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41.
目的研究床上体操配合音疗对脑卒中早期患者偏瘫肢体功能的影响.方法将100例脑卒中偏瘫患者分为2组,常规组(n=50),常规+训练组(n=50).常规组给予常规内科治疗护理.常规+训练组除常规内科治疗护理外,根据患者肢体运动功能情况选择适合不同时期的床上体操和音疗训练,治疗前后予Brunnstrom法运动功能评估,日常生活活动能力Barthel指数评估,心理评估.结果治疗前2组日常生活活动能力、肢体运动功能、心理评估无差异,治疗后1个月常规+训练组日常生活活动能力(Barthel指数)、运动功能(Brunnstrom法)明显高于常规组(P<0.05).常规+训练组的恐怖、抑郁、强迫、焦虑症状得到明显改善(P<0.05).常规组治疗护理组抑郁、强迫、焦虑症状无明显改善(P>0.05),仅恐怖症状有改善(P<0.05).结论音乐床上体操对脑卒中早期偏瘫肢体功能恢复和心理障碍治疗有明显作用,有利于提高患者的生活质量.  相似文献   
42.
Over the last years, electronic cigarettes (ECs) have become more popular, particularly in individuals who want to give up smoking tobacco. The aim of the present study was to assess the influence of the different e-smoking liquids on the viability and proliferation of human periodontal ligament fibroblasts. For this study six test solutions with components from ECs were selected: lime-, hazelnut- and menthol-flavored liquids, nicotine, propylene glycol, and PBS as control group. The fibroblasts were incubated up to 96 h with the different liquids, and cell viability was measured by using the PrestoBlue® reagent, the ATP detection and the migration assay. Fluorescence staining was carried out to visualize cell growth and morphology. Data were statistically analyzed by two-tailed one-way ANOVA. The cell viability assay showed that the proliferation rates of the cells incubated with nicotine or the various flavored liquids of the e-cigarettes were reduced in comparison to the controls, though not all reductions were statistically significant. After an incubation of 96 h with the menthol-flavored liquid the fibroblasts were statistically significant reduced (p?相似文献   
43.
目的:观察中药大黄治疗后肢体高能量枪弹伤犬脑神经元c-Jun蛋白表达的变化,从分子生物水平上探讨中药大黄治疗肢体火器伤后远达效应的脑保护途径。方法:实验于2001-07/12在解放军第四军医大学西京医院实验外科完成。18只杂种犬,以M-193,5.56mm制式弹射击犬双后肢肌肉丰满处,随机分为对照组、大黄治疗组,每组分伤后2,6,10h3个时间点,每个时间点3只。对照组伤后应用无菌注射用水鼻饲,大黄治疗组应用中药大黄的乙醇及水提液鼻饲,采用免疫组化方法观察两组伤后2,6,10h远隔部位脑组织脑神经元中c-Jun蛋白的表达变化。结果:18只杂种犬均进入结果分析。伤后2,6,10h大黄治疗组脑神经元中c-Jun蛋白显著少于对照组[(8.7±1.2),(14.2±1.7)个/单位面积;(3.7±2.5),(21.6±2.1)个/单位面积;(11.6±1.4),(19.2±1.9)个/单位面积,P<0.01]。结论:中药大黄提取液能够抑制肢体枪弹伤后脑神经元c-Jun蛋白的表达。  相似文献   
44.
目的:研究促皮质激素释放激素(corticotrophin releasing hormone,CRF)在豚鼠结肠肌间神经丛的表达和生理功能。方法:RT-PCR、免疫荧光组织化学染色检测CRF在结肠肠肌层神经丛的表达;细胞内电生理记录结合生物素示踪法研究CRF在肠道的生理功能。结果:豚鼠的肠肌间神经丛有CRF mRNA的表达;豚鼠结肠肠肌间神经丛中有表达CRF的神经元,其形态均为DogielⅠ型神经元。CRF对豚鼠结肠肌间神经丛有很强的兴奋作用,可诱发慢的兴奋性去极化反应,而且CRF所兴奋的神经元均为表达CRFI受体的神经元。结论:CRF是肠道神经系统的兴奋性神经递质。  相似文献   
45.
Signs of physical dependence as a consequence of long-term drug use and a moderate abuse liability limit benzodiazepine clinical usefulness. Growing evidence suggests a role for voltage-gated calcium channel (VGCC) regulation in mediating a range of chronic drug effects from drug withdrawal phenomena to dependence on a variety of drugs of abuse. High voltage-activated (HVA) calcium currents were measured in whole-cell recordings from acutely isolated hippocampal CA1 neurons after a 1-week flurazepam (FZP) treatment that results in withdrawal-anxiety. An approximately 1.8-fold increase in Ca(2+) current density was detected immediately after and up to 2 days but not 3 or 4 days after drug withdrawal. Current density was unchanged after acute desalkyl-FZP treatment. A significant negative shift of the half-maximal potential of activation of HVA currents was also observed but steady-state inactivation remained unchanged. FZP and diazepam showed use- and concentration-dependent inhibition of Ca(2+) currents in hippocampal cultured cells following depolarizing trains (FZP, IC(50) = 1.8 microM; diazepam, IC(50) = 36 microM), pointing to an additional mechanism by which benzodiazepines modulate HVA Ca(2+) channels. Systemic preinjection of nimodipine (10 mg/kg), an L-type (L)-VGCC antagonist, prevented the benzodiazepine-induced increase in alpha-amino-3-hydroxy-5-methylisoxasole-4-propionic acid receptor (AMPAR)-mediated miniature excitatory postsynaptic current in CA1 neurons 2 days after FZP withdrawal, suggesting that AMPAR potentiation, previously linked to withdrawal-anxiety may require enhanced L-VGCC-mediated Ca(2+) influx. Taken together with prior work, these findings suggest that enhanced Ca(2+) entry through HVA Ca(2+) channels may contribute to hippocampal AMPAR plasticity and serve as a potential mechanism underlying benzodiazepine physical dependence.  相似文献   
46.
[目的]探讨经颈静脉肝内门腔静脉内支架分流术(TIPSS)后病人的生命质量。[方法]采用问卷调查方法,对30例TIPSS病人进行生命质量调查及自编问卷调查,对发现的问题给予积极的护理支持。[结果]生理、心理、环境领域维度得分较术前明显上升,社会关系领域维度则下降,差异有统计学意义(P〈0.05)。[结论]对TIPSS术后病人实施心理疏导,重视病人的随访咨询,定期评估和干预,帮助病人有效应对,可以有效提高病人的生命质量。  相似文献   
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Purpose

