Effect of xeroderma pigmentosum group D gene on proliferation of human umbilical arterial smooth muscle cells induced by Ox-LDL

AIM: To investigate the effects of xeroderma pigmentosum group D (XPD) gene on the proliferation of human umbilical arterial smooth muscle cells (HUASMCs) induced by oxidized low-density lipoprotein (Ox-LDL). METHODS: The recombinant plasmid pEGFP-N2/XPD was transfected into HUASMCs by liposome. The cells were divided into blank control group, pEGFP-N2 group, pEGFP-N2/XPD group, Ox-LDL group, Ox-LDL+pEGFP-N2 group and Ox-LDL+pEGFP-N2/XPD group. The proliferation rate of the cells was detected by MTT and EdU assays. The apoptotic rate and cell cycle distribution were analyzed by flow cytometry. The protein levels of XPD, caspase-3, Bcl-2 and Bax were determined by Western blot. RESULTS: Compared with blank control group, the expression of XPD was increased in pEGFP-N2/XPD group (P<0.05). According to the results of MTT and EdU assays, the cell proliferation in pEGFP-N2/XPD group was reduced compared with blank control group (P<0.05). Compared with Ox-LDL group, the cell proliferation in Ox-LDL+pEGFP-N2/XPD group was significantly inhibited (P<0.05). According to the results of flow cytometry, the cell proportion of S phase decreased and the G₀/G₁-phase cell proportion increased significantly in pEGFP-N2/XPD group and Ox-LDL+pEGFP-N2/XPD group compared with blank control group and Ox-LDL group, repectively (P<0.05). Compared with blank control group and Ox-LDL group, the protein level of Bcl-2 decreased and the protein levels of Bax and cleaved caspase-3 increased in pEGFP-N2/XPD group and Ox-LDL+pEGFP-N2/XPD group, respectively (P<0.05). CONCLUSION: XPD inhibits the proliferation of HUASMCs and promotes their apoptosis, and reduces the promoting effect of Ox-LDL on the proliferation of HUVSMCs. XPD may be the target for treatment of atherosclerosis.     

基于TRIZ的方草捆收集车集捆装置设计

针对方草捆收集车集捆装置工作稳定性较差的问题，利用TRIZ系统分析方法及ProInnovator软件对集捆装置进行分析，提出了改进方案，对改进方案进行综合评价，得到了最优方案。      

Dexmedetomidine attenuates acute alcoholic hepatic injury in mice

AIM: To investigate the effects of dexmedetomidine (DEX) on acute alcoholic hepatic injury in mice and to explore the possible mechanisms. METHODS: Kunming mice (n=50) were randomly divided into 5 groups (n=10): normal saline control (NS) group, acute alcoholic hepatic injury model (E) group, low-dose (10 μg/kg) DEX (E+L) group, medium-dose (50 μg/kg) DEX (E+M) group and high-dose (100 μg/kg) DEX (E+H) group. The animals were sacrificed at 6 h after gavage of alcohol or normal saline. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) were measured. The livers were removed for evaluation of histological characteristics and determining the content of tumor necrosis factor-α (TNF-α) amd interleukin-1β (IL-1β) in the liver tissues by ELISA. The expression levels of cytochrome P450 2E1 (CYP2E1) and nuclear factor-κB (NF-κB) in the liver tissues were evaluated by Western blot. RESULTS: Compared with NS group, the levels of ALT, AST and TG were obviously increased in E group, which were obviously decreased in E+M and E+H groups. Compared with NS group, the levels of TNF-α, IL-1β and MDA were obviously increase in E group, which were obviously decreased in E+M and E+H groups. Compared with NS group, the activity of SOD and the content of GSH were obviously decreased in E group, which were obviously increased in E+M and E+H groups. Compared with NS group, the expression of CYP2E1 and NF-κB was obviously increase in E group, which was obviously decreased in E+M and E+H groups. Compared with NS group, ethanol induced marked liver histological injury, which was less pronounced in E+M and E+H groups. CONCLUSION: DEX has a protective effect on mouse liver with acute alcoholic injury by the involvement in the processes of antioxidation and antiinflammation, and its mechanism may be associated with the inhibition of CYP2E1 and NF-κB expression.     

