铝电解槽节能的基本原理就是降低电解槽运行电压U和提高电流效率η。一般状态下获得较低电解槽电压的方法是通过电解槽母线优化配置获得小于5Gs的Bzave,但是研究发现,在采取通用母线配置方法获得小于5Gs的Bzave的条件下,电解槽的磁流体...铝电解槽节能的基本原理就是降低电解槽运行电压U和提高电流效率η。一般状态下获得较低电解槽电压的方法是通过电解槽母线优化配置获得小于5Gs的Bzave,但是研究发现,在采取通用母线配置方法获得小于5Gs的Bzave的条件下,电解槽的磁流体流速却较快,对炉帮的冲刷大而存在漏槽风险。在流速满足设计要求的条件下,Bzave值又难以满足小于5Gs的磁流体高稳定技术条件。本文深度剖析直流电耗达到12 000 k Wh/t.Al以下所采取的更进一步提高电解槽稳定性——抑制铝液层水平电流、曲面阴极降低流速、槽内衬保温匹配低电压等节能技术以及提高电流效率——氧化铝质量、电解质成分控制的关键技术问题。并对电解槽深度节能问题进行分析和探讨。展开更多
Objective: To elucidate the relation between human tissue factor pathwayinhibitor-2 (TFPI-2) expression and ovarian tumor migration and invasion. Methods: Human TFPI-2expression vector pBos-Cite-neo/TFPI-2 was transfe...Objective: To elucidate the relation between human tissue factor pathwayinhibitor-2 (TFPI-2) expression and ovarian tumor migration and invasion. Methods: Human TFPI-2expression vector pBos-Cite-neo/TFPI-2 was transfected into ovarian tumor cells line A2780- Afterthe transfected cells were selected by G418, transfected and nontransfected cells were screened forTFPI-2 mRNA and protein by reverse transcription-polymerase chain reaction and Western blotanalysis, respectively. The number of transfected or nontransfected cells passing through membraneof Boyden chamber was counted as the basis assessing tumor cells migratory and invasive behaviors.Results: Expression of mRNA and protein of TFPI-2 was detectable in transfected cells. In invasionassay, the number of TFPI-2-expressing cells to traverse a Matrigel-coated membrane was obviouslydecreased compared with that of nonexpressing cells (59.3±6.5 vs 109.7±5.5, P 【 0.01); While inmigration assay, no significant difference through a noncoated membrane was observed amongtransfected and nontransfected cells (114.7±8.6 vs 127.3±7.1, P 】 0.05). Conclusion: Expression ofTFPI-2 may strongly inhibit the invasive ability of ovarian tumor cells in vitro, but has no effecton the migratory ability which provides an experimental basis for genotherapy of human ovariantumor.展开更多
Emerging evidence has shown the association of aberrantly expressed microRNAs （miRNAs） with tumor development and progression. However, little is known about the potential role of miRNAs in gastric carcinogenesis. H...Emerging evidence has shown the association of aberrantly expressed microRNAs （miRNAs） with tumor development and progression. However, little is known about the potential role of miRNAs in gastric carcinogenesis. Here, we performed miRNA microarray to screen miRNAs differentially expressed in the paired gastric cancer and their adjacent nontumor tissues and found that miR-375 was greatly downregulated in gastric cancer tissues. Quantitative real-time PCR analysis verified that miR-375 expression was significantly decreased in more than 90% of primary gastric cancers compared with their nontumor counterparts from patients undergoing gastric resection. Overexpression of miR-375 significantly inhibited gastric cancer cell proliferation in vitro and in vivo. Forced expression of miR-375 in gastric cancer cells significantly reduced the protein level of Janus kinase 2 （JAK2） and repressed the activity of a luciferase reporter carrying the 3＇-untranslated region of JAK2, which was abolished by mutation of the predicted miR-375-binding site, indicating that JAK2 may be a miR-375 target gene. Either inhibition of JAK2 activity by AG490 or silencing of JAK2 by RNAi suppressed gastric cancer cell proliferation resembling that of miR-375 overexpression. Moreover, ectopic expression of JAK2 can partially reverse the inhibition of cell proliferation caused by miR-375. Finally, we found a significant inverse correlation between miR-375 expression and JAK2 protein level in gastric cancer. Thus, these data suggest that miR-375 may function as a tumor suppressor to regulate gastric cancer cell proliferation potentially by targeting the JAK2 oncogene, implicating a role of miR-375 in the pathogenesis of gastric cancer.展开更多
