卫藏藏族、康巴藏族和安多藏族女青年唇形特征

目的 探讨藏族女青年的唇形特征。 方法 根据知情同意原则,以自愿参加的藏族女青年为研究对象,有效样本542例,年龄18～23岁,平均年龄（20.42±1.34）岁。利用直角规直接测量被测者的口裂宽和唇高,并计算唇指数。 结果 藏族女青年唇高均值为（18.01±4.29）mm,口裂宽均值为（49.40±5.55）mm,唇指数均值为（36.60±8.21）mm。康巴藏族的唇高和唇指数均值与卫藏藏族和安多藏族比较差异均有显著性（P<0.01）,卫藏藏族的口裂宽均值与安多藏族比较差异均有显著性（P＜0.01）。唇高与年龄成负性相关（r=-0.124,P<0.01）,唇指数与年龄成负性相关（r=-0.155,P<0.01）,口裂宽与年龄相关性无统计学意义（P＞0.05）。 结论 康巴藏族唇高较高,安多藏族具有更阔的口裂宽。藏族女青年唇高和唇指数随年龄递增而减小,唇形特征以中唇型（69.2%）和宽口裂（73.6%）为主。     

HGF与PGE2在 RA-ILD患者血清中的表达水平及意义

目的 通过检测肝细胞生长因子（HGF）和前列腺素E2（PGE2）在类风湿关节炎合并肺间质病变（RA-ILD）患者血清中的表达水平,探讨其在RA-ILD中的意义.方法 采用ELISA法检测100例RA（包括50例RA-ILD）和50例健康体检者血清HGF、PGE2的表达水平.结果 RA-ILD组中HGF、PGE2的含量均低于非肺间质病变RA组及对照组,差异有统计学意义（P＜0.05）;且HGF与PGE2呈正相关关系,二者均与疾病活动性指标DAS28评分呈负相关关系.结论 HGF和PGE2参与RA ILD的发生发展过程;HGF和PGE2可作为判断RA-ILD活动期的指标,也可作为筛查RA-ILD指标之一,同时为RA-ILD提供一种新的治疗方法.     

Maturational atrioventricular nodal physiology in the mouse

INTRODUCTION: Dual AV nodal physiology is characterized by discontinuous conduction from the atrium to His bundle during programmed atrial extrastimulus testing (A2V2 conduction curves), AV nodal echo beats, and induction of AV nodal reentry tachycardia (AVNRT). The purpose of this study was to characterize in vivo murine maturational AV nodal conduction properties and determine the frequency of dual AV nodal physiology and inducible AVNRT. METHODS AND RESULTS: A complete transvenous in vivo electrophysiologic study was performed on 30 immature and 19 mature mice. Assessment of AV nodal conduction included (1) surface ECG and intracardiac atrial and ventricular electrograms; (2) decremental atrial pacing to the point of Wenckebach block and 2:1 conduction; and (3) programmed premature atrial extrastimuli to determine AV effective refractory periods (AVERP), construct A2V2 conduction curves, and attempt arrhythmia induction. The mean Wenckebach block interval was 73 +/- 12 msec, 2:1 block pacing cycle length was 61 +/- 11 msec, and mean AVERP100 was 54 +/- 11 msec. The frequency of dual AV nodal physiology increased with chronologic age, with discontinuous A2V2 conduction curves or AV nodal echo beats in 27% of young mice < 8 weeks and 58% in adult mice (P = 0.03). CONCLUSION: These data suggest that mice, similar to humans, have maturation of AV nodal physiology, but they do not have inducible AVNRT. Characterization of murine electrophysiology may be of value in studying genetically modified animals with AV conduction abnormalities. Furthermore, extrapolation to humans may help explain the relative rarity of AVNRT in the younger pediatric population.     

Botulinum neurotoxin type A inhibits synaptic vesicle 2 expression in breast cancer cell lines

Aim: It is known that botulinum neurotoxin type A (BoNTA) improves some kinds of cancer (e.g. prostate) and that synaptic vesicle glycoprotein 2 (SV2) is the molecular target of this neurotoxin. Besides having potential therapeutic value, this glycoprotein has recently been proposed as a molecular marker for several types of cancer. Although the mechanisms of cancer development and the improvement found with botulinum treatment are not well understood, the formation of the botulinum-SV2 complex may influence the presence and distribution of SV2 and the function of vesicles. To date, there are no reports on the possible effect of botulinum on breast cancer of unknown causes, which have a great impact on women’s health. Thus we determined the presence of SV2 in three breast cancer cell lines and the alterations found with botulinum application. Materials and methods: With and without adding 10 units of botulinum, SV2 protein expression was determined by optical densitometry in T47D, MDA-MB-231 and MDA-MB-453 cell lines and the distribution of SV2 was observed with immunochemistry (hematoxylin staining). Results: The SV2 protein was abundant in the cancer cells herein tested, and maximally so in T47D. In all three cancer cell lines botulinum diminished SV2 expression, which was found mostly in the cell periphery. Conclusion: SV2 could be a molecular marker in breast cancer. Its expression and distribution is regulated by botulinum, suggesting an interesting control mechanism for SV2 expression and a possible alternative therapy. Further studies are needed in this sense.     

