Calcification and ossification of chronic encapsulated intracerebral haematoma: case report.

We report a case of calcified chronic encapsulated intracerebral haematoma (ICH) in a 29-year-old female who presented with progressive left sided weakness and intermittent seizures since childhood. The preoperative magnetic resonance (MR) imaging of the head initially suggested that a partially thrombosed aneurysm or vascular malformation was present. However, no vascular stain was found on the digital subtraction angiography (DSA) of both the carotid and vertebral arteries. The excised mass was histologically diagnosed as a chronic ICH. We traced the patient's medical history and found that at the age of one she sustained a head injury after a fall. So far, to our knowledge, no case of epilepsy secondary to a calcified chronic encapsulated ICH occurring 28 years after head injury has been reported. Calcified chronic encapsulated ICH concomitant with new bone formation within is even rarer. The possible pathogenesis of this case is discussed.     

猪心脏移植缺血再灌注损伤中NO和NOS的表达

①目的　了解猪同种原位心脏移植术后早期一氧化氮 (NO)、一氧化氮合酶 (NOS)含量的变化 ,及其与早期缺血再灌注损伤的关系。②方法　建立猪同种原位心脏移植模型。供心在移植前低温保存 (Thomas液 ,4℃ ) 4h ,移植成功心脏复搏后 2h取材。应用组织化学方法测定心肌组织中NO、NOS的含量 ,应用核酸原位末端标记法 (TUNEL)测定心肌细胞凋亡指数 ,作为评价心肌缺血再灌注损伤的指标。以正常心肌及单纯缺血心肌组织作为对照。③结果　移植后心肌组织NO、NOS的含量较缺血组与正常组低 ,差异有显著意义 (F =2 7.2 2 9、16 .2 0 3,q =5 .716～ 6 .4 12 ,P <0 .0 1)。移植组心肌细胞凋亡指数与正常组及缺血组比较明显升高 ,差异有显著性(F =16 3.884 ,q =7.4 82、6 .975 ,P <0 .0 1)。心肌组织NO、NOS含量与心肌细胞凋亡指数呈负相关关系 (r =- 0 .886、- 0 .795 ,P <0 .0 1)。④结论　猪心脏移植后早期心肌缺血再灌注损伤所致的细胞死亡主要表现为心肌细胞凋亡 ;再灌注期间内源性NO、NOS的减少参与了心脏移植后早期缺血再灌注损伤的发生     

跟痛症的发病机制与临床诊断方法

跟痛症是一种临床常见多发疾病，以中老年患者居多，对于其发病机制与临床诊断鉴别方法不同的学者有着不同的见解。结合周福贻教授的理论与临床经验从发病机制、诊断、鉴别诊断及辅助检查等方面对跟痛症加以阐述。     

左双腔支气管导管管端位置与吸气峰压变化的关系

目的 观测无隆突钩双腔支气管导管(DLT)管端位置与吸气峰压(Ppeak)以及肺顺应性环形状改变的关系，探讨用Ppeak和顺应性环的变化评估DLT管端位置的可行性。方法 拟行右侧剖胸手术的成年患者32例，静脉诱导后插入左Mallinckrodt DLT，吸入氧化亚氮和地氟醚维持麻醉。按纤维支气管镜(FOB)确认DLT管端位置和通气方式将观测过程分为四个阶段：第一阶段(S1)，管端位置正确的双肺通气；第二阶段(S2)，管端位置正确的左侧单肺通气；第三阶段(S3)，管端插入左下支气管(置管过深)的左侧单肺通气；第四阶段(S。)，管端处在左支气管开口(置管偏浅)的左侧单肺通气。每阶段均机械通气15min。结果 回归方程预计插管深度与FOB检查符合者占71．9％。S2时Ppeak值比S1时增加50．8％，肺顺应性(Cdyn)值减少36．2％；S3时Ppeak值比S1时增加87．4％，Cdyn值减少56．8％。PV环曲线斜率向右明显移位，环体显著延长。结论 用无隆突钩DLT行肺隔离，在无FOB定位的条件时，联合应用听诊法、回归方程预计插管深度、动态监测气道峰压和P-V环的变化综合评估，可提高DLT管端的正确到位率。单肺通气的气道峰压超过双肺通气时的1．65倍，且气道峰压超过25cm H2O．应高度怀疑DLT管端发生过深移位。     

多层螺旋CT尿路造影在尿路梗阻性疾病中的临床应用

目的探讨多层螺旋CT尿路造影在泌尿系梗阻性疾病诊断中的应用价值。方法对48例泌尿系统梗阻性疾病者,分别进行多层螺旋CT平扫及多时相期CT增强扫描。对增强后各期图像进行相关处理,以不同的三维重建方式获得CTA、CTU影像。所有病例均经临床及手术证实。结果48例中肾脏及输尿管先天畸形者15例;输尿管阴性结石致肾盂输尿管积水者4例;泌尿系炎症者5例;肾及输尿管、膀胱结核6例;外源性压迫导致肾盂及输尿管积水者8例;泌尿系肿瘤者10例。结论多层螺旋CT泌尿系造影对尿路梗阻性疾病的诊断具有很高的应用价值。     

