Objective To investigate the expression and clinical significance of apoptotic protease activating factor 1 (Apaf-1) and bax in prostate cancer (PCa) and benign prostatic hyperplasia (BPH). Methods Immunohistochemistry was used to detect the expression of Apaf-1 and bax in the tissues from 45 PCa patients and 60 BPH patients. Results The positive rates of Apaf-1 and bax in PCa tissues were 22.22%(10/45) and 20.00 % (9/45), respectively, while those in BPH tissues were 48.33 % (29/60) and 46.67 % (28/60). There was a statistically significant difference in the expressions of Apaf-1 and bax between two groups (P< 0.05). The expressions of Apaf-1 and bax were not correlated with the age of patients and distant metastasis (P>0.05), but they were correlated with the pathological grade and clinical stage of PCa (P< 0.05). The expressions of Apaf-1 and bax in PCa tissues were lower than those in BPH tissues. There was a positive correlation between the expression of Apaf-1 and bax (r=0.535, P<0.01). Conclusion Apaf-1 and bax might be correlated with the carcinogenesis and development of PCa.

Background Cooking oil fumes are closely related to immune response, and adipose tissue also plays an important role in immune regulation. At present, the biological effect and mechanism of inflammation of adipose tissue induced by oil fume exposure are not clear yet. Objective To investigate the inflammatory effect of different exposure duration of cooking fumes on adipose tissue in mice and explore the role of Nod-like receptor pyrin domain 3 (NLRP3)/cysteinyl aspartate specific proteinase 1 (Caspase 1)/interleukin (IL)-1β signaling pathway. Methods Forty 8-week-old female C57BL/6J mice were randomly divided into 3-day control group (CON₃ group), 7-day control group (CON₇ group), 3-day oil fume exposure group (COF₃ group), and 7-day oil fume exposure group (COF₇ group), with 10 mice in each group. The mice were exposed to oil fumes in a cooking oil fume formation and exposure equipment (COFFEE) for 20 min, followed by a 10-min pause, 1 h a day for consecutive 3 d or 7 d. General condition of mice was observed and body weight was measured every day. After exposure, blood was sampled from the eyeball. Serum levels of IL-6, IL-27, and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA). The adipose tissue of mice was collected and observed after hematoxylin-eosin (HE) staining. The percentages of CD4⁺ and CD8⁺T cells in adipose tissue were detected by flow cytometry. Real-time quantitative PCR (RT-qPCR) was used to detect the expression levels of nuclear factor-κB (NF-κB), NLRP3, Caspase 1, and IL-1β in adipose tissue. Western blot was used to detect the expression levels of NLRP3, Caspase 1, and IL-1β in adipose. Results Compared with the corresponding control group, serum IL-6, IL-27, and IL-1β contents in the COF₃ group and the COF₇ group were significantly increased (P<0.05) except IL-6 in the COF₃ group, and the levels in the COF₇ group were significantly higher than those in the COF₃ group (P<0.05). Vacuolar lipid droplets in adipocytes decreased, cytoplasm shrank, and inflammatory cells infiltrated in the COF₇ group after HE staining. The flow cytometry results showed that the proportions of CD4⁺ and CD8⁺T cells in adipocytes of the COF₃ group and the COF₇ group were increased compared to the corresponding control group, with a significant increase in the COF₇ group (P<0.05), and the CD4⁺/CD8⁺T ratio also significantly increased progressively in the two groups (P<0.05). The results of RT-qPCR showed that compared with the corresponding control group, the mRNA expression levels of NF-κB, NLRP3, Caspase 1, and IL-1β in adipose tissue of mice in the COF₃ group and the COF₇ group were significantly increased (P<0.05, P<0.01). The mRNA expression levels of mice in each exposure group gradually increased over time. The Western blot results showed that compared with the corresponding control group, the protein expressions of NLRP3 and Caspase 1 in the COF₃ group were significantly increased (P<0.01), and the expression of IL-1β protein also increased but without statistical significance. The protein expressions of NLRP3, Caspase 1, and IL-1β in the COF₇ group were significantly higher than those in the CON₇ group (P<0.05, P<0.01). Conclusion Acute exposure to cooking oil fumes can induce significant inflammatory response in adipose tissue, and the effect gradually increases with the extension of exposure time. The mechanism of action may be related to the activation of NLRP3 inflammasome signaling pathway.

Objective To investigate the effect of intravenous infusion of lidocaine on postoperative analgesia in patients undergoing laparoscopic total hysterectomy.Methods Eighty patients aged 28-65 years undergoing laparoscopic total hysterectomy were randomly divided into 2 groups (n=40 each):lidocaine group (group L) and control group (group C).In group L,patients assigned to received an intravenous bolus infusion of 1.5 mg/kg of lidocaine,then followed by 2 mg·kg-1 ·h-1 until the end of operation.Group C received an equal volume of normal saline (100 ml).The patients received patient-controlled intravenous analgesia (PCIA) of snfentanil after surgery,maintaining VAS score≤3.The Ramsay sedation scores and Bruggrmann comfort scale (BCS) at 2,4,8,12,24 and 48 h after operation were recorded.The consumption of sufentanil within 24 h after operation,the dose of extra sufentanil,the number of delivered doses,the times of postoperative firstly flatus and defecation,the incidence of postoperative nausea and vomiting,and total hospital stay were also observed.Results Compared with group C,the Ramsay sedation scores and BCS was increased,the consumption of sufentanil within 24 h after operation [(34.8±5.8)μg vs (49.8±12.5)μg],the dose of extra sufentanil [(22.5 ± 2.6) μg vs (46.2 ± 3.8) μg],the number of delivered doses [(20 ± 4)times vs (48± 6) times] was significantly decreased (P ＜ 0.05),the time of postoperative firstly flatus [(17±6)h vs (27±7)h] and defecation [(26±8)h vs (47±9)h] and total hospital stay [(4.5±0.5)d vs (5.6±0.8)d] was significantly shortened (P＜0.05),and the incidence of postoperative nausea (5％ vs 20％) were significantly decreased (P＜0.05) in group L.Conclusion Intravenous infusion of lidocaine can enhance postoperative analgesia and reduce the volume of opioid analgesics,and was beneficial for peristalsis and hospital for patients undergoing laparoscopic total hysterectomy.

