全髋关节置换者深静脉血栓形成早期血浆细胞因子及细胞间黏附分子的变化

目的：全髋关节置换者深静脉血栓形成是由内皮细胞损伤、血小板激活和凝血瀑布反应与抗凝、纤溶等机制共同作用的结果。了解全髋关节置换者深静脉血栓形成患者早期血浆炎症细胞因子表达以及细胞间黏附分子水平的变化，寻找相关预警指标。 方法：①实验对象：选择2005-05/2007-05在沈阳市第七人民医院骨科住院进行全髋关节置换术治疗患者77例，83 髋，男45例，女32例，年龄39~78岁，平均（65.09±18.74）岁。全部患者对全髋关节置换治疗知情同意，并自愿接受超声影像学检查以及各类实验室血清标本采集。施术者为同一组从事骨科临床工作≥ 7年的具有中级或副高级职称的骨科医生。②主要材料：全髋关节假体选用美国史赛克（中国）有限公司和北京普鲁复星外科植入物有限公司生产的APL非骨水泥柄和Muller骨水泥柄假体。材料采用精密锻造钛合金，表面用真空等离子钛或钛加羟基磷灰石喷涂，符合欧洲EN46001标准。③实验方法：入选对象均在全髋关节置换后1~7 d采用彩色多普勒超声检查下肢深静脉血流通畅情况。采用酶联免疫吸附法测定白细胞CD18的表达，放射免疫方法测定血清肿瘤坏死因子α、白细胞介素6 和白细胞介素10浓度。酶联免疫吸附法测定血浆可溶性细胞间黏附分子1和可溶性血管细胞间黏附分子1浓度。 结果：①全髋关节置换中，超声检查发现深静脉血栓26例（血栓组），未发现静脉血栓者51例（对照组）。②血栓组全髋关节置换后1 d和3 d肿瘤坏死因子α、白细胞介素6 和白细胞介素10炎症细胞因子表达指标明显高于对照组（P均 < 0.01~0.05）。③全髋关节置换后1 d和3 d时血栓组CD18、可溶性细胞间黏附分子1和可溶性血管细胞间黏附分子1表达明显高于对照组（P均 < 0.01~0.05）。 结论：全髋关节置换后深静脉血栓形成患者早期相关血浆炎症细胞因子表达增强，细胞间黏附分子浓度明显增高，这些表现可能与深静脉血栓形成发生有关。     

全髋关节置换后早期创伤局部引流血和循环血中的相关细胞因子水平

背景：对于全髋关节置换后创伤早期的应激阶段,创伤局部和全身细胞因子动态变化规律的研究还鲜见报道。 目的：观察全髋关节置换后早期无菌性炎症阶段创伤局部引流血和全身循环血中相关细胞因子水平的动态变化。 方法：选取行全髋关节置换患者9例,分别在关闭伤口时、置换后1,4和24 h采集静脉血样本以及创伤局部引流血液样本;采用酶联免疫吸附法分别测定血清中白细胞介素6,肿瘤坏死因子α,白细胞介素1β和白细胞介素17水平。 结果与结论：全髋关节置换后早期创伤局部引流血和循环血中白细胞介素6水平均明显升高,并且在各个时间点上创伤局部引流血中白细胞介素6水平均高于循环血(P < 0.05);置换后早期循环血中肿瘤坏死因子α水平明显升高,创伤局部引流血肿瘤坏死因子α的水平无明显变化,但仍高于循环血中的水平(P < 0.05);白细胞介素1β和白细胞介素17的水平在置换后无显著改变,且在创伤局部和循环中的含量无显著性差异。结果提示在全髋关节置换后急性无菌性炎症阶段,循环血中炎性细胞因子的水平不会直接反映局部的炎症反应。     

