血管内皮生长因子和微血管密度与乳腺浸润性导管癌生物学行为的关系

目的探讨血管内皮生长因子和微血管密度与乳腺浸润性导管癌生物学行为的关系。方法应用免疫组化方法检测55例术前未作过化疗的乳腺浸润性导管癌组织中血管内皮生长因子(VEGF)、微血管密度(MVD)的表达,与乳腺癌的临床分期、淋巴结转移等生物学行为进行统计学分析。结果 (1)乳腺浸润性导管癌组织中MVD值与淋巴结转移、临床分期密切相关(P0.05);(2)VEGF主要表达于肿瘤细胞胞浆或胞膜,与乳腺浸润性导管癌淋巴结转移、临床分期有关(P0.05);(3)乳腺浸润性导管癌VEGF表达与MVD值密切相关(P0.05)。结论 VEGF表达与乳腺浸润性导管癌的血管生成和侵袭转移关系密切。MVD和VEGF的检测可以用于乳腺浸润性导管癌的预后判断。     

乳腺浸润性导管癌雌、孕激素受体及人类上皮生长因子受体表达与超声特征的关系

目的 探讨乳腺浸润性导管癌(IDC)患者雌激素受体(ER)、孕激素受体(PR)、人类上皮生长因子受体(HER-2)表达水平与灰阶超声特征的相关性.方法 对术前应用超声检查的73例IDC患者的灰阶超声图像特征与术后标本经免疫组织化学染色检测ER、PR、HER一2表达情况进行对比研究.结果 肿瘤有毛刺(蟹足)征、周边高回声晕、肿瘤后方衰减组ER阳性表达率高于肿瘤无毛刺(蟹足)征、无周边高回声晕、肿瘤后方无衰减组,差异有统计学意义(P＜0.01);肿瘤内微钙化、腋窝肿大淋巴结组HER-2表达阳性率高于肿瘤内无微钙化、腋窝无肿大淋巴结组,差异有统计学意义(P＜0.05).结论 ER、HER-2表达与IDC灰阶超声特征之间存在相关性,灰阶超声征象可对部分乳腺浸润性导管癌的预后及生物学特性作出初步判断.     

乳腺浸润性导管癌ER、PR表达的临床病理意义

目的 :探讨乳腺浸润性导管癌ER、PR表达的临床病理意义。方法 :采用免疫组织化学Envision二步法检测乳腺浸润性导管癌ER、PR表达情况。结果 :6 0例乳腺浸润性导管癌ER、PR阳性表达在乳腺癌发病年龄、肿瘤大小、有无淋巴结转移和肿瘤分级间差异均有显著性 (P <0 0 5 )。结论 :ER、PR阳性表达与乳腺浸润性导管癌的病理组织学分级、有无腋窝淋巴结转移和患者预后相关。     

Ezrin和E-cadherin在乳腺浸润性导管癌中的表达及临床意义

目的:Ezrin是一种细胞骨架连接蛋白,参与调节肿瘤细胞的生长和转移。本研究通过检测Ezrin和钙黏素E(E-cadherin)在浸润性乳腺导管癌中的表达情况,探讨其在淋巴结转移中的意义。方法:采用免疫组织化学SP法检测60例浸润性乳腺导管癌病理组织切片中Ezrin和E-cadherin的表达。结果:Ezrin在21例无转移的癌组织中10例异常表达(48%),19例有转移的癌组织中14例异常表达(74%)。E-cadherin在无转移的癌组织中9例异常表达(43%),而在有转移的癌组织中13例异常表达(68%)。Ezrin异常表达与E-cadherin异常表达有显著的正相关性(r=0.898,P=0.038)。结论:Ezrin和E-cadherin与乳腺导管癌的浸润和转移密切相关,可以作为预测浸润性乳腺导管癌淋巴结转移的重要肿瘤标志物。     

Beclin 1在乳腺浸润性导管癌中的表达及其与Ki67的关系

目的探讨自噬相关基因Beclin 1和增殖相关基因Ki67编码的蛋白在乳腺浸润性导管癌中的表达情况。方法选取乳腺浸润性导管癌患者64例。采用免疫组化法检测癌组织及对应的癌旁组织中Beclin 1和Ki67蛋白的表达,同时采用免疫荧光法和免疫印迹法检测癌组织及对应癌旁组织中Beclin1蛋白的表达。结果癌组织中Beclin 1的阳性表达率(43.8%)明显低于癌旁组织(98.5%)(P0.05),而Ki67的阳性表达率(76.6%)则高于癌旁组织(0.00%)(P0.05)。癌组织中Beclin 1蛋白表达与Ki67蛋白表达呈负相关(r=-0.256,P0.05)。Beclin 1蛋白表达与乳腺浸润性导管癌病理分级、有无淋巴结转移有关(P0.05),与肿瘤直径、年龄、雌激素受体(ER)、孕激素受体(PR)、人类表皮生长因子受体2(HER-2)均无关(P0.05)。Ki67蛋白表达与乳腺浸润性导管癌病理分级、肿瘤直径有关(P0.05),与有无淋巴结转移、年龄、ER、PR、HER-2均无关(P0.05)。免疫荧光法检测结果显示癌组织中Beclin 1蛋白的阳性表达率(30.0%)明显低于癌旁组织(100.0%)(P0.05)。免疫印迹法检测结果显示癌旁组织中Beclin l蛋白的相对表达量为0.43±0.12,明显高于癌组织(0.20±0.18)(P0.05)。结论乳腺浸润性导管癌组织中Beclin 1蛋白表达明显降低,Ki67蛋白表达明显升高。     

