目的 分析以大量腹水为首发临床表现的儿童嗜酸细胞性胃肠炎(Eosinophilic Gastroenteritis,EG)诊治特点.方法 对安徽医科大学第一附属医院2014年1月至2020年4月的3例EG病儿临床特点、实验室检查、胃镜、病理以及诊治经过进行回顾性分析.结果 3例病儿均为年长儿,为EG浆膜型病变,临床表现主要为腹胀、腹水;外周血及骨髓细胞学检查显示嗜酸性粒细胞(EoS)显著增多,治疗前3例病儿外周血EoS计数分别是(9.84,9.84,8.48)×109/L;胃镜检查显示胃窦及十二指肠黏膜充血水肿明显、可见充血出血斑;病理检查在胃窦黏膜固有层可见大量EoS浸润.予以饮食回避、抗过敏、激素治疗,1周内病儿症状明显缓解.结论 浆膜型EG病儿主要以大量腹水为首发临床表现,外周血EoS显著升高,确诊依靠内镜下病理检查,饮食疗法结合激素治疗有显著疗效.

To study the clinical features of infectious mononucleosis (IM) caused by Epstein-Barr virus (EBV) mixed with Mycoplasma pneumonia (MP) or/and cytomegalovirus (CMV)infection, collected 201 hospitalized children who met the IM diagnostic criteria, the clinical manifestations, laboratory tests, complications, treatment, and outcome were compared among EBV infection alone and EBV mixed with MP or/and CMV infection. Most of the children with IM were preschoolers, more frequently occurred in boys than girls. EBV patients with MP had the longest duration of fever. When mixed pathogen infections were involved, the white blood cell count of preschool children was significantly increased, while splenomegaly was more common in older children. In the cases of EBV infection alone, abnormal liver function was positively correlated with age (P=0.044). Mixed pathogen infections were more common in children with IM, occurring in all age groups, and some clinical characteristics were related to the age of onset and the pathogen of the infection.

目的 探索翻转课堂教学模式在儿科学临床技能培训中的应用效果.方法 选取安徽医科大学临床医学专业学生作为研究对象,分为对照组30例,采用传统教学法;观察组30例,采用翻转课堂教学模式.比较两组的儿科临床技能考核和理论知识成绩以及教学满意度调查结果.结果 观察组操作技能考核和理论知识成绩均明显高于对照组(P<0.001).观察组对教学模式认同度、学习兴趣、培养自主学习能力及理论知识和临床实践结合度的满意度明显高于对照组(P<0.001).结论 翻转课堂应用于儿科学临床技能培训中效果显著,可提高学生的学习兴趣,有利于自主学习能力的培养.

目的:分析小儿消化性疾病的胃电图变化及与临床病理特征和胃镜特征的关联性.方法:选取2018年1月至2019年5月我院儿科收治的经胃镜和病理学两种方式诊断为消化性疾病的患儿54例为观察组,另选取无胃肠道疾病的健康儿童40例为对照组.比较两组胃电图参数(频率均值和波幅均值),54例胃电图诊断后纤维胃镜检查结果,分析消化性疾病患儿HP感染与临床病理特征、溃疡面积的关系.结果:各组胃病患者胃电慢波频率均值各不相同(P＜0.05),三组患者胃电慢波波幅均值相比差异具有统计学意义(P＜0.05);且浅表性胃炎组、胆汁反流性胃炎组患者胃电慢波频率均值、胃电慢波波幅均显著低于胃溃疡组(P＜0.05);浅表性胃炎组患者胃电慢波频率均值显著低于胆汁反流性胃炎组(P＜0.05).胆汁反流性胃炎组患者胃电慢波波幅显著低于浅表性胃炎组(P＜0.05).胃镜检查结果显示,其中浅表性胃炎的诊断符合率较高,达90.00％,胃溃疡符合率为60.71％,胆汁反流性胃炎符合率为83.33％.HP检测结果显示,HP阳性患儿占总例数的77.78 ％(42/54),HP阴性患儿占总例数的22.22 ％(12/54);HP阳性组患儿淋巴滤泡形成、胃黏膜萎缩、胃黏膜炎性活动的发生率明显高于HP阴性组,差异具有统计学意义(P＜0.01);HP阳性组溃疡范围＞2 cm的患儿比例明显高于HP阴性患儿,差异具有统计学意义(P＜0.01).结论:小儿消化性疾病胃电图存在餐后NSWP的下降及节律过缓的上升,胃电图检查和胃镜检查在诊断上有较高的符合率,HP感染科引起胃黏膜组织学改变,可作为小儿消化性疾病的靶向治疗.

