Constant-current anodization of pure aluminum was carried out in non-corrosive capacitor working electrolytes to study the formation mechanism of nanopores in the anodic oxide films.Through comparative experiments,nan...Constant-current anodization of pure aluminum was carried out in non-corrosive capacitor working electrolytes to study the formation mechanism of nanopores in the anodic oxide films.Through comparative experiments,nanopores are found in the anodic films formed in the electrolytes after high-temperature storage(HTS)at 130°C for 240 h.A comparison of the voltage-time curves suggests that the formation of nanopores results from the decrease in formation efficiency of anodic oxide films rather than the corrosion of the electrolytes.FT-IR and UV spectra analysis shows that carboxylate and ethylene glycol in electrolytes can easily react by esterification at high temperatures.Combining the electronic current theory and oxygen bubble mold effect,the change in electrolyte composition could increase the electronic current in the anodizing process.The electronic current decreases the formation efficiency of anodic oxide films,and oxygen bubbles accompanying electronic current lead to the formation of nanopores in the dense films.The continuous electronic current and oxygen bubbles are the prerequisites for the formation of porous anodic oxides rather than the traditional field-assisted dissolution model.展开更多
目的:采用Meta分析方法评价相干光断层扫描血管成像(OCTA)对湿性年龄相关性黄斑变性(wARMD)患者脉络膜新生血管(CNV)的诊断价值。方法:计算机检索PubMed、Embase、Web of science、Cochrane library、CNKI、Wanfang、CBM和VIP数据库建库...目的:采用Meta分析方法评价相干光断层扫描血管成像(OCTA)对湿性年龄相关性黄斑变性(wARMD)患者脉络膜新生血管(CNV)的诊断价值。方法:计算机检索PubMed、Embase、Web of science、Cochrane library、CNKI、Wanfang、CBM和VIP数据库建库至2020-10-27关于OCTA诊断wARMD患者CNV的相关研究。由两位研究员独立筛选文献、提取资料并采用QUADAS-2工具评价纳入研究的偏倚风险,使用Meta-Disc 1.4及Stata 16.0软件进行Meta分析。结果:纳入文献11篇,患者995眼。OCTA诊断wARMD患者CNV的Meta分析结果显示,合并灵敏度、特异度、阳性似然比、阴性似然比、诊断比值比、sROC曲线下面积和阳性验后概率依次为0.88[95%CI(0.83,0.92)]、0.95[95%CI(0.85,0.99)]、18.45[95%CI(5.36,63.52)]、0.12[95%CI(0.08,0.18)]、152.73[95%CI(36.39,641.05)]、0.95[95%CI(0.92,0.96)]和0.96。结论:相干光断层扫描血管成像用于诊断wARMD患者CNV具有较高价值,尤其适用于wARMD的早期诊断。展开更多
AIM: To examine the effect of aqueous fructus aurantii immaturus(FAI) extracts on the intestinal plexus of cathartic colons.METHODS: Cathartic colons were induced in rats with dahuang,a laxative used in traditional Ch...AIM: To examine the effect of aqueous fructus aurantii immaturus(FAI) extracts on the intestinal plexus of cathartic colons.METHODS: Cathartic colons were induced in rats with dahuang,a laxative used in traditional Chinese medicine. Once the model was established(after approximately 12 wk),rats were administered mosapride(1.54 mg/kg) or various doses of aqueous FAI extracts(1-4 g/kg) for 14 d. Transit function was assessed using an ink propulsion test. Rats were then sacrificed,and the ultramicrostructure of colonic tissue was examined using transmission electron microscopy. The expression of the 5-hydroxytryptamine receptor 4(5-HTR4) and neurofilament-H was assessed in colon tissues using real-time PCR,Western blot,and immunohistochemistry.RESULTS: Mosapride and high dose(4 g/kg) of aqueous FAI extracts significantly improved the bowel movement in cathartic colons compared to untreated model colons as measured by the intestinal transit rate(70.06 ± 7.25 and 72.02 ± 8.74,respectively,vs 64.12 ± 5.19; P < 0.05 for both). Compared to controls,the ultramicrostructure of cathartic colons showed signsof neural degeneration. Treatment with mosapride and aqueous FAI extracts resulted in recovery of ultrastructural pathology. Treatment with mosapride alone upregulated