替米沙坦对压力负荷过重所致心衰大鼠心肌ACE2和AT1R表达的影响

目的 探讨替米沙坦对压力负荷过重所致心衰大鼠血管紧张素Ⅱ(AngⅡ)、心肌血管紧张素Ⅱ1型受体(AT1R)、血管紧张素转化酶2(ACE2)及MAS蛋白表达的影响。方法 采用SD雄性大鼠通过腹主动脉缩窄术构建压力负荷性心肌肥厚致心力衰竭(HF)模型。将大鼠随机分为假手术对照组(n=12)、HF模型组(n=12)和替米沙坦干预组(n=12)。替米沙坦干预组每天给予替米沙坦连续8周,检测各组大鼠血流动力学参数、心脏指数、血浆AngⅡ含量、心肌中AT1R、ACE2和MAS蛋白的表达情况。结果 HF模型组心脏指数、血流动力学指标、血浆AngⅡ的含量及心肌AT1R、ACE2蛋白的表达明显升高(P<0.01),MAS蛋白表达明显下降(P<0.01);替米沙坦干预组心脏指数、血流动力学指标明显下降(P<0.01),血浆AngⅡ的含量及心肌AT1R蛋白的表达明显下降(P<0.01),而MAS和ACE2蛋白的表达明显升高(P<0.01)。结论 应用替米沙坦可明显改善HF大鼠心室重构,可能与AngⅡ和AT1R的下调,而MAS和ACE2的上调有关。     

早幼粒细胞白血病蛋白在Bowen病、皮肤鳞状细胞癌及皮肤基底细胞癌组织中的表达

目的作为肿瘤抑制因子,早幼粒细胞白血病（PML）蛋白在Bowen病(BD)、皮肤鳞状细胞癌（SCC）及皮肤基底细胞癌
(BCC)组织中的表达关系、以及PML 蛋白与他们的临床预后关系不明,本研究旨在探讨PML蛋白在其中的作用机制。方法用
免疫组化方法检测正常皮肤组织、BD、SCC及BCC皮损组织中PML蛋白的表达。结果正常人皮肤组织中,PML蛋白不表达
（阴性）;BCC皮损中,全层几乎无PML蛋白的表达(细胞核阳性率为8.69%,细胞质阳性率为4.35%);Bowen病及Ⅰ~Ⅱ级SCC
皮损中,细胞核及细胞质均明显表达PML 蛋白,且细胞核中的表达显著高于Ⅲ~Ⅳ级SCC。结论PML蛋白的过度表达在鳞状
细胞癌发病的早期阶段起关键作用,可能与SCC的发生和转移有关。
     

脂肪肝与血脂和转氨酶关系的调查研究

目的:通过体检研究脂肪肝的患病情况及脂肪肝患者血清血脂与转氨酶的关系。方法:随机抽取2003年度西安地区某设计院体检表1285份进行血脂、转氨酶、脂肪肝统计分析。结果:脂肪肝患者随年龄增长有增加的趋势,且男性高于女性。高脂血症者的脂肪肝患病率高于血脂正常者,且脂肪肝患者多见甘油三酯(TG)升高。脂肪肝患者AST、ALT显著高于健康对照组。结论:对于健康人群年度体检肝功能、血脂及腹部B超,在脂肪肝的早发现、早治疗、疗效观察、预后判断上,均有重要的临床意义。     

类风湿关节炎滑膜细胞凋亡及相关基因Fas表达的研究

目的:研究类风湿关节炎(RheumatoidArthritis,RA)患者滑膜组织中细胞凋亡及相关基因蛋白Fas的表达和意义。方法:采用免疫组织化学方法,对9例患者及8例正常对照滑膜组织中凋亡细胞及Fas的表达进行检测。结果:RA患者滑膜组织中细胞凋亡率明显低于对照组,而Fas阳性的细胞百分比却明显高于对照组。结论:RA患者滑膜组织中细胞凋亡的减少可能是导致滑膜过度增生进而关节功能丧失的原因之一,Fas表达虽增多但不能直接诱导细胞凋亡。     

