Background:Hand, foot, and mouth disease (HFMD) complicated by encephalitis is a severe condition with an acute onset, yet its pathogenesis remains incompletely understood. This study aimed to investigate the role of platelet miR-223-3p in HFMD complicated by encephalitis. We sought to determine its expression dynamics, verify its direct target F-box and WD repeat domain containing 7 (FBXW7), and elucidate its functional impact on neuronal apoptosis, thereby exploring a novel microRNA (miRNA) mediated mechanism in the pathogenesis of this severe complication. Methods:We initially enrolled 20 children with HFMD complicated by encephalitis and 20 with uncomplicated HFMD. Platelet miRNA expression profiles were analyzed by high-throughput sequencing. Bioinformatics tools predicted key target genes, which were validated in a larger cohort (n=70) using reverse transcription quantitative polymerase chain reaction (RT-qPCR). Gain- and loss-of-function models were established in SK-N-SH neuroblastoma cells by transfecting with an miR-223-3p mimic or inhibitor. A dual-luciferase reporter assay confirmed the direct targeting of FBXW7. The effects on apoptosis were assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and by measuring the protein levels of B-cell lymphoma 2 (Bcl-2), BCL2-associated X protein (Bax), and cleaved cysteinyl aspartate specific proteinase-3 (caspase-3) via Western blot. Rescue experiments with an FBXW7 overexpression plasmid (OE-FBXW7) were performed to confirm the specific pathway. Results:Platelet miR-223-3p was identified as the most significantly upregulated miRNA in the encephalitis group. Its expression was elevated in the acute phase but decreased during recovery (P<0.05). A significant negative correlation was observed between acute-phase miR-223-3p and whole-blood FBXW7 expression. Both messenger RNA (mRNA) and protein levels of FBXW7 were reduced by the miR-223-3p mimic and increased by its inhibitor (P<0.05). The dual-luciferase assay confirmed FBXW7 as a direct target. Functionally, miR-223-3p overexpression suppressed apoptosis, as evidenced by decreased TUNEL-positive cells, increased Bcl-2, and decreased Bax and cleaved caspase-3 (P<0.05). Conversely, both miR-223-3p inhibition and FBXW7 overexpression promoted apoptosis, and FBXW7 overexpression effectively reversed the anti-apoptotic effect of the miR-223-3p mimic. Conclusions:Our study demonstrates that platelet miR-223-3p is significantly upregulated in HFMD complicated by encephalitis. It promotes the pathogenesis of this condition by directly targeting FBXW7 and inhibiting mitochondrial pathway-mediated apoptosis. These findings highlight a novel role for platelet miRNAs in the neuropathogenesis of HFMD and suggest the miR-223-3p/FBXW7 axis as a potential therapeutic target.

This study aimed to assess differences in peripheral blood platelet indices including platelet count (PLT), mean platelet volume (MPV), platelet distribution width (PDW), and the platelet-to-lymphocyte ratio (PLR) between children with hand, foot and mouth disease (HFMD) complicated by encephalitis and those with uncomplicated HFMD. A further objective was to develop a robust predictive model for HFMD complicated by encephalitis, specifically designed for resource-limited clinical settings. This retrospective study enrolled children with HFMD who were hospitalized at the Children’s Hospital of Soochow University between January 2015 and December 2020. The participants were categorized into two groups: an encephalitis group (HFMD complicated by encephalitis) and a control group (those with uncomplicated HFMD). The baseline data, clinical features and platelet indices of the children in the two groups were then compared. Binary logistic regression analysis was used to identify the risk factors for HFMD complicated by encephalitis, and a nomogram prediction model for HFMD complicated by encephalitis was developed based on these risk factors. The risk factors in children with HFMD complicated by encephalitis included fever for more than 3 days, listlessness, headache, limb myoclonus, positive neck resistance and/or pathological signs, and certain PLT, PDW, and PLR values. These risk factors were used to construct a simple and practical nomogram prediction model for HFMD complicated by encephalitis, which demonstrated strong predictive performance with an area under the curve (AUC) of 0.902, along with satisfactory calibration and stability upon validation. The nomogram prediction model of platelet indices (PLT, PDW and PLR) combined with clinical risk factors demonstrated a robust predictive capacity for HFMD complicated by encephalitis. Not applicable.

