儿童感觉统合失调及其影响因素的调查分析

目的 研究儿童感觉统合失调与学习障碍及环境因素的关系。方法 采用感觉统合评定量表和学习障碍(PRS)筛查量表，分别对755名学龄儿童进行检测、分析。结果 感觉统合严重失调率为13．25％；感觉统合正常与失调儿童的学习障碍有统计学差异(P＜0．005)；其中在LD儿童中感觉统合失调率占63．51％；感觉统合失调与母孕期的情绪、是否足月顺产、出生后的喂养方式、居住环境、孩子1岁内有无高热、家长对孩子的态度及期待等因素有关(P＜0．05)。结论 儿童感觉统合失调与环境因素、学习障碍有一定的关系。     

广州港1997～2002年中小学生营养状况分析

目的 了解广州港中小学生的营养状况。方法 收集1997-2002年广州港4所中小学生的体检资料。结果 广州港4所中小学生平均营养不良发病率为23．39％，肥胖发病率为6．34％。营养不良发病率有逐年下降的趋势，而肥胖发病率则有逐年上升的趋势。男女性别间差异有显性意义(P＜0．01)。结论 中小学生营养不良与肥胖同时存在。今后的学生营养工作应防治中小学生营养不良与肥胖并举，全面推行以学校为中心的全民营养教育。     

呼和浩特地区11070名中,小学生视力调查分析

本文共测试了１１０７０名呼和浩特市城区和在区中、小学生的视力。结果是：引起学生视力低下的主要原因为近视，且近视的检出率和重度近视随年龄增长而增加，特别是在１３～１８岁年龄组更为明显；近视检出率城区学生明显高于农区学生（μ＞２．５８，ｐ＜０．０１），但是，无论城区学生或农区学生，女生的检出率分别都明显高于男生（μ＞２．５８，Ｐ＜０．０１）。     

大学生应对方式研究

介绍了大学生应对方式研究现状．重点阐述了大学生常用的应对方式、影响因素及应对方式对大学生心理健康的影响。     

基于学习体验的医学生智慧教室使用需求调查

为了更加准确地了解医学生智慧教室的使用需求,为智慧教室管理者在制定智慧教室环境优化策略时提供科学依据,本研究采用问卷调查法,从硬件设施、信息技术、教学法、医学智慧教室特色功能4个维度23项指标展开调查,采用KANO模型分析技术和满意度、重要度象限图对1 074份问卷进行数据分析。发现23项需求指标中,必备属性6项、期望属性7项、魅力属性9项、无差异属性1项。根据KANO模型理论重要度排序,智慧教室管理者应首先改善必备属性相关指标质量,优先提升期望属性相关指标质量,最后满足魅力属性相关指标需求。文章从学校顶层设计、教师和管理者3个层面提出了智慧教室相关政策和建设建议。     

阶梯式带教配合个体化考核在高职院校护理实训教学中的应用

目的 探讨阶梯式带教配合个体化考核在高职院校护理实训教学中的应用效果。方法 选取2020级高职护理专业护生219人,随机分为对照组（107人）与试验组（112人）,均在第一学期开设护理实训课程。对照组采用传统教学,试验组采用阶梯式带教配合个体化考核教学。对比两组护生教学后的理论知识与实践技能考核成绩、教学前后的综合护理能力,并比较两组护生对教学的肯定度。以SPSS 22.0进行t检验和卡方检验。结果 教学后试验组学生的理论知识与实践技能考核成绩各分项成绩及总分[（89.68±3.58） vs. （82.56±3.35）;（91.75±3.01） vs. （85.36±2.58）]均高于对照组（P<0.05）;教学前两组护生的综合护理能力比较差异无统计学意义,教学后的综合护理能力均高于教学前,且试验组护生的综合护理能力各分项成绩及总分[（86.53±2.61） vs. （80.32±2.31）]高于对照组（P<0.05）;教学后试验组护生对教学方法激发学习兴趣与积极性、提高自学能力、提高综合素养、提高理论知识运用能力、提高临床思维能力的肯定度均高于对照组（P<0.05）。结论 在高职院校护理实训教学中应用阶梯式带教配合个体化考核,可提高学生学习成绩及综合护理能力,并可提高其对教学的肯定度,可推广应用。     

An action of disodium cromoglycate: inhibition of cyclic 3',5'-AMP phosphodiesterase.

