Research on Energy Consumption of Traditional Natural Villages in Transition: A Case Study in Zhejiang Province

Traditional agriculture is in the direction of increasing integration of the primary industry, secondary industry, and tertiary industry in Zhejiang province. A survey was undertaken on energy consumption of traditional natural villages by taking Anji Ligeng village for an example. This paper firstly studied rural buildings, rural family structure, occupants’ activity and the usage of household appliances in the form of a questionnaire. Then, the household energy resource structure and energy consumption structure were analyzed and compared with other surveys. The results show that, the electric energy consumption was 6 kWh/(m2•a), which was far less than urban residential household. In rural household energy resource structure, the proportion of non-commercial energy resource was higher than commercial energy resource. Firewood accounted for 83%, electricity for 12%, LPG for 3% and solar energy for 2%. In building energy consumption structure, cooking and hot water took up 33%, appliances 31%, lighting 20%, heating 12%, cooling 4%. In all influential factors, frequently used area, number of air conditioner per household and building function were obviously correlated with energy consumption;income, building shape factor and window to wall area ratio had no correlation with energy consumption in the low energy consumption area.

基于体细胞突变数据库筛选免疫原性结直肠癌高频新抗原的方法

结直肠癌是世界高发和高致死率的恶性肿瘤。靶向新抗原的免疫治疗已被证实可以诱导癌症患者肿瘤持续消退,但这些特异性新抗原,仅适用于个体精准治疗。随着大量的高频肿瘤基因突变被发现,这些与突变相关的高频新抗原可覆盖更多人群,具有较强的临床意义。然而目前结直肠癌中是否也存在高频新抗原仍不清楚。本研究利用来源于321个结直肠癌患者的体细胞突变数据库,联合1种标准过滤和7种预测算法,筛选并获得了25个基于中国人高频分型HLA-A^*1101限制性的高频新抗原,它们均具有高亲和力(IC50<50 nmol/L)和高呈递分值(>0.90);其中,除了阳性对照多肽KRAS_G12V8-16外,11个高频新抗原能够在体外诱导细胞毒性T淋巴细胞(cytotoxic T lymphocyte,CTL)分泌γ干扰素(interferon gamma,IFN-γ),证实具有免疫原性。选取免疫原性最强的新抗原C1orf170_S418G413-421及阳性对照多肽KRAS_G12V8-16体外刺激T细胞,利用流式细胞分选及单细胞转录组测序技术,获得其特异性CTL的免疫组库信息,所构建的TCR-T(T-cell receptor engineered T cell)能够识别新抗原并分泌细胞因子。以上结果表明,本研究开发了一种利用体细胞数据库预测并体外筛选验证具有免疫原性高频新抗原的方法,为结直肠癌及其他癌种的多肽、DC(dendritic cells)疫苗、TCR-like抗体、TCR-T等免疫治疗提供了重要的多肽靶点和TCR信息,具有实际的临床应用价值。

RNA-seq analysis of protective effect of epicatechin gallate on H_(2)O_(2)-induced oxidative injury in PC12 cells

Epicatechin gallate(ECG)is one of the polyphenolic compounds and has attracted much attention due to its various bioactivities.In this study,the neuroprotective eff ect of ECG against H_(2)O_(2)-induced oxidative injury in PC12 cells as well as the possible mechanisms were investigated.Cell viability was determined by MTT assay.The differentially expressed genes(DEGs),GO enrichment,and KEGG enrichment were analyzed to explore the mechanism of ECG against H_(2)O_(2)-induced oxidative injury by using the RNA-seq method.Finally,the change in the cell cycle was analyzed by fl ow cytometry.H_(2)O_(2)(400-1200μmol/L)inhibited the cell viability in a concentration-dependent manner.ECG(6-150μmol/L)eff ectively attenuated the H_(2)O_(2)-induced decrease in cell viability.RNA-seq analysis showed that ECG regulated 1058 coexpressed DEGs.GO enrichment analysis showed that the cellular component was the dominant group after ECG treatment.KEGG analysis showed that the cell cycle,fanconi anemia pathway,and homologous recombination were the important pathways for ECG in improving H_(2)O_(2)-induced oxidative injury and 28 coexpressed DEGs in the cell cycle pathway were summarized.Finally,cell cycle analysis also proved that ECG improved H_(2)O_(2)-induced cell cycle arrest in the G2/M phase.Our present study demonstrated that ECG attenuated H_(2)O_(2)-induced neurologic oxidative damage by multiple modulatory mechanisms at the molecular transcription level.These fi ndings provide new insights for further study of the molecular mechanism of the neuroprotection of ECG.