Objective To investigate the effect of intestinal flora from children with Irritable Bowel Syndrome (IBS) on intestinal motility and acid-sensitive ion channel expression in mice. Methods Fecal samples of children with IBS identified according to Rome Ⅳcriteria and healthy children were collected and made into fecal microbiota solution. A pseudo-aseptic mouse model was established, mice were randomly divided into two groups:the control group was given fecal microbiota solution of healthy children,and the experimental group was given fecal microbiota solution of IBS children. The intestinal propulsion rate was measured, Serum Motilin (MOT) and Gastrin (Gas) were determined by ELISA, the expression and distribution of ASICs in intestinal tissues of mice were determined by immunohistochemistry. Results Compared with the control group, intestinal propulsion rate, serum MOT and Gas level were significantly reduced in the experimental group (P＜0.05), the expression of ASIC3 in the small intestine and colon of mice from experimental group was significantly increased (P＜0.05);the expression of ASIC3 in small intestine and colon was negatively correlated with the intestinal propulsion rate (P＜0.05). Conclusions Intestinal flora of children with IBS can promote the expression of ASIC3 in intestinal tissue of mice, and the effect of intestinal microorganism on intestinal motility may be related to the activation of ASICs.

Previous studies show that the proliferation of human mesangial cells (HMCs) played a significant part in the pathogenesis of Henoch-Schönlein purpura nephritis (HSPN). The aim of this study was to explore the proliferation of HMCs induced by IgA1 isolated from the sera of HSP patients. HMCs were cultured in three different types of media, including IgA1 from patients with HSP (HSP IgA1 group), healthy children (healthy IgA1 group) and medium (control group). The proliferation of HMCs incubated with IgA1 was determined by cell counting kit-8 assay and bromodeoxyuridine incorporation. The expression of ERK1/2 and phosphatidylinositol 3 kinase/protein kinase B/mammalian targets of the rapamycin (PI3K/AKt/mTOR) signals and transferrin receptor (TfR/CD71) was detected with the methods of immunoblotting. The results indicated that the proliferation of HMCs significantly increased in the HSP IgA1 group compared with that in the control group or the healthy IgA1 group (P < 0.001). Moreover, we found that IgA1 isolated from HSP patients activated ERK and PI3K/AKt/mTOR signals, and markedly increased TfR/CD71 expression in HMCs. These effects induced by IgA1 isolated from patients with HSP were inhibited by human TfR polyclonal antibody (hTfR pAb) and soluble human transferrin receptor (sTfR), indicating that IgA1-induced HMC proliferation and ERK1/2 and PI3K/AKt/mTOR activation were dependent on TfR/CD71 engagement. Altogether, these data suggested that TfR/CD71 overexpression and ERK1/2 and PI3K/AKt/mTOR activation were engaged in HMC proliferation induced by IgA1 from HSP patients, which might be related to the mesangial injury of HSPN.

