食用菌生产企业社会责任与财务绩效的互动关系分析

食用菌生产企业的社会责任是决定企业可持续发展的关键因素,同时对企业的财务绩效存在多方面影响。基于已有文献研究结论,通过构建回归模型对食用菌生产企业社会责任与财务绩效的相关性进行分析。结果表明,食用菌生产企业对股东、供应商、消费者、政府和社区所承担的社会责任与财务绩效具有正相关关系;而食用菌生产企业对员工承担的社会责任与财务绩效的相关性不显著。     

湖南省粮食产量波动的影响因素分析及预测

旨在维护国家稳定,为预判粮食生产前景、提高粮食生产效率、保障粮食安全提供理论依据。利用湖南省统计数据,运用灰色关联分析法筛选关联性较强的影响因素,并建立GM(1,N)预测模型预测粮食产量。2008—2017年与湖南省粮食产量关联度最大的影响因素是粮食作物播种面积和农业机械总动力;科技因素是影响2008—2017年湖南省粮食产量的主要因素,其次是自然因素,社会因素;2018—2027年湖南省粮食产量有较小波动,且农业机械总动力和财政农业支出影响较大;农业机械总动力在前后十年对粮食产量都有较重要的影响,越来越占据主导地位。粮食产量受国家政策的影响,受农业机械总动力影响最大,维持产量水平需高度重视农业机械化水平,稳步提高粮食作物播种面积。     

不同浓度NAA/6BA配比对不同品种甘薯茎尖培养特性的影响

为明确不同品种甘薯茎尖培养的最佳NAA/6BA配比,设置0.1 mg/L/2.5 mg/L、0.2 mg/L/2.5 mg/L、0.2 mg/L/1.0 mg/L 3组NAA/6BA浓度配比处理,观测不同浓度激素处理对‘北京553’、‘红香蕉’、‘苏薯8号’、‘烟薯25’、‘安吉芋’、‘济徐23’、‘渝紫7号’、‘商薯19’茎尖培养成苗率、愈伤组织直径、不定根数目、叶片数和植株高度的影响,同时调查不同品种试管苗的移栽成活率。结果表明,‘红香蕉’、‘济徐23’、‘渝紫7号’、‘商薯19’在0.1 mg/L/2.5 mg/L的处理下培养效率最高;‘安吉芋’在0.2 mg/L/2.5 mg/L的处理下培养效率最高;‘苏薯8号’、‘北京553’、‘烟薯25’在0.2 mg/L/1.0 mg/L的处理下培养效率最高。因此,在甘薯茎尖培养过程中,不同甘薯品种适宜的NAA/6BA配比存在显著差异,在实际生产中应根据品种特性来进行调整激素的用量和比例。     

通过GbF3’H基因单独沉默及其与GbCHI和GbDFR基因共沉默研究其在海岛棉中抗枯萎病功能

【目的】通过沉默海岛棉GbF3’H基因及共沉默GbF3’H、GbCHI和Gb DFR基因,研究其在海岛棉抗枯萎病中的作用。【方法】以海岛棉抗病材料06-146为研究对象,GhCLA1基因为阳性对照,空载体为阴性对照,构建海岛棉TRV2-Gb F3’H沉默载体,协同课题组前期构建的TRV2-CHI和TRV2-DFR载体,利用病毒诱导的基因沉默技术(Virus-induced gene silencing,VIGS)分别进行Gb F3’H基因单独沉默以及GbF3’H、GbCHI和Gb DFR这3种基因共沉默试验。通过实时荧光定量聚合酶链式反应(Quantitative real time-polymerase chain reaction,q RT-PCR)分析各处理样品中基因沉默情况;设置室内接种枯萎病菌试验测定病情指数,分析各沉默材料对枯萎病的抗性差异。【结果】q RT-PCR结果显示,海岛棉GbF3’H基因沉默后其在海岛棉根、茎和叶中的表达量比空载体对照低,Gb F3’H、GbCHI和GbDFR这3种基因共沉默后其在海岛棉根、茎和叶中的表达量均比空载体对照低。病情指数调查结果显示,野生型<空载体对照相似文献   

