LiNiO2 was prepared by reaction of stoichiometric amounts of thoroughly mixed LiOH· H2O and preoxidation nanometer scale Ni3O2（OH）4 powders in O2 at the temperature of 700℃ for 6h. The products were tested by ...LiNiO2 was prepared by reaction of stoichiometric amounts of thoroughly mixed LiOH· H2O and preoxidation nanometer scale Ni3O2（OH）4 powders in O2 at the temperature of 700℃ for 6h. The products were tested by XRD, XPS, SEM and electrochemistry methods. It was shown that product was LiNiO2 single phase, and the valence of nickel was + 3; the average size of it was 40nm; its initial charge specific capacity is 168mAh· g- 1 and the coulomb efficiency is 90% ; the second charge specific capacity is 160mAh· g- 1 and the coulomb efficiency is 96% .展开更多
目的绒毛外滋养细胞焦亡是否参与子痫前期的发生发展值得探讨。文章旨在构建H 2 O 2诱导滋养细胞焦亡模型,探讨绒毛外滋养细胞焦亡是否参与子痫前期的发生发展,为探究子痫前期发病机制提供新的方向。方法人滋养细胞HTR-8/SVneo培养于164...目的绒毛外滋养细胞焦亡是否参与子痫前期的发生发展值得探讨。文章旨在构建H 2 O 2诱导滋养细胞焦亡模型,探讨绒毛外滋养细胞焦亡是否参与子痫前期的发生发展,为探究子痫前期发病机制提供新的方向。方法人滋养细胞HTR-8/SVneo培养于1640+10%胎牛血清+1%抗生素中,培养12 h后,给予H 2 O 2(100、150、200、250μmol/L)处理细胞(2、4、6、12 h),对照为1640+10%胎牛血清+1%抗生素正常培养细胞。提取细胞总蛋白,Western blot检测焦亡相关分子蛋白水平的表达;RT-qPCR检测细胞中焦亡相关分子mRNA水平;倒置相差显微镜观察细胞形态学改变。结果当H 2 O 2为150μmol/L,处理人滋养细胞4 h时,焦亡相关分子NLRP3、caspase1、Cleaved caspase1、GSDMD及IL-1β的蛋白水平明显高于对照,随着作用时间的延长及浓度的增加,蛋白质表达水平被抑制;当H 2 O 2为150μmol/L,作用2 h时,焦亡经典通路中上游“启动”信号关键分子NLRP3及IL-1β的mRNA水平较对照明显升高(P<0.000);4 h时,焦亡经典通路中的关键分子GSDMD的mRNA水平及下游炎症因子IL-18的mRNA水平明显高于对照组(P<0.05)。通过焦亡相关分子mRNA水平的逆向验证,H 2 O 2诱导滋养细胞焦亡模型最佳条件为150μmol/L和4 h,在该条件下,光镜下可明显看到细胞肿胀、碎裂及质膜气泡形成等细胞焦亡典型改变。结论体外成功建立了氧化应激反应诱导滋养细胞焦亡模型,模拟了氧化应激反应诱导滋养细胞发生焦亡损伤的病生理过程,为后续子痫前期发病机制的研究提供实验基础。展开更多
Objective Proprionibacterium acnes(P.acnes)-induced inflammatory responses,proliferation and differentiation of keratinocytes contribute to the progression of acne vulgaris(AV).P.acnes was found to enhance the product...Objective Proprionibacterium acnes(P.acnes)-induced inflammatory responses,proliferation and differentiation of keratinocytes contribute to the progression of acne vulgaris(AV).P.acnes was found to enhance the production of interleukin-8(IL-8)by keratinocytes.This study aimed to investigate the role of IL-8 in P.acnes-induced proliferation and differentiation of keratinocytes and the underlying mechanism.Methods The P.acnes-stimulated HaCaT cell(a human keratinocyte cell line)model was established.Western blotting and immunofluorescence were performed to detect the expression of the IL-8 receptors C-X-C motif chemokine receptor 1(CXCR1)and C-X-C motif chemokine receptor 2(CXCR2)on HaCaT cells.Cell counting kit-8(CCK-8)assay,5-ethynyl-20-deoxyuridine(EdU)assay and Western blotting were performed to examine the effects of IL-8/CXCR2 axis on the proliferation and differentiation of HaCaT cells treated with P.acnes,the IL-8 neutralizing antibody,the CXCR2 antagonist(SB225002),or the CXCR1/CXCR2 antagonist(G31P).Western blotting,nuclear and cytoplasmic separation,CCK-8 assay,and EdU assay were employed to determine the downstream pathway of CXCR2 after P.acnes-stimulated HaCaT cells were treated with the CXCR2 antagonist,the protein kinase B(AKT)antagonist(AZD5363),or the constitutively active forkhead box O1(FOXO1)mutant.Finally,autophagy markers