癌抗原125联合癌抗原199检测对子宫内膜异位诊断价值分析

目的探讨癌抗原125（CA125）联合癌抗原199（CA199）检测对子宫内膜异位（EMs）的诊断价值。方法以我院收治的EMs病患48例、卵巢上皮癌（EOC）患者44例、卵巢良性肿瘤（BOT）36例为研究对象。检测研究对象血清癌抗原125、癌抗原199。结果血清CA125、CA199均从BOT组患者、EMs组患者到EOC组患者呈显著增加趋势（P〈0.05）;血清CA125、CA199联合检测对EMs、EOC的诊断灵敏度明显高于单项检测（P〈0.05）,但特异性、准确度较单项指标略有下降。结论CA125联合CA199可提高EMs诊断灵敏度,可作为EMs的辅助诊断指标。     

超声联合肿瘤标志物CA125、CA199在卵巢肿瘤诊断中的价值

目的 探讨超声检查联合肿瘤标志物在卵巢良、恶性肿瘤鉴别诊断中的价值。方法 回顾性分析经手术病理证实的80例（100个肿块）卵巢良、恶性肿瘤或盆腔其他性质肿块的超声征象,结合肿瘤标记物CA125及CA199的含量,对其进行统计学分析。结果 超声检查对术前卵巢肿瘤的诊断符合率为89．29％,肿瘤标志物CA125、CA199的诊断符合率81．03％,超声检查联合肿瘤标志物CA125、CA199检测的诊断符合率为92．83％,且联合诊断的符合率高于该两种方法单独使用时,差异有统计学意义（P〈0．05）。结论 超声检查卵巢肿瘤二维结构与血流频谱特征,结合检测血清CA125、CA199水平可弥补该两种方法单独诊断时的不足,是鉴别卵巢肿瘤良、恶性的一种良好方法,具有较大的临床应用价值。     

血清CA125等4种肿瘤标志物联合检测对胸腔积液鉴别诊断的意义

目的：探讨肿瘤标志物联合检测在良、恶性胸腔积液鉴别诊断中鲫临床意义。方法：采集有胸腔积液患者的血清样本80例，其中恶性胸腔积液患者48例，良性胸腔积液患者32例，用多肿瘤标志物蛋白芯片检测系统检测血清CA125、CA153、CA99和CEA的含量。结果：恶性胸腔积液组血清CA125、CA153、CA199和CEA的水平明显高于良性胸腔积液组（P〈0．02）；联合检测可提高恶性胸腔积液诊断率。结论：肿瘤标志物CA125、CA153、CA199和CEA的联合检测，对胸腔积液的鉴别诊断有较好的临床价值。     

血清肿瘤标志物联合检测对乳腺癌诊断的临床价值

目的探讨4种血清肿瘤标志物联合检测对乳腺癌诊断的临床应用价值。方法对92例乳腺癌和35例良性乳腺疾病患者以及40例健康女性体检者的血清恶性肿瘤生长因子（TSGF）、CA125、CA153和癌胚抗原（CEA）进行测定,观察肿瘤标志物联合检测对乳腺癌的诊断价值。结果乳腺癌组4种肿瘤标志物水平均显著高于良性乳腺疾病组和正常对照组（P〈0.01）;4种肿瘤标志物联合检测的灵敏度和特异度分别为88.9%、79.3%,均高于单项检测。结论肿瘤标志物联合检测可提高对乳腺癌诊断的灵敏度和特异度,对乳腺癌的鉴别诊断提供依据。     

CA19-9、AFP和CEA联合检测在消化道恶性肿瘤诊断中的价值

甲胎蛋白（AFP）和癌胚抗原（CEA）是消化道恶性肿瘤比较传统的特异性相对较高的肿瘤标志物。近年来，癌抗原19-9（CA19-9）作为恶性肿瘤生物学标志的研究已经日趋深入，国内外均有报道。多数研究表明，CA19—9在许多恶性肿瘤血清中会升高，因此我们采用血清CA19—9、AFP和CEA联合检测以提高对消化道恶性肿瘤的实验室阳性检出率，协助临床医生对该类疾病作出诊断。     

肿瘤标志物CEA、CA19—9、CA50在联合诊断胰腺癌中的价值

目的研究与胰腺癌有关的三种肿瘤标志物癌胚抗原（CEA）、癌抗原19—9（CA19—9）、癌抗原50（CA50）在胰腺癌诊断中的价值。方法采用放免法同时测定36例正常体检者、30例慢性胰腺炎患者、41例胰腺癌患者血清中CEA、CA19-9、CAS0值。结果胰腺癌患者血清中CEA、CA19—9、CAS0与正常人及慢性胰腺炎患者比较有显著性差异（P〈0．01）。CEA、CA19-9、CAS0单独检测时敏感性分别为38．6％、80.8％、78．2％，联合检测特异性达98．6％。结论CEA、CA19—9、CA50三种肿瘤标志物联合应用比单项应用提高了对胰腺癌的诊断价值。     

