b to a specific response element of microRNA in the 3'UTR region of EphA2 mRNA