经皮集束电极射频消融治疗小肝癌

目的 探讨经皮集束电极射频消融(radiofrequency ablation,RFA)对小肝癌(直径≤3cm)的治疗效果。方法利用RF-2000TM肿瘤射频治疗系统,在B超引导下对21例小肝癌患者24个肿块进行经皮肝穿刺射频热凝治疗,并用B超及CT检查以了解RFA治疗效果,随访观察其复发和生存情况。结果 RFA治疗后100％(20/20)的肿块血供消失(另4个治疗前即无血供),且2,4个肿块呈完全凝固性坏死(100％)。随访6月-3年,21侧中存活19例,半年生存率100％。存活的19例中,已有5例生存半年,4例生存1年,6例生存2年,4例生存3年。结论 集束电极RFA治疗小肝癌创伤小,安全,疗效可靠。     

米铂的合成工艺改进

本研究对米铂(1)的合成工艺进行了改进。十四烷酸(2)和氢氧化钠在乙酸乙酯/纯化水混合溶剂中反应,经静置析晶得十四烷酸钠(3)。3和奥沙利铂(4)在水中反应,经静置析晶、抽滤、热纯化水淋洗和精制后得1,纯度达99.91%,总收率79%(以2计),并且将1中3和草酸的含量均降至0.05%以下。优化后的工艺对原料2的质量要求降低:同系物十至十六烷酸单杂含量不超过0.2%,各杂质含量之和不超过1.0%即可得到合格产品,后处理简单,易于工业化生产。     

异种鼠原位肝移植模型的改进

目的:建立金黄地鼠到大鼠异种原位肝移植模型,使异种肝移植模型能够普及应用. 方法:共施行99例金黄地鼠到大鼠原位肝移植,其中44例采用Kamada方法,55例采用改进方法(即受体肝分步切除的二袖套法原位肝移植),对两种术式的操作时间、无肝期及手术成功率等进行了比较. 结果:Kamada方法受体手术时间(44.1±4.5) min、无肝期(17.1±2.2) min、肝下下腔静脉和门静脉套接时间均3.5 min、手术成功率88.6% (39/44),改进方法所需时间分别为(39.2±3.7) min, (13.9±1.2) min, 1 min,手术成功率87.3% (48/55). 结论:改进的受体肝分步切除的二袖套法金黄地鼠到大鼠异种原位肝移植术,能缩短无肝期和手术时间,是异种肝移植研究较简单、易行、稳定的动物模型.     

地塞米松对体外嗜酸粒细胞白介素3、白介素5和GM-CSF受体的共同β受体mRNA表达的影响及意义

目的 观察地塞米松对哮喘豚鼠体外不同密度嗜酸粒细胞(EOS)凋亡及IL-3、IL-5和粒细胞-巨噬细胞集落刺激因子受体的共同β受体(βcR)mRNA表达的影响.探讨地塞米松促进哮喘EOS凋亡的机制.方法 卵蛋白激发哮喘豚鼠动物模型48 h后行支气管肺泡灌洗,分离低密度EOS(HEOS)及正常密度EOS(NEOS).HEOS及NEOS分别与地塞米松(10-10～10-5mol/L)共培养24 h,以原位杂交方法检测不同密度EOS的βcR mRNA表达,3'末端脱氧核苷转移酶介导的脱氧三磷酸尿苷缺口末端标记法检测细胞凋亡.结果 地塞米松干预24 h后,可见EOS凋亡增加的同时,不同密度EOS中βcR mRNA表达下降,并与地塞米松浓度呈剂量依赖性.βcR表达与EOS凋亡呈负相关(P<0.05).结论 地塞米松可抑制不同密度EOS表达βcR,抑制其细胞因子活动,促进EOS凋亡.地塞米松可以通过增加EOS中βcR表达调节EOS凋亡.     

Definitive Surgery for Perforated Peptic Ulcer in Malaysia1

Seventy-three cases of perforated peptic ulcer (51 duodenal and 22 gastric) are reviewed. The condition is common in the Chinese, but rare in Malays, Indians, Pakistanis and Ceylonese. Simple closure is followed by a high recurrence rate. Emergency definitive surgery is safe. Difficulties with follow-up of patients favour a wider use of emergency definitive surgery for perforated peptic ulcer in Malaysia.     

