不同体积分数血清对培养原代破骨细胞噬骨能力的影响

目的:改变培养液中血清的浓度,观察破骨细胞形态结构,并比较不同体积分数血清对培养的原代破骨细胞噬骨能力的影响。方法:实验于2007-03/06在沈阳医学院中心实验室完成。①实验材料:选取清洁级新生24hWistar大鼠6只;胎牛血清(天津灏洋);新鲜成年牛股骨皮质(市售)。②实验过程:取新鲜成年牛股骨皮质,用磨片机磨成厚50μm的1cm×1cm骨片;取新生大鼠四肢长骨,分离破骨细胞,并用不同体积分数血清(分别为0,0.05,0.1,0.15,0.2,0.25)培养原代破骨细胞。③实验评估:第1,6天倒置显微镜下计数,第3天取细胞玻片观察细胞形态结构;扫描电镜观察不同体积分数血清培养的破骨细胞在牛骨皮质上产生骨陷凹面积的差异。结果:①破骨细胞的分离培养结果:分离培养的破骨细胞数量较少,体积大,胞浆丰满,细胞突起延展,细胞核呈圆形或椭圆形,积聚在细胞中央或排列在细胞周边。②不同体积分数血清培养液中骨片上吸收陷窝深度比较:随着培养液中血清体积分数的增加,骨片上陷窝深度逐渐增加,在培养液中血清体积分数为0.15时,骨片上陷窝最深,此后随着培养基血清体积分数的增加,形成骨陷凹的深度无明显增加。结论:血清体积分数为0.15培养基培养的破骨细胞在牛皮质骨片上产生骨陷凹最深,噬骨能力最强。     

Mesenchymal hamartoma of the liver: radiologic-pathologic correlation

Mesenchymal hamartoma of the liver (MHL) is an uncommon cystic mass of infancy that is a developmental anomaly rather than a neoplasm. Fourteen cases of MHL were retrospectively reviewed. Grossly, MHL is a solitary mass with cystic spaces of variable size. Patients are seen initially with painless progressive abdominal enlargement. On plain films, MHL appears as a large, noncalcified mass in the right upper quadrant. Scintigraphy is helpful in confirming its hepatic origin. Ultrasonography and computed tomography demonstrate a large multiloculated mass with considerable variation in the size of septa and cystic spaces. Angiographically, MHL is avascular or hypovascular. Recognition of these radiographic findings allows a correct diagnosis to be made in many cases. With resection, the prognosis is excellent.     

HPLC定量分析麦迪霉素

麦迪霉素是链霉菌发酵的次级代谢产物,在发酵过程中往往产生一系列结构相似、性质相仿的同系物,而当菌种或生产工艺不同时,都会使产品中各组分间的比例有明显不同,从而带来一些质量问题。为了考察国产麦迪霉素的质量,本文较系统地研究了反相高效液相色谱分离和测定麦迪霉素的条件,选用了日立胶3050柱,以甲醇—0.01mol/L磷酸盐缓冲液(pH5.8)(45:55)作流动相,较满意地分离、测定了麦迪霉素。方法快速、准确。     

Pregnancy with concomitant chorangioma and placental vascular malformation with mesenchymal hyperplasia

We present two pregnancies associated with normal live births and the unusual concomitance of chorangioma and placental vascular malformation with mesenchymal hyperplasia. The enlarged placenta had the characteristic findings of chorangioma, dilated and varicose chorionic vessels and multiple vesicle-like villi containing hyaluronic acid. The vesicle-like villi showed diploid cellular DNA contents. Molecular genetic analysis using the polymerase chain reaction amplification of polymorphic microsatellite markers confirmed genetic identity among the chorangioma, the vesicle-like villi and the fetus. Both pregnancies were complicated by polyhydramnios, pre-term labour and prematurity. One neonate suffered from anaemia and thrombocytopenia. Another neonate suffered from haemangiomatosis. Our cases demonstrate that concomitant chorangioma and placental mesenchymal hyperplasia are genetically identical to the fetus and can coexist with a normal viable fetus. Since haemangiomas, chorangiomas, chorionic vessels and villi mesenchymal cells are all derived from the mesoderm, a combination of fetal haemangiomas, placental vascular malformation, chorangiomas and placental mesenchymal hyperplasia may represent a mixed form of congenital malformation of the mesoderm.      

