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排序方式: 共有893条查询结果,搜索用时 15 毫秒
81.
82.
目的探讨柴芩承气汤(Chai Qin Cheng Qi Decoction,CQCQD)对急性坏死性胰腺炎(acute necrotizingpancreatitis,ANP)小鼠白细胞介素-6(interleukin-6,IL-6)、白细胞介素-10(interleukin-10,IL-10)水平及胰腺病理改变的影响。方法将30只昆明小鼠随机分成对照组、ANP组及CQCQD组,每组10只。ANP模型采用8%L-精氨酸溶液腹腔注射,4.0mg·g-1·1h-1×2制作。CQCQD组予以CQCQD制剂0.1ml/10g灌胃,1次/2h,观察其第6h的血清IL-6、IL-10水平及胰腺病理改变。结果 ANP组血清IL-6水平(1589.63±377.28)pg/ml高于对照组(927.46±210.42)pg/ml,P<0.05,也高于CQCQD组(1107.73±351.62)pg/ml,P<0.05,对照组血清IL-6水平与CQCQD组相比较,无统计学差异(P>0.05)。ANP组血清IL-10水平(920.64±101.68)pg/ml与对照组(1083.77±142.85)pg/ml相比较无统计学差异(P>0.05),ANP组血清IL-10水平低于CQCQD组(1177.84±201.72)pg/ml,P<0.05,对照组血清IL-10水平与CQCQD组相比较,无统计学差异(P>0.05)。ANP组胰腺病理评分(6.20±1.65)高于对照组(1.00±1.11),P<0.01,也高于CQCQD组(4.50±0.54),P<0.05。对照组胰腺病理评分低于CQCQD组(P<0.01)。结论 CQCQD可降低ANP小鼠IL-6水平,升高血清IL-10水平,减轻ANP小鼠胰腺的损伤。 相似文献
83.
目的 研究内皮素受体B(ETR-B)在人恶性黑素瘤中的表达及内皮素3对黑素瘤细胞A375的体外促生长效应。方法 采用免疫组化SP法检测ETR-B在黑素瘤组织中的表达,用RT-PCR法检测ETR-B基因在人恶性黑素瘤细胞A375和SK-mel-1中的表达,用MTT比色法检测不同浓度内皮素3对黑素瘤细胞A375的体外促增殖活性。结果 ETR-B在41例恶性黑素瘤和23例色素痣中的阳性率分别为78.05%和8.69%,两组间差异有统计学意义,P < 0.05。15例原位和26例Ⅰ ~ Ⅳ期恶性黑素瘤ETR-B阳性表达率分别为53.33%和92.31%,两组比较,P < 0.05。13例转移性恶性黑素瘤(Ⅲ ~ Ⅳ期)中ETR-B阳性表达率100%,28例未转移者(0 ~ Ⅱ期)的阳性表达率为67.86%,两组比较,P < 0.05。ETR-B基因在人恶性黑素瘤细胞A375和SK-mel-1中均有表达;内皮素3对黑素瘤细胞A375在体外具有很强的促增殖作用,且促增殖能力呈内皮素3浓度依赖性。结论 内皮素3/ETR-B在促黑素瘤细胞生长中有重要作用 相似文献
84.
