替硝唑葡萄糖注射液的稳定性研究

采用反相ＨＰＬＣ法测定替硝唑葡萄糖注射液中替硝唑的含量，用加温加速实验研究该制剂的热稳定动力学。结果表明，替硝唑的热降解反应为一级动力学过程，在５０、６５、８０、９５℃时的降解速度常数分别为５．５８×１０－４、２．６６×１０－３、８．１０×１０－３、２．８２×１０－２ｄ－１，为８．３年，半衰期为３９．５年。     

Apopotic gene Bax expression in carotid plaque

The expression of BAX in carotid atherosclcrosis and its regulation is far from defined. Objectives To investigate BAX expression in stable/fibrous and instable/vulnerable carotid plaque and its clinical significance. Methods 25 cases of carotid plaque specimens obtained from endarterectomy were divided into two groups, stable/fibrous 14 cases, vulnerable/instable 11 cases; aortic artery and its branches from hepatic transplantation donors 6 case as control. The expression of proapoptotic BAX was detected by immunohistochemistry (IHC), in situ hybridization(ISH) and in situ TdT dUTP nick end labeling (TUNEL). Results 5 eases of BAX ( ) were detected by ICH and ISH, 4 case of TUNEL ( ) were detected by TUNEL in stable/fibrous carotid plaque, while 10 cases were BAX ( )by IHC(P<0.05) , 11 case by ISH and 9 case by TUNEL were detected in instable/vulnerable carotid plaque (P<0.01), respectively. The intensity of BAX ( ) cells by IHC and ISH was 8.63±2.62 and 10.32±3.12 in fibrous plaques, whereas 122±21.64 and 152±23.35 in vulnerable plaques, respectively. No expression of BAX was found in controlled group. Conclusion The higher expression of Bax in vulnerable carotid plaque may be one mechanisms in molecular pathogenesis of carotid atherosclerosis which affect plaque stability and be the cause of higher incidence of stroke than fibrous carotid plaques, the regulation of BAX expression in different stage of atherosclerosis may provide targets in gene therapy for carotid atherosclerosis.     

前列腺癌去势术前后雄性激素变化的研究

目的 :观察前列腺癌去势术前后雄性激素的变化。　方法 :16例前列腺癌病人在手术前后分别采集血清样本 ,用放射免疫法测定睾酮 (T)、游离睾酮 (FT)、双氢睾酮 (DHT)的含量 ,进行对比分析。　结果 :手术前后 ,血清中T、FT、DHT浓度有非常明显的差异 ,手术后分别下降 92 .2 7%、92 .2 6%、5 8.3 6% ,以T、FT下降为主。根据 2次测定的结果采用配对t检验方法 ,P <0 .0 0 1。　结论 :去势术后 ,去除了血清中绝大部分T、FT ,而DHT仅下降5 8.3 6% ,应当继续使用雄性激素受体竞争剂 ,阻止残存的雄性激素作用     

PCBP1:一种在多水平上参与基因表达调控的蛋白因子

多聚胞嘧啶结合蛋白1 (poly C binding protein-1,PCBP1),属于RNA结合蛋白亚家族,因其具有同RNA的多聚胞嘧啶(poly C)区域特异的结合活性而得名.目前该亚家族共有5个成员:hnRNP K(heterogeneous nuclear ribonucleoprotein K)、PCBP1、PCBP2、PCBP3和PCBP4.PCBP1蛋白在多个水平参与基因的表达调控,如转录、mRNA加工、mRNA的转运、mRNA稳定以及翻译水平调控等.本文对PCBP1基因的结构和生物学功能进行了综述.     

负载乳腺癌抗原单核细胞来源树突状细胞迁移能力的调控因素研究

目的：体外培养乳腺癌抗原负载的人单核细胞来源DC，应用不同刺激因子使其表面CCR7表达上调，在体外观察其迁移能力。方法：用rhGM-CSF和rhIL-4诱导MoDCs，并负载乳腺癌抗原后，分别与PGE2、LTC4或Bryo-1共培养，检测其表型及其功能变化。结果：PGE2、LTC4和Bryo-1在体外不影响MoDCs刺激淋巴细胞增殖能力和自体特异性淋巴细胞杀伤活性。与对照组MoDCs相比，PGE2和LTC4作用MoDCs后CD86表达增高，可以上调CCR7 mRBA和蛋白表达（P〈0．05）。PGE2可以使MoDCs对其配体CCL19和CCL21反应性增强（P〈0．05），而LTC4仅能使MoDCs对CCL19反应性增强。Bryo-1虽然可以促进MoDCs成熟，使其CCR7 mRNA表达增强，但在CCR7蛋白表达、迁移能力方面与对照组相似。结论：以PGE2和LTC4作用MoDCs后可以通过上调其CCR7表达，促进其迁移趋化能力。     

