常规检查淋巴结阴性No.7组胃癌患者的淋巴结微转移研究

目的探讨常规病理检查无淋巴结转移的胃癌淋巴结微转移的特点,并分析微转移与各种临床病理因素的关系.方法应用淋巴结组织连续切片和端粒酶 RT-PCR ELISA方法检测 46例胃癌患者常规病理检查无淋巴结转移的 No.7组淋巴结 138个,并结合胃癌患者的临床病理资料进行统计学分析.结果本组 13例(28.3%) 32枚淋巴结(23.2%)经连续切片检出有微转移;而端粒酶阳性表达为 20例(43.5%) 49枚淋巴结(35.5%).端粒酶 RT-PCR ELISA检测敏感性为 100%,特异性为 84%,阳性预测值为 65%,阴性预测值为 100%,诊断准确率为 88%.淋巴结微转移与患者年龄、性别、原发肿瘤部位、组织学类型和转移淋巴结分型无关(P >0.05),但与原发肿瘤大体类型、大小及是否浸透浆膜有关(P< 0.05).结论对常规病理检查无淋巴结转移的胃癌患者,为客观评价胃癌临床病理分期及其预后,有必要监测其微转移,端粒酶 RT-PCR ELISA方法可以作为传统组织学检查方法的补充.     

可切除胃癌的前哨淋巴结示踪研究

目的 探讨前哨淋巴结活检在胃癌中的临床价值.方法 回顾性分析2003年1月至2006年6月46例行D2根治术的胃癌患者进行亚甲蓝前哨淋巴结活检的临床资料.结果 38例成功识别前哨淋巴结.前哨淋巴结敏感性、假阴性、准确性、特异性、阴性预测值及阳性预测值分别为69%(18/26)、31%(8/26)、79%(30/38)、100%(12/12)、60%(12/20)、100%(12/12).pT1期、TNM Ⅰ期和肿瘤直径<4 cm的患者,敏感性、准确性和阴性预测值均高达100%.肿瘤部位和淋巴结转移程度影响活检成功率,而肿瘤浸润深度、临床分期、淋巴结转移程度影响活检的敏感性、准确性和阴性预测值.结论 亚甲蓝前哨淋巴结活检在胃癌中的应用是可行的,早期患者的敏感性、准确性和可靠性高.     

胃癌根治术中肿大淋巴结的分析

目的　研究胃癌根治手术中肿大淋巴结实际转移状况并分析淋巴结切除范围与预后的关系。方法　查阅手术记录和术后病理报告并进行 5年随访。记录肿大淋巴结数 ,比较近端胃、远端胃和全胃切除术的淋巴结切除数目并分析其与预后的关系。结果　本组 15 5例胃癌标本中 ,共摘取淋巴结 3 3 0 5枚 (平均 2 1.3 2枚 /例 ) ;肿大淋巴结 10 3 7枚 (平均 6.69枚 /例 ) ;转移淋巴结 42 3枚 (平均 2 .73枚 /例 )。在 15 5例获 5年随访的患者中 ,行D2式手术 10 9例 ,D3式 46例 ,5年生存分别是 3 7例和 11例。结论　手术中肿大淋巴结不一定是转移淋巴结 ;胃癌根治术中淋巴结清扫范围不应盲目扩大 ,而应根据术中冰冻病检结果判断。     