硅暴露对铜和锌尿排泄的影响

硅的职业性暴露可能导致肾小球及近球小管组织结构的改变。对有硅暴露的不吸烟工人进行尿铜、尿锌含量的检测,探讨其与肾组织学改变以及与工龄之间的关系。通过测定尿中微量白蛋白含量反映肾小球功能,测定尿中α1-微球蛋白含量来判定近球小管重吸收功能,测定尿液中细胞内谷胱甘肽S转移酶(GST)活性来判定近球小管结构的完整性。此外,还测定尿铜、锌和肌酐的含量。结果显示,硅暴露组与对照组比较发现,所有检测的指标均显著性升高。尿铜、锌含量与肾小球及近球小管结构和功能及工龄之间呈显著性相关。职业性硅暴露可能导致铜和锌以蛋白一金属复合物的形式从尿中丢失,这些必需微量元素在尿中的含量可以作为检验肾功能失常与否的生物学标记。尿液GST含量也许可以作为判定近球小管损伤的有用标志。     

低硒、低碘及联合对亲代和子代大鼠骨、软骨生长的影响

Objective To study the effects of selenium deficiency,iodine deficiency and combined selenium and iodine deficiency on bone and cartilage growth in the parental and the first filial generation rats. Methods Forty-eight weanling healthy SD rats were randomly divided into selenium deficieney, iodine deficiency, combined selenium and iodine deficiency and control groups according to their body mass. These rats were fed with selenium deficiency, iodine deficiency, combined selenium and iodine deficiency, and normal fodder, respectively. The parental rats (about 3 months old) were mated in each group 8 weeks after the beginning of the experiment. Right tibias and left knee joints were collected when the parental generation rats were about 6 months and the first filial generation rats were about 3 months old. Tibial length, mid-shaft tibial diameter, and articular cartilage diameters of the right tibias were measured by vernier caliper. Left knee joints were embedded and cut into sections and the thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in growth plate cartilage were observed under the light microscope. Results The selenium deficiency had significant effect on serum selenium level of the parental and the first filial generation rats(F value were 239.56,232.68, P< 0.01), and also on serum T4 level of the first filial generation rats(F value were 6.95, P < 0.05). The iodine deficiency had significant effect on serum T3 and T4 level in the two generations rats(F value were 14.11,14.05,30.29,34.53, P < 0.01 ). There were interactions between selenium deficiency and iodine deficiency on serum T4 level in the first filial generation rats (F= 5.99, P< 0.05). The serum selenium of selenium deficiency group[ (30.28 ± 6.34), (43.95 ± 9.75)μg/L],combined selenium and iodine deficiency group[ (30.33 ± 5.18), (35.40 ± 3.16)μg/L] were significantly lower than iodine deficiency group[(345.83 ± 29.55), (245.24 ± 9.95)μg/L] and the controls[ (358.64 ± 30.50), (236.50 ±9.75) μg/L] in the two generations. The serum T3 of combined selenium and iodine deficiency group [(0.55 ± 0.05 ),(0.88 ± 0.14)nmol/L] were significantly lower than the controls[(0.75 ± 0.08), (1.26 ± 0.26)nmol/L] in the two generations. The serum T4 of iodine deficiency [ (24.11 ± 2.29), (42.10 ± 8.92) nmol/L ] and combined selenium and iodine deficiency group[ (20.66 ± 1.93), (26.55 ± 5.98)nmol/L] were significantly lower than the controls[ (36.15 ±2.74), (52.79 ± 8.84)nmol/L] and selenium deficiency group[ (28.12 ± 3.33), (52.02 ± ll.99)nmol/L] in the two generations. The selenium deficiency and iodine deficiency had significant effect on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in first filial generation rats(F values were 24.31,6.98,40.76,56.15,25.24,82.82, 10.07,5.57, P <0.05 or <0.01). There were interactions between selenium deficiency and iodine deficiency on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes (F values were 5.68,24.86,41.82,9.12, P <0.05 or <0.01 ). The tibial length of the selenium deficiency group[ (33.17 ± 0.34)mm] and combined selenium and iodine deficiency group[ (31.30 ± 0.87)mm] were significantly lower than the controls[ (34.12 ± 0.32)mm, P< 0.05]. Thickness of the growth plate cartilage [ (1.60 ± 0.18)mm ], layers of proliferative chondrocyte (8.54 ± 0.81), and hypertrophic chondrocyte (4.95 ± 0.37)of the combined selenium and iodine deficiency group were significantly decreased when compared to the selenium deficiency group[ (3.03 ± 0.10)mm, 14.68 ± 0.84,6.60 ± 0.31], iodine deficiency group[ (2.90 ± 0.09)mm, 13.75 ±0.33,6.61 ± 0.84 ] and the controls [ (3.19 ± 0.09) mm, 14.94 ± 0.36, 6.64 ± 0.26, P <0.05]. Thickness of the growth plate cartilage, layers of proliferative chondrocyte of the iodine deficiency group were lower than the controls(P<0.05). Conclusions Selenium deficiency impair tibial growth in first filial generation rats, iodine deficiency retarded the chondroncyte proliferation and decreases the thickness of growth plate cartilage in first filial generation rats, and combined selenium and iodine deficiency significantly impair the growth of bone and cartilage in first filial generation rats.     

