健脾补肾方增加β-catenin、Runx2表达而促进骨质疏松性骨折愈合的疗效观察

目的研究健脾补肾方促进骨质疏松性骨折愈合的疗效机制,探讨"脾肾相关"、"先后天之本"中医理论在骨质疏松性骨折防治中的运用。方法建立去卵巢骨质疏松性骨折小鼠模型,随机分为7、14、28d 3个时间点,每个时间点分生理盐水、健脾补肾方2组。于骨折术后第2天给予相应药物灌胃治疗,分别于治疗3个时间点后处死小鼠,取材,进行影像学观察和病理组织学染色。结果 X-ray、Micro-CT结果显示,健脾补肾组7、14、28d均可促进骨痂形成及骨折愈合;Micro-CT定量分析显示,健脾补肾组7、14d骨痂BV/TV、Conn.D、mean/density of TV、mean/density of BV均明显高于生理盐水组(P0.05);有限元分析结果提示,健脾补肾组28d骨折部位刚度、弹性模量结果均高于生理盐水组(P0.05);HE染色、ABH/OG染色结果显示,健脾补肾方可以促进骨折部位早、中期膜内成骨和软骨内成骨,加速骨折愈合;免疫组化染色结果显示,健脾补肾方能增加骨痂部位β-catenin、Runx2的表达,促进骨折愈合。结论健脾补肾方可以促进骨质疏松性骨折的愈合,其机制可能与增加β-catenin、Runx2的表达相关。     

Charcot-Marie-Tooth病患者血清PMP22抗体、IL-6和TNF-α水平的研究

目的检测Charcot-Marie-Tooth(CMT)病患者血清周围髓鞘蛋白22(PMP22)抗体、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平,以探讨是否有免疫学机制参与CMT的病理生理过程。方法以人工合成PMP22胞外片段作为多肽抗原,用双抗体酶标法检测9名CMT1A患者和7名CMTX1患者血清PMP22抗体,同时检测IL-6和TNF-α水平;11名吉兰-巴雷综合征(GBS)患者和20名性别、年龄相匹配的正常人作对照。结果55.6%CMT1A患者和57.1%CMTX1患者PMP22抗体阳性,63.6%GBS患者和10%正常对照PMP22抗体阳性。正常对照组和CMT患者血清IL-6和TNF-α水平差异无统计学意义(P>0.05)。结论CMT1A患者PMP22抗体阳性与性别、年龄和病程均无关,但在CMTX1家系中,该抗体与性别相关(男性患者阳性),这可能是导致CMTX1家系中男性患者临床症状明显重于女性患者的原因之一。在CMT1A中,PMP22抗体的存在可能是对神经损伤的继发性反应而不是原发性病理过程,在CMTX1家系中存在继发性的免疫过程。此症可能不存在细胞因子介导的免疫损害。     

The lipoprotein-associated coagulation inhibitor that inhibits the factor VII-tissue factor complex also inhibits factor Xa: insight into its possible mechanism of action

Blood coagulation is initiated when plasma factor VII(a) binds to its essential cofactor tissue factor (TF) and proteolytically activates factors X and IX. Progressive inhibition of TF activity occurs upon its addition to plasma. This process is reversible and requires the presence of VII(a), catalytically active Xa, Ca2+, and another component that appears to be associated with the lipoproteins in plasma, a lipoprotein-associated coagulation inhibitor (LACI). A protein, LACI(HG2), possessing the same inhibitory properties as LACI, has recently been isolated from the conditioned media of cultured human liver cells (HepG2). Rabbit antisera raised against a synthetic peptide based on the N-terminal sequence of LACI(HG2) and purified IgG from a rabbit immunized with intact LACI(HG2) inhibit the LACI activity in human serum. In a reaction mixture containing VIIa, Xa, Ca2+, and purified LACI(HG2), the apparent half-life (t1/2) for TF activity was 20 seconds. The presence of heparin accelerated the initial rate of inhibition threefold. Antithrombin III alpha alone had no effect, but antithrombin III alpha with heparin abrogated the TF inhibition. LACI(HG2) also inhibited Xa with an apparent t1/2 of 50 seconds. Heparin enhanced the rate of Xa inhibition 2.5-fold, whereas phospholipids and Ca2+ slowed the reaction 2.5-fold. Xa inhibition was demonstrable with both chromogenic substrate (S-2222) and bioassays, but no complex between Xa and LACI(HG2) could be visualized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Nondenaturing PAGE, however, showed that LACI(HG2) bound to Xa but not to X or Xa inactivated by diisopropyl fluorophosphate. Thus, LACI(HG2) appears to bind to Xa at or near its active site. Bovine factor Xa lacking its gamma-carboxyglutamic acid-containing domain, BXa(-GD), through treatment with alpha-chymotrypsin, was used to further investigate the Xa requirement for VIIa/TF inhibition by LACI(HG2). LACI(HG2) bound to BXa(-GD) and inhibited its catalytic activity against a small molecular substrate (Spectrozyme Xa), though at a rate approximately sevenfold slower than native BXa. Preincubation of LACI(HG2) with saturating concentrations of BXa(-GD) markedly retarded the subsequent inhibition of BXa. The VII(a)/TF complex was not inhibited by LACI(HG2) in the presence of BXa(-GD), and further, preincubation of LACI(HG2) with BXa(-GD) slowed the inhibition of VIIa/TF after the addition of native Xa. The results are consistent with the hypothesis that inhibition of VII(a)/TF involves the formation of a VIIa-TF-XA-LACI complex that requires the GD of XA.(ABSTRACT TRUNCATED AT 400 WORDS)     

