The outbreak of coronavirus named COVID-19, initially identified in Wuhan, China in December 2019, has spread rapidly at the global scale. Most countries have rapidly stopped almost all activities including industry, services and transportation of goods and people, thus decreasing air pollution in an unprecedented way, and providing a unique opportunity to study air pollutants. While satellite data have provided visual evidence for the global reduction in air pollution such as nitrogen dioxide (NO 2) worldwide, precise and quantitative information is missing at the local scale. Here we studied changes in particulate matter (PM 2.5 , PM 10), carbon monoxide (CO), NO 2 , sulfur dioxide (SO 2) and ozone (O 3) at 10 urban sites in Hangzhou, a city of 7.03 million inhabitants, and at 1 rural site, before city lockdown, January 1-23, during city lockdown, January 24-February 15, and during resumption, February 16-28, in 2020. Results show that city lockdown induced a sharp decrease in PM 2.5 , PM 10 , CO, and NO 2 concentrations at both urban and rural sites. The NO 2 decrease is explained by reduction in traffic emissions in the urban areas, and by lower regional transport in rural areas during lockdown, as expected. SO 2 concentrations decreased from 6.3 to 5.3 μg m −3 in the city, but increased surprisingly from 4.7 to 5.8 μg m −3 at the rural site: this increase is attributed both to higher coal consumption for heating and emissions from traditional fireworks of the Spring Eve and Lantern Festivals during lockdown. Unexpectedly, O 3 concentrations increased by 145% from 24.6 to 60.6 μg m −3 in the urban area, and from 42.0 to 62.9 μg m −3 in the rural area during the lockdown. This finding is explained by the weakening of chemical titration of O 3 by NO due to reductions of NO x fresh emissions during the non-photochemical reaction period from 20:00 PM to 9:00 AM (local time). During the lockdown, compared to the same period in 2019, the daily average concentrations in the city decreased by 42.7% for PM 2.5 , 47.9% for PM 10 , 28.6% for SO 2 , 22.3% for CO and 58.4% for NO 2 , which is obviously explained by the absence of city activities. Overall, we observed not only the expected reduction in some atmospheric pollutants (PM, SO 2 , CO, NO 2), but also unexpected increases in SO 2 in the rural areas and of ozone (O 3) in both urban and rural areas, the latter being paradoxically due to the reduction in nitrogen oxide levels. In other words, the city lockdown has improved air quality by reducing PM 2.5 , PM 10 , CO, and NO 2 , but has also decreased air quality by augmenting O 3 and SO 2 .
Background: As a neutral lipid and prominent component of the Western diet, cholesterol levels might be a risk factor for prostate cancer. However, current evidence has been inconsistent. This meta-analysis aimed to evaluate the association between blood cholesterol levels and the risk of prostate cancer.Methods: An extensive search was performed in MEDLINE and EMBASE for prospective studies that have reported the association between total cholesterol (TC), high-density lipoprotein cholesterol (HDL), and low-density lipoprotein cholesterol (LDL) levels in blood and risk of prostate cancer. Random-effects models were used to summarize the study-specific results.Results: Fourteen studies were included in this meta-analysis. In the meta-analysis, the summarized risk ratios (RR) for the highest to lowest cholesterol levels were as follows: 1.05 [95%
Our RNAseq analyses revealed that ZIP4 is a top gene up-regulated in more aggressive ovarian cancer cells. ZIP4's role in cancer stem cells has not been reported in any type of cancer. In addition, the role and regulation of ZIP4, a zinc transporter, have been studied in the context of extracellular zinc transporting. Factors other than zinc with ZIP4 regulatory effects are essentially unknown. ZIP4 expression and its regulation in epithelial ovarian cancer cells was assessed by immunoblotting, quantitative PCR, or immunohistochemistry staining in human ovarian tissues. Cancer stem cell-related activities were examined to evaluate the role of ZIP4 in human high-grade serous ovarian cancer cells in vitro and in vivo. RNAi and CRISPR techniques were used to knockdown or knockout ZIP4 and related genes. Ovarian cancer tissues overexpressed ZIP4 when compared with normal and benign tissues. ZIP4 knockout significantly reduced several cancer stem cell-related activities in EOC cells, including proliferation, anoikis-resistance, colony-formation, spheroid-formation, drug-resistance, and side-population in vitro. ZIP4-expressing side-population highly expressed known CSC markers ALDH1 and OCT4. ZIP4 knockout dramatically reduced tumorigenesis and ZIP4 overexpression increased tumorigenesis in vivo. In addition, the ZIP4-expressing side-population had the tumor initiating activity. Moreover, the oncolipid lysophosphatic acid effectively up-regulated ZIP4 expression via the nuclear receptor peroxisome proliferator-activated receptor gamma and lysophosphatic acid 's promoting effects in cancer stem cell-related activities in HGSOC cells was at least partially mediated by ZIP4 in an extracellular zinc-independent manner. Our critical data imply that ZIP4 is a new and important cancer stem cell regulator in ovarian cancer. Our data also provide an innovative interpretation for the apparent disconnection between low levels of zinc and up-regulation of ZIP4 in ovarian cancer tissues.
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