Deletion of galectin-3 in the host attenuates metastasis of murine melanoma by modulating tumor adhesion and NK cell activity

Galectin-3, a β galactoside–binding lectin, plays an important role in the processes relevant to tumorigenesis such as malignant cell transformation, invasion and metastasis. We have investigated whether deletion of Galectin-3 in the host affects the metastasis of B16F1 malignant melanoma. Galectin-3-deficient (Gal-3^−/−) mice are more resistant to metastatic malignant melanoma as evaluated by number and size of metastatic colonies in the lung. In vitro assays showed lower number of attached malignant cells in the tissue section derived from Gal-3^−/− mice. Furthermore, lack of Galectin-3 correlates with higher serum levels of IFN-γ and IL-17 in tumor bearing hosts. Interestingly, spleens of Gal-3^−/− mice have lower number of Foxp3⁺ T cells after injection of B16F1 melanoma cells. Finally, we found that while CD8⁺ T cell and adherent cell cytotoxicity were similar, there was greater cytotoxic activity of splenic NK cells of Gal-3^−/− mice compared with “wild-type” (Gal-3 ^+/+ ) mice. Despite the reduction in total number of CD3ε⁻NK1.1⁺, Gal-3^−/− mice constitutively have a significantly higher percentage of effective cytotoxic CD27^highCD11b^high NK cells as well as the percentage of immature CD27^highCD11b^low NK cells. In contrast, CD27^lowCD11b^high less functionally exhausted NK cells and NK cells bearing inhibitory KLRG1 receptor were more numerous in Gal-3 ^+/+ mice. It appears that lack of Galectin-3 affects tumor metastasis by at least two independent mechanisms: by a decrease in binding of melanoma cells onto target tissue and by enhanced NK-mediated anti-tumor response suggesting that Galectin-3 may be considered as therapeutic target.     

The impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen treatment in breast cancer patients

Tamoxifen is a standard therapeutical treatment in patients with estrogen receptor positive breast carcinoma. However, less than 50% of estrogen receptor positive breast cancers do not respond to tamoxifen treatment whereas 40% of tumors that initially respond to treatment develop resistance over time. The underlying mechanisms for tamoxifen resistance are probably multifactorial but remain largely unknown. The primary aim of this study was to investigate the impact of PTEN tumor suppressor gene on acquiring resistance to tamoxifen by analyzing loss of heterozygosity (LOH) and immunohystochemical expression of PTEN in 49 primary breast carcinomas of patients treated with tamoxifen as the only adjuvant therapy. The effect of PTEN inactivation on breast cancer progression and disease outcome was also analyzed. Reduced or completely lost PTEN expression was observed in 55.1% of samples, while 63.3% of samples displayed LOH of PTEN gene. Inactivation of PTEN immunoexpression significantly correlated with the PTEN loss of heterozygosity, suggesting LOH as the most important genetic mechanism for the reduction or complete loss of PTEN expression in primary breast carcinoma. Most importantly, LOH of PTEN and consequential reduction of its immunoexpression showed significant correlation with the recurrence of the disease. Besides, our study revealed that LOH of PTEN tumor suppressor was significantly associated with shorter disease free survival, breast cancer specific survival and overall survival. In summary, our results imply that LOH of PTEN could be used as a good prognostic characteristic for the outcome of breast cancer patients treated with tamoxifen.     

Experimental research on production and uptake sites of TNFα in rats with acute hemorrhagic necrotic pancreatitis

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ST2 deletion enhances innate and acquired immunity to murine mammary carcinoma

