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71.
72.
Cheng-Fang Yen Yu-Min Chen Jen-Wen Cheng Tai-Ling Liu Tzu-Yu Huang Peng-Wei Wang Pinchen Yang Wen-Jiun Chou 《Child psychiatry and human development》2014,45(3):338-347
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
73.
Kexin Guo Xiaojie Mou Jinsha Huang Nian Xiong Hongge Li 《Journal of molecular neuroscience : MN》2014,54(1):41-48
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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75.
Lingling Kong MD Jian Cheng MD Xiuping Ding MD Baosheng Li MD PhD Jian Zhang PhD Hongsheng Li PhD Wei Huang PhD Tao Zhou MD Hongfu Sun MD 《The breast journal》2014,20(2):116-124
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
76.
Louis L. Huang David J. Nikolic-Paterson Yingjie Han Elyce Ozols Frank Y. Ma Morag J. Young Greg H. Tesch 《Journal of the American Society of Nephrology : JASN》2014,25(10):2231-2240
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.2–6 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.7–9The 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.14–16 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
77.
【摘要】〓结直肠癌是常见的消化道恶性肿瘤,传统治疗以外科手术为主,辅以放、化疗,术后5年生存率仅为50%左右。近年来结直肠癌基因治疗备受人们青睐,且有许多研究成果成功运用于临床。目前对结直肠癌基因治的方法主要有原癌基因治疗、抑癌基因治疗、免疫基因治疗以及多基因联合治疗等。 相似文献
78.
79.
老年脑卒中偏瘫患者的平衡训练 总被引:11,自引:4,他引:11
对109例老年脑卒中偏瘫患者平衡训练进行观察,发现患者经训练后,各项能力都有明显改善。与老年前期组相比无差别。训练对恢复运动及日常生活活动很有价值。观察还表明,平衡能力由高到低呈规律性变化,对指导平衡训练及判断预后有参考作用。 相似文献
80.