慢病毒介导NDRG2基因过表达抑制人膀胱癌T24细胞的侵袭和迁移

目的： 观察N-Myc下游调节基因-2（N-Myc downstream-regulated gene 2, NDRG2）过表达对人膀胱癌T24细胞体外侵袭和迁移的影响。 方法： 采用携带NDRG2基因的慢病毒Lenti-NDRG2感染T24细胞,构建稳定过表达NDRG2的细胞株。Western blotting检测T24细胞中NDRG2、基质金属蛋白酶（matrix metalloproteinase,MMP）-2和MMP-9的表达,Transwell体外迁移和侵袭实验观察过表达NDRG2对T24细胞体外迁移和侵袭的影响。 结果： 建立了稳定过表达NDRG2的T24细胞株。与Lenti-Lacz组和空白对照组相比,Lenti-NDRG2组NDRG2蛋白的表达\[(30.1±1.27) vs (9.9±1.24)、(8.2±1.28), P<001\]明显提高;Lenti-NDRG2组MMP-2 \[(13.5±1.32) vs (30.7±1.29)、(28.8±1.30), 均P<0.01\]和MMP-9 \[(11.7±127) vs (25.2±1.28)、(26.4±1.31), 均P<0.01\]的表达明显降低;Lenti-NDRG2组T24细胞的侵袭细胞数\[(18.1±3.4) vs (88.5±4.2)、(90.2±4.1)个,均P<0.01\]和迁移细胞数\[(20.1±3.5) vs (109.4±5.6)、(113.0±4.9)个,均P<0.01\]明显减少。 结论： 慢病毒介导的NDRG2基因过表达可能通过降低MMP-2和MMP-9的表达而抑制人膀胱癌T24细胞的转移与侵袭。     

慢病毒介导 EGFL7 沉默对肺癌A549细胞体外生物学行为的影响

目的：通过慢病毒介导沉默表皮生长因子样结构域7基因 (epidermal growth factor-like domain 7, EGFL7 )在肺癌A549细胞的表达,探讨 EGFL7对A549细胞的增殖、凋亡、侵袭和血管生成的影响。 方法： 利用慢病毒介导靶向 EGFL7的shRNA 转染A549细胞,实验分三组： LV-RNAi组（转染LV-RNAi）,LV-NC组（转染空病毒）和对照组（A549细胞）。Real-time PCR和Western blotting分别检测LV-RNAi感染对A549细胞 EGFL7 mRNA和蛋白水平表达的影响,MTT法和流式细胞术分别检测沉默〖STBX〗EGFL7〖STBZ〗对A549细胞增殖和凋亡的影响,Transwell侵袭实验和鸡胚绒毛尿囊膜（chick embryo chorioallantoic membrane,CAM）实验分别检测沉默 EGFL7 对A549细胞侵袭和血管生成能力的影响。 结果： 慢病毒稳定高效地转染A549细胞,LV-RNAi组细胞内 EGFL7 mRNA\[（0.18±0.03） vs （0.98±0.05）、（1.03±0.09）,P<0.05\]和蛋白表达较LV-NC组和对照组显著降低。与LV-NC组及对照组相比,沉默EGFL7 对LV-RNAi组A549细胞的增殖活力\[感染120 h 时：（073±0.22） vs （0.79±0.08） vs （0.81±0.11）,P>0.05\]与和凋亡率\[感染120 h 时：（1.92%±0.06） vs （2.11%±0.07） vs （1.85%±0.13）, P>0.05\]均无显著影响;同时,LV-RNAi组A549细胞侵袭入下室细胞数\[（61.7±14.5） vs （272.8±215）、（286.6±40.0）/mm2,P<0.05\]与血管生成指数\[（31.7±4.1） vs （96.3±4.4）、（103.3±6.5）,P<0.05\]均显著减少。 结论： 沉默 EGFL 基因能够抑制A549细胞侵袭和血管生成能力,但不影响其增殖与凋亡。     

