Chang-Chong Li

分析轻度胃肠炎伴婴幼儿良性惊厥（BICE）的临床特点及预后。 对436例BICE患儿的临床资料进行回顾性分析，并对其中206例患儿进行1.5~7年的预后随访，邀请部分家长完成Weiss功能缺陷量表以评价患儿远期的社会功能。 患儿发病年龄多在13~24月龄；发病时间多在9月至次年2月；惊厥主要表现为全身强直-阵挛发作，多在发病24 h内发作，每次持续时间多在5 min内，可有丛集性发作。206例患儿随访过程中，除1例仍有癎样放电，其余脑电图复查均恢复正常，所有患儿家属认为患儿智力正常，无明显性格改变。基于部分BICE患儿家长填写的Weiss功能缺陷量表显示，BICE患儿的远期社会功能与年龄、性别相匹配的健康对照儿童比较差异无统计学意义。 BICE多发生于1~2岁婴幼儿，多表现为短暂的全面性发作，部分可表现为丛集性发作，但极少进展为癫癎，预后良好。

探讨肺炎链球菌（SP）感染时短腭、肺及鼻咽上皮克隆1（SPLUNC1）的宿主防御作用，及白藜芦醇（Res）对SPLUNC1表达的影响，为SP感染性疾病的治疗提供新的思路。 根据感染复数（MOI）不同将SP感染BEAS-2B细胞分为对照组、MOI20 SP组和MOI50 SP组；根据Res药物浓度不同将Res预处理MOI20 SP感染BEAS-2B细胞分为12.5Res+SP组、25Res+SP组、50Res+SP组（Res终浓度分别为12.5 μmol/L、25 μmol/L、50 μmol/L）。通过CCK-8法检测细胞活性，并选出SP、Res最佳作用浓度及时间。正式实验分为对照组、Res组、SP组和Res+SP组，采用实时定量PCR法和ELISA法检测各组SPLUNC1 mRNA及蛋白表达。 随SP感染时间延长，细胞活性呈降低趋势；与对照组和MOI20 SP组相比，MOI50 SP组细胞活性有下降趋势；与MOI20 SP组相比，25Res+SP组细胞活性增强（ P 0.05）。 SP感染可以诱导SPLUNC1表达，发挥宿主防御作用，Res可以在感染发生时上调SPLUNC1的表达，以浓度及时间依赖的方式加强细胞保护。

比较儿童流感病毒A型(ⅣA)、B型(ⅣB)致下呼吸道感染(LRTI)的流行特点及临床特征。 回顾性分析2010~2014年收住在温州医科大学附属育英儿童医院的366例流感病毒(Ⅳ)阳性的LRTI患儿的临床资料, 其中ⅣA阳性272例, ⅣB阳性94例。 Ⅳ多在每年12月至次年3月流行, 以ⅣA为主, 且ⅣA隔年7月或9月有小流行, ⅣB呈隔年12月至次年3月流行。单纯ⅣA致LRTI患儿白细胞计数、白细胞升高比例、血钠异常比例、血钾异常比例高于单纯ⅣB致LRTI患儿(P < 0.05), 但两组患儿在年龄、性别、基础疾病、临床表现、合并细菌及非典型病原体感染率方面差异无统计学意义(P > 0.05)。ⅣB合并呼吸道合胞病毒(RSV)感染率高于ⅣA(P < 0.01)。 ⅣA每年冬春季节流行, 隔年夏季有小流行; ⅣB呈隔年冬春季节流行。ⅣA引起白细胞升高、电解质紊乱较ⅣB多见, ⅣB感染患儿更易合并RSV感染, 但两种病毒所致LRTI患儿临床表现相似。

This study investigated the association between obesity and obstructive sleep apnea (OSA) in preschool and school-age children. Parents of obese and randomly chosen normal weight children completed a questionnaire on sleep-related symptoms, demography, family, and medical history. All subjects were invited to undergo polysomnography (PSG). OSA cases were defined as obstructive apnea hypopnea index (OAHI) ≥1. A total of 5930 children were studied with 9.5 % obese (11.9 % boys/6.1 % girls), 205/2680 preschool and 360/3250 school children. There were 1030 children (535 obese/495 normal weight) who underwent PSG. OSA was higher in obese children and obese school children had higher OAHI, arousal index, and shorter total sleep time. However, there was no positive correlation between OSA and body mass index (BMI). The main risk factors for OSA in preschool children were adenotonsillar hypertrophy and recurrent respiratory tract infection. The main cause for OSA in school children was a history of parental snoring and obesity. Mallampati scores and sleep-related symptoms were found to be associated with OSA in both preschool and school children.

Airway smooth muscle cells (ASMCs) play a key role in the process of asthma airway remodeling. Urotensin II (UII) and transforming growth factor (TGF)-β are potent mitogens for ASMCs proliferation. The study was aimed to determine whether UII-upregulated TGF-β-mediated ASMCs proliferation and extracellular signal-regulated kinase (ERK) was required for such an effect. OVA-sensitized rats were challenged to induce asthma. Lung morphology and airway dynamic parameters were monitored. ASMCs from control and asthma rats were purified for the measurement of UII and TGF-β1 expression. In vitro experiments were conducted to determine the direct effect of UII on TGF-β1 expression by ASMCs. Finally, U0126, an ERK inhibitor was used to examine the role of ERK pathway in UII mediated TGF-β1 upregulation. We found that both UII and TGF-β1 were upregulated in asthma lung tissues. In vitro study on ASMCs further revealed that UII may render its effect on ASMCs cells through the upregulation of TGF-β1. Data also supported the conclusion that ERK pathway was required, but not sufficient in UII-induced TGF-β1 upregulation. The current study provides new evidence that UII is involved in the TGF-β mediated mitogenic effect on ASMCs. UII, at least partially, uses ERK pathway to render such effect.

Apart from airway inflammation, airway remodeling is one of the main pathological features of asthma. However, it remains unclear when airway remodeling starts in children and whether it could be a potential therapeutic target in asthma. We have reviewed the recent literature regarding structural changes after airway remodeling, the relationship between airway inflammation and airway remodeling, the relationship between childhood asthma and airway remodeling, and the role of long-term medication in asthma treatment for airway remodeling. The relationship between airway inflammation and airway remodeling is still controversial. A number of morphological and pathological studies have confirmed that airway remodeling occurs not only in adult asthma, but also in childhood asthma. It develops early in the disease process of asthma. At present, long-term medication in asthma treatment mainly focuses on anti-inflammation. However, there are no therapeutic interventions that revert airway remodeling once it is established. Airway remodeling may provide a possible new therapeutic target in the management of asthma. It is imperative to strengthen the research in developing new medications specifically for asthma airway remodeling. Prevention and treatment of airway remodeling become top priority in future asthma research.