Efficacy of atrial antitachycardia pacing using the Medtronic AT500 pacemaker in patients with congenital heart disease

Patients with congenital heart disease are vulnerable to atrial tachyarrhythmias, especially after atrial surgeries. We evaluated the efficacy of atrial arrhythmia detection and antitachycardia pacing (ATP) using the Medtronic AT500 pacemaker in 28 patients with congenital heart disease (age 30 +/- 18 years). Of 15 patients with atrial arrhythmias, 14 had atrial tachycardia events that were appropriately detected. ATP was enabled for 167 treatable episodes, successfully converting 90 (54%). Rhythms classified as ventricular tachycardia were detected 127 times, yet most were actually atrial or sinus tachycardia with 1:1 atrioventricular conduction. Atrial tachycardias in congenital heart disease are amenable to ATP algorithms in the AT500 pacemaker.     

Comparison of two murine models of familial hypertrophic cardiomyopathy

Although sarcomere protein gene mutations cause familial hypertrophic cardiomyopathy (FHC), individuals bearing a mutant cardiac myosin binding protein C (MyBP-C) gene usually have a better prognosis than individuals bearing beta-cardiac myosin heavy chain (MHC) gene mutations. Heterozygous mice bearing a cardiac MHC missense mutation (alphaMHC(403/+) or a cardiac MyBP-C mutation (MyBP-C(t/+)) were constructed as murine FHC models using homologous recombination in embryonic stem cells. We have compared cardiac structure and function of these mouse strains by several methods to further define mechanisms that determine the severity of FHC. Both strains demonstrated progressive left ventricular (LV) hypertrophy; however, by age 30 weeks, alphaMHC(403/+) mice demonstrated considerably more LV hypertrophy than MyBP-C(t/+) mice. In older heterozygous mice, hypertrophy continued to be more severe in the alphaMHC(403/+) mice than in the MyBP-C(t/+) mice. Consistent with this finding, hearts from 50-week-old alphaMHC(403/+) mice demonstrated increased expression of molecular markers of cardiac hypertrophy, but MyBP-C(t/+) hearts did not demonstrate expression of these molecular markers until the mice were >125 weeks old. Electrophysiological evaluation indicated that MyBP-C(t/+) mice are not as likely to have inducible ventricular tachycardia as alphaMHC(403/+) mice. In addition, cardiac function of alphaMHC(403/+) mice is significantly impaired before the development of LV hypertrophy, whereas cardiac function of MyBP-C(t/+) mice is not impaired even after the development of cardiac hypertrophy. Because these murine FHC models mimic their human counterparts, we propose that similar murine models will be useful for predicting the clinical consequences of other FHC-causing mutations. These data suggest that both electrophysiological and cardiac function studies may enable more definitive risk stratification in FHC patients.     

糖尿病合并慢性鼻窦炎患者鼻分泌物培养结果分析

目的分析糖尿病合并慢性鼻窦炎患者鼻分泌物病原菌分布及耐药性,为临床合理使用抗菌药物提供依据。方法以医院2012年1月-2014年10月收治的297例糖尿病合并慢性鼻窦炎患者为研究对象,调查分析感染病原菌种类及药敏试验结果。结果 297份标本中237份检出病原菌,阳性率为79.8%;共分离鉴定病原菌256株,其中革兰阳性菌占61.7%,主要包括表皮葡萄球菌39.8%、金黄色葡萄球菌8.2%和肺炎链球菌5.9%,革兰阴性菌占38.3%,主要包括产气肠杆菌10.9%、肺炎克雷伯菌7.4%和大肠埃希菌5.9%,革兰阳性菌对青霉素G和红霉素耐药率较高,耐药率分别为78.5%和67.1%,革兰阴性菌对头孢唑林、庆大霉素、氨苄西林、氨曲南和哌拉西林高度耐药,耐药率为77.6%~92.9%。结论糖尿病合并慢性鼻窦炎患者鼻分泌物病原菌检出率较高,且病原菌表现为耐多药特性,应加强其病原菌及耐药性监测,掌握病原菌分布及其耐药性,为临床选用抗菌药物提供依据。     