含AFP基因调控序列的pAFP-P53-EGFP质粒诱导AFP阳性肝癌细胞凋亡

目的：观察含AFP基因调控序列的载体对AFP阳性肝癌细胞的靶向致凋亡作用。方法：将AFP启动子、沉默子和远端增强子Ⅲ组合为1.2 kb的AFP基因调控序列,构建pAFPEGFP载体,分别转染人肝癌HepG2（AFP阳性）、人肝癌SMMC7721（AFP阴性）和人宫颈癌HeLa（AFP阴性）细胞,荧光显微镜下观察EGFP荧光蛋白表达强度。引入P〖STBX〗53〖STBZ〗基因片段,构建pAFPP53EGFP重组质粒,转染HepG2、SMMC7721和HeLa细胞,Western blotting检测各组细胞P53蛋白的表达,流式细胞术分析各组细胞凋亡率及细胞周期。结果：成功构建了pAFPEGFP和pAFPP53EGFP重组质粒。pAFPEGFP转染后,AFP阳性的HepG2细胞中EGFP荧光蛋白表达显著高于AFP阴性的SMMC7721和HeLa细胞。pAFPP53EGFP转染后,HepG2细胞中P53蛋白的表达量明显高于SMMC7721和HeLa细胞;HepG2细胞的G1期细胞及细胞凋亡率明显高于SMMC7721和HeLa细胞\[(66.7±0.25)% vs（50.5±0.18）%,（51.0±0.20）%,P<0.05;（2.65±008）% vs（0.42±003）%,（0.39±0.02）%,P<0.05\], 但S期细胞明显低于转染后SMMC7721和HeLa细胞\[(20.1±022)% vs（29.8±018）%,（37.8±0.21）%,P<0.05\]。结论：含AFP基因调控序列的pAFPP53EGFP载体可专一性地作用于AFP阳性肝癌细胞,引起肝癌细胞周期阻滞和凋亡。     

Bestrophin 3高表达促进人肝癌细胞株HepG2的凋亡

目的：研究Bestrophin 3高表达对人肝癌细胞株HepG2凋亡能力的影响,并初步探讨其作用机制。 方法： 将Bestrophin 3腺病毒以感染复数(multiplicity of infection, MOI)10、20、40、80转染HepG2细胞株,Western blotting检测转染细胞内Bestrophin 3的表达,确定最佳MOI值。设对照组（未转染病毒）、LacZ组（转染携带LacZ的对照腺病毒载体）、Ad-Best3组（以最佳MOI值转染Bestrophin 3腺病毒）,CCK-8法和流式细胞术分别检测Bestrophin 3过表达对HepG2细胞增殖、凋亡的影响,Western blotting检测Bestrophin 3过表达对HepG2细胞内Bcl-2、Bax以及细胞色素C表达的影响,JC-1染色观察Bestrophin 3过表达对HepG2细胞线粒体膜电位的影响。 结果： Bestrophin 3腺病毒转染HepG2细胞的最佳MOI为40,转染后细胞过表达Bestrophin 3。Ad-Best3组的细胞存活率显著低于对照组和LacZ组\[(79.37±1.76)% vs (98.67±3.02)%、(99.67±325)%,均P<0.05\],而其细胞凋亡率显著升高\[（29.47±2.37）% vs （5.47±0.37）%,（4.95±0.44）%,均P<0.05\]。 Ad-Best3组HepG2细胞内Bcl-2的蛋白表达显著减少,Bax的蛋白表达显著增加,导致Bcl-2/Bax比值显著降低（0.32±0047 vs 1.00±000, P<0.05）;Ad-Best3组HepG2细胞的线粒体膜电位显著降低 \[(0.64±0.09)% vs （1.00±0.00)%, P<0.05\],同时线粒体中细胞色素C明显减少（P<0.05）,而细胞质中细胞色素C水平显著升高（P<0.05）。结论：过表达Bestrophin 3可能通过促使线粒体释放细胞色素C从而促进肝癌细胞株HepG2的凋亡。     

