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61.
摘要 目的:探讨脑电双频指数(BIS)监测下右美托咪定联合七氟醚对颅内动脉瘤介入栓塞术患者苏醒质量、血清氧化应激指标和神经损伤标志物的影响。方法:采用随机数字表法,将我院2019年3月-2021年6月期间收治的80例颅内动脉瘤介入栓塞术患者分为研究组(BIS监测下右美托咪定联合七氟醚,n=40)和对照组(BIS监测下七氟醚,n=40),观察两组血流动力学、苏醒质量、血清氧化应激指标和神经损伤标志物水平变化。记录两组围术期间不良反应发生状况。结果:气管插管后1 min(T1)~拔管后10 min(T4)时点,两组平均动脉压(MAP)、心率(HR)升高后下降,但研究组低于对照组同时点(P<0.05)。与对照组比较,研究组苏醒时间、恢复呼吸时间、拔管时间较短(P<0.05)。T1~T4时点,两组超氧化物歧化酶(SOD)、过氧化氢酶(CAT)水平下降后升高,但研究组较对照组同时点高(P<0.05)。术后1 d,两组人脑髓鞘碱性蛋白(MBP)、神经元特异性烯醇化酶(NSE)、S100?茁水平升高,但研究组低于对照组同时点(P<0.05)。对照组、研究组的不良反应发生率组间对比无显著性差异(P>0.05)。结论:BIS监测下七氟醚联合右美托咪定应用于颅内动脉瘤介入栓塞术患者中,可提高苏醒质量,减轻氧化应激水平和神经损伤程度,稳定血流动力学波动。  相似文献   
62.
摘要 目的:探讨自体输血与异体输血对创伤性颅脑损伤(TBI)开颅手术患者凝血功能、细胞免疫功能和神经损伤标志物的影响。方法:回顾性分析2019年4月~2022年5月期间在本院行开颅手术的120例TBI患者的临床资料。根据输血方式的不同将患者分为异体输血组(n=58,异体输血)和自体输血组(n=62,自体输血),观察两组临床指标、细胞免疫功能、凝血功能、神经损伤标志物和不良反应发生率情况。结果:两组患者手术出血量、输血量、输注含凝血成分血制品比例对比,差异无统计学意义(P>0.05)。自体输血组出院时CD3+、CD4+、CD4+/CD8+高于异体输血组,CD8+低于异体输血组(P<0.05)。两组出院时凝血酶原时间(PT)、凝血酶时间(TT)、纤维蛋白原(FIB)、活化部分凝血活酶时间(APTT)组间对比无统计学差异(P>0.05)。自体输血组出院时S100钙结合蛋白B(S100B)、神经胶质原纤维酸性蛋白(GFAP)、神经元特异性烯醇化酶(NSE)低于异体输血组(P<0.05)。两组不良反应发生率组间比较无差异(P>0.05)。结论:自体输血用于TBI开颅手术患者,对患者的凝血功能影响较小,同时还可改善机体细胞免疫功能,降低神经损伤标志物水平。  相似文献   
63.
摘要 目的:对比关节镜下双排缝合桥固定和单排固定治疗肩袖全层撕裂的疗效,并分析术后早期再撕裂的危险因素。方法:回顾性分析广州中医药大学附属北碚中医院2018年1月~2021年12月期间收治的200例肩袖全层撕裂患者的临床资料,根据手术方案的不同分为A组(n=97,接受单排固定治疗)和B组(n=103,接受双排缝合桥固定治疗)。对比两组的疼痛、肩关节功能情况、肩关节活动度及术后早期再撕裂发生率。采用单因素和多因素Logistic回归分析肩袖全层撕裂患者术后早期再撕裂的危险因素。结果:术后6个月,B组视觉疼痛模拟评分量表(VAS)评分低于A组,美国加州大学肩关节评分系统(UCLA)评分、美国肩肘外科医师学会(ASES)评分高于A组(P<0.05)。术后6个月,B组前屈、外展、体侧外旋角度大于A组(P<0.05)。B组的术后早期再撕裂总发生率低于A组(P<0.05)。术后早期再撕裂的发生与糖尿病史、撕裂大小、吸烟史、年龄、术前肌肉质量、性别、脂肪浸润、注射皮质类固醇有关(P<0.05)。多因素Logistic回归分析结果显示:年龄≥60岁、性别为男性、吸烟史、糖尿病史、撕裂大小为巨大型再撕裂、脂肪浸润、注射皮质类固醇是术后早期再撕裂发生的危险因素(P<0.05)。结论:关节镜下双排缝合桥固定治疗肩袖全层撕裂,可更好的减轻疼痛症状,改善关节功能和关节活动度。此外,糖尿病史、脂肪浸润、吸烟史、高龄、撕裂大小为巨大型再撕裂、男性、注射皮质类固醇等是肩袖全层撕裂患者术后早期再撕裂的危险因素。  相似文献   
64.
