儿童期单纯肥胖症的行为治疗

为研究适合中国肥胖儿童的行为治疗方案及效果，对２４例（男女各１２例）１３岁单纯肥胖儿童进行３年行为治疗纵向研究。２４名同年龄、性别、年级非肥胖儿童为正常对照组。观测参数有身高、体重、四处皮脂、腰、臀围及其比例、有氧运动能力（最大耐受时间和运动距离）。体育测试成绩包括引体向上、跳远、８００米跑、仰卧起坐，满分为３０分。按运动处方每天运动２小时，每周５天。在医生指导下肥胖儿童写行为分析和行为矫正方案。有关肥胖指标年减少率（男／女）体脂含量为２３％～４２％，肥胖度２．８％～２．１％，腰／臀比２．５％～２．６％，四处皮脂和５．７％女０．８％～１．０％），有氧能力明显进步。体育成绩肥胖干预组３０％达满分，７０％为２７～２９分。肥胖对照组６０％为２０分，３０％为１５～１９分。提示儿童期单纯肥胖症的干预方案应以健康教育和运动处方为基础，行为治疗为核心技术；在家庭日常生活中持续进行，家长、教师、医务人员应共同参与。     

重组人绒毛膜促性腺激素β-亚基对C57BL小鼠免疫应答反应及抗血清特征的研究

采用福氏性剂，对C57BL小鼠进行重组hCGβ和天然hCGβ免疫应签反应的比较研究，结果表明：两者引发的抗血清性质相似，与hCG有较高的亲和力（K（γβ）≈5．86×108／mol／L，Kaβ≈8．18×108／mol／L）；抗血清能有效地抑制（125）I－hCG与睾丸受体的结合，结果提示重组hCGβ抗血清与天然hCGβ抗血清相似，具有中和hCG的生物活性能力，重组hCGβ可作为免疫避孕疫苗的抗原。     

消瘀散消肿止痛作用的实验观察

消瘀散在临床运用中有较好的消肿止痛之功效．为了证实其药理作用，作者用大白鼠建立急性软组织损伤和血肿的实验模型，使用消疾散进行治疗。观察结果表明该药能够有效抑制创伤性无菌性炎症反应，促进血肿吸收，提高实验动物的痛阈值；而且药效随作用时间的延长而逐渐增加。实验结果为该药的消肿止痛作用提供了科学依据。     

小鼠自然老化过程中耳蜗的糖代谢障碍

应用定量组织化学技术分析了ＣＢＡ和Ｃ５７ＢＬ小鼠耳蜗中糖元代谢的改变，发现１８个月和３６个月龄ＣＢＡ小鼠的毛细胞和血管纹中，糖元含量比６周龄ＣＢＡ正常小鼠明显增高，说明在自然老化ＣＢＡ小鼠耳蜗中存在糖元储积现象。     

灰鼠疆孔内听神经纤维的定量观察

目的为了观察正常灰鼠和卡铂（Ｃａｒｂｏｐｌａｔｉｎ）耳中毒灰鼠耳蜗单个疆孔（ｈａｂｅｎｕｌａｐｅｒｆｏｒａｔａ）内的神经纤维数量。方法１２只灰鼠中６只按１００ｍｇ／ｋｇ腹腔注射卡铂２次，６只作正常对照，３个月后处死，沿蜗轴平面作半薄切片，甲苯胺蓝－美蓝染色后光镜观察，组间统计学比较采用ｔ检验。结果正常灰鼠的神经纤维数量在耳蜗不同部位有所不同，其中在底回起始段每个疆孔中通过９３．７±１２．２（ｘ±ｓ，下同）根神经纤维，底回末段为１８１．５±３０．４，第二回中段为１２９．７±２７．８，顶回中段为７５．８±１３．２。应用加倍大剂量卡铂将内毛细胞和Ｉ型螺旋神经元全部破坏后，疆孔内残存的神经纤维数仅占正常值的七分之一。结论疆孔内七分之六的神经是支配内毛细胞的Ｉ型神经元。     

