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21.
目的 评价脊髓胶质细胞在小鼠骨癌痛形成中的作用.方法 健康雄性C3H/He小鼠40只,周龄8~10周,体重18~22 g,随机分为4组(n=10):假手术组(S组)、骨癌痛组(B组)、PBS组(P组)和米诺环素组(M组).S组跟骨骨髓腔内注射PBS 10 μl;余3组跟骨骨髓腔内注射含2×105个骨纤维肉瘤细胞的PBS 10 μl制备骨癌痛模型,于造模前即刻开始PBS组鞘内注射PBS 5μl,M组鞘内注射米诺环素(用PBS溶解为0.2 mmol/L)5μl,1次/d,连续11 d.于造模前1 d、造模后即刻、3、5、7、9、11 d时测定机械痛阈;于造模后3、7、9、11 d机械痛阈测定结束后测定冷痛阈.痛阈测定结束后处死小鼠,取脊髓组织,测定神经胶质纤维酸性蛋白(GFAP)和CD11b的表达水平.结果 与S组比较,B组和P组造模后3-11 d时、M组造模后3、5 d时机械痛阈升高,B组、P组和M组造模后7~11 d时冷痛阈升高,脊髓CD11b和GFAP表达上调(P<0.05).与B组比较,M组造模后3-11 d时机械痛阈降低,造模后7-11 d时冷痛阈降低,脊髓CD11b和GFAP表达下调(P<0.05).结论 脊髓胶质细胞(星形胶质细胞和小胶质细胞)的激活参与了小鼠骨癌痛的形成.  相似文献   
22.
Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.  相似文献   
23.
椎间盘病变是引起临床疼痛症状的常见原因。近年来,交感神经在退变腰椎间盘的分布逐步被阐明,腰椎间盘病变累及交感神经在腰椎间盘源性疼痛的发病机制中的作用越来越受到重视。椎间盘退变,髓核外漏会导致神经张入腰椎间盘内及神经炎性反应的发生,这种变化也构成了腰椎间盘源性疼痛的基础。本文就交感神经在退变腰椎间盘的分布及腰椎间盘源性疼痛的发病机制进行综述。  相似文献   
24.
Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.  相似文献   
25.
Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.  相似文献   
26.
A型肉毒毒素治疗带状疱疹后神经痛的临床观察   总被引:1,自引:0,他引:1  
目的观察A型肉毒毒素治疗带状疱疹后神经痛的临床疗效和不良反应。方法重度带状疱疹后神经痛患者29例,应用A型肉毒毒素进行皮内注射治疗,问卷调查记录每例带状疱疹后神经痛患者治疗前、治疗后1,2,4,8周带状疱疹后神经痛疼痛严重程度,观察不良反应。结果A型肉毒毒素治疗后1周,带状疱疹后神经痛疼痛严重程度均较治疗前明显下降(P〈0.01),疗效可至少维持8周,且不良反应轻微、短暂。结论A型肉毒毒素皮内注射治疗带状疱疹后神经痛临床疗效显著,不良反应轻微、短暂,值得临床研究。  相似文献   
27.
目的 比较低温等离子消融术和射频热凝术治疗三叉神经痛的有效性和安全性.方法 收集2020年5-12月首都医科大学宣武医院疼痛科收治的行三叉神经外周支毁损治疗三叉神经痛患者的临床资料行回顾性分析.其中52例接受超声引导下三叉神经外周支低温等离子消融术治疗(A组),38例接受超声引导下射频热凝术治疗(B组).对比2组术前及...  相似文献   
28.
目的 探讨肉毒毒素A(BoNT-A)对神经病理性疼痛大鼠疼痛行为学及脊髓背角Fos蛋白表达的影响.方法 建立雄性SD大鼠慢性坐骨神经结扎(CCI)疼痛模型,CCI术后第3天开始,同侧肢体足底皮下注射BoNT-A 30 U/kg和等容积生理盐水,给药前、给药后1、3、5、7、14 d,采用von-Frey纤维细丝机械刺激法和热辐射刺激法评定大鼠机械刺激缩足反射阈值(MWT)和热刺激缩足反射潜伏期(TWL),观察大鼠疼痛行为学变化,根据变化结果,给药后第5天取相应脊髓节段标本,运用免疫组织化学法观察脊髓背角Fos蛋白表达.结果 CCI神经病理性疼痛模型大鼠建立后,CCI组同侧MWT和TWL均明显降低,且脊髓水平Fos蛋白表达明显增多;同侧足底注射BoNT-A 30 U/kg后,其MWT和TWL,均显著增加,脊髓水平Fos蛋白表达明显减少.结论 足底注射BoNT-A抑制脊髓水平Fos蛋白的表达,能减轻神经病理性疼痛模型大鼠的机械性触诱发痛和热痛觉过敏.  相似文献   
29.
脊髓损伤(spinal cord injury,SCI)是指由于外界直接或间接因素导致的相应脊髓节段出现各种运动、感觉、括约肌功能障碍、肌张力异常及病理反射等相应改变.过去的研究大多集中于运动和感觉的恢复;但是部分患者在脊髓损伤后会发生顽固性神经痛,并且常面临疼痛治疗困难.近年来,随着研究的深入,脊髓损伤后中枢性疼痛对患者生存质量的影响,越来越受到重视.Onnelly等报道[1]:脊髓损伤后疼痛的发生率高达77%-86%.  相似文献   
30.
目的观察低温等离子消融术治疗三叉神经痛(TN)的有效性及安全性。方法回顾性分析127例三叉神经第2、3支病变TN患者,其中72例接受C臂X线机引导下低温等离子消融治疗(A组),55例接受C臂X线机引导下射频热凝术治疗(B组)。对比2组术前、出院时及术后1、3、6和12个月的疼痛数字量表(NRS)评分、面部麻木程度巴罗神经学研究所(BNI)分级及并发症。结果2组间各时间点NRS评分差异无统计学意义(P均>0.05)。出院时及术后1个月,A组患者面部麻木程度BNI分级均低于B组(P均<0.05)。2组间口腔溃疡、咀嚼肌肌力减退、眼部症状、温度觉敏化及耳鸣发生率差异均无统计学意义(P均>0.05)。结论C臂X线机引导下低温等离子消融与射频热凝术对缓解TN患者疼痛效果相仿,而降低术后短期面部麻木程度效果更好。  相似文献   
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