大鼠肾移植模型技术的改进

目的 为开展器官移植的实验研究，建立了大鼠异体肾移植模型。方法使用Wistar大鼠分别作为供者和受者，采用原位低温灌洗，肾动脉带一小段主动脉，肾静脉带一小段下腔静脉、输尿管末端带一直径约为0．5cm的膀胱瓣的供者手术方式；受者主动脉与供者主动脉、受者下腔静脉与供者下腔静脉进行端侧吻合，在受者膀胱上剪去一膀胱瓣与供者相同大小的圆瓣，然后进行一层膀胱吻合。结果 第一阶段为实验探索阶段，经过半年近150次的实验摸索，克服了移植物灌洗、血管吻合、膀胱吻合等技术难关，终于建立了比较稳定的大鼠同种异体肾移植模型。第二阶段为模型成熟阶段，冷热缺血时间、血管吻合的速度以及手术时间都比第一阶段有所缩短。手术成功率为85％左右，动物死亡的原因主要为血管吻合口出血、灌洗不良、休克、血栓形成以及膀胱漏尿致弥漫性腹膜炎等。结论 此模型容易掌握，可以在条件比较简单的实验室开展，除常规显微外科器械外不需要特殊的器械或设备。     

4-Aminopyridine induces the release of neuropeptide Y (NPY) to produce an atropine- and tetrodotoxin-resistant contraction in rabbit isolated jejunum

4-Aminopyridine (4-AP) induced an atropine- and tetrodotoxin (TTX)-insensitive contraction (resistant contraction), in a concentration-dependent manner, in the isolated jejunum of rabbits. The failure of specific antagonists of histamine, serotonin and substance P to affect this resistant contraction ruled out the participation of histamine, serotonin and/or substance P. Antiserum against neuropeptide Y (NPY) reduced this resistant contraction in a concentration-dependent manner and inhibited the action of 4-AP totally at a high concentration (1.25% dilution) whereas normal serum lacked this ability. This suggested that the release of NPY was involved in this 4-AP-induced resistant contraction. Radioimmunoassay of NPY-like immunoreactivity in isolated synaptosomal preparations indicated that 4-AP possessed the ability to induce the release of NPY. However, guanethidine did not affect the actions of 4-AP, indicating that NPY is released mainly from non-adrenergic nerves. Our results indicate that 4-AP induces the release of NPY from non-adrenergic nerves to produce an atropine- and TTX-resistant contraction in the isolated jejunum of rabbits.     

Monokines produced by macrophages stimulate the growth of osteoblasts

We have previously reported that the J774A.1 macrophage-like tumor cell line produces two potent monokines which stimulate the growth of osteoblasts and chondrocytes. These growth factors, which have an affinity for heparin-agarose, have been termed HEP I (a 30 Kd PDGF-like molecule) and HEP II (an approximately 20 Kd molecule), respectively, based on their elution profile. Unlike HEP I, HEP II does not stimulate the growth of fibroblasts. Extensive biological and chromatographic studies disclosed that HEP II appears to be a unique bone cell mitogen unlike any known growth factor, including the FGFs, IL-1s, and TNFs, EGF, IGF-I and -II, TGF-beta, beta 2 microglobulin, G-CSF, CSF-1 and GM-CSF. To characterize more fully the effects of the macrophage-derived monokines on osteoblast growth and function, clones were derived from calvaria explant cultures. Two clones, SDFRC-2.05 and SDFRC-3, were developed and found to exhibit osteoblastic characteristics, including high levels of alkaline phosphatase, synthesis of type I but not type III collagen, and an increased intracellular cAMP production in response to PTH. The SDFRC-3 cells exhibited a polygonal morphology like that of the explant-derived cells while SDFRC-2.05 cells exhibited a more fibroblastic morphology. When tested on the explant cultures and clones, HEP I and HEP II were found to stimulate DNA synthesis and increase protein per culture, but decreased alkaline phosphatase activity. Clone SDFRC-3 was found to be more responsive to HEP II than clone SDFRC-2.05. Both monokines were found to be more potent mitogens for bone cells than TGF-beta. HEP II, but not HEP I or TGF-beta, induced a transformation of bone cells from a polygonal to a fibroblastic morphology, suggesting the induction of migration prior to proliferation. Thus, macrophages may be responsible not only for bone repair but also for ensuring the linkage of bone formation to resorption during physiological remodeling.