Phenolic Compound Profiles in Grape Skins of Cabernet Sauvignon, Merlot, Syrah and Marselan Cultivated in the Shacheng Area (China)

The phenolic compounds in the grape skins of Cabernet Sauvignon (CS), Merlot (ML), Syrah (SY) and Marselan (MS) from Shacheng, in China, were compared using HPLC-MS/MS. The results showed that the types and levels of phenolic compounds varied greatly with cultivars. Malvidin derivatives were the main anthocyanins. CS and ML showed a higher content of malvidin-3-O-(6-O-acetyl)-glucoside than malvidin-3-O-(trans-6-O- coumaryl)-glucoside, while SY and MS differed from CS and ML. ML had higher delphinidin and cyanidin derivatives, SY had higher peonidin derivatives, while malvidin and petunidin were higher in MS. The total content of flavonols, flavan-3-ols, phenolic acids and stilbenes in grape skins showed no difference among CS, ML and MS. Isorhamnetin-3-O-glucoside (CS, ML, MY), quercetin-3O-glucoside (SY), procyanidin trimer (SY, MS), procyanidin dimer (CS, ML), syringetin-3-O-glucoside, trans-cinnamic acid and resveratrol were the most abundant non-anthocyanin phenolic compounds. Cluster analysis showed that CS and ML, and SY and MS had similar phenolic profiles

Precision Measurement of the Proton Flux in Primary Cosmic Rays from Rigidity 1 GV to 1.8 TV with the Alpha Magnetic Spectrometer on the International Space Station

A precise measurement of the proton flux in primary cosmic rays with rigidity (momentum/charge) from 1 GV to 1.8 TV is presented based on 300 million events. Knowledge of the rigidity dependence of the proton flux is important in understanding the origin, acceleration, and propagation of cosmic rays. We present the detailed variation with rigidity of the flux spectral index for the first time. The spectral index progressively hardens at high rigidities.</p

Ambient air pollution and homocysteine: Current epidemiological evidence and a call for further research.

Elevated blood homocysteine (Hcy) is an independent risk factor for cardiovascular disease. A growing number of studies have evaluated the link between air pollution and blood Hcy levels, but the results are inconsistent. To date, no systematic review of the published studies has been conducted yet. We aimed to provide a comprehensive overview of these studies. We systematically searched three international databases (PubMed, Web of Science, and Embase) and four Chinese databases (Wanfang, CNKI, CBM, and VIP) for peer-reviewed epidemiological studies investigating associations between ambient air pollutants and Hcy levels published before December 2019. We screened literature, extracted data, assessed methodological quality, and evaluated the risk of bias of the included studies. Of 1157 identified articles, 10 were finally included in this systematic review. Most were cross-sectional studies and were performed in developed countries. Particulate matter with aerodynamic diameters less than 2.5 mu m (PM2.5) and/or 10 mu m (PM10) were investigated in all of the included studies. Overall, the evidence generally supports a positive association between higher PM concentrations and elevated Hcy levels. However, high heterogeneity in terms of study participants, study design, exposure duration, and particle components and sources, low methodological quality and probable high risk of bias in some studies, and limited literature number precluded us from drawing a robust conclusion. Associations between Hcy and gaseous pollutants were explored in only one or two studies, and the results were inconclusive. Additional, well-designed studies remain required to validate the association between air pollution and Hcy

Ambient air pollution and depression: A systematic review with meta-analysis up to 2019.

Although epidemiological studies have evaluated the associations of ambient air pollution with depression, the results remained mixed. To clarify the nature of the association, we performed a comprehensive systematic review and meta-analysis with the Inverse Variance Heterogeneity (IVhet) model to estimate the effect of ambient air pollution on depression. Three English and four Chinese databases were searched for epidemiologic studies investigating associations of ambient particulate (diameter &lt;= 2.5 mu m (PM2.5), &lt;= 10 mu m (PM10)) and gaseous (nitric oxide (NO), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2) and ozone (O-3)) air pollutants with depression. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were calculated to evaluate the strength of the associations. We identified 22 eligible studies from 10 countries of the world. Under the IVhet model, per 10 mu g/m(3) increase in long-term exposure to PM2.5 (OR: 1.12, 95% CI: 0.97-1.29, I-2: 51.6), PM10 (OR: 1.04, 95% CI: 0.88-1.25, I-2: 85.7), and NO2 (OR: 1.05, 95% CI: 0.83-1.34, I-2: 83.6), as well as short-term exposure to PM2.5 (OR: 1.01, 95% CI: 0.99-1.04, I-2: 51.6), PM10 (OR: 1.01, 95% CI: 0.98-1.04, I-2: 86.7), SO2 (OR: 1.03, 95% CI: 0.99-1.07, I-2: 71.2), and O-3 (OR: 1.01, 95% CI: 0.99-1.03, I-2: 82.2) was not significantly associated with depression. However, we observed significant association between short-term NO2 exposure (per 10 mu g/m(3) increase) and depression (OR: 1.02, 95% CI: 1.00-1.04, I-2: 65.4). However, the heterogeneity was high for all of the pooled estimates, which reduced credibility of the cumulative evidence. Additionally, publication bias was detected for six of eight meta-estimates. In conclusion, short-term exposure to NO2, but not other air pollutants, was significantly associated with depression. Given the limitations, a larger meta-analysis incorporating future well-designed longitudinal studies, and investigations into potential biologic mechanisms, will be necessary for a more definitive result

Long-term self-renewing human epicardial cells generated from pluripotent stem cells under defined xeno-free conditions

Therapeutic cell differentiatio

Examining markers in 8q24 to explain differences in evidence for association with cleft lip with/without cleft palate between Asians and Europeans

10.1002/gepi.21633Genetic Epidemiology364392-399GENY