老年单侧全髋关节置换与下肢深静脉血栓形成

背景：下肢深静脉血栓形成是全髋关节置换患者围手术期严重的并发症,其发生率较高。目前尚不清楚原发病对老年全髋关节置换后下肢深静脉血栓形成的影响。 目的：观察不同原发病对老年全髋关节置换后下肢深静脉血栓形成的影响。 方法：选择单侧全髋关节置换患者147例,年龄64~93岁,根据原发病不同分为2组：骨折组68例,置换前经历了创伤,均为股骨颈骨折患者;骨病组79例,术前未经历过创伤。根据患者生理年龄、置换前社会活动能力、骨质情况、预期寿命等选择全髋假体,其中采用生物学假体5例,混合型假体12例,其他全部采用骨水泥型假体。对术后出现患肢肿胀和/或疼痛,下肢伴有或不伴有Homans征/ Neuhofs征阳性的患者常规应用加压超声技术进行超声多谱勒检查。 结果与结论：骨折组置换后32例出现患侧肢体肿胀,伴有疼痛者20例,出现Homans征/ Neuhofs征15例,经超声多普勒检查证实29例下肢下肢深静脉血栓形成阳性;股骨颈骨折后行全髋关节置换1例,无下肢深静脉血栓形成临床症状,于置换后17 d猝死,尸检证实为伤侧下肢混合型下肢深静脉血栓形成合并肺栓塞;骨病组置换后20例出现患侧肢体肿胀,伴有疼痛者11例,出现Homans征/ Neuhofs征9例,经超声多普勒检查证实20例下肢深静脉血栓形成阳性。股骨颈骨折患者比骨病组患者具有更高的血液凝固状态,下肢深静脉血栓形成发生率更高(P < 0.05)。提示股骨颈骨折是老年全髋关节置换后下肢深静脉血栓形成发生的高危因素。     

关节置换后血清白细胞介素 6，8，10及C-反应蛋白表达与深静脉血栓形成

背景：血管内皮细胞损伤、血流缓慢、血液高凝状态、白细胞流变特性异常是关节置换后深静脉血栓形成的重要因素。 目的：分析关节置换后血清白细胞介素 6,8,10、C-反应蛋白表达特点及与深静脉血栓形成的关系。 方法：检测68例关节置换患者置换前后血清白细胞介素6,8,10及C-反应蛋白浓度,并以超声检测确定是否有下肢深静脉血栓形成。 结果与结论：血栓形成组关节置换后1,3 d白细胞介素6,8,10、C-反应蛋白质量浓度明显高于无血栓组(P < 0.05),说明炎症因子参与了血栓形成,及时监测上述指标变化有助于预防血栓形成;血栓形成组置换后1,3 d白细胞介素6,8,10、C-反应蛋白质量浓度明显高于置换前1 d(P < 0.05),置换后5 d上述指标基本接近置换前水平(P > 0.05)。说明关节置换后血液由高凝状态逐渐降低的过程,尤其是置换后3 d是抗炎抗凝治疗的关键。     

全髋关节置换后深静脉血栓栓塞与APACHEⅡ评分：98例资料回顾

背景：全髋关节置换后发生深静脉血栓栓塞的发生存在多种危险因素,且涉及多个临床学科,目前尚缺乏系统、可靠的评分预测系统。但临床上早期可以通过深静脉多普勒超声来判断其发生情况。急性生理学与慢性健康评定标准(APACHEⅡ)在国内外已被广泛用于对ICU危重患者病情严重程度的分析和预后评估。 目的：评价APACHEⅡ评分与全髋关节置换后深静脉血栓栓塞的相关性。 方法：回顾性分析2000/2005解放军401医院全髋关节置换病例98例(106髋)的动态APACHEⅡ评分,包括置换前、发生深静脉血栓时及出现肺栓塞时,比较深静脉血栓栓塞症发生组与未发生组的APACHEⅡ评分差异,以及深静脉血栓栓塞症患者中发生肺栓塞组与未发生肺栓塞组的APACHEⅡ评分差异。 结果与结论：发生深静脉血栓栓塞症组与未发生深静脉血栓栓塞症组置换前APACHEⅡ评分差异无显著性意义(P > 0.05)。深静脉血栓栓塞症患者中肺栓塞组APACHEⅡ评分明显高于未发生肺栓塞组(P < 0.05)。提示APACHEⅡ评分与早期深静脉血栓栓塞症的发生无明显相关性;但深静脉血栓栓塞症发生后,APACHEⅡ评分与肺栓塞发生有相关性,且APACHEⅡ评分分值越高,肺栓塞发生风险越大。     