MicroRNAs （miRNAs） are endogenous, small, non-coding RNAs, which are capable of silencing gene expression at the post-transcriptional level. In this study, we report that miR-205 is significantly underexpressed in b...MicroRNAs （miRNAs） are endogenous, small, non-coding RNAs, which are capable of silencing gene expression at the post-transcriptional level. In this study, we report that miR-205 is significantly underexpressed in breast tumor compared to the matched normal breast tissue. Similarly, breast cancer cell lines, including MCF-7 and MDA-MB- 231, express a lower level miR-205 than the non-malignant MCF-10A cells. Of interest, ectopic expression of miR-205 significantly inhibits cell proliferation and anchorage independent growth, as well as cell invasion. Furthermore, miR- 205 was shown to suppress lung metastasis in an animal model. Finally, western blot combined with the luciferase reporter assays demonstrate that ErbB3 and vascular endothelial growth factor A （VEGF-A） are direct targets for miR-205, and this miR-205-mediated suppression is likely through the direct interaction with the putative miR-205 binding site in the 3＇-untranslated region （3＇-UTR） of ErbB3 and VEGF-A. Together, these results suggest that miR- 205 is a tumor suppressor in breast cancer.展开更多
文摘去泛素化酶（deubiquitinating enzymes， DUBs）能对抗泛素连接酶（ubiquitin ligases），从而调节靶信号分子的泛素化和稳定性。在果蝇体内，泛素-蛋白酶体系统在调节凋亡方面发挥关键作用，最明显的是通过控制主要的凋亡调节因子--果蝇凋亡抑制蛋白1（Drosophila inhibitor of apoptosis protein 1， DIAP1）的丰度来调节凋亡。虽然基于DIAP1的泛素化机制已被广泛研究，但是DUBs在控制DIAP1活性中的确切作用仍未得到充分研究。
文摘铝电解槽节能的基本原理就是降低电解槽运行电压U和提高电流效率η。一般状态下获得较低电解槽电压的方法是通过电解槽母线优化配置获得小于5Gs的Bzave,但是研究发现,在采取通用母线配置方法获得小于5Gs的Bzave的条件下,电解槽的磁流体流速却较快,对炉帮的冲刷大而存在漏槽风险。在流速满足设计要求的条件下,Bzave值又难以满足小于5Gs的磁流体高稳定技术条件。本文深度剖析直流电耗达到12 000 k Wh/t.Al以下所采取的更进一步提高电解槽稳定性——抑制铝液层水平电流、曲面阴极降低流速、槽内衬保温匹配低电压等节能技术以及提高电流效率——氧化铝质量、电解质成分控制的关键技术问题。并对电解槽深度节能问题进行分析和探讨。
文摘Objective: To elucidate the relation between human tissue factor pathwayinhibitor-2 (TFPI-2) expression and ovarian tumor migration and invasion. Methods: Human TFPI-2expression vector pBos-Cite-neo/TFPI-2 was transfected into ovarian tumor cells line A2780- Afterthe transfected cells were selected by G418, transfected and nontransfected cells were screened forTFPI-2 mRNA and protein by reverse transcription-polymerase chain reaction and Western blotanalysis, respectively. The number of transfected or nontransfected cells passing through membraneof Boyden chamber was counted as the basis assessing tumor cells migratory and invasive behaviors.Results: Expression of mRNA and protein of TFPI-2 was detectable in transfected cells. In invasionassay, the number of TFPI-2-expressing cells to traverse a Matrigel-coated membrane was obviouslydecreased compared with that of nonexpressing cells (59.3±6.5 vs 109.7±5.5, P 【 0.01); While inmigration assay, no significant difference through a noncoated membrane was observed amongtransfected and nontransfected cells (114.7±8.6 vs 127.3±7.1, P 】 0.05). Conclusion: Expression ofTFPI-2 may strongly inhibit the invasive ability of ovarian tumor cells in vitro, but has no effecton the migratory ability which provides an experimental basis for genotherapy of human ovariantumor.