脂肪肝与血脂、转氨酶关系的调查

1 对象和方法 西安地区某设计院2003年体检1285例(排除各种肝炎患及携带)，男性785例．女性500例，年龄20—70岁．采血前停止饮酒，低脂饮食，空腹12h以上．采取清晨静脉血3mL，分离血清，用日本7170全自动生化分析仪和日本第一化学试剂检查AST，ALT，TC和TG，转氨酶采用速率比浊法，血脂采用氧化酶法，用美国Cicuson公司生产的XP10高档彩色超声诊断分析仪，     

T-2毒素和硒对人软骨蛋白聚糖酶的影响

目的 研究T-2毒素和硒对人软骨蛋白聚糖代谢的影响.方法 体外培养胎儿软骨细胞,根据施加的实验措施将其分为8组,对照组(T-2毒素:0 mg/L,硒:0 mg/L)、1、10、20μg/L T-2毒素组、加硒(0.1mg/L)组、1、10、20 μg/L T-2毒素加硒(0.1 mg/L)组,每组设3个平行样.在T-2毒素和(或)硒作用5d后,采用免疫蛋白印迹法检测软骨细胞蛋白聚糖的蛋白表达水平,用RT-PCR方法检测软骨细胞蛋白聚糖酶-1和蛋白聚糖酶-2的mRNA表达水平.结果 硒、T-2毒素对蛋白聚糖的蛋白表达量、蛋白聚糖酶-1 mRNA表达水平、蛋白聚糖酶-2的mRNA表达水平有影响(F=0.294、27.71,107.45、362.25,34.68、22.26,P均＜0.05),硒与T-2毒素存在交互作用(F=79.99、230.76、388.33,P均＜0.05),表现为拮抗作用.在硒水平为0 mg/L时,1、10、20 μg/L的T-2毒素组蛋白聚糖的蛋白表达(0.278±0.015、0.235±0.029、0.195±0.028)均低于0 mg/L的T-2毒素组(0.472±0.0358,P均＜0.05);在硒水平为0.1 mg/L时,1、10、20 μg/L的T-2毒素组的蛋白聚糖的蛋白表达(0.399±0.028、0.299±0.020、0.263±0.019)均高于0 mg/L的T-2毒素组(0.197±0.018,P均＜0.05).在T-2毒素分别为1、10、20μg/L时,0.1 mg/L硒组的蛋白聚糖的蛋白表达均高于0 mg/L硒组(P均＜ 0.05).在硒水平为0 mg/L时,1、10、20μg/L的T-2毒素组蛋白聚糖酶-1 mRNA表达(0.535±0.033、1.071±0.043、1.454±0.058)均高于0 mg/L的T-2毒素组(0.481±0.023,P均＜0.05);在硒水平为0.1 mg/L时,1、10、20μg/L的T-2毒素组的蛋白聚糖酶-1 mRNA表达(1.057±0.048、0.555±0.036、0.902±0.045)均高于0 mg/L的T-2毒素组(0.346±0.020,P均＜0.05).