发育期大鼠高热惊厥前后海马γ-氨基丁酸B受体亚基表达的变化

目的：研究高热惊厥(febrile seizures，FS)对发育期大鼠脑内γ-氨基丁酸(γ-aminobutyric acid，GABA)B受体亚基GABABR1与GABARR2蛋白表达的影响。方法：采用热水浴诱导大鼠高热惊厥模型。隔日诱导惊厥1次，共诱导10次，末次惊厥后24h处死大鼠。发育期大鼠随机分为3组：对照组(n＝24)，1次高热处理组(n＝28)，10次高热处理组(n＝40)。高热处理组根据是否出现惊厥再分为1次高热惊厥组(FS1，n＝16)与1次高热未惊厥组(F1，n＝12)，10次高热惊厥组(FS10，n＝15)与10次高热未惊厥组(F10，n＝13)。采用免疫组化方法观察不同次数高热惊厥大鼠脑内GABABR1与GABABR2蛋白表达的变化。结果：FS10大鼠海马齿状回、CAl-CA3区GABABRl和GABABR2蛋白表达明显低于F10、F1、FSl和对照组；F10大鼠上述脑区GABABRl和GABABR2蛋白表达低于F1、FS1和对照组；F1及FS1大鼠与对照组相比差异无显著性；海马各区GABABR1与GABABR2表达的改变大部分平行，但10次高热惊厥后GABABR2在CA1—CA3区下降更明显，而GABABR1在齿状回下降更明显。结论：反复高热惊厥及反复高热均可使发育期大鼠脑内GABABR亚基蛋白表达降低，高热惊厥的影响较单纯高热更为明显，提示GABABR亚单位与发育期大鼠高热惊厥及其脑损伤密切相关。GABABR1与GABABR2改变的不平行可能与受体亚单位组合的可塑性改变有关，这种改变可能导致抑制功能的改变。     

便携式多普勒血管探测仪在皮瓣移植中的应用

目的 :研究皮瓣移植前简单、可靠的血管探测的方法。方法 :在皮瓣移植前 ,以 HADECO ES-1 0 0 0 SPM多普勒血管探测仪对皮瓣血管蒂及皮动脉进行探测 ,与术中皮动脉探查结果进行比较 ,考察术前血管探测的准确性和意义。结果 :皮瓣血管蒂及皮动脉术前探测与术中探查结果完全一致。结论 :便携式血管多普勒仪是皮瓣移植前 ,简单、可靠的血管探测的仪器 ,根据探测结果进行皮瓣设计 ,有效地降低了手术失败的风险     

Acute effects of serotonin on rat bladder contractility.

INTRODUCTION: The purpose of this study is to investigate in vitro the effects of serotonin on the rat detrusor. In particular, it examines which drugs inhibit the serotonin-induced detrusor contractions. MATERIALS AND METHODS: Isometric tension changes of isolated rat bladder muscle strips were recorded in an organ bath using a force transducer. Acute effects of serotonin (0.0001-0.01 mM) on resting tension were assessed. Electrical field stimulation (EFS); bethanechol (0.0001-0.01 mM); ATP (1-3 mM)- or KCl (63.5-254 mM)-induced contractions using an application in an organ bath were compared with serotonin-induced contractions. In order to examine the action mechanism of serotonin-induced stimulation, EFS-, bethanechol-, ATP- or KCl-induced contraction on serotonin treatment (0.001 mM) was assessed and serotonin (0.001-0.1 mM) was cumulatively added to the organ bath following preincubation with propranolol, ketanserin, tropisetron, propiverine, sodium nitroprusside or doxazosin. RESULTS: The serotonin-induced response has two phases: an initial transient contraction and a prolonged tonic phase. Serotonin produced a reversible and dose-dependent contraction of the detrusor strips. Responses to bethanechol significantly increased with a concentration of 0.001 mM serotonin (p < 0.05). There was no effect on the responses to ATP, KCl, or EFS on 0.001 mM serotonin. The 5-HT(2) receptor is mainly responsible for serotonin-induced contractions of the detrusor (p < 0.05), while the 5-HT(1) receptor is partially responsible. Doxazosin and propiverine each significantly suppressed the response to serotonin, while sodium nitroprusside and tropisetron each had no effect (p < 0.05). CONCLUSIONS: Because the 5-HT(2) antagonist blocked the effect of serotonin-induced bladder contractions and the stimulation of the adrenoreceptors, the 5-HT(2) antagonist seems to improve lower urinary tract symptoms.     