Disodium cromoglycate (DSCG) prevents allergic asthma by inhibiting the release of chemical mediators of immediate-type allergic reactions. The mechanism of this action is unclear and prompted us to examine the effect of DSCG on cyclic adenosine 3',5'-monophosphate (cAMP), the implicated regulator of IgE-mediated reactions. We used the peripheral blood lymphocyte as a model to mirror the biochemical events occurring in the allergic shock organs. Isolated peripheral blood lymphocytes from perennial allergic asthmatic children receiving only DSCG had significantly (p less than 0.005) lower phosphodiesterase (PDE) activity (mean 1.05 +/- 0.17 SE per 10(6) cells) than normal individuals (2.93 +/- 0.14) and allergic children receiving methylxanthines (4.08 +/- 0.28) or no medications (3.58 +/- 0.2). DSCG (10 mug/ml) significantly lowered PDE activity in normal lymphocytes (p less than 0.005) in a beef heart extract (p less than 0.001), and 100 mug/ml lowered PDE activity in fetal rabbit lung homogenates (p less than 0.001). DSCG (10 mug/ml) significantly elevated (p less than 0.01) cAMP concentration in normal human lymphocytes (118 +/- 38 vs 30 +/- 10 picomoles cAMP/10(6) lymphocytes). Thus, DSCG appears to inhibit chemical mediator release by increasing intracellular cAMP through the inhibition of cAMP PDE.     

家庭因素对医学新生适应能力的影响

目的 :探讨家庭因素对医学新生适应能力的影响。方法 :使用“一般情况问卷”、“大学生适应情况调查表”、“父母养育方式问卷”、“家庭环境量表中文版”对三所医学院校新生 5 5 6人进行调查。通过单因素分析和多元回归分析等方法 ,筛选影响新生适应能力的主要家庭因素。结果 :入学新生四个月后仍有9 7%不能适应大学学习 ,3 6 %不适应大学生活 ,11 9%不适应大学的人际关系。女生差于男生。父母情感温暖、亲密度、成功性、娱乐性与适应得分呈低度正相关 (r =0 16～ 0 2 4) ,而父母严厉惩罚、拒绝否认、过度保护、矛盾性、控制性呈低度负相关 (r =-0 15～ 0 2 4)。多元逐步回归显示 :矛盾性、娱乐性、组织性、控制性、父亲过度保护是影响医学新生适应能力的主要因素 (r =3 8～ 2 1)。结论 :家庭背景对新生的适应能力有显著影响     

Effects of theophylline,terbutaline, and prednisone on antigen-induced bronchospasm and mediator release

Eleven subjects demonstrating clinical, skin, and inhalation sensitivity to grass or ragweed pollen underwent serial inhalation challenges, with and without orally administered theophylline, terbutaline, and prednisone. Comparisons of antigen sensitivity and mediator release were made during these challenges. All three drugs significantly reduced antigen sensitivity (PD₂₀ inhalation units increasing from 670 to ≧ 3,280). Peak plasma histamine levels after antigen challenge decreased from 11.4 ng/ml to ≦ 3.4 ng/ml during all drug administrations. Similarly, the percent increase in serum neutrophil chemotactic activity (NCA) also decreased, from 96% to ≦ 36% during drug administrations. However, even at antigen doses resulting in bronchospasm during drug administration the systemic appearance of NCA and histamine were reduced. We conclude that prednisone, theophylline, and terbutaline significantly reduce antigen-induced bronchospasm and mediator release. The occurrence of bronchospasm despite the inhibition of histamine and NCA suggests either that the local concentration of these mediators are critical or that other mediators produce the bronchospasm observed.     

