目的:使用国产图迈机器人行腹腔镜根治性前列腺切除手术,观察其安全性及使用效果。方法:收集2023年1月至2023年5月前列腺癌患者40例,患者均行机器人辅助腹腔镜根治性前列腺切除术,采取保留膀胱颈和最大长度功能性尿道的手术方法。按使...目的:使用国产图迈机器人行腹腔镜根治性前列腺切除手术,观察其安全性及使用效果。方法:收集2023年1月至2023年5月前列腺癌患者40例,患者均行机器人辅助腹腔镜根治性前列腺切除术,采取保留膀胱颈和最大长度功能性尿道的手术方法。按使用机器人系统不同,分为观察组(图迈机器人组)和对照组(达芬奇机器人组),观察机械臂安装时间、腔内手术时间、尿道吻合时间、术中出血量、术后尿控等指标。结果:所有患者均顺利完成手术,观察组和对照组机械臂中位安装时间分别为6 min vs 5 min(P>0.05),腔内手术中位时间分别为146 min vs 130 min(P<0.05),尿道吻合中位时间分别为19 min vs 16 min(P<0.05),术中中位出血量分别为200 ml vs 150 ml(P>0.05)。术后即刻、1个月、3个月、6个月尿控恢复率分别为9/15(60.0%)vs 16/25(64.0%)、12/15(80.0%)vs 19/25(76.0%)、14/15(93.3%)vs 23/25(92.0%),15/15(100%)vs 24/25(96%),两组比较无显著差异(P>0.05)。结论:国产图迈机器人系统行腹腔镜根治性前列腺切除手术安全可靠,术后尿控效果满意。展开更多
ZnO nanorods with different morphologies were fabricated through a simple reaction method. They were characterized by means of powder x-ray diffraction (XRD), field emission scanning electron microscopy (FE-SEM) and e...ZnO nanorods with different morphologies were fabricated through a simple reaction method. They were characterized by means of powder x-ray diffraction (XRD), field emission scanning electron microscopy (FE-SEM) and ener-gy-dispersive x-ray (EDX) spectroscopy. FE-SEM images have shown that the shapes of the ZnO nanorods included straight nanorods, spear-like nanorods with sawtooth-shaped surfaces and lotus root-like nanorods. XRD and EDX indicated that all the nanorods are composed of hexagonal ZnO.展开更多
Tetrandrine (Tet), the main active constituent of Stephania tetrandra root, has been demonstrated to alleviate adjuvant-induced arthritis in rats. The present study was designed to investigate the effects of Tet on ...Tetrandrine (Tet), the main active constituent of Stephania tetrandra root, has been demonstrated to alleviate adjuvant-induced arthritis in rats. The present study was designed to investigate the effects of Tet on the migration and invasion of rheumatoid arthritis fibroblast-like synovioeytes (RA-FLS) and explore the underlying mechanisms. By using cultures of primary FLS isolated from synoviums of RA patients and cell line MH7A, Tet (0.3, 1 μmol L-1) was proven to significantly impede migration and invasion of RA-FLS, but not cell proliferation. Tet also greatly reduced the activation and expressions of matrix degrading enzymes MMP-2/9, the expression of F-actin and the activation of FAK, which controlled the morphologic changes in migration process of FLS. To identify the key signaling pathways by which Tet exerts anti-migration effect, the specific inhibitors of multiple signaling pathways LY294002, Triciribine, SP600125, U0126, SB203580, and PDTC (against PI3K, Akt, JNK, ERK, p38 MAPK and NF-kB-p65, respectively) were used. Among them, LY294002, Triciribine, and SP600125 were shown to obviously inhibit the migration of MH7A cells. Consistently, Tet was able to down-regulate the activation of Akt and JNK as demonstrated by Western blotting assay. Moreover, Tet could reduce the expressions of migration-related proteins Rho GTPases Rac 1, Cdc42, and RhoA in MH7A cells. In conclusion, Tet can impede the migration and invasion of RA-FLS, which provides a plausible explanation for its protective effect on RA. The underlying mechanisms involve the reduction of the expressions of Racl, Cdc42, and RhoA, inhibition of the activation of Akt and JNK, and subsequent down-regulation of activation and/or expressions of MMP-2/9, F-actin, and FAK.展开更多