血清CEA、CA199、CA125、CA153、AFP联合检测对胃癌的诊断价值

目的 探讨血清癌胚抗原（ CEA） 、糖链抗原199（ CA199） 、糖链抗原125（CA125）、糖链抗原153（CA153）、甲胎蛋白（AFP）单检和联检在胃癌中的诊断价值.方法采用化学发光免疫分析法检测50 例胃癌患者和65 例正常对照组的血清CEA、CA199、CA125、CA153、AFP的含量,分析五种肿瘤标志物单个检测和联合检测的敏感度、特异度.结果 胃癌患者的血清CEA、CA199、CA125的含量明显高于正常对照组（P＜0.05）;采用单项肿瘤标志物诊断胃癌时,灵敏度最高的为CEA和CA199,特异度最高的为CA153,ROC曲线下面积最大的为CEA;采用不同肿瘤标志物的组合诊断胃癌时,灵敏度和特异度均较好的为CEA、CA199与CA125组成的组合.联合检测和单独检测相比,敏感度显著提高,特异度有所下降.结论 联合检测可提高胃癌诊断的敏感度,为早期诊断及早期治疗提供有力的依据.     

多肿瘤标志物蛋白芯片检测系统在消化道恶性肿瘤的临床应用价值

目的研究多肿瘤标志物蛋白芯片检测系统在消化道恶性肿瘤的普查、诊断及预后判断的临床价值。方法采用C-12蛋白芯片技术检测96例常见消化道恶性肿瘤患者组,87例消化道良性疾病患者组,120例健康查体者组血清中12项肿瘤标志物表达水平及阳性率,及51例消化道恶性肿瘤患者术后12项肿瘤标志物表达水平。结果消化道恶性肿瘤组肿瘤标志物C-12检测结果及阳性率明显高于良性疾病组及健康查体组,差异有显著性（P〈0.05）;12项联合检测阳性率（61.1%-82.3%）明显高于单项检测阳性率（27.72%-70.5%）;消化道恶性肿瘤患者术前及部分患者术后C-12检测结果比较,差异也有显著性（P〈0.05）;C-12中CA199、CEA、CA242、FER、AFP、CA125、CA153等7项在恶性消化道肿瘤中表达明显高于其余几项肿瘤标志物（P〈0.05）。结论多肿瘤标志物蛋白芯片检测系统用于恶性消化道肿瘤的普查、早期诊断及术后疗效观察,有一定的临床价值。     

探讨肿瘤标志物在结直肠癌患者中的诊断价值

目的 探讨肿瘤标志物癌胚抗原（carcinoembryonic antigen,CEA）、糖类抗原（carbohydrateantigen,CA）19-9、CA724在结直肠癌中的诊断价值.方法 收集2011年1月-2012年5月期间在我院确诊为结直肠癌的患者153例为患者组,同期选择67例健康体检者作为对照组,检测其血清CEA、CA19-9、CA724水平,按检测结果将患者组分为肿标阳性组和肿标阴性组,并对检测结果进行统计学分析.结果 三项肿瘤标志物检测水平在肿标阳性组、肿标阴性组及对照组间差异均有统计学意义（P均＜ 0.05）,肿标阳性组三项肿瘤标志物水平均高于肿标阴性组及对照组,且差异均有统计学意义（P均＜0.05）.三项肿瘤标志物诊断结直肠癌患者的阳性率分别为32.09％、14.18％、11.94％,三项联合检测的阳性率为43.28％.肿标阳性组、肿标阴性组患者手术前后血清CEA水平差异均有统计学意义（P均＜0.05）,而CA19-9水平在两组患者手术前后差异均无统计学意义（P均＞0.05）,血清CA724水平在肿标阳性组患者手术前后差异有统计学意义（P＜0.05）,而在肿标阴性组患者手术前后差异无统计学意义（P＞ 0.05）.处于不同Dukes分期的结直肠癌患者血清CEA、CA19-9、CA724水平差异均无统计学意义（P均＞ 0.05）.在不同Dukes分期患者中,三项肿瘤标志物联合检测的阳性率均在40％左右.结论 三项肿瘤标志物在结直肠癌中的诊断阳性率均较低,建议临床高度怀疑结直肠癌的患者,即使在各肿瘤标志物均为阴性的情况下,也应及早接受肠镜检查,以免贻误病情.对于已手术的患者,定期监测肿瘤标志物可作为其术后评估指标.     

