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排序方式: 共有744条查询结果,搜索用时 468 毫秒
1.
《Cryobiology》2019
The aim of the study was to investigate the effects of endovascular hypothermia on mitochondrial biogenesis in a pig model of prolonged cardiac arrest (CA). Ventricular fibrillation was electrically induced, and animals were left untreated for 10 min; then after 6min of cardiopulmonary resuscitation (CPR), defibrillation was attempted. 25 animals that were successfully resuscitated were randomized into three groups: Sham group (SG, 5, no CA), normal temperature group (NTG, 5 for 12 h observation and 5 for 24 h observation), and endovascular hypothermia group (EHG, 5 for 12 h observation and 5 for 24 h observation). The core temperatures (Tc) in the EHG were maintained at 34 ± 0.5 °C for 6 h by an endovascular hypothermia device (Coolgard 3000), then actively increased at the speed of 0.5 °C per hour during the next 6 h to achieve a normal body temperature, while Tc were maintained at 37.5 ± 0.5 °C in the NTG. Cardiac and mitochondrial functions, the quantification of myocardial mitochondrial DNA (mtDNA), peroxisome proliferator-activated receptor coactivator-1α (PGC-1α), nuclear respiratory factor (NRF)-1, and NRF-2 were examined. Results showed that myocardial and mitochondrial injury and dysfunction increased significantly at 12 h and 24 h after CA. Endovascular hypothermia offered a method to rapidly achieve the target temperature and provide stable target temperature management (TTM). Cardiac outcomes were improved and myocardial injuries were alleviated with endovascular hypothermia. Compared with NTG, endovascular hypothermia significantly increased mitochondrial activity and biogenesis by amplifying mitochondrial biogenesis factors’ expressions, including PGC-1α, NRF-1, and NRF-2. In conclusions, endovascular hypothermia after CA alleviated myocardial and mitochondrial dysfunction, and was associated with increasing mitochondrial biogenesis. 相似文献
2.
Francis G. Spinale Rupak Mukherjee Juozas A. Zavadzkas Christine N. Koval Shenikqua Bouges Robert E. Stroud Lawrence W. Dobrucki Albert J. Sinusas 《The Journal of biological chemistry》2010,285(39):30316-30327
The membrane type-1 matrix metalloproteinase (MT1-MMP) is a unique member of the MMP family, but induction patterns and consequences of MT1-MMP overexpression (MT1-MMPexp), in a left ventricular (LV) remodeling process such as myocardial infarction (MI), have not been explored. MT1-MMP promoter activity (murine luciferase reporter) increased 20-fold at 3 days and 50-fold at 14 days post-MI. MI was then induced in mice with cardiac restricted MT1-MMPexp (n = 58) and wild type (WT, n = 60). Post-MI survival was reduced (67% versus 46%, p < 0.05), and LV ejection fraction was lower in the post-MI MT1-MMPexp mice compared with WT (41 ± 2 versus 32 ± 2%,p < 0.05). In the post-MI MT1-MMPexp mice, LV myocardial MMP activity, as assessed by radiotracer uptake, and MT1-MMP-specific proteolytic activity using a specific fluorogenic assay were both increased by 2-fold. LV collagen content was increased by nearly 2-fold in the post-MI MT1-MMPexp compared with WT. Using a validated fluorogenic construct, it was discovered that MT1-MMP proteolytically processed the pro-fibrotic molecule, latency-associated transforming growth factor-1 binding protein (LTBP-1), and MT1-MMP-specific LTBP-1 proteolytic activity was increased by 4-fold in the post-MI MT1-MMPexp group. Early and persistent MT1-MMP promoter activity occurred post-MI, and increased myocardial MT1-MMP levels resulted in poor survival, worsening of LV function, and significant fibrosis. A molecular mechanism for the adverse LV matrix remodeling with MT1-MMP induction is increased processing of pro-fibrotic signaling molecules. Thus, a proteolytically diverse portfolio exists for MT1-MMP within the myocardium and likely plays a mechanistic role in adverse LV remodeling. 相似文献
3.
