基质金属蛋白酶与肺癌转移的关系

基质金属蛋白酶(matrix metalloproteinases，MMPs)是一组锌离子依赖的蛋白水解酶，在ECM降解中起着重要作用。目前研究表明，MMPs活性异常不仅能促进肿瘤血管形成，还是人类多种肿瘤侵袭和转移的必要条件。本文就与肺癌侵袭和转移有关的MMPs研究作一综述。     

富氧对海拔3700m高原人体运动心力储备的影响

目的　探讨富氧对高原人体运动心力储备方面的影响。方法　对海拔 3 70 0m高原的 1 2名健康青年富氧 (氧浓度为 2 4%～ 2 5 %)前后分别进行踏阶运动 ,采用心力监护仪采集和记录心动周期和心力信息 ,把完成规定运动量运动后第一心音 (S1 )幅值对安静时S1 幅值增加的相应倍数评估心肌收缩能力储备指数 (CCRI) ;利用舒张期和收缩期时限数据计算舒张期 /收缩期比值 (D/S比 )。结果　运动后较安静时HR ,D/S ,S1 幅值均增高 ,有非常显著性差异 (P <0 .0 1 ) ;富氧运动较未富氧运动CCRI,D/S ,S1 幅值增高 ,有显著性差异 (P <0 .0 5 ) ,HR无统计学意义 (P >0 .0 5 )。结论　高原低氧环境下心脏储备主要是心肌收缩能力储备而不是心率储备。富氧对增强机体心力储备具有重要作用     

胶质细胞瘤复发前后Cyclin D1和P16的表达

目的　探讨CyclinD1,P16在胶质瘤复发前后表达改变及其意义。方法　采用免疫组织化学LsABC法对 4 5例复发胶质瘤瘤组织、瘤旁脑组织和 10例正常脑组织CyclinD1,P16蛋白表达进行检测 ,统计分析CyclinD1,P16表达水平与胶质瘤分级、肿瘤复发的关系。结果　正常脑组织 ,瘤旁脑组织和胶质瘤组织CyclinD1表达依次升高 ,而P16的表达依次下降 ;肿瘤复发CyclinD1表达增强 ,P16的表达减弱。结论　CyclinD1与P16的表达与胶质瘤恶性进程和复发密切相关。     

长沙市小学生焦虑障碍现状调查

目的　初步了解小学儿童焦虑障碍的患病现况。方法　使用焦虑性情绪障碍筛查表 (SCARED)调查长沙市某小学 2～ 6年级的 5 6 5名小学生 ,并对量表总分≥划界分 (2 3分 )的学生进行面谈。结果　在 5 6 5名小学生 (男生2 90名 ,女生 2 75名 )中 ,SCARED筛查阳性的有 14 0名 ,占总人数的 2 4 78%。使用中国精神障碍分类与诊断标准 (第三版 ) (CCMD 3)对筛查阳性者进行面谈 ,发现符合焦虑障碍诊断标准的 32例 (男 15 ,女 17) ,患病率为 5 6 6 % ,其中儿童分离性焦虑症 7例 ,患病率为 1 2 4 % ;儿童广泛焦虑症 11例 (1 95 % ) ;儿童恐惧症 10例 (1 77% ) ;儿童社交恐惧症 14例(2 4 8% ) ;有 8例存在 2～ 3种焦虑障碍共病 ;无 1例诊断为学校恐怖症、选择性缄默症和惊恐发作。结论　在儿童中焦虑情绪存在较普遍 ,这对儿童的学习、行为、自我意识造成不良影响 ,应予以积极干预。     

彩超引导介入治疗腘窝囊肿23例

目的探讨彩超引导下腘窝囊肿介入治疗的价值。方法在彩超引导下穿刺囊肿并抽尽囊液，生理盐水反复冲洗囊腔后注入无水乙醇，5min后抽出，反复2～3次。结果23例中22例穿刺一次治愈，1例穿刺2次治愈。23例随访6个月，无复发。结论彩超引导下介入治疗腘窝囊肿操作简便，创伤轻微，安全可靠，效果显著，可重复操作。     

人抵抗素基因cDNA的克隆

目的克隆人抵抗素基因(hRETN)cDNA,为进一步研究RETN的结构和功能提供实验基础.方法应用RT-PCR方法从中国人网膜脂肪垫总RNA中扩增出RETN 基因cDNA,克隆入载体pMD18-T中,形成重组载体pMD18-T/hRETN.通过蓝白斑筛选出阳性克隆,限制性内切酶酶切鉴定后对其进行测序.结果从脂肪组织总RNA中扩增得到363 bp片段hRETN基因,其cDNA序列与Genbank hRETN基因序列基本相同.结论成功地克隆中国人hRETN cDNA.     