基金Supplementary information is linked to the online version of the paper on Cell Research website.Acknowledgments This work was supported by the National Natural Scientific Foundation of China （30901714, 30671070 and 30771107）, the Ministry of Science and Technology of China （2007CB914500）, the Ministry of Education of China （NCET-06-0530）, the Ministry of Health of China （WKJ2006-2-014）, the Postdoctoral Science Foundation of China （20070421179）, the Department of Science and Technology of Zhejiang Province （2009F80032）, and the Natural Scientific Foundation of Zhejiang Province, China （R205291, Y206103 and 2007R10G2010103）.
文摘Emerging evidence has shown the association of aberrantly expressed microRNAs （miRNAs） with tumor development and progression. However, little is known about the potential role of miRNAs in gastric carcinogenesis. Here, we performed miRNA microarray to screen miRNAs differentially expressed in the paired gastric cancer and their adjacent nontumor tissues and found that miR-375 was greatly downregulated in gastric cancer tissues. Quantitative real-time PCR analysis verified that miR-375 expression was significantly decreased in more than 90% of primary gastric cancers compared with their nontumor counterparts from patients undergoing gastric resection. Overexpression of miR-375 significantly inhibited gastric cancer cell proliferation in vitro and in vivo. Forced expression of miR-375 in gastric cancer cells significantly reduced the protein level of Janus kinase 2 （JAK2） and repressed the activity of a luciferase reporter carrying the 3＇-untranslated region of JAK2, which was abolished by mutation of the predicted miR-375-binding site, indicating that JAK2 may be a miR-375 target gene. Either inhibition of JAK2 activity by AG490 or silencing of JAK2 by RNAi suppressed gastric cancer cell proliferation resembling that of miR-375 overexpression. Moreover, ectopic expression of JAK2 can partially reverse the inhibition of cell proliferation caused by miR-375. Finally, we found a significant inverse correlation between miR-375 expression and JAK2 protein level in gastric cancer. Thus, these data suggest that miR-375 may function as a tumor suppressor to regulate gastric cancer cell proliferation potentially by targeting the JAK2 oncogene, implicating a role of miR-375 in the pathogenesis of gastric cancer.
文摘MicroRNAs （miRNAs） are endogenous, small, non-coding RNAs, which are capable of silencing gene expression at the post-transcriptional level. In this study, we report that miR-205 is significantly underexpressed in breast tumor compared to the matched normal breast tissue. Similarly, breast cancer cell lines, including MCF-7 and MDA-MB- 231, express a lower level miR-205 than the non-malignant MCF-10A cells. Of interest, ectopic expression of miR-205 significantly inhibits cell proliferation and anchorage independent growth, as well as cell invasion. Furthermore, miR- 205 was shown to suppress lung metastasis in an animal model. Finally, western blot combined with the luciferase reporter assays demonstrate that ErbB3 and vascular endothelial growth factor A （VEGF-A） are direct targets for miR-205, and this miR-205-mediated suppression is likely through the direct interaction with the putative miR-205 binding site in the 3＇-untranslated region （3＇-UTR） of ErbB3 and VEGF-A. Together, these results suggest that miR- 205 is a tumor suppressor in breast cancer.