Dual β-Catenin and γ-Catenin Loss in Hepatocytes Impacts Their Polarity through Altered Transforming Growth Factor-β and Hepatocyte Nuclear Factor 4α Signaling

Hepatocytes are highly polarized epithelia. Loss of hepatocyte polarity is associated with various liver diseases, including cholestasis. However, the molecular underpinnings of hepatocyte polarization remain poorly understood. Loss of β-catenin at adherens junctions is compensated by γ-catenin and dual loss of both catenins in double knockouts (DKOs) in mice liver leads to progressive intrahepatic cholestasis. However, the clinical relevance of this observation, and further phenotypic characterization of the phenotype, is important. Herein, simultaneous loss of β-catenin and γ-catenin was identified in a subset of liver samples from patients of progressive familial intrahepatic cholestasis and primary sclerosing cholangitis. Hepatocytes in DKO mice exhibited defects in apical-basolateral localization of polarity proteins, impaired bile canaliculi formation, and loss of microvilli. Loss of polarity in DKO livers manifested as epithelial-mesenchymal transition, increased hepatocyte proliferation, and suppression of hepatocyte differentiation, which was associated with up-regulation of transforming growth factor-β signaling and repression of hepatocyte nuclear factor 4α expression and activity. In conclusion, concomitant loss of the two catenins in the liver may play a pathogenic role in subsets of cholangiopathies. The findings also support a previously unknown role of β-catenin and γ-catenin in the maintenance of hepatocyte polarity. Improved understanding of the regulation of hepatocyte polarization processes by β-catenin and γ-catenin may potentially benefit development of new therapies for cholestasis.

A hallmark of epithelial cells is polarization, which is achieved by the orchestration of external cues, such as cellular contact, extracellular matrix, signal transduction, growth factors, and spatial organization.¹ Hepatocytes in the liver show a unique polarity by forming several apical and basolateral poles within a cell.² The apical poles of adjacent hepatocytes form a continuous network of bile canaliculi into which bile is secreted, whereas the basolateral membrane domain forms the sinusoidal pole, which secretes various components, such as proteins or drugs, into the blood circulation.³ Loss of hepatic polarity has been associated with several cholestatic and developmental disorders, including progressive familial intrahepatic cholestasis (PFIC) and primary sclerosing cholangitis (PSC).^4,5 Although the molecular mechanisms governing hepatocyte polarity have been extensively studied in the in vitro systems, there is still a significant gap in our understanding of how polarity is established within the context of tissue during development or maintained during homeostasis.^6,7 Similarly, the molecular pathways contributing to hepatic polarity are not entirely understood, and a better comprehension of hepatic polarity regulation is thus warranted.Previous studies have confirmed the role of hepatocellular junctions, such as tight and gap junctions, in the maintenance of hepatocyte polarity.^8,9 Studies done in vitro and in vivo have shown that loss of junctional proteins, such as zonula occludens protein (ZO)-1, junctional adhesion molecule-A, and claudins, lead to impairment of polarity and distorted bile canaliculi formation.10, 11, 12, 13 In addition, proteins involved in tight junction assembly, such as liver kinase B1, are also involved in polarity maintenance.¹⁴ Among adherens junction proteins, various in vitro cell culture models have confirmed the role of E-cadherin in the regulation of hepatocyte polarity, possibly through its interaction with β-catenin.^15,16 However, there is a lack of an in vivo model to study the role of adherens junction proteins in hepatocyte polarity and their misexpression contributing to various liver diseases.β-Catenin plays diverse functions in the liver during development, regeneration, zonation, and tumorigenesis.17, 18, 19 The relative contribution of β-catenin as part of the adherens junction is challenging to study because like in other tissues, γ-catenin compensates for the β-catenin loss in the liver.^20,21 To address this redundancy, we previously reported a hepatocyte-specific β-catenin and γ-catenin double-knockout (DKO) mouse model was reported.²² Simultaneous deletion of β-catenin and γ-catenin in mice livers led to cholestasis, partially through the breach of cell-cell junctions. However, more comprehensive understanding of the molecular underpinnings of the phenotype is needed.In the current study, prior preclinical findings of dual β-catenin and γ-catenin loss were extended to a subset of PFIC and PSC patients. In vivo studies using the murine model with hepatocyte-specific dual loss of β-catenin and γ-catenin showed complete loss of hepatocyte polarity compared to the wild-type controls (CONs). Loss of polarity in DKO liver was accompanied by epithelial-mesenchymal transition (EMT), activation of transforming growth factor (TGF)-β signaling, and reduced expression of hepatocyte nuclear factor 4α (HNF4α). Our findings suggest that β-catenin and γ-catenin and in turn adherens junction integrity, are critical for the maintenance of hepatocyte polarity, and any perturbations in this process can contribute to the pathogenesis of cholestatic liver disease.