nm23-H1基因转染对人胆管癌细胞系QBC939体外浸润能力的影响

目的：探讨nm23-H1基因转染对人胆管癌细胞系QBC939体外浸润能力的影响。方法：将含有全长nm23-H1 cDNA的真核表达载体通过脂腩体法转染人胆管癌细胞系。结果：转染成功的QBC939细胞，其nm23-Hl基因的mRNA、蛋白表达明显增加，转染nm23-H1基因的胆管癌细胞体外浸润能力下降，穿越matrigel的细胞数明显低于亲本QBC939细胞，代表浸润能力的IV型胶原酶（MMP-9）分泌量下降。结论：nm23-Hl基因可以抑制胆管癌细胞的体外浸润能力。     

常用消毒剂及自来水对弓形虫速殖子活力的影响

目的了解常用消毒剂及自来水对弓形虫速殖子活力的影响。方法将各种消毒剂分别加入等体积含弓形虫速殖子的小鼠腹水中，在不同时间内观察虫体胎盘蓝（trypanblue）着色率及活动率，并将经消毒剂处理不同时间的速殖予接种昆明鼠，观察速殖子能否在接种鼠体内复苏繁殖，导致小鼠死亡。用类似方法观察自来水时速殖子的影响。结果除甲醛个速殖子在常用浓度的不同消毒剂中，lmin月台盘蓝着色率均为100％，活动率为0。经消毒剂处理1min的速殖子接种小鼠后，各组接种鼠（包括甲醛处理组）无一死亡。经自来水处理4h的速殖子接种小鼠后仍能在小鼠体内复苏繁殖，小鼠于接种1wk内全部死亡。结论弓形虫速殖子对常用消毒剂均很敏感；而在自来水中途殖子可保持感染力4h以上。     

加锌对大鼠脑内微量元素的影响

用SD雌性成年大鼠20只,随机分为实验组和对照组各10只。加锌40d后,用原子吸收分光光度计(日本津岛)分别测定了两组大鼠大脑皮质感觉运动区和海马CA3区的微量元素Zn、Cu、Fe和轻金属Mg的含量。结果表明:在大脑皮质感觉运动区,两组大鼠的诸元素含量无显著变化;在海马CA3区,两组大鼠的微量元素Zn、Cu、Fe的含量也无显著变化(P>0.05),但轻金属Mg的含量却发生了显著的变化,表现为对照组明显高于实验组(P<0.05)。     

Clinical and hormonal effects of chronic gonadotropin-releasing hormone agonist treatment in polycystic ovarian disease

Previously, we reported that short term administration of a highly potent GnRH agonist (GnRHa) for 1 month to patients with polycystic ovarian disease (PCO) resulted in complete suppression of ovarian steroidogenesis without measurable effects on adrenal steroid production. This new study was designed to evaluate the effects of long term GnRHa administration in PCO patients with respect to their hormone secretion patterns and clinical responses. Eight PCO patients and 10 ovulatory women with endometriosis were treated daily with sc injections of [D-His6-(imBzl]),Pro9-NEt]GnRH (GnRHa; 100 micrograms) for 6 months. Their results were compared to hormone values in 8 women who had undergone bilateral oophorectomies. In response to GnRHa, PCO and ovulatory women had rises of serum LH at 1 month, after which it gradually declined to baseline. In both groups FSH secretion was suppressed throughout treatment. Serum estradiol, estrone, progesterone, 17-hydroxyprogesterone, androstenedione, and testosterone levels markedly decreased to values found in oophorectomized women by 1 month and remained low thereafter. In contrast, serum pregnenolone and 17-hydroxypregnenolone were partially suppressed, and dehydroepiandrosterone, dehydroepiandrosterone sulfate, and cortisol levels did not change. Clinically, hyperplastic endometrial histology in three PCO patients reverted to an inactive pattern, and proliferative endometrium in two other PCO patients became inactive in one and did not change in the other. Regression of proliferative endometrial histology occurred in all ovulatory women. Vaginal bleeding occurred in all women studied during the first month of GnRHa administration, after which all but one PCO patient became amenorrheic. Hot flashes were noted by all ovulatory women and by four of eight PCO patients. All PCO patients noted subjective reduction of skin oiliness, and five had decreased hair growth. We conclude that in premenopausal women: 1) chronic GnRHa administration results in apparently complete persistent suppression of ovarian steroid secretion; 2) adrenal steroid secretion is not influenced directly or indirectly; and 3) its use may be helpful in the treatment of endometrial hyperplasia and ovarian androgen excess in women with PCO.