胃癌患者淋巴结转移危险因素分析及患者预后分析

目的分析胃癌患者淋巴结转移的相关危险因素，以及对患者生存状况的影响。 方法选取2014年3月至2016年3月收治的125例胃癌患者作为此次研究对象，对其进行回顾性分析，所有研究对象均经病理确诊行根治手术治疗。依照淋巴结是否转移进行分组，91例患者纳入未转移组，34例纳入转移组。将研究数据均纳入SPSS20.0软件中进行整理分析，两组患者各临床指标的计数资料用"例"表示，行χ²检验，首先将P<0.05各项指标进行Logistic单因素回归分析，得出淋巴结转移的危险因素，后进行Logistic多因素分析。以P<0.05表示差异具有统计学意义。 结果单因素分析结果显示：肿瘤病灶直径、分化程度、浸润深度、有无脉管侵犯以及有无神经侵犯等因素是淋巴结转移的危险因素(P<0.05)；多因素回归分析证实，肿瘤直径、肿瘤浸润深度、有无脉管侵犯以及有无神经侵犯是影响淋巴结转移的独立危险因素(P<0.05)；随访结果表明，发生淋巴结转移的患者2年生存率均明显低于未转移患者，差异有统计学意义(P<0.05)。 结论在胃癌患者中，肿瘤大小、脉管侵犯、神经侵犯以及肿瘤的浸润深度是胃癌患者淋巴结转移的独立危险因素，发生淋巴结转移患者其生存时间以及生存率均有明显降低，对患者的预后造成一定的影响和威胁。     

实时荧光定量PCR检测胃癌淋巴结微转移及其临床意义

目的使用实时荧光定量PCR(qRT-PCR)法检测胃癌淋巴结的微转移情况,并探讨微转移的临床意义。方法收集我院2010年1～6月期间40例行胃癌根治术切除的281枚和10例行胃十二指肠溃疡手术切除的39枚,共计320枚淋巴结标本,以CEA、CK-19和CK-20为引物进行qRT-PCR检测其微转移情况,并分析微转移的临床病理特点。结果 40例胃癌患者中有28例(70.00%)、31枚(15.35%,31/202)淋巴结检测出有微转移。10例胃溃疡的39枚淋巴结标本,HE染色检测和qRT-PCR检测均为阴性。淋巴结微转移的阳性率与肿瘤分化程度、浸润深度和临床分期有关(P<0.05)。结论 qRT-PCR是检测胃癌淋巴结微转移敏感且特异的方法,对胃癌临床分期、判断预后以及治疗方案选择具有重要意义。     

胃癌D2根治术淋巴结切除数目与预后的关系

目的研究胃癌根治术淋巴结清扫数目与预后的关系。方法对1996年1月至2005年1月期间457例胃癌根治术患者的临床资料进行回顾性分析。结果淋巴结转移组中,切除淋巴结超过20枚组患者其1、3、5年生存率分别为82.4%、49.0%和33.4%;切除淋巴结16～20枚组者则分别为71.5%、49.7%和40.1%。无淋巴结转移组中,切除淋巴结超过20枚组患者1、3、5年生存率分别为98.2%、92.7%和84.7%;切除淋巴结16～20枚组者则分别为94.0%、89.7%和81.4%。淋巴结清扫16～20枚与20枚以上者,无论有无淋巴结转移,生存率比较差异均无统计学意义(P>0.05)。结论胃癌根治术清扫淋巴结16～20枚即可。除非发现转移,否则不必过度追求淋巴结清扫。     

进展期胃癌 No.12淋巴结转移规律对手术范围的指导意义

目的分析进展期胃癌 No.12淋巴结的转移规律,为肝十二指肠韧带淋巴结切除范围提供参考依据。方法选择2013年1月至2014年12月行根治性切除手术的进展期胃癌217例,记录每例病人的淋巴结总数,计算总体淋巴结转移率及 No.12a,12p 和 No.12b 淋巴结转移率,并分析No.12p 淋巴结转移的相关危险因素。结果217例手术标本共检出淋巴结9490枚(16~107枚),平均(43.73±14.05)枚/例。217例中164例有淋巴结转移,总体淋巴结转移率为75.58%,其中61例(28.11%)有 No.12淋巴结转移。61例 No.12淋巴结转移病例中,50例(23.04%)发现 No.12a 淋巴结转移,26例(11.98%)发现 No.12p 淋巴结转移,仅 1例(0.46%)发现 No.12b 淋巴结转移。No.12p 淋巴结转移的相关危险因素有肿瘤部位、肿瘤侵犯深度、No.5及 No.12a 淋巴结转移。结论进展期胃癌的 No.12淋巴结转移有明显规律,有助于指导肝十二指肠韧带淋巴结切除范围。     

