介入导管动脉化学药物治疗对直肠癌根治术后患者生存率的影响

目的 观察介入导管动脉化学药物治疗对直肠癌根治术后患者生存率的影响。方法 采用介入导管动脉化学药物治疗（下称化疗）代替全身化疗治疗直肠癌根治术后患者５６例。化疗药物为每次顺铂３０￣４０ｍｇ／ｍ＾２、５－氟尿嘧啶５００￣７５０ｍｇ／ｍ＾２、丝裂霉素４￣５ｍｇ／，＾２。结果 治疗后无大出血、肠坏死、肝肾功能障碍等严重并发症。经阴访，治疗组１、２、３、４、５年的生存率分别为９４．６％（５３／５６）、８２     

术前介入化疗对直肠癌细胞凋亡和增殖的影响

目的 观察术前介入化疗对直肠癌的疗效及对细胞凋亡和细胞增殖的时相变化的影响。方法 对１２例直肠癌患者术前应用Ｓｅｌｄｉｎｇｅｒ法经皮股动脉穿刺插管,选择肿瘤供血脉一次性化疗药物,５－氟脲嘧啶６００ｍｇ／ｍ＾２,丝裂霉素Ｃ１５ｍｇ／ｍ＾２,阿霉素３５ｍｇ／ｍ＾３。分别于化疗前,化疗后２４、４８、７２小时和７￣１０天取肿瘤组织,应用末端脱氧核苷酸转移酶介导的原位标记法（ＴＵＮＥＬ）检测凋亡细胞,应用免     

诺维本治疗恶性胸腔积液的疗效观察

目的：观察诺维本治疗恶性胸腔积液的疗效。以便寻找更安全有效的药物,及早控制病情,提高患者的生活质量。方法：晚期肺癌患者４２例,晚期乳腺癌患者１２例,所有患者分为诺维本治疗组（２０组）,其他药物治疗组（２５例）。所有患者行胸腔闭式引流术,诺维本２５ｍｇ／ｍ＾２,博莱霉素４０ｍｇ／ｍ＾２,顺铂６０ｍｇ／ｍ＾２,丝裂霉素６ｍｇ／ｍ＾２,长春花碱２ｍｇ／ｍ＾２,均用２％利多卡因５～１０ｍｌ溶解,将药物注入     

消化系统恶性肿瘤术后丝裂霉素和5-氟脲嘧啶的腹腔化学治疗

目的 减少中晚期消化系统恶性肿瘤术后腹腔内复发和肝转移率。方法 术后将患者随机分成腹腔化疗组（观察组）和静脉化疗组（对照组）,观察组５２例,将丝裂霉素６！１０ｍｇ／ｍ＾２和５氟脲嘧啶１￣１．５ｇ／ｍ＾２加入按２０ｍｌ／ｋｇ的生理盐水中,经左右下腹穿刺置管灌注腹腔。对照组５３例,用ＭＭＣ４￣６ｍｇ／ｍ＾２＋ＮＳ２０－３０ｍｌ静脉注及５－Ｆｕ０．７５￣１ｇ／ｍ＾２＋５％葡萄糖注射液５００ｍｌ静脉点滴治     

术前区域动态灌注化疗治疗乳癌

目的 评价术前动脉灌注化疗药物在乳癌治疗中的作用。方法 采用Ｓｅｌｄｉｎｇｅｒ江经皮股动脉穿刺,将导管置于锁肌下动脉与胸廓内动脉开口交界处的近侧,用充气止血带高于患者收缩压阻断患侧肱动脉血流后,注入化疗药物。根据病人情况３－４周重复灌注化疗１次。化疗方案：吡喃阿霉素,或阿霉素,或表阿霉素５０－７０ｍｇ／ｍ＾３,卡铂３００－４００ｍｇ／ｍ＾２,５氟－脲嘧啶（５－Ｆｕ）７５０－１０００ｍｇ／ｍ＾２,甲     