Objective: The aim of this study is to compare laboratory parameters between incomplete Kawasaki disease (IKD) and sepsis, and to evaluate the predictive value of common laboratory parameters in distinguishing IKD from sepsis. Methods: A retrospective analysis was conducted on medical records of patients diagnosed with Kawasaki disease or sepsis between January 2021 and December 2023. A total of 207 cases of IKD and 315 cases of sepsis were included in this study. Clinical data were analyzed to identify intergroup differences. Results: Significant intergroup differences (P < 0. 05) were observed in blood platelet (PLT) count, procalcitonin, aspartate aminotransferase, alanine aminotransferase (ALT), urea nitrogen, creatinine, C-reactive protein, fibrinogen (Fib), and D-dimer levels. Markers with statistically significant variations relevant to the diagnosis of IKD were identified using binary logistic regression analysis. Receiver operating characteristic curve analysis demonstrated areas under the curve of 0. 771 for PLT, 0. 800 for ALT, and 0. 755 for Fib. A combined assessment of these markers resulted in improved sensitivity and specificity. Conclusion: PLT, ALT, and Fib can serve as laboratory markers for distinguishing IKD from sepsis and offer diagnostic reference value. Their combined assessment may improve the predictive accuracy for IKD.

Nitric oxide (NO), a gaseous free radical produced from L-arginine catalyzed by NO synthase, functions as an important signaling molecule in the human body. Its antiviral activity was confirmed in the 1990s, and has been studied more extensively since the outbreak of the SARS pandemic in 2003. In the fight against the ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, some recent studies have revealed the potential of NO in the treatment of coronavirus disease 2019 (COVID-19). The progress in this field, including several noteworthy clinical trials of inhaled NO for the treatment of COVID-19 and the emergency approval of NO nasal spray by the regulatory agencies of Israel, Bahrain, Thailand and Indonesia for the treatment of COVID-19 pneumonia, offers a new perspective for addressing the raging coronavirus infection and greatly broadens the clinical application of NO therapy. This review aims to explore the underlying molecular mechanisms of NO-based therapy against SARS-CoV-2, including direct viral inhibition, immune regulation, and protection against pulmonary and cardiovascular symptoms. Furthermore, the potential therapeutic applications of inhaled NO, NO donors and drugs involved in the NO pathway are discussed. In the context of a global vaccination campaign and newly proposed strategy of "coexistence with COVID-19," the advantages of NO therapies as symptomatic and adjuvant treatments are expected to deliver breakthroughs in the treatment of COVID-19.

Objective: Kawasaki disease (KD) is an acute vasculitis that typically occurs in young children and may lead to coronary artery lesions (CALs), but the precise mechanisms that trigger this illness are unclear. We hope to identify some clues to the pathogenesis of KD through clinical sample analysis. Methods: We included 12 children who had been diagnosed with KD coronary artery lesions (KD-CALs) or KD-no coronary artery lesions (KD-nCALs) and investigated the transcriptome variations of patients with KD in the acute and subacute stages. Further, we enrolled 12 new patients with KD and investigated the expression of CD14 mRNA and the downstream genes A20, A1/BF1_1, and I kappa Boc, via real-time quantitative PCR (qRT-PCR). In addition, we established an animal model of KD-induced coronary inflammation and measured the protein levels of mCD14, I kappa Boc and IL-6 on Day 7 and 14 after completion of modelling. Then, molecular docking was applied to analyse the binding power of the chemical compounds with mCD14. Results: The KD-CALs group contained 62 differentially expressed genes (DEGs), which were enriched in the nuclear factor kappa-B (NF-kappa B) signalling pathway. CD14 mRNA was upregulated in the acute stage, which caused an increase in expression of the downstream genes A20, A1/BF1_1, and I kappa Boc. Molecular docking revealed that the best docking medicine with mCD14 was lupenone. On Day 14 after modelling, there was significant inflammation with infiltration of lymphocytes and macrophages in the coronary endothelium of the mice. Compared with those in the Day 7 group and the control group, the levels of mCD14, I kappa Boc and IL-6 proteins in the coronary endothelium significantly increased in mice in the Day 14 group. Conclusions: CD14 mRNA may regulate I kappa Boc expression and subsequently activate the NF-kappa B signalling pathway, ultimately causing vasculitis. CD14 mRNA participates in the occurrence of coronary artery injury, and its protein product mCD14 may be a potential therapeutic target for KD-CALs.