胃癌病人脉管内癌栓与临床病理因素及预后的关系

目的分析胃癌病人脉管内癌栓与淋巴结转移等病理特征的关系及其对疾病预后影响。方法回顾性分析375例胃癌病人术后临床及病理资料,其中脉管内癌栓阳性者54例,阴性者321例,分析脉管内癌栓与疾病分期、淋巴结转移等的关系,并比较同期癌栓阳性组与阴性组病人3年及5年生存率的差异。结果不同UICC分期、肿瘤浸润深度、组织分化程度、淋巴结转移程度胃癌病人脉管内癌栓的发生率比较,差异皆有显著意义（χ^2=7.355-20.066,P〈0.05）。脉管内癌栓阴性病人Ⅰb＋Ⅱ期、Ⅲ期的3年、5年生存率高于同期阳性组,差异有统计学意义（χ^2=3.950-5.632,P〈0.05）。结论脉管内癌栓是胃癌病人重要的预后因素,应予以高度重视。     

Serum digoxin concentration in a neonate with renal and hepatic impairment

Abstract This report demonstrates the questionable usefulness of monitoring digoxin concentrations using the available immunoassays in some clinical situations. The patient reported here showed three characteristics (being a neonate with hepatic and renal impairment) that are associated with the presence of digoxin-like immunoreactive substances. The patient's serum digoxin concentration continued to rise to a peak of 43.7 nmol/L (34.1 ng/mL), 19 days after administration of the drug was discontinued.     

急性肺栓塞后线粒体前凋亡蛋白的表达及其促细胞凋亡机制研究

目的 研究大鼠急性肺栓塞(APE)后肺组织中线粒体前凋亡蛋白(ARTS)的表达变化及其诱导的细胞凋亡.方法 采用自体血栓栓塞颈总动脉制备大鼠APE模型.分别在APE前(对照)和APE后1、8、24和48 h开胸取肺脏.常规提取肺组织的总RNA和总蛋白,用半定量逆转录-聚合酶链反应(RT-PCR)方法检测ARTS mRNA表达水平,用蛋白质免疫印迹法(Western blotting)进一步验证ARTS以及ARTS诱导凋亡相关蛋白Bcl-2、Bcl-xL、XIAP和H2Ax的表达变化,用免疫组化法检测肺组织中ARTS在APE前后的表达变化及其组织分布情况,用原位末端缺刻标记法(TUNEL)检测肺组织内细胞凋亡情况.结果 APE后ARTS的mRNA及蛋白表达水平均升高,于1 h和48 h升高最明显(P相似文献   

Protein kinase A-mediated phosphorylation of cMyBP-C increases proximity of myosin heads to actin in resting myocardium

Protein kinase A-mediated (PKA) phosphorylation of cardiac myosin binding protein C (cMyBP-C) accelerates the kinetics of cross-bridge cycling and may relieve the tether-like constraint of myosin heads imposed by cMyBP-C. We favor a mechanism in which cMyBP-C modulates cross-bridge cycling kinetics by regulating the proximity and interaction of myosin and actin. To test this idea, we used synchrotron low-angle x-ray diffraction to measure interthick filament lattice spacing and the equatorial intensity ratio, I(11)/I(10), in skinned trabeculae isolated from wild-type and cMyBP-C null (cMyBP-C(-/-)) mice. In wild-type myocardium, PKA treatment appeared to result in radial or azimuthal displacement of cross-bridges away from the thick filaments as indicated by an increase (approximately 50%) in I(11)/I(10) (0.22+/-0.03 versus 0.33+/-0.03). Conversely, PKA treatment did not affect cross-bridge disposition in mice lacking cMyBP-C, because there was no difference in I(11)/I(10) between untreated and PKA-treated cMyBP-C(-/-) myocardium (0.40+/-0.06 versus 0.42+/-0.05). Although lattice spacing did not change after treatment in wild-type (45.68+/-0.84 nm versus 45.64+/-0.64 nm), treatment of cMyBP-C(-/-) myocardium increased lattice spacing (46.80+/-0.92 nm versus 49.61+/-0.59 nm). This result is consistent with the idea that the myofilament lattice expands after PKA phosphorylation of cardiac troponin I, and when present, cMyBP-C, may stabilize the lattice. These data support our hypothesis that tethering of cross-bridges by cMyBP-C is relieved by phosphorylation of PKA sites in cMyBP-C, thereby increasing the proximity of cross-bridges to actin and increasing the probability of interaction with actin on contraction.