A study of pre-antibiotic bacteriology in 125 patients with necrotizing enterocolitis

Over a five-year period, 125 newborns with necrotizing enterocolitis (NEC) were managed by us. Their mean birthweight was 1700 g and mean maturity was 32 weeks. Before commencement of antibiotics, routine septic work-up was done in order to define the bacterial spectrum and antibiotic sensitivity. The study includes aerobic and anaerobic cultures of gastric and pharyngeal aspirates, blood cultures, umbilical swabs and culture of umbilical catheter tips in relevant cases. Peritoneal swab results were also analyzed if laparotomy was performed. Positive cultures were present in 45 patients (36%) with 55 positive specimens. Fifteen types of organism were isolated: the commonest was Enterobacter (29%), followed by E. coli (14.5%) and Klebsiella (13%). They were resistant to ampicillin and first-generation cephalosporin. These organisms were usually opportunistic pathogens. Overgrowth of them may be the cause of NEC. Regular review of the antibiotic sensitivity of these organisms allows prompt and appropriate choice of antibiotics. At the same time, antibiotic sensitivity for these organisms was analyzed to guide us in the choice of antibiotic therapy.     

Beta 3 integrin-mediated fibrin clot retraction by nucleated cells: differing behavior of alpha IIb beta 3 and alpha v beta 3

Fibrin clot retraction may be important in resolution of thrombi and, in platelets, is mediated by integrin alpha IIb beta 3 (GPIIb-IIIa). Nucleated cells that lack alpha IIb beta 3 can retract fibrin clots, and we now report that integrin alpha v beta 3 can support this process. In addition, we compared the capacities of recombinant beta 3 integrins to mediate clot retraction in Chinese hamster ovary and M21 melanoma cells. We found that alpha v beta 3, but not alpha IIb beta 3, could spontaneously support retraction. Transferring the cytoplasmic domain of alpha v to alpha IIb enabled the resulting chimeric alpha IIb beta 3 to support clot retraction. The capacity of the alpha v cytoplasmic domain to support clot retraction was not caused by activation of the ligand binding function of alpha IIb beta 3 or by enhancement of alpha IIb beta 3's capacity to stimulate the formation of focal adhesions or the tyrosine phosphorylation of pp125FAK. These experiments define requirements for alpha IIb beta 3-mediating clot retraction, establish the capacity of alpha v beta 3 to mediate this process, and suggest differing functional roles of the alpha v and alpha IIb cytoplasmic domains.     

大鼠肠系膜淋巴微循环在急性微循环障碍时的变化

目的:采用局部滴加肾上腺素造成大鼠肠系膜微循环障碍模型,观察急性微循环障碍时淋巴微循环的变化。方法:实验于2006-04/07在河北北方学院医学院病理生理实验室完成。①实验分组:Wistar雄性大鼠20只,随机分为肾上腺素组和生理盐水组,每组10只。②实验方法:肾上腺素组依次由低浓度向高浓度用微量灌流泵从肠系膜局部滴加给药,给药浓度为0.1,1,10mg/L,速度为15滴/min,,每次给药间隔为30min;生理盐水组,在肾上腺素组的相对应时间肠系膜滴加生理盐水。两组大鼠在滴加后5min进行指标测量。③实验指标:测量急性微循环障碍时大鼠肠系膜淋巴管最大舒张口径、最大收缩口径和静态口径;记录大鼠肠系膜淋巴管收缩频率、收缩期时间、舒张期时间;计算大鼠肠系膜淋巴管收缩活性指数、总收缩活性指数、淋巴动力学指数。结果:20只大鼠均进入结果分析。①肠系膜淋巴管口径:给药前,肾上腺素组与生理盐水组肠系膜淋巴管静态口径、最大收缩口径及最大舒张口径组差异无显著性(P>0.05),肠系膜滴加不同浓度肾上腺素后,淋巴管静态口径、最大舒张口径小于给药前及生理盐水组(P<0.05),而生理盐水组淋巴管口径无明显变化。②肠系膜淋巴管收缩周期:活体淋巴微循环观察可见肠系膜淋巴管呈自主节律性收缩,平均收缩频率为(4.50±1.08)次/min,肠系膜滴加肾上腺素后,淋巴管收缩频率及舒张期时间明显低于给药前及生理盐水组(P<0.05)。③肠系膜淋巴管收缩指数:给药前,肾上腺素组肠系膜淋巴管收缩活性指数、总收缩活性指数、淋巴动力学指数与生理盐水组比较差异无显著性(P>0.05)。肠系膜滴加不同浓度肾上腺素后,3个收缩性指数明显低于给药前及对照组水平(P<0.05),而滴加生理盐水后,收缩指数无明显变化。结论:急性微循环时大鼠肠系膜淋巴微循环明显障碍。     

