行气散外敷治疗结核性肠梗阻的疗效观察

目的:探讨中西医结合治疗结核性腹膜炎伴粘连性肠梗阻的疗效。方法:96例结核性腹膜炎合并肠梗阻患者随机分为治疗组及对照组,每组各48例,治疗组及对照组均在抗痨治疗的基础上给予常规禁食、持续胃肠减压、抗感染、补液支持等治疗,治疗组则在此基础上加用中药行气散外敷治疗。结果:治疗组疗效有效率为91.67%,优于对照组的64.60%(P<0.05);且治疗组的住院时间与对照组相比明显缩短,优于对照组(P<0.05)。结论:西医常规治疗的基础上结合中药行气散外敷治疗,具有良好的临床效果,在抗痨治疗的基础上能有效缓解肠梗阻,同时缩短住院时间,值得在临床上推广应用。     

血瘀证候模型小型猪视网膜血管血氧饱和度的研究

目的:对比血瘀证组和对照组巴马小型猪眼底视网膜血管血氧饱和度,探讨血瘀证候模型小型猪眼底视网膜血管血氧饱和度的改变。方法:12只小型猪,随机分为血瘀证组6只和对照组6只,正常喂养7d后进行眼底视网膜血管血氧饱和度检测并进行血液生化指标基线检测。第8d,血瘀证组耳缘静脉给予10%高分子右旋糖酐溶液5mL/kg,隔日1次,共7次;对照组正常饲养。第21d,再次检测2组眼底视网膜血管血氧饱和度及血液生化指标并进行统计分析。实验结束后分别摘除2组小型猪眼球,用于做视网膜切片和视网膜消化铺片并对其结果进行分析。结果:血瘀证候模型建立后,血液指标FIB、PT、APTT较前降低(P<0.05),TT较前出现升高(P<0.05);ESR、血浆黏度、红细胞压积、红细胞变形指数、红细胞聚集指数升高(P<0.05);全血还原黏度升高(P<0.05)。本实验初步评估了巴马小型猪眼底视网膜血管血氧饱和度,其视网膜静脉血氧饱和度范围大致为(74.67±6.12)%,动脉血氧饱和度大致范围为(110.91±8.52)%。与对照组相比,血瘀证组小型猪SvO2、鼻上SvO2、颞侧SvO2值降低(P<0.05),鼻下SvO2值明显降低(P<0.01),颞侧SaO2值降低(P<0.05),SaO2-SvO2、SaO2/SvO2均升高(P<0.05)。视网膜切片HE结果及视网膜消化铺片结果显示,血瘀证组巴马小猪视网膜神经纤维层厚度增加,轻度水肿,内皮细胞计数及周细胞计数降低(P<0.05)。结论:高分子右旋糖酐溶液建立血瘀证候动物模型,引起红细胞聚集,血液黏稠度增高,血流缓慢,造成微循环缺氧状态,对视网膜静脉血氧饱和度的影响比视网膜动脉血氧饱和度更加明显。     

The BH3-mimetic GX15-070 induces autophagy,potentiates the cytotoxicity of carboplatin and 5-fluorouracil in esophageal carcinoma cells

Despite improvements in both surgical techniques and radio- and chemo-therapy regimens, the prognosis of esophageal cancer is poor. In pursuit of novel effective strategy, this study examined the effect of the BH3-mimetic GX15-070 on esophageal carcinoma cells. We discovered that GX15-070 inhibited the growth of esophageal cancer cells. There was synergism between GX15-070 and carboplatin or 5-fluorouracil. GX15-070 induced autophagy in esophagus cancer cell line EC9706 and osteosarcoma cancer cell line U2OS. 3-methyladenine and chloroquine, inhibitors of autophagy with distinct mechanisms, potentiated the cytotoxicity of GX15-070. In conclusion, GX15-070 inhibits growth of esophageal cancer cells.     

生长抑素及其2型受体与胰腺癌

生长抑素在体内有着广泛的生物学活性。研究表明,生长抑索及其类似物可以和生长抑素2型受体（SSTR2）结合发挥直接抗肿瘤细胞增殖的作用。少部分胰腺癌组织中存在着SSTR2的表达,大多数不表达SSTR2的胰腺癌则通过在细胞表面的再表达也可发挥抑制肿瘤生长的作用。现就胰腺癌中生长抑素及SSTR2的研究进展作一综述。     

ERK5和MMP-9在骨肉瘤中的表达及其临床意义

  目的  探讨细胞外信号调节激酶5（extracellular signal-regulated kinase 5,ERK5）蛋白和基质金属蛋白酶-9（matrix metallo proteinase-9,MMP-9）在骨肉瘤组织中的表达及其临床意义。  方法  选取71例骨肉瘤组织和40例正常骨组织,采用免疫组织化学法检测ERK5和MMP-9的表达,并分析ERK5和MMP-9的表达与骨肉瘤患者临床病理特征及预后之间的关系。  结果  骨肉瘤组织中ERK5和MMP-9阳性表达率分别为85.9%（61/71）、74.65%（53/71）,均明显高于正常骨组织中阳性表达率12.5%（5/40）、10.0%（4/40）,差异均具有统计学意义（均P < 0.05）。ERK5和MMP-9的阳性表达与Enneking分期和转移相关（均P < 0.05）。Ka-plan-Meier生存分析显示在骨肉瘤组织中ERK5、MMP-9的阳性表达组患者生存时间均短于阴性表达组（均P < 0.05）。单因素Cox回归分析发现,肿瘤大小、Enneking分期、转移、ERK5和MMP-9阳性表达与患者总生存时间相关（均P < 0.05）;多因素分析证实Enneking分期、转移、ERK5和MMP-9蛋白的阳性表达可作为骨肉瘤患者独立的预后因子（均P < 0.05）。  结论  ERK5和MMP-9在骨肉瘤组织中高表达,与骨肉瘤的病理特征及预后相关;二者可能在骨肉瘤发生发展的过程中起着重要作用。      