Ibuprofen, a nonsteroidal anti-inflammatory drug, is considered a safe and effective analgesic for treating different types of pain and joint disorders. Dexibuprofen, S-(+)-ibuprofen, is the single pharmacologically active enantiomer of ibuprofen. It is more potent than the racemic formulation of ibuprofen in terms of analgesic and anti-inflammatory properties and causes less acute gastric damage. For the first time, in the present single-dose, randomized, open-label, 2-period crossover study, the safety and pharmacokinetic (PK) characteristics of a single-dose dexibuprofen injection (0.2 g) were evaluated in healthy Chinese subjects and compared with the PK characteristics of a 0.2-g ibuprofen injection. Five consecutive men and women were randomly administered a single dose of the 0.2-g ibuprofen or 0.2-g dexibuprofen injection after fasting in every period during the 5-day interval. Then, plasma samples were collected for liquid chromatography-tandem mass spectrometric analysis. WinNonlin software was used for calculating the PK parameters. The geometric mean ratios of the 0.2-g dexibuprofen injection/ibuprofen injection for maximal plasma concentration, area under the plasma concentration-time curve (AUC) from time 0 to the last quantifiable time point, and AUC from time 0 to infinity were 184.6%, 136.9%, and 134.4%, respectively. The dexibuprofen plasma exposure of the 0.15-g dexibuprofen injection was comparable to that of the 0.2-g ibuprofen injection, calculated using AUC from time 0 to infinity.

目的 分析 598 例川崎病(KD)急性期超声心动图,探讨KD心脏并发症特点.方法 回顾性分析2018 年 11 月至 2020 年 10 月苏州大学附属儿童医院收治的 598 例KD患儿的超声心动图,分析冠状动脉病变(CAL)发生率和心脏损害发生率.结果 KD急性期CAL发生率为36.5%,男性、年龄<6个月、静脉注射免疫球蛋白(IVIG)无反应型KD患儿CAL发生率升高(P<0.05);心包积液发生率为8.4%,CAL患儿高于NCAL患儿(P<0.05);左室扩大发生率为 10.5%,男性高于女性(P<0.05),>3 岁患儿高于<6个月及6个月～3 岁患儿(P<0.05);左室收缩功能不全发生率为 3.0%,>3岁患儿高于<6个月及6个月～3 岁患儿(P<0.05);瓣膜反流发生率为 20.7%,KD左室收缩功能不全患儿心包积液、瓣膜反流及左室扩大发生率均升高(P<0.05).结论 男性、年龄<6 个月、IVIG无反应为KD并发CAL高危因素.KD合并心包积液CAL发生率高,大年龄儿童更易出现左室扩大及左室收缩功能不全,左室收缩功能不全患儿有KD休克综合征的临床表现.

OBJECTIVES:To study the biological processes and functions of serum exosomes in children in the acute stage of Kawasaki disease (KD), so as to provide new biomarkers for the early diagnosis of KD.METHODS:In this prospective study, 13 children with KD who were treated in Children's Hospital of Soochow University from June 2019 to August 2020 were enrolled as the KD group, and 13 children who were hospitalized due to bacterial infection during the same period were enrolled as the control group. Whole blood was collected on the next morning after admission, serum samples were obtained by centrifugation, and exosomes were extracted through ultracentrifugation. Serum exosomes were analyzed by label-free quantitative proteomics, and differentially expressed proteins (DEPs) were screened out for functional enrichment analysis. A protein-protein interaction (PPI) network was plotted, and unique proteins were validated by targeted proteomics.RESULTS:A total of 131 DEPs were screened out for the two groups, among which 27 proteins were detected in both groups. There were 48 unique DEPs in the KD group, among which 23 were upregulated and 25 were downregulated, and these proteins acted on "complement and coagulation cascades" and "the MAPK signaling pathway". Validation by targeted proteomics showed that FGG, SERPING1, C1R, C1QA, IGHG4, and C1QC proteins were quantifiable in the KD group. A total of 29 proteins were only expressed in the control group, among which 12 were upregulated and 17 were downregulated. Four proteins were quantifiable based on targeted proteomics, i.e., VWF, ECM1, F13A1, and TTR. A PPI network was plotted for each group. In the KD group, FGG and C1QC had close interaction with other proteins, while in the control group, VWF had close interaction with other proteins.CONCLUSIONS:The serum exosomes FGG and C1QC in children in the acute stage of KD are expected to become the biomarkers for the early diagnosis of KD. For children with unexplained fever, detection of FGG, C1QC1, and VWF may help with etiological screening.