姜黄素对人多发性骨髓瘤ARH-77细胞外源性凋亡通路的影响

目的：探讨姜黄素（curcumin,Cur）对人多发性骨髓瘤ARH-77细胞外源性凋亡通路的影响。方法：ARH-77细胞经6.25、12.5、25、50、100、200 μmol/L Cur处理12、24、48 h,MTT法检测Cur对ARH-77细胞增殖的抑制作用,Hoechst 33258染色法观察Cur处理24 h后ARH-77细胞凋亡的形态学改变,流式细胞术检测ARH-77细胞周期和Fas/FasL、TRAIL/TRAIL-R的表达,分光光度法检测ARH-77细胞caspase-8的活性。结果：Cur对ARH-77细胞的增殖有时间和剂量依赖的抑制作用。25 μmol/L Cur处理ARH-77细胞可观察到凋亡小体,Cur阻滞细胞周期于G0/G1期,并且有凋亡峰。其促凋亡作用呈浓度依赖性,6.25、12.5、25 μmol/L Cur作用24 h后,ARH-77细胞凋亡率均显著高于对照组\[（10.35±0.35）%、（14.35±1.34）%、（36.65±1.06）% vs（3.83±0.32）%,F=500.432, P=0.000\];实验组细胞内caspase 8的活化程度均显著高于对照组\[（0223±0.018）、（0.263±0.019）、（0.240±0.035） vs （0.154±0.007）;F=9.059,P=20.03\]。12.5 μmol/L Cur作用24 h后,ARH-77细胞表面Fas\[（99.05±0.49）% vs（92.10±0.70）%,t=15.404, P=0.000\]、FasL \[（9.05±0.78）% vs（1.73±119）%,t=9.487, P=0.008\]、TRAIL\[（1.35±0.07）% vs（0.55±0.07）%,t=-11.317, P=0.008\]、DR4、DcR1和DcR2的表达均显著升高,DR5表达显著降低\[（0.95±0.07）% vs（7.70±0.29）%,t=32.742, P=0.001\];进一步提升Cur浓度至25 μmol/L,却降低了DcR1\[（4.35±120）% vs （14.25±021）%;t=5.692, P=0.008\]及DcR2\[（0.75±0.21）% vs （1.65±071）%;t=11.470, P=0.03\]的表达。结论：Cur能明显抑制人多发性骨髓瘤ARH-77细胞的增殖,其机制可能与激活外源性凋亡通路从而诱导细胞凋亡有关。     

miRNA-21调节PTEN表达影响宫颈癌HeLa细胞的生物学行为

目的： 探讨抑制miRNA-21表达对宫颈癌HeLa细胞中PTEN的表达及细胞增殖、侵袭能力的影响。 方 法： 以脂质体介导anti-miRNA-21（anti-miRNA-21转染组）、anti-miRNA-21-neg（阴性对照组）转染HeLa细胞,同时设空白对照组（未转染组）。应用Real-time PCR技术检测3组细胞中miRNA-21的表达,Western blotting 检测3组细胞中PTEN的表达,MTT法检测3组细胞的增殖能力,Transwell实验检测3组细胞的侵袭能力。结果： Anti-miR-21转染组与阴性对照组相比,HeLa细胞中miRNA-21的表达量明显降低\[（0.187±0.027）vs （0.861±0.144）,P＜0.01\]。转染 anti-miRNA-21 96 h后,HeLa细胞增殖抑制率明显升高\[（49.44±1.97）% vs （4.36±0.64）%,P＜0.01\]。Anti-miR-21转染组与阴性、空白对照相比, Hela细胞的侵袭细胞数明显减少\[（29.4±2.1）vs （40.4±2.9）、（41.2±2.6）个,均P＜0.01\];PTEN蛋白的表达则明显增加\[（1766.00±35.56）vs（726.00±5.48）、（729.25±17.73）,均P<0.01\]。 结论： 抑制miRNA-21的表达后,宫颈癌HeLa细胞增殖、侵袭能力明显下降,其机制可能与上调PTEN的表达有一定关系。     

