肝门部胆管癌165例的诊断与外科治疗

目的 总结肝门部胆管癌的诊断及外科治疗.方法 回顾性分析1972-2001年收治的肝门部胆管癌165例的临床资料.结果 根据不同时期的发病例数、手术切除率不同,分为前15年第一阶段及后15年的第二阶段.首发症状为上腹不适或闷痛、胀痛、乏力、食欲减退及进行性黄疸.B超、CT、MRI和MRCP是无损伤诊断的首选方法;若显示肝内胆管扩张或诊断肝外梗阻性黄疸,则应行PTC（27例）、MRCP（15例）或ERCP（78例）.本组手术切除73例,切除率44.2%,其中根治性切除38例;非根治性切除35例.第一阶段切除15例,切除率27.3%;第二阶段切除58例,切除率52.7%.本组54例得到随访,其中根治性切除术5年生存率39.5%,非根治性切除术为14.3%;未切除的62例得到随访,均于1～1.5年死亡.结论 一旦诊断为肝门部胆管癌,就应积极剖腹探查,不要延误切除时机.手术切除是治疗肝门部胆管癌的最有效的治疗方法.     

肝癌胆管内转移致阻塞性黄疸的外科治疗

目的: 探讨外科手术治疗原发性肝癌胆管内转移致阻塞性黄疸的疗效.方法: 自1944年1月至1997年10月间对21例原发性肝癌胆管内转移致阻塞性黄疸的患者进行了外科手术治疗.其中行总胆管切开取癌栓者19例,行肝动脉插管化疗者4例,行肝动脉结扎者10例,行肝叶切除者2例.结果: 患者平均生存时间为8.5个月,最长存活时间为18个月.结论: 外科治疗明显改善了患者生活质量,提高了生存时间.     

高血压病患者血清载脂蛋白与主动脉壁厚度和视网膜动脉硬化的关系

从住院的高血压病患者中选择高脂血症者７６例（高脂组），血脂正常者５２例（对照组）。同时进行血清载脂蛋白（ａｐｏ）、主动脉壁厚度（ＡＷＴ）及眼底检查。结果：与对照组比较，高脂组血清ａｐｏＢ、ＡＷＴ、视网膜动脉硬化（ＲＡＳ）程度及冠心病患病率均显著增加，ａｐｏＡＩ及ａｐｏＡＩ／ａｐｏＢ均显著降低。相关分析显示，ＡＷＴ与ＲＡＳ呈正相关；ＡＷＴ和ＲＡＳ各自与ａｐｏＢ呈正相关，与ａｐｏＡＩ、ａｐｏＡＩ／ａｐｏＢ呈负相关（均Ｐ＜０．０１）。经逐步回归，筛选对ＡＷＴ和ＲＡＳ有显著作用的血脂指标均为ａｐｏＡＩ／ａｐｏＢ。提示ａｐｏＡＩ／ａｐｏＢ是反映Ａｓ疾病较可靠的血脂指标。     

Application of support vector machine classifiers to preoperative risk stratification with myocardial perfusion scintigraphy

BACKGROUND: Myocardial perfusion single-photon emission computed tomography (SPECT) has been used for risk stratification before non-cardiac surgery. However, few authors have used mathematical models for evaluating the likelihood of perioperative cardiac events. METHODS AND RESULTS: This retrospective cohort study collected data of 1,351 patients referred for SPECT before non-cardiac surgery. We generated binary classifiers using support vector machine (SVM) and conventional linear models for predicting perioperative cardiac events. We used clinical and surgical risk, and SPECT findings as input data, and the occurrence of all and hard cardiac events as output data. The area under the receiver-operating characteristic curve (AUC) was calculated for assessing the prediction accuracy. The AUC values were 0.884 and 0.748 in the SVM and linear models, respectively in predicting all cardiac events with clinical and surgical risk, and SPECT variables. The values were 0.861 (SVM) and 0.677 (linear) when not using SPECT data as input. In hard events, the AUC values were 0.892 (SVM) and 0.864 (linear) with SPECT, and 0.867 (SVM) and 0.768 (linear) without SPECT. CONCLUSION: The SVM was superior to the linear model in risk stratification. We also found an incremental prognostic value of SPECT results over information about clinical and surgical risk.     

