含2-N,N-二甲氨基嘧啶环与噻吩环结构的共轭聚合物的合成及其性能

合成了一种新型单体2-N,N-二甲氨基-4,6-二氯嘧啶(ADNP).以二氯-1,3-双(二苯基磷)丙烷基镍(Ⅱ)作催化剂,通过2,5-二溴噻吩格氏试剂与该单体共聚得到了一种新型共轭聚合物,聚[(2-N,N-二甲胺基嘧啶-4,6-二)-2,5-噻吩](PThPm).采用FT-IR、1H-NMR等测试手段对新型单体与共聚物的结构进行了表征,并用UV-Vis、荧光光谱、X射线衍射、循环伏安、热重分析(TGA)等测试方法对单体和共聚物进行了性能分析.结果表明:共聚物在420 nm处出现UV-Vis吸收峰,在528 nm处出现荧光发射峰;共聚物的DMF溶液存在酸致变色现象,加入CF3COOH和CH3SO3H后,溶液由淡绿黄色转变为淡红色,UV-Vis吸收峰发生红移;PThPm共聚物有一定的结晶性和热稳定性;在-1.8～ 1.8 V之间出现电致变色现象,电极周围的溶液颜色从深蓝色变成深红色.     

早期氧气面罩雾化给氧对纠正重型颅脑损伤患者低氧血症的影响效果观察

目的探讨氧气面罩雾化给氧方式对重型颅脑损伤患者低氧血症的可行性及安全性,以促进患者早日康复。方法将收治98例重型颅脑损伤患者随机分为观察组48例和对照组50例,在常规治疗的同时,观察组采用氧气面罩接雾化器给氧方式进行给氧;对照组采用鼻塞导管湿纱布覆盖口鼻进行给氧。结果观察组其动脉血氧饱和度、氧分压明显提高。2组病死率比较差异明显,而2组患者的心率、血压、pH、PaCO2比较差异不明显。结论氧气面罩雾化器给氧能快速、有效纠正重型颅脑损伤患者缺氧状态,纠正低氧血症。     

Fragile X syndrome: clinical,cytogenetic and molecular screening among autism spectrum disorder children in Indonesia

Fragile X testing is a priority in the evaluation of autism spectrum disorders (ASD) cases because identification of the FMR1 mutation leads to new treatment options. This study is focused on determining the prevalence of the FMR1 gene mutation among ASD cases in Indonesia. DSM‐IV‐TR criteria were administered to diagnose ASD; symptom severity was classified using the Childhood Autism Rating Scale. Cytogenetic analysis, polymerase chain reaction, and Southern blot for FMR1 gene analysis were carried out to confirm the diagnosis of fragile X syndrome. The fragile X site and FMR1 full mutation allele were identified in 3 out of 65 (4.6%) and 4 out of 65 (6.15%) children aged 3–17 years (57 boys and 8 girls), respectively. The Fragile X laboratory workup is essential in the evaluation of patients with ASD. Molecular analysis is most accurate, while cytogenetic documentation of the fragile X site can also be useful if molecular testing is not available.     

婴儿先天性心脏病体外循环术后肾损伤分析

目的：探讨婴儿先天性心脏病（简称先心病）体外循环（CPB）术后肾损伤情况。方法：选取我院2009年10月至2010年7月期间CPB下行先心病手术的婴儿40 例，分别于转流前、手术结束时、术后2 h、术后6 h、术后24 h用酶联免疫吸附法（ELISA）检测血清肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、半胱氨酸蛋白酶抑制剂C (CysC)和尿N-乙酰-β-D氨基葡萄糖苷酶(NAG)浓度。常规生化方法检测术前及术后血清肌酐（Cr）及尿素氮（BUN）浓度。结果：术前与术后血清Cr及BUN均在正常范围内；血清TNF-α、IL-6和尿NAG浓度在CPB后均有显著性升高（P<0.05）。相关性分析提示血清TNF-α分别与尿NAG、血清CysC呈正相关（r分别为0.195，0.190，均P<0.05），血清IL-6与尿NAG亦呈正相关（r=0.278，P<0.01）；血清CysC和尿NAG检测出肾损伤的阳性率显著高于血清Cr或BUN(均P<0.01)。结论：CPB能引起婴儿急性肾损伤，可能与血清中TNF-α和IL-6的浓度增高相关。血清CysC和尿NAG可作为反映肾功能变化较敏感的指标。     

破骨细胞的骨吸收机制

破骨细胞是一种巨大的多核细胞,起源于单核巨噬细胞/单核系造血前体细胞,在骨吸收过程中发挥重要作用。破骨细胞的形成和活性异常可导致骨质疏松、类风湿关节炎、关节置换后假体无菌性松动等许多疾病,因此破骨细胞是治疗这些疾病的靶点之一。目前对破骨细胞的分化形成研究较多,但对破骨细胞如何识别、降解骨组织方面的研究较少。骨盐被认为是破骨细胞识别的重要成分,但是近年来的研究发现骨基质不是破骨细胞激活的必需成分,玻连蛋白包被的培养皿也能使破骨细胞出现骨吸收的特有形态,玻连蛋白对破骨细胞的激活有重要的作用。此外,最近的研究证明骨基质降解产物的吞入和分泌对破骨细胞的分化和功能的保持有重要意义。这些分子机制的研究可能为骨骼疾病提供新的治疗靶点。     

There are no association between IgE levels and symptoms of anxiety and depression in the adult female general population. The Hordaland Health Study (HUSK)

There are multiple reports of increased prevalence of anxiety and depression in patients with asthma, eczema and rhinitis. Suggested biological mechanisms underlying these associations most commonly involve IgE. However, the association between anxiety/depression and IgE has hardly been studied, and the aim of the present study will therefore be to examine the hypothesized association between anxiety/depression and IgE in a general adult female population. A sub-sample of 374 female participants in a population-based general health study in Norway (the Hordaland Health Study) with participation rate 70% was screened for total and allergen-specific IgE. Anxiety and depression were measured employing the Hospital Anxiety and Depression Scale (HADS). This design ensured adequate statistical power, and the population-approach ensured satisfactory variance in both IgE and anxiety/depression. No association between case level or symptom load of anxiety/depression and total or allergen-specific IgE was found. Non-significant tendencies were both positive and negative. This finding was robust across continuous and categorical statistical approaches. Our finding does not question the commonly reported associations between anxiety/depression and asthma, rhinitis and eczema. We do, however, question the relevance of IgE as an aetiological factor in the biological chain underlying these associations.