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为您找到包含“免疫性血小板减少症”的内容共10

吴晓勇,陈广雷,王云龙,曾强武,安仕刚

2016-08-19

免疫性血小板减少(ITP)是一种获得性自身免疫性出血疾病,其特点为血小板破坏增多和生生成不足。ITP发病涉及复杂免疫失调,近年来研究表明T细胞亚群免疫异常在ITP免疫发病机制中起核心中医,Th细胞

国家自然科学基金项目(81260539

贵州省高校优秀科技创新人才支持计划(黔教合KY字[2013]139号

贵阳中医学院第一附属医院苗医药科,贵阳贵阳,550001,贵阳中医学院研究生院,贵州贵阳,550002,贵阳中医学院研究生院,贵州贵阳,550002,贵阳中医学院第一附属医院检验科,贵州贵阳,550001,贵阳中医学院第一附属医院检验科,贵州贵阳,550001

#临床医学#

陶莉莉,潘莹,王会平,陶千山,卞恒娟,翟志敏

2014-01-10

通过检测初诊成人免疫性血小板减少(ITP)患者外周血T细胞亚群的表达及调节性T细胞(Treg)水平,探讨患者T细胞免疫状态与发病机制的关系。以26例ITP患者及10例健康体检者作为研究对象,运用

安徽医科大学第二附属医院血液内科,合肥 230601,安徽医科大学第二附属医院血液内科,合肥 230601,安徽医科大学第二附属医院血液内科,合肥 230601,安徽医科大学第二附属医院血液内科,合肥 230601,安徽医科大学第二附属医院血液内科,合肥 230601,安徽医科大学第二附属医院血液内科,合肥 230601

#临床医学#

吴晓勇,陈广雷,王云龙,李成龙,毕莲,陈育,陈蕾蕾

2016-08-12

免疫性血小板减少(ITP) 是一种免疫介导的血小板破坏增多、血小板生成不足,以皮肤粘膜出血为特征的自身免疫性疾病。现代中西医血液病专家共识将ITP的中医病名命名为"紫癜病"。近年来,中医药治疗

贵州省高校优秀科技创新人才支持计划(黔教合KY字[2013]139号

国家自然科学基金项目(81260539

贵阳中医学院第一附属医院,贵州贵阳,550001,贵阳中医学院研究生院,贵州贵阳,550002,贵阳中医学院研究生院,贵州贵阳,550002,贵阳中医学院研究生院,贵州贵阳,550002,贵阳中医学院第一附属医院,贵州贵阳,550001,贵阳中医学院第一附属医院,贵州贵阳,550001,贵阳中医学院学报编辑部,贵州贵阳,550025

#中医学与中药学#

吴晓勇,陈广雷,王云龙,毕莲,陈蕾蕾

2016-08-19

免疫性血小板减少(immune thrombocytopenia,ITP)是一种免疫介导的以血小板减少和皮肤粘膜出血为特征的自身免疫性疾病。现代医学家将ITP中医病名称为"紫癜病"。慢性ITP中医

基金项目:国家自然科学基金项目(81260539

贵州省高校优秀科技创新人才支持计划(黔教合KY字[2013]139号

贵阳中医学院第一附属医院,贵州贵阳,550001,贵阳中医学院研究生院,贵州贵阳,550002,贵阳中医学院研究生院,贵州贵阳,550002,贵阳中医学院第一附属医院,贵州贵阳,550001,贵阳中医学院学报编辑部,贵州贵阳,550025

#中医学与中药学#

王珺,张玲,张雅月,马薇,陈科,陈信义,侯丽

2017-09-12

目的:观察健脾益气摄血颗粒改善"脾不统血证(脾气虚)"型免疫性血小板减少(ITP)患者症状及止血疗效。方法:应用中央随机对照、多中心临床试验方法,将符合病例入选标准的ITP患者按3:3:2分为中药