Background Kawasaki disease (KD) is a self-limiting vasculitis with an unknown etiology. It has been reported that breastfeeding has a potential protective effect on KD development. However, whether breastfeeding has an effect on the development of coronary artery lesions (CALs) remains unclear. Methods We retrospectively reviewed the medical records of patients with the main diagnosis of KD hospitalized in our hospital from May 2017 to November 2018. Standardized telephone interviews were carried out to obtain feeding practices before KD was onset. Results Two hundred and ninety-three (51.6%) were exclusively breastfed, 223 (39.3%) were partially breastfed and 52 (9.2%) were formula fed. There were no significant differences in the characteristics regarding age, gender, incomplete KD, intravenous immunoglobulin (IVIG) resistance, and the laboratory variables among the three groups. With formula feeding as a reference, patients exclusively breastfed and partially breastfed seemed to have a higher incidence of CALs, even after adjusting confounders, but were not statistically significant. After grouping patients who were older than six months into formula feeding, partial breastfeeding for < 2 months, partial breastfeeding for ≥ 2 and < 4 months, partial breastfeeding for ≥ 4 and < 6 months and exclusively breastfeeding based on the length of breastfeeding, the results remained the same ( P > 0.05). Conclusions Breastfeeding has no protective effect on the development of CALs in KD.

目的 探讨急性期川崎病(KD)患儿外周血树突状细胞(DC)亚群的变化及意义.方法 回顾性分析2020年12月—2021年5月就诊的初发急性期KD患儿的临床资料.KD患儿分别于静脉注射用免疫球蛋白(IVIG)治疗前、后取血,采用流式细胞术检测外周血DC亚群浆细胞样树突状细胞(pDC)及CD 1 c+髓样树突状细胞(mDC)数量和比例及表面功能分子HLA-DR、CD 86、CD 40蛋白表达水平.选择同期健康体检儿童作为对照组.结果 KD组患儿32例,男19例、女13例,中位年龄37.0(22.3～58.5)月.对照组23例,男14例、女9例,中位年龄52.0(30.0～65.0)月.KD组患儿IVIG治疗前、治疗后的pDC、CD 1 c+mDC占外周血总DC比例均低于对照组,治疗后组CD 1 c+mDC占外周血总DC比例高于治疗前;治疗前组pDC、CD 1 c+mDC数量低于对照组和治疗后组,差异均有统计学意义(P<0.05).治疗前组pDC表面CD 86、CD 40表达以及CD 1 c+mDC表面HLA-DR、CD 86水平均低于对照组和治疗后组,差异有统计学意义(P<0.05).急性期KD患儿pDC和CD 1 c+mDC数量与C反应蛋白、中性粒细胞与淋巴细胞比值均呈显著负相关(P<0.05);CD 1 c+mDC细胞数量与血沉也呈显著负相关(P<0.05).结论 KD患儿外周血循环中pDC和CD 1 c+mDC存在数量不足及功能受损,pDC和CD 1 c+mDC可能参与了KD的发病过程.

目的 通过收集苏州大学附属儿童医院进行24 h动态血压监测(ambulatory blood pressure monitoring,ABPM)的高血压儿童住院期间的临床资料,分析不同儿童高血压的特点,为临床诊治儿童高血压提供临床思路.方法 选取2018年04月—2020年12月在苏州大学附属儿童医院住院期间采用动态血压仪进行24 h ABPM的高血压患儿为研究对象.按病因分为白大衣组、原发性组、继发性组.用卡方检验或秩和检验统计方法分析三组患儿的性别,年龄,身体质量指数(BMI),24 h、白天、夜间平均收缩压(SBP)及舒张压(DBP)水平,24 h血压负荷,24 h、白天、夜间SBP及DBP负荷,夜间SBP、DBP下降率的差异;用二元Logistic回归方法分析年龄、性别、BMI与血压的相关性.结果 116例高血压患儿中,每组性别上男性居多,但三组间性别、年龄差异无统计学意义(P>0.05),身高、体重、BMI组间差异均有统计学意义(P<0.05),原发性组的身高、体重、BMI均高于白大衣组与继发性组.继发性组的夜间SBP、DBP下降率明显低于其他组,继发性组的昼夜节律明显消失.血压负荷、夜间DBP负荷,继发性组明显高于原发性组.夜间DBP,继发性组明显高于原发性组,差异有统计学意义(P<0.05).原发性组中BMI与血压呈正相关(P<0.05).结论 高血压儿童中,超重、肥胖更多见于原发性高血压.夜间血压升高、DBP平均血压的升高、夜间DBP异常更多见于继发性高血压.继发性高血压的昼夜节律明显消失.原发性高血压者BMI与血压呈正相关.