CXCR1 signaling promotes tumor progression in various cancers, and clinical trial has proved efficacy of CXCR1 inhibitor in metastatic breast cancer. Therefore, we investigated the prognostic value of CXCR1 in patients with metastatic renal cell carcinoma (mRCC) receiving tyrosine kinase inhibitors (TKIs) therapy.

Materials and Methods

Patients treated with sunitinib or sorafenib were retrospectively enrolled (n = 111). CXCR1 expression was assessed by immunohistochemical staining of tissue microarrays of primary tumor, and its association with prognosis and therapeutic response were evaluated. To explore possible mechanism related to CXCR1 expression, gene set enrichment analysis was performed based on The Cancer Genome Atlas cohort.

Results

High CXCR1 expression was associated with poorer overall survival (P = 0.015) and was an independent prognostic factor for patients with mRCC treated by TKIs (Hazard Ratio = 1.683, 95% Confidence Interval: 1.109–2.553, P = 0.014). CXCR1 expression was also associated with worse therapeutic response of TKIs (P = 0.017). Thirteen pathways, including hypoxia and angiogenesis, were identified to be enriched in CXCR1 positive patients.

Conclusions

High CXCR1 expression indicates reduced benefit from TKIs therapy in patients with mRCC. The mechanism may be attributed to the enriched pathways of hypoxia and angiogenesis in CXCR1 positive patients. CXCR1 may be a potential therapeutic target for mRCC, but further studies are required.  相似文献   
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