Objective To investigate the effects ofendothelin-1 (ET-1) and endothelin-3 (ET-3) on the expression of transformation growth factor-beta 1 (TGF-β1) and phosphorylation of Smad 3 in malignant melanoma cell line, A375. Methods Cultured A375 cells were classified into 5 groups, i.e. control group (no stimulation), ET-1 group (stimulated with ET-1), ET-1+BQ123 group (treated with ET-1 and BQ123),ET-1 + BQ788 group (treated with ET-1 and BQ788), ET-3 group (stimulated with ET-3), to receive different stimulation. The working concentrations were 0, 0.1, 1, 10, 100 nmol/L for ET-1 and ET-3, 10 μmol/L for BQ123 and BQ788. After another 12- and 24-hour culture, ELISA, RT-PCR and Western blot were used to detect the expression of TGF-β1 protein and mRNA as well as phosphorylated Smad 3 (P-Smad 3). Results The expression of TGF-β1 in A375 cells was up-regulated by ET-1, but down-regulated by ET-3, and both of the effects were in a concentration-dependent manner. Under the stimulation with ET-1 and ET-3 of 100 nmol/L, the level of TGF-β1 reached 1289.38 ± 89.42 ng/L per 105 cells and 85.09 ± 9.37 ng/L per 105 cells, respectively, significantly different from that in unstimulated cells (both P < 0.05). BQ123 signifi-cantly blocked the up-regnlatory effect of ET-1 on the expression TGF-β1 protein(P < 0.05), but BQ788 had no significant influence on the effect, so was the case with TGF-β1 mRNA. Western blot revealed that ET-1significantly elevated the expression of P-Smad 3 in A375 cells (P <0.05), and the elevation was significantly inhibited by BQ123, but not by BQ788. The expression of P-Smad 3 was statistically decreased by ET-3 in A375 cells (P <0.05). Conclusions The expression of TGF-β1 could be enhanced by ET-1, but suppressed by ET-3. It is likely that endothelin receptor A mediates the phosphorylation of Smad 3 induced by ET-1. 相似文献
85.
Objective To investigate the effects ofendothelin-1 (ET-1) and endothelin-3 (ET-3) on the expression of transformation growth factor-beta 1 (TGF-β1) and phosphorylation of Smad 3 in malignant melanoma cell line, A375. Methods Cultured A375 cells were classified into 5 groups, i.e. control group (no stimulation), ET-1 group (stimulated with ET-1), ET-1+BQ123 group (treated with ET-1 and BQ123),ET-1 + BQ788 group (treated with ET-1 and BQ788), ET-3 group (stimulated with ET-3), to receive different stimulation. The working concentrations were 0, 0.1, 1, 10, 100 nmol/L for ET-1 and ET-3, 10 μmol/L for BQ123 and BQ788. After another 12- and 24-hour culture, ELISA, RT-PCR and Western blot were used to detect the expression of TGF-β1 protein and mRNA as well as phosphorylated Smad 3 (P-Smad 3). Results The expression of TGF-β1 in A375 cells was up-regulated by ET-1, but down-regulated by ET-3, and both of the effects were in a concentration-dependent manner. Under the stimulation with ET-1 and ET-3 of 100 nmol/L, the level of TGF-β1 reached 1289.38 ± 89.42 ng/L per 105 cells and 85.09 ± 9.37 ng/L per 105 cells, respectively, significantly different from that in unstimulated cells (both P < 0.05). BQ123 signifi-cantly blocked the up-regnlatory effect of ET-1 on the expression TGF-β1 protein(P < 0.05), but BQ788 had no significant influence on the effect, so was the case with TGF-β1 mRNA. Western blot revealed that ET-1significantly elevated the expression of P-Smad 3 in A375 cells (P <0.05), and the elevation was significantly inhibited by BQ123, but not by BQ788. The expression of P-Smad 3 was statistically decreased by ET-3 in A375 cells (P <0.05). Conclusions The expression of TGF-β1 could be enhanced by ET-1, but suppressed by ET-3. It is likely that endothelin receptor A mediates the phosphorylation of Smad 3 induced by ET-1. 相似文献
86.