Zhejiang Provincial Hospital of TCM of Zhejiang Chinese Medical University,Dongzhimen Hospital of Beijing University of Chinese Medicine,Dongzhimen Hospital of Beijing University of Chinese Medicine,Dongzhimen Hospital of Beijing University of Chinese Medicine,Dongzhimen Hospital of Beijing University of Chinese Medicine,Dongzhimen Hospital of Beijing University of Chinese Medicine,Dongzhimen Hospital of Beijing University of Chinese Medicine

#中医学与中药学#

李慧媛,周芳芳,杨仁池

2017-01-05

CD40/CD40L 是一对重要的共刺激分子,参与多种自身免疫性疾病的发生。近年来研究发现CD40L 在一些自身免疫性疾病女性患者中高表达。因而本研究中我们检测CD40L 在原发免疫性血小板减少

高等学校博士学科点专项科研基金(新教师类

中国医学科学院血液病医院(血液学研究所),中国医学科学院血液病医院(血液学研究所),中国医学科学院血液病医院(血液学研究所)

#临床医学#

陈科,张雅月,赵宁,马薇,陈信义

2017-08-08

目的:基于脑肠轴平衡学说,从血液神经递质角度探讨从脾论治ITP新机制。方法:采用中央随机对照、多中心临床试验方法,将272例符合脾不统血证候的ITP患者随机分A、B、C三组。A组给予健脾益气摄血配方颗粒,每次1袋,每日2次;C组强的松首次剂量按1-1.5mg/(kgod),早8点顿服;B组配方颗粒、强的松用量、用法同上。21天为1疗程。结果:①三组治疗后外周血小板分度评分值组间比较,具有统计学意义(p<0.05)。各组间两两比较,A组与B组比较,具有统计学意义(p<0.05);A组与C组比较,具有统计学意义(p<0.05)。②第7天与第1天出血分级评分值比较,A组、B组均具有统计学意义(p<0.05)。第14天、第21天分别与第1天出血分级评分值比较,三组均具有统计学意义(p<0.05)。③治疗前后β-EP测定值比较,A组、B组均有统计学意义(p<0.05)。⑤三组治疗前后VIP测定值比较,具有统计学意义(p<0.05);治疗后较治疗前的变化值组间比较,有统计学意义(p<0.05)。其中,A、B两组分别和C组两两比较,有统计学意义(p<0.05)。结论:健脾益气摄血方可能通过调控血液神经递质激活机体止血机制。

北京中医药大学东直门医院,北京,100700,北京中医药大学东直门医院,北京,100700,北京中医药大学东直门医院,北京,100700,北京中医药大学东直门医院,北京,100700,北京中医药大学东直门医院,北京,100700

#中医学与中药学#

冀学斌,李丽珍,朱媛媛,侯明

2013-09-17

目的 筛选出血浆中含有抑制血小板粘附功能的血小板GPIb自身抗体的ITP患者,为人源化抗GPIb基因工程抗体的研制做准备。方法 用改良MAIPA法检测28例ITP患者血浆有无血小板GPIb自身抗体;用血小板粘附试验研究抗GPIb自身抗体对血小板粘附功能的影响。结果28例ITP患者中 5例(17.86%)抗GPIb自身抗体阳性,1例(3.57%)明显抑制血小板粘附功能。结论 少数抗血小板GPIb自身抗体可抑制血小板粘附功能。