the gene and protein expression of 5-HTR4 compared to untreated controls(P < 0.05 for both). Treatment with aqueous FAI extracts(≥ 2 g/kg) increased 5-HTR4 m RNA levels(P < 0.05),but no change in protein level was observed by Western blot or immunohistochemistry. The m RNA and protein levels of neurofilament-H were significantly increased with mosapride and ≥ 2 g/kg aqueous FAI extracts compared to controls(P < 0.05 for all).CONCLUSION: Aqueous FAI extracts and mosapride strengthen bowel movement in cathartic colons via increasing the expression of 5-HTR4 and neurofilament-H.展开更多
AIM To explore the significance of corticotropin-releasing hormone(CRH)-receptor(R)2 in mucosal healing of dextran sulfate sodium(DSS)-induced colitis and the effect of Tong-Xie-Yao-Fang(TXYF) on CRH-R2 expression and...AIM To explore the significance of corticotropin-releasing hormone(CRH)-receptor(R)2 in mucosal healing of dextran sulfate sodium(DSS)-induced colitis and the effect of Tong-Xie-Yao-Fang(TXYF) on CRH-R2 expression and regulation.METHODS Ulcerative colitis was induced in mice by administration of 3%(w/v) DSS for 7 d. Once the model was established,mice were administered urocortin-2(30 μg/kg), a peptide which binds exclusively to CRH-R2, or various doses of aqueous TXYF extracts(2.8-11.2 g/kg), a CRH-R2 antagonist Astressin(Ast)2B(20 μg/kg), Ast2B + Ucn2, or Ast2B with various doses of aqueous TXYF extracts for 9 d. Colonic mucosal permeability was then evaluated by measuring the fluorescence intensity in serum. The colitis disease activity index(DAI), histology, body weight loss and colon length were assessed to evaluate the condition of colitis. Terminal deoxynucleotidyl transferase d UTP nick-end labeling was used to detect apoptosis of the intestinal epithelial cells. The expression level of Ki-67 represented the proliferation of colonic epithelial cells and was detected by immunohistochemistry. The expression levels of inflammation cytokines IL-6, TNF-α and CXCL-1 were examined in colon tissues using real-time PCR and ELISA kits.RESULTS Compared with the DSS group, mice treated with the CRH-R2 antagonist Ast2B showed greater loss of body weight, shorter colon lengths(4.90 ± 0.32 vs 6.21 ± 0.34 cm, P < 0.05), and higher DAI(3.61 ± 0.53 vs 2.42 ± 0.32, P < 0.05) and histological scores(11.50 ± 1.05 vs 8.33 ± 1.03, P < 0.05). Additionally, the Ast2B group showed increased intestinal permeability(2.76 ± 0.11 μg/mL vs 1.47 ± 0.11 μg/mL, P < 0.001), improved secretion of inflammatory cytokines in colon tissue, and reduced colonic epithelial cell proliferation(4.97 ± 4.25 vs 22.51 ± 8.22, P < 0.05). Increased apoptosis(1422.39 ± 90.71 vs 983.01 ± 98.17, P < 0.001) was also demonstrated. The Ucn2 group demonstrated lower DAI(0.87 ± 0.55 vs 2.42 ± 0.32, P < 0.001) and histological scores(4.33 ± 1.50 vs 8.33 ± 1.03, P < 0.05). Diminished weight loss, longer colon length(9.58 ± 0.62 vs 6.21 ± 0.34 cm, P < 0.001), reduced intestinal permeability(0.75 ± 0.07 vs 1.47 ± 0.11 μg/mL, P < 0.001), inhibited secretion of inflammatory cytokines in colon tissue and increased colonic epithelial cell proliferation(90.04 ± 15.50 vs 22.51 ± 8.22, P < 0.01) were all observed. Reduced apoptosis(149.55 ± 21.68 vs 983.01 ± 98.17, P < 0.05) was also observed. However, significant statistical differences in the results of the Ast2 B group and Ast2 B + Ucn2 group were observed. TXYF was also found to ameliorate symptoms of DSS-induced colitis in mice and to promote mucosal repair like Ucn2. There were significant differences between the Ast2B + TXYF groups and the TXYF groups.CONCLUSION CRH-R2 activates the intestinal mucosal antiinflammatory response by regulating migration, proliferation and apoptosis of intestinal epithelial cells in colitisinduced mice, and plays an important antiinflammatory role. TXYF promotes mucosal repair in colitis mice by regulating CRH-R2.展开更多
基金financially supported by the National Natural Science Foundation of China(Nos.51777097,51577093)。
文摘Constant-current anodization of pure aluminum was carried out in non-corrosive capacitor working electrolytes to study the formation mechanism of nanopores in the anodic oxide films.Through comparative experiments,nanopores are found in the anodic films formed in the electrolytes after high-temperature storage(HTS)at 130°C for 240 h.A comparison of the voltage-time curves suggests that the formation of nanopores results from the decrease in formation efficiency of anodic oxide films rather than the corrosion of the electrolytes.FT-IR and UV spectra analysis shows that carboxylate and ethylene glycol in electrolytes can easily react by esterification at high temperatures.Combining the electronic current theory and oxygen bubble mold effect,the change in electrolyte composition could increase the electronic current in the anodizing process.The electronic current decreases the formation efficiency of anodic oxide films,and oxygen bubbles accompanying electronic current lead to the formation of nanopores in the dense films.The continuous electronic current and oxygen bubbles are the prerequisites for the formation of porous anodic oxides rather than the traditional field-assisted dissolution model.
基金Supported by National Natural Science Foundation of China,No.81473506Natural Science Foundation of Zhejiang Province,No.LY13H030011State Administration of Traditional Chinese Medicine of Zhejiang Province,No.2013ZB050
文摘AIM: To examine the effect of aqueous fructus aurantii immaturus(FAI) extracts on the intestinal plexus of cathartic colons.METHODS: Cathartic colons were induced in rats with dahuang,a laxative used in traditional Chinese medicine. Once the model was established(after approximately 12 wk),rats were administered mosapride(1.54 mg/kg) or various doses of aqueous FAI extracts(1-4 g/kg) for 14 d. Transit function was assessed using an ink propulsion test. Rats were then sacrificed,and the ultramicrostructure of colonic tissue was examined using transmission electron microscopy. The expression of the 5-hydroxytryptamine receptor 4(5-HTR4) and neurofilament-H was assessed in colon tissues using real-time PCR,Western blot,and immunohistochemistry.RESULTS: Mosapride and high dose(4 g/kg) of aqueous FAI extracts significantly improved the bowel movement in cathartic colons compared to untreated model colons as measured by the intestinal transit rate(70.06 ± 7.25 and 72.02 ± 8.74,respectively,vs 64.12 ± 5.19; P < 0.05 for both). Compared to controls,the ultramicrostructure of cathartic colons showed signsof neural degeneration. Treatment with mosapride and aqueous FAI extracts resulted in recovery of ultrastructural pathology. Treatment with mosapride alone upregulated the gene and protein expression of 5-HTR4 compared to untreated controls(P < 0.05 for both). Treatment with aqueous FAI extracts(≥ 2 g/kg) increased 5-HTR4 m RNA levels(P < 0.05),but no change in protein level was observed by Western blot or immunohistochemistry. The m RNA and protein levels of neurofilament-H were significantly increased with mosapride and ≥ 2 g/kg aqueous FAI extracts compared to controls(P < 0.05 for all).CONCLUSION: Aqueous FAI extracts and mosapride strengthen bowel movement in cathartic colons via increasing the expression of 5-HTR4 and neurofilament-H.