小檗碱对有机阴离子转运体抑制作用及双向跨膜转运研究

目的 研究小檗碱对有机阴离子转运体（OATs）的抑制作用及其双向跨膜转运情况。方法 应用由转染试剂Lipo 3 000介导的动物细胞转基因方法、经筛选得到人有机阴离子转运体OAT1、OAT2、OAT3、OAT4、OAT7和URAT1高表达单克隆细胞株;以野生型（WT）细胞为对照组,用各转运体放射性同位素标记底物和抑制剂验证其转运活性;观察100 μmol/L小檗碱对各转运体的抑制作用,并测定小檗碱对URAT1转运活性的半数抑制浓度（IC₅₀）。通过Caco-2细胞模型研究小檗碱的双向跨膜转运情况。结果 100 μmol/L小檗碱使OAT1、OAT2、OAT3、OAT4、OAT7和URAT1相对转运活性分别下降至（70.48±4.23）%、（69.13±1.28）%、（72.12±3.28）%、（79.77±6.49）%、（69.51±5.99）%、（38.4±2.67）%;小檗碱对URAT1抑制作用的IC₅₀为13.6 μmol/L;在50和100 μmol/L浓度下,小檗碱在顶侧（AP侧）-基底侧（BL侧）方向的跨膜渗透率P_app（A-B）分别为0.28×10^-6 cm/s和0.40×10^-6 cm/s,其相对应的外排率分别为3.18和3.15。结论 小檗碱对URAT1的抑制作用较强,对OAT1、OAT2、OAT3、OAT4、OAT7抑制作用相对较弱,小檗碱是一些外排蛋白的底物,为预测小檗碱可能发生的药物-药物相互作用、解释生物利用度低提供了理论依据。     

Impact of manufacturer advisories and FDA recalls of implantable cardioverter defibrillator generators in pediatric and congenital heart disease patients

Introduction: Recalls of implantable cardioverter defibrillator (ICD) generators have affected many patients. No information is available regarding the impact specifically on pediatric and congenital heart disease (CHD) patients. This study was undertaken to determine implications of ICD manufacturers’ advisories and recalls on children and CHD patients. Methods: The first part of this study involved single‐center review of patients who underwent ICD placement between 2000 and 2005. Patients with ICDs affected by the 2005 advisories/recalls were reviewed for incidence of explantation, malfunction and complications. Secondly, members of the Pediatric and Congenital Electrophysiology Society (PACES) were queried for patients with affected devices, incidences of explantation, malfunction, and explant‐related complications. Data were pooled for aggregate summary. Results: Among 233 patients who underwent ICD implantation at our institution during the study period, 58 (25%) patients had advisory/recalled devices and 13 of 58 (22%) underwent explantation following 3.1 ± 1.3 years implant duration. No defects were identified by the manufacturer. No patients experienced complications requiring reintervention or rehospitalization. Questionnaire responses were received from 22 PACES institutions, included 177 patients with affected devices, of which 76 (43%) were removed. One patient died from complications following revision, and 1 patient had complications requiring reoperation. Two explanted devices had loose headers; no other defects were discovered. Taken together, 2 of 89 explanted devices were defective, and 2 complications occurred from explantation. Conclusions: Advisories and recalls affect substantial numbers of pediatric and CHD patients. A significant proportion underwent explantation. Although complications are infrequent, there are important medical, psychosocial, and financial impacts associated with ICD replacement.     

基于药物转运体的小白菊内酯衍生物ACT001的跨膜转运机制和耐药性研究

目的 从药物转运体角度探讨小白菊内酯衍生物ACT001的跨膜转运机制,并阐明ACT001可能产生的耐药性机制。方法 采用人药物转运体高表达单克隆细胞株/囊泡、人结肠腺癌细胞（Caco-2、LS-180）,使用q RT-PCR、Western blotting、LC-MS/MS放射性同位素示踪等技术手段,共同研究ACT001的跨膜转运机制和耐药性。结果 小白菊内酯衍生物ACT001能够抑制外排转运体BCRP的转运活性,其半数抑制浓度（half inhibitory concentration,IC50）为48.6μmol/L。ACT001在Caco-2细胞单层上的外排率为2.95,添加乳腺癌耐药蛋白（breast cancer resistance protein,BCRP）抑制剂Ko143可使外排率降至0.807;添加P糖蛋白（P-glycoprotein,P-gp）抑制剂盐酸维拉帕米对ACT001的外排率没有影响。在LS-180细胞中添加10μmol/L的ACT001诱导72 h,可使P-gp和BCRP的m RNA表达水平分别提高8.89、8.21倍,蛋白相对表达量分别提高3.76、...