实验性哮喘豚鼠初级传入系统和中枢内NKB的变化(英文)

本文应用放射免疫分析方法，测定了16只哮喘豚鼠初级传入系统和中枢内神经激肽β（NKB）的水平。结果表明，与正常对照组（结状神经书3228±11．89，C7～C8段脊神经节23．63±13．26，T1～T2段脊神经节24．25±1819，T3～T5段脊神经节25．53±12．34，C7～T5段脊髓后角28．65±16．59，孤束核26．34±18．36Pg／gwettissue）相比较，哮喘豚鼠初级传入系统和中枢内（结状神经节43．26±12．35，C7～C段脊神经节32．53±17．63，T1～T2段神经书32.25±20．65，T3～T5段脊神经节34．36±15．33，C7～T5段脊髓后角39．53±2028，孤束核3662±17．85Pg／gwettissue）NKB的含量明显高于对照组（P＜0．05）。结合NKB在呼吸道的作用，这些结果提示，初级传入系统和中枢内的NKB可能参与哮喘发病的病理生理机制。     

NGF对哮喘小鼠气道阻力和肺组织Akt/PKB表达的影响

目的探讨NGF介导的Akt/PKB信号转导通路在哮喘小鼠发病中的作用。方法BALB/c小鼠30只,按随机数字表法随机分为正常对照组、哮喘组、NGF阻断组。利用An iRes2005肺功能仪测小鼠气道阻力,运用免疫组织化学方法测定Akt/PKB的组织表达,M etamoph图像分析系统对结果进行分析。结果哮喘小鼠吸气阻力和呼气阻力明显高于正常组小鼠(P<0.01),NGF阻断组小鼠吸气阻力和呼气阻力明显低于哮喘组。免疫组织化学染色结果显示哮喘组Akt/PKB在肺组织炎性细胞的表达及AK t/PKB阳性炎症细胞数明显多于正常对照组(P<0.05),而NGF阻断组则明显低于哮喘组(P<0.05)。结论NGF介导哮喘气道高反应和炎症反应,Akt/PKB参与了哮喘发病中NGF介导的信号传导。     

神经激肽A免疫反应在哮喘豚鼠脊髓中的定量分析

用免疫细胞化学ＡＢＣ法结合显微图像定量分析，研究了神经激肽Ａ（ＮＫＡ）免疫反应物在哮喘豚鼠脊髓中的分布及其变化。结果表明，ＮＫＡ免疫反应纤维及终末分布于豚鼠Ｃ７～Ｔ５段脊髓后角Ⅰ～Ⅲ层和背外侧索核区，ＮＫＡ样阳性免疫反应物的平均密度在前者为４２．２％，后者为３７．２％；它们的平均灰度值分别为１３４．７和９２．９，与对照组（平均密度分别为２７．２％和２４．９％，平均灰度值分别为１９９．９和１２９．２）比较均有显著性差别（Ｐ＜０．０１）。这些研究结果提示脊髓内ＮＫＡ可能参与了哮喘发作的神经病理生理机制，是其发作的重要因素之一。     

不停跳冠状动脉旁路移植术中应用MostCare/PRAM监测系统进行血流动力学监测的临床研究

目的探究Most Care/PRAM系统监测下不停跳冠状动脉旁路移植术(OPCABG)患者术中血流动力学变化情况和预后分析。方法纳入2016年10月至2017年1月安贞医院89例OPCABG患者,其中男53例、女36例,年龄(60.50±8.40)岁。记录术中血流动力学变化情况。按是否发生心肌梗死、低心排血量等严重循环不良事件,分为平稳组和严重循环不良事件组,进行相关分析。结果手术全程监测完整血流动力学数据患者65例,开胸前和关胸后被动抬高试验的每搏量(SV)升高均值分别为23.00%±3.20%和29.40%±3.70%。麻醉、开胸、应用肝素时、搭桥中、应用鱼精蛋白时、关胸和术毕7个时间段,SV明显下降,外周血管阻力指数(SVRI)持续显著增加,最大压力梯度(d P/d T)和心脏循环效率(CCE)在麻醉后明显下降,搭桥时下降到最低,其后逐渐升高;每搏量变异率(SVV)和脉压变异率(PPV)在麻醉后下降,开胸后一直升高。89例患者发生严重循环不良事件共9例,其中4例死亡。严重循环不良事件组术中基础SVRI、SVV和PPV均显著高于平稳组(P<0.05),CCE、d P/d T和SV差异无统计学意义(P>0.05)。术中基础SVRI、CCE、d P/d T、SVV、PPV和SV均值与预后指标均无明显相关性。结论OPCABG术中易出现血流动力学的改变,因此,OPCABG术中宜应用Most Care/PRAM仪进行血流动力学监测,并及时纠正血流动力学异常。     

