Variation of photosynthetic performance, nutrient uptake, and elemental composition of different generations and different thallus parts of Saccharina japonica

In order to illustrate the physiological variation of different generations and different thallus parts of Saccharina japonica, physiological parameters such as maximum and effective PSII photochemical efficiency, nutrient uptake, and elemental composition were determined in the laboratory. Photosynthetic analysis in different generations indicated that, although gametophytes had higher pigment contents than the sporophyte, they had lower values of F _v/F _m and ΔF/F′_m. The highest Chl a/Chl c ratio was found in sporophyte generation (3.98?±?0.01) and in the basal part of fresh thallus (2.66?±?0.02). The sporophyte had significantly higher values of nitrate uptake but lower values of phosphorus uptake than the gametophytes. The contents of nitrogen and carbon as well as C/N in gametophytes were significantly higher than those in sporophytes. In addition, the basal part of the S. japonica thallus had the highest C content (22.31?±?1.50 %) but the lowest N content (2.02?±?0.16 %), as well as the highest value of C/N (11.02?±?0.34).     

Histochemical Studies of the Non‐Host Resistance and the Role of Actin Cytoskeleton in Pepper Against Colletotrichum orbiculare

The penetration process and defence reactions (hypersensitive response, oxidative burst and cell wall fortification) of Colletotrichum orbiculare were studied histochemically on pepper cultivar ‘A11’ (non‐host) and susceptible cucumber cultivar ‘Changchun Thorn’ (host). The results indicate that C. orbiculare could hardly penetrate the non‐host pepper leaves. It was papillae rather than hypersensitive response and H₂O₂ that played an important role in resisting the colonization and development of C. orbiculare on the non‐host pepper. The depolymerization of the actin microfilament weakened the papilla deposition of pepper and allowed successful penetration of the non‐adapted C. orbiculare, suggesting that the actin cytoskeleton of pepper is significant in preventing the invasion of the non‐host pathogen C. orbiculare.     

EZH2在乳腺癌中的表达及其临床意义

目的 探讨EZH2在乳腺癌中的表达及其临床意义.方法 用免疫组化的方法研究105例乳腺癌中EZH2蛋白表达情况,并进一步探讨其与乳腺癌临床病理因素及其预后的关系.结果 EZH2蛋白在乳腺癌组织中表达明显高于乳腺良性疾病,其表达与患者年龄、肿瘤大小、TNM分期、PR和c-erbB-2表达无关(P＞0.05),与淋巴结转移、病理组织学分级、ER表达及乳腺癌预后相关(P＜0.05).EZH2蛋白表达在三阴性乳腺癌中表达明显高于非三阴性乳腺癌(P＜0.05).结论 EZH2在乳腺癌淋巴结转移及侵袭中扮演一定的角色,其与乳腺癌预后相关,与ER阴性的乳腺癌发生发展有关.     

沙眼衣原体感染诱导小鼠生殖道局部促炎性细胞因子的表达情况

建立小鼠生殖道沙眼衣原体感染模型,观察小鼠生殖道局部促炎性细胞因子的表达。将小鼠生物型沙眼衣原体C. muridarum 1＆#215;104 IFU阴道接种于C57B6背景雌性小鼠,取感染后阴道拭子做沙眼衣原体培养,计算IFU,监测小鼠感染和病原体清除情况;80 d后处死小鼠,检测子宫输卵管病理改变;ELISA检测感染过程中小鼠生殖道促炎性细胞因子IL-1α、IL-6、MIP-2和TNF-α产生情况。小鼠感染在第3至第15天维持较高水平,然后病原体被逐渐清除,整个病程约3~5周;病理检测显示子宫输卵有严重炎症、管腔扩张积水,狭窄等;于感染后第3天检测到局部IL-1α、IL-6、MIP-2分泌,第7天达高峰,然后逐渐下降至正常水平（ IL-6于11 d恢复正常,IL-1α和 MIP-2于15 d恢复正常）。 TNF-α仅在第7天检测到高水平表达。相对于TNF-α和IL-6,IL-1α和MIP-2维持时间较长。成功建立沙眼衣原体感染小鼠生殖道模型,沙眼衣原体急性感染可诱导小鼠生殖道局部分泌IL-1α、IL-6、MIP-2和TNF-α。     

酒精发酵过程中酿酒酵母耐受环境胁迫的研究进展

提高酿酒酵母细胞耐受环境胁迫（高渗透压、高浓度酒精和高温）的能力对酒精工业生产具有重要的意义。对提高酿酒酵母耐受性的研究方法和策略的发展历程进行了综述。基因组学、转录组学和蛋白质组学等现代组学技术在这一领域的研究获得了广泛的应用。这些技术将提供期待的信息,去理性改造并获得更加耐受胁迫的工业酵母菌株。     