Background:Hand, foot, and mouth disease (HFMD) caused by coxsackievirus A6 (CV-A6) has become prevalent in many parts of the world. It is commonly referred to as atypical HFMD which more likely to present as bullous lesions. Compared with traditional HFMD, its misdiagnosis rate is relatively high, which brings difficulties to clinical diagnosis. We retrospectively analyze the clinical characteristics of children with HFMD with bullous lesions caused by CV-A6.Methods:The study included 68 children with atypical HFMD caused by CV-A6 who were hospitalized from 2018 to 2020. Data of the children including age, sex, month of HFMD onset, the morphologies and distribution of rashes, the details of fever, the presence or absence of onychomadesis, and laboratory test results were analyzed and compared between an infant group (<1 year), a toddler group (1-<3 years), and a preschool group (3-<6 years).Results:Of the 68 children, 67 were younger than 5 years old, with a male to female ratio of 1.62:1. The disease peaked in the period from June to September. With 75.0% of the infant group had more than three kinds of rashes; 95.0% of the preschool group had rashes in more than five locations. These differences were statistically significant (P<0.05). All children had fever. The peak fever in the toddler group was lower (P=0.033). No critical cases were observed in any of the groups. Of the 61 children who were successfully followed up, 68.9% developed onychomadesis within 2-3 weeks. The proportion of cases with abnormal liver function was 83.3%, 41.7%, and 10.0% in the infant, toddler, and preschool groups (P<0.001). The proportion of cases with increased serum creatine kinase MB isoenzyme (CK-MB) were significantly higher in the toddler group (P<0.05).Conclusions:Atypical HFMD caused by CV-A6 infection usually occurred in children under 5 years old. The morphologies of the rashes in the infant group changed more, while the rashes in the preschool group was more widely distributed. The incidence of critical cases was low. More than half of the cases can develop onychomadesis in the recovery period. Organ damage was relatively mild in the preschool group.

Fluoroquinolones are an important class of antimicrobial agents to manage infectious diseases. However, knowledge about how host bile acids are modified by fluoroquinolones is limited. We investigated and compared the impact of fluoroquinolones on circulating bile acid profiles and gut microbiota from in vivo studies. We administered ciprofloxacin (100 mg/kg/day) or moxifloxacin (40 mg/kg/day) orally to male Wistar rats for seven days. Fifteen bile acids (BAs) from the serum and large intestine were quantified by HPLC-MS/MS. The diversity of gut microbiota after ciprofloxacin and moxifloxacin treatment was analyzed using high-throughput, next-generation sequencing technology. The two fluoroquinolone-treated groups had different BA profiles. Ciprofloxacin significantly reduced the hydrophobicity index of the BA pool, reduced secondary BAs, and increased taurine-conjugated primary BAs in both the serum and large intestine as compared with moxifloxacin. Besides, ciprofloxacin treatment altered intestinal microbiota with a remarkable increase in Firmicutes to Bacteroidetes ratio, while moxifloxacin exerted no effect. What we found suggests that different fluoroquinolones have a distinct effect on the host BAs metabolism and intestinal bacteria, and therefore provide guidance on the selection of fluoroquinolones to treat infectious diseases.

