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91.
目的:探讨非医学指征剖宫产儿童在本顿视觉保持测验中的视知觉、视觉记忆、视觉结构能力等认知特征,分析剖宫产对儿童神经心理的影响,为控制人为剖宫产率提供理论支持。方法:于2003-09/10整群选取广州市几所小学三、四年级儿童作为调查对象。共发放自编的“分娩情况和一般家庭情况”调查问卷727份,回收663份,根据回收问卷中分娩方式情况,筛查出非医学指征性剖宫产儿童63例,作为剖宫产组,选择与剖宫产组儿童年龄、性别、学校、班级及家庭一般情况无显著性差异的正常阴道分娩儿童156人作为对照组。应用国内修订版本顿视觉保持测验对两组儿童的视觉记忆保持能力、视觉结构能力和延迟记忆能力进行测试,该测验的测具包括无意义的图卡片C、D、E式各10张,分为4种测验方法,A法、B法为每一图卡片呈现10s或5s后让被试默画,C法为让被试临摹图卡片,D法为每一图卡片呈现10s后间隔15s再让被试默画,本测试采用C式B法,D式C法和E式D法,采用个别施测方式,分别记录两组儿童测验的正确分(每一图卡根据全或无的原则记1或0分,总分范围0~10之间)及错误次数(错误类型分为遗漏、变形、持续、旋转、位置错误和大小错误6个范畴),基本资料进行两组间的成组t检验。结果:所有调查对象全部进入结果分析,无脱落。本顿视觉保持测验结果显示剖宫产儿童在E式D法测验中的得分低于对照组(P<0.05);在D式C法中“位置”错误类型的出现次数多于对照组(P<0.05),在E式D法中“位置”和“变形”错误类型的出现次数较对照组明显偏高(P<0.05)。结论:剖宫产儿童的视觉空间结构能力及视觉延时回忆能力存在缺陷,视空间工作记忆、视觉结构与视觉统和功能不足。  相似文献   
92.
Schizophrenia is a common mental disorder with high heritability and strong genetic heterogeneity. Common disease-common variants hypothesis predicts that schizophrenia is attributable in part to common genetic variants. However, recent studies have clearly demonstrated that copy number variations (CNVs) also play pivotal roles in schizophrenia susceptibility and explain a proportion of missing heritability. Though numerous CNVs have been identified, many of the regions affected by CNVs show poor overlapping among different studies, and it is not known whether the genes disrupted by CNVs contribute to the risk of schizophrenia. By using cumulative scoring, we systematically prioritized the genes affected by CNVs in schizophrenia. We identified 8 top genes that are frequently disrupted by CNVs, including NRXN1, CHRNA7, BCL9, CYFIP1, GJA8, NDE1, SNAP29, and GJA5. Integration of genes affected by CNVs with known schizophrenia susceptibility genes (from previous genetic linkage and association studies) reveals that many genes disrupted by CNVs are also associated with schizophrenia. Further protein-protein interaction (PPI) analysis indicates that protein products of genes affected by CNVs frequently interact with known schizophrenia-associated proteins. Finally, systematic integration of CNVs prioritization data with genetic association and PPI data identifies key schizophrenia candidate genes. Our results provide a global overview of genes impacted by CNVs in schizophrenia and reveal a densely interconnected molecular network of de novo CNVs in schizophrenia. Though the prioritized top genes represent promising schizophrenia risk genes, further work with different prioritization methods and independent samples is needed to confirm these findings. Nevertheless, the identified key candidate genes may have important roles in the pathogenesis of schizophrenia, and further functional characterization of these genes may provide pivotal targets for future therapeutics and diagnostics.Key words: schizophrenia, copy number variation, prioritization, integrative analysis, NRXN1, CHRNA7  相似文献   
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The aims of this intervention study were to examine the effects of individual cognitive-behavioral therapy (CBT) based on the modified Coping Cat Program on improving anxiety symptoms and behavioral problems in Taiwanese children with anxiety disorders and parenting stress perceived by their mothers. A total of 24 children with anxiety disorders in the treatment group completed the 17-session individual CBT based on the modified Coping Cat Program, and 26 children in the control group received the treatment as usual intervention. The Taiwanese version of the MASC (MASC-T), the Child Behavior Checklist for Ages 6–18 (CBCL/6-18) and the Chinese version of the Parenting Stress Index (C-PSI) were applied to assess the severities of anxiety symptoms, behavioral problems and parenting stress, respectively. The effects of CBT on improving anxiety symptoms, behavioral problems and parenting stress were examined by using linear mixed-effect model with maximum likelihood estimation. The results indicated that the CBT significantly improved the severities of MASC-T Physical Symptoms and Social Anxiety subscales, CBCL/6-18 DSM-oriented Anxiety Problem subscale, and C-PSI Child domains Mood and Adaptability subscales. Individual CBT based on the modified Coping Cat Program can potentially improve anxiety symptoms in Taiwanese children with anxiety disorders and some child domains of parenting stress perceived by their mothers.  相似文献   
97.
