天津市1999-2021年0~14岁儿童伤害死亡谱及城乡差异分析

目的 分析天津市0~14岁儿童伤害死亡谱的特征、变化情况及城乡差异。方法 1999-2021年天津市儿童伤害死亡数据来源于天津市全人口全死因监测数据库,计算不同亚组人群和主要伤害原因的构成比、粗死亡率和标化死亡率并比较城乡差异。采用Cochran-Armitage趋势检验分析死亡原因构成比的时间变化趋势。采用Joinpoint回归分析变化趋势,计算平均年变化百分比（AAPC）。伤害死亡风险的季节差异用死亡率比值及其95%CI表示。结果 1999-2021年,伤害是天津市0~14岁儿童的第3位死因。农村儿童死于医疗卫生机构的比例为31.08%,低于城市的37.82%。儿童伤害的总体标化死亡率呈下降趋势（AAPC=-5.54%,P<0.001）。溺水和道路交通伤害的标化死亡率在城市和农村地区呈下降趋势（P<0.001）。意外中毒的标化死亡率仅在农村地区呈下降趋势（AAPC=-8.09%,P<0.001）,在城市地区无明显变化趋势（P>0.05）。自杀标化死亡率在城市地区无明显变化趋势（P>0.05）,在10~14岁农村儿童中呈上升趋势（AAPC=4.58%）。跌倒/坠落标化死亡率在城市和农村地区均无明显变化趋势（P>0.05）。伤害死亡的总体风险和溺水死亡风险在城乡均为夏季最高;道路交通伤害在城市为秋季最高,在农村为夏季最高;意外中毒死亡风险在城乡均为冬季最高。结论 近年来天津市儿童伤害死亡情况得到明显改善。城市和农村地区的儿童伤害死亡水平仍存在较大差异,在未来政策制定中,应充分考虑缩小城乡差距。     

15例原发性淀粉样变性的临床与病理分析

目的 加强对有突出肾损害的原发性淀粉样变性的认识,提高诊断水平。方法 对１５例有突出肾损害的原发性淀粉样变性病例资料从多脏器受累情况。骨髓穿刺及活检。血／尿蛋白电泳和电泳及治疗预后等方面进行总结和分析。结果 肾脏、消化、循环和血液系统有不同程度受累,部分病例有骨髓浆细胞增生,血／尿中检出单克隆蛋白。结论本病肾损害有一定特点,尤其特异性的肾脏病理改变可明确诊断 。     

家庭环境因素对青少年精神分裂症的影响

目的 探讨精神分裂症和家庭环境的关系。方法 用自编“家庭环境调查问卷”、修订的父母养育方式评价量表（ＥＭＢＵ）对８２例青少年患者和８２个正常青少年家庭进行调查,用Ｃａｍｂｅｒｗｅｌｌ家庭会谈表（ＣＦＩ）评定患者亲属的情感表达（ＥＥ）水平。结果 （１）病例组父母关系、亲子关系差,父母有不良行为习惯者多（Ｐ〈０．０５）;家庭性患者父母文化水平低、经济收入低、健康状况差（Ｐ〈０．０１）。（２）病例组父母     

微血管舒张功能障碍及体外反搏的改善作用

目的：通过测定微血管血流灌注来反映微血管的舒张功能,同时观察体外反搏治疗改善冠心病患者微血管舒张功能障碍的效果。方法：应用激光多普勒血流量计（ＬＤＦ） ,测量５８ 个被观察者的前臂皮肤在反应性充血前后微血管血流灌注增加比值,评价血流介导的微血管舒张功能。结果：冠心病组、高胆固醇血症组及吸烟组微血管舒张功能明显低于对照组,比值分别为１．８３±０．３７、２．６３±０．５１、３．１９ ±０．５６ 比３．５６±０．３６ ;Ｐ分别＜ ０．０１,＜０．０１,＜ ０．０５。冠心病组反搏治疗前后比,其微血管的舒张功能明显提高,比值为１．８３±０．３７ 比２．５４±０．４３; Ｐ＜０．０１。结论：ＬＤＦ可检测冠心病患者明显的微血管舒张功能障碍及高胆固醇血症者和吸烟者微血管功能的异常;体外反搏治疗可改善冠心病患者的微血管舒张功能。     

大鼠局灶性脑缺血模型及其与C反应蛋白变化的关系

目的 改进大鼠大脑中动脉梗塞法,建立更接近于临床缺血性脑卒中及其再扩灌注的可靠模型,并观察其与血甭Ｃ反应蛋白变化的。方法沿大鼠右颈内动脉插入长２．１￣２．３ｃｍ直径０．２０５ｍｍ的单股尼龙丝,直达大脑中动脉起始部开口,阻断其血流,观察大鼠神经病学改变及脑组织形态学变化,并测定血清Ｃ反应蛋白含量。结果 术后大鼠表现特殊体态及典型追尾征,６ｈ大脑中动脉供血区出现缺血性外观（ＴＴＣ染色）及相应组织学变化     