Inhibition of stromal‐interacting molecule 1‐mediated store‐operated Ca2+ entry as a novel strategy for the treatment of acquired imatinib‐resistant gastrointestinal stromal tumors

Imatinib has revolutionized the treatment of gastrointestinal stromal tumors (GIST); however, primary and secondary resistance to imatinib is still a major cause of treatment failure. Multiple mechanisms are involved in this progression. In the present study, we reported a novel mechanism for the acquired resistance to imatinib, which was induced by enhanced Ca²⁺ influx via stromal‐interacting molecule 1 (STIM1)‐mediated store‐operated Ca²⁺ entry (SOCE). We found that the STIM1 expression level was related to the acquired resistance to imatinib in our studied cohort. The function of STIM1 in imatinib‐resistant GIST cells was also confirmed both in vivo and in vitro. The results showed that STIM1 overexpression contributed to SOCE and drug response in imatinib‐sensitive GIST cells. Blockage of SOCE by STIM1 knockdown suppressed the proliferation of imatinib‐resistant GIST cell lines and xenografts. In addition, STIM1‐mediated SOCE exerted an antiapoptotic effect via the MEK/ERK pathway. The results from this study provide a basis for further research into potential novel therapeutic strategies in acquired imatinib‐resistant GIST.     

The Significance of Low Serum Pepsinogen Levels to Detect Stomach Cancer Associated with Extensive Chronic Gastritis in Japanese Subjects

Serum pepsinogen levels were measured in 137 stomach cancer patients and compared with those of 288 normal cancer-free subjects. The serum pepsinogen levels of stomach cancer patients, especially pepsinogen I and the pepsinogen I/pepsinogen II ratio were significantly lower than those of normal controls and correlated well with the extent of chronic gastritis associated with the cancerous stomach. These results were in good accordance with the results of previous studies indicating that the cancer derived from the stomach where chronic gastritis/intestinal metaplasia is extensive. The high sensitivity and specificity of this non-invasive serum test to detect chronic gastritis suggested the possibility of its application to the mass screening of stomach cancer.     

艾迪注射液对肺癌细胞A549放射增敏作用的实验研究

目的研究艾迪注射液对人肺腺癌细A549放射增敏作用及机制。方法（1）MTT法测定药物对细胞的抑制作用,计算半数抑制浓度IC50。（2）应用集落形成法观察药物对细胞的放射增敏作用。（3）流式细胞仪分析药物对细胞周期分布、凋亡的影响。结果药物作用48小时后,细胞生长受到抑制,且细胞抑制率随药物浓度的升高而增加。IC50为16.04 mg/mL。加药照射组与单纯照射组比较,细胞存活率下降,药物有放射增敏作用,随药物作用时间的延长放射增敏作用增强。单纯照射组、加药24小时、48小时后照射组三组D0值依次为2.13 Gy、2.04 Gy、1.64 Gy,Dq值依次为2.88 Gy、1.68 Gy、1.51 Gy,加药24小时及48小时后照射组放射增敏比SERD0分别为1.04、1.3,SERDq分别为1.71、1.91。流式细胞仪检测药物作用后G2/M期细胞增加,细胞凋亡率升高,药物作用时间延长以上变化更显著。结论艾迪注射液对肺癌细胞A549有抑制作用及放射增敏作用,其放射增敏作用机制可能为抑制细胞亚致死损伤修复,阻滞细胞于G2/M期,诱导细胞凋亡。     

去甲氧柔红霉素治疗急性髓细胞白血病45例临床疗效分析

[目的]比较去甲氧柔红霉素（IDA）和柔红霉素（DNR）治疗急性髓细胞白血病（AML）的临床疗效和不良反应。[方法]85例初治AML患者按诱导缓解方案随机分成2组,其中IDA联合阿糖胞苷（IA）组45例,DNR联合阿糖胞苷（DA）组40例。IA组诱导化疗方案为去甲氧柔红霉素10～12mg/（m2.d）,d1～3,阿糖胞苷100～150mg/（m2.d）,d1~7。DA组诱导化疗方案为柔红霉素40～60mg/（m2.d）,d1～3,阿糖胞苷100～150mg/（m2.d）,d1～7。观察两组疗效和不良反应。[结果]1个疗程结束后IA组有效率88.9%,完全缓解率82.2%,DA组有效率70.0%,完全缓解率57.5%,两组间有效率、完全缓解率差异有统计学意义（P〈0.05）。化疗的不良反应主要为骨髓抑制和粒细胞缺乏所致的感染,未见严重的非血液系统不良反应,两组不良反应发生率差异无统计学意义（P〉0.05）。[结论]去甲氧柔红霉素的诱导方案比用柔红霉素的方案具有更高的完全缓解率,且不良反应可耐受。