乳腺浸润性导管癌63例临床病理分析

目的 探讨乳腺浸润性导管癌与ER、PR、C-erbB-2表达相关性.方法 应用免疫组化技术S-P法检测分析63例术后、术中病理证实为乳腺浸润性导管癌的ER、PR、C-erbB-2表达.结果 63例乳腺浸润性导管癌中ER、PR、C-erbB-2的阳性表达率分别是62.5％、67.1％、44.2％,ER、PR共同阳性率为64.2％; C-erbB-2阳性表达率与有无淋巴结转移有关;ER、PR与C-erbB-2表达呈负相关(P＜0.01).结论 ER、PR、C-erbB-2联合检测可作为乳腺癌预后指标,同时有助于制定患者术后的个体化治疗方案.     

HER2在乳腺浸润性导管癌中的表达及意义

目的:观察人类表皮生长因子2(简称HER2)在乳腺浸润性导管癌组织中的表达,探讨HER2表达与其淋巴结转移的关系及意义。方法:采用免疫组织化学技术检测15例正常乳腺组织和60例原发性乳腺浸润性导管癌中HER2基因的表达。结果:乳腺浸润性导管癌组织HER2表达总阳性率为67%,有淋巴结转移者其阳性率(65.22%)明显高于无淋巴结转移者(35.14%)(P<0.05);uPAR阳性的癌组织中HER2表达阳性率显著升高[(84.21±36.36)%,P<0.05],uPAR与HER2之间的表达高度相关。结论:HER2蛋白在乳腺浸润性导管癌中高度表达,且其过度表达与乳腺浸润性导管癌淋巴结转移有关。     

E-cadherin蛋白在乳腺导管癌中的表达及意义

目的 探讨E-cadherin蛋白在乳腺导管癌中的表达及意义.方法 采用免疫组化方法 检测E-cadherin蛋白在53例乳腺浸润性导管癌、25例导管内癌组织和13例乳腺囊性增生病组织中的表达.结果 E-cadherin蛋白在乳腺囊性增生组织、导管内癌及乳腺浸润性导癌中表达逐渐升高,差异有统计学意义.在浸润性导管癌中其表达与病理分级、脉管浸润和腋窝淋巴结转移显著相关.结论 E-cadherin与乳腺浸润性导管癌的发生、发展及淋巴结转移关系密切.     

肺腺癌中表皮生长因子受体基因突变及表皮生长因子受体2、血管内皮生长因子的表达及与临床的关系

目的 探讨肺腺癌中表皮生长因子受体(EGFR)基因突变及人表皮生长因子受体2(HER-2)、血管内皮生长因子(VEGF)的表达与临床病理因素间的关系。方法 采用ARMS-PCR法检测10例正常肺组织及49例肺腺癌组织的EGFR基因突变的情况,同时应用免疫组织化学方法检测HER-2和VEGF蛋白表达水平。结果 (1)肺腺癌组织标本EGFR基因突变率及HER-2、VEGF蛋白表达率均比正常肺组织高(χ2=10.875 6,P=0.001;χ2=12.456 0,P=0.000;χ2=6.775 2,P=0.009)。(2)EGFR突变的发生与患者性别、是否吸烟有关(P0.05),与年龄、肿块大小、肿瘤分化程度、有无淋巴结转移、TNM分期、有无胸膜浸润无关(P0.05)。HER-2与VEGF蛋白表达均与肿瘤的分化程度、肿块大小、TNM分期、有无淋巴结转移、有无胸膜浸润相关(P0.05),与患者性别、年龄、有无吸烟史无关(P0.05)。(3)肺腺癌中HER-2与VEGF的表达呈正相关(r=0.376 4,P=0.007 7)。结论 EGFR突变与肺腺癌的发生密切相关,其在女性、非吸烟者的高表达有重要的临床意义。HER-2和VEGF在肺癌的发生、发展、转移中起协同作用,有助于临床评估预后,并为肺腺癌的新分子靶向治疗提供理论依据。     

乳腺癌组织中HER-2、VEGF和Ki67的表达及临床意义

目的探讨人表皮生长因子受体-2(HER-2)、血管内皮生长因子(VEGF)和Ki67在乳腺癌组织中的表达及其与临床病理因素的关系。方法采用免疫组化法检测49例乳腺癌患者组织中HER-2、VEGF和Ki67的表达。结果 HER-2、VEGF和Ki67在乳腺癌组织中的阳性表达率分别为36.7%、69.4%、79.6%;HER-2在乳腺癌组织学分级和淋巴结转移中的表达差异有统计学意义(P<0.05);VEGF在乳腺癌淋巴结转移中的表达有显著差异(P<0.05);Ki67表达在乳腺癌组织学分级中的差异有统计学意义(P<0.05)。结论 HER-2、VEGF和Ki67与乳腺癌的发生、发展密切相关,联合检测可作为判定乳腺癌预后的评估指标。     

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.     

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