Red cell loss following orthopedic surgery: the case against postoperative blood salvage

BACKGROUND: Expensive devices have been developed for the collection and transfusion of blood salvaged after hip or knee arthroplasty. STUDY DESIGN AND METHODS: The volume of salvaged red cells was measured for the first 6 hours after operation. This volume was compared to total red cell loss during hospitalization and to the volume of allogeneic red cells transfused. RESULTS: Mean postoperative red cell loss in 31 patients following hip replacement was 55 +/− 29 mL and that in 20 patients following knee replacement was 121 +/− 50 mL. The 6-hour wound drainage represented 8.7 and 16.8 percent of overall red cell loss during hospitalization for hip and knee replacement, respectively. The transfusion of postoperatively salvaged red cells would have supplanted transfusion of less than one-third of a unit of allogenic blood after hip replacement and two-thirds of a unit after knee replacement. Only three patients (5.9%) lost red cell volume in the drainage equivalent to or in excess of 1 unit of red cells (180 mL). The volume of red cells salvaged postoperatively bore no relationship to perioperative red cell losses as a whole. CONCLUSION: The relatively small red cell loss in the postoperative period in most arthroplasty patients does not appear to justify the routine use of this technique for the recovery of autologous blood.     

脂多糖诱导体外培养骨骼肌卫星细胞表达肝细胞生长因子的变化

目的:研究证实,在众多生长因子中,肝细胞生长因子无论在体外还是体内都可以激活静止状态的肌卫星细胞,修复受损肌肉。采用脂多糖刺激体外培养的骨骼肌卫星细胞,观察肌卫星细胞产生肝细胞生长因子以及肌卫星细胞增殖分化的变化。方法:实验于2006-07/2007-05在华中科技大学同济医学院同济医院创伤外科实验室完成。①实验材料:健康SD成年雄性大鼠,体质量150～200g,由华中科技大学同济医学院实验动物中心提供。实验过程中对动物处置符合实验动物伦理学标准。②实验方法:分离SD大鼠后肢部分股四头肌肉进行骨骼肌卫星细胞的培养。取第2代细胞爬片,待细胞增殖到80%密度时,丙酮固定细胞,常规处理后进行α-sarcometricactin细胞免疫化学染色鉴定,以成纤维细胞作为阴性对照。取第3代骨骼肌卫星细胞,应用0,5,10,20mg/L脂多糖刺激体外培养的大鼠骨骼肌卫星细胞,采用ELISA方法测细胞培养液中的肝细胞生长因子的浓度。取第4代骨骼肌卫星细胞,用含体积分数为0.10胎牛血清的培养基配制成单个细胞悬液,调整浓度为5×107L-1,分成两组,一组加入10mg/L脂多糖,另一组不加任何干预。采用噻唑蓝(MTT)法测定卫星细胞的增殖率。结果:①以未经脂多糖处理的无血清培养基培养的肌肉卫星细胞培养液为对照,将对照组和5,10,20mg/L脂多糖处理组比较,各实验组肝细胞生长因子浓度明显高于对照组(P<0.05)。②5,10,20mg/L脂多糖刺激骨骼肌卫星细胞分泌的肝细胞生长因子水平差异无显著性。③肝细胞生长因子在脂多糖刺激后36h分泌浓度最高。④脂多糖刺激肌卫星细胞的增殖分化明显高于未经刺激的肌卫星细胞。结论:①脂多糖可诱导骨骼肌卫星细胞自分泌肝细胞生长因子。②不同质量浓度脂多糖培养基中肝细胞生长因子水平差异无统计学意义。③脂多糖具有促进骨骼肌卫星细胞增殖分化的效应。     

大肠癌免疫组化表达与临床病理的关系

目的:探讨大肠癌CEA、P53、nm23、Ki-67、MRP免疫组化表达特点和相互关系,及其与临床病理的关系．方法:回顾性分析2003-01／2006-07我院收治的73例大肠癌患者的临床病理及随访资料,并对其石蜡标本采用免疫组化SP染色法检测CEA、P53、nm23、Ki-67、MRP,分析其免疫组化特点及其与临床病理之间的关系．结果:CEA、P53、nm23、Ki-67、MRP在大肠癌中的阳性表达率依次为82．2％、68．5％、75.3％、84．9％和64．4％．CEA、MRP与大肠癌患者的各因素无统计学差异．P53、Ki-67和nm23与肿瘤的Dukes分期和淋巴结转移有关, P53、Ki-67在Dukes C、D期的阳性表达率(依次为82．8％和100％1明显高于Dukes A、B期者(59．1％和75．0％)(P<0．05),而nm23在Dukes C、D期的阳性表达率(58．6％)明显低于Dukes A、B期者(86．4％)(P<0．05)．CEA与nm23的表达呈明显的负相关(r=-0．296,P=0．011),而P53和Ki-67表达之间呈现明显的正相关(r= 0．308,P=0．008),其他各指标间的表达无相关性．nm23、P53和Ki-67与预后因素关系明显,nm23在生存期≥3 a患者的阳性表达率(92．9%)高于生存期<3 a者(71．2％)(P<0．05),而P53和Ki-67在生存期≥3 a患者的阳性表达率(依次为42．9％和64.3％)明显低于生存期<3 a者(74．6％和89．8％)(P<0．05)．结论:P53、Ki-67和nm23的表达与大肠癌的侵袭转移和预后密切相关．CEA可能是大肠癌的侵袭转移的促进因素．MRP所引起的耐药机制是一个相对独立的机制．CEA、P53、nm23、Ki-67可作为判断大肠癌恶性程度、侵袭转移以及预后的指标．     