Clinical significance of KLF15 expression in human lung adenocarcinoma

AIM: To explore the clinical significance of Krüpple-like factor 15 (KLF15) protein expression in the patients with lung adenocarcinoma for exploring the therapeutic and prognositic biomarkers of lung cancer. METHODS: Four cases of lung adenocarcinoma tissues and matched adjacent tissues were collected from our hospital, and the expression of KLF15 protein in these tissues was analyzed by Western blot. At the same time, 72 cases of archived paraffin-embedded samples and clinical data of the patients with lung adenocarcinoma were also collected. The KLF15 protein expression in the archived paraffin-embedded lung adenocarcinoma samples was detected by immunohistochemical staining. The correlations between KLF15 protein expression and clinical characteristics of the patients including prognosis were also analyzed. In addition, the KLF15 protein was up-regulated in A549 cells, and then the effects of KLF15 protein on the viability of the cells were measured by CCK-8 assay. RESULTS: The protein expression of KLF15 in the 4 cases of lung adenocarcinoma tissues was significantly lower than that in matched paracancerous tissues. Fifty-three cases of lung adenocarcinoma specimens showed low expression or no expression of KLF15 protein in total 72 cases (73.6%). The 5-year survival rate of the patients with high expression of KLF15 protein in their specimens was higher than that of the patients with the low expression of KLF15 protein (P<0.01), and the expression of KLF15 protein was significantly correlated with the pathological staging (P<0.01) and T stage (P<0.01) of the patients with lung adenocarcinoma. Furthermore, the low expression of KLF15 protein was an important poor prognostic indicator of the patients. Up-regulation of KLF15 protein in the A549 cells significantly inhibited the growth of the cells. CONCLUSION: KLF15 inhibits the growth of lung adenocarcinoma cells. It could be used as a therapeutic target and a prognostic biomarker for the patients with lung adenocarcinoma.     

Effect of hypercapnia on lysyl oxidase-dependent collagen cross-linking and hypoxia-induced pulmonary hypertension in rat

AIM: To investigate the effect of hypercapnia on hypoxia-induced pulmonary hypertension and the changes of lysyl oxidase (LOX) and extracellular matrix collagen cross-links in the rat. METHODS: Sprague-Dawley rats were randomly divided into 4 groups:normoxia group, hypoxia group, hypercapnia group and hypoxia+hypercapnia group. LOX activity was detected by fluorescence spectrophotometry. LOX protein expression was detected by immunohistochemistry and Western blot. The mRNA expression of LOX in the pulmonary artery was detected by real-time PCR. RESULTS: The levels of mean pulmonary artery pressure (mPAP), RV/(LV+S) and WA/TA in hypoxia group were significantly higher than those in normoxia group (P<0.01). Moreover, the levels of mPAP and RV/(LV+S) in hypoxia+hypercapnia group were significantly lower than those in hypoxia group (P<0.01). However, no significant difference of mPAP and RV/(LV+S) between hypercapnia group and normoxia group was observed. In hypoxia group, the collagen cross-links in the lung tissue was significantly higher than that in normoxia group and hypercapnia group (P<0.01). Importantly, collagen cross-links in the lung tissue of hypoxia+hypercapnia group was significantly lower than that in hypoxia group (P<0.01). There was no significant difference in collagen cross-links between hypercapnia group and normoxia group. The expression of LOX at mRNA and protein levels and its activity in the pulmonary arteries of hypoxia group were significantly increased as compared with normoxia group (P<0.01). Furthermore, the expression of LOX at mRNA and protein levels and its activity in the pulmonary arteries in hypoxia+hypercapnia group were lower than those in hypoxia group (P<0.01). CONCLUSION: Hypoxia not only up-regulates LOX but also promotes collagen cross-linking in the rat lung, which contributes to the development of pulmonary hypertension. Hypercapnia inhibits hypoxia-induced LOX expression and collagen cross-linking, therefore impairing the progress in hypoxia-induced pulmonary hypertension.     

