大数据背景下高职院校数据素养教育研究——基于广东省科技干部学院商科学生的抽样调查

[目的/意义]针对高职数据素养教育缺位的现状,以师生对数据素养的认知情况为培养现状的分析依据,为高职院校建立科学合理的数据素养培养体系、建设相应的课程体系、合理分配有限教学资源提供参考。[方法/过程]基于已有的数据素养指标体系,构建高职院校数据素养评价体系,采用问卷的方式调查高职学生的数据意识、数据收集、数据组织与管理、数据分析、数据利用与归档、数据伦理6个方面的认知与能力,结合文献提出“三阶递进”式的高职数据素养教育体系。[结果/结论]师生总体具备一定的数据意识,但对商业数据的有效获取能力比较缺乏。具备基础的数据分析能力及表达能力,数据价值的深度挖掘能力不足。数据收集、组织与管理、分析、利用与归档能力认知在群体间的差异明显,认为应从“底层-进阶-高级”3个层次进行教育体系的设计,提升数据素养综合能力。     

基于多源数据的华北平原夏玉米种植区划研究

精准识别农业生产环境信息和农业生产特征,对气象、土壤和作物等多源数据进行综合分类,是提高农业资源利用效率和优化农业种植结构的基础。本研究基于近20年（1998~2017年）气象数据和华北五省的玉米单产统计数据,首先构建了华北平原气候资源和玉米生产时空分布特征数据库,研究区内的降雨量、活动积温、日照时数、太阳辐射和玉米单产均存在显著的时空变化;利用作物精细种植区划方法,将华北平原夏玉米种植区分为极不适宜区、不适宜区、较适宜区、适宜区、极适宜区五大类,各类面积分别占总体的比例约为10%、11%、25%、30%、24%;进一步通过环境类别归属度分析方法,将每一大类分为5小类,概率大于75%的相对稳定区域约占总面积的63%,小于75%的波动区域约占37%;极不适宜区、不适宜区和较适宜区,三类时空分布比较稳定,隶属度为100%分别占各类面积的87.67%、70.41%和84.28%,波动区主要发生在极适宜区和适宜区,以及适宜区和较适宜区之间。本研究构建的华北平原夏玉米精细区划结果,对提高研究区资源利用效率和优化玉米产业布局具有重要的指导意义。     

河西荒漠灌区紫花苜蓿施肥效应及其基于数据包络分析法的经济效益研究

为科学准确地评判河西走廊苜蓿主产区紫花苜蓿饲草生产中施肥措施对其产品质量及生产收益的影响,本研究以“甘农3号”紫花苜蓿为材料,通过2016、2017年2年田间试验,以该区域紫花苜蓿饲草生产的平衡施肥推荐方案(N 103.5 kg·hm^-2、P₂O₅ 105 kg·hm^-2、K₂O 90 kg·hm^-2)为对照,探讨了不施肥及3种不完全施肥(缺氮偏施、缺磷偏施、缺钾偏施)处理下紫花苜蓿的生产性能,并采用数据包络分析法(DEA)对其经济效益进行分析。结果表明:与不施肥相比,施肥措施各处理均显著提高紫花苜蓿产量、蛋白总量,降低其酸性洗涤纤维和中性洗涤纤维,提高了相对饲用价值,从而改善了紫花苜蓿品质,并有效增加了经济效益;与氮、磷、钾平衡施肥相比,各偏肥处理的紫花苜蓿产量和品质均显著低于平衡施肥,尤以缺磷偏施的降幅最大,2016、2017年2年的产量和蛋白总量降幅分别达到25.9%、25.7%和33.4%、33.1%。因此,磷是河西荒漠灌区紫花苜蓿饲草生产的养分限制因子,氮、磷、钾对该地区紫花苜蓿生产性能影响顺序为:磷>氮>钾。运用数据包络分析法(DEA)分析出河西荒漠灌区紫花苜蓿的施肥效应为氮、磷、钾平衡施肥的经济效益最优,为DEA有效;不完全施肥的3个评价单元及不施肥评价单元为DEA无效,其中,不施肥经济效益最低,3个不完全施肥评价单元中的缺磷偏肥的紫花苜蓿经济效益比缺氮偏肥和缺钾偏肥更低;另外还以DEA模型推算出不同施肥措施下紫花苜蓿饲草生产经济效益改进的具体方案,其中,不施肥的紫花苜蓿饲草生产需调整的幅度最大,调整额度达10678.88 CNY·hm^-2,各施肥措施需调整的幅度排序为:不施肥>缺磷偏施>缺氮偏施>缺钾偏施。     

基于区块链的食用菌质量安全溯源系统设计

为了实现食用菌质量安全溯源,在食用菌质量安全溯源系统现状的基础上,利用区块链技术的去中心化分布式存储结构,保证了食用菌溯源数据的安全可靠。基于区块链技术设计了食用菌质量安全溯源系统,给出了追溯体系的总体架构和主要业务流程,有针对性地解决了食用菌溯源系统中存在问题。实现了食用菌全周期全流程的信息溯源,为消费者提供了真实、可靠的溯源信息。     

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.     

Effect of HMGA2 gene on high glucose-induced apoptosis of renal tubular epithelial cells by regulating Notch signaling pathway

AIM:To investigate the effect of HMGA2 down-regulation on apoptosis and Notch signaling pathway in renal tubular epithelial cells exposed to high glucose (HG). METHODS:D-glucose at 5, 10, 20 and 30 mmol/L was used to stimulate human renal tubular epithelial HK-2 cells for 2 h, and D-glucose at 30 mmol/L was used to stimulate the HK-2 cells for 10 min, 60 min and 120 min. The protein expression of HMGA2 was determined by Western blot. The HK-2 cells were divided into normal glucose (NG) group, HG group, HG+si-HMGA2 group and HG+NC group, in which siRNA was transfected by Lipofectamine^TM 2000 for 48 h. Flow cytometry was used to analyze the apoptotic rate, reactive oxygen species (ROS) assay kit was used to detect ROS content, and Western blot was used to detect the protein levels of Notch1, Hes1 and Bcl-2. The HK-2 cells were treated with the Notch signaling pathway inhibitor DAPT, and then the cells were divided into HG group, HG+DAPT group and HG+si-HMGA2+DAPT group. The apoptotic rate was analyzed by flow cytometry. RESULTS:Exposure of the HK-2 cells to D-glucose at different concentrations for different time significantly increased the expression of HMGA2 (P<0.05). Compared with NG group, the protein expression of HMGA2, Notch1 and Hes1 in HG group was increased, the expression of Bcl-2/Bax was decreased, the apoptotic rate was increased, and the content of ROS was increased obviously (P<0.05). Compared with HG group, the protein expression of HMGA2, Notch1 and Hes1 of HG+si-HMGA2 group was decreased, the expression of Bcl-2/Bax was increased, the apoptotic rate was decreased, and the content of ROS was decreased significantly (P<0.05). The apoptotic rate in HG+DAPT group was significantly lower than that in HG group, while the apoptotic rate in HG+si-HMGA2+DAPT group was significantly lower than that in HG+DAPT group (P<0.05). CONCLUSION:Down-regulation of HMGA2 expression inhibits the apoptosis of renal tubular epithelial cells by regulating Notch signaling pathway and decreasing ROS production.     

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.