Objective: To evaluate the value of combined interferon β (IFN-β) and platelet (PLT) detection for Kawasaki disease (KD) identification. Methods: Forty-four children who were newly diagnosed with KD were selected as the KD group. They were divided into acute phase of KD and subacute phase of KD. They were also separated into groups with and without coronary artery disease (CAD) (CAD+ and CAD–, respectively). Meanwhile, 44 children hospitalized with febrile disease and 44 healthy children were selected as a febrile control group and normal control group, whom were attended to at Children's Hospital of Soochow University at the same time. We detected the concentration of IFN-β and PLT of peripheral blood serum for all three groups and analyzed the difference. Results: At acute and subacute phases of KD, both IFN-β and PLT are higher than both the febrile control group and healthy control group, especially at subacute phase; the difference between groups was statistically significant, P < 0.05. Receiver operating characteristic (ROC) curve showed that the areas under the ROC curve (AUCs) of IFN-β and PLT at acute phase of KD were 0.81 and 0.72, respectively; the sensitivity and specificity were 97.22 and 63.64%, and 57.89 and 73.86%, respectively. The AUCs of combined IFN-β and PLT were 0.81 at acute phase and 0.96 at subacute phase of KD, with sensitivity and specificity of 97.22 and 55.26%, and 86.36 and 100%, respectively. The cutoff value of combined IFN-β and PLT detection was IFN-β = 3.51 pg/ml and PLT = 303 × 10 9 /L at acute phase of KD, IFN-β = 4.21 pg/ml and PLT = 368 × 10 9 /L at subacute phase from plot vs. criterion values. However, there are no significant differences between the CAD– group and the CAD+ group for combined IFN-β and PLT, both P > 0.5, neither at acute nor at subacute phase of KD. Conclusion: Combined IFN-β and PLT detection is an efficient biomarker for KD identification. The cutoff values are IFN-β = 3.51 pg/ml and PLT = 303 × 10 9 /L at acute phase of KD and IFN-β = 4.21 pg/ml and PLT = 368 × 10 9 /L at subacute phase.

目的 报告1例RAF1基因突变致Noonan综合征(NS)的临床特征,增加对RAF1基因突变表型谱的认识.方法 收集患儿的临床资料,包括病史特点、相关实验室检查和家族史等.采用外显子捕获的方法对患儿及其父母进行全外显子高通量测序,并进行生物信息学分析,通过Sanger测序对高通量测序结果进行验证.结果 患儿女,9岁,发育落后,头发稀疏卷曲,前额宽大突出,鼻梁扁平,眼距宽,双侧眼裂向外下略倾斜,上睑下垂.彩色多普勒超声心动图显示房间隔缺损,室间隔与左室肥厚.心电图提示:房性早搏,房性心动过速,测序发现RAF1基因c.770C>T(p.S257L)杂合突变,其父母均未携带,为突变.Sanger法验证了上述测序结果.结论 RAF1基因突变可出现NS表型,而房性心律失常可能是RAF1基因突变型NS的一个新的表型谱.

Background Our study aimed to explore the anxiety levels and possible associated factors in the pediatric medical staff in Jiangsu province during an outbreak of Coronavirus Disease 2019 (COVID-19). Methods Pediatric medical staff (n=534) from nine hospitals in Jiangsu province were enrolled. Their anxiety levels and quality of sleep were assessed using the online SAS and PSQI questionnaires. Results The prevalence of anxiety was 14.0% among the medical staff. In children’s hospital staff, anxiety levels in outpatient and emergency departments were significantly higher than those in inpatient departments, except for the intensive care unit. The SAS scores were significantly associated with educational background, professional title, lifestyle, and physical condition. Stepwise multiple linear regression showed that physical condition, lifestyle, attention to the epidemic, professional title, and educational background all had a linear relationship with the individual’s anxiety levels. Pearson correlation analysis showed that sleep quality was moderately associated with anxiety levels. Conclusions The prevalence of anxiety was 14.0% in pediatric medical staff in Jiangsu province during an outbreak of COVID-19. Department, professional title, and educational background were associated with anxiety levels in these workers. More attention should be paid to staff who are in poor health, and this anxiety can also be accompanied by poor sleep quality. Peer support can assist with anxiety relief.

为了在儿科医学教学中培养学生的思维能力,适应复杂的临床工作,急需改变以往传统的应试教学模式.基于思维教学理论的相关研究,根据斯滕伯格的三元思维教育观,从激发学生兴趣、直接讲授、中英文教学、PBL法、布置自学内容、增加临床技能实验室的实践课、增设文学课等方面,提高学生的分析能力、创造能力和实践能力.