EGCG对人肝癌细胞的抑制作用及其可能的机制

目的：观察表没食子儿茶素没食子酸酯\[(-)-epigallocatechin-3-gallate, EGCG\]对体外培养的人肝癌细胞株生物学特性的影响,研究其作用效果与血红素氧合酶-1（hemeoxygenase-1, HO-1）及相关信号分子的关系,探讨其作用机制。方法：利用MTT法检测EGCG对HepG2、Sk-hep1、SMMC7721等肝癌细胞增殖的影响,并用吖啶橙/溴化乙锭（AO/EB）双染法观察肝癌细胞的形态学变化,流式细胞术检测EGCG作用后Sk-hep1细胞周期的变化,Real-time PCR和Western blotting法检测EGCG作用后Sk-hep1细胞中HO-1、IL-10及TNF-α等信号分子表达的变化。结果：EGCG作用后,3株肝癌细胞贴壁细胞数量显著少于对照组,凋亡细胞数增多\[HepG2:（16.33±3.51) vs (3.67±1.15)个,P<0.01）,Sk-hep1:（18.33±2.31) vs (2.33±208)个,P<0.01）,SMMC7721: （15.33±3.06) vs (3.33±2.08)个,P<0.01）\]。实验组Sk-hep1细胞G2/M期比例明显高于对照组\[（34.33±8.09）% vs （3.07±2.32）%,P<0.01\]。设对照组基准值为1.00,实验组Sk-hep1细胞中HO-1、IL-10、及TNF-α的mRNA相对表达水平依次为（0.58±0.15）、（5.91±1.11）、（5.29±1.14）,差别均有统计学意义(P<001）;与对照组相比,实验组HO-1蛋白表达水平明显下调（0.16±0.04 vs 0.33±0.08,P<0.05）,IL-10（0.42±0.06 vs 0.24±0.08, P=0034,P<0.05）和TNF-α蛋白（0.95±0.17 vs 0.58±008,P<0.05）表达水平明显上调。结论：EGCG可抑制肝癌细胞增殖及诱导细胞凋亡,并将Sk-hep1细胞阻滞在G2/M期,其机制可能与HO-1、IL-10、TNF-α等炎症信号分子表达的变化有关。     

TLR4信号通过对miR-21的表达调控影响乳腺癌4T1细胞的凋亡和增殖

目的：探讨TLR4信号对乳腺癌4T1细胞株中miR-21表达的影响及调控机制,研究miR-21对乳腺癌细胞凋亡和增殖的影响。方法：体外培养乳腺癌细胞株4T1,以TLR4配体LPS刺激6、12、18、24 h,实时荧光定量PCR检测4T1细胞中miR-21的表达变化。Western blotting 检测TLR4信号活化后4T1细胞中NF-κBp65的表达和磷酸化情况;应用NF-κB抑制剂PDTC预处理30 min,实时荧光定量PCR检测4T1细胞中miR-21的变化。转染miR-21抑制剂和阴性对照后, Annexin-V/PI双标法检测4T1细胞凋亡情况,MTT法检测4T1细胞增殖情况。结果：LPS刺激致TLR4信号活化能够时间依赖性地上调miR-21的表达(18 h时: 207±0.33 vs 1; t=5.61, P=0.03),TLR4信号能够时间依赖性地上调NF-κB的活化,NF-κB抑制剂PDTC能明显抑制TLR4信号诱导的4T1细胞的miR-21上调(0.70±0.10 vs 2.14±0.32; t=-7.357,P=0.002)。与阴性对照组相比,miR-21抑制剂组4T1细胞的凋亡率明显增高\[(24.2±2.4)% vs (14.8±5.1)%; t=2.891, P=0.044\],4T1细胞的增殖能力明显降低(042±0.02 vs 0.55±0.01;t=-8.528, P=0.001)。结论：TLR4信号通路的活化能够上调乳腺癌4T1细胞中miR-21的表达,其机制与NF-κB的活化有关;靶向抑制miR-21能有效促进4T1细胞的凋亡、抑制4T1细胞增殖。     