L. Hove-Madsen H. Gesser 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1989,159(1):61-69
Summary Isolated heart ventricular preparations from rainbow trout were electrically stimulated to contraction. Following a temporary change in stimulation rate from 0.2 Hz to a higher value, the force fell to a minimum after which it increased and levelled off. Upon the return to 0.2 Hz a further transient increase in force appeared. The latter two responses were stimulated by an increased extracellular K+, which is known to inactivate the Na+ channel. The initial negative inotropic effect, in contrast to the two subsequent positive effects, was associated with a parallel decrease in amplitude of the action potential measured in 15 mM K+, used as an index of the Ca2+ influx. One micromolar (1 M) ryanodine did not affect either the negative or the positive responses due to an increase in stimulation rate, but depressed the force developed after prolonged periods of rest. Ten micromolar (10 M) adrenaline strongly inhibited the positive effects of an elevation of frequency. An elevation of extracellular Na+ from 141 to 166 mM had a similar effect. In conclusion, the positive effects occurring in 15 mM K+ do not seem to depend on the initial Na+ current. They may nevertheless depend on changes of the cellular Na+ balance as suggested by the effects of adrenaline, K+ and Na+. The functional role of the sarcoplasmic reticulum is unclear. 相似文献
4.
Peter W. Achterberg Peter P. de Tombe Eef Harmsen Jan Willem de Jong 《Biochimica et Biophysica Acta (BBA)/General Subjects》1985,840(3):393-400
(1) The coronary vasodilator adenosine can be formed in the heart by breakdown of AMP or S-adenosylhomocysteine (SAdoHcy). The purpose of this study was to get insight into the relative importance of these routes of adenosine formation in both the normoxic and the ischemic heart. (2) A novel HPLC method was used to determine myocardial adenosine and SAdoHcy. Accumulation of SAdoHcy was induced in isolated rat hearts by perfusion with L-homocysteine thiolactone or L-homocysteine. The release of adenosine, inosine, hypoxanthine, xanthine and uric acid was determined. Additional in vitro experiments were performed to determine the kinteic parameters of S-adenosylhomocysteine hydrolase. (3) During normoxia the thiolactone caused a concentration-dependent increase in SAdoHcy. At 2000 μM of the thiolactone an SAdoHcy accumulation of 0.49 nmol/min per g wet weight was found during normoxia. L-Homocysteine (200 μM) caused an increased of 0.37 and 4.17 nmol SAdony/soc per g wet weight during normaxia and ischemia, respectively. (4) The adenosine concentration in ischemic hearts was significantly lower when homocysteine was infused (6.2 vs. 115 nmol/g; P < 0.05). Purine release was increased 4-fold during ischemia. (5) The Km for hydrolysis of SAdoHcy was about 12 μM. At in vitro conditions favoring near-maximal SAdoHcy synthesis (72 μM adenosine, 1.8 mM homocysteine), the synthesis rate in homogenates was 10 nmol/min per g wet weight. (6) From the combined in vitro and perfusion studies, we comclude that S-adenosylhomocysteine hydrolase can contribute significantly to adenosine production in normoxic rat heart, but not during ischemia. 相似文献
5.
X-ray fluorescence spectrometry and atomic absorption spectrometry were used in a quantitative study of zinc, copper, and
magnesium in 71 postmortal human hearts. Samples were obtained from individuals who had demonstrated no previous clinical
or subsequent pathological findings of myocardial infarction and from victims of a recent or an old infarction. A significant
difference (p<0.001) in the elemental levels was observed between the noninfarct and the recent infarct groups. The noninfarct group had
higher cardiac levels of all three elements. However, the difference in elemental concentrations between the noninfarct and
the old-infarct groups was not significant. Cardiac levels of zinc (p<0.001) and copper (p<0.01) were significantly greater in the old-infarct group than in the recent-infarct group. Magnesium levels were higher
in the recent-and-old-infarct group than in the recent infarct group (p<0.01). It is possible that the elements are redistributed during myocardial infarction, and that uptake of these elements
(from the serum pool) by the heart may be important in maintaining myocardial integrity and function. 相似文献
6.