异丙酚不同给药方法辅助硬膜外阻滞时的血浆浓度与镇静作用

目的：探讨异丙酚最适给药方法，在４２例硬外麻醉下行上腹部手术的患者研究了三种给药法的血浆浓度和临床效应。方法：组１异丙酚负荷量１．５ｍｇ／ｋｇ，３ｍｉｎ后开始维持量３．７５ｍｇ．ｋｇ＾－１．ｈ＾－１，组２负荷量０．７５ｍｇ／ｋｇ，随之接与组１相同的维持量，组３以０．１５ｍｇ．ｋｇ＾－１．ｍｉｎ＾－１，６ｍｉｎ为负荷１ｍｉｎ内注入异丙酚１５ｍｇ并将维持量增加０．７５ｍｇ．ｋｇ＾－１．ｈ＾－１。结果．     

胃恶性肿瘤术前介入治疗的基础和临床研究

观察胃恶性肿瘤术前介入治疗的临床疗效探讨及其作用机制。方法：对４２０例胃恶性肿瘤患者术前采用Ｓｅｌｄｉｎｇｅｒ选择性动脉插管法进行化疗,方案为： ５－ＦＵ５００～７５０ｍｇ／ｍ２,表阿霉素４０ｍｇ／ｍ２,丝裂霉素１０ｍｇ／ｍ２或顺铂６０ｍｇ／ｍ２,直接注入肿瘤的主要供血动脉。动脉化疗后７～１０天,全部病人接受了手术治疗,对切除的标本进行详细组织病理学研究,观察介入治疗后的组织病理学改变。结果：本组总有效率为７２．８％,３例显效。经对比研究发现,介入治疗后小动脉炎和血管周围炎引起的肿瘤组织血供障碍和肿瘤组织病理性坏死是产生治疗效果的主要原因之一。结论：胃恶性肿瘤术前介入治疗效果明显,副作用轻,可以成为胃恶性肿瘤总体治疗中的一种重要的辅助治疗方法。     

自体骨髓移植保护下对耐药性ⅢB期骨肉瘤实施超大剂量化疗

目的：在大一化疗无效的ⅢＢ期骨肉瘤中探讨克服耐药，提高疗效的方法，并为将此疗法应用于ⅡＢ期骨肉瘤做准备。方法：在４例既往大剂量化疗无效的ⅢＢ期骨肉瘤中进行化疗，化疗前，取自体骨髓血备用，化疗后，于氨甲喋呤血药浓度小于１．０×１０＾－７ｍｏｌ／Ｌ时，回输自体骨髓血。设计化疗方案氨甲喋呤５００ｍｇ／ｋｇ，阿霉素２５－７５ｍｇ／ｍ＾２，长春新碱１．５ｍｇ／ｍ＾２。结果：４例患化疗后胸痛、胸闷症状缓解或     

紫杉醇加顺铂治疗非小细胞肺癌临床观察

目的：观察新型抗癌药紫杉醇治疗肺小细胞肺癌临床疗效及毒副作用。方法：紫杉醇１３５ｍｇ／ｍ＾２，顺铂６０ｍｇ／ｍ＾２，３－４周一次，２－３周期为一疗程，并随机分国产紫素和进口泰素比较，结果１０例患者完全缓解（ＣＲ）１例，部分缓解（ＰＲ）４例总有效率５０％，其中紫素ＰＲ３便，有效率６０％，泰素ＣＲ，ＰＲ各１例，有效率４０％。全部病例未发现严重毒副作用，结论：紫杉醇加顺铂治疗非小细胞肺明显疗效，副作用小     

他克莫司抗同种肾移植排斥反应的临床研究(附136例报道)

目的 研究他克莫司（ＦＫ５０６）在同种肾移植术后抗排斥反应的效果及毒副作用。方法 １３６例肾移植患者在术后２４ｈ开始服用ＦＫ５０６,起始量０．１５ｍｇ．ｋｇ＾－１,ｄ＾－１,同时口服霉酚酸酯（ＭＭＦ）１．０ｇ／ｄ、泼尼松（Ｐｒｅｄ）３０ｍｇ／ｄ。观察ＦＫ５０６的治疗效果、理想的治疗窗及毒副反应。结果 肾移植术后１３６例应用ＦＫ５０６的患者中,肾功能２～７ｄ恢复正常为９６例,８～１５ｄ恢复正常为２３     

