胸段食管鳞癌淋巴结转移规律探究

目的探讨胸段食管鳞癌淋巴结转移规律及其影响因素,以指导淋巴结清扫方式。方法回顾分析漳州市医院2010年4月至2012年7月手术治疗的328例胸段食管鳞癌的临床病理资料,探讨淋巴结转移规律及其影响因素。结果全组328例共清扫淋巴结9937枚,平均30．3枚／例。共437枚、153例有淋巴结转移,转移率46．65％;其中喉返神经旁淋巴结转移18．30％,10．46％喉返神经旁淋巴结为唯一转移部位。胸段食管癌淋巴结转移与肿瘤部位、长度、分化程度及浸润深度明显相关。胸上段食管癌淋巴结转移方向主要向上纵隔及下颈部;胸中段食管癌颈、胸、腹均可发生淋巴结转移;胸下段食管癌主要向腹腔、中下纵隔转移。结论食管上段鳞癌,颈部淋巴结转移率高,应行三野淋巴结清扫;下段食管癌清扫重点在腹腔、中下纵隔;中段鳞癌应提倡进行个体化清扫和适度清扫;分化程度差,浸润程度深的病例应适当扩大清扫范围。胸段食管癌喉返神经旁淋巴结转移率高,均应行喉返神经旁淋巴结清扫。     

食管癌淋巴结转移特点及其危险因素

目的 探讨食管癌淋巴结转移情况及其危险因素,为外科手术行淋巴结清扫提供参考。方法回顾总结2006年1月至2010年12月在复旦大学附属肿瘤医院胸外科行三野淋巴结清扫食管癌根治术308例患者的临床资料．分析淋巴结的转移规律及特点。结果308例患者平均清扫淋巴结（35．6±14．5）枚,197例（64％）患者出现淋巴结转移。Logistic单因素分析结果显示,脉管（淋巴管及血管）侵犯（P=0．019）及肿瘤浸润深度（P〈0．001）是发生淋巴结转移的危险因素。各站淋巴结中,胸部气管旁淋巴结转移率最高（25．0％）。上段食管癌腹部淋巴结转移率显著低于中段或下段食管癌（P=0．001）,而各段食管癌颈胸部淋巴结转移率比较,差异无统计学意义（P〉0．05）。颈胸部和颈胸腹部淋巴结转移率分别为14．6％和11．0％,而颈腹部和胸腹部则分别为3．6％和4．9％。脉管侵犯（P〈0．001）和胸部气管旁淋巴结转移（P=0．014）是食管癌发生颈部淋巴结转移的危险因素。结论食管癌淋巴结转移具有上、下双向和跳跃性的特点．胸部气管旁淋巴结转移可作为行颈部淋巴结清扫的指征。     

177例胸段食管癌淋巴结转移规律研究

目的探讨胸段食管癌淋巴结转移规律及影响因素,为食管癌淋巴结清扫提供参考。方法回顾性分析我科2015~2016年行食管癌根治术177例胸段食管癌患者的临床资料,其中男125例、女52例,中位年龄64(18~86)岁。排除颈段食管癌及胃食管交接部肿瘤,分析胸段食管癌不同病变部位淋巴结转移情况及淋巴结转移与肿瘤病理类型、浸润深度、分化程度、病变长度的关系。结果 177例患者中,76例发生淋巴结转移,淋巴结转移率为42.9%(76/177)。手术共清扫4 977枚淋巴结,转移361枚,淋巴结转移度为7.3%(361/4 977)。胸段食管癌淋巴结转移率与肿瘤位置、病变长度无关(P0.05),而与肿瘤浸润深度及分化程度有关(P0.05)。结论胸段食管癌早期容易发生淋巴结转移,我们应根据食管癌淋巴结转移的特点,规范、系统及有重点地进行淋巴结清扫。     

胸段食管鳞癌淋巴结合理廓清范围的探讨

目的通过分析胸段食管鳞癌淋巴结转移方式、转移规律及其与相关病理因素的关系,探讨淋巴结合理廓清范围。方法对117例胸段食管鳞癌患者行食管癌手术中摘除有癌转移的淋巴结155枚,采用logistic回归分析临床病理因素与淋巴结转移的关系。结果胸段食管鳞癌患者无论肿瘤病理类型和临床状态如何,均有淋巴结转移。肿瘤分化程度和浸润深度对淋巴结转移率有明显的影响,肿瘤分化越低,浸润深度越深,淋巴结转移率越高。纵隔淋巴结转移多位于隆突下和癌旁,腹腔淋巴结转移多发生于胃左血管旁及胃小弯处。结论对胸段食管鳞癌应行常规胸、腹两野淋巴结清扫,尤其对T3和T4的患者,对有颈部淋巴结转移的患者应行颈、胸、腹三野淋巴结清扫;手术中对颈部可疑淋巴结转移的患者可行活组织冰冻病理检查。尽可能达到根治,提高手术疗效。     