不同血液净化方式对尿毒症病人皮肤瘙痒疗效的研究进展

对尿毒症病人皮肤瘙痒的原因以及不同血液净化方式对皮肤瘙痒的治疗效果进行综述,旨在为临床医务人员针对尿毒症皮肤瘙痒病人选择最优的透析方式提供科学依据.     

循环肿瘤细胞的检测方法及其在肺癌临床中的应用

目前研究肺癌转移过程中最主要的切入点是循环肿瘤细胞,循环肿瘤细胞的研究已经受到了社会各界的广泛关注。预测循环肿瘤细胞的存在自十九世纪末“种子,土壤”学说开始。就目前而言,对循环肿瘤细胞的分析已经建立了可靠的、重复性好的检测方法以及分析方法。就目前而言,在临床上被广泛使用的是Cel Search检测方法。循环肿瘤细胞的计数可以有效的指导转移性肿瘤患者的预后评估分析。与此同时可以有效的反应出肿瘤药物的使用效果,同时对肿瘤的复发发挥着非常显著的检测效果。     

Hyperbaric oxygen therapy improves cognitive functioning after brain injury

Hyperbaric oxygen therapy has been widely applied and recognized in the treatment of brain injury; however, the correlation between the protective effect of hyperbaric oxygen therapy and changes of metabolites in the brain remains unclear. To investigate the effect and potential mechanism of hy- perbaric oxygen therapy on cognitive functioning in rats, we established traumatic brain injury models using Feeney＇s free falling method. We treated rat models with hyperbaric oxygen therapy at 0.2 MPa for 60 minutes per day. The Morris water maze test for spatial navigation showed that the average escape latency was significantly prolonged and cognitive function decreased in rats with brain injury. After treatment with hyperbaric oxygen therapy for 1 and 2 weeks, the rats＇ spatial learning and memory abilities were improved. Hydrogen proton magnetic resonance spectroscopy analysis showed that the N-acetylaspartate/creatine ratio in the hippocampal CA3 region was sig- nificantly increased at 1 week, and the N-acetylaspartate/choline ratio was significantly increased at 2 weeks after hyperbaric oxygen therapy. Nissl staining and immunohistochemical staining showed that the number of nerve cells and Nissl bodies in the hippocampal CA3 region was significantly increased, and glial fibrillary acidic protein positive cells were decreased after a 2-week hyperbaric oxygen therapy treatment. Our findings indicate that hyperbaric oxygen therapy significantly im- proves cognitive functioning in rats with traumatic brain injury, and the potential mechanism is me- diated by metabolic changes and nerve cell restoration in the hippocampal CA3 region.     