雷公藤内酯醇对人胰腺癌PANC-1细胞的抑制作用及其可能的机制

目的： 通过体内外实验观察雷公藤内酯醇（triptolide,TPL）对人胰腺癌PANC-1细胞生长和凋亡的抑制作用,并分析其对Toll样受体4（Toll-like receptor 4,TLR4）、血管内皮细胞生长因子（vascular endothelial cell growth factor,VEGF）的表达和肿瘤血管生成的影响。 方法： 以0、20、40、80 ng/ml的TPL作用于PANC-1细胞,MTT法和流式细胞术分别检测TPL对PANC-1细胞增殖和凋亡的影响,Western blotting检测TPL作用后PANC-1细胞中TLR4和VEGF的表达。建立PANC-1细胞裸鼠荷瘤模型并随机分为TPL组、PBS组,测量移植瘤的体积变化,治疗35 d后摘取瘤块,免疫组织化学方法检测移植瘤组织内TLR4、VEGF和CD31的表达,并计算微血管密度（microvessel density,MVD）。 结果： 与0 ng/ml组相比,PANC-1细胞经20、40和80 ng/ml的TPL处理24 h后,细胞凋亡率均显著升高\[（4.7±1.0）%、（10.5±2.0）%、（21.1±4.2）% vs （2.6±05）%,P<0.05或P<0.01\];48 h后,细胞增殖率均显著下降\[（68.0±5.3）%、（59.6±5.0）%、（51.6±4.2）% vs （99.6±5.2）%,均P<0.01\],并较相同浓度TPL处理24 h时显著降低（P<0.05或P<0.01）。80 ng/ml TPL组处理后PANC-1细胞中TLR4蛋白\[(20.2±4.7)% vs (57.5±63)%,P<0.01\]和VEGF蛋白\[ (35.8±4.0)% vs (92.1±8.3)%,P<0.01\]的表达量显著低于未处理组。TPL治疗组第34天的裸鼠移植瘤体积显著小于PBS对照组\[（510.9±79.8）vs（1 220.6±127.2）mm3,P<0.01\];TPL治疗组移植瘤组织内的TLR4、VEGF表达均显著低于PBS组\[（3.2±0.6) vs (6.7±1.1),(3.7±0.7) vs (7.1±1.2);均P<0.01）,其MVD也显著低于PBS组\[(12.2±4.0) vs (22.7±5.6),P<0.01\]。 结论： TPL能够抑制人胰腺癌PANC-1细胞及其裸鼠移植瘤的生长,并促进PANC-1细胞凋亡,其机制可能与TPL抑制TLR4、VEGF表达及肿瘤血管生成有关。     

miRNA-210对人乳腺癌细胞增殖、迁移和侵袭的影响

目的： 探讨miRNA-210（miR-210）在人乳腺癌组织中的表达及其对人乳腺癌细胞MDA-MB-231增殖、迁移和侵袭的影响。 方法： 收集2011年10月至2012年6月期间昆明医科大学第一附属医院20例乳腺癌患者组织标本,real-time PCR检测乳腺癌组织和癌旁组织以及乳腺癌细胞MDA-MB-231和正常乳腺细胞MCF-10a中miR-210的表达。采用LipofectamineTM 2000将miR-210 inhibitor转染至MDA-MB-231细胞中,通过荧光显微镜检测miR-210的转染效率,MTT和软琼脂克隆形成实验检测MDA-MB-231细胞的增殖,流式细胞术检测细胞周期和凋亡,Transwell法检测细胞的迁移、侵袭能力。 结果： miR-210在乳腺癌组织和MDA-MB-231细胞中的表达水平均显著高于癌旁组织和正常乳腺细胞（P<0.01）。miR-210 inhibitor成功转染MDA-MB-231细胞,转染效率为（88.29±2.98）%,转染miR-210 inhibitor后MDA-MB-231细胞的增殖和克隆形成能力明显减弱（P<0.05）,被阻滞于G0/G1期的细胞数明显增多\[（64.23±3.12）% vs （55.53±0.96）%,P<0.01\],凋亡细胞比例也显著增加\[（31.90±3.05）% vs （15.98±0.63）%,P<0.01\],细胞的迁移\[（291.00±43.12） vs （1137.38±83.49）个,P<001\]、侵袭\[（131.63±32.01） vs （647.88±31.20）个,P<0.01\]均受到明显抑制。 结论： miR-210在乳腺癌组织和细胞中过表达,转染miR-210 inhibitor后乳腺癌细胞MDA-MB-231的增殖、迁移和侵袭能力明显减弱。     