Background: Inflammatory bowel disease (IBD) is a chronic recurrent inflammatory disease of gastrointestinal tract including ulcerative colitis (UC) and Crohn's disease (CD). It is unclear whether there is a causal association between unsaturated fatty acids and IBD. Aims: A two⁃sample Mendelian randomization analysis was used to explore the causal association between unsaturated fatty acids and IBD. Methods: The data of the genome⁃wide association study (GWAS) of unsaturated fatty acids and IBD were obtained from web⁃based public databases. Two⁃sample Mendelian randomization analysis was performed by using inverse⁃variance weighted analysis, and weight median estimator and MR⁃Egger regression were conducted to validate the association of the causal effect. The causality of unsaturated fatty acids on the risk of IBD was evaluated by OR and 95% CI. Results: No direct causal association was found between ω⁃6 fatty acids and CD, and a direct causal association was found with UC. Inverse⁃variance weighted analysis showed a 16% increase in the risk of UC for each standard deviation increase in ω⁃6 fatty acid gene levels (OR=1.16, 95% CI: 1.00⁃1.36, P=0.04). However, no causal association was found between ω⁃3 fatty acids, monounsaturated fatty acids and IBD. Conclusions: ω⁃6 fatty acids may be only causally associated with UC, and no causal association is found between ω⁃3 fatty acids, monounsaturated fatty acids and IBD.

[摘 要] 目的：探讨橙花叔醇通过Wnt-β-catenin通路抑制黑色素瘤A-375和WM-115细胞恶性生物学行为的分子机制。方法: 体外培养黑色素瘤细胞A-375和WM-115，用不同浓度的橙花叔醇处理，采用SRB法和克隆形成实验、FCM术、Transwell实验和细胞划痕实验、DCFH-DA染色法、qPCR和WB法分别检测橙花叔醇对A-375和WM-115细胞的增殖能力、细胞周期和凋亡、迁移能力、活性氧（ROS）水平和Wnt-β-catenin通路及其下游相关基因和相关蛋白表达的影响。利用ULCAN和GEPIA2数据库分析黑色素瘤中Wnt-β-catenin通路的激活与患者预后的关系。结果：与对照组比较，橙花叔醇处理组A-375和WM-115细胞的增殖能力受明显抑制（均P<0.01）、细胞周期阻滞于G2/M期（P<0.05或P<0.01）、细胞凋亡率增加（均P<0.01）、迁移能力降低（P<0.05或P<0.01）、ROS水平升高（均P<0.01）、Wnt-β-catenin通路被抑制而其下游基因和蛋白表达明显上调（均P<0.01）。数据库数据分析显示，WNT1基因高表达患者OS低于低表达患者（P<0.01）。结论：橙花叔醇通过上调A-375和WM-115细胞中ROS水平影响Wnt-β-catenin通路，从而抑制其恶性生物学行为；Wnt-β-catenin通路可能是黑色素瘤治疗的潜在靶点。

Background It is unclear if there is any combined effect of air pollutants and non-optimal temperature on metabolic syndrome, or any molecular mechanisms of related signaling pathways in the process, which requires urgent systematic research. Objective To observe the effects of combined exposure to PM_2.5 and non-optimal temperature on metabolic damage at gene and protein levels in mice, and elucidate the role of related signaling pathway in crucial organs. Methods A total of 60 six-week-old male C57BL/6J mice were randomly divided into six groups: a normal temperature-filter air group (T_N-FA), a normal temperature-concentrated PM_2.5 group (T_N-PM), a heat-filter air group (T_H-FA), a heat-concentrated PM_2.5 group (T_H-PM), a cold-filter air group (T_C-FA), and a cold-concentrated PM_2.5 group (T_C-PM). The Shanghai Meteorological and Environmental Animal Exposure System (Shanghai-METAS) was used to provide combined exposure settings of air types [concentrated PM_2.5 and filter air (FA)] and temperatures [normal (22°C), cold (4°C), and heat (30°C)] for 4 weeks. Skeletal muscle and white adipose tissue (WAT) of the mice were sampled at the end of exposure, and transcriptomics and Western blot (WB) assay were adopted to observe selected gene and protein expression levels in the samples respectively. Results The transcriptomics results indicated that the PM_2.5 exposure enhanced the number of differentially expressed genes. Specifically, 4820 genes were differentially expressed in the T_N-PM mice compared to the T_N-FA mice at normal temperature, and 1143 genes were differentially expressed in the Tc-PM mice compared to the Tc-FA mice in the cold environment. The phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway and the endoplasmic reticulum protein processing pathway were identified as the most significant pathways in metabolic injury resulting from combined exposure to PM_2.5 and non-optimal temperature exposure. The WB results showed that exposure to PM_2.5 in the normal temperature and the cold environments led to a significant increase in the expression of p-AKT in WAT (P<0.01, P<0.05) and a significant decrease in the expression of GLUT4 (P<0.05, P<0.01). In skeletal muscle, exposure to PM_2.5 led to a significant decrease in GLUT4 (P<0.05) in all environments, with a consistent trend of change as observed in WAT. Conclusion Cold/heat exposure might promote PM_2.5-induced metabolic disorder through suppression of the AKT/GLUT4 pathway, aggravating metabolic damage.