The top cited articles on glioma stem cells in Web of Science

BACKGROUND: Glioma is the most common intracranial tumor and has a poor patient prognosis. The presence of brain tumor stem cells was gradually being understood and recognized, which might be beneficial for the treatment of glioma. OBJECTIVE: To use bibliometric indexes to track study focuses on glioma stem cell, and to investigate the relationships among geographic origin, impact factors, and highly cited articles indexed in Web of Science. METHODS: A list of citation classics for glioma stem cells was generated by searching the database of Web of Science-Expanded using the terms "glioma stem cell" or "glioma, stem cell’" or "brain tumor stem cell". The top 63 cited research articles which were cited more than 100 times were retrieved by reading the abstract or full text if needed. Each eligible article was reviewed for basic information on subject categories, country of origin, journals, authors, and source of journals. Inclusive criteria: (1) articles in the field of glioma stem cells which was cited more than 100 times; (2) fundamental research on humans or animals, clinical trials and case reports; (3) research article; (4) year of publication: 1899-2012; and (5) citation database: Science Citation Index-Expanded. Exclusive criteria: (1) articles needing to be manually searched or accessed only by telephone; (2) unpublished articles; and (3) reviews, conference proceedings, as well as corrected papers. RESULTS: Of 2 040 articles published, the 63 top-cited articles were published between 1992 and 2010. The number of citations ranged from 100 to 1 754, with a mean of 280 citations per article. These citation classics came from nineteen countries, of which 46 articles came from the United States. Duke University and University of California, San Francisco led the list of classics with seven papers each. The 63 top-cited articles were published in 28 journals, predominantly Cancer Research and Cancer Cell, followed by Cell Stem Cell and Nature. CONCLUSION: Our bibliometric analysis provides a historical perspective on the progress of glioma stem cell research. Articles originating from outstanding institutions of the United States and published in high-impact journals are most likely to be cited.     

TACE分别联合放射性125I粒子植入与射频消融治疗乏血供肝癌

目的探讨TACE联合放射性~(125)I粒子植入与TACE联合经皮射频消融(RFA)治疗乏血供肝癌的临床疗效。方法回顾性分析46例乏血供肝癌患者资料,其中25例(30个病灶)接受TACE联合放射性~(125)I粒子植入治疗(A组),21例(27个病灶)接受TACE联合RFA治疗(B组)。比较两组疗效及并发症情况。结果治疗后3个月,B组临床有效率(RR)为96.30%(26/27),明显高于A组[86.67%(26/30),χ~2=8.694,P0.05];直径≤3cm的病灶中,A、B组的RR均为100%(8/8、10/10);在直径3~5cm的病灶中,A、B组的RR分别为81.82%(18/22)、94.12%(16/17),差异无统计学意义(χ~2=5.837,P0.05)。治疗后6个月,A、B组的RR分别为93.33%(28/30)、96.30%(26/27),差异无统计学意义(χ~2=3.422,P0.05);直径≤3cm的病灶中,A、B组的RR均为100%(8/8、10/10);直径3~5cm的病灶中,A、B组的RR分别为90.91%(20/22)、94.12%(16/17),差异无统计学意义(χ~2=2.716,P0.05)。两组术后并发症差异无统计学意义(P均0.05),均未出现严重并发症。结论 TACE联合放射性~(125)I粒子植入与TACE联合RFA均为乏血供肝癌安全、有效的治疗方法,TACE联合RFA相对近期疗效更优。     

Cofilin participates in regulating alpha-epithelial sodium channel by interaction with 14-3-3 isoforms

Renal epithelial sodium channel (ENaC) plays a crucial role in maintaining homeostasis and sodium absorption. While insulin participates in controlling sodium transport across the renal epithelium, the underlying molecular mechanism remain unclear. In this study, we found that insulin increased the expression and function of alpha-epithelial sodium channel (α-ENaC) as well as phosphorylation of cofilin, a family of actin-binding proteins which disassembles actin filaments, in mouse cortical collecting duct (mpkCCD_c14) cells. The wild-type (WT) cofilin and its constitutively phosphorylated form (S3D), but not its constitutively non-phosphorylable form (S3A), contributed to the elevated expression on α-ENaC. Overexpression of 14-3-3ε, β, or γ increased the expression of α-ENaC and cofilin phosphorylation, which was blunted by knockdown of 14-3-3ε, β, or γ. Moreover, it was found that insulin increased the interaction between cofilin and 14-3-3 isoforms, which indicated relevance of 14-3-3 isoforms with cofilin. Furthermore, LIMK1/SSH1 pathway was involved in regulation of cofilin and α-ENaC expression by insulin. The results from this work indicate that cofilin participates in the regulation of α-ENaC by interaction with 14-3-3 isoforms.