体外循环状态下血液肿瘤坏死因子α、白细胞介素８、白细胞介素１０水平的变化★

目的：心脏移植、心脏直视手术过程中的体外循环状态可导致各种炎症介质含量升高，强烈的炎症反应可引起肺损伤。肺开放策略可改善体外循环后肺损伤，观察肺开放策略对体外循环术后呼吸功能及肿瘤坏死因子α、白细胞介素8、白细胞介素10水平的影响。 方法：①选择2005-10/2007-10于南通大学第二附属医院心胸外科在全麻、低温、体外循环下行心内直视手术的患者60例，所有患者对实验及治疗方案均知情同意。②将60例患者按随机数字表法分为常规机械通气组、早期肺开放组及晚期肺开放组，每组20例。早期肺开放组在气管插管后实施肺开放策略，晚期肺开放组到达ICU后30 min实施肺开放策略。③应用酶联免疫吸附反应技术于术前、体外循环后及到达ICU后3，5，24，48 h测定血清肿瘤坏死因子α、白细胞介素8、白细胞介素10水平。 结果：患者60例全部进入结果分析。①体外循环后各组患者血清肿瘤坏死因子α、白细胞介素8、白细胞介素10水平均较术前显著升高（P < 0.01）。②体外循环后早期肺开放组肿瘤坏死因子α水平上升幅度低于晚期肺开放、常规机械通气组（P < 0.01）；体外循环后早期肺开放组肿瘤坏死因子α水平逐渐下降，晚期肺开放、常规机械通气组肿瘤坏死因子α水平进一步上升。③血清白细胞介素8水平在期肺开放组、晚期肺开放组呈下降趋势，但常规机械通气组血清白细胞介素8水平各时点均高于术前（P < 0.01）。④白细胞介素10水平只在早期肺开放组呈下降趋势。 结论：肺开放策略可减少体外循环后炎性细胞因子的释放，从而减轻体外循环相关肺损伤，早期实施肺开放策略优于晚期实施。     

人工髋关节置换后的深静脉血栓形成：发生因素及其预防策略

目的：近年来有关人工髋关节置换后深静脉血栓形成的研究很多。文章总结人工髋关节置换后深静脉血栓形成的因素及预防措施。 方法：由第一作者应用计算机检索维普数据库(http://www.cqvip.com/)与髋关节置换后深静脉血栓发生有关的文献，检索时限为1994-01/2009-10。检索关键词：髋关节置换，深静脉血栓。纳入标准：①髋关节置换后深静脉血栓形成因素。②深静脉血栓形成的诊断标准及诊断方法。③预防人工髋关节置换后深静脉血栓发生的措施。排除标准：重复研究或较陈旧文章。依据纳入排除标准共保留相关文献25篇。 结果: 目前国内外对于人工髋关节置换后下肢深静脉血栓形成的发病机制与危险因素基本已达成一致意见，发病机制主要有：血液高凝状态、静脉血流缓慢(或郁滞)、血管壁的损伤。高龄、心脑血管病、静脉曲张或静脉手术是并发深静脉血栓的危险因素。人工髋关节置换后深静脉血栓的预防性治疗主要有机械性和药物性预防两种方法，机械性疗法无药物不良反应，易被患者接受，但对高风险患者治疗效果尚不能肯定，需结合药物预防性治疗以获得较确切的治疗效果。低分子肝素已成为人们预防术后深静脉血栓形成的首选药物，是目前最常用、效果最可靠的手段。 结论：对人工关节置换后深静脉血栓的影响因素和预防性治疗已受到医务界的极大关注，掌握人工髋关节置换后发生深静脉血栓的发生机制、相关因素以及预防措施等知识，对降低深静脉血栓的发生率有重要意义。     