Matrix metalloproteinase expressions in arteriosclerotic aneurysmal disease

Medial degeneration of extracellular matrix (ECM) proteins in the wall of abdominal aortas results in smooth muscle cell destruction, a loss of architectural integrity, and abdominal aortic aneurysm (AAA) formation. It has been theorized that an imbalance between proteinases and their naturally occurring inhibitors is the cause of these observed histologic abnormalities. Therefore, the purpose of this investigation was to determine if differences in the matrix metalloproteinase (MMP) -2 and -9, tissue inhibitor of metalloproteinase-1 (TIMP-1), tissue-type plasminogen activator (tPA), and urokinase-type plasminogen activator (uPA) protein and activity levels existed between infrarenal AAA and normal abdominal aortic tissue specimens. Between November 1995 and January 1997, 10 patients undergoing elective infrarenal AAA repair had a portion of their aneurysm walls snap frozen in liquid nitrogen and processed for subsequent western blot or zymographic analysis. Tissue specimens from 6 normal abdominal aortas obtained from fresh cadaver specimens were similarly processed and served as controls. Protein levels for MMP-2, MMP-9, TIMP-1, uPA, and tPA were analyzed by western blotting. The degree of MMP-2 and MMP-9 gelatinolytic activity was analyzed by zymography. Detection and immunolocalization for MMP-2, MMP-9 and CD68 was performed on tissue sections of AAA and normal infrarenal abdominal aortas fixed in 10% formalin. MMP-9 and tPA protein levels were increased in AAAs compared to controls by western blotting. However, uPA levels were slightly increased in controls. No differences in TIMP-1 protein levels were identified. Similarly, zymography demonstrated increased MMP-2 and MMP-9 gelatinolytic activity in AAAs compared to controls (p < or = 0.05). CD68-positive cells (macrophages) in the adventitia and media demonstrated immunoreactivity to MMP-9. This investigation demonstrated increased MMP-9 proteinase activity and tPA protein levels in the walls of AAAs, as well as inflammatory leukocyte invasion of the adventitia and media compared to controls. These data suggest that leukocyte-derived MMP-9 is associated with aortic wall degeneration and aneurysm formation. Furthermore, activation of MMP-9 may be caused by increased tPA levels in the walls of AAAs.     

基质金属蛋白酶在腹主动脉瘤组织中的表达

目的探查基质金属蛋白酶类（MMPs）在腹主动脉瘤（AAA）组织中产生的源泉。方法采用间质胶原酶（MMP-1）和明胶酶以MMP-9）的mRNA探针在20例AAA组织及4例正常人腹主动脉组织的切片上行原位杂交实验结果MMP-1及MMP-9在巨噬细胞、平滑肌细胞和淋巴细胞均有表达,其中巨噬细胞的MMPs表达强烈。结论MMPs在AAA的形成和扩张中发挥重要作用,炎性细胞是产生MMPS的主要源泉,并影响问质细胞的MMPS表达。     

