运动感觉神经阻滞分离与患者自控镇痛技术用于肌腱修复与重建手术的临床研究

目的　探讨运动感觉神经阻滞分离与患者自控镇痛 (PCA)技术用于肌腱修复与重建手术以及术后主、被动功能锻炼的可行性。方法　 2 10例患者 ,均采用 0 2 5 %布比卡因、0 0 6 2 5mg/ml罂粟碱和 0 2 5mg/ml地塞米松混合液作腋路臂丛运动感觉神经阻滞分离麻醉药物 ,随机分为A、B和C 3组 ,每组 70例患者。A组为空白对照组 ,B、C组为实验组。B组患者自控静脉镇痛 (PCIA)泵药液为曲马多 0 0 1～ 0 0 15mg/kg、恩丹西酮 0 0 5～ 0 10mg/kg ,C组在B组PCIA泵用药基础上加用咪唑安定 0 15～ 0 30mg/kg ,泵液均加生理盐水至 10 0ml,阻滞注药后开启。PCA设置 :背景剂量 2ml/h ,单次剂量 2ml,锁定时间 6 0min ,维持时间 4 8h。比较阻滞注药后 1、2、3、6、12h等 5个时点运动感觉阻滞深度及开泵后即刻、12、2 4、4 8h 4个时点视觉模拟评分法 (VAS)、镇静评分法 (Ramesay)评分相关数值。结果　 3组患者 1、2、3h 3个时点运动阻滞深度逐渐增强 ,6和 12h 2个时点明显减弱 ;感觉阻滞深度均满意 ,VAS、Ramesay评分 ,2 4、4 8h 2个时点镇痛、镇静深度 ,A组 相似文献   

实验性髓核突出诱致神经根性疼痛机理的探讨

目的 探索单纯自体髓核组织放置于神经根邻近,并与神经根接触后对大鼠后爪机械刺激痛觉敏感性的影响。方法 取大鼠自体尾椎髓核组织无压迫下置于腰4和腰5神经根旁并与神经根相接触,术后不同的时间点观察大鼠双侧后爪机械刺激敏感性的变化;同时采用HE染色方法观察髓核组织和神经根的变化。结果 无明显机械压迫情况下,自体髓核组织与神经根接触后可诱导大鼠术侧后爪出现明显的机械性痛觉敏感性的升高;HE染色显示髓核组织发生了明显的炎性改变,邻近神经根出现空泡变性。结论 髓核组织自身介导的炎症反应可能参与机械性痛觉敏感性的发生。除机械因素外,突出髓核组织发生的炎症反应也可能是腰椎间盘突出所致坐骨神经痛的原因。     

Enhancing performance of protein and gene name recognizers with filtering and integration strategies

Named entity (NE) recognition is a fundamental task in biological relationship mining. This paper considers protein/gene collocates extracted from biological corpora as restrictions to enhance the precision rate of protein/gene name recognition. In addition, we integrate the results of multiple NE recognizers to improve the recall rates. Yapex and KeX, and ABGene and Idgene are taken as examples of protein and gene name recognizers, respectively. The precision of Yapex increases from 70.90 to 85.84% at the low expense of the recall rate (i.e., it only decreases 2.44%) when collocates are incorporated. When both filtering and integration strategies are employed together, the Yapex-based integration with KeX shows good performance, i.e., the F-score increases by 7.83% compared to the pure Yapex method. The results of gene recognition show the same tendency. The ABGene-based integration with Idgene shows a 10.18% F-score increase compared to the pure ABGene method. These successful methodologies can be easily extended to other name finders in biological documents.     

单核细胞RAGE表达上调:慢性肾功能衰竭微炎症的机制

目的探讨慢性肾功能衰竭(CRF)时细胞表面晚期糖基化终产物(AGE)受体(RAGE)的表达及其在单核细胞介导的炎症反应中的作用。方法96例非糖尿病CRF患者的断面队列研究。用密度梯度离心加免疫磁珠法分离外周血单核细胞(PMC),用特异性抗RAGE抗体染色、流式细胞仪检测PMC表面RAGE表达,Scatchard印迹法分析PMC结合AGE的位点数和亲和力,用ELISA法测定循环新蝶呤、TNF-α、C反应蛋白(CRP)和AGE水平。结果CRF患者PMC表面RAGE表达明显上调并随肾功能恶化而增加(r^2=0．73),RAGE上调程度与血浆AGE水平呈正相关(r=0．71);CRF患者PMC与AGE的结合位点数和亲和力明显高于正常人,在相同剂量AGE刺激下,CRF患者PMC生成的TNF-α明显多于正常PMC,且AGE诱导的TNF-α分泌可被抗RAGE抗体所抑制;患者PMC表面RAGE表达水平与循环TNF-α水平呈正相关(r=0．61),与单核细胞活化标志物——新蝶呤(r=0．65)和急性时相反应蛋白——CRP(r=0．44)呈正相关。结论CRF患者RAGE表达增加,RAGE上调可能通过促发炎症正反馈环导致单核细胞持续活化,从而参与CRF由单核细胞介导的全身微炎症反应。     

Hybrid retroviral vector with MCK enhancers inserted in LTR for stable and specific expression of human factor IX in skeletal muscle