胸段食管癌喉返神经旁淋巴结转移特点及临床意义

目的 探讨胸段食管癌喉返神经旁淋巴结转移特点及临床发生率,为术后准确分期、制定后续治疗方案和判断预后提供依据.方法 回顾性分析2007年3月至2010年2月,124例行胸段食管癌切除合并喉返神经旁淋巴结清扫术病人的临床和病理资料.结果 124例中34例出现了喉返神经旁淋巴结转移,34例共清扫了297枚淋巴结,47枚淋巴结有转移,其转移率为27.41%(34/124例),转移度为15.82%(47/297枚).34例有转移者中,高分化食管癌4例,中分化食管癌13例,低分化食管癌17例;低分化食管癌比高、中分化食管癌更易发生喉返神经旁淋巴结转移.上段食管癌9例、中段20例、下段5例,上段食管癌喉返神经旁淋巴结转移率为30%,中段为29%,下段为20%,上、中段食管癌喉返神经旁淋巴结转移率明显高于下段食管癌;T2 6例,T1 27例,T2的转移率为23.08%(6/26例),T3的转移率为28.72%(27/94例),两组转移率基本相似,P>0.05.11例术后出现声嘶,发生率为8.87%(11/124例),7例3个月后恢复.结论 胸段食管癌病例有近1/3发生喉返神经旁淋巴结转移,尤其是胸上段、低分化、浸润深(T2 以上)的食管癌更易发生.     

胸段食管癌喉返神经旁淋巴结转移特点及临床意义

目的 探讨胸段食管癌喉返神经旁淋巴结转移特点及临床发生率,为术后准确分期、制定后续治疗方案和判断预后提供依据.方法 回顾性分析2007年3月至2010年2月,124例行胸段食管癌切除合并喉返神经旁淋巴结清扫术病人的临床和病理资料.结果 124例中34例出现了喉返神经旁淋巴结转移,34例共清扫了297枚淋巴结,47枚淋巴结有转移,其转移率为27.41%(34/124例),转移度为15.82%(47/297枚).34例有转移者中,高分化食管癌4例,中分化食管癌13例,低分化食管癌17例;低分化食管癌比高、中分化食管癌更易发生喉返神经旁淋巴结转移.上段食管癌9例、中段20例、下段5例,上段食管癌喉返神经旁淋巴结转移率为30%,中段为29%,下段为20%,上、中段食管癌喉返神经旁淋巴结转移率明显高于下段食管癌;T2 6例,T1 27例,T2的转移率为23.08%(6/26例),T3的转移率为28.72%(27/94例),两组转移率基本相似,P>0.05.11例术后出现声嘶,发生率为8.87%(11/124例),7例3个月后恢复.结论 胸段食管癌病例有近1/3发生喉返神经旁淋巴结转移,尤其是胸上段、低分化、浸润深(T2 以上)的食管癌更易发生.     

胸段食管癌淋巴结转移特点的临床研究

目的 探讨胸段食管癌淋巴结转移的规律和特点,从而为其手术入路和淋巴结清扫范围提供参考.方法 回顾性分析2009年1月至2012年12月间中南大学湘雅医学院附属肿瘤医院胸外科收治的72例胸段食管癌患者的临床资料,所有病例均行右胸入路手术. 记录各组淋巴结的清扫及转移情况,并分析淋巴结转移的影响因素.结果 72例患者中,有48例出现淋巴结转移,淋巴结转移率为66.7％;清扫淋巴结总数为1495枚,转移181枚,淋巴结转移度为12.1％,平均每例清扫淋巴结20.8枚.在各组淋巴结中,右喉返神经旁（1R组）淋巴结转移率最高,达30.6％（22/72）.左喉返神经旁淋巴结（2L组、4L组和5组） 转移率为12.5％（9/72）.淋巴结转移率与肿瘤大小和浸润深度有关（均P＜0.05）,而与病变部位和分化程度无关（P＞0.05）.结论 胸段食管癌淋巴结转移以右喉返神经旁淋巴结转移为主,故其手术最佳入路应是右胸入路,淋巴结清扫则应以右、左喉返神经旁淋巴结为重点的系统纵隔、腹野淋巴结清扫.     

胸段食管癌颈部及上纵隔淋巴结转移

探讨胸段食管癌颈部及上纵隔淋结转移规律。方法采用颈,胸,腹三切口施行胸段食管癌手术６１６例,同时施行三区域淋巴洁清扫。结果：中及上纵隔淋巴结转移率和转移度分别为５７．１％和２１．５％。结论胸段食管癌必须重颈部及上纵隔淋巴结清扫。     