Rapamycin suppresses experimental aortic aneurysm growth

OBJECTIVE: Inflammatory modulators are important in the pathogenesis of aneurysmal disease. Gene expression profiling of experimental abdominal aortic aneurysm (AAA) tissue demonstrated upregulation of the FK506BP12 (rapamycin binding protein) gene product. Rapamycin is a potent immunosuppressor that prevents recurrent stenosis. However, its effect on aneurysm formation has not been studied. We therefore examined the effect of rapamycin in an experimental rat AAA model. METHODS: Adult male Wistar rats underwent elastase infusion into isolated infrarenal aortas to create experimental aneurysms. Rats were randomized to receive either rapamycin or placebo via gastric lavage daily starting on the day of surgery. On postoperative day 7 the aneurysm was measured, the infrarenal aorta was harvested, and the rats were euthanized. NF kappa B was measured with Western blotting as a marker of inflammation. Matrix metalloproteinase (MMP)-9 protein levels were measured. Hematoxylin-eosin and elastin staining were used to examine tissue inflammation and elastin preservation. RESULTS: Aneurysms were significantly smaller in diameter in the rapamycin-treated group (3.3 +/- 0.7 mm vs 4.5 +/- 0.5 mm; P <.0001). NF kappa B levels were significantly reduced by 64% +/- 14% in rapamycin-treated aortas (P =.023). MMP-9 was reduced in rapamycin-treated aortas by 54% +/- 22% (P =.043). Hematoxylin-eosin and elastin staining showed no changes in inflammatory infiltrate or degradation of elastin fibers in elastase-infused aortic segments in rapamycin-treated rats. CONCLUSION: Rapamycin significantly reduces the rate of aneurysm expansion in the experimental AAA rat model by 40%. Biochemical evidence suggests that this is related to suppression of inflammatory signaling and decreased MMP-9 levels. Rapamycin could provide a new treatment for small aneurysms. CLINICAL RELEVANCE: Human aortic aneurysms are characterized histologically by an inflammatory infiltrate with severe proteolytic destruction. Rapamycin is an immunosuppressive agent commonly used to control transplant rejection and intimal hyperplasia by modulating the inflammatory cascade. In this experimental model rapamycin suppressed aneurysm expansion, decreased NF kappa B activation (a marker of inflammation), and decreased matrix metalloproteinase-9 levels. It is hoped that rapamycin or other similar anti-inflammatory drugs will one day be able to control aneurysm expansion in patients     

Inflammatory abdominal aortic aneurysm: close relationship to IgG4-related periaortitis

Inflammatory abdominal aortic aneurysm (AAA) is a member of a family of disorders referred to as "chronic periaortitis" together with retroperitoneal fibrosis. Retroperitoneal fibrosis is included in IgG4-related disease, which is characterized by numerous infiltrating IgG4-positive plasma cells and high serum IgG4 concentrations. However, the relationship between IgG4-related disease and inflammatory AAA has not been documented. In this study, we examined the clinicopathologic characteristics of inflammatory (10 cases) and atherosclerotic (22 cases) AAAs, based on the hypothesis that inflammatory AAA might be related to IgG4-related disease. Cases of inflammatory AAA could be classified into 2 groups based on immunostaining of IgG4. Four patients showed diffuse infiltration of abundant IgG4-positive plasma cells (IgG4-related cases), whereas the remaining 6 cases of inflammatory AAA and all cases of atherosclerotic AAA had only a few IgG4-positive plasma cells (non-IgG4-related cases). IgG4-related inflammatory AAA was pathologically characterized by the frequent infiltration of eosinophils, lymph follicle formation, perineural inflammatory extension, and inconspicuous infiltration of neutrophils compared with non-IgG4-related inflammatory AAA. Obliterative phlebitis, which is venous occlusion with inflammatory cell infiltration, is observed in all IgG4-related cases. In addition, serum IgG4 concentrations were significantly higher in IgG4-related inflammatory AAA (109 to 559 mg/dL, normal range: 4 to 110 mg/dL) than non-IgG4-related inflammatory AAA (32 to 59 mg/dL) and all atherosclerotic AAA (12 to 83 mg/dL). In conclusion, inflammatory AAAs might be classified into 2 groups: IgG4-related or nonrelated. The former might be one of the IgG4-related diseases, and could be included in IgG4-related periaortitis together with retroperitoneal fibrosis.     

他莫昔芬对大鼠腹主动脉瘤形成的抑制作用

目的 观察他莫昔芬对大鼠腹主动脉瘤(AAA)形成的影响及作用机制.方法 40只雄性Wistar大鼠随机分成2组,实验组他莫昔芬预给药7 d(每天15 mg/kg体重),建立A从灌注模制.术后7 d切取腹主动脉.一计算腹主动脉直径变化率,苏木素-伊红(HE)染色观察动脉壁炎性细胞浸润,Verhoff染色观察动脉壁弹性纤维,免疫组织化学观察动脉壁基质金属蛋白酶(MMP)-2,9及巨噬细胞的表达.结果 他莫昔芬明显抑制AAA的形成,抑制率95%～99%.动脉壁内炎性细胞浸润明显减少,弹力纤维破坏受到抑制,MMP-2,9及巨噬细胞的表达受到抑制.结论 他莫昔芬通过抑制大鼠腹主动脉壁内早期的炎症反应和MMPS的表达,抑制大鼠AAA的形成.     

