DIAGNOSTIC IMPLICATIONS OF IMMUNOHISTOCHEMICAL MARKERS IN UTERINE SMOOTH MUSCLE TUMORS

Objective: To evaluate the diagnostic implications of immunohistochemieal markers in uterine smooth muscle tumors. Methods: Formalin-fixed paraffin-embedded tissue blocks were selected from 17 uterine leiomyosarcomas, 40 uterine unusual leiomyomas and 25 uterine usual leiomyomas. Utilizing immunohistochemical techniques with antigen retrieval, serial sections of each tumor for immunoreactivity with myogenic markers, ovarian steroid receptors, CD44v3, proliferating cell nuclear antigen and mast cells were assessed. Results: Although the myogenic markers and CD44v3 showed less frequent positivity in uterine leiomyosarcomas than those in unusual leiomyomas,they were not reliable markers for differentiating leiomyosarcoma from leiomyoma. Uterine leiomyosarcoma tended to have lower ovarian steroid receptors immunoreactivity rates than leiomyoma. Leiomyoma tended to have a higher quantity of intratumoral mast cells than leiomyosarcoma, while the expression of proliferating cell nuclear antigen was lower in them. Conclusion: Because the estimation of mitotic count was subject to significant variation, the immunohistochemical expression of ovarian steroid receptors, mast cells and proliferating cell nuclear antigen seemed to be helpful for the discrimination of unusual leiomyoma from leiomyosarcoma.     

ICAM-1 deficiency suppresses host allosensitization and rejection of MHC-disparate corneal transplants

BACKGROUND: We used a murine model of orthotopic corneal transplantation to determine whether host deficiency in ICAM-1 promotes survival of corneal grafts with different degrees of allodisparity. METHODS: ICAM-1-/- and wild-type C57BL/6 (ICAM-1+/+) received corneal grafts from the following strains of mice: BALB/c (fully mismatched), BALB.b (mismatched at multiple minor H only), or B10.D2 [including major histocompatibility complex (MHC) mismatch]. Graft rejection, induction of allospecific delayed-type hypersensitivity (DTH) responses, and leukocytic infiltration of grafts were measured. RESULTS: There were no differences in long-term survival of allografts that were either fully mismatched or had only minor H disparity in ICAM-1+/+ vs. ICAM-1-/-hosts. However, whereas B10.D2 grafts were accepted in only 58% of the ICAM-1+/+ hosts, graft survival in ICAM-1-/- recipients was 100% (P=0.006). Moreover, none of the ICAM-1-/- mice receiving B10.D2 grafts developed allospecific DTH. CONCLUSIONS: Prolonged survival seen in MHC-mismatched grafts in ICAM-1-/- mice, along with a suppressed DTH response to donor alloantigens after transplantation, suggest that ICAM-1 is associated with recipient sensitization to MHC alloantigens.     

嗜铬细胞瘤临床诊治

目的 提高嗜铬细胞瘤的诊治水平。方法 总结１９５８年至１９９８年间经手术和病理证实的嗜铬细胞瘤２８６例。结果 本组２２０例患者肿瘤位于肾上腺,６６例位于肾上腺外。在２９例恶性嗜铬细胞瘤中,７例位于肾上腺,２２例位于肾上腺外。１９例为静止型嗜铬细胞瘤。手术切除肿瘤２８１例。结论 对潜在的儿茶酚胺性心肌病的防治可降低手术死亡率。恶性嗜铬细胞瘤的诊断要靠长期严密的随访。     

心外管道全腔肺动脉吻合术的临床应用

目的 评价心外管道全腔肺动脉吻合术的临床应用价值。方法 １９９８年６月～１９９９年８月,１０例先天性心脏复杂畸形的患者接受了心外管道全腔肺动脉吻合术。包括单心室８例,均伴有完全性大动脉转位;右心室发育不良２例。均在全麻低温体外循环下手术。结果 患者全部治愈出院。术后随访６～１８个月,无晚期死亡。所有患者症状消失,无静脉压明显升高现象,超声检查显示心外管道血流通畅,无血栓形成;心电图检查显示无严重心     

Clinical observation of 82 cases of enuresis treated by ginger-partitioned moxibustion plus cupping therapy

Purpose: To observe the clinical therapeutic effect in the treatment of enuresis by ginger-partitioned moxibustion plus cupping therapy.Methods: Ginger-partitioned moxibustion was applied on Guanyuan (CV 4) and bilateral Zusanli (ST 36) and cupping therapy was applied on Shenque (CV 8) in the treatment of 82 cases of enuresis, in comparison with 76 cases treated by Chinese herbal medicine.Results: The effective rate was 84.1% in the treatment by ginger-partitioned moxibustion plus cupping therapy and was 64.5% in the treatment by Chinese herbal medicine.Conclusion: Ginger-partitioned moxibustion plus cupping therapy was better than Chinese herbal medicine in the treatment of enuresis (P<0.05). Translator: HUANG Guo-qi     

化学诱导大鼠多发肾囊肿伴肾肿瘤及肾组织DNA损伤的表达

目的 观察化学药物大鼠多发肾囊肿伴肾肿瘤模型的诱发情况和ＤＮＡ损伤标记物８－羟基脱氧鸟苷（８－ＯＨｄＧ）在其肾组织的表达。方法 用２－氨基４,５－二苯噻唑（ＤＰＴ）和Ｎ－亚硝基吗啉（ＮＮＭ）诱发和人类获得性肾囊肿（ＡＣＤＫ）伴肾癌相似的大鼠动物模型,并用免疫组化方法（ＬＳＡＢ法）检查８－ＯＨｄＧ在大鼠肾组织的表达。结果在本实验中,ＮＮＭ组３／１０的大鼠诱发肾肿瘤出现,在ＤＰＴ／ＮＮＭ组的９只大鼠均     