Microglia cells have been reported to mediate hypoxia-induced inflammation through the production of proinflammatory cytokines, including interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and IL-6. Given the fact that the activation of the type 2 cannabinoid receptor (CB2R) provides antioxidative and anti-inflammatory results, it is suspected that its selective agonist, trans-caryophyllene (TC), may have protective effects against hypoxia-induced neuroinflammatory responses. In this study, TC was found to significantly inhibit hypoxia-induced cytotoxicity as well as the release of proinflammatory cytokines, including IL-1β, TNF-α, and IL-6, through activation of BV2 microglia following hypoxic exposure (1 % O2, 24 h). Furthermore, TC significantly inhibited hypoxia-induced generation of reactive oxygen species (ROS) in mitochondria as well as the activation of nuclear factor kappa B (NF-κB) in microglia. Importantly, TC’s effects on inhibiting the activation of NF-κB and the secretion of inflammatory cytokines can be abolished by muting the CB2R using small RNA interference. These observations indicate that TC suppresses the hypoxia-induced neuroinflammatory response through inhibition of NF-κB activation in microglia. Therefore, TC may be beneficial in preventing hypoxia-induced neuroinflammation.  相似文献   
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To compare the treatment outcomes between accelerated partial breast irradiation (APBI) and conventional whole‐breast irradiation (WBI) and to explore the efficacy and safety of APBI as an adjuvant treatment for early‐stage breast cancer who received breast‐conserving therapy. Eligible studies were identified on Medline, Embase, and the Cochrane Library updated to July 10, 2012. Comparative studies were considered for inclusion. Analyses were carried out using Stata software. Eleven comparative studies with a total of 7,097 patients were included. The meta‐analysis showed that there were no statistically significant differences between group APBI and group WBI associated with the supraclavicular failure, distant metastasis, overall survival, and disease‐free survival, while local recurrence (LR) and axillary failure (AF) increased in group APBI. The sensitivity analysis indicated that both the LR and AF were not statistically significant difference between the two groups. In the subgroup analysis, LR was statistically significantly higher in group APBI for patients with the age <60, large tumor size, and unknown margin status. APBI is a safe treatment modality and could become a potential option for the delivery of adjuvant radiation therapy in patients receiving breast‐conserving therapy, especially for the suitable group that was classified by the American Society of Radiation Oncology Consensus Panel.  相似文献   
100.
Clinical and experimental studies have shown that mineralocorticoid receptor (MR) antagonists substantially reduce kidney injury. However, the specific cellular targets and mechanisms by which MR antagonists protect against kidney injury must be identified. We used conditional gene deletion of MR signaling in myeloid cells (MRflox/flox LysMCre mice; MyMRKO) or podocytes (MRflox/flox PodCre mice; PodMRKO) to establish the role of MR in these cell types in the development of mouse GN. Accelerated anti–glomerular basement membrane GN was examined in groups of mice: MyMRKO, PodMRKO, wild-type (WT) littermates, and WT mice receiving eplerenone (100 mg/kg twice a day; EPL-treated). At day 15 of disease, WT mice had glomerular crescents (37%±5%), severe proteinuria, and a 6-fold increase in serum cystatin-C. MyMRKO, PodMRKO, and EPL-treated mice with GN displayed proteinuria similar to that in these disease controls. However, MyMRKO and EPL-treated groups had a 35% reduction in serum cystatin-C levels and reduced crescent numbers compared with WT mice, whereas PodMRKO mice were not protected. The protection observed in MyMRKO mice appeared to result predominantly from reduced recruitment of macrophages and neutrophils into the inflamed kidney. Suppression of kidney leukocyte accumulation in MyMRKO mice correlated with reductions in gene expression of proinflammatory molecules (TNF-α, inducible nitric oxide synthase, chemokine (C-C motif) ligand 2, matrix metalloproteinase-12), tubular damage, and renal fibrosis and was similar in EPL-treated mice. In conclusion, MR signaling in myeloid cells, but not podocytes, contributes to the progression of renal injury in mouse GN, and myeloid deficiency of MR provides protection similar to eplerenone in this disease.Mineralocorticoid receptor (MR) antagonists are known to inhibit renal and cardiovascular disease (CVD) by direct blockade of MR in tissues and by reducing hypertension.1 They can also suppress kidney damage in animal models of GN and diabetic nephropathy without affecting BP.26 In addition, MR antagonists provide added protection against proteinuria and loss of renal function when used with standard antihypertensive therapies in patients with diabetic and nondiabetic CKD.79The clinical use of MR antagonists is limited by the development of hyperkalemia due to the importance of the MR in tubular regulation of salt balance.10 This consequence of MR blockade in the distal tubule is most evident during renal impairment and can require a reduction in the dosage of MR antagonist or withdrawal of the agent as a therapy.7,8 The specific renal cell types that are targeted by MR antagonists to reduce injury during kidney disease have not been clearly identified. Establishing the identity of these cells is an important step toward developing more selective inhibitors of MR signaling that do not interfere with tubular cell function.Animal studies demonstrate that the protection afforded by MR antagonists in GN and diabetic nephropathy is associated with reductions in renal inflammation, proteinuria, and glomerular injury.2,3,5,11 These studies also link MR blockade to suppression of leukocyte recruitment and podocyte injury. This suggests that the major pathologic effects of MR signaling may occur in podocytes and inflammatory cells.Recent in vitro studies have suggested that MR signaling can induce apoptosis in podocytes and oxidative stress in macrophages,12,13 which supports a role for MR signaling in these cell types in kidney disease. In addition, an MR deficiency in myeloid cells protects against cardiovascular injury and ischemic cerebral infarcts by reducing inflammation and fibrosis.1416 However, no in vivo studies have identified whether MR signaling in podocytes or macrophages is specifically important to the development of kidney disease.In this study, we created mice with a selective genetic deficiency of MR in myeloid cells or podocytes and used these strains to evaluate the hypothesis that MR signaling in macrophages or podocytes is required for the development of renal injury in a normotensive model of progressive GN.  相似文献   
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