Extracellular matrix of cultured bovine aortic endothelial cells contains functionally active type 1 plasminogen activator inhibitor

The extracellular matrix (ECM) of cultured bovine aortic endothelial cells (BAEs) was analyzed by immunoblotting and reverse fibrin autography and shown to contain type 1 plasminogen activator inhibitor (PAI-1). Most PAI-1 in the ECM formed complexes with exogenously added tissue-type plasminogen activator (tPA), demonstrating that this PAI-1 was functionally active. The resulting tPA/PAI-1 complexes were recovered in the reaction solution, indicating that the PAI-1 in such complexes no longer bound to ECM. The PAI-1 could not be removed by incubating ECM in high salt (2 mol/L NaCl), sugars (1 mol/L galactose, 1 mol/L mannose), glycosaminoglycans (10 mmol/L heparin, 10 mmol/L dermatan sulfate), or epsilon-aminocaproic acid (0.1 mol/L). However, PAI-1 could be extracted from ECM by treatment with either arginine (0.5 mol/L) or potassium thiocyanate (2 mol/L), or by incubation under acidic conditions (pH 2.5). ECM depleted of PAI-1 by acid extraction was able to bind both the active and latent forms of PAI-1. In this instance, most of the bound PAI-1 did not form complexes with tPA, indicating that the latent form was not activated as a consequence of binding to ECM. Although the PAI-1 activity in conditioned medium decayed with a half-life (t 1/2) of less than 3 hours, the t 1/2 of ECM- associated PAI-1 was greater than 24 hours. These data suggest that PAI- 1 is produced by cultured BAEs in an active form and is then either released into the medium where it is rapidly inactivated or into the subendothelium where it binds to ECM. The specific binding of PAI-1 to ECM protects it from this inactivation.     

Familial hemiplegic migraine: a clinical comparison of families linked and unlinked to chromosome 19

We compared the clinical characteristics of 50 patients from three unrelated families with familial hemiplegic migraine (FHM) linked to chromosome 19, with those of 20 patients from two families with FHM not linked to chromosome 19. We found no significant differences for age at onset, frequency and duration of attacks, duration of the paresis, and occurrence of basilar migraine symptoms. In the linked families, significantly more patients reported unconsciousness during attacks (39%, vs 15%; p<0.05) and provocation of attacks by mild head trauma (70% vs 40%; p< 0.05). In one linked family patients also displayed chronic progressive cerebellar ataxia, whereas in one unlinked family benign infantile convulsions occurred in addition to FHM. Interestingly, so far an association with cerebellar ataxia was only described in chromosome 19-linked families. FHM linked to chromosome 19 and FHM unlinked to chromosome 19 do not differ with respect to clinical features.     

Defective opsonization in multiple myeloma

The mechanisms responsible for the unusual susceptibility of multiple myeloma (MM) patients to infections are incompletely defined. Since MM is associated with decreased production of normal serum proteins, we investigated the possibility that the production of opsonins might also be impaired. The neutrophil chemiluminescence assay of opsonization was used to evaluate the ability of serum from patients with MM to opsonize zymosan. It was found that sera from 18 MM patients exerted only 50% +/- 2.5% (mean +/- SEM) of the opsonic activity found in 18 control sera (p less than 0.001). In mixture experiments, untreated normal serum completely restored the opsonic activity of MM serum, suggesting a deficiency of opsonic factors rather than an inhibitor. In other mixture experiments, heat-inactivated normal serum only partially corrected the opsonic defect in MM serum. Serum from three patients had low C3 levels, and treatment of particles with these resulted in a greater opsonic defect than the patient population as a whole (p less than 0.02). No correlation between the opsonic defect and infections was established over an 18-mo period. These data suggest that MM serum lacks both heat-stable and heat-labile opsonic activity, the direct clinical significance of which remains to be clarified. However, these studies support the concept that defective host resistance in MM may be multifactoral, combining opsonic abnormalities with other defects previously described.     

Proximal femoral focal deficiency: radiologic analysis of 49 cases

Proximal femoral focal deficiency, an uncommon congenital anomaly, necessitates early radiologic classification for surgical planning and treatment. Objective radiographic criteria, including femoral length index, acetabular depth index, acetabular angle index, and shape of the proximal femur were determined in 49 patients before cartilaginous ossification of the femoral capital epiphysis; final classification was based on follow-up radiographs or findings at arthrography or surgery. These parameters were analyzed to determine the accuracy and contributions of each in classification. Correct classification into one of three groups was possible in 86% of cases with use of three of the parameters: femoral length index, acetabular depth index, and shape of the proximal femur. The acetabular angle was found to contribute insignificantly to classification. Magnetic resonance imaging, used in only one case, depicted the nonossified cartilaginous femoral capital epiphysis, thus obviating the need for invasive diagnostic procedures and facilitating early classification.