五种免疫相关性心血管疾病的免疫学研究

对扩张型心肌病、风湿性心脏病，原发性高血压，冠心病及肥厚型心肌病进行外周血清可溶性白细胞介素２受体，Ｔ淋巴细胞亚群及自然杀伤细胞活性的检测，并与健康对照组比较，结果显示：ＤＣＭ组，ＲＨＤ组及ＥＨＴ组的ｓＩＬ－２Ｒ明显高于ＮＣ组，而ＤＣＭ、ＲＨＤ风湿活动组的ＮＫ活性低于ＮＣ组，ＥＨＴ组ＮＫ活性高于ＮＣ组。     

微波体模

用水、盐,聚氯乙烯粉和羧甲基纤维钠四种材料配制成一种适用的微波体模(模拟肌肉组织)。该体模的复介电系数在300～2500MHz范围内与实际人体肌肉组织的误差≤5％。这种体模的优点是材料立足国内,价廉,室温下配制,使用方便。本文也给出这种体模的温度特性,稳定性和热学特性,供电磁场生物效应和微波热疗等研究使用。     

The neuroprotective effects of K252a through inhibiting MLK3/MKK7/JNK3 signaling pathway on ischemic brain injury in rat hippocampal CA1 region

It has been well documented that the activation of c-Jun N-terminal protein kinase (JNK) pathway and caspase-3 signal are involved in the delayed neuronal cell death in cerebral ischemia. In this study, we first detected the activation pattern of JNK signaling including mixed lineage kinase (MLK)3, mitogen-activated protein kinase kinase (MKK)7 and JNK3 in hippocampal CA1 and CA3/DG regions at various time points after 15 min of ischemia. These results indicated that cerebral ischemia induced the continuous activation of MLK3/MKK7/JNK3 cascade, which all had two active waves only in the CA1 region. We also detected the phosphorylation of JNK substrates c-Jun and Bcl-2, and the activation of a key protease of caspase-3 in CA1 region, which only had one active peak, respectively. Because K252a has recently been shown to be a potent inhibitor of MLK3 activity both in vivo and in vitro, we further examined the possible effects and mechanism of this interesting drug in cerebral ischemia. In our present paper, we found that administration of K252a 20 min prior to ischemia inhibited MLK3/MKK7/JNK3 signaling, Bcl-2 phosphorylation, the activation of c-Jun and caspase-3, but had no significant effects on these protein expressions. Additionally, pretreatment of K252a significantly increased the number of the surviving CA1 pyramidal cells at 5 days of reperfusion. Our results suggest that K252a play a neuroprotective role in ischemic injury via inhibition of the JNK pathway, involving the death effector of caspase-3. Thus, JNK signaling may eventually emerge as a prime target for novel therapeutic approaches to treatment of ischemic stroke, and K252a may serve as a potential and important neuroprotectant in therapeutic aspect in ischemic stroke.     

咪唑安定、异丙酚对体外循环期酸碱平衡的影响

目的 观察异丙酚和咪唑安定在体外循环麻醉中对术前和术中的酸碱度的影响.方法 40例先天性心脏病患者随机分为两组(异丙酚组、咪唑安定组),监测手术前、主动脉阻断10 min和复温至31℃时血气指标等的动态变化.结果与手术前比,主动脉阻断10 min和复温后,血液pH、PaCO2、HCO3-、BEB两组均有明显变化(P＜0.05),但两组间差异无显著性(P＞0.05).结论异丙酚和咪唑安定在体外循环麻醉中其对酸碱度无明显的影响.     

