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41.
Indwelling intravascular catheters provide convenient access to healthcare personnel and also recreational intravenous drug users who inject suspensions of oral medications. A nine‐case series of autopsies of clinically stable decedents with indwelling catheters and sudden death is herein presented. Pulmonary histologic findings were consistent with intravenous administration of oral medications in all cases. In eight, the mechanism of death was directly attributed to occlusive vascular embolization of foreign material, with or without contribution of acute drug toxicity. In one, the mechanism of death was solely attributed to acute drug toxicity. Acute, massive embolization of foreign material may explain sudden death by vascular obstruction, whereas chronic repeated injections lead to obliteration of the pulmonary vasculature, increased pulmonary vascular resistance, and cardiac failure. Therefore, a complete autopsy with histologic examination of the lungs and toxicology testing is recommended in patients with indwelling catheters to determine the cause and mechanism of death.  相似文献   
42.
This case concerns a sudden death of a patient with Chiari I malformation. A 17‐year‐old female was seen unconscious then fell off a motorbike during the vehicle acceleration. The girl was confirmed dead on the way to hospital, being previously asymptomatic and with a clean medical record. Autopsy findings showed an extremely extra‐long cerebellar tonsillar herniation in the left side and unexplained multiple small cavities in cerebral hemispheres. Microscopic findings revealed loss and abnormal migration of the Purkinje cells, as well as capillary congestion in the herniated tonsil. The cause and mechanisms of this sudden death are considered as the cardiopulmonary dysfunction and arrest resulted from compression of the medulla and cervical cord, which was induced by both the positional insult and minor head trauma. In addition, this study stresses the importance of cervical cord examination in the case of unexpected sudden death following road accidents.  相似文献   
43.
目的 观察肺抑瘤膏联合树突状细胞-细胞因子诱导的杀伤细胞(dendritic cells-cytokine induced killer cells, DC-CIK)治疗晚期肺腺癌的临床疗效。方法 将46例晚期肺腺癌患者随机分为观察组(肺抑瘤膏联合DC-CIK治疗)和对照组(化学疗法联合免疫支持治疗),治疗4个月后观察患者临床主症、卡氏功能状态量表(Karnofskys performance scale, KPS)评分及血清血管内皮生长因子(vascular endothelial growth factor,VEGF)的改变。结果 治疗后,观察组咳嗽、咳血、胸痛、气短、乏力、纳呆的好转率显著高于对照组(P<0.05,或P<0.01);观察组在提高KPS评分及降低血清VEGF水平方面显著优于对照组(P<0.05,或P<0.01)。结论 肺抑瘤膏联合DC-CIK治疗可有效改善晚期肺腺癌患者临床症状,提高生存质量,并能显著降低患者血清VEGF。  相似文献   
44.
目的 观察微RNA-21(microRNA-21,miR-21)对p38丝裂原活化的蛋白激酶(p38 mitogen-activated protein kinase, p38-MAPK)信号通路的调控作用,探究丹皮酚(paeonol, Pae)抑制血管内皮细胞(vascular endothelial cell, VEC)损伤的机制。方法 组织块预消化贴壁法培养大鼠VEC;氧化低密度脂蛋白(oxidized low-density lipoprotein, ox-LDL)诱导VEC的损伤;用HiPerFect试剂将miR-21模拟物或抑制剂转染进入VEC;免疫印迹法检测p38 MAPK信号通路相关蛋白的表达;酶联免疫吸附试验检测VEC中肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)的水平。结果 ox-LDL明显提高VEC中Ras、p-MKK3/6、p-p38蛋白表达水平,并诱导VEC分泌TNF-α;miR-21高表达可升高TNF-α水平及Ras、p-MKK3/6、p-p38蛋白表达水平;Pae明显降低损伤的VEC分泌TNF-α水平,且抑制由miR-21高表达引起的TNF-α水平上升及p38 MAPK信号通路的激活。结论 Pae可抑制miR-21介导的p38 MAPK信号通路,减少ox-LDL诱导的VEC中TNF-α的分泌。  相似文献   
45.
目的 复制拟血管性痴呆(vascular dementia,VD)模型,探讨针刺百会、人中、大椎穴对大鼠学习记忆能力及血清和海马内乙酰胆碱酯酶(acetylcholinesterase,AchE)含量的影响.方法 用双侧颈总动脉缺血再灌注法复制VD大鼠模型,将VD大鼠随机分为模型组、针刺组和西药组.采用大鼠跳台试验检测...  相似文献   
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