Schwannomas of Head and Neck and Review of Literature

Benign nerve cell tumours have been given various names like schwannoma, neurilemmoma, neurinoma, neurofibroma, spindle cell tumours etc. Extra cranial head and neck schwannomas usually present as solitary and well-demarcated lesions. The lesion can cause secondary symptoms, such as nasal obstruction, dysphasia, and hoarseness, depending upon the location of the lesion. Fine needle aspiration cytology, CT scans, and MRI may be of limited help in the diagnosis of schwannomas. The treatment is complete surgical excision of the benign tumour and postoperative histopathological examination establishes the final diagnosis.     

A comparative study of knowledge and awareness of colorectal and breast cancerA comparative study of knowledge and awareness of colorectal and breast cancer

Aims: To assess and compare knowledge and awareness of colorectal cancer and breast cancer in a sample of the general population. Methods: Eleven hundred visitors to six different outpatient clinics, in a University Hospital, were given a study-specific questionnaire, based on educational material from the British Association of Cancer United Patients (CancerBACUP). The questionnaire consisted of 12 statements on the incidence, presentation, detection, treatment and prognosis of colorectal and breast cancer. Results: One thousand and sixty-eight individuals returned the questionnaire. One thousand and four completed questionnaires were analysed. The mean age (SD) of respondents was 50.1 (17.2) years, and the male to female ratio was 2:3. Respondents had read more about breast than about colorectal cancer (60.3%vs 32.4%,P <0.0001, McNemar's test). The proportion of correct answers for each statement on breast cancer was higher than for answers to corresponding items on colorectal cancer. Mean overall scores (95% CI) for breast and colorectal cancer were 88.1 (86.9, 89.2) and 64.4 (62.5, 66.3) respectively, the mean difference (95% CI) being 23.7 (22.0, 25.5). Scores were higher for breast cancer irrespective of age or gender. Conclusion: There is a low level of understanding of colorectal cancer in the general population when compared to breast cancer. This highlights the importance of public education in this common cancer.     

甲状腺手术的技巧及副损伤的预防和处置

鉴于甲状腺手术是普外科的常见手术，为求其日渐完美，以有益于病人，现根据作者的体会，并结合阅读相关文献，就其手术操作、喉返神经处理、甲状旁腺处理进行扼要阐述。     

miRNA与肿瘤侵袭转移

目前,microRNA (miRNA)已成为肿瘤研究中最基本的参与者,主要通过与靶标基因3 'UTR(非翻译区)的完全或不完全配对,降解靶标基因mRNA或抑制其翻译,从而参与调控个体发育、细胞凋亡、增殖及分化等生命活动.miRNA作为调控基因表达的重要分子在肿瘤侵袭转移中的作用越来越受到重视,表明miRNA在肿瘤侵袭和转移中的作用机制具有重要的理论意义,同时也可为肿瘤的诊断和治疗提供新方法.本文就miRNA通过调控上皮间质转化及肿瘤干细胞导致肿瘤侵袭转移的最新研究进展作一综述.     

Quality of life and care in leukemia,myeloma and non-malignant disease. Opinions of patients and relatives,and effects of geography and time

In a questionnaire study 140 subjects answered 4200 questions in 1980 and 1986. They consisted of patients with myeloma, acute leukemia, lung carcinoma, and non-malignant disease and their relatives. In 22 additional cases the questionnaire was not answered. The results show that myeloma patients are less content with the general care than leukemia patients (P < 0.05). Similarly, relatives of deceased myeloma patients are less satisfied with the information given to them than relatives of deceased leukemia patients (P < 0.001). The information has improved with time, however, since the patients were more satisfied in 1986 than in 1980 (P < 0.001) and relatives of myeloma patients still alive were more satisfied than relatives of patients who had died earlier (P < 0.001).     