Background Retroviral vectors have been widely used to introduce foreign into various target cells in vitro, thus showing relatively high systemic delivery efficiency of various transgene products. The authors investigated the stability and efficiency of skeletal muscle-specific hybrid retroviral vectors in expression of human factor IX (FIX) in vitro and iv vivo.Methods FIX cDNA in LIXSN vector was replaced with a FIX minigene containing splicing donor and splicing acceptor sequence of first intron of human FIX gene. Two copies of muscle creatine kinase enhancer (MCK, Me2) were inserted in forward or reverse orientation at Nhel site of 3‘ long terminal repeat (LTR), resulting in two hybrid vectors, which were designated as LMe2lXm2SN (F) and LMe2lXm2SN(R), respectively. The vectors were tested in vitro and in vivo for stability and musclespecificity of factor IX expression with SCID mice.Results Muscle cells carrying vector with Me2 expressed significantly higher levels of FIX (up to 1800 ng/106.24h) than those without Me2, thus suggesting that Me2 could specifically increase expression level of FIX in muscle cells. Myoblasts transduced with LMe2lXm2SN(R) produced much less FIX in vivo in SCID mice than LMe2lXm2SN(F). One or two copies of Me2 sequence were deleted in myoblasts transduced with LMe2lXm2SN(R) without changing the orientation of Me2.Conclusions LTR inserted with MCK enhancers can specifically increase human FIX expression in skeletal muscle cells in vitro and in vivo, and MCK enhancer should be positioned in the same orientation as that of LTR promoter.     

Electron paramagnetic resonance in monitoring of nitric oxide production after kidney transplantation in rats

Background Much research has been focused on ischemia/reperfusion injury (IRI) to the transplanted organs. As a free radical, nitric oxide （NO） plays an important role in IRI. In this study, the production of NO and its functions during IRI were monitored in rat models after allotransplantation of kidney grafts.Methods Of 75 male LEW rats, 30 served as donors, and the remaining 45 rats were divided into three groups (15 rats in each group): controls (group 1), kidney allotransplantation followed by bilateral nephrectomy during reperfusion (group 2), 2 hours before operation, donors and recipients were treated with N（G）-nitro L-arginine methyl ester (L-NAME), a NO synthase inhibitor, at a dose of 30 mg/kg (group 3). Bilateral nephrectomies were performed while kidney grafts were reperfused. The kidney grafts were hypothemically stored for 24 hours. The production of NO before and after reperfusion was measured by electron paramagnetic resonance (EPR). The creatinine level, the glomerular filtration rate (GFR) and the protein carbonyl content in tissue samples were recorded on the first and the fifth day after operation. The data were evaluated by one-way analysis of variance. Differences were considered to be statistically significant when a P value was less than 0.05.Results After reperfusion for 15 minutes, the production of NO increased remarkably and kept increasing till 120 minutes, after which the level returned to normal. In group 3, which was pretreated with L-NAME, creatinine levels were higher than those in group 2 at the 24th hour (4.10±0.50 mg/dl vs. 3.77±0.42 mg/dl, P<0.05) and the 120th hour (3.19±0.79 mg/dl vs. 2.22±0.53 mg/dl, P<0.05). GFR levels in group 3 were lower than those in group 2 at the 24th hour (0.50±0.12 ml/min vs. 0.71±0.19 ml/min, P<0.05) and the 120th hour (0.59±0.38 ml/min vs. 1.27±0.23 ml/min, P<0.01). The content of protein carbonyl in tissue samples of group 3 was lower than that in group 2 at the 24th hour (29.01±7.02 nmol/mg protein vs. 49.39±13.13 nmol/mg protein, P<0.05), but was higher than that at the 120th hour (75.71±16.74 nmol/mg protein vs. 57.93±15.32 nmol/mg protein, P<0.05).Conclusions After transplantation of hypothemically stored kidney grafts, the increased NO production in the early stage has protective effects on the transplanted kidney. Application of L-NAME to inhibit NO production is harmful to the recovery of the renal functions of kidney grafts.     

Prevention of macrophage adhesion molecule-1 (Mac-1)-dependent neutrophil firm adhesion by taxifolin through impairment of protein kinase-dependent NADPH oxidase activation and antagonism of G protein-mediated calcium influx

Taxifolin has been reported to down-regulate the expression of intercellular adhesion molecule-1 (ICAM-1), a receptor-mediating firm adhesion with beta2 integrin (e.g., Mac-1) expressed on leukocytes. To evaluate whether taxifolin could modulate Mac-1-dependent firm adhesion by neutrophils, and the possible mechanism(s) underlying its anti-inflammatory action, its effects on N-formyl-methionyl-leucyl-phenylalanine (fMLP) or phorbol-12-myristate-13-acetate (PMA)-activated peripheral human neutrophils were studied. Pretreatment with taxifolin (1-100 microM) concentration-dependently diminished fMLP- or (PMA)-induced Mac-1-dependent firm adhesion and upexpression of surface Mac-1. Mobilisation of intracellular calcium and production of reactive oxygen species (ROS) signal the upexpression of Mac-1 and firm adhesion by neutrophils. Taxifolin impeded the calcium influx induced by fMLP (a receptor-mediated activator) or AlF(4)(-) (a G protein-mediated activator). Taxifolin also effectively inhibited the fMLP- or PMA-induced ROS production with 50% inhibitory concentration (IC(50)) less than 10microM, possibly through impairing the activation of NADPH oxidase, a major ROS-generating enzyme in neutrophils, by restricting the activation of p38 mitogen-activated protein kinase (p38 MAPK) and protein kinase C (PKC). In conclusion, we propose that impairment of ROS production by NADPH oxidase through interfering with p38 MAPK- and/or PKC-dependent signals, and antagonism of G protein-mediated calcium influx may account for the inhibition of Mac-1-dependent neutrophil firm adhesion that confers taxifolin the anti-inflammatory activity.