中药桔丙酯联合降糖治疗对2型糖尿病患者甲襞微循环及血液流变学的影响

目的观察中药桔丙酯注射液联合降糖治疗对2型糖尿病甲襞微循环及血液流变学的影响,探讨其治疗机制.方法于2005-10/2006-08选择河北北方学院附属校医院、张家口市第一人民医院门诊及住院收治的2型糖尿病患者48例,为治疗组.应用注射用桔丙酯治疗,桔丙酯180 mg,次,1次,d,连用2周;健康志愿者30例为对照组.采用微循环显微镜,于治疗前后常规检查左手第4指甲襞第一排管袢,按田牛加权积分法对16项指标综合定量分析,判断疗效和甲襞微循环的变化.同时观察2型糖尿病患者治疗前后血液流变学各项指标的变化.结果①治疗组治疗前甲襞微循环及血液流变学各项指标均表现为不同程度的异常,治疗后甲襞微循环及血液流变学各项指标明显改善.甲襞微循环由治疗前的中、重度异常恢复到大致正常,治疗后总积分值低于治疗前(分别为1.52±0.69,4.52±0.82,t=3.96,P＜0.05).②血液流变学指标变化表明,血浆黏度、全血黏度、纤维蛋白原及红细胞电泳等各指标经桔丙酯治疗后均明显降低(P＜0 05).结论中药桔丙酯联合降糖治疗能够明显改善2型糖尿病患者血流变异常及微循环障碍.     

丰富环境刺激对缺氧缺血性脑损伤大鼠脑超微结构改变及神经丝蛋白表达的影响

目的:观察丰富环境刺激对缺氧缺血性脑损伤大鼠脑超微结构及神经丝蛋白(NF)的影响。方法:实验于2005-03/2006-06在新桥医院中心实验室完成。取7日龄健康SD大鼠52只随机分为3组:①丰富环境干预组:20只,采用Rice法建立缺氧缺血性脑损伤模型,予早期抚触(15min/次,2次/d)和丰富环境(2h/次,1次/d)刺激共28d。②缺氧缺血非干预组:20只,同前造模,造模后不干预。③正常对照组:12只,不造模,不干预。饲养至1月龄时各组随机选10只进行Morris水迷宫测试学习记忆功能;行为学测定后处死大鼠取脑,免疫组织化学方法观察海马神经丝蛋白的染色情况,借助自动图像分析系统对其进行定量分析;利用透射电镜观察海马神经元超微结构、神经丝蛋白及突触情况。结果:52只进入结果分析。①隐匿平台逃避潜伏期(学习能力):缺氧缺血非干预组较正常对照组明显延长[(39.98±7.86),(26.12±4.03)s,P<0.001],丰富环境干预组较缺氧缺血非干预组缩短[(29.06±5.11)s,P<0.01],与正常对照组无差异。②跨越平台次数(记忆能力):缺氧缺血非干预组明显少于正常对照组[(2.13±1.33),(4.91±2.01)次,P<0.001],丰富环境干预组多于缺氧缺血非干预组[(4.45±1.59)次,P<0.01],与正常对照组无差异。③缺氧缺血非干预组左侧与右侧脑组织NF-H积分吸光度值之比值明显小于正常对照组和丰富环境干预组(0.398±0.110,0.975±0.011,0.821±0.138,P<0.01),后2组比较无差异。④超微结构显示缺氧缺血非干预组海马神经细胞固缩改变,线粒体肿胀,神经丝数量减少,排列稀疏,突触数量减少;丰富环境干预组海马神经元和突触无明显异常。结论:早期抚触及丰富环境刺激可以促进缺血缺氧的脑损伤恢复,脑组织神经网络重建及脑的可塑性增加是其可能的机制之一。     