人His6-IFNγ/TNFβ(His6γ-TNFNβ)融合蛋白(包涵体)的分离、纯化与复性研究

应用pET28(含T_7lac启动子和His6-tag)质粒,将人γTNFβ融合基因与之组建成pETγLT表达质粒,并转化于E.coliBL21(DE3).本文对pETγLT/ BL21(DE3)工程菌的His6-γTNFβ重组产物进行了诱导表达,分离纯化的研究.结果表明,该工程菌用LB培养基在37℃扩增至OD_(590)为0.5左右,加IPTG(终浓度为1mmol/L)诱导5小时,此时His6-γTNFβ的表达量可占菌体总蛋白的45%.重组产物绝大多数以IBs形式存在于菌体中.工程菌经反复超声破碎、高速离心,得IBs粗制品后,再经含2mol/L脲的缓冲液洗涤可得到相对纯净的IBs.然后用7mol/L脲变性溶解IBs,离心取上清,进行Ni~(2 )-Sepharose 6B柱一步法亲和层析,可得到电泳纯度为95%的His6-γTNFβ,经稀释复性和用凝血酶切去His6-tag的产物,其细胞毒活性为(1.2～2.0)×10~7U/mgp,抗病毒活性为(6.0～6.6)×10~6U/map.     

盐酸恩丹西酮预防化疗所致呕吐Ⅱ期临床研究

观察国产５－ＨＴ３阻滞剂－盐酸恩丹西酮预防化疗所致呕吐的临床疗效。方法：采用随机自身交替对照方法分为两组观察，接受顺铂联合化疗组及非顺铂联合化疗组各２５例。盐酸恩丹西酮８ｍｇ，化疗前１５分钟静注，恩丹西酮８ｍｇ，化疗后８小时口吸口服。对照组：胃复安２０ｍｇ，化疗前１５分钟肌注，胃复安８ｍｇ化疗后８小时口服。     

Synthesis and evaluation of 6-[(18)F]fluoro-3-(2(S)-azetidinylmethoxy)pyridine as a PET tracer for nicotinic acetylcholine receptors

Both ABT-594 ((R)-2-chloro-5-(2-azetidinylmethoxy)pyridine) and A-85380 (3-[2(S)-2-azetidinylmethoxy]pyridine), novel nicotinic agonists that possess potent non-opioid analgesic properties, have high affinity for neuronal nicotinic acetylcholine receptors (nAChR) but do not elicit the pronounced toxicity of epibatidine. 6-[(18)F]Fluoro-3-(2(S)-azetidinylmethoxy)pyridine (6-[(18)F]fluoro-A-85380), a F-18 labeled analogue of these two compounds, is therefore a promising radioligand for positron emission tomography (PET) studies in humans. The use of trimethylammonium as a leaving group in nucleophilic aromatic substitution reactions has proven to be a versatile and efficient strategy, and offers several advantages over other leaving groups. Here, we report the synthetic strategy for the preparation of a precursor, as a trimethylammonium iodide salt, and its use in the radiosynthesis to 6-[(18)F]fluoro-A-85380. Preliminary compartative PET studies of 6-[(18)F]fluoro-A-85380 and 2-[(18)F]fluoro-A-85380 were carried out in baboon to examine their suitability as tracers for studying nAChR system.     

Increased chromatid-type chromosomal aberrations in mouse m5S cells exposed to power-line frequency magnetic fields

PURPOSE: To investigate the induction of chromosomal aberrations in mouse m5S cells after exposure to power-line frequency magnetic fields (extremely low frequency magnetic fields; ELFMF) at high-flux densities. MATERIAL AND METHOD: m5S cells were either untreated or pretreated during the G1 phase with mitomycin C (MMC, 1 microM) for 1 h or 3 Gy X-rays, and then exposed to ELFMF at three different flux densities (5 and 50 mT at 60 Hz, 400 mT at 50 Hz) for 40 h. Unexposed control cells were incubated for the same period in a conventional CO2 incubator. Chromosomal aberrations were analysed in the first post-treatment metaphases. Cell kinetics were assessed by DNA flow cytometry and the mitotic index. RESULTS AND CONCLUSIONS: ELFMF enhanced the formation of spontaneous and MMC- or X-ray-induced chromosomal aberrations, in a flux-density-dependent manner. Statistically significant increases in the frequency of chromosomal aberrations were observed in cells exposed to 400 mT ELFMF with respect to unexposed controls. The aberrations induced by ELFMF were mostly chromatid-type, not chromosome-type. The cells exposed to 400 mT ELFMF exhibited a three-fold higher level of chromatid-type aberrations than did the unexposed cells. Flow cytometric and mitotic index analyses revealed that the S or G2 arrest following MMC or X-irradiation was more profound in ELFMF-exposed cells than in unexposed cells. Our results suggest that ELFMF can interfere with post-replication repair, resulting in increased levels of chromatid-type chromosomal aberrations induced spontaneously and by DNA damaging agents.