Objective To investigate the effects ofendothelin-1 (ET-1) and endothelin-3 (ET-3) on the expression of transformation growth factor-beta 1 (TGF-β1) and phosphorylation of Smad 3 in malignant melanoma cell line, A375. Methods Cultured A375 cells were classified into 5 groups, i.e. control group (no stimulation), ET-1 group (stimulated with ET-1), ET-1+BQ123 group (treated with ET-1 and BQ123),ET-1 + BQ788 group (treated with ET-1 and BQ788), ET-3 group (stimulated with ET-3), to receive different stimulation. The working concentrations were 0, 0.1, 1, 10, 100 nmol/L for ET-1 and ET-3, 10 μmol/L for BQ123 and BQ788. After another 12- and 24-hour culture, ELISA, RT-PCR and Western blot were used to detect the expression of TGF-β1 protein and mRNA as well as phosphorylated Smad 3 (P-Smad 3). Results The expression of TGF-β1 in A375 cells was up-regulated by ET-1, but down-regulated by ET-3, and both of the effects were in a concentration-dependent manner. Under the stimulation with ET-1 and ET-3 of 100 nmol/L, the level of TGF-β1 reached 1289.38 ± 89.42 ng/L per 105 cells and 85.09 ± 9.37 ng/L per 105 cells, respectively, significantly different from that in unstimulated cells (both P < 0.05). BQ123 signifi-cantly blocked the up-regnlatory effect of ET-1 on the expression TGF-β1 protein(P < 0.05), but BQ788 had no significant influence on the effect, so was the case with TGF-β1 mRNA. Western blot revealed that ET-1significantly elevated the expression of P-Smad 3 in A375 cells (P <0.05), and the elevation was significantly inhibited by BQ123, but not by BQ788. The expression of P-Smad 3 was statistically decreased by ET-3 in A375 cells (P <0.05). Conclusions The expression of TGF-β1 could be enhanced by ET-1, but suppressed by ET-3. It is likely that endothelin receptor A mediates the phosphorylation of Smad 3 induced by ET-1. 相似文献
87.
目的探讨FIPL1-PDGFRα阴性高嗜酸性粒细胞综合征患者的临床特征。方法对7例FIPL1-PDGFRα阴性高嗜酸性粒细胞综合征患者的病史、临床表现和实验室检查结果以及治疗进行综合分析。结果FIPL1-PDGFRα阴性高嗜酸性粒细胞综合征的诊断需要排除反应性和继发性因素,分为克隆性和特发性。临床表现为外周血嗜酸性粒细胞增高和受累器官相应症状。以激素作为一线治疗。结论不明原因嗜酸性粒细胞明显升高伴个或多个器官损害的患者应警惕高嗜酸性粒细胞综合征。FIPL1-PDGFRα阴性的高嗜酸性粒细胞综合征足量使用激素可取得较好疗效。 相似文献
88.
89.
目的 探讨伴EB病毒(EBV)感染的淋巴瘤继发噬血细胞综合征(HPS)的临床特征。方法 分析4例伴EB病毒感染的淋巴瘤继发HPS患者的临床资料,并文献复习。结果 3例患者初诊为EBV继发HPS,4例患者最终均诊断为T细胞淋巴瘤。临床共同特点为发热、脾大、全血细胞减少、铁蛋白升高和低纤维蛋白原血症,浅表淋巴结肿大不明显,3例患者存在肝功能异常。4例患者抗EBV治疗后EBV-DNA均无明显下降。4例患者采用甲泼尼龙联合环孢素、依托泊苷或氟达拉滨治疗HPS,其中1例患者在激素减量过程中复发,规范化疗后HPS得以控制。结论 伴EBV感染的淋巴瘤继发HPS易被误诊为单纯EBV感染继发HPS。临床抗病毒效果欠佳或治疗过程中出现HPS反复需要警惕潜在淋巴瘤可能,需要多次取材送病理检查,甚至进行PET-CT检查积极寻找原发病,此类疾病的治疗原则是在积极治疗控制HPS后立即开始针对淋巴瘤的规范化疗。 相似文献
90.
提睾肌耻骨束及其临床意义 总被引:2,自引:0,他引:2
目的:通过对100例腹股沟区标本的解剖观察,研究疝的发病和疝修补术的复发的解剖学因素。方法:用福尔马林固定的尸体常规解剖和4 ̄10倍的解剖放大镜进行观察。疝修被术中使用25 ̄50mA-V(毫安-伏)电刺激此肌刺观察生理反应。结果:发现自提睾肌发生一肌束,由外上向内下以腱膜性结构抵止于耻骨结节,将其命名为“提睾肌耻骨束”,出现率为100%,此肌束由生殖股神经的生殖支支配。用直流电刺激此肌刺或生殖股神 相似文献