Although the etiology of inflammatory bowel disease is still tmcertain, increasing evidence indicates that the excessive activation of NLRP3 inflammasome plays a major role. Norisoboldine (NOR), an alkaloid isolated...Although the etiology of inflammatory bowel disease is still tmcertain, increasing evidence indicates that the excessive activation of NLRP3 inflammasome plays a major role. Norisoboldine (NOR), an alkaloid isolated from Radix Linderae, has previously been demonstrated to inhibit inflammation and IL-1,8 production. The present study was to examine the effect of NOR on colitis and the underlying mechanism related to NLRP3 inflammasome activation. Our results showed that NOR alleviated colitis symptom in mice induced by 2, 4, 6-trinitrobenzene sulfonic acid (TNBS). Moreover, it significantly reduced expressions of cleaved IL-lfl, NLRP3 and cleaved Caspase-1 but not ASC in colons of mice. In THP-1 cells, NOR suppressed the expressions of NLRP3, cleaved Caspase-1 and cleaved IL-1β but not ASC induced by lipopolysaccharide (LPS) and adenosine triphosphate (ATP). Furthermore, NOR could activate aryl hydrocarbon receptor (AhR) in THP-1 cells, inducing CYP1A1 mRNA expression, and promoting dissociation of AhR/HSP90 complexes, association of AhR and ARNT, AhR nuclear translocation, XRE reporter activity and binding activity of AhR/ARNT/XRE. Both siAhR and a-naphthoflavone (a-NF) markedly diminished the inhibition of NOR on NLRP3 inflammasome activation. In addition, NOR elevated Nrf2 level and reduced ROS level in LPS- and ATP-stimulated THP-1 cells, which was reversed by either siAhR or α-NF treatment. Finally, correlations between activation of AhR and attenuation of colitis, inhibition of NLRP3 inflammasome activation and up-regulation of Nrf2 level in colons were validated in mice with TNBS-induced colitis. Taken together, NOR ameliorated TNBS-induced colitis in mice through inhibiting NLRP3 inflammasome activation via regulating AhR/Nrf2/ROS signaling pathway.展开更多
文摘目的:使用国产图迈机器人行腹腔镜根治性前列腺切除手术,观察其安全性及使用效果。方法:收集2023年1月至2023年5月前列腺癌患者40例,患者均行机器人辅助腹腔镜根治性前列腺切除术,采取保留膀胱颈和最大长度功能性尿道的手术方法。按使用机器人系统不同,分为观察组(图迈机器人组)和对照组(达芬奇机器人组),观察机械臂安装时间、腔内手术时间、尿道吻合时间、术中出血量、术后尿控等指标。结果:所有患者均顺利完成手术,观察组和对照组机械臂中位安装时间分别为6 min vs 5 min(P>0.05),腔内手术中位时间分别为146 min vs 130 min(P<0.05),尿道吻合中位时间分别为19 min vs 16 min(P<0.05),术中中位出血量分别为200 ml vs 150 ml(P>0.05)。术后即刻、1个月、3个月、6个月尿控恢复率分别为9/15(60.0%)vs 16/25(64.0%)、12/15(80.0%)vs 19/25(76.0%)、14/15(93.3%)vs 23/25(92.0%),15/15(100%)vs 24/25(96%),两组比较无显著差异(P>0.05)。结论:国产图迈机器人系统行腹腔镜根治性前列腺切除手术安全可靠,术后尿控效果满意。
基金Supported by the National Natural Science Foundation of China under Grant Nos.59925206,10044001 and 59972040the Foundation of the Chinese Academy of Sciences under Grant No.KY951-AI-205-05.
文摘ZnO nanorods with different morphologies were fabricated through a simple reaction method. They were characterized by means of powder x-ray diffraction (XRD), field emission scanning electron microscopy (FE-SEM) and ener-gy-dispersive x-ray (EDX) spectroscopy. FE-SEM images have shown that the shapes of the ZnO nanorods included straight nanorods, spear-like nanorods with sawtooth-shaped surfaces and lotus root-like nanorods. XRD and EDX indicated that all the nanorods are composed of hexagonal ZnO.