Differences in mitochondrial membrane composition and ultrastructure were studied after storage of cauliflower ( Brassica oleracea , L., Botrytis group) for 5 days at 25°C in air or under controlled atmospheres: 3% O2, 21% O2+ 15% CO2 or 3% O2+ 15% CO2. In air, postharvest senescence involved a 20% decrease in mitochondrial phospholipid content. A large reduction in the relative abundance of phosphati-dylcholine (PC) and in the degree of unsaturation of PC and phosphatidyl ethanolamine (PE) was observed. However, the degree of unsaturation increased in cardiolipin (CL). Storage under 3% O2 did not prevent phospholipid breakdown. Low O2 prevented the relative decrease in PC observed during storage in air and the loss of linoleic acid from PC, but not from PE. This relative protection offered by the low O2 atmosphere was lost under 3% O2+ 15% CO2. The high CO2 atmospheres caused twice as much loss in phospholipids as that observed during storage in air. Extensive loss of mitochondrial protein, a marked decrease in phospholipid to protein ratio, and electron micrograph observations suggest structural alterations in the presence of high CO2.  相似文献   
65.
Ectopic ion channels developed locally at the injury site after nerve damage by light ligation around common sciatic nerve of the rats. Different channel types have different processes of formation, accumulation and degeneration. During the first three days after injury, mechanically activated channels that are modulated by Ca++ channel activities first appeared. As the nerve fibers begin to be excited by TEA, a blocker of K+ channels, suggesting that the accumulation of K+ channels, the responsibility of mechanically activated channels was declining. Onset of K+ channels was from the 3rd postoperative day and lasted up to the fiftieth day. This time course of K+ channel development was closely related to allodynia and hyperalgesia of neuropathic animal behaviour. The results suggest that chronic contraction injury induces a dynamic change in the ectopic mechanically activated channels and K+ channels at the injury site of nerve and there is an interchange in the development time courses of the mechanic  相似文献   
66.
为了解决高氧预适应(HyperoxicpreconditioningHOP)对大鼠心肌缺血再灌注时自由基的影响,本实验将实验组大鼠放入高压氧舱内,每日吸80-85%氧气(1atm)6h,连续7d。利用Langendorf装置做成心肌缺血再灌注模型,采用电子自旋共振技术测定自由基含量。实验动物随机分为二组,第一组为对照组:缺血10min,再灌注60min。第二组为HOP组:缺血10min,再灌注60min。实验观察冠脉回流液中自由基PBN加合物含量。结果表明:在再灌注过程中,1、5、10min3个时间点,HOP组PBN加合物含量较对照组明显减少。提示:HOP能减少缺血再灌注时自由基的产生。  相似文献   
67.
本实验采用D-氨基半乳糖(D-GalN)诱导的大鼠急性肝损伤模型,观察大鼠肝脏组织化学的变化,探讨肝炎平对急性肝损伤的保护作用。实验分为四组,即正常对照组、模型组、肝炎平及肝得健保护组。结果表明:肝炎平对肝细胞膜系统有一定的保护作用。肝炎平组和肝得健组SDH、CCO及ChE活性明显高于模型组,且与正常对照组相近。本实验模型组ACP的活性明显高于正常组,而肝炎平组ACP的活性明显低于模型组,与正常对照组无显著性差异。提示:肝炎平可显著改善因D-氨基半乳糖所致肝损害的作用。且其对肝细胞的保护作用与肝得健一致。  相似文献   
68.