Isolated muscle cells from adult rat heart have been used to study the relationship between myocardial glucose transport and the activity of the Na+/K+ pump. 86Rb+-uptake by cardiac cells was found to be linear up to 2 min with a steady-state reached by 40–60 min, and was used to monitor the activity of the Na+/K+ pump. Ouabain (10?3 mol/I) inhibited the steady-state uptake of 86Rb+ by more than 90%. Both, the ouabain-sensitive and ouabain-insensitive 86Rb+-uptake by cardiac cells were found to be unaffected by insulin treatment under conditions where a significant stimulation of 3-O-methylglucose transport occurred. 86Rb+-uptake was markedly reduced by the presence of calcium and/or magnesium, but remained unresponsive towards insulin treatment. Inhibition of the Na+/K+ pump activity by ouabain and a concomitant shift in the intracellular Na+:K+ ratio did not affect basal or insulin stimulated rates of 3-O-methylglucose transport in cardiac myocytes. The data argue against a functional relationship between the myocardial Na+/K+ pump and the glucose transport system. 相似文献
7.
David R. Thompson Jurgen E. Pohl Yiu-Yu S. Tse Robert W. Hiorns 《International journal of biometeorology》1996,39(3):116-120
Analysis of the time of onset of chest pain in 2254 patients with a myocardial infarction admitted to a coronary care unit in Leicester during a 10-year period shows an association with temperature and humidity. During both the most cold and humid times of the year, the relationship is a strong one. A generalized linear model with a log link was used to fit the data and the backward elimination selection procedure suggested a humid, cold day might help to trigger the occurrence of myocardial infarction. In addition, cold weather was found to have a stronger effect on the male population while those men aged between 50 and 70 years were more sensitive to the effect of high humidity. 相似文献
8.
本文利用ESR技术研究了心肌线粒体酶修饰下的脂质过氧化和脂类自由基,以及(-)-EGCG的抑制作用。结果表明:4-POBN能捕集lipoxygengse诱发心肌线粒体产生的自由基,得到6条线谱的脂类自由基和4条线谱捕集物,(-)-EGCG对该体系中使用的1ipoxyenase活性无影响,对所产生的自由基有明显的清除作用,并呈量效关系。对脂质过氧化的抑制作用,在本试验浓度范围内随浓度增加变化不大,最大抑制率约20%。 相似文献
9.
利用大鼠肝脏线粒体为材料,以琥珀酸为底物,研究了不同浓度的丹参酮Ⅱ-A磺酸钠对线粒体态4、态3呼吸及呼吸控制率,线粒体跨膜电位,线粒体呼吸链复合体(Ⅱ+Ⅲ)电子传递及质子转移活性的影响。结果证明丹参酮ⅡA-磺酸钠是线粒体呼吸链复合体(Ⅱ+Ⅲ)的有效抑制剂。文中对丹参酮ⅡA-磺酸钠在心肌缺血再灌注过程中的保护作用的分子机理进行了讨论。 相似文献
10.
摘要 目的:研究丙泊酚联合七氟醚麻醉在先天性心脏病介入手术患儿中的心肌保护作用及对苏醒质量和应激反应的影响。方法:选择2020年1月~2022年4月期间在苏州大学附属儿童医院接受先天性心脏病介入手术患儿96例,按照双色球法将患儿分为对照组(n=48,接受瑞芬太尼、丙泊酚麻醉)和观察组(n=48,接受丙泊酚、七氟醚麻醉)。对比两组患儿心率、呼吸频率、平均动脉压、苏醒质量、心肌损伤指标、应激反应指标和不良反应发生率。结果:两组置喉罩时(T1)~拔除喉罩(T4)时间点心率、呼吸频率、平均动脉压下降后升高,观察组高于对照组同时间点(P<0.05)。观察组的苏醒时间、拔管时间均短于对照组(P<0.05)。两组术毕、术后24 h肌酸磷酸激酶同工酶(CK-MB)、心肌肌钙蛋白(cTnI)升高后下降,观察组低于对照组同时间点(P<0.05)。两组术毕、术后24 h血糖、皮质醇升高后下降,观察组低于对照组同时间点(P<0.05)。两组不良反应发生率组间对比,差异不显著(P>0.05)。结论:丙泊酚联合七氟醚麻醉应用于先天性心脏病介入手术中,可减轻患儿的应激反应,稳定机体血流动力学波动,同时还可发挥心肌保护作用,提高苏醒质量。 相似文献