Palmitic acid as an excipient in implants for sustained release of insulin

Sustained-release implants for insulin can be made by compressing a powder admixture with palmitic acid as the excipient. At less than 20%, insulin does not disperse uniformly in the admixture. The size distribution of the excipient particles obtained after grinding for 15 min does not affect the sustained release action. When tested in a 33 d period, an 1/8-size piece (approximately 25 mg) implant cut from a pellet disc containing 20% insulin which is 13 mm in diameter and 1.5 mm thick released 0.12-0.17 mg insulin/d in diabetic Wistar rats. The 1/8-size piece containing 20% insulin or a rod of similar weight with a diameter of 3 mm, which can be inserted by a trocar, was optimal for the implant to provide a service-life of 49 +/- 7 d. The service-life decreased with progressive reduction in implant size. The implant functioned just as well subcutaneously or intraperitoneally and was eroded subcutaneously by 33.6-53.1% in 33 d. The glycosylated haemoglobin contents of diabetic animals on implant therapy which had a blood glucose level of 4.7 +/- 2.5 mmol/l were in a range of 6.2-8.9% compared to the control value of greater than 13% with chronic hyperglycemia. The overall results indicated that the implant was a promising alternative to daily insulin injections.     

中国部分地区妇幼卫生信息系统的现状分析

本文通过研究卫生 项目地区报表资料和现场调查 ,对项目地区妇幼卫生信息系统的建设及运作情况进行了分析 ,并对报表数据质量进行了评价。分析显示 :卫 项目推动了贫困地区信息系统建设 ,项目地区已建立起系统的妇幼卫生信息管理体系 ,但分析也反映出项目地区妇幼卫生常规报表的数据质量仍存在一定问题。分析结果提示 ,应进一步加强妇幼卫生信息系统建设 ,提高妇幼卫生统计信息专业队伍的业务水平。     

糖耐量减低患者胰岛素抵抗与颈动脉粥样斑块的相关性分析

目的　探讨胰岛素抵抗 (IR)在糖耐量减低 (IGT)大血管并发症中的作用。方法　测定 1 2 0名IGT患者和 96名糖耐量正常(NGT)对照者的空腹血糖 (FBG)、胆固醇 (TC)、甘油三酯 (TG)、胰岛素 (FINS)及餐后 2h血糖 (PBG) ,并测量身高、体重、腰围、臀围 ,计算相对胰岛素敏感指数 (RISI)、体重指数 (BMI)、腰臀比 (WHR) ,结合其颈动脉多普勒超声检测结果进行对比分析。结果　IGT组及NGT组颈动脉粥样斑块发生率有显著性差异 (P <0 .0 0 1 ) ,斑块面积与RISI呈负相关 (r =- 0 .45 ,P <0 .0 1 ) ,与餐后 2h血糖 (r =0 .39,P <0 .0 1 )、BMI(r=0 .48,P <0 .0 1 )及WHR(r=0 .41 ,P <0 .0 1 )正相关 ,而与TG、FBG、TC、FINS无相关性 (P >0 .0 5)。IGT组患者有斑块和无斑块者之间RISI、WHR、BMI、餐后 2h血糖、TG之间也存在显著性差异 (P <0 .0 1 )。结论　胰岛素抵抗与颈动脉粥样硬化的发生密切相关 ,是IGT患者发生大血管并发症的重要原因。     

Extracellular signal regulated kinases 1/2 signal pathway and responses of astrocytes after diffuse brain injury