MicroRNA-30a inhibits cell proliferation in a sepsis-induced acute kidney injury model by targeting the YAP-TEAD complex

Background Acute kidney injury(AKI)is a primary feature of renal complications in patients with sepsis.MicroRNA(miRNA/miR)-30a is an essential regulator of cardiovascular diseases,tumors,phagocytosis,and other physical processes,but whether it participates in sepsis-induced AKI(sepsis-AKI)is unknown.We aimed to elucidate the functions and molecular mechanism underlying miR-30a activity in sepsis-AKI.Methods The classical cecal ligation and puncture(CLP)method and lipopolysaccharide(LPS)-induced Human Kidney 2(HK-2)cells were used to establish in vivo and in vitro sepsis-AKI models.Specific pathogen-free and mature male Sprague-Dawley(SD)rats,aged 6–8 weeks(weight 200–250 g),were randomly divided into five-time phase subgroups.Fluid resuscitation with 30 mL/kg 37°C saline was administered after the operation,without antibiotics.Formalin-fixed,paraffin-embedded kidney sections were stained with hematoxylin and eosin.SD rat kidney tissue samples were collected for analysis by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay.HK-2 cells were transfected with hsa-miR-30a-3p mimics or inhibitors,and compared with untreated normal controls.RNA,protein,and cell viability were evaluated by quantitative reverse transcription-polymerase chain reaction(qRT-PCR),western blot,and cell counting kit-8 methods.A Dual-Luciferase Assay Kit(Promega)was used to measure luciferase activity 48 h after transfection with miR-30a-3p mimics.Results Expression levels of miR-30a-3p and miR-30a-5p in renal tissues of the sepsis group were significantly reduced at 12 h and 24 h(P<0.05).Tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β)were significantly increased in renal tissue 3 h after the operation in rats(P<0.05),and gradually decreased 6 h,12 h,and 24 h after CLP.Levels of miR-30a-5p and miR-30a-3p were significantly down-regulated at 3 h after LPS treatment(P<0.05),and gradually decreased in HK-2 cells.One hour after LPS(10µg/mL)treatment,TNF-αand IL-1βlevels in HK-2 cells were significantly up-regulated(P<0.05),and they were markedly down-regulated after 3 h(P<0.05).IL-6 expression levels began to rise after LPS treatment of cells,peaked at 6 h(P<0.05),and then decreased to the initial level within a few hours.Stimulation with 10µg/mL LPS promoted HK-2 cells proliferation,which was inhibited after miR-30a-3p-mimic transfection.Bioinformatics prediction identified 37 potential miR-30a-3p target genes,including transcriptional enhanced associate domain 1(TEAD1).After transfection of HK-2 cells with miR-30a-3p mimics and miR-30a-3p inhibitor,TEAD1 transcript was significantly up-and down-regulated,respectively(both P<0.05).After LPS treatment(24 h),expression of TEAD1 in the inhibitors group was significantly increased(P<0.01),while that in the mimics group was significantly suppressed(P<0.01).In the dual luciferase reporter experiment,miR-30a-3p overexpression decreased fluorescence intensity(P<0.01)from TEAD1-wt-containing plasmids,but did not influence fluorescence intensity from TEAD1-muta-containing plasmids.LPS may promote HK-2 cells proliferation through the miR-30a-3p/TEAD1 pathway.Conclusion In a background of expression of inflammatory factors,including TNF-α,IL-1β,and IL-6,which were transiently increased in the sepsis-AKI model,miR-30a was down-regulated.Down-regulated miR-30a-3p may promote cell proliferation by targeting TEAD1 in LPS-induced HK-2 cells,demonstrating its potential as a biomarker for early sepsis-AKI diagnosis.

Visible light-promoted aerobic oxidative cleavage and cyclization of olefins to access 3-hydroxyisoindolinones

A convenient and environmentally friendly synthetic route from 2-vinylbenzimide to 3-hydroxy-isoindolinones through visible light-promoted transformations via iron/disulfide catalysis and molecular oxygen oxidation has been developed.A range of 3-hydroxy-isoindolinones was obtained in moderate to good yields,which exhibit excellent functional group compatibility and broad substrate scope.Further mechanistic investigations proved that dioxetane might be a key intermediate being involved in the reaction.