稀释药物时抽吸无菌空气的研究

在同一治疗室内，分别采集密封无菌空瓶中、酒精灯蓝色火焰中和治疗室内空气，将以上三种空气分别注入无菌的１０％葡萄糖注射液中，在其滴注的不同时间作细菌培养；又将抽吸的这三种空气分别注入无菌的１０％葡萄糖注射液中，再各抽出无菌溶液稀释药物，将稀释药物与１０％葡萄糖注射液配伍后，在其滴注的不同时间作细菌培养。结果表明，密封无菌空瓶中、酒精灯蓝色火焰中抽吸的空气所稀释药物无细菌生氏；而治疗室内抽吸的空气稀释药物有细菌生长。提示：稀释药物抽吸空气应在密封无菌空瓶中采集；并在稀释药物过程中将此空气保留在无菌注射器针筒内再使用。     

中药治疗354例成人股骨头无菌性坏死

根据临床及 x 线表现,结合骨功能检查,按 Flcet 分类法,将成人股骨头无菌性坏死分型、分期。突出肾主骨理论,进行中医辨证分型,结合病因病机拟治则及处方用药。全部采用保守疗法。随访354例患者,治愈率59.89%,显效率29.37%,好转率5.93%,无效率4.80%。作者提出中药可激活坏死的骨质,使塌陷的股骨头修复,展示中药治疗此病的优越性。     

The interaction of the macrophage and the osteoblast in the pathophysiology of aseptic loosening of joint replacements

Macrophage phagocytosis of cement particles with production of inflammatory mediators is a component of the underlying mechanism of aseptic loosening of joint prostheses. Prostaglandin E₂ (PGE₂), a bone resorbing mediator, has been implicated in the loosening process. Investigations have shown that macrophage phagocytosis of cement particles leads to production of bone-resorbing mediators other than PGE₂. In this study, conditioned medium from macrophages exposed to crushed simplex cement particles stimulated osteoblasts to release radiolabeled arachidonic acid and metabolites. Incubation of osteoblasts in conditioned medium from macrophages exposed to cement particles small enough to be phagocytized increased PGE₂ release 80-fold over unexposed osteoblasts (P<0.001). Incubation of osteoblasts in conditioned medium from macrophages exposed to particles too large to be phagocytized, or to bone cement filtrate, did not stimulate PGE₂ release. We propose that the role of the macrophage in aseptic loosening is primarily to recognize the mechanical failure of the cement mantle by phagocytosis of cement particles and subsequent production of small amounts of specific mediators. These mediators stimulate surrounding osteoblasts to secrete PGE₂, which then amplifies the inflammatory response and ultimately results in bone resorption and aseptic loosening.     

Perspectives: Applications of a biomechanical model of the endochondral ossification mechanism

A biomechanical model of endochondral ossification (Frost and Jee, 1994. Anat. Rec., 240:435–446) can help to explain: (1) some differences in fracture patterns in children and adults, (2) increased fractures during the human adolescent growth spurt, (3) localization of stress fractures and pseudofractures to cortical instead of trabecular bone, (4) increased bone mass in adult-acquired and childhood obesity, (5) subchondral bone densification and osteopenia in some arthroses, (6) why and where mammals lose spongiosa with aging, (7) why, as percents of the original bone stock, metaphyseal trabecular bone losses with aging usually exceed cortical bone losses, (8) why osteochondritis dissecans and aseptic necroses of bone localize in epiphyses instead of metaphyses, (9) some features of growth plate histology in rickets and the chondrodystrophies, (10) why spontaneous fractures in osteoporotic patients affect vertebral more than metaphyseal spongiosa, (11) why osteopenias develop in most chronic, debilitating diseases, and (12) why histomorphometric values can differ in iliac bone biopsies obtained by the “vertical” Jamshidi and “horizontal” Bordier-Meunier techniques. © 1994 Wiley-Liss, Inc.     

Lymphocytic choriomeningitis in Michigan

We summarize the first reported case of acquired lymphocytic choriomeningitis virus (LCMV) infection in Michigan to be investigated by public health authorities and provide evidence of the focal nature of LCMV infection in domestic rodents. Results of serologic and virologic testing in rodents contrasted, and negative serologic test results should be confirmed by tissue testing.     

人工关节无菌性松动动物模型中EphB4-EphrinB2的表达

目的：建立并评价聚甲基丙烯酸甲酯（PMMA）微粒诱导的小鼠air-pouch人工关节无菌性松动模型,并且分析核激活因子受体配体（RANKL）与EphB4-EphrinB2在此模型中表达及意义。方法：在10周大小的雌性近交系BALB／c小鼠背部皮下单点注射无菌空气形成气囊,后将气囊中植入同种系小鼠颅骨骨片。术后实验组和对照组小鼠气囊内分别注射PMMA微粒溶液和生理盐水,15d后处死小鼠,将气囊和植入颅骨骨片一并取出,进行组织学观察。并行RANKL及EphB4-EphrinB2免疫组化检测。结果：HE染色实验组标本囊壁增厚、炎性细胞浸润增多,颅骨表面有明显的骨吸收;免疫组化显示实验组中RANKL的表达增高,EphrinB2-EphB4的表达降低。结论：小鼠air—pouch模型能方便、经济、有效的模拟人工关节松动的病理过程;实验组中RANKL的高表达显示骨溶解效应增强,EphB4-EphrinB2双向信号蛋白的低表达显示骨形成作用被抑制,验证了骨稳态的失衡是导致关节松动发生的重要机制。     