基金supported by the National Natural Science Foundation of China(No.81373426)the Priority Academic Program Development of Jiangsu Higher Education Institutions
文摘Tetrandrine (Tet), the main active constituent of Stephania tetrandra root, has been demonstrated to alleviate adjuvant-induced arthritis in rats. The present study was designed to investigate the effects of Tet on the migration and invasion of rheumatoid arthritis fibroblast-like synovioeytes (RA-FLS) and explore the underlying mechanisms. By using cultures of primary FLS isolated from synoviums of RA patients and cell line MH7A, Tet (0.3, 1 μmol L-1) was proven to significantly impede migration and invasion of RA-FLS, but not cell proliferation. Tet also greatly reduced the activation and expressions of matrix degrading enzymes MMP-2/9, the expression of F-actin and the activation of FAK, which controlled the morphologic changes in migration process of FLS. To identify the key signaling pathways by which Tet exerts anti-migration effect, the specific inhibitors of multiple signaling pathways LY294002, Triciribine, SP600125, U0126, SB203580, and PDTC (against PI3K, Akt, JNK, ERK, p38 MAPK and NF-kB-p65, respectively) were used. Among them, LY294002, Triciribine, and SP600125 were shown to obviously inhibit the migration of MH7A cells. Consistently, Tet was able to down-regulate the activation of Akt and JNK as demonstrated by Western blotting assay. Moreover, Tet could reduce the expressions of migration-related proteins Rho GTPases Rac 1, Cdc42, and RhoA in MH7A cells. In conclusion, Tet can impede the migration and invasion of RA-FLS, which provides a plausible explanation for its protective effect on RA. The underlying mechanisms involve the reduction of the expressions of Racl, Cdc42, and RhoA, inhibition of the activation of Akt and JNK, and subsequent down-regulation of activation and/or expressions of MMP-2/9, F-actin, and FAK.
基金supported by the Natural Science Foundation of Jiangsu Province of China(No.BK20140662)partially supported by the National Natural Science Foundation of China(No.81503319)the Priority Academic Program Development of Jiangsu Higher Education Institutions
文摘Although the etiology of inflammatory bowel disease is still tmcertain, increasing evidence indicates that the excessive activation of NLRP3 inflammasome plays a major role. Norisoboldine (NOR), an alkaloid isolated from Radix Linderae, has previously been demonstrated to inhibit inflammation and IL-1,8 production. The present study was to examine the effect of NOR on colitis and the underlying mechanism related to NLRP3 inflammasome activation. Our results showed that NOR alleviated colitis symptom in mice induced by 2, 4, 6-trinitrobenzene sulfonic acid (TNBS). Moreover, it significantly reduced expressions of cleaved IL-lfl, NLRP3 and cleaved Caspase-1 but not ASC in colons of mice. In THP-1 cells, NOR suppressed the expressions of NLRP3, cleaved Caspase-1 and cleaved IL-1β but not ASC induced by lipopolysaccharide (LPS) and adenosine triphosphate (ATP). Furthermore, NOR could activate aryl hydrocarbon receptor (AhR) in THP-1 cells, inducing CYP1A1 mRNA expression, and promoting dissociation of AhR/HSP90 complexes, association of AhR and ARNT, AhR nuclear translocation, XRE reporter activity and binding activity of AhR/ARNT/XRE. Both siAhR and a-naphthoflavone (a-NF) markedly diminished the inhibition of NOR on NLRP3 inflammasome activation. In addition, NOR elevated Nrf2 level and reduced ROS level in LPS- and ATP-stimulated THP-1 cells, which was reversed by either siAhR or α-NF treatment. Finally, correlations between activation of AhR and attenuation of colitis, inhibition of NLRP3 inflammasome activation and up-regulation of Nrf2 level in colons were validated in mice with TNBS-induced colitis. Taken together, NOR ameliorated TNBS-induced colitis in mice through inhibiting NLRP3 inflammasome activation via regulating AhR/Nrf2/ROS signaling pathway.