were measured in HaCaT cells following the transfection of the FOXO1 mutant or treatment with the autophagy inhibitor 3-methyladenine(3-MA).Results The expression levels of CXCR1 and CXCR2 were significantly increased on the membrane of HaCaT cells following P.acnes stimulation.The IL-8/CXCR2 axis predominantly promoted the proliferation and differentiation of P.acnes-induced HaCaT cells by activating AKT/FOXO1/autophagy signaling.In brief,IL-8 bound to its receptor CXCR2 on the membrane of keratinocytes to activate the AKT/FOXO1 axis.Subsequently,phosphorylated FOXO1 facilitated autophagy to promote the proliferation and differentiation of P.acnes-induced keratinocytes.Conclusion This study demonstrated the novel autocrine effect of IL-8 on the proliferation and differentiation of P.acnes-induced keratinocytes,suggesting a potential therapeutic target for AV.展开更多
A S 2O 2- 8/ZrO 2 Al 2O 3 type solid superacid catalyst was prepared from ZrOCl 2·8H 2O, AlCl 3· 6H 2O and (NH 4) 2S 2O 8 by coprecipitation, maceration and calcination processes. Their crystal structures an...A S 2O 2- 8/ZrO 2 Al 2O 3 type solid superacid catalyst was prepared from ZrOCl 2·8H 2O, AlCl 3· 6H 2O and (NH 4) 2S 2O 8 by coprecipitation, maceration and calcination processes. Their crystal structures and acidities were determined by XRD and Hammett method, respectively. The activity of the catalyst was studied as function of Al 2O 3 content, calcination temperature and time in the esterification of acetic acid with butanol, and a conversion of 96 5% was obtained. The catalyst gave also higher yields in syntheses of ketals and acetals: cyclohexanone ethylene ketal(86 2%), acetophenone ethylene ketal(78 5%), acetylacetic ester ketal(88 5%), benzaldehyde glycol acetal(76 3%). The chemical structures of the products were confirmed by IR spectra.展开更多
文摘LiNiO2 was prepared by reaction of stoichiometric amounts of thoroughly mixed LiOH· H2O and preoxidation nanometer scale Ni3O2（OH）4 powders in O2 at the temperature of 700℃ for 6h. The products were tested by XRD, XPS, SEM and electrochemistry methods. It was shown that product was LiNiO2 single phase, and the valence of nickel was + 3; the average size of it was 40nm; its initial charge specific capacity is 168mAh· g- 1 and the coulomb efficiency is 90% ; the second charge specific capacity is 160mAh· g- 1 and the coulomb efficiency is 96% .
文摘目的绒毛外滋养细胞焦亡是否参与子痫前期的发生发展值得探讨。文章旨在构建H 2 O 2诱导滋养细胞焦亡模型,探讨绒毛外滋养细胞焦亡是否参与子痫前期的发生发展,为探究子痫前期发病机制提供新的方向。方法人滋养细胞HTR-8/SVneo培养于1640+10%胎牛血清+1%抗生素中,培养12 h后,给予H 2 O 2(100、150、200、250μmol/L)处理细胞(2、4、6、12 h),对照为1640+10%胎牛血清+1%抗生素正常培养细胞。提取细胞总蛋白,Western blot检测焦亡相关分子蛋白水平的表达;RT-qPCR检测细胞中焦亡相关分子mRNA水平;倒置相差显微镜观察细胞形态学改变。结果当H 2 O 2为150μmol/L,处理人滋养细胞4 h时,焦亡相关分子NLRP3、caspase1、Cleaved caspase1、GSDMD及IL-1β的蛋白水平明显高于对照,随着作用时间的延长及浓度的增加,蛋白质表达水平被抑制;当H 2 O 2为150μmol/L,作用2 h时,焦亡经典通路中上游“启动”信号关键分子NLRP3及IL-1β的mRNA水平较对照明显升高(P<0.000);4 h时,焦亡经典通路中的关键分子GSDMD的mRNA水平及下游炎症因子IL-18的mRNA水平明显高于对照组(P<0.05)。通过焦亡相关分子mRNA水平的逆向验证,H 2 O 2诱导滋养细胞焦亡模型最佳条件为150μmol/L和4 h,在该条件下,光镜下可明显看到细胞肿胀、碎裂及质膜气泡形成等细胞焦亡典型改变。结论体外成功建立了氧化应激反应诱导滋养细胞焦亡模型,模拟了氧化应激反应诱导滋养细胞发生焦亡损伤的病生理过程,为后续子痫前期发病机制的研究提供实验基础。
基金supported by the National Natural Science Foundation of China(No.82103756).
文摘Objective Proprionibacterium acnes(P.acnes)-induced inflammatory responses,proliferation and differentiation of keratinocytes contribute to the progression of acne vulgaris(AV).P.acnes was found to enhance the production of interleukin-8(IL-8)by keratinocytes.This study aimed to investigate the role of IL-8 in P.acnes-induced proliferation and differentiation of keratinocytes and the underlying mechanism.Methods The P.acnes-stimulated HaCaT cell(a human keratinocyte cell line)model was established.Western blotting and immunofluorescence were performed to detect the expression of the IL-8 receptors C-X-C motif chemokine receptor 1(CXCR1)and C-X-C motif chemokine receptor 2(CXCR2)on HaCaT cells.Cell counting kit-8(CCK-8)assay,5-ethynyl-20-deoxyuridine(EdU)assay and Western blotting were performed to examine the effects of IL-8/CXCR2 axis on the proliferation and differentiation of HaCaT cells treated with P.acnes,the IL-8 neutralizing antibody,the CXCR2 antagonist(SB225002),or the CXCR1/CXCR2 antagonist(G31P).Western blotting,nuclear and cytoplasmic separation,CCK-8 assay,and EdU assay were employed to determine the downstream pathway of CXCR2 after P.acnes-stimulated HaCaT cells were treated with the CXCR2 antagonist,the protein kinase B(AKT)antagonist(AZD5363),or the constitutively active forkhead box O1(FOXO1)mutant.Finally,autophagy markers were measured in HaCaT cells following the transfection of the FOXO1 mutant or treatment with the autophagy inhibitor 3-methyladenine(3-MA).Results The expression levels of CXCR1 and CXCR2 were significantly increased on the membrane of HaCaT cells following P.acnes stimulation.The IL-8/CXCR2 axis predominantly promoted the proliferation and differentiation of P.acnes-induced HaCaT cells by activating AKT/FOXO1/autophagy signaling.In brief,IL-8 bound to its receptor CXCR2 on the membrane of keratinocytes to activate the AKT/FOXO1 axis.Subsequently,phosphorylated FOXO1 facilitated autophagy to promote the proliferation and differentiation of P.acnes-induced keratinocytes.Conclusion This study demonstrated the novel autocrine effect of IL-8 on the proliferation and differentiation of P.acnes-induced keratinocytes,suggesting a potential therapeutic target for AV.
基金Project supported by Technology-Innovation and Results-transformation of Jiangsu Province(BA2008049)The State Key Laboratory of Materialsoriented Chemical Engineering(KL09-11)~~
文摘A S 2O 2- 8/ZrO 2 Al 2O 3 type solid superacid catalyst was prepared from ZrOCl 2·8H 2O, AlCl 3· 6H 2O and (NH 4) 2S 2O 8 by coprecipitation, maceration and calcination processes. Their crystal structures and acidities were determined by XRD and Hammett method, respectively. The activity of the catalyst was studied as function of Al 2O 3 content, calcination temperature and time in the esterification of acetic acid with butanol, and a conversion of 96 5% was obtained. The catalyst gave also higher yields in syntheses of ketals and acetals: cyclohexanone ethylene ketal(86 2%), acetophenone ethylene ketal(78 5%), acetylacetic ester ketal(88 5%), benzaldehyde glycol acetal(76 3%). The chemical structures of the products were confirmed by IR spectra.
