颈椎病手术中脊髓损伤的原因及处理

目的探讨颈椎病术中脊髓损伤的原因及处理方法。方法我科2005年3月至2007年10月手术治疗279例颈椎病,对术中出现脊髓损伤的5例患者的临床资料进行回顾性分析。结果279例患者中5例发生脊髓损伤,发生率为1.79%。颈前路颈椎病手术中发生4例,后路单开门颈椎管扩大成形术中发生1例。经过清除血肿,甲基强的松龙等药物的及时治疗,5例患者逐渐恢复。结论颈椎病前、后路手术中均可能发生脊髓损伤,如能及时治疗,预后较好。     

结核分枝杆菌Rv1009基因蛋白的克隆和表达

目的 克隆表达结核分枝杆菌促Rv1009基因,序列测定正确后进行融合、表达.方法 采用热启动聚合酶链反应（Polymerase Chain Reaction,PCR）从结核分枝杆菌H37Rv基因组中扩增出Rv1009编码基因,用限制性内切酶消化后插入pGEX 4T-2载体中,将重组质粒转化大肠杆菌BL21（DE3）,目的基因经IPTG诱导,表达Rv1009基因蛋白.结果 经PCR扩增在1300bp处发现一条目的片段,获得了结核分枝杆菌H37Rv株Rv1009基因蛋白,经诱导后高效表达分子量为64KD的外源蛋白,与预期分子量大小一致,凝胶自动扫描分析,在A600值为0.6,IPTG终浓度为0.3 mmol/L,诱导表达3 h时融合蛋白表达量即达峰值,占菌体总蛋白的22.8%.结论 构建了结核分枝杆菌Rv1009基因重组表达载体,获得了RPF样融合蛋白的高效表达,为今后深入研究奠定了基础.     

Leukaemia Inhibitory Factor or Related Factors Promote the Differentiation of Neuronal and Astrocytic Precursors within the Developing Murine Spinal Cord

Previously we have shown that leukaemia inhibitory factor (LIF) potentiates the development of murine spinal cord neurons in vitro , suggesting that it, or related factors, may play an important regulatory role in neuronal development. We have further investigated this role and show here that the generation of neurons in cultures of embryonic day 10 spinal cord cells is inhibited by antibodies to the β subunit of the LIF receptor. Since there are more undifferentiated precursors in antibody-treated cultures than in control and LIF-treated cultures, it is concluded that the primary action of LIF, or related molecules, is to promote neuronal differentiation, not precursor survival. In addition, the failure of LIF to support neuronal survival in the period immediately following differentiation suggests that the increased numbers of neurons generated with LIF are not attributable to its neurotrophic action. By selecting neuronal precursors on the basis of their inability to express class I major histocompatibility complex molecules, it was shown that LIF acted directly upon these cells and not via an intermediary cell. LIF also appears to be involved in regulating the differentiation of astrocytes, since it increases the number of glial fibrillary protein (GFAP)-positive cells present in the cultures and since the spontaneous production of GFAP-positive cells is blocked by antibodies to the LIF β receptor. These findings suggest that LIF or related factors promote the differentiation of neural precursors in the spinal cord, but that they are not involved in preferentially promoting precursors down a specific differentiation pathway.     

脊髓血管畸形合并胸腔血管畸形

脊髓血管畸形的临床发病率较低,仅为颅内血管畸形或脊髓新生物的1/10左右.本病可能与其它组织的血管异常同时存在,如皮肤血管痣(Cobb综合征),皮肤、粘膜病变,和Klipple-Trenaunay-Weber综合征等.本文报告的与胸腔血管畸形同时存在的脊髓血管畸形,我们尚未见诸报道.本文还结合文献就脊髓血管畸形导致脊髓功能损害的病理生理作了阐述.     