上颌骨缝牵张的组织学变化

目的:观察缝牵张过程中环上颌骨缝的组织反应和组织再生机制。方法:实验于2005-03/09在解放军第四军医大学口腔医学院颌面外科实验室完成。15周龄杂种犬12只,随机数字法分为实验组8只,对照组4只。实验组安置口外自制牵引支架,自鼻腭孔引出牵引钩,橡皮圈连接牵引支架和牵引钩,向前持续弹性牵引,牵引力约600g。牵引1周和4周时,各处死实验组犬4只和对照组犬2只,对前颌缝,腭横缝,颧颌缝,颧颞缝区组织作大体观察和组织学观察。结果:实验犬12只均进入结果分析。①骨缝区成骨主要发生在侧带与骨缘之间,缝牵张初期骨缘外侧出现囊状分离带,成骨细胞与成纤维细胞大量增殖,新骨与结缔组织纤维排列方向与牵引力方向基本平行。②中央带纤维较致密,在牵引过程中,纤维排列方式未发生明显变化,而起到了屏障作用,阻止了缝骨性融合的发生。③牵张早期,缝区组织同时可见Ⅰ和Ⅲ型胶原,随后成骨细胞在Ⅲ型胶原基质的基础上分泌沉积Ⅰ型胶原而成骨,最终Ⅲ型胶原降解,Ⅰ型胶原完全代替Ⅲ型胶原成为骨基质的主要成份。缝区组织天狼猩红染色未见Ⅱ型胶原。结论:缝牵张成骨是以膜内成骨方式为主,无明显的软骨内成骨现象。中央带具有屏障作用,阻止牵张过程中骨缝发生骨性融合。     

评价Ti-6Al-7Nb合金的细胞相容性及其组织相容性

目的:评价Ti-6Al-7Nb合金的细胞相容性和组织相容性。方法:实验于2006-05/10在解放军第四军医大学口腔生物学实验室完成。实验分组:①细胞毒性试验:按照GB/T16886.5-2003《医疗器械生物学评价》体外细胞毒性的试验方法进行。分为5组:Ti-6Al-7Nb合金组、Ti-6Al-4V合金组、纯钛组、纯铅组、空白对照组。将对数生长期的L-929细胞用胰蛋白酶消化后制备成浓度为1×107L-1的细胞悬液,接种于培养板,待细胞贴壁生长后弃去原培养液。磷酸盐缓冲液冲洗后分别加入4种金属材料的浸提液和空白对照组的DMEM培养液。培养1,3,5,7d在倒置相差显微镜下观察细胞形态。每孔加入MTT后继续培养,抽出浸提液,磷酸盐缓冲液冲洗后加入二甲基亚砜,在490nm波长下用酶联免疫检测仪上测定吸光度值(A值),计算细胞相对增殖率,相对增殖率=(实验组A值/空白对照组A值)×100%。相对增殖率为≥100%,80%￣99%,50%￣79%,30%￣49%,0￣29%时细胞毒性分别为0,1,2,3,4级。②急性溶血性试验:抽取新西兰兔血10mL,制成新鲜抗凝稀释兔血。将Ti-6Al-7Nb合金、Ti-6Al-4V合金各5g浸泡入10mL生理盐水的试管。阳性对照组及阴性对照组分别为10mL的蒸馏水及生理盐水。每个试管中加0.2mL稀释兔血,离心后取上清液,用分光光度计在波长为545nm波长下测吸光度值,计算溶血率,溶血率=(Dt-Dnc)/(Dpc-Dnc)×100%。Dt,Dnc,Dpc分别代表Ti-6Al-7Nb合金组或Ti-6Al-4V合金组、阴性对照组、阳性对照组的A值。③短期皮下埋植试验:在10只新西兰大白兔皮下至肌肉间制备皮囊植入材料。囊底至切口>10mm,两皮囊间相隔>10mm,使植入材料相互之间不接触。每只兔植入4种金属材料各1个。于术后1,4,12周麻醉后处死动物各3只,取材料周围组织行苏木精-伊红染色,观察炎性细胞数量及种类,使用电子测量尺Version1.0测量纤维包膜厚度。参照GB/T16175-1996中的评价标准确定组织反应程度,其反应程度主要通过试验区组织中炎性细胞数量及种类变化,纤维包膜形成与否及厚度变化评价。结果:①细胞毒性评价:3种钛金属材料浸泡7d时L-929细胞形态正常,生长近汇合,排列密集规则;纯铅组可见大量细胞死亡。浸泡7d时Ti-6Al-7Nb、Ti-6Al-4V、纯钛、纯铅相对增殖率分别为100%,97%,101%,9%。经过评价,Ti-6Al-7Nb合金和纯钛的细胞毒性为0级,Ti-6Al-4V合金为1级,纯铅为4级。②细胞相容性评价:Ti-6Al-7Nb合金组、Ti-6Al-4V合金组溶血率分别0.95%,1.08%,低于国家标准规定的5%界限,无明显的急性溶血性。③组织相容性评价:肉眼可见材料被纤维包膜包裹,3组钛金属周围包膜透明且较薄,纯铅组包膜较厚呈半透明乳白色。术后12周时3种钛金属材料周围炎性细胞密度较低,包膜致密且进一步变薄。纯铅组炎性细胞数量及包膜厚度均较3种钛金属为高,组织反应较重。Ti-6Al-7Nb合金和纯钛炎性细胞/组织反应程度均为Ⅰ级,Ti-6Al-4V合金分别为Ⅰ、Ⅱ级,纯铅分别为Ⅱ、Ⅲ级。结论:Ti-6Al-7Nb合金具有良好的细胞相容性和组织相容性,是一种理想的生物医用钛合金。     