Abstract: The adenylyl cyclase-cyclic AMP (cAMP) second messenger pathway has been proposed to regulate myelin gene expression; however, a clear correlation between endogenous cAMP levels and myelin-specific mRNA levels has never been demonstrated during the induction or maintenance of differentiation by the myelinating Schwann cell. Endogenous cAMP levels decreased to 8–10% of normal nerve by 3 days after crush or permanent transection injury of adult rat sciatic nerve. Whereas levels remained low after transection injury, cAMP levels reached only 27% of the normal values by 35 days after crush injury. Because P0 mRNA levels were 60% of normal levels by 14 days and 100% by 21 days after crush injury, cAMP increased only well after P0 gene induction. cAMP, therefore, does not appear to trigger myelin gene induction but may be involved in myelin assembly or maintenance. Forskolin, an activator of adenylyl cyclase, increased endoneurial cAMP levels only in the normal nerve, and in the crushed nerve beginning at 16 days after injury, but at no time in the transected nerve. Only by treating transected nerve with 3-isobutyl-1-methylxanthine (IBMX), an inhibitor of cAMP phosphodiesterases, in combination with forskolin was it possible to increase cAMP levels. No induction of myelin genes, however, was observed with short- or long-term treatment with IBMX and forskolin in the transected nerve. A three-fold increase in phosphodiesterase activity was observed at 35 days after both injuries, and a nonmyelinated nerve was shown to have even higher activity. These experiments, therefore, suggest an important role for phosphodiesterase in the inactivation of this second messenger-dependent stimuli when Schwann cells are non-myelinating, such as after sciatic nerve injury or in the nonmyelinated nerve, which again implies that cAMP may be required for the maintenance of the myelin sheath.  相似文献   
69.
Abstract: Lateral fluid-percussion brain injury in rats results in cognitive deficits, motor dysfunction, and selective hippocampal cell loss. Neurotrophic factors have been shown to have potential therapeutic applications in neurodegenerative diseases, and nerve growth factor (NGF) has been shown to be neuroprotective in models of excitotoxicity. This study evaluated the neuroprotective efficacy of intracerebral NGF infusion after traumatic brain injury. Male Sprague-Dawley rats received lateral fluid-percussion brain injury of moderate severity (2.1–2.3 atm). A miniosmotic pump was implanted 24 h after injury to infuse NGF (n = 34) or vehicle (n = 16) directly into the region of maximal cortical injury. Infusions of NGF continued until the animal was killed at 72 h, 1 week, or 2 weeks after injury. Animals were evaluated for cognitive dysfunction (Morris Water Maze) and regional neuronal cell loss (Nissl staining) at each of the three time points. Animals surviving for 1 or 2 weeks were also evaluated for neurobehavioral motor function. Although an improvement in memory scores was not observed at 72 h after injury, animals receiving NGF infusions showed significantly improved memory scores when tested at 1 or 2 weeks after injury compared with injured animals receiving vehicle infusions ( p < 0.05). Motor scores and CA3 hippocampal cell loss were not significantly different in any group of NGF-treated animals when compared with controls. These data suggest that NGF administration, in the acute, posttraumatic period following fluid-percussion brain injury, may have potential in improving post-traumatic cognitive deficits.  相似文献   
70.
Lipid composition and pigment content in bell pepper ( Capsicum annuum L. cv. Bell Tower) fruit that were freshly harvested, chilled 14 days at 2° C. or chilled and then transferred to 20 °C for 3 days ("rewarmed") were determined. There was slight to moderate loss of membrane glycerolipids during chilling, with much greater losses after chilled fruit was rewarmed. Galactolipid (GL) loss exceeded that of phospholipid (PL). The ratio of monogalactosyl -to digalactosyl-diacylglycerol did not change in chilled or in rewarmed fruit, and there was no chlorophyll loss, but the amount of neutral carotenes declined during chilling and dropped further alter rewarming. Only minor changes in total membrane sterols (TMS = free sterols + steryl glycosides + acylated steryl glycosides) were noted in chilled and in rewarmed fruit (a small increase followed by a small decrease), but major changes occurred in sterol glycosylation and esterification. The ratio of stigmasterol to sitosterol increased during chilling and rose further after rewarming. Due to PL loss, the ratios of TMS and free sterols to PL increased in rewarmed fruit. The ratio of linolenate (18:3) to linoleate (18:2) rose during chilling and after rewarming in all fatty-acyl lipids (GL. PL. and acylated steryl glycosides), but the unsaturation index increased only in GL. These results indicate that most membrane damage occurs after rewarming of chilled fruit and that the chloroplasts are especially chilling sensitive.  相似文献   
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