红霉素、阿仑膦酸钠抑制磨损颗粒对小鼠巨噬细胞分泌白细胞介素1，6及肿瘤坏死因子α的影响*

背景：阿仑膦酸钠的抗骨吸收作用是通过其对破骨细胞的抑制作用完成的,近年亦有报道证实红霉素有直接抑制破骨细胞的作用。 目的：观察阿仑膦酸钠和红霉素抑制钛颗粒刺激巨噬细胞分泌肿瘤坏死因子α、白细胞介素1,6的作用。 方法：分离、培养小鼠腹腔巨噬细胞,14 h后分为红霉素组及阿仑膦酸钠组,每组分为6个亚组。红霉素组：A组：仅为巨噬细胞;B组：巨噬细胞+钛颗粒;C组：巨噬细胞+钛颗粒+红霉素1 μg/L;D组：巨噬细胞+钛颗粒+红霉素10 μg/L;E组：巨噬细胞+钛颗粒+红霉素100 μg/L;F组：巨噬细胞+钛颗粒+红霉素1 000 μg/L。阿仑膦酸钠组分组及剂量同红霉素组。培养24 h后,用酶联免疫法检测细胞培养上清液中白细胞介素1,6及肿瘤坏死因子α的质量浓度。 结果与结论：B组白细胞介素1,6及肿瘤坏死因子α的质量浓度明显高于其他组(P < 0.05),F组白细胞介素1,6及肿瘤坏死因子α的质量浓度明显低于C组(P < 0.05)。同剂量阿仑膦酸钠和红霉素组间差异无显著性意义(P > 0.05)。提示钛颗粒可以刺激巨噬细胞分泌大量的白细胞介素1,6及肿瘤坏死因子α,红霉素、阿仑膦酸钠能够呈剂量依赖型地有效抑制钛颗粒诱导的巨噬细胞分泌白细胞介素1,6及肿瘤坏死因子α。     

复合组织及血清肿瘤坏死因子α、白细胞介素10表达与大鼠喉移植急性排斥反应的相关性

背景：喉移植后致炎细胞因子(肿瘤坏死因子α、γ-干扰素等)和抗炎细胞因子(白细胞介素10、白细胞介素4等)之间的相互作用会发生哪些变化呢？ 目的：观察肿瘤坏死因子α、白细胞介素10在大鼠喉移植急性排斥反应期移植喉组织的不同部位和血清中的表达变化,评价其血清水平在预测急性排斥反应中的作用。 方法：进行Wistar→SD大鼠喉移植,移植后依照注射环孢霉素A剂量不同随机分为3组：0 mg组、5 mg组及10 mg组,以未进行喉移植的SD大鼠为正常对照组。 结果与结论：各组移植后第3,7,11天肿瘤坏死因子α、白细胞介素10血清浓度的变化与移植后各相应时间点黏膜上皮及黏膜下层组织中其表达水平的变化均呈正相关。提示,供体喉的高抗原性主要集中于喉的黏膜上皮层及黏膜下层组织;血清肿瘤坏死因子α和白细胞介素10的浓度可以作为预测喉移植术后急性排斥反应的指标。     

全髋置换后深静脉血栓的预防

目的：比较低分子肝素和吲哚美辛对预防全髋置换后深静脉血栓发生的疗效。 方法：选择北京世纪坛医院骨科收治的股骨头无菌坏死患者120例,男62例,女58例,年龄38~82岁,平均66.9岁;均计划行全髋置换。全部患者随机分为3组,对照组(n=41)：没有接受抗凝预防治疗;低分子肝素组(n=40)：接受低分子肝素治疗,以患者的体质量计算,给予皮下注射范围1 900~3 800 U/d;吲哚美辛组(n=39)：接受吲哚美辛治疗,剂量为 2次/d,口服25 mg/次,均从置换前1 d至出院当天。对比观察各组患者全髋置换后深静脉血栓的发生情况。 结果：120例患者在全髋置换后第1周行彩色多普勒超声检查,发现65例患者有深静脉血栓(54%),其中18例深静脉血栓发生在非手术侧肢体。在手术侧肢体发生深静脉血栓的患者中18例有临床症状(28%),在非手术侧肢体发生深静脉血栓的患者均未见临床症状。对照组深静脉血栓的发生率为71%,明显高于低分子肝素组48%和吲哚美辛组45%(P < 0.05)。 结论：全髋置换前应用低分子肝素或吲哚美辛明显降低了深静脉血栓发生。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -