二尖瓣脱垂的外科治疗

报道５７例二尖瓣脱垂（ＭＶＰ０不同术式的外科治疗效果。手术随机分为３组;传统的二尖瓣成形组,Ｇｏｒｅ－Ｔｅｘ线人工腱索替换组和瓣膜置换组。结果显示,Ⅱ组和Ⅲ组术后每搏二尖瓣返流量明显少于Ⅰ组。各组术后长期随访机能状况均明显改善。ＭＶＰ的外科治疗应首选二尖瓣成形;而Ｇｏｒｅ－Ｔｅｘ线人工腱索替换和人造瓣环盛开有方法安全可靠,其效果优于传统的腱索成形,并可避免瓣膜置换术后长期抗凝的并发症。     

P53与ras癌基因产物对直肠癌的诊断价值

目的提高直肠癌术前活检的诊断率。方法5年来手术治疗的168例直肠癌病人中,有20例（11．9％）第一次手术前活检不能明确诊断。对其中17例患者的活检组织石蜡标本（实验组）和10例正常肠粘膜活检标本（对照组）进行常规病理、P53与ras癌基因产物检测。结果实验组中P53与ras基因表达阳性率分别为71％与47％,阳性率均高于常规病理,有显著性差异。17例标本中,11例为不典型增生,5例仅有慢性炎症。不典型增生的P53与ras基因表达分别为11例和7例,而慢性炎症则全部为阴性。二者之间,两种基因表达阳性率均有显著差异。实验结果还显示P53与ras基因表达有较好的一致性。对照组的10例正常肠粘膜的活检标本P53与ras基因检测结果均阴性,与实验组比较,P53阳性率有显著差异。结论P53与ras基因表达检测,可以作为常规病理的补充,提高直肠良恶性病变的鉴别力。     

CART: from gene to function

CART was identified as a novel mRNA regulated by psychostimulant drugs. CART peptides appear to be neurotransmitters involved in a variety of functions such as feeding. The mouse gene has been characterized and localized to Chromosome 13. The processing of CART peptides is evident in Western blotting studies.     

Expression of intercellular adhesion molecule 1 (ICAM-1) is reduced in permanent focal cerebral ischemic mouse brain using an adenoviral vector to induce overexpression of interleukin-1 receptor antagonist

Our previous studies have demonstrated that overexpression of recombinant human interleukin-1 receptor antagonist protein (IL-1ra) via gene transfer can reduce ischemic brain injury. However, the mechanism of action of IL-1ra in ischemia is unclear. Since interleukin-1 can up-regulate intercellular adhesion molecules in endothelium, the present study was designed to determine whether overexpression of the IL-1ra can reduce the expression of intercellular adhesion molecule-1 (ICAM-1) after ischemic injury. Normal saline or adenovirus vector (1x109 particles) encoding the human IL-1ra gene (Ad.RSVIL-1ra) or the Escherichia coli LacZ gene (Ad.RSVlacZ) was injected into the right lateral cerebral ventricle of adult CD-1 mice. After five days, permanent middle cerebral artery occlusion (MCAO) was achieved for 24 h using an intraluminal suture. Cerebral blood flow was monitored by transcranial laser Doppler flowmetry to verify the occlusion. ICAM-1 protein was quantified using Western blot analysis and localized using immunohistochemistry. After MCAO, surface blood flow in the ischemic hemisphere was decreased to 9-11% of the baseline. There were fewer ICAM-1 positive vessels in the ischemic cortex of the Ad.RSVIL-1ra transfected mice than in the Ad.RSVlacZ transfected and saline treated mice (138+/-19 vs. 249+/-25, 284+/-22, p<0.05). Western blot analysis shows that ICAM-1 protein decreased 50-60% in the Ad. RSVIL-1ra group compared to the other two groups. There were no significant differences in the numbers of positive vessels in the ischemic basal ganglia and contralateral hemisphere among the three groups. Our studies suggest that IL-1ra overexpression can down-regulate the expression of ICAM-1 in the ipsilateral cortex in ischemic mice. Interleukin-1 may play an important role in the activation of inflammatory reaction during focal cerebral ischemia by promoting leukocyte adhesion on the endothelium cells.     

敏感期内、末单眼斜视和剥夺猫视觉系统脑源性神经营养因子表达机理研究

目的观察和研究敏感期内、末不同时限单眼斜视
(monocularstrabismus,MS)和单眼剥夺(monoculardeprivation,
MD)幼猫视皮质、外侧膝状体的脑源性神经营养因子(brain
derivedneurotrophicfactor,BDNF)的可塑性变化。从形态学、分
子神经生物学角度探讨不同时限MS和MD幼猫视     

Cochlear degeneration in guinea pigs after repeated hyperbaric exposures.

The effects of repeated hyperbaric exposures on inner ear function and morphology in guinea pigs were investigated with auditory electrophysiological testing, histopathological and electron microscopic techniques associated with enzyme histochemical method. The results showed that repeated hyperbaric exposures, though considered "safe," did cause damage to the cochlear system. Possible causes of the pathology include direct effects of repeated compression and decompression on the ear, and the possibility of inner ear decompression sickness and barotrauma cannot be excluded.     

β-内酰胺酶抑制短肽SIPIS04-01的表达、纯化与抑制作用测定

通过酵母双杂交系统从一个随机DNA片段文库中筛选到一个编码能与β-内酰胺酶结合的短肽SIPIS04—01的DNA序列，将它克隆到pGEX-4T-1的多克隆位点中，得到重组质粒pYG205。当用适量的IPTG诱导后，携带pYG205的E．coli DH5α能表达短肽SIPIS04-01-GST融合蛋白。利用谷胱甘肽Sepharose 4B亲和层析介质分离纯化短肽SIPIS04-01-GST融合蛋白，经凝血酶切割并分离纯化后，体外试验表明短肽SIPIS04-01具有抑制β-内酰胺酶的作用。