一种新的胃癌淋巴结分期方案

目的比较AJCC/UICC 1997年第五版胃癌TNM分期中的N分期与以淋巴结转移度为标准的新N分期. 方法行D2或D3术式的胃癌(皆无远处转移)标本用透光法摘取淋巴结,分别按2种方法分期,新法中N1为淋巴结转移度0.01%～10.00%, N2为10.01%～25.00%,N3为＞25.00%.全组随访,资料经统计学处理. 结果本组78例患者共取得淋巴结5388 枚,平均每例69枚(范围30～157枚).全组淋巴结转移率75.64%(59/78).新分期N0、N 1、N2、N3期患者3年生存率分别为100%、68.42%、7.58%、6.78%(χ2=35.85 0,P<0.01, r=0.95). 结论淋巴结转移度是一相对数,在预后的判断上,优于淋巴结转移数目.     

IHC和RT-PCR法对检测胃癌区域淋巴结微转移的价值及其意义

目的 探讨免疫组织化学方法(IHC)和逆转录聚合酶链反应(RT-PCR)两种方法对检测胃癌区域淋巴结微转移的临床价值及意义.方法 对85例胃癌根治性手术切除的淋巴结转移患者的临床资料进行了回顾性分析.共切取淋巴结1835枚,每例平均切除21.7枚.采用IHC和RT-PCR法检测细胞角蛋白20(CK20)的表达,研究淋巴结微转移与临床病理参数和预后的关系.结果 患者的淋巴结转移率经IHC法和RT-PCR法检测从HE染色的75.3%分别上升为83.5%和90.6%.经IHC和RT-PCR法检测重新分期率分别为18.8%和37.6%.淋巴结微转移的发生与肿瘤大小、部位无关·与肿瘤Lauren分型和浸润深度密切相关.82例完成随访,平均随访时间为21.2个月.微转移与预后无明显关系.结论 IHC和RT-PCR法是检测胃癌淋巴结微转移的有效手段,能准确判断临未分期,可为制定治疗方案提供依据.     

进展期胃癌的淋巴结转移特点及其临床意义

目的探讨进展期胃癌的淋巴结转移特点及临床意义。方法对2002年4月至2003年7月期间进行胃癌根治淋巴结清扫手术的91例患者的手术切除标本进行解剖，收集切除的淋巴结，逐枚进行病理组织学和免疫组织化学检查，判断淋巴结是否转移并计算淋巴结转移率。分析淋巴结转移率与肿瘤大小、TNM分期、Borrmann分型、肿瘤部位和淋巴结清扫范围等方面的关系。结果91例胃癌患者中淋巴结转移阳性63例（69．2％）。共收获3149枚淋巴结，平均每例34．6枚。肿瘤直径小于3cm者淋巴结转移率较3cm以上者低（P〈0．05）。TNM分期中Ⅲa和Ⅳ期患者淋巴结转移率均为100％，其转移度在30．3％～58．4％之间，较Ⅰ、Ⅱ期者高（P〈0．001）；Borrmann分型中Ⅲ型病例的淋巴结转移率（79．6％）较其他型患者高，而Ⅳ型患者淋巴结转移度（35．3％）最高（P〈0．05）。施行D3淋巴结清扫手术患者的淋巴结转移率和转移度（88．2％、38．0％）均高于D1、D2术患者（P〈0．05）。17例（18．7％）患者常规病理检查发现有183枚淋巴结微转移，肿瘤各部位与淋巴结微转移的关系差异无统计学意义（P〉0．05）。近端胃癌淋巴结转移主要在第1、2、3、5、7、8、9、12、13和16组，以8组转移度为最高（68．1％）；中部胃癌淋巴结转移主要在第1、3、7、12、13和16组，其中最高转移度为第3组（47．6％）；远侧胃癌淋巴结转移主要见于1、2．3、5、6、12、13和16组，其中第16组转移度为最高（83．3％）。结论淋巴结转移率和转移度与胃癌的恶性程度密切相关，因此D3淋巴结清扫手术对某些进展期胃癌患者值得考虑使用。     

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.