芦荟大黄素及芦荟提取物的诱变性和抗诱变性

目的:用L5178Y小鼠淋巴瘤细胞体外微核试验评价芦荟大黄素和芦荟提取物的诱变和抗诱变作用,为其安全性评价提供依据。方法:设溶剂对照、阳性对照和抗诱变对照,芦荟大黄素和芦荟提取物诱变和抗诱变试验各设4个剂量组,处理L5178Y细胞12 h后按常规方法进行体外微核试验分析。结果:较高浓度(6.67μg/ml)的芦荟大黄素可致微核细胞率增加,与对照组比较,差异有统计学意义(P0.05);而芦荟提取物未见此效应。在一定剂量范围内,芦荟大黄素(0.22～6μg/ml)和芦荟提取物(20～180μg/ml)对甲磺酸甲酯(MMS)所致微核细胞率均有一定程度的拮抗作用,与对照组比较,差异有统计学意义(P0.01)。结论:芦荟大黄素具有一定的诱变作用,而在本实验剂量范围内的芦荟提取物未见遗传毒性。两种受试物在一定范围内均能较好地拮抗MMS所致的染色体损伤。     

Comparison of the Efficacy and Safety of Ceftibuten and Cefaclor in the Treatment of Pneumonia and Bronchiectasis

Summary

In a multicentre, international study of 187 adult patients with bacterial pneumonia or bronchiectasis, the safety and efficacy of a regimen of 200 mg ceftibuten administered twice-daily was compared with cefaclor given in a dosage of 500 mg three times a day. Of the 94 evaluable patients, 66 received ceftibuten and 28 received cefaclor. The overall bacteriological response was similar in the two treatment groups with elimination of the original pathogen in 91% and 89% of the patients receiving ceftibuten and cefaclor, respectively. The overall clinical response mirrored the bacteriological results with a successful clinical outcome in 92% of ceftibuten-treated patients compared with 93% in patients receiving cefaclor. Adverse experiences were, in general, few and mild, being reported in 8% and 17% of patients receiving ceftibuten and cefaclor, respectively.     

Erythrocyte levels of cadmium and lead and risk of B-cell non-Hodgkin lymphoma and multiple myeloma

Cadmium and lead are persistent environmental toxins that are known or probable carcinogens, based on evidence for causality for nonhematologic cancers. Associations of these metals with risk of non-Hodgkin lymphoma (NHL) and multiple myeloma (MM) are unknown but biologically plausible. To examine the associations of circulating levels of lead and cadmium exposure with risk of B-cell NHL (B-NHL) and multiple myeloma, we conducted a nested case-control study among 299 incident B-cell NHLs and 76 MM cases within the Cancer Prevention Study-II Nutrition Cohort (CPS-II NC). Each case was incidence-density matched to two eligible controls on age, race, sex and blood draw date. Conditional logistic regression was used to estimate relative risks (RR) and 95% confidence intervals (CI) for lymphoid malignancies overall and stratified by subtype. We observed a significant positive association between high erythrocyte lead concentration and risk of lymphoid malignancies overall (RR = 1.16, 95% CI: 1.02-1.33 per 17.6 μg/L (1 standard deviation [SD])) and follicular lymphoma in particular (RR = 1.80, 95% CI: 1.15-2.80 per SD). In contrast, there was no association between erythrocyte cadmium and risk of B-NHL (RR = 0.89, 95% CI: 0.75-1.06 per 0.37 μg/L [1 SD]), or any B-NHL subtypes; but a strong inverse association with MM risk (RR = 0.59, 95% CI: 0.38-0.89, per SD). Results from our study suggest a positive association between erythrocyte lead level and risk of lymphoid malignancies and a possible inverse association between cadmium and myeloma. Additional research is needed to confirm and further explore these findings.     

Cytologic classification of precancer and cancer of the endometrium and esophagus and of malignant lymphomas

The paper discusses cytological classifications of precancer and cancer of the endometrium, esophagus and malignant lymphomas presented by cytologists from five Soviet research institutes of oncology. The classifications were based on the data of 4400 cases in conformity with WHO histologic classifications.