百合花色及相关育种研究进展

花色是百合属植物重要的观赏性状之一。目前世界上对百合种质创新研究大力开发,但在花色创新方面进入瓶颈期。我国百合种质资源丰富,但种质创新发展相对缓慢。花色创新更是在起步阶段。该研究总结了百合花色的相关研究成果,并对百合花色育种进行了综述和展望,以期为进一步开展百合的花色创新提供参考依据。     

桔小实蝇在云南蒙自地区的发生规律研究

桔小实蝇寄主范围广、繁殖量大、危害重,是世界性的重要检疫害虫。本文通过调查分析,研究了云南蒙自市的海拔、防治措施、果树种类三因素对桔小实蝇种群动态的影响。结果表明,桔小实蝇在1412 m低海拔地区的种群数量大于1608 m和1700 m高海拔地区的,这说明海拔越高,桔小实蝇种群数量越小,危害也越小。根据在相似海拔地区相同果园桔小实蝇种群数量的比较,发现严格按照本课题组探索的防治措施做好桔小实蝇防治能收到良好的效果。蒙自市的水果成熟期不同,随着各种水果的成熟,桔小实蝇种群动态会出现多个峰值,3~5月桔小实蝇种群高峰期主要出现在枇杷园,7~10月主要出现在石榴园、小红枣园和水蜜桃园。对桔小实蝇在蒙自种群动态的调查,能够为下一步防治措施的制定做好准备。     

氨氮胁迫对四鼻须鲤鱼肝脏GST酶活力的影响

实验采用生态毒理学方法,以NH4Cl为实验药物,设置0、50、150和250mg/L实验浓度。通过对野生和养殖群体的四鼻须鲤鱼氨氮对肝脏谷胱甘肽巯基转移酶（GST）活力的影响,比较两个群体抗氨氮能力。结果表明：在相同的氨氮浓度和胁迫时间下,四鼻须鲤鱼养殖群体GST酶活力的变化趋势与野生群体大致相同。除250mg/L浓度组在胁迫5d和10d时,野生群体酶活性略低于养殖群体外,在其余时间点的野生群体酶活性均高于养殖群体,而且,在高浓度氨氮胁迫下,野生群体肝脏的GST酶活性达到峰值的时间比养殖群体更短,显示出较强的抗氨氮能力。     

保护地蔬菜灰霉病菌的菌系分布及致病力分化测定

以山东省寿光市保护地栽培蔬菜上分离的30个灰霉病菌菌株为试材,采用菌落培养性状观察和菌饼活体接种法,研究灰霉病菌的菌系划分及对黄瓜叶片的致病力差异。结果表明:供试菌株划分为菌核型、菌丝型和孢子型3个菌系,不同菌株对黄瓜叶片的致病力分化显著,致病力强弱与寄主植物无显著相关性;强致病力菌株以菌核型为主,菌丝型和孢子型菌株致病力相对较弱。     

长期定位施不同氮源有机肥替代部分含氮化肥对陇东旱塬冬小麦产量和水分利用效率的影响

在陇东黄土旱塬覆盖黑垆土大田,利用陇鉴301进行了连续10年的定位试验,观测长期施用不同氮源有机肥(发酵有机肥、农家肥)或小麦秸秆还田各处理对冬小麦产量相关性状和水分利用效率的影响。结果显示,小麦产量和水分利用效率年际间变化较大,与降雨量有直接关系;不同有机氮源替代部分含氮化肥处理对提高冬小麦产量和水分利用效率具有明显作用。在干旱、平水和丰水年型,较不施肥对照分别增产53.1%~103.7%、40.3%~79.3%和73.1%~94.8%,较单施化肥对照分别增产6.6%~41.8%、7.0%~36.8%和-2.9%~9.3%。以发酵有机肥做替代物处理的产量和水分利用效率最高,增产幅度最大,10年平均产量较不施肥和单施化肥对照分别增加88.9%和25.4%,水分利用效率和边际水分利用率也最高,分别为10.8 kg mm~(-1) hm~(-2)和1.03 kg m~(-3);并且产量构成因素和植株生理指标也优于其他处理。因此,发酵有机肥是陇东半湿润偏旱雨养农业区(年降水量约550 mm)冬小麦生产上替代部分含氮化肥的首选有机氮源。