Objective To investigate the effect of intestinal flora in children with functional constipation (FC) on expression of acid-sensitive Ion channel 3(ASIC3) in rats and their regulation in intestinal motility. Methods Faeces of FC children identified according to RomeⅣ criteria and healthy children from the First Affiliated Hospital of Anhui Medical University from December 2017 to June 2018 were collected, and then made into fecal microbiota solution.A pseudo - sterile rat model was established, according to the random number table method, and the rats were randomly divided into the treatment group and the control group, with 12 rats in each group, then the treatment group was given fecal microbiota solution of the children with FC and the control group was given fecal microbiota solution of the healthy children.The visceral sensitivity and intestinal propulsion rate of rats were determined by means of abdominal withdrawal reflex (AWR), while the intestinal microorganism of rats and children with FC were determined by 16SrDNA high-throughput sequencing, and the expressions of ASIC3 of intestinal in mRNA and protein were determined by adopting fluorescence quantitative PCR and Western blot. Results The species and quantity of intestinal flora of the children with FC and rats implanted with FC faecal bacteria were reduced(all P<0.05), and firmicutes and bacteroidetes were the main bacteria; compared to the control group, the small intestine propulsion rate(52% vs.74%) and visceral sensitivity(78 mmHg vs.63 mmHg) of the treated group were significantly decreased compared with those in the control group (all P<0.05); the mRNA (0.003 1±0.000 8 vs.0.012 4±0.002 5) and protein levels of ASIC3 (0.013 2±0.001 9 vs.0.072 1±0.008 7) in the small intestine were down-regulated significantly(all P<0.05); and the mRNA (0.002 8±0.000 7 vs.0.009 4±0.001 1) and protein levels of ASIC3(0.038 2±0.004 5 vs.0.089 7±0.009 4) in the colon were down-regulated significantly(all P<0.05). Conclusions Children with FC have intestinal flora disorder, and intestinal flora of FC children may affect intestinal motility by down-regulating the expression of intestinal ASIC3 in rats. Key words: Acid-sensitive ion channels; Intestinal flora; Visceral sensitivity; Intestinal motility; High throughput sequencing

Foreign bodies ingestion are common in children due to their the natural tendency to put things in mouth. Coins, batteries, small toys, safety pins and fish bones are some of the most common culprits. A retrospective study of 1,334 swallowing cases found that 80% of blunt, relatively small ingested foreign bodies pass through the gastrointestinal tract with no significant complications (1). However, the other 20% comprised of sharp, pointed, relatively larger objects and these became lodged in the gastrointestinal tract, causing an range of complications requiring emergency intervention (2). This article is protected by copyright. All rights reserved.

Henoch-Schönlein purpura is a common small vessel vasculitis in children. Acute pancreatitis rarely presents as a complication of Henoch-Schönlein purpura and has not been well characterized.

BACKGROUND Acid-sensing ion channels (ASICs) are ligand-gated cation channels activated by extracellular protons. However, the role of ASICs in kidney diseases remains uncertain. This study investigated ASICs expression in kidney tissues and their role in the development of Henoch-Schönlein purpura nephritis (HSPN). MATERIAL AND METHODS The expression of ASIC subunits was examined by immunochemical techniques in the kidney tissue from HSPN patients. Acid-induced ASICs expression in cultured renal tubular epithelial cells was determined by quantitative RT-PCR analysis. The expression of K7 and K18 protein in renal tubular epithelial cells was used to evaluate acid-induced cell injury. In addition, we observed the effect of blocking ASICs on acid-induced cell injury to assess the role of ASICs in renal tubular epithelial cell injury. RESULTS The results showed that ASIC1, ASIC2, and ASIC3 proteins were obviously expressed in renal tubular cells from HSPN patients. ASIC1 expression and 24-h urine protein level were higher in the pathological grade ISKD III group than in the ISKD II group. ASIC1, ASIC2, and ASIC3 mRNA, and K7 and K18 protein expression in cultured renal tubular epithelial cells were increased when exposed to pH 6.5. K7 and K18 protein expression was closely related to ASIC1 expression, and ASICs blockers reduced K7 and K18 protein expression in tubular epithelial cells. CONCLUSIONS These findings suggest ASICs are most highly expressed in renal tubular cells of HSPN patients, which is closely related to renal tubular injury. ASICs might be involved in the development of HSPN.