股骨偏心距重建与全髋关节置换术后关节功能的相关性

目的:股骨偏心距的恢复和重建,在髋关节软组织张力的平衡中具有非常重要的作用,是调节软组织平衡的主要手段。分析重建股骨偏心距与人工全髋关节置换术后关节功能恢复的关系。方法:选择2004-01/2005-06北京大学人民医院骨关节科收治的单侧髋关节置换患者76例,随访资料均完整,患者对治疗方案均知情同意。随访时间16￣29个月,平均23.2个月。手术均采用髋关节外侧入路,使用Zweymüller双锥形螺旋臼及SL-PLUS矩形直柄(颈干角135°,股骨头假体的直径均为28mm)。术前和术后随访时拍摄双髋正侧位X射线片,测量股骨偏心距、髋外展肌力臂及双下肢长度;记录手术前后髋关节活动度及Harris评分,分析股骨偏心距与其他指标的相关性。结果:76例患者全部进入结果分析。①股骨偏心距与髋外展肌力臂具有正相关性(r=0.523,P<0.001)。②髋关节术后活动度、Harris评分与股骨偏心距均存在明显回归相关关系(r=0.419,0.326,P<0.001)。③股骨偏心距重建与否对下肢长度的影响存在显著性意义(χ2=4.62,P<0.01)。结论:人工全髋关节置换术中股骨偏心距重建与髋外展肌的力臂增加、髋关节的活动度、功能改善及稳定性增强呈正相关。     

Infliximab and methotrexate as induction therapy in patients with early rheumatoid arthritis

OBJECTIVE: To evaluate the efficacy of infliximab plus methotrexate (MTX) as induction therapy in patients with early rheumatoid arthritis (RA). METHODS: Disease-modifying antirheumatic drug (DMARD)-naive patients with active, early RA who were included as group 4 of the BeSt study were initially treated with infliximab (3 mg/kg) in combination with MTX (25 mg/week). The Disease Activity Score (DAS) was measured every 3 months. In patients with persistent low disease activity (DAS 2.4, the infliximab dosage was increased (maximum 10 mg/kg), and they were subsequently switched to another DMARD. Except for intraarticular administration, corticosteroids were not permitted. Functional ability and the modified Sharp/van der Heijde score were determined after 2 years of therapy. RESULTS: Of the 120 patients, 67 responders (56%) had persistent low disease activity and discontinued infliximab after a median of 9.9 months, with a median MTX dosage of 10 mg/week after 2 years. Ten other patients experienced a disease flare after discontinuation and resumed infliximab after a median of 3.7 months. Thirteen patients did not achieve persistent low disease activity and received infliximab at various dosages. Treatment was unsuccessful in 30 patients. In the 67 responders, the progression of joint damage was lower than in the 30 patients in whom treatment failed. CONCLUSION: Fifty-six percent of patients with active early RA, initially treated with infliximab plus MTX, could discontinue infliximab after achieving a DAS of 相似文献