电针足三里对脓毒症大鼠小肠促炎症因子、二胺氧化酶活性及组织含水率的影响

目的:探讨电针足三里(ST36)对脓毒症大鼠促炎症因子所致小肠损伤的抑制作用.方法:采用盲肠结扎穿孔术(CLP)制备大鼠脓毒症模型, 取♂SD大鼠32只, 随机分为CLP+电针(EA)足三里组(CLP+EA组)、CLP+假电针(shame EA)(CLP+SEA)组、迷走神经切断(VA)+CLP(VA+CLP)组和迷切后CLP再电针(VA+CLP+EA组)组, 每组8只. EA组持续针刺双侧足三里30 min, 强度为2 mA, 2-100 Hz.CLP/SEA组采用相同频率和强度刺激非经非穴(足三里外侧旁开0.5 cm)30 min. VA组先手术切断腹腔迷走神经再CLP. 各组大鼠于CLP术后6 h处死取空肠组织, 检测TNF-α和NO含量、髓过氧化物(MPO)和二胺氧化酶活性及肠组织含水率.结果:采用盲肠结扎穿孔术后6 h, 与其余3组相比, CLP/EA组小肠组织促炎因子TNF-α、NO、MPO水平和组织含水率均显著降低、DAO活性显著升高(均P<0.05). VA+CLP组和VA+CLP+EA组TNF-α、NO和MPO水平显著高于CLP+SEA组(748.80±112.45 pg/g protein,737.58±100.56 pg/g protein vs 560.23±82.25pg/g protein; 1.32±0.15 μmol/g protein, 1.12±0.24 μmol/g protein vs 0.97±0.12 μmol/gprotein; 0.57±0.06 U/g, 0.61±0.12 U/g vs 0.45±0.07 U/g, 均P<0.05), DAO活性显著低于CLP+SEA组(0.07±0.02 U/L, 0.06±0.04 U/Lvs 0.12±0.04 U/L,均P<0.05); VA+CLP+EA组、VA+CLP组、CLP+SEA组上述指标的变化无统计学差别.结论:电针足三里显著抑制CLP大鼠小肠促炎症因子水平, 减轻肠组织水肿和功能损害.     

Progress in accelerated measles control in the People's Republic of China, 1991-2000

Measles incidence decreased dramatically following widespread use of measles vaccine in China in 1965. To evaluate continued progress in accelerated measles control, data on measles cases reported to the National Notifiable Disease Reporting System during 1991 to 2000 were analyzed. From 1991-1995 to 1996-2000, average annual measles incidence decreased from 9.0 to 5.7 cases per 100,000 population, mortality rates fell from <0.3 to 0.1 deaths per million population, and the percentage of China's total population residing in provinces with a measles incidence of <2 cases per 100,000 population and having a measles elimination goal increased from 21% to 29%. Incidence rates were highest in western provinces and in infants and young children. Additional attention must be focused on western provinces and toward ensuring that all infants are immunized. Achieving high routine two-dose coverage with measles vaccine and enforcing school entry requirements may be highly effective strategies to support further gains in measles control.     

CD19-targeting liposomes containing imatinib efficiently kill Philadelphia chromosome-positive acute lymphoblastic leukemia cells

Patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) have poor prognosis despite intensive therapeutic intervention. Recently, imatinib, a BCR-ABL tyrosine kinase inhibitor, has been proven to be an effective treatment for Ph(+) ALL, but nearly all patients rapidly acquire resistance. High-dose imatinib administration might overcome this resistance; however, systemic toxicities would likely limit this approach. Therefore, a new delivery system allowing for the specific targeting of imatinib is urgently needed. Because almost all Ph(+) ALL cells express CD19 on their surface, we have developed an immunoliposome carrying anti-CD19 antibody (CD19-liposomes). The internalization efficiency of the CD19-liposomes approached 100% in all Ph(+) ALL cells but was very low in CD19(-) cells. The cytocidal effect of imatinib-encapsulated CD19-liposomes (imatinib-CD19-liposomes) on Ph(+) ALL cell lines and primary leukemia cells from patients with Ph(+) ALL was much greater than that of imatinib with or without control liposomes. Importantly, the imatinib-CD19-liposomes did not affect the colony formation of CD34(+) hematopoietic cells, even at inhibitory concentration of free imatinib. Taken together, these data clearly demonstrate that the imatinib-CD19-liposomes induced specific and efficient death of Ph(+) ALL cells. This new therapeutic approach might be a useful treatment for Ph(+) ALL with fewer side effects than free imatinib.     