Objective To observe the expression of acid-sensing ion channels ( ASICs) of renal tissue from He-noch-Sch?nlein purpura nephritis( HSPN) and IgA nephropathy( IgAN) patients and its relationship with pathologi-cal damages. Methods The study was based on the paraffin-embedded renal tissues from 13 Henoch-Sch?nlein purpura nephritis patients, 11 IgA nephropathy patients and the 7 nomal persons. The expression of ASICs in the tissues from HSPN and IgAN patients was examined by immunohistochemical staining, while the expression of ASICs in the renal tissues was observed under microscope light by integral optical density( IOD) . And then, the re-lationship was analyzed between ASICs expressions and pathological damages according to the outcome. Results① The HSPN and IgAN patients’ ASICs were widely expressed in kidney tubules, only few were expressed in glo-meruli;②The HSPN and IgAN patients’ ASICs expressions were more than that of the control group(P<0. 01), ASIC1 and ASIC2 expressions of IgAN tissue were more than that of the HSPN group ( P<0. 05 );③The relation-ship between ASICs expression and 24 h urinary protein quantity with pathological grade Ⅲ was significantly more than pathological gradeⅡboth in HSPN and IgAN(P<0. 01);④ASIC1 expression was positively correlated with 24 h urinary protein quantity both in HSPN and IgAN. Conclusion ASICs express in both HSPN and IgAN pa-tients’ renal tissues, especially in their renal tubules. The expression is related to pathological grade and urinary protein production, which suggests that ASICs could participate in the pathological process of kidney damage.

Objective To observe the expression of acid -sensing ion channels (ASICs) in renal tissues from patients with Henoch -Sch?nlein purpura nephritis (HSPN) and to explore the action and mechanism of ASICs in the inflammatory injury of renal tissues. Methods Immunohistochemical methods were used to investigate the expression and localization of ASICs in renal tissue from patients with HSPN and patients with dropsical nephritis.The expressions of ASICs were semiquantitatively assessed by the percentage of posi-tive area of ASIC1a, ASIC2a, and ASIC3.The correlation between expression of ASICs and quantity of 24 -hour urinary protein was analyzed.According to different expressions of α1 -MG and β2 -MG in the test of urine trace protein, patients with HSPN were divid-ed into two groups.The expressions of ASICs in renal tubules of those two groups were assessed respectively.Results Immunohisto-chemical analysis revealed that higher expression of ASIC1a, ASIC2a and ASIC3 was noted in renal tubules from patients with HSPN. The expression of ASIC3 in patients with HSPN was positively correlated with quantity of 24 -hour urinary protein.Compared with the group with normal expressions of α1 -MG and β2 -MG, the expression of ASIC3 was significantly increased in the group with abnormal expressions of α1 -MG and β2 -MG (P <0.01) and higher expression of ASIC2a was noted in the group with abnormal expressions ofα1 -MG (P <0.01).Conclusions This study suggested an excitive role of ASICs in the pathogenesis of the injury of renal tubules in patients with HSPN.The expression of ASICs may be related to the production of proteinuria, especially microalbuminuria.

BACKGROUND:Asctites is rare in eosinophilic gastroenteritis.CASE CHARACTERISTICS:An 11-year-old boy who presented with abdominal pain and ascites.OBSERVATION:Peripheral blood examination revealed eosinophilia; serum IgE levels were raised. Biopsy from gastric antrum revealed marked eosinophilic infiltration of mucosa.OUTCOME:The childs symptoms and clinical findings improved after corticosteroids and anti-allergy treatment for 2 weeks.MESSAGE:Children presenting with unexplained gastrointestinal symptoms in the presence of ascites should be investigated for the gastrointestinal tract allergic disease.