NF-κB p65的敲减加重结肠上皮HCT116细胞氧化损伤

炎症细胞诱导的活性氧类生成和肠道氧化应激与慢性炎症性肠疾病以及结直肠肿瘤的发病密切相关。NF-κB信号通路参与氧化应激反应以及在结直肠炎症和肿瘤发生中的作用还并不完全清楚。本研究将化学合成一对编码小干扰RNA 序列、靶向人NF-κB 基因的长60 bp寡核苷酸链定向克隆至pSUPER小干扰RNA表达载体中,通过单酶切、双酶切及测序证实重组RNA干扰载体构建成功. 将构建成功的质粒转染至结肠上皮细胞HCT116中敲减p65,分别采用Western blot方法检测NF-κB p65蛋白表达水平,（3-(4,5-二甲基噻唑-2)-3,5-二苯基四氮唑溴盐（MTT）方法检测细胞存活情况. 结果显示,pSUPER-NF-κB p65载体可特异性下调NF-κB p65蛋白表达;下调p65表达可导致过氧化氢诱导的HCT116内活性氧类物质生成增高,存活细胞数目显著减少,氧化损伤加重。研究表明,在人结肠上皮细胞内NF-κB p65通路的抑制显著加重了结肠上皮细胞氧化损伤情况.     

A set of microRNAs mediate direct conversion of human umbilical cord lining-derived mesenchymal stem cells into hepatocytes

In a previous study, we elucidated the specific microRNA (miRNA) profile of hepatic differentiation. In this study, we aimed to clarify the instructive role of six overexpressed miRNAs (miR-1246, miR-1290, miR-148a, miR-30a, miR-424 and miR-542-5p) during hepatic differentiation of human umbilical cord lining-derived mesenchymal stem cells (hMSCs) and to test whether overexpression of any of these miRNAs is sufficient to induce differentiation of the hMSCs into hepatocyte-like cells. Before hepatic differentiation, hMSCs were infected with a lentivirus containing a miRNA inhibitor sequence. We found that downregulation of any one of the six hepatic differentiation-specific miRNAs can inhibit HGF-induced hepatic differentiation including albumin expression and LDL uptake. Although overexpression of any one of the six miRNAs alone or liver-enriched miR-122 cannot initiate hepatic differentiation, ectopic overexpression of seven miRNAs (miR-1246, miR-1290, miR-148a, miR-30a, miR-424, miR-542-5p and miR-122) together can stimulate hMSC conversion into functionally mature induced hepatocytes (iHep). Additionally, after transplantation of the iHep cells into mice with CCL4-induced liver injury, we found that iHep not only can improve liver function but it also can restore injured livers. The findings from this study indicate that miRNAs have the capability of directly converting hMSCs to a hepatocyte phenotype in vitro.     

Patulin induces pro-survival functions via autophagy inhibition and p62 accumulation

Patulin (PAT) is one of the most common mycotoxins found in moldy fruits. Skin contact is one of the most likely exposure routes of PAT. Investigation of dermal toxicity of PAT is clearly needed and has been highlighted by WHO. In the present study, using human keratinocyte HaCaT cells as a model, we found that treatment with PAT caused an increased autophagosome accumulation. Measurements of autophagic flux demonstrated that the accumulation of autophagosomes by PAT was not directly due to enhanced autophagosome formation but due to inhibition of autophagosome degradation. Reductions in the activities of the lysosomal enzymes cathepsin B and cathepsin D by PAT might contribute to this inhibitory effect. Consistent with this, inhibition of autophagosome degradation by PAT resulted in accumulation of p62 that functioned as a pro-survival signal. The pro-survival function of p62 was found to be attributed to reactive oxygen species-mediated cytoprotective endoplasmic reticulum (ER) stress response. ER stress exerted cytoprotective effect via extracellular signal-regulated kinase1/2-dependent B-cell CLL/lymphoma 2-associated agonist of cell death inhibitory phosphorylation. Given the critical role of autophagy and its substrate p62 in carcinogenesis, our findings may have important implications in PAT-induced skin carcinogenesis.     

Cancer-initiating cells derived from human rectal adenocarcinoma tissues carry mesenchymal phenotypes and resist drug therapies

Accumulating evidence indicates that cancer-initiating cells (CICs) are responsible for cancer initiation, relapse, and metastasis. Colorectal carcinoma (CRC) is typically classified into proximal colon, distal colon, and rectal cancer. The gradual changes in CRC molecular features within the bowel may have considerable implications in colon and rectal CICs. Unfortunately, limited information is available on CICs derived from rectal cancer, although colon CICs have been described. Here we identified rectal CICs (R-CICs) that possess differentiation potential in tumors derived from patients with rectal adenocarcinoma. The R-CICs carried both CD44 and CD54 surface markers, while R-CICs and their immediate progenies carried potential epithelial–mesenchymal transition characteristics. These R-CICs generated tumors similar to their tumor of origin when injected into immunodeficient mice, differentiated into rectal epithelial cells in vitro, and were capable of self-renewal both in vitro and in vivo. More importantly, subpopulations of R-CICs resisted both 5-fluorouracil/calcium folinate/oxaliplatin (FolFox) and cetuximab treatment, which are the most common therapeutic regimens used for patients with advanced or metastatic rectal cancer. Thus, the identification, expansion, and properties of R-CICs provide an ideal cellular model to further investigate tumor progression and determine therapeutic resistance in these patients.