金属离子对成骨细胞凋亡、细胞周期分布及ALP分泌的影响

目的金属磨损产物对人工关节的无菌性松动有影响,通过观察Co2+、Cr3+对小鼠成骨细胞凋亡、细胞周期以及在离子刺激下对成骨细胞分泌ALP的影响,为防治人工关节置换术后假体周围骨溶解提供实验依据。方法体外培养小鼠颅骨成骨细胞MC3T3-E1至第3～5代,调整细胞密度至5×105个/mL,根据干预方法不同将细胞分为两组。实验组:成骨细胞于含10%FBS的α-MEM培养基中培养,待细胞完全贴壁后,加入CoCl2与CrCl3混合溶液;对照组:成骨细胞于含10%FBS的α-MEM培养基中培养。于培养12、24、48h后,采用流式细胞仪检测细胞凋亡率及周期分布,ELISA法检测培养上清液中ALP含量。结果培养12、24、48h,实验组凋亡率分别为13.90%±0.52%、14.80%±0.41%、13.40%±0.26%,对照组分别为8.56%±0.31%、8.19%±0.24%、2.15%±0.11%,差异均有统计学意义(P<0.05)。各时间点实验组细胞G2M期分布比例明显较对照组降低,G0G1期分布比例较对照组增多,差异均有统计学意义(P<0.05)。培养12、24、48h,实验组ALP含量检测吸光度(A)值分别为0.955±0.052、0.624±0.041、0.498±0.026,对照组分别为1.664±0.041、1.986±0.024、2.192±0.041,两组比较差异均有统计学意义(P<0.05)。结论 Co2+、Cr3+对成骨细胞的细胞周期分布有明显影响,抑制其增殖,使细胞大部分处于G0G1期,同时增加其凋亡率,抑制成骨细胞释放ALP。     

肿瘤型假体无菌性松动翻修术后疗效观察

目的探讨采用普通长柄假体或同种异体骨假体复合物(allograft-prosthesis composite,APC)翻修治疗肿瘤型假体无菌性松动的疗效。方法 2002年1月-2008年6月,收治14例肿瘤型假体无菌性松动患者。男8例,女6例;年龄21～70岁,平均43.9岁。肿瘤部位:股骨远端8例,股骨近端2例,胫骨近端4例。假体置换术后6～31年出现患肢疼痛,负重和行走时加重;6例出现患肢短缩畸形。术前参照美国骨与软组织肿瘤协会(MSTS)功能评分系统行关节功能评分为(16.36±1.50)分。X线片检查见假体明显松动和下沉。出现症状至入院时间为3～9年,平均4.5年。7例骨量严重丢失(骨皮质厚度减少>50%)、假体下沉>2 cm、假体穿破骨皮质或即将穿破骨皮质者采用APC翻修;7例骨量丢失不严重(骨皮质厚度减少<50%)者,采用订制普通长柄假体翻修。结果患者切口均Ⅰ期愈合;2例出现腓总神经一过性麻木,对症治疗后3个月内恢复。患者术后均获随访,随访时间2年2个月～7年,平均3.6年。翻修术后患者术前疼痛症状均缓解,关节功能改善。术后12个月MSTS功能评分为(23.43±2.56)分,与术前比较差异有统计学意义(t=8.910,P=0.024)。X线片检查示,术后12个月2例采用普通长柄假体翻修患者出现骨水泥周围无症状透亮线,无假体松动和周围感染等并发症;其余患者未见明显异常。结论肿瘤型假体无菌性松动后再次行翻修重建肢体功能可行,根据患者骨量丢失情况选择APC或普通长柄假体翻修,可获较好疗效。     

Aseptic meningitis and ischemic stroke in relapsing polychondritis

Relapsing polychondritis (RP) is a rare disease characterized by recurrent inflammation of cartilaginous structures. Its involvement of central nervous system is uncommon. We report the case of a 71-year-old woman whose initial manifestations were RP and meningitis and whose subsequent attack of RP was associated with a left cerebral infarction. The patient responded to steroid therapy in both attacks of RP.     

一株引起无菌性脑膜脑炎柯萨奇B组3型病毒的分离和VP1基因分析

目的对一株从无菌性脑膜脑炎患者中分离到的柯萨奇B组3型病毒(coxsackie virus B3,CVB3)分离株KMA103-09进行VP1区的基因特征分析。方法采用Hep-2、RD细胞对患者粪便标本进行病毒分离,肠道病毒组合血清进行鉴别,反转录-聚合酶链反应(RT-PCR)扩增病毒目的片段,测序后进行VP1基因分析,用Mega4.1等软件分析处理。结果肠道病毒组合血清鉴别为柯萨奇病毒B组3型(Cox.B3),从病毒性脑膜脑炎患者粪便标本中,分离到CVB3,其VP1区的核苷酸长度为849bp,未发现核苷酸插入与丢失。与山东04433/SD/CHN/2004/CB3株、山东05280/SD/CHN/2005/CB3株及山东YZ127/SD/CHN/2005/CB3株氨基酸同源,与其余国内分离株同源性高于为99.29%,与国外毒株的同源性为95.41%~96.47%。在进化树上与AM06HZ/SD/CHN/2006/CB3株显示在同一个分支上。结论分离的肠道病毒为柯萨奇病毒B组3型(Cox.B3),分离株(KMA103-09)VP1区变异较小。