艾纳香中的黄酮类化合物及其抗菌活性

为明确艾纳香抗菌药效物质基础,采用硅胶柱色谱, 凝胶色谱和反相色谱等技术从艾纳香乙酸乙酯部位中分离获得15个单体化合物,经波谱学鉴定分别为：3,3°,5-三羟基-4°,7-二甲氧基二氢黄酮 (1)、4°,5-二羟基-3,3°,7-三甲氧基黄酮 (2)、艾纳香素 (3)、3,5,3°,4°-四羟基-7-甲氧基黄酮 (4)、香叶木素 (5)、3°,4°,5-三羟基-3,7-二甲氧基黄酮 (6)、异鼠李素 (7)、chrysosplenol C (8)、金丝桃苷 (9)、异槲皮苷 (10)、3°,5,7-三羟基-4°-甲氧基二氢黄酮 (11)、sakuranetin (12)、pilloin (13)、5,7,3°,4°-四羟基-3-甲氧基黄酮 (14)、5-羟基-3,7,3°,4°-四甲氧基黄酮 (15),其中化合物7、11、12和13为首次从该植物中分得。抗菌活性评价结果显示：化合物1、3、6、8和12对3株细菌具有不同程度的抑制活性,其中化合物3对金黄色葡萄球菌抑制活性最强, 最低抑菌浓度MIC值为32 μg/mL。     

Up-regulation of miR-181a attenuates releases of CSE-induced pro-inflammatory factors and expression of collagen IV,fibronectin and α-SMA in human bronchial epithelial cells

AIM: To investigate the effect and potential mechanism of microRNA-181a (miR-181a) on cigarette smoke extract (CSE)-induced the productions of pro-inflammatory factors and the expression of collagen IV, fibronectin and α-smooth muscle actin (α-SMA) in human bronchial epithelial cells (HBECs). METHODS: CSE-induced miR-181a expression was detected by RT-qPCR in the HBECs. After tansfected with miR-181a mimic, the releases of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and transforming growth factor-β1 (TGF-β1) were measured by ELISA, the protein expression of collagen IV, fibronectin and α-SMA was determined by Western blot. The activation of NF-κB/TGF-β1/Smad3 pathway was also evaluated by Western blot. RESULTS: CSE increased the levels of TNF-α, IL-1β, IL-6 and TGF-β1 and the expression of collagen IV, fibronectin and α-SMA, and decreased the expression of miR-181a in the HBECs (P<0.05). However, transfected with miR-181a mimic partially prevented the releases of TNF-α, IL-1β, IL-6 and TGF-β1, and inhibited the expression of collagen IV, fibronectin and α-SMA (P<0.05). Additionally, the activation of NF-κB/TGF-β1/Smad3 evoked by CSE was attenuated after transfected with miR-181a mimic. CONCLUSION: Up-regulation of miR-181a prevents the releases of CSE-induced pro-inflammatory factors and expression of collagen IV, fibronectin and α-SMA in the HBECs, and its mechanism may be related to the inhibition of NF-κB/TGF-β1/Smad3 pathway.     

SIRT1 promotes autophagy of pancreatic cancer cells induced by hypoxia via regulating FOXO1/RAB7 signaling pathway

AIM: To investigate the effect of SIRT1 on the autophagy of pancreatic cancer cells under hypoxia condition, and to analyze the underlying mechanism of regulating FOXO1/RAB7 signaling pathway. METHODS: Western blot and immunofluorescence methods were used to determine the expression of SIRT1 in the pancreatic cancer cells. The small interfering RNA targeting SIRT1 and SIRT1 over-expression plasmid were transfected into the pancreatic cancer Panc-1 cells. Confocal microscopy was used to detect the LC3 expression. Western blot was used to analyze the protein levels of LC3, p62 and FOXO1/RAB7 signaling pathway-related molecules. Co-immunoprecipitation was used to detected the protein interaction between SIRT1 and FOXO1. RESULTS: The expression level of SIRT1 in the nucleus of Panc-1 cells was increased under hypoxia condition. Compared with negative control under hypoxia condition, knock-down of SIRT1 expression attenuated the autophagy flux in the pancreatic cancer Panc-1 cells (P<0.05). Over-expression of SIRT1 increased the protein levels of FOXO1 and RAB7. On the contrary, knock-down of SIRT1 expression inhibited the protein levels of FOXO1 and RAB7. The protein interaction between SIRT1 and FOXO1 in the pancreatic cancer cells was observed. CONCLUSION: SIRT1 in pancreatic cancer Panc-1 cells under hypoxia condition is over-expressed in the nucleus. Down-regulation of SIRT1 inhibits autophagy and its mechanism may be related to FOXO1/RAB7 signaling pathway.     

331份四川小麦品种(系)在甘肃陇南抗条锈性表现及利用价值

2014年-2017年度先后对331份四川省小麦生产品种(系)在温室进行苗期人工接种条锈菌混合菌鉴定和甘谷试验站大田成株期分别接种CYR32、CYR33、CYR34、G22-14、中4-1和混合菌鉴定,同时在甘谷试验站和汪川良种场两地进行自然诱发鉴定。结果发现:在人工接种条件下,苗期、成株期表现抗病的分别有‘XK201465’等36份和‘XK20132’等72份材料,分别占10.88%和21.75%;有‘XK62483’等11份材料全生育期表现抗病,占3.32%;两地三年自然诱发鉴定发现,仅有‘XK20132’等5份材料在两地均表现抗病,有‘川农17’等30份材料具有慢条锈性。对供鉴材料在甘肃陇南的利用前景进行了分析。     

Effect of miR-29b-mediated TGF-β/Smad signaling pathway on progression of hepatic fibrosis in rats

AIM: To investigate the role of microRNA-29b (miR-29b)-mediated TGF-β/Smad signaling pathway in the activation of hepatic stellate cells (HSC) and its effect on the progression of hepatic fibrosis in rats.METHODS: Hepatic liver fibrosis rat model was established, and its HSC were isolated. Normal rat HSC were also obtained and identified in vitro. RT-qPCR and Western blot were used to detect the alterations of miR-29b, TGF-β/Smad signaling pathway-related proteins and liver fibrosis marker proteins in the acquired cells. Finally, the direct targeting binding of miR-29b to TGF-β1 was identified by dual-luciferase reporter assay system.RESULTS: With the activation of HSC, the expression of miR-29b gradually decreased (P<0.01), while the expression of collagen type I and α-smooth muscle actin gradually increased (P<0.01). At the same time, the expression of Smad2/3/4 was significantly increased, and the expression of Smad7 was significantly decreased (P<0.01). Dual-luciferase reporter assay showed that miR-29b bound directly to "UCUCUCCGU" in the 3'UTR of TGF-β1, indicating that TGF-β1 was a downstream target gene of miR-29b.CONCLUSION: miR-29b may be involved in the inhibition of HSC activation and migration, thereby inhibiting the process of liver fibrosis. The biological function of miR-29b may be through the direct targeting of TGF-β1, thus regulating and inhibiting the TGF-β/Smad signaling pathway.     

Role of ghrelin in cell protection by up-regulating HSP70 through ERK1/2 signaling pathway in PC12 cells

AIM:To study the role of ghrelin in cell protection by up-regulating heat shock protein 70 (HSP70) and inhibiting apoptosis induced by oxidative stress through extracellular regulated protein kinases 1/2 (ERK1/2) signaling pathway in the PC12 cells. METHODS:Sodium nitoprusside (SNP) was used to induce oxidative stress injury in the PC12 cells. The cultured PC12 cells were divided into SNP-injured group (incubated with SNP at 0.5 mmol/L for 6, 12, 18 and 24 h), ghrelin pretreatment group (ghrelin at 100 nmol/L was given 30 min before adding SNP); HSP70 inhibitor group (quercetin at 10 μmol/L was added 60 min before ghrelin treatment), ERK inhibitor group (ERK 1/2 inhibitor PD98059 was added 60 min before ghrelin treatment) and control group (added same amount of culture medium only). The apoptotic rate was detected by flow cytometry. The protein expression was determined by Western blot and immunocytochemistry. RESULTS:Compared with control group, the apoptotic rate of PC12 cells in SNP-injured group was significantly increased (P<0.05). Compared with SNP-injured group, ghrelin (100 nmol/L) pretreatment significantly inhibited SNP-induced apoptosis of PC12 cells (P<0.05), and significantly up-regulated the protein expression of HSP70 (P<0.05). Time-effect analysis showed that ghrelin had the most significant effect at 18 h after SNP injury. Quercetin, an inhibitor of HSP 70, significantly reduced the anti-apoptotic effect of ghrelin (P<0.05). Ghrelin pretreatment promoted the phosphorylation of ERK1/2. ERK1/2 inhibitor PD98059 significantly inhibited the effects of ghrelin on up-regulation of HSP70 expression (P<0.05). CONCLUSION:Ghrelin upregulates the expression of HSP70 and inhibits the apoptosis in the PC12 cells induced by oxidative stress by promoting the phosphorylation of ERK1/2.