胸段食管鳞癌淋巴结的转移规律及危险因素分析

目的:分析影响胸段食管鳞癌淋巴结转移的规律及相关危险因素,为外科手术方式的选择及临床治疗提供参考依据。方法:回顾分析2017年1月至2018年12月为180例胸段食管鳞癌患者行胸腹腔镜联合食管癌根治术的临床资料,术中接受二野或三野淋巴结清扫术,将发生淋巴结转移的89例患者作为观察组,未发生淋巴结转移的91例患者作为对照组,统计淋巴结转移率、淋巴结转移位置;并对肿瘤位置、患者年龄、性别、肿瘤大小、肿瘤浸润深度、是否有脉管内癌栓等因素进行单因素分析,对有统计学意义的因素进行多因素Logistic回归分析。结果:胸段食管癌转移率为49.4%,单因素分析显示,肿瘤大小、肿瘤分化、肿瘤浸润深度、脉管癌栓对淋巴结转移的影响有统计学意义(P<0.05);对上述因素进行多因素Logistic回归分析,结果显示肿瘤分化、肿瘤大小、肿瘤浸润深度、脉管内癌栓是影响胸段食管鳞癌转移的独立因素(P<0.05)。结论:胸段食管鳞癌淋巴结转移率较高,食管癌术中进行完整、彻底的二野或三野清扫是非常有必要的;淋巴结转移的相关危险因素为肿瘤分化、肿瘤大小、肿瘤浸润深度、脉管内癌栓等。     

选择性颈胸腹三野淋巴结清扫治疗胸段食管鳞癌

目的 研究胸段食管鳞癌的淋巴结转移规律，探讨合适的淋巴结清扫范围。方法 87例接受食管次全切除术的胸段食管鳞癌患者，根据术前食管腔内超声和颈部超声检查结果，选择性进行胸腹二野或颈胸腹三野淋巴结清扫。结果 超声发现颈部淋巴结肿大并行三野清扫35例（40．2％，三野清扫组），其中原发肿瘤位于胸上段食管者的比例（16／24例，66．7％）显著高于中、下段肿瘤者（19／63例，30．2％）（P=0．002）。三野清扫术扫除淋巴结13．7组／例，显著多于二野清扫组（52例，59．8％）的10．5组／例（P〈0．001）。术后病理检测三野清扫组转移淋巴结1．5组／例，也显著多于二野清扫组的0．8组／例（P〈0．01）。颈淋巴结转移（pM1-LN）17例（占全组19．5％，占三野清扫组48．6％），有区域淋巴结转移者的颈淋巴结转移比例（15／48例，31．3％）显著高于无区域淋巴结转移者（2／39例，5．1％）（P〈0．01）。上、中、下纵隔及上腹部的淋巴结转移率分别为25．3％、23．O％、5．7％和24．1％，颈淋巴结转移与上纵隔（P〈0．01）及中纵隔（P〈0．01）淋巴结转移显著相关，但与下纵隔及上腹部淋巴结转移无关。三野清扫组术后并发症发生率（60．0％）显著高于二野清扫组（34．6％，P=0．020）。喉返神经损伤发生率两组差异无统计学意义（P〉0．05）；但喉返神经损伤者吻合口瘘发生率（7／13例，53．8％）显著高于无喉返神经损伤者（10／74例，13．5％，P=0．001）。术后死亡率两组差异无统计学意义（P〉0．05）。结论 应对肿瘤位于胸上段食管、或上纵隔及中纵隔淋巴结已发生转移的食管癌患者在超声指导下进行选择性颈胸腹三野淋巴结清扫术，以降低手术风险、提高手术根治效果。     

杭州健康女性定量骨超声测定原发性骨质疏松

目的 评价杭州健康女性骨超声速度(SOS)值随增龄减少和骨质疏松患病率，建立杭州地区女性骨超声速度值参考数据库。方法 定量超声法测定1208例杭州地区健康女性桡骨远端(RAD)，第3指骨近节(PLX)，第V跖骨(MTR)和胫骨中段(TIB)的超声速度值。结果 RAD、PLX、MTR和TIBSOS峰值(Peak of SOS)均出现在40-45岁，TJB的SOS峰值出现在35—40岁，此后随年龄增长而下降。绝经后妇女在绝经后早期和晚期各有1个SOS快速减少期，前见于桡骨近端，平均年减少率为2．4％，后见于胫骨中段，平均年减少率为1．8％。各部位骨SOS累积减少率随年龄增长而增加，到85岁4部位累积减少为13％-18％。60岁以后骨质疏松性症(OP)检出率为45％-70％，OP检出率以桡骨远端最高，60-70岁平均为67％，第3指骨近端次之约50％，胫骨中段最低为36％；75岁以后分别为70％，65％和45％。结论 全身各部位骨超声速度值到达峰值的年龄不同，峰值也各有差异。绝经后妇女骨超声速度值随年龄增加减少较快，应予激素和补钙治疗，桡骨远端为本地区SOS检测和OP检出的敏感部位。     

Importance of echocardiography in prognosis of surgical outcomes in cholecystitis in elderly patients

The authors propose to use more often echocardiography (EchoCG) in examination of elderly (over 60 years) of age patients with cholecystitis that permits to increase surgical activity to 92.4%. Left ventricular ejection fraction is the most informative. When this fraction is lower than 45% surgery must be recommended on vital indications only. EchoCG was used in 155 patients with cholecystitis, 131 of them were operated. 2 (1.52%) patients died due to acute cardio-vascular insufficiency and pulmonary artery thromboembolism.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

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.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

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.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

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.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

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.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

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.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

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.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

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.