哇巴因与地高辛对大鼠肝脏钠泵A亚单位基因表达的影响

目的　观察哇巴因与地高辛对大鼠肝脏钠泵基因表达的影响 .方法　分别给大鼠注射哇巴因 (2 0 μg· kg- 1·d- 1 )、地高辛 (32 μg·kg- 1·d- 1 )和生理盐水 (1m L· kg- 1·d- 1 ) ,观察给药后 6wk大鼠血压的动态变化 ;并分别应用分子生物学 RT- PCR及免疫组织化学技术 ,探讨各组大鼠肝脏钠泵 α1 ,α2 及 α3 亚单位 m RNA及蛋白水平基因表达的改变 .结果　给予哇巴因 2 wk后大鼠血压开始升高 ,至 6 wk时明显高于生理盐水组 (17.7± 1.2 ) vs(15 .4± 1.1) k Pa,P<0 .0 1) ,而实验过程中地高辛组血压与对照组比较差异不明显 .无论是在 m RNA水平还是在蛋白水平 ,哇巴因对大鼠肝脏钠泵α1 亚单位表达无影响 ,而地高辛使α1 亚单位表达增强 ;两组大鼠 α2 亚单位表达均无改变 ;哇巴因使 α3 亚单位蛋白水平表达减弱 ,而 m RNA水平增强 ,地高辛组大鼠肝脏钠泵 α3 亚单位无论在 m RNA水平及蛋白水平表达均增强 .结论　哇巴因在高血压发病中可能起着重要作用 ;哇巴因与地高辛可导致不同的钠泵基因表达改变 ,为进一步揭示内源性哇巴因生理与病理作用以及洋地黄类药物药理与毒理作用的分子机制提供了理论及实验依据     

磷酸钛钾激光声带切除术不同术式的临床特点

目的 探讨支撑喉镜下磷酸钛钾（ｐｏｔａｓｉｕｍ ｔｉｔａｎｉｕｍ ｐｈｏｓｐｈａｔｅ,ＫＴＰ）激光声带切除术不同术式的选择及愈合过程中的临床特点。方法 选择７６例早期声门型喉癌行ＫＴＰ激光声带切除术,对不同术式术后喉内结构恢复过程、音质变化等进行随访观察记录。结果 Ⅰ型术式１１例,３个月后恢复喉的正常结构及功能;Ⅱ型术式５０例,３个月后有声带样粘膜皱襞（以下称新声带）形成,基本恢复喉的结构;Ⅲ型术     

U-Patch GAN: A Medical Image Fusion Method Based on GAN

Journal of Digital Imaging - Although medical imaging is frequently used to diagnose diseases, in complex diagnostic situations, specialists typically need to look at different modalities of image...     

Microsomal casein kinase II in endoplasmic reticulum- and Golgi apparatus-rich fractions of ROS 17/2.8 osteoblast-like cells: An enzyme that modifies osteopontin

Osteopontin is an acidic phosphoprotein containing casein kinase II (CKII) phosphorylatable sites and an acidic amino acid cluster. The metabolically ³²P-labelings of both serines and threonines in vitro in osteopontin immunoprecipitated from rat osteoblast-like ROS 17/2.8 cells may suggest that casein kinase II catalyzes this modification. The enzyme occurs in microsomal fractions of rat osteoblast-like ROS 17/2.8 cells. Subcellular fractions containing endoplasmic reticulum and Golgi apparatus were isolated by differential centrifugation and were identified according to their ultrastructures and the presence of marker enzymes such as glucose-6-phosphatase and thiamine pyrophosphatase, respectively. Both fractions phosphorylated the partially dephosphorylated osteopontin and the specific substrate peptide RRREEETEEE. Endoplasmic reticulum-catalyzed peptide phosphorylation was 2.7 times lower than that of Golgi although both endoplasmic reticulum- and Golgi-catalyzed peptide reactions were 50% inhibited by 20 and 100 ng/ml heparin, respectively. Western blot analysis revealed that both fractions contained osteopontin and microsomal CKII. Furthermore, microsomal CKII was immunogold-labeled in endoplasmic reticulum and Golgi apparatus. Heparin inhibition and utilization of [-³²P]GTP as a phosphate donor by both fractions confirmed their capacity to phosphorylate osteopontin. The results suggest that microsomal CKII modifies the acidie matrix proteins during transportation. These matrix phosphoproteins may participate in the mineralization process of hard tissues.     

医疗机构产权制度改革及其监管

本文从产权的角度出发,对当前的医疗机构改革进行了分析,并对医疗机构自主经营、企业化经营过程中可能出现的一些问题,提出了政府作为财产的最终所有者应加强对医疗机构经营状况的监管。