Objectives: To explore the characteristics of Kawasaki disease (KD) under 6 months and to investigate the possible indications of incomplete KD (iKD). Methods: The medical records of KD patients hospitalized in Children's Hospital of Soochow University from January 2007 to December 2017 were retrospectively reviewed and analyzed. A total of 50 cases of urinary tract infection (UTI) and 50 cases of adenovirus (ADV)-infected patients under 6 months that were age and gender-matched with the main complaint of high fever were selected as controls. Results: A total of 1,872 KD patients were enrolled. Among them, 194 (10.4%) were infantile patients under 6 months. There were 72 (37.1%) and 494 (29.4%) iKD in patients younger and older than 6 months, respectively (P < 0.05). Although patients under 6 months had a shorter fever duration before immunoglobulin (IVIG) treatment, a larger proportion of these patients had IVIG resistance and coronary artery lesions. They also tended to have higher platelet (PLT) counts and C-reactive protein (CRP) and lower hemoglobin (Hb), percentage of neutrophils (N%), albumin and serum sodium. When we compared iKD under 6 months with UTI and ADV-infected patients, significant differences were found in white blood cells (WBC), Hb, PLT, CRP, N% and serum albumin (P < 0.05). After adjusting the confounders, Hb < 105.5 g/L, CRP > 22.7 mg/L, N% > 47.4 and PLT > 496 × 109/L were indications of iKD when compared with ADV infection (area under the curve [AUC]: 0.872, 0.939, 0.707, and 0.684, respectively). N% > 51.8 and albumin < 39.0 g/L were indications of iKD when compared with UTI (AUC: 0.627 and 0.832, respectively). Conclusions: Infantile KD patients under 6 months had their own particularity. Laboratory variables could be good indications of iKD when compared with UTI and ADV infection.

目的:探讨血管内皮细胞生长因子(VEGF)基因多态性与手足口病脑炎易感性关系。方法:采用病例对照的方式，通过Taqman探针法测定手足口病中145例普通患儿和91例脑炎患儿的VEGF基因启动子区＋405G/C、-460T/C、＋936T/C位点的多态性分布，并进行对比分析。结果:VEGF＋405G/C位点中，脑炎组和普通组的基因型分布均为GG、GC和CC，两组基因型比较无显著差异( χ2＝3.882， P＝0.144)，脑炎组G、C等位基因频率43.96%、56.04%，普通组G、C等位基因频率为53.45%、46.55%，脑炎组C等位基因频率显著高于普通组，差异有统计学意义( χ2＝4.03， P＝0.047)；VEGF-460T/C位点中，脑炎组和普通组的基因型分布均为TT、TC和CC，两组基因型比较无显著差异( χ2＝3.948， P＝0.139)，脑炎组的T、C等位基因频率为78.57%、21.43%，普通组T、C等位基因频率为70.34%、29.66%，脑炎组T等位基因频率显著高于普通组，差异有统计学意义( χ2＝3.851， P＝0.049)；VEGF＋936T/C位点中，脑炎组和普通组的基因型分布均为TT、TC和CC，组间差异无统计学意义( χ2＝1.272，0.530)，两组的T、C等位基因频率比较差异无统计学意义( χ2＝0.395， P＝0.597)。 结论:VEGF＋405C基因、-460T基因可能是手足口病脑炎的易患基因，干预和阻断VEGF可能成为手足口病脑炎的一种治疗新靶点。

目的 分析新生儿房性心动过速(atrial tachycardia,AT)的临床特征、治疗及预后.方法 回顾分析新生儿科2011年4月—2019年2月收治的24例新生儿AT的临床资料.结果 24例新生儿中,4例早产儿,20例足月儿,男20例,女4例,日龄2 h～28 d,中位日龄2 d.所有患儿给予美托洛尔联合西地兰或地高辛治疗后,均能有效减少AT的发生.24例患儿随访示均能恢复窦性心律,部分患儿转律后有频发房性早搏发生,予美托洛尔或联合地高辛口服后能有效减少房性早搏,并于1岁左右明显好转.结论 AT是新生儿期重要的心律失常,美托洛尔或联合洋地黄类药物治疗新生儿AT具有较好的疗效.新生儿AT可能是自限性疾病.