肝硬化门静脉高压症患者肝脏组织α1紧上腺素受体亚型的mRNA表达

目的 探讨肝硬化门静脉高压症患者肝脏组织α１肾上腺素受体亚型ｍＲＮＡ的表达。方法 应用半定量逆转录聚合酶链反应检测了１２例乙型肝炎后肝硬化门静脉高压症患者和１５例无高血压,无肝脏疾患的胆石症或胃肠道肿瘤患者肝脏组织α１肾上腺素受体亚型ｍＲＮＡ的表达。在同一体系中同时逆转录并扩增α１肾上腺素受体亚型特异性片段和内参ＧＡＰＤＨ片段,以二者的积分密度比值作为该受体亚型的ｍＲＮＡ相对表达量。结果 肝脏组织     

Overexpression of oncogenic STK15/BTAK/Aurora A kinase in human pancreatic cancer.

PURPOSE: Multiple chromosome abnormalities, including gain of chromosome20q, have been detected frequently in human pancreatic cancers. Overexpression of the STK15/BTAK/Aurora A gene located on chromosome 20q13, which encodes a centrosome-associated serine/threonine kinase, has been shown to induce chromosomal instability, leading to aneuploidy and cell transformation in multiple in vitro experimental systems. The purpose of this study was to investigate the expression and copy number alteration of STK15 in pancreatic cancer. EXPERIMENTAL DESIGN: STK15 expression at both the mRNA and protein levels together with the copy number of STK15 gene was measured in nine pancreatic carcinoma cell lines: (a) HPAF-II; (b) Aspc-1; (c) Panc-1; (d) Panc-3; (e) Panc-28; (f) Panc-48; (g) HS766T; (h) MIAPaCa-2; and (i) BxPc3. STK15 protein expression was also examined in normal pancreatic tissues and tumors by Western blotting and immunohistochemistry. RESULTS: STK15 was overexpressed in all of the nine cell lines examined, but gene amplification was infrequent. Western Blot analysis of primary tumor tissues revealed 2-10 times overexpression of STK15 protein compared with normal adjacent tissues from pancreatic cancer patients. Concurrent overexpression of cdc20, an STK15-associated protein, and reduced expression of cdc25, a mitosis-activating protein phosphatase, were detected in the same tumor samples. Elevated STK15 protein expression was detected in 22 of 38 tumor sections (58%) from pancreatic cancer patients. The extent of STK15 expression was not significantly correlated with the size, degree of differentiation, and metastasis status of the tumors. CONCLUSIONS: These results show that STK15 is overexpressed in pancreatic tumors and carcinoma cell lines and suggest that overexpression of STK15 may play a role in pancreatic carcinogenesis.     

Survivin反义RNA真核表达载体的构建及鉴定

目的 为了特异封闭白血病细胞survivin的表达，抑制其功能，本实验构建了survivin反义核酸载体并导入白血病细胞系中。方法 应用RT—PCR获得survivin的cDNA片段，反向插入pcDNA3质粒载体中；经限制性酶切和测序鉴定所构建的反义核酸是否正确；采用电转染方法将重组体导入HL—60细胞中；RT—PCR技术检测转染细胞survivin表达的变化。结果 经限制性酶切和测序鉴定证明survivin反义核酸已成功构建；RT—PCR产物电泳结果显示，与转染前细胞、空质粒转染细胞相比，转染survivin反义核酸的细胞survivin mRNA水平明显降低。结论 本实验已成功建立了survivin反义核酸真核表达载体，而且在白血病细胞系中发挥了特异封闭作用，为进一步研究survivin反义核酸在白血病治疗中的作用提供了实验基础。     

Inhibition of human leukemia in an animal model with human antibodies directed against vascular endothelial growth factor receptor 2. Correlation between antibody affinity and biological activity.

Vascular endothelial growth factor (VEGF) and its receptors (VEGFR) have been implicated in promoting solid tumor growth and metastasis via stimulating tumor-associated angiogenesis. We recently showed that certain 'liquid' tumors such as leukemia not only produce VEGF, but also express functional VEGFR, resulting in an autocrine loop for tumor growth and propagation. A chimeric anti-VEGFR2 (or kinase insert domain-containing receptor, KDR) antibody, IMC-1C11, was shown to be able to inhibit VEGF-induced proliferation of human leukemia cells in vitro, and to prolong survival of nonobese diabetic-severe combined immune deficient (NOD-SCID) mice inoculated with human leukemia cells. Here we produced two fully human anti-KDR antibodies (IgG1), IMC-2C6 and IMC-1121, from Fab fragments originally isolated from a large antibody phage display library. These antibodies bind specifically to KDR with high affinities: 50 and 200 pM for IMC-1121 and IMC-2C6, respectively, as compared to 270 pM for IMC-1C11. Like IMC-1C11, both human antibodies block VEGF/KDR interaction with an IC(50) of approximately 1 nM, but IMC-1121 is a more potent inhibitor to VEGF-stimulated proliferation of human endothelial cells. These anti-KDR antibodies strongly inhibited VEGF-induced migration of human leukemia cells in vitro, and when administered in vivo, significantly prolonged survival of NOD-SCID mice inoculated with human leukemia cells. It is noteworthy that the mice treated with antibody of the highest affinity, IMC-1121, survived the longest period of time, followed by mice treated with IMC-2C6 and IMC-1C11. Taken together, our data suggest that anti-KDR antibodies may have broad applications in the treatment of both solid tumors and leukemia. It further underscores the efforts to identify antibodies of high affinity for enhanced antiangiogenic and antitumor activities.