多肿瘤标志物蛋白芯片检测系统对消化道肿瘤诊断的价值评价

目的探讨多肿瘤标志物蛋白芯片检测系统在诊断消化系统肿瘤的应用价值。方法使用多肿瘤标志物蛋白芯片检测系统（C-12）检测173例消化道恶性肿瘤患者及其中60例肿瘤术后患者、225例消化道良性疾病患者、82例健康体检者血清中12项肿瘤标志物表达水平。结果消化道恶性肿瘤组肿瘤标志物C-12检测阳性率明显高于良性疾病组及健康体检组,有显著性差异（P〈0.01）;除胰腺癌外,12项联合检测阳性率明显高于单项标志物阳性率（P〈0.05）;60例肿瘤患者6项肿瘤标志物（CA19-9、CEA、CA242、AFP、CA125、CA15-3）血清水平术后均低于术前,并有显著性差异（P〈0.05）。结论运用蛋白芯片技术检测多肿瘤标志物可以明显提高恶性肿瘤诊断的灵敏度,可用于高危人群的早期消化系统肿瘤筛查,以及肿瘤治疗后的疗效观察。     

Effect of 5-fluorouracil, mitoxantrone, methotrexate, and vincristine on the antibacterial activity of ceftriaxone, ceftazidime, cefotiam, piperacillin, and netilmicin

Using the checkerboard agar dilution technique, antibacterial activity and in vitro interactions of 4 antineoplastic agents and 5 antimicrobial drugs were examined against 56 strains of 7 bacterial species. 5-fluorouracil was found to inhibit all strains of Staphylococcus aureus and of Staphylococcus epidermidis at a concentration of 0.8 micrograms/ml or less. 84% of all gram-negative strains were inhibited synergistically when 5-fluorouracil was combined with beta-lactam antibiotics. Methotrexate and cefotiam were antagonistic in 42% of all combinations, especially when tested against Escherichia coli and Klebsiella pneumoniae.     

Susceptibilities of non-Pseudomonas aeruginosa gram-negative nonfermentative rods to ciprofloxacin, ofloxacin, levofloxacin, D-ofloxacin, sparfloxacin, ceftazidime, piperacillin, piperacillin-tazobactam, trimethoprim-sulfamethoxazole, and imipenem.

Agar dilution MICs of 10 agents against 410 non-Pseudomonas aeruginosa gram-negative nonfermentative rods were determined. MICs at which 50 and 90% of the isolates were inhibited, respectively, were as follows (in micrograms per milliliter): sparfloxacin, 0.5 and 8.0; levofloxacin, 1.0 and 8.0; ciprofloxacin, 2.0 and 32.0; ofloxacin, 2.0 and 32.0; D-ofloxacin, 32.0 and > 64.0; ceftazidime, 8.0 and 64.0; piperacillin with or without tazobactam, 16.0 and > 64.0; trimethoprim-sulfamethoxazole, 0.5 and > 64.0; imipenem, 2.0 and > 64.0. With the exception of those for Stenotrophomonas maltophilia, Burkholderia cepacia, and Alcaligenes faecalis-A. odorans, agar dilution MICs for all strains tested were within 1 dilution of inhibitory (bacteriostatic) levels as determined by time-kill methodology.     

Comparative ototoxicity of ribostamycin, dactimicin, dibekacin, kanamycin, amikacin, tobramycin, gentamicin, sisomicin and netilmicin in the inner ear of guinea pigs

Nine aminoglycoside antibiotics, ribostamycin (RSM), dactimicin (DAC), dibekacin (DKB), kanamycin (KM), amikacin (AMK), netilmicin (NTL), tobramycin (TOB), gentamicin (GM) and sisomicin (SISO) were administered intramuscularly to guinea pigs for 4 weeks, and ototoxicity and drug concentration in the inner ear fluid were determined. RSM and DAC showed the weakest ototoxicity against the cochlea and vestibular organs. AMK and KM were more toxic to cochlea than vestibular organs. DKB, TOM, GM and SISO were equally toxic to vestibular organs and cochlea. NTL was more toxic to vestibular organs than cochlea. As judged from the pinna reflex response and hair cell damage in the cochlea, the order of auditory toxicity was the following: SISO greater than GM greater than TOB greater than AMK greater than DKB greater than KM greater than NTL, DAC RSM, whereas the vestibular toxicity was in the following order: SISO greater than GM greater than DKB greater than TOB greater than NTL greater than AMK greater than KM greater than DAC, RSM. RSM, causing the weakest ototoxicity, showed a low drug concentration in the inner ear fluid, while GM, causing severe ototoxicity, showed the highest drug level under the same conditions.     

Reviews of books, videos, CDs, audiotapes, web sites, and more, written by emergency nurses

Zimmermann PG. Philadelphia: Hanley & Belfus, 2002, 243 pp, ISBN 1-56053-529-6.     

In vitro activity of piperacillin, ticarcillin, mezlocillin, ticarcillin-clavulanic acid, aztreonam, ceftazidime, azlocillin, cefoperazone, and thienamycin against Pseudomonas aeruginosa

The in vitro susceptibility of 103 well-characterized strains of Pseudomonas aeruginosa to nine antimicrobial agents was assessed by means of the Kirby-Bauer disk diffusion assay and the microtiter minimal inhibitory concentration assay. The antimicrobials, from the most to the least active against P aeruginosa, were thienamycin greater than ceftazidime greater than piperacillin greater than azlocillin greater than cefoperazone greater than aztreonam greater than ticarcillin greater than ticarcillin-clavulanic acid greater than mezlocillin. The resistance patterns of the antimicrobial agents suggest that P aeruginosa resistant to a penicillin, cephalosporin, or aztreonam may be susceptible to thienamycin.