ST2 is a member of the IL-1 receptor family and IL-33 was recently identified as its natural ligand. The IL-33/ST2 pathway regulates Th1/Th2 immune responses in autoimmune and inflammatory conditions, but the role of ST2 signaling in tumor growth and metastasis has not been investigated. We aimed to investigate whether ST2 gene deletion affects tumor appearance, growth, and metastasis, and antitumor immunity in an experimental metastatic breast cancer model. Deletion of ST2 in BALB/c mice bearing mammary carcinoma attenuated tumor growth and metastasis, which was accompanied by increased serum levels of IL-17, IFN-γ, and TNF-α and decreased IL-4. Tumor-bearing ST2-/- mice had significantly higher percentages of activated CD27high CD11bhigh NK cells, CD69+ and KLRG- NK cells and higher cytotoxic activity of splenocytes, NK cells, and CD8+ T cells in vitro. A significantly higher number of NK cells expressing IFN-γ were found in ST2-/- mice compared with WT recipients. In vivo depletion of CD8+ or NK cells revealed a key role for NK cells in enhanced antitumor immunity in ST2-/- mice. We report for the first time that suppressed breast cancer progression and metastasis in mice lacking ST2 corresponds mainly with enhanced cytotoxic activity of NK cells, and increased systemic Th1/Th17 cytokines.     

慢性前列腺炎患者前列腺液环氧化酶2细胞表达和炎性因子水平变化与中药前列安栓治疗效果的相关性

目的:观察慢性前列腺炎患者前列腺液环氧化酶2细胞表达和炎性因子水平变化与中药前列安栓临床疗效的关系。方法:①选择2005-05/2006-05川北医学院附属医院泌尿外科住院的慢性前列腺炎男性患者43例,年龄25～67岁。均符合世界卫生组织慢性前列腺炎分类诊断标准,且均对治疗方案和检测指标知情同意。随机将患者分为抗生素组20例(对照组)和前列安栓组23例(治疗组)。分组干预:对照组口服罗红霉素胶囊(武汉同济现代医药有限公司)治疗,150mg/次,2次/d;治疗组在此基础上给予前列安栓(丽珠集团丽珠制药厂,国药准字Z10980066,主要成分有黄柏、虎杖、泽兰、栀子、大黄等)局部治疗,1次/d,晚间入睡前纳入肛门内3～5cm。②治疗前及治疗4周后对临床有关症状尿频、排尿不尽感、尿痛、会阴涨痛进行观察并记录,检查前列腺压痛。于治疗前,治疗1,2,3,4周后应用尿流动力仪进行尿流率检测(最大尿流率、平均尿流率),进行前列腺液细胞环氧化酶2免疫组化染色及白细胞介素6、丙二醛、肿瘤坏死因子α含量和超氧化物歧化酶活性检测。400倍视野下计环氧化酶2阳性细胞数及阳性率。疗程结束后评价疗效。③计数资料差异比较采用χ2检验,计量资料差异比较采用t检验。结果:因对照组1例患者未能完成第3周的治疗,最终进入治疗3周后的结果分析42例。①疗效:治疗组总有效率明显高于对照组[47%(9/19),83%(19/23),χ2=5.815,P<0.05]。②治疗后症状和体征改善情况:治疗组尿频、排尿不尽感、尿痛、会阴胀痛及前列腺压痛改善率明显高于对照组(χ2=6.617～10.756,P<0.05～0.01)。③尿流率测定结果:对照组治疗2～4周后和治疗组治疗1～4周后最大尿流率和平均尿流率明显大于治疗前(t=2.567～6.478,P<0.05～0.01),治疗组治疗2～4周后明显大于对照组(t=2.368～5.593,P<0.05～0.01)。④前列腺液细胞环氧化酶2阳性细胞数和阳性率:对照组治疗2～4周后和治疗组治疗1～4周后明显少于或低于治疗前(t=2.124～6.372,P<0.05～0.01),治疗组治疗2～4周后明显少于或低于对照组(t=3.617～5.545,P<0.01)。⑤前列腺液炎性因子、丙二醛含量和超氧化物歧化酶活性变化:对照组治疗2～4周后和治疗组治疗1～4周后前列腺液白细胞介素6、丙二醛、肿瘤坏死因子α含量明显低于治疗前,超氧化物歧化酶含量明显高于治疗前(t=2.364～5.569,P<0.05～0.01)。治疗组治疗2～4周后前列腺液白细胞介素6、丙二醛、肿瘤坏死因子α含量明显低于对照组,超氧化物歧化酶含量明显高于对照组(t=2.028～6.127,P<0.05～0.01)。结论:环氧化酶2表达和炎性因子及丙二醛、超氧化物歧体酶活性变化在慢性前列腺炎的发生发展中起重要作用,前列安栓应用可通过改善上述指标起到减轻临床症状和体征的作用。