高等学校博士学科点专项科研基金资助课题(20100131120058

山东省自然科学基金(ZR2010CQ040

山东大学齐鲁医院血液科,济南 250012,山东大学齐鲁医院血液科,山东大学齐鲁医院血液科,山东大学齐鲁医院血液科

#临床医学#

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LI Huiyuan,YANG Renchi

Toll like receptor 4 takes part in the activation of immune cells and triggers a pro-inflammatory response by activating of the nuclear factor-κB pathway, thus dysregulation in TLR4 signaling might be associated with autoimmunity. Consideration the effects of TLR4 +896A/G and +1196C/T single-nucleotide polymorphisms (SNPs) on TLR4 signaling and abnormal expression of TLR4 on monocytes from patients with primary immune thrombocytopenia (ITP), we speculated there was an association between the TLR4 polymorphisms and genetic susceptibility to ITP in a Chinese Han population. Therefore, we analyzed the +896A/G and +1196C/T SNP by sequencing in 151 ITP patients and 152 healthy controls. The result showed that the mutated alleles in the +896A/G and +1196C/T site were not detected in both ITP patients and normal controls. Therefore, for TLR4 +896A/G site, the allele frequencies were 100% for A and 0 for G, the genotype frequencies were 100% for AA, 0 for AG and 0 for GG. For TLR4 +1196 C/T site, the allele frequencies were 100% for C and 0 for T. the genotype frequencies were 100% for CC, 0 for CT and 0 for TT. In conclusion, the TLR4 +896 G and +1196 T alleles have a markedly reduced frequency in northern Chinese population, and the gene polymorphisms neither for TLR4 +896A/G nor for +1196C/T site may be associated with susceptibility to ITP in a Chinese Han population.)

2015-10-08

This work was supported in part by grants of National Natural Science Foundation of China (81270581

State Key Laboratory of Experimental Haematology, Institute of Haematology and Blood Disease Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College , State Key Laboratory of Experimental Haematology, Institute of Haematology and Blood Disease Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, 300020

#Clinical Medicine#

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XU Linlin,FU Haixia,ZHANG Jiamin,FENG Feier,WANG Qianming,WANG Chencong,ZHU Xiaolu,XUE Jing,CHEN Qi,LIU Xiao,KONG Yuan,XU Lanping,LIU Kaiyan,HUANG Xiaojun,ZHANG Xiaohui

IImmune thrombocytopenia (ITP) is an autoimmune disease in which dendritic cells (DCs) play a crucial role in the break-down of self-tolerance. Studies have identified the function ofmesenchymal stem cells (MSCs)in promoting the development of regulatory DCs(regDCs). Our previous work revealed that MSCs in ITP exerted senescence, apoptosis and impaired immunosuppressive effects on T and B cells. However, it is unclear whether the effectsof MSCs onregDCinduction are altered in ITP. Our datademonstrated thatMSCs in ITP were impaired in inhibiting CD1a+DC and CD14+DC differentiation from CD34+hematopoietic progenitor cells (CD34+HPCs). DCs differentiated with MSCs in ITP exhibited an increased expression of costimulatory molecules CD80/CD86 and secretion of pro-inflammatory IL-12.Accordingly,the tolerogenic characteristics were deficient in DCs induced by MSCs in ITP.DCs differentiated with MSCs in ITP exhibitedan impaired ability to inhibit CD3+T cell proliferation, to suppressT helper (Th)1cellsdifferentiation and to induce anergic and regulatory T cells(Tregs).Theexpression of Notch signaling components was measuredinMSCs in ITP. Reduced expression of the ligand Jagged-1, the receptor Notch-1 intracellular domain(NICD-1) and the target gene Hes-1wasidentifiedin MSCs in ITP.The addition of biologically active Jagged-1 to CD34+HPCswas observed to promoteregDC differentiation.When cultured on Jagged-1-coated plates, MSCs in ITP showed an enhancement of theNotch-1 pathway activation, Jagged-1 expression and thefunctionin inducing regDCs.Pretreatment with all-trans retinoic acid(ATRA) was found to partially restore the capacity of MSCs in both ITP patients and healthy controls in inducing CD34+-derived regDCs. Our data elucidated that MSCs in ITP were impaired in inducing CD34+-regDCs, which was associated with the Notch-1/Jagged-1 signaling pathway. ATRA could partially correct the impairment of MSCs, suggesting that ATRA could serve as a potential therapeutic alternativefor ITP.

2017-05-10

高等学校博士学科点专项科研基金(20130001120078

Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking University Institute of Hematology, Beijing 100044,Peking University People’s Hospital, Peking Universi

#Clinical Medicine#

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