丹参对心肌缺血和再灌注损伤的保护作用

采用在家兔全麻、开胸、自主呼吸和自主心律的条件下,结扎冠脉左室支造成急性心肌缺血模型,进而松开结扎结形成再灌注损伤模型。对心肌缺血和再灌注损伤的组织脂质过氧化物含量和局部血流量变化进行测定,同时辅以心电图监护;以丹参注射液为保护剂观察其作用效果。结果表明,随着缺血时间的延续,心肌脂质过氧化物含量逐渐增加;当缺血60分钟后再灌注30分钟,脂质过氧化物含量仍继续上升,明显高于缺血60分钟组,但与缺血90分钟组比较则无显著差异;其缺血区局部组织血流量再灌注后仅恢复53.2%。给予丹参保护的再灌注组,其缺血区组织脂质过氧化物含量较再灌注损伤组下降56.0%(P<0.005),而局部组织血流量恢复则提高32.0%(P<0.001)。     

To die or not to die for neurons in ischemia,traumatic brain injury and epilepsy: a review on the stress-activated signaling pathways and apoptotic pathways

After a severe episode of ischemia, traumatic brain injury (TBI) or epilepsy, it is typical to find necrotic cell death within the injury core. In addition, a substantial number of neurons in regions surrounding the injury core have been observed to die via the programmed cell death (PCD) pathways due to secondary effects derived from the various types of insults. Apart from the cell loss in the injury core, cell death in regions surrounding the injury core may also contribute to significant losses in neurological functions. In fact, it is the injured neurons in these regions around the injury core that treatments are targeting to preserve. In this review, we present our cumulated understanding of stress-activated signaling pathways and apoptotic pathways in the research areas of ischemic injury, TBI and epilepsy and that gathered from concerted research efforts in oncology and other diseases. However, it is obvious that our understanding of these pathways in the context of acute brain injury is at its infancy stage and merits further investigation. Hopefully, this added research effort will provide a more detailed knowledge from which better therapeutic strategies can be developed to treat these acute brain injuries.     

心肌缺血／再灌注损伤时相性变化的电子示踪研究

本文以结扎家兔冠状动脉左室支为心肌缺血模型,应用镧电子示踪技术,生物体视学定量分析等方法,观察了心肌缺血不同时间再灌注后细胞膜系及线粒体超微结构以及镧示踪所提示的线粒体的功能变化等特点。结果表明,在心肌缺血20分时,细胞膜通透性升高,镧粒子进入细胞,再灌注时更为严重,即出现再灌注损伤。此时镧粒子多集于肌浆管。随缺血时间延长(30—40分),变化愈趋严重,缺血40分后再灌注,镧粒子大量涌入线粒体。而缺血60分,特别是再灌注时,心肌细胞严重破坏,几乎无完整线粒体,其中亦很少有镧颗粒。说明在此情况下的再灌损伤已属不可逆性。膜通透性的变化是由外及里的,即先肌膜而后为细胞内膜。就线粒体来讲则是先外膜而后内膜。实验结果提出可逆性(早期)再灌注损伤期,及不可逆性再灌注损伤期(晚期)的概念。     

Loss of imprinting of IGF2 and H19 in osteosarcoma is accompanied by reciprocal methylation changes of a CTCF-binding site

The adjacent insulin-like growth factor 2 (IGF2) and H19 genes are imprinted in most normal human tissues, but imprinting is often lost in tumors. The mechanisms involved in maintenance of imprinting (MOI) and loss of imprinting (LOI) are unresolved. We show here that osteosarcoma (OS) tumors with IGF2/H19 MOI exhibit allele-specific differential methylation of a CTCF-binding site upstream of H19. LOI of IGF2 or H19 in OS occurs in a mutually exclusive manner, and occurs with monoallelic expression of the other gene. Bisulfite sequencing reveals IGF2 LOI occurs with biallelic CpG methylation of the CTCF-binding site, while H19 LOI occurs with biallelic hypomethylation of this site. Our data demonstrate that IGF2 LOI and H19 LOI are accompanied by reciprocal methylation changes at a critical CTCF-binding site. We propose a model in which incomplete gain or loss of methylation at this CTCF-binding site during tumorigenesis explains the complex and often conflicting expression patterns of IGF2 and H19 in tumors.