Single-acquisition chemical-shift imaging of a binary system with use of stimulated echoes

A method for separating binary chemical-shift components with a single image data acquisition by means of stimulated echoes is demonstrated. With a strategy analogous to the modified Dixon method, three stimulated echoes were acquired to form three complex images. In each of the images, the complex pixel intensities were imparted, by design of the pulse sequence, with a phase factor carrying chemical-shift or field inhomogeneity information. With these three images, true fat/water separation can be obtained in biologic tissues. Studies at high field strength (4.7 T) on a toluene phantom, a pseudo-binary chemical-shift system, were used to evaluate the applicability of the method. Its clinical feasibility was demonstrated on a healthy human subject in a 0.6-T whole-body imaging system.     

原发性肉碱缺乏致脂质沉积性肌病的临床与病理特点

目的 分析原发性肉碱缺乏致脂质沉积性肌病（LSM）的临床与病理特点。方法 回顾性分析4例可能LSM患者的临床资料。结果 本组患者为亚急性或慢性起病，主要表现为近端肌无力，疲劳不能耐受；血清肌酶有不同程度的升高；肌电图示肌源性损害；病理检查示肌纤维内可见大量细小空泡和裂隙形成；MGT染色无破碎红纤维，油红O染色显示空泡为大量脂滴充填；受累纤维以Ⅰ型纤维为主。电镜证实肌纤维内脂滴堆积，可伴有线粒体的轻度增多。改善能量和糖皮质激素治疗有效。结论原发性肉碱缺乏致LSM是一种以易疲劳和肌无力为主要临床表现的脂质代谢障碍性肌病，病理改变以肌纤维内脂滴堆积为主，一般不伴有线粒体结构的明显异常。糖皮质激素治疗可获得良好疗效。     

以光敏性癫痫为主要表现的肌阵挛性癫痫伴肌肉破碎红纤维综合征一家系分析

目的研究1个以光敏性癫痫为主要表现的肌阵挛性癫痫伴肌肉破碎红纤维综合征(MERRF)家系的临床特点、遗传学特征。方法整理一个以光敏性癫痫为主要表现的肌阵挛性癫痫伴肌肉破碎红纤维综合征家系的临床表现、辅助检查及影像学资料,分析其临床特点和遗传特征。结果该家系呈母系遗传,共4人(包括先证者3个同辈,1个子代)出现肌阵挛表现,先证者以光敏性癫痫为主要表现,其肌肉活检可见典型的破碎红纤维(RRF),先证者的线粒体DNA提示8344位点由A突变为G。结论 MERRF家系少见,可以光敏性肌阵挛癫痫为主要表现。     

武警某机动部队幽门螺杆菌感染情况的调查分析

  目的 了解武警某机动部队官兵幽门螺杆菌(helicobacter pylori,Hp)感染情况及其影响因素。 方法 随机抽取武警某总队机动部队官兵912名,填写一般情况问卷调查表,采用¹³C呼气试验进行Hp检测,对感染者相关因素进行统计学分析。 结果 912名受检官兵Hp感染率为56.5%,其中<20、20~30、≥30年龄组Hp感染率分别为53.2%,56.1%和64.5%,三组比较差异无统计学意义(P>0.05)。大学及大学以上文化程度Hp感染率为30.4%,明显低于高中及以下文化程度的62.4%,差异有统计学意义(P<0.001)。40.7%的干部感染了幽门螺杆菌,明显低于战士的58.1%,差异有统计学意义(P=0.002)。入伍前居住城市者与居住农村者感染率差异有统计学意义(P<0.001)。 结论 武警机动部队Hp感染率高于国内平均水平,文化程度、职务因素及其入伍前居住环境对Hp感染有明显的影响。