儿童手足口病502例临床分型探讨

目的探讨手足口病临床分型特点。方法回顾性分析502例儿童手足口病的临床分型特点。结果轻型和重型病例在年龄、性别和皮疹的分布上无明显差异性。重型病例中发热持续〉72h占54例（55.67％）、肢体抖动占69例（71.13％）、膝反射亢进40例（41.24％）、呕吐17例（17.53％）、白细胞〉15×10^9／L占21例（21.65％）、血糖升高〉9mmol／L占19例（19.59％）,均明显高于轻型组（P〈0.05）。而心功酶增高率无明显差别（P=-0.27）。结论肢体抖动、膝反射亢进及呕吐对诊断重型病例较具临床特征性,而心功酶升高与否对于分型无指导意义。     

血管性痴呆的证候观察分析

对符合血管性痴呆（ＶＤ）诊断标准的１０５例患者进行了较为系统的证候调查及随访观察。研究发现,根据病情演变性质不同,ＶＤ可分三个期,即平台期、波动期和下滑期,各期证候特点及演变趋势各不相同。分析表明：肾精气虚、痰瘀阻络为ＶＤ发病的基础,痰瘀蕴积、生风化火、酿生毒邪、浊毒伤络、败坏脑髓形体为ＶＤ发生发展的关键。提出：ＶＤ临床辨证先分期、再分型,有助于从整体上定位、定性,把握疾病演变转归趋势,对确立符合ＶＤ发生发展规律的辨证治疗方案具有重要意义     

旧院区改造规划的探索——山东菏泽市第二人民医院门诊病房楼设计方案

文章以山东省菏泽市第二人民医院门诊病房楼的拆建工程为例，介绍该医院采用整体规划、分期实施的设计构思，分享对旧院区进行拆建改造设计的经验，以供其他改造的医院参考。     

The «Amish» NM_000256.3:c.3330+2T>G splice variant in MYBPC3 associated with hypertrophic cardiomyopathy is an ancient Swiss mutation

MYBPC3 is the most frequently mutated gene in hypertrophic cardiomyopathy (HCM). Several loss-of-function founder variants have been reported in MYBPC3 from various geographic regions, altogether suggestive of a modest or absent effect of these variants on reproductive fitness. One of them, a MYBPC3 splice variant, NM_000256.3:c.3330+2T > G, was first described in homozygous state in newborns presenting with a severe, recessive form of HCM among the Amish population and was later associated with adult-onset dominant HCM in heterozygous carriers. We here report this splice variant in heterozygous state in eight unrelated Swiss families with HCM, making it the most prevalent cardiomyopathy variant in western Switzerland. This variant was identified in patients using targeted (n = 5) or full-genome sequencing (n = 3). Given the prevalence of this variant in the Old Order Amish, Mennonites and Swiss populations, and given that both Amish and Mennonites founders originated from the Bern Canton in Switzerland, the MYBPC3, NM_000256.3:c.3330+2T > G variant appears to be of Swiss origin. Neighboring regions that hosted the first Amish settlements (Alsace, South Germany) should be on the lookout for that variant. The existence of MYBPC3 founder variants in different populations suggests that individuals with early-onset clinical disease may be the tip of the iceberg of a much larger number of asymptomatic carriers. Alternatively, reproductive fitness could even be slightly increased in some variant carriers to compensate for the reduction of fitness in the more severely affected ones, but this remains to be investigated.