BACKGROUND: The treatment of diffuse brain injury during an acute period is focused on relieving degrees of secondary brain injury. Generation and development of pathological changes of secondary brain injury depend on signal conduction, so down-regulating over response of astrocyte through interfering a key link of signal conduction pathway may bring a new thinking for the treatment of diffuse brain injury. OBJECTIVE: To observe the effect of over activity of extracellular signal regulated kinases 1/2 (ERK1/2) signal pathway on the response of astrocyte during an acute period of diffuse brain injury. DESIGN: Completely randomized grouping and controlled animal study. SETTINGS: Department of Neurosurgery, the Third Affiliated Hospital, Nanchang University; Department of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: A total of 158 healthy male SD rats, of 11 weeks old, weighing 320–370 g, were provided by Experimental Animal Faulty, Tongji Medical College, Huazhong University of Science and Technology. Rabbit-anti-phosphorylated ERK1/2 (pERK1/2) polyclonal antibody was provided by R&D Company; rabbit-anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, SP immunohistochemical kit and horseradish peroxidase (HRP)-labeled goat-anti-rabbit IgG by Santa Cruz Company; specific inhibitor U0126 of ERK1/2 signal pathway by Alexis Company. METHODS: The experiment was carried out in the Laboratory of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from September 2004 to March 2006. ① Detection of pERK1/2 expression: A total of 110 rats were randomly divided into sham operation group (n =5), model group (n =35), high-dosage U0126 group (n =35) and low-dosage U0126 group (n =35). Rats in the sham operation group were only treated with incision of epicranium and fixation of backup plate, but not hit. Rats in the model group were used to establish diffuse brain injury models based on Marmarou free falling body without drug intervention. Rats in the high- and low-dosage U0126 groups were injected into caudal vein with 0.1 and 0.05 mg/kg U0126, respectively, and then, rats were hit to establish injured models. Every 5 rats were collected from model, high- and low-dosage U0126 groups at 5, 30 minutes, 3, 12, 24, 72 hours and 7 days after diffuse brain injury to detect pERK1/2 expression in cortex of parietal lobe based on Western blot technique. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Another 48 rats were randomly divided into sham operation group (n =3), model group (n =15), high-dosage U0126 group (n =15) and low-dosage U0126 group (n =15). The intervention and administration were dealt as the same as those mentioned above. Every 3 rats were collected from model, high- and low-dosage U0126 groups at 30 minutes, 3, 12, 24 and 72 hours after model establishment to observe the distribution of pERK1/2 and postive GFAP cells in brain tissue which was cut from coronal section at Bregma –4.8 mm layer with immunohistochemical staining. MAIN OUTCOME MEASURES: pERK1/2 expression in cortex of parietal lobe and distribution of pERK1/2 and positive GFAP cells in brain tissues. RESULTS: ① pERK1/2 expression: After diffuse brain injury, pERK1/2 expression in cortex of parietal lobe was rapidly increased in the model group, reached at peak at 5 minutes and then decreased gradually. But the expression was still in a high level until the 72nd hour and fallen to the basic level on the 7th day. pERK1/2 level was lower in high- and low-dosage U0126 groups than that in model group at various time points (P < 0.01); meanwhile, pERK1/2 level was lower in high-dosage U0126 group than that in low-dosage U0126 group. The results showed that there was a certain dosage dependence on pERK1/2 expression. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Positive expression of pERK1/2 lasted in brain tissue from 30 minutes to 72 hours after diffuse brain injury (P < 0.05). In addition, from 30 minutes to 3 hours, brown-yellow stained cells were mainly distributed in plasma, but rarely in nucleus. A lot of positive cells had tree-like apophysis, which was similar to neurons. With the time passing by, more and more nuclei manifested positive stains; moreover, nuclei mainly manifested positive staining until 24 hours after diffuse brain injury. Immune-positive pERK1/2 cells were widely distributed in brain tissue, especially mainly in binding site between deep cortex and cerebral white matter, and then in hippocampus. In addition, ependymal cell and vascular endothelial cells of choroids plexus also manifested strongly positive staining. As compared with model group, positive cells were decreased gradually in high- and low-dosage U0126 groups. However, number of positive cells was less in high-dosage U0126 group than that in low-dosage U0126 group. CONCLUSION: Diffuse brain injury strongly induces the activity of ERK1/2 signal pathway and response of astrocyte; in addition, U0126 can inhibit response of glial cells during an acute period, and the effect manifests dosage dependence.