超声照射对声振微泡稳定性的影响

目的与方法造影剂微泡浓度、大小是影响心肌声学显影最重要因素。本研究采用２×２×４析因分析法分析不同超声照射条件对造影剂微泡浓度及直径的影响,即声波频率、能量以及照射时间对微泡浓度、大小的单独及交互作用。为临床行静脉心肌声学造影检查时选择适宜的超声照射条件提供参考。结果能量越大、照射时间越长,微泡破坏越多,平均直径越小：照射频率对微泡浓度影响不大,但影响微泡大小,频率越高,微泡越小。结论为减少超声照射对微泡的破坏,提高心肌声学造影效果,应尽可能选用低能量、低频率超声波,并减少不必要的照射时间。     

Optimizing contrast-enhanced abdominal CT in infants and children using bolus tracking

OBJECTIVE: Manual administration of IV contrast material results in unpredictable injection rates. Our purpose was to determine the effect of bolus tracking on overall abdominal helical CT scan quality, particularly on hepatic enhancement, in children with manually administered contrast media. MATERIALS AND METHODS: We compared 33 abdominal helical CT scans of 29 children in whom bolus tracking was used with 22 CT scans of a control group of 21 children in whom bolus tracking was not used. All contrast material was administered by manual injection. Qualitative assessment was made of organ and vessel enhancement and overall scan appearance. Quantitative assessment using region-of-interest cursors was performed at three anatomic levels, and the results for the two groups of children were compared. RESULTS: Qualitative comparison of enhancement parameters between the bolus tracking group (number given first) and the control group (number given second) yielded the following: splenic artifact in 9% versus 23% (p = .24); inferior vena cava flow artifact in 3% versus 27% (p = .01); scanning during the nephrographic phase in 89% versus 59% (p = .02); and good quality grade in 79% versus 64% (p = .23). Significantly greater hepatic enhancement (as measured in mean Hounsfield units) was achieved in the bolus tracking group than in the control group at the superior (48.5 versus 28.6; p < .001), middle (47.9 versus 32.3; p < .001), and inferior (48.2 versus 36.5; p = .01) levels. Hepatic enhancement increased significantly from the superior to the inferior level in the control group (p < .02), whereas enhancement was homogeneous in the bolus tracking group (p > .50). CONCLUSION: Bolus tracking provides improved contrast enhancement, including significantly greater hepatic enhancement, during abdominal helical CT in children in whom the rate of injection of contrast material is unpredictable.     

Polymorphisms at - 174 and in the 3' flanking region of interleukin-6 (IL-6) gene in patients with myasthenia gravis

We examined the bi-allelic polymorphism at - 174 in the promoter region and the polymorphism in the 3' flanking AT rich region of the interleukin-6 (IL-6) gene in Swedish patients with myasthenia gravis (MG) and ethnically matched healthy individuals. There was no association between the polymorphisms and the disease. There was no relation of the polymorphisms to the clinical variables, the thymic histopathologies, the level of serum acetylcholine receptor antibodies or the concentrations of IgG and its subclasses. Our data yield no evidence for the IL-6 gene contributing to the disease susceptibility.     

Opioid peptide receptor studies, 11: involvement of Tyr148, Trp318 and His319 of the rat mu-opioid receptor in binding of mu-selective ligands

Previous data obtained with the cloned rat mu opioid receptor demonstrated that the "super-potent" opiates, ohmefentanyl (RTI-4614-4) and its four enantiomers, differ in binding affinity, potency, efficacy, and intrinsic efficacy. Molecular modeling (Tang et al., 1996) of fentanyl derivatives binding to the mu receptor suggests that Asp147, Tyr148, Trp318, and His319 are important residues for binding. According to this model, Asp147 interacts with the positively charged opiate agonist to form potent electrostatic and hydrogen-bonding interactions. In this study, the role of weak electrostatic and hydrogen-bonding "pi-pi" interactions of the O atom of the carbonyl group and the phenyl ring structures of RTI-4614-4 and its four enantiomers with residues Tyr148, Trp318, and His319 were explored via site-directed mutagenesis. Tyr148 (in transmembrane helix 3 {TMH3}), Trp318 (TMH7), and His319 (TMH7) were individually replaced with phenylalanine or alanine. Receptors transiently expressed in COS-7 cells were labeled with [125I]IOXY according to published procedures. Mutation of Tyr148 to phenylalanine reduced the binding affinities of some mu-selective agonists (2-7 fold) but did not alter the affinities of DAMGO, naloxone, and the non-selective opiates etorphine and buprenorphine. In contrast, this mutation significantly increased the binding affinities (decreased the Kd values) of [D-Ala2,D-Leu5]enkephalin, IOXY, and dermorphin. Mutation of Trp318 decreased opioid receptor binding to almost undetectable levels. Substitution of alanine for His319 significantly reduced binding affinities for the opioid ligands tested (1.3- to 48-fold), but did not alter the affinities of naloxone and bremazocine. These results indicate the importance of Tyrl48 and His319 for the binding of fentanyl derivatives to the mu receptor. Functional studies using the mutant receptors will provide additional insight into the mechanism of action of RTI-4614-4 and its four enantiomers.