在硒水平为0 mg/L时,1、10、20μg/L的T-2毒素组蛋白聚糖酶-2 mRNA表达(0.596±0.038、0.656±0.033、0.949±0.049)均高于0 mg/L的T-2毒素组(0.387±0.020,P均＜0.05);在硒水平为0.1 mg/L时,1、10、20μg/L的T-2毒素组的蛋白聚糖酶-2 mRNA表达(0.600±0.040、0.453±0.031、0.164±0.011)均低于0 mg/L的T-2毒素组(1.021±0.046,P均＜0.05);在T-2毒素分别为10、20μg/L时,0.1 mg/L硒组的蛋白聚糖酶-1和蛋白聚糖酶-2 mRNA表达均低于0 mg/L硒组(P均＜ 0.05).结论 T-2毒素通过上调蛋白聚糖的主要代谢酶蛋白聚糖酶-1和蛋白聚糖酶-2达到降解蛋白聚糖的作用,微量元素硒对T-2毒索引起的软骨细胞蛋白聚糖降解有一定保护作用.     

原发性胆囊癌的CT诊断(附56例报告)

目的：研究胆囊癌的CT诊断。资料和方法：对照病理回顾分析56例胆囊癌的CT表现。结果:胆囊壁不规则增厚32％；胆囊腔内结节21％；胆囊区肿块46％；肝侵犯52％；胆管扩张53％；胆结石27％；淋巴转移34％。结论：1、胆囊癌CT分型为厚壁型、腔内结节型、肿块型，各型为病理发展中不同的阶段。2、直接侵犯肝脏及胆管受侵扩散为胆囊癌主要转移方式。3、CT对诊断中晚期胆囊癌及判断浸润范围有价值，尤其是增强扫描。     

骨康宁对维甲酸骨质疏松大鼠的骨形态计量学和生物力学影响

目的 探讨中药骨康宁对维甲酸骨质疏松大鼠的骨形态计量学和生物力学影响.方法 选用45只雌性SD 大鼠, 5～6月龄, 按体重随机分为正常对照组10只和骨质疏松模型组35只.以维甲酸诱导骨质疏松后,骨质疏松模型组的大鼠处死7只,其骨皮质菲薄,部分吸收,骨髓腔增宽,松质骨骨纹理稀疏、变细,证实骨质疏松模型复制成功.剩余28只大鼠再随机分为骨质疏松模型组(9只) 、骨康宁治疗组(骨康宁组,10只)和雌激素治疗阳性对照组(9只)3组.正常组大鼠及骨质疏松模型组给予常规饲料及蒸馏水,骨康宁组给予中药骨康宁治疗,雌激素组给予雌激素治疗.用形态计量学、骨生物力学、骨密度等实验技术,观察骨康宁的治疗效果.结果 经骨康宁治疗后,骨质疏松大鼠的平均骨小梁数、平均骨小梁宽、骨皮质指数、股骨骨密度、股骨的最大变形能力等与骨质疏松模型组比较明显增加(P<0.05),有显著性差异,与正常组和雌激素组比较无显著性差异.结论 骨康宁对维甲酸诱导的大鼠骨质疏松有一定的治疗作用.