Expression of Helicobacter pylori AlpA protein and its immunogenicity

AIM: To construct a recombinant strain which expresses adhesin AlpA of Helicobacter pylori (H pylori) and to study the immunogenicity of adhesin AlpA. METHODS: Gene Ab, which was amplified from H pylori chromosomal DNA by PCR technique, was sequenced and the biological information was analyzed, and inserted into the Nco I and Not I restriction fragments of the expression vector pET-22b(+) using T4 DNA ligase. The resulting plasmid pET-AlpA was transformed into competent E.coli BL21(DE3) cells using ampicillin resistance for selection. Recombinant strains were incubated in 5 mL LB with 100 μg/mL ampicillin overnight at 37 ℃. Sonication of BL21(DE3)pET-22b(+)/AlpA was analyzed by Western blot to detect AlpA immunogenicity. RESULTS: The gene encoding AlpA protein was amplified by PCR with chromosomal DNA of H pylori Sydney strain (SS1) as templates. It revealed that AlpA DNA fragment amplified by PCR had approximately 1 500 nucleotides, compatible with the previous reports. The recombinant plasmid pET-22b(+)/AB was successfully constructed. DNA sequencing showed one open reading frame with the length of 588 bp. It encoded seven conservative regions that showed good antigenicity and hydrophobicity by Parker and Welling method. Furthermore, INTERNET EXPASY, NNPREDICT and ISREC predicted that it was a porin-like structure consisting of β-pleated sheets that were embedded in the outer membrane. BLAST analyzed 836 767 protein sequences and found that the similar sequences were all belonging to H pylori OMP sequences. SDS-PAGE and scan analysis showed that the molecular weight of AB was 22.5 ku and recombinant protein amounted to 29% of the total bacterial protein, among which dissolved expression amounted to 21.9% of sonicated supernatant. The rAB purity amounted to 96% through affinity chromatography. Western blot analysis of rAB confirmed that it could be specially recognized by serum form rabbit immunized with AlpA and H pylori infected. CONCLUSION: Adhesin AlpA recombinant protein may be a potential vaccine for control and treatment of H pylori infection.     

过氧化还原蛋白6对细菌脂多糖诱导的小鼠急性肺损伤氧化应激的保护作用

目的探讨过氧化还原蛋白Peroxiredoxin(Prdx)6对细菌脂多糖(LPS)诱导的小鼠急性肺损伤氧化应激的作用及机制。方法应用PCR法对Prdx6基因敲除小鼠行基因型鉴定并应用免疫组织化学法测定Prdx6蛋白在肺脏的表达。将雄性Prdx6基因敲除型小鼠（18只）按随机数字表法分入Prdx6敲除型对照组（9只）、Prdx6敲除型LPS 24 h组（9只）;将雄性野生型C57BL/6J小鼠（18只）按随机数字表法分入野生型对照组（9只）、野生型LPS 24 h组（9只）。各LPS组小鼠气管滴注LPS(5 mg/kg)制备急性肺损伤模型,于给药后24 h分别行肺脏病理检测,BCA法测定BALF内蛋白浓度,比色法测定肺脏总超氧化物歧化酶(T-SOD)活力和过氧化氢、羰基化蛋白和总抗氧化能力(TAOC),TBA法测定丙二醛的表达。结果Prdx6基因敲除小鼠肺组织免疫组织化学法未检测到Prdx6蛋白表达。两种属小鼠LPS组肺脏病理可见炎症细胞浸润、肺泡间隔增厚及肺泡内出血,Prdx6敲除型较野生型小鼠病理损伤更重。LPS刺激后,野生型LPS 24 h组BALF内的蛋白浓度为(441±54) mg/L,高于野生型对照组的(168±20) mg/L(t=-4.71,P＜0.01);Prdx6敲除型LPS 24 h组为(770±66)mg/L,高于野生型LPS 24 h组（t=-3.69,P＜0.01）。野生型LPS 24 h组T-SOD为(16.0±1.2) U/mg,低于野生型对照组的(26.5±3.9) U/mg(t=-6.22,P＜0.01);Prdx6敲除型LPS24 h组为(14.5±5.3)U/mg,与野生型LPS 24 h组差异无统计学意义（t=-0.56,P=0.60）。野生型LPS 24 h组肺脏过氧化氢和丙二醛[分别为(52.3±7.8)nmol/g和(3.3±0.5)nmol/mg]高于野生型对照组[分别为(29.5±3.2)nmok/g和(1.6±0.8)nmol/mg],差异有统计学意义（t值分别为-4.25和-5.94,均P＜0.01）,Prdx6敲除型LPS 24 h组[分别为(73.5±12.4)nmol/g和(5.9±0.9)nmol/mg],均高于野生型LPS24 h组（t值分别为-3.01和-6.01,均P＜0.05）。野生型LPS24 h组肺脏蛋白羰基为(6.9±1.2)nmol/mg,与野生型对照组的(6.1±0.9)nmol/mg差异无统计学意义(t=-1.62,P=0.15);Prdx6敲除型LPS 24 h组为(8.9±0.9)nmol/mg,高于野生型LPS 24 h组(t=-2.76,P＜0.05)。野生型LPS 24 h组肺脏TAOC为(4.7±0.6) U/mg,低于野生型对照组的(6.5±0.4) U/mg(t =3.35,P＜0.01);Prdx6敲除型LPS 24 h组为(3.9 ±0.4) U/mg,低于野生型LPS24 h组(t =2.44,P=0.04)。Prdx6敲除型对照组与其野生型对照组以上参数表达差异无统计学意义。结论在LPS诱导的肺损伤中,Prdx6基因缺失增加了活性氧的产生,加重了氧化应激反应,从而使肺损伤恶化。