基金Supported by National Natural Science Foundation of China,No.81473506Natural Science Foundation of Zhejiang Province,No.LY13H030011 and No.LY17H290009+2 种基金State Administration of Traditional Chinese Medicine of Zhejiang Province,No.2013ZB050Department of Zhejiang Province to Build Funded Project,No.WKJ-ZJ-1531Zhejiang TCM Science and Technology Project,No.2016ZB047,No.2017ZA056 and No.2018ZB046
文摘AIM To explore the significance of corticotropin-releasing hormone(CRH)-receptor(R)2 in mucosal healing of dextran sulfate sodium(DSS)-induced colitis and the effect of Tong-Xie-Yao-Fang(TXYF) on CRH-R2 expression and regulation.METHODS Ulcerative colitis was induced in mice by administration of 3%(w/v) DSS for 7 d. Once the model was established,mice were administered urocortin-2(30 μg/kg), a peptide which binds exclusively to CRH-R2, or various doses of aqueous TXYF extracts(2.8-11.2 g/kg), a CRH-R2 antagonist Astressin(Ast)2B(20 μg/kg), Ast2B + Ucn2, or Ast2B with various doses of aqueous TXYF extracts for 9 d. Colonic mucosal permeability was then evaluated by measuring the fluorescence intensity in serum. The colitis disease activity index(DAI), histology, body weight loss and colon length were assessed to evaluate the condition of colitis. Terminal deoxynucleotidyl transferase d UTP nick-end labeling was used to detect apoptosis of the intestinal epithelial cells. The expression level of Ki-67 represented the proliferation of colonic epithelial cells and was detected by immunohistochemistry. The expression levels of inflammation cytokines IL-6, TNF-α and CXCL-1 were examined in colon tissues using real-time PCR and ELISA kits.RESULTS Compared with the DSS group, mice treated with the CRH-R2 antagonist Ast2B showed greater loss of body weight, shorter colon lengths(4.90 ± 0.32 vs 6.21 ± 0.34 cm, P < 0.05), and higher DAI(3.61 ± 0.53 vs 2.42 ± 0.32, P < 0.05) and histological scores(11.50 ± 1.05 vs 8.33 ± 1.03, P < 0.05). Additionally, the Ast2B group showed increased intestinal permeability(2.76 ± 0.11 μg/mL vs 1.47 ± 0.11 μg/mL, P < 0.001), improved secretion of inflammatory cytokines in colon tissue, and reduced colonic epithelial cell proliferation(4.97 ± 4.25 vs 22.51 ± 8.22, P < 0.05). Increased apoptosis(1422.39 ± 90.71 vs 983.01 ± 98.17, P < 0.001) was also demonstrated. The Ucn2 group demonstrated lower DAI(0.87 ± 0.55 vs 2.42 ± 0.32, P < 0.001) and histological scores(4.33 ± 1.50 vs 8.33 ± 1.03, P < 0.05). Diminished weight loss, longer colon length(9.58 ± 0.62 vs 6.21 ± 0.34 cm, P < 0.001), reduced intestinal permeability(0.75 ± 0.07 vs 1.47 ± 0.11 μg/mL, P < 0.001), inhibited secretion of inflammatory cytokines in colon tissue and increased colonic epithelial cell proliferation(90.04 ± 15.50 vs 22.51 ± 8.22, P < 0.01) were all observed. Reduced apoptosis(149.55 ± 21.68 vs 983.01 ± 98.17, P < 0.05) was also observed. However, significant statistical differences in the results of the Ast2 B group and Ast2 B + Ucn2 group were observed. TXYF was also found to ameliorate symptoms of DSS-induced colitis in mice and to promote mucosal repair like Ucn2. There were significant differences between the Ast2B + TXYF groups and the TXYF groups.CONCLUSION CRH-R2 activates the intestinal mucosal antiinflammatory response by regulating migration, proliferation and apoptosis of intestinal epithelial cells in colitisinduced mice, and plays an important antiinflammatory role. TXYF promotes mucosal repair in colitis mice by regulating CRH-R2.
