Background: Stroke is one of the leading causes of death and disability for adult men and women worldwide, and a number of studies have explored the influences of smoking on stroke. However, few studies have discussed the relationship between stroke and smoking with consideration of the following factors: sex, the number of cigarettes smoked per day, stroke subtype, and the follow-up duration. Consequently, we aimed to extend previous work by using a systematic review to explore the relationship between stroke and cigarette smoking in reference to the above factors. Methods: A systematic review was conducted using the PubMed, Embase, and Cochrane Central Register databases and the following search criteria: [“stroke” (MeSH) and “smoking” (MeSH)]. All analyses were conducted with Stata, and funnel plots and Egger regression asymmetry tests were used to assess publication bias. Results: The meta-analysis included 14 studies involving 303134 subjects. According to the meta-analysis, smokers had an overall increased risk of stroke compared with nonsmokers, with a pooled odds ratio (OR) of 1.61 (95% confidence interval [CI]: 1.34–1.93, P < .001). A subgroup analysis conducted based on smoking status revealed ORs of 1.92 (95% CI: 1.49–2.48) for current smokers and 1.30 (95% CI: 0.93–1.81) for former smokers. In addition, the relationship between stroke of any type and smoking status was also statistically significant; current smokers had an increased risk of stoke compared with nonsmokers (OR: 1.46, 95% CI: 1.04–2.07, P < .001), which was influenced by sex (men: OR: 1.54, 95% CI: 1.11–2.13, P = .002; women: OR: 1.88, 95% CI: 1.45–2.44, P < .023). From the analysis, we also observed that passive smoking increased the overall risk of stroke by 45% (OR: 1.45, 95% CI: 1.0–2.11, P < .05). Based on the dose-response meta-analysis, the risk of stroke increased by 12% for each increment of 5 cigarettes per day.

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Dendrobium catenatum Lindley is a precious plant with both dietary and medicinal applications. However, the antiproliferative activity of D. catenatum-derived peptides has not been investigated. In this study, the whole proteins of D. catenatum were extracted, hydrolysis with three proteases (alcalase 2.4L, alcalase 37017 and trypsin) was performed, and gel filtration chromatography was employed to obtain nine fractions. Fraction A3 possessed the best antiproliferative activity in vitro, with percentage inhibitions of 73.38%, 78.91% and 86.8% against HepG-2, SGC-7901 and MCF-7 cancer cells, respectively, and an inhibition of only 5.52% against L-O2 normal liver cells at 500 μg mL(-1). Subsequently, mass spectrometry revealed the existence of 10 alcalase-derived peptides in fraction A3, and the sequences of the three most abundant peptides were determined by de novo sequencing as: RHPFDGPLLPPGD, RCGVNAFLPKSYLVHFGWKLLFHFD and KPEEVGGAGDRWTC. Moreover, these peptides were synthesized and their antiproliferative activities in vitro were also confirmed. This suggests that fraction A3 may be promising for use in food and pharmaceutical applications.

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The aim of this study was to investigate the mechanism by which growth arrestspecific transcript 5 (GAS5) regulates bladder cancer cells. Bladder cancer samples were collected and tested for experiment. Dual-luciferase reporter assay was used to verify the downstream target genes for GAS5 and miR-21. The expression level of GAS5 was decreased and that of miR-21 was increased, indicating a negative correlation between the two. Patients with high GAS5 level and low miR-21 level had relatively longer survival rates. GAS5 inhibited bladder cancer cells proliferation and promoted apoptosis, and miR-21 had the opposite effects. MiR-21 was a direct target for GAS5, whereas phosphatase and tensin homolog (PTEN) was a direct target gene of miR-21. Low expression of miR-21 could reverse the proliferative and antiapoptotic effects caused by GAS5 silencing. High levels of GAS5 and low levels of miR-21 might be associated with a higher survival rate in bladder cancer patients.GAS5 could exert antiproliferative and proapoptotic effects on bladder cancer cells through miR-21 and PTEN. K E Y W O R D Sbladder cancer, growth arrest-specific transcript 5, long noncoding RNAs, miR-21 | 2847 CHEN Et al.