ObjectiveTo investigate the etiological factors of abdominal palns and improve the diagnosis.Methods 200 hospitalized cases with abdominal palns as chief manifastation during from January 2012 to February 2014 were analyzed, including etiological factors, symptoms, physical signs and laboratory ifndings.Results Surgical acute abdomen was seen in<2 year, mesenteric lymphadenitis was seen in 2-5 year, Henoch-Schonlein purpura was seen in>5-12 year, gastritis was seen in>12 year.Conclusions The causes of acute abdomen are complex and various. More attention needs to be pald about early diagnosis.

[目的]探讨钙敏感受体(Calcium-sensing receptor,CaR)在淤胆型肝炎小鼠肝组织中的表达.[方法]采用ANIT(80 mg/kg,po)制备小鼠淤胆型肝炎模型,检测给予ANIT 24 h、48 h后小鼠血清ALT、ALP及BA水平,HE染色观察肝脏病理组织学改变,免疫组化检测CaR在淤胆型肝炎小鼠肝组织中的表达.[结果]给予ANIT 24h、48 h后,小鼠血清ALT、ALP及BA水平逐渐升高,48 h后明显上升;病理结果显示48 h后,肝细胞坏死明显;免疫组化结果显示淤胆型肝炎小鼠肝组织中CaR的表达明显增强.[结论]CaR在淤胆型肝炎小鼠肝脏组织中存在高表达,且可能与淤胆的发生有关.

OBJECTIVE It had been shown that apoptosis of vascular endothelial cells played an important role in the pathogenesis of HSP. The present study was designed to investigate the apoptosis of vascular endothelial cells induced by isolated IgA1 from sera of HSP patients. METHODS HUVEC were cultured in 3 different types of media with IgA1 from HSP patients, normal healthy children and simply medium (blank control). Serum IgA1 was purified by jacalin affinity chromatography. The rates of apoptosis in HUVEC incubated with IgA1 were determined by the TUNEL method and flow cytometry, respectively. The expression of bax/bcl-2 and p53 was detected with the methods of Real-time PCR and Westernblot, respectively. RESULT The results showed that the apoptosis rate of HUVEC by IgA1 isolated from HSP patients was higher than that the normal controls (14.77±2.23% vs 9.97±1.48%) and blank controls (14.77±2.23% vs 2.25±0.77%) (P <0.01). Moreover the rate of HUVEC by IgA1 from normal healthy children was higher than the blank controls (9.97±1.48% vs 2.25±0.77%) (P <0.01). In addition, the bax and P53 expression were up-regulated and the Bcl-2 expression was down-regulated in HUVEC co-cultured with IgA1 isolated from HSP patients for 24 hours. CONCLUSIONS These findings suggested that IgA1 from HSP patients could induce the apoptosis of HUVEC, which might be related to the vascular endothelial injury of HSP.