Haemodynamic changes during spinal anaesthesia with slow continuous infusion or single dose of plain bupivacaine

Forty elderly patients, scheduled for orthopaedic surgery of the hip or knee were studied. Twenty patients received a single-dose spinal anaesthesia with 3 ml of plain 0.5% bupivacaine (SDSA group). Twenty patients received continuous spinal anaesthesia using a 32- or 22-gauge catheter. A bolus of 1.0 ml of plain 0.5% bupivacaine was given to ten patients and 0.5 ml to another ten, continued by an infusion at a rate of 2 ml/h. The spread of analgesia and haemodynamic changes (central venous pressure, arterial pressures, need for sympathomimetic medication) were registered. The mean dose of bupivacaine was 2.9 ml (range 1.5-5 ml) in the CSA group (3.0 ml in the SDSA group). Eight patients in the CSA group needed medication for pain during surgery compared to five patients in the SDSA group (n.s.). The median level of pinprick analgesia at 60 min was T11 in the CSA and T6.5 in the SDSA group (P less than 0.01). The mean maximum decreases in CVP and MAP were quite similar in the CSA and SDSA group (2.1 vs 2.8 mmHg (0.3 vs 0.4 kPa) and 17 vs 21 mmHg (2.3 vs 2.8 kPa), respectively) (n.s.). Six patients in the SDSA group and four patients in the CSA group needed sympathomimetic medication. It is concluded that titration of bupivacaine for spinal anaesthesia caused only minor haemodynamic changes which were similar to those after single-dose spinal bupivacaine.     

HBV、TB合并感染时抗TB治疗对肝功能的影响

目的:探讨乙型肝炎病毒(HBV)、结核(TB)杆菌合并感染时抗TB药物所致肝损伤的临床及组织学特点。方法:单纯TB感染者45例,TB合并HBV感染者35例,前4月均服用异烟肼、利福平、吡嗪酰胺、乙胺丁醇,后2月服用异烟肼、利福平。每2～4周复查肝功能、HBV标记物、T细胞亚群等指标,部分患者进行了肝穿刺病理检查。结果:TB HBV组肝功能异常发生率为34.3%,较单纯TB组高,发生时间较单纯TB组早半月,发生平均年龄小8岁;谷丙转氨酶水平、肝组织学炎症积分均较TB组高(P<0.05);肝功能异常者中80%为HBeAb阳性,T细胞免疫功能紊乱较重,CD4 细胞明显减少(P<0.05)。结论:HBV、TB合并感染时,抗TB药物的肝毒性增强,治疗过程中应及时复查肝功能。     

Diagnostic imaging of spinal cord lesions

Magnetic resonance imaging (MRI) has greatly facilitated morphologic evaluation of spinal cord lesions. Eleven cases representative of inflammatory, demyelinating, neoplastic and vascular diseases, are presented which illustrate and summarize important abnormal features in spinal cord imaging, particularly MR findings. Recently, specialised techniques such as MR angiography, fat-inhibiting methods, dynamic MRI and functional imaging have been developed. These methods have facilitated not only lesion diagnosis but also qualitative assessment, and are being used to analyze pathophysiology. Comprehensive diagnoses based on such modalities may be important in determining indications for surgery or defining the extent of surgery or the intensity of other treatments.     

Experimental study of spinal cord compression by epidural tumors using electron probe X-ray microanalysis and confocal laser scanning microscopy

Changes in the nerve fibers of the spinal cord were studied in rat experimental epidural tumor models. Light microscopy showed demyelinization in all with rats paraparesis and paraplegia. Cross-sectional views of nerve fibers stained with 3,3dipentyloxacarbo-cyanine iodide, obtained by confocal laser scanning microscopy, showed distorted, shrunken fibers with a low fluorescence intensity. Changes in the electrolyte contents of nerve fibers were studied by electron probe X-ray microanalysis. The K concentration in axons and the myelin sheath was increased in the paraparesis group, but was decreased in the paraplegia group. These findings suggest that, in the paraparesis group, compression of the spinal cord damaged cell membrane channels, which subsequently caused an increase in intracellular K, a decline in the action potential, and low-intensity fluorescence of nerve fibers. On the other hand, in the paraplegia group, destruction of cell membranes caused a decrease in intracellular K until it approached the extracellular level. This reduced both the action potential and the fluorescence intensity. As Ca and Mg concentrations in both axons and the myelin sheath increased in relation to the severity of neurologic damage, it appears that these electrolytes may also play an important role in damage to nerve fibers.