硫酸寡聚糖复合物对实验性腹主动脉瘤的抑制作用

目的 观察乙酰肝素酶抑制剂PI-88对腹主动脉瘤形成的抑制作用。方法 利用豚鼠-SD大鼠异种移植腹主动脉瘤模型，于移植术后4周内连续PI-88治疗；术后4周利用Northem blot杂交和免疫组化技术，检测移植腹主动脉直径、乙酰肝素酶表达、微血管增生及炎性细胞浸润程度。结果 与非治疗组相比，治疗组腹主动脉乙酰肝素酶表达、移植血管直径、微血管增生及炎性细胞浸润程度均显著降低，但仍高于阴性对照组。结论 PI-88可通过抑制乙酰肝素酶作用，控制腹主动脉瘤形成。     

腹主动脉瘤发病机理的实验研究 Ⅱ.基质金属蛋白酶-9在大鼠腹主动脉瘤模型中的动态表达

目的 :检测MMP 9在大鼠正常动脉及动脉瘤模型组织中的动态表达 ,以探讨其在腹主动脉瘤发病机制中的作用。方法 :Wistar大鼠 5 4只 ,随机均分为 1组正常对照组、4组灌注对照组和 4组实验组。实验组腹主动脉灌注弹力蛋白酶 (2 5U ml) 2ml,灌注对照组灌注生理盐水 2ml,分别于术前、术后即刻、2d、7d、14d测量腹主动脉直径 ,并采用免疫组织化学和分子原位杂交技术动态检测腹主动脉组织中MMP 9的表达。结果 :正常及灌注对照组腹主动脉组织中均未发现MMP 9,而实验组弹力蛋白酶灌注后2～ 14dMMP 9均有不同程度升高 ,第 7d达到高峰 ,第 14d有所回落。结论 :MMP 9分泌的增加可能与炎症反应有关 ,且为腹主动脉瘤形成中不可或缺的一步。     

血红素氧合酶-1在早期腹主动脉瘤中的动态表达

目的探讨早期腹主动脉瘤(AAA)的发病机制。方法建立大鼠腹主动脉瘤模型,于术后3、7、14、28d取材,观察主动脉的扩张情况,弹力纤维染色观察弹力纤维的损伤;原位分子杂交检测动脉壁中血红素氧合酶(HO)1mRNA的动态表达,免疫组织化学染色检测细胞间黏附分子(ICAM)-1及巨噬细胞特异性抗原CD68的蛋白表达。结果在AAA组织中,HO1mRNA表达于3d出现,14d达到高峰,为(33.9±6.9)%,与其他时段相比,差异有统计学意义(P<0.01)。ICAM1及CD68蛋白表达分别于7、14d达到高峰(P<0.01)。结论HO-1在早期腹主动脉瘤组织中表达增强,伴随着弹力纤维损伤和炎性细胞浸润。     

u-PA和明胶酶A、B蛋白在人腹主动脉瘤组织中表达的研究

目的 探讨尿激酶型纤溶酶原活化物(u-PA)和明胶酶A、B在腹主动脉瘤(AAA)组织中蛋白的表达和产生的来源。方法 用u-PA和明胶酶A(MMP-2)、明胶酶B(MMP-9)的单克隆抗体,以免疫组织化学SABC方法在10例AAA组织和10例正常腹主动脉组织的切片上控测u-PA和MMP-2、MMP-9抗原(蛋白)。结果 u-PA和MMP-9蛋白在AAA组织中主要浸润于中层和外膜巨噬细胞表达,在正常腹主动脉组织中无表达,MMP-2蛋白在AAA组织中主要由中层平滑肌细胞表达,在正常腹主动脉组织中无表达。结论 由巨噬细胞产生的u-PA直接激活,并调节MMP-2和MMP-9的活性,在AAA的形成、扩张和破裂中起着关键性的作用。