An 11-year-old boy presented with an acute headache, vomiting, blurred vision, and seizure. Five years ago, he was diagnosed with hemolytic uremic syndrome (HUS). Half a year before, urine protein reappeared and prednisone was initiated at 2 mg/kg and was now reduced to 0.5 mg/kg. His blood pressure (BP) was not regularly examined during therapy. At admission, his BP was 194/122 mm Hg. On physical examination, he had the presence of typical Cushing's appearance. His pupils were equal and round but poorly reactive to light. A neurological examination revealed obvious confusion and increased muscle tension in all four limbs. Laboratory examination revealed a hemoglobin level of 149 g/L, a platelet count of 332×109/L, and a reticulocyte level of 3.9%. Results from serum biochemical tests were within normal limits. Urine microscopy showed protein 3+ and no red blood cells. Serum complement component 3 (C3) and C4 levels were normal. Findings from electroencephalography showed abnormality signs of the brain. Findings from magnetic resonance imaging (MRI) demonstrated bilateral multiple abnormal signals in the occipital and parietal lobes (Figure). The patient was diagnosed with HUS in combination with reversible posterior leukoencephalopathy syndrome (RPLS). To control sequelae, diazepam (0.3 mg/kg) at 1 mg/min and a 20% mannitol solution at 1.5 g/kg was immediately given intravenously. Aggressive antihypertensive therapy with intravenous administration of sodium nitroprusside (2 μg/kg/min) was initiated. The patient's BP decreased to around 120/80 mm Hg and his consciousness recovered to normal on day 2 after admission. The intravenous antihypertensive therapy was switched to nifedipine orally and HUS treatment with corticosteroid was started. Twenty-two days later, the MRI abnormalities had diminished and the patient was discharged with no neurological symptoms. The boy had three possible risk factors for the presence of RPLS, including hypertension, proinflammatory cytokines, and cytotoxic effects of immunosuppressive agents on the vascular endothelium: (1) sudden elevated BP that exceeded the autoregulatory capacity of the brain vasculature leading to a marked increase in cerebral blood flow; (2) the presence of proinflammatory cytokines could induce inflammatory reaction in tissue and aggregate the impairment of endothelium cells1; and (3) immunosuppressive agents2, 3 could directly intoxicate the endothelium cells. In the present case, the patient's BP may have increased as a result of the boy's transient headache and blurred vision before admission. At his follow-up admission, we detected hypertension. More importantly, MRI findings were in accordance with the radiologic abnormalities of RPLS. Typical MRI findings in RPLS are of bilateral white matter abnormalities in vascular watershed areas in the posterior regions of both cerebral hemispheres, affecting mostly the occipital and parietal lobes.4-6 Therefore, hypertension was the most accepted trigger of RPLS in our patient. Prompt diagnosis and treatment of RPLS are essential to avoid irreversible brain damage. The typical clinical signs consist of seizure, consciousness impairment, headaches, visual abnormalities, and focal neurological signs; however, clinical symptoms alone are insufficient to rule out alternative causes and confirm the diagnosis. It has come to increasingly rely on MRI abnormalities. The brain MRI of our patient confirmed our diagnosis (Figure). The treatment and control of the factors causing RPLS7 including controlling hypertension, discontinuing or decreasing cytotoxic/immunosuppressive drugs, and controlling seizure were beneficial for improving prognostic implications. Hypertension control was an important part of the patient's symptomatic management. In this case, initial intravenous sodium nitroprusside and subsequent oral nifedipine effectively controlled hypertension in our patient. Little evidence exists on the prognosis of RPLS in children with kidney diseases. According to data in 20 children by Kenji Ishikura and colleagues,8 most patients recovered well within a few weeks after proper management and only a few cases showed neurological consequences or imaging abnormalities. The outcome of our patient was relatively satisfactory despite reports of poor prognosis associated with HUS; however, the long prognosis of this case was needed to be further investigated. RPLS is prevalent in children with kidney disease and it should be suspected when potential neurological complications are present. MRI is helpful in the early detection of RPLS, and prompt management significantly reduces mortality and improves prognosis.

T-cell immunoglobulin-containing and mucin-domain-containing molecule-3 (Tim-3) was identified nearly 10 years ago as a negative regulatory molecule that specifically identifies T helper 1 cells in both mice and humans. Recently, identification of Galectin-9 as a ligand for Tim-3 has established the Tim-3–Galectin-9 pathway as an important regulator in the CD8+ T-cell exhaustion that takes place in chronic immune conditions such as chronic viral infection and cancer in both humans and experimental models. In addition, association of Tim-3 polymorphisms with susceptibility to several autoimmune diseases has been identified. Recent work has explored the role of Tim-3 in hepatitis B virus (HBV) infection, and the results indicate that Tim-3 may represent a novel target for the treatment of HBV infection. In this review, we will discuss the Tim-3 pathway and the therapeutic potential of modulating the pathway in HBV infection.