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361.
采用水热法将聚丙烯酰胺(PAM)和十六烷基三甲基溴化铵(CTMAB)作为软性模板合成样品Ni(OH)2-PAM,Ni(OH)2-CTMAB和Ni(OH)2.在PAM和CTMAB的作用下,合成出来的样品有了更多的介孔,并且展现出了较宽的尺寸分布.通过扫描电镜(SEM)可以观察到不同的形貌.Ni(OH)2-PAM和Ni(OH)2-CTMAB基电极在1 A/g的放电密度下的比电容分别是1200 F/g和757 F/g,这大大地高于没加水溶性材料合成的Ni(OH)2样品基的电极的比电容,只有113 F/g.因此,适当的添加一些水溶性材料能够提高电极材料的电化学性能. 相似文献
362.
363.
在鼓泡吸收反应器中,以过硫酸盐溶液为氧化剂吸收脱除烟气中NO,以双膜理论为基础,研究了吸收过程中的传质动力学。对NO的氧化吸收过程进行了分析,建立了气液传质模型,测定了动力学参数:比相界面(a)和气相传质系数(KG)。结果显示:温度为75 oC,过硫酸盐溶液浓度在0.05-0.2M范围内,NO浓度≤1 000 ppm,NO的反应级数为0.5,过硫酸钠的反应级数为1,并确定了过硫酸盐溶液吸收NO总的传质速率方程。 相似文献
364.
在电化学阻抗测试中,电极作为传递信号的载体,电极与材料的接触程度,也即之间存在的接触电阻的大小,直接影响到了电化学阻抗及其阻抗谱所拟合等效电路参数的结果。通过对粉土、灰土分别在不同电极间压力和不同电极面积的正交试验下,所测得的阻抗|Z|和接触电阻R_0,来探求R_0与|Z|及其等效电路参数的关系。研究表明:电化学阻抗谱呈现非Randles模型的材料,可以提出类似于材料电阻率ρ_m的材料阻抗率ρ来表征材料的特性;同时ρ可以用其相对应的R_0与参数α的乘积表示。α随着电极间压力的增大而缓慢增大,随着电极面积的增大而急剧增大,随着材料压缩模量E_s的增大而减小;随着电极间压力的增大,其ρ、R_0、|Z|以及等效电路参数溶液电阻R_s、电荷转移电阻R_t在不断减小,而其双电层电容C_d在不断增大;随着电极面积的增大,其R_0、C_d在不断减小,而其ρ、|Z|、R_s和R_t在不断增大;随着材料E_s、ρ_m的增大,其ρ、R_0、R_s和R_t在不断增大,而其C_d不断减小。 相似文献
365.
为了提高氧化锌(ZnO)压敏电阻的电学性能,采用常规烧结并在ZnO压敏电阻中掺杂预先合成的BiSbO4和Zn2SiO4,研究不同掺杂比例对ZnO压敏电阻的微观结构、电学性能、通流能力的影响.结果表明:ZnO压敏电阻在掺杂BiSbO4和Zn2SiO4后,能够有效抑制ZnO晶粒变大,晶体结构变得致密均匀,致密性有所提高,有效提高压敏特性和通流能力.BiSbO4和Zn2SiO4掺杂比例为3∶1的样品综合性能比较优异,样品的致密度为5.58 g·cm-3,压敏电位梯度达到425 V·mm-1,非线性系数为70,漏电流为1.2×10-7 A·cm-2,能量耐受能力达到334.21 J·cm-3,残压比为2.5. 相似文献
366.
刘瑛 《内蒙古民族大学学报(自然科学版)》1999,(2)
本文研制的电极是在铂丝上涂双层聚合膜而制成的一种甘草次酸涂丝药物电极。该电极制作简便,性能较佳,具有较强的应用价值。 相似文献
367.
Endothelium-derived nitric oxide and vascular physiology and pathology 总被引:13,自引:0,他引:13
J.-F. Arnal A.-T. Dinh-Xuan M. Pueyo B. Darblade J. Rami 《Cellular and molecular life sciences : CMLS》1999,55(8-9):1078-1087
In 1980, Furchgott and Zawadzki demonstrated that the relaxation of vascular smooth muscle cells in response to acetylcholine
is dependent on the anatomical integrity of the endothelium. Endothelium-derived relaxing factor was identified 7 years later
as the free radical gas nitric oxide (NO). In endothelium, the amino acid L-arginine is converted to L-citrulline and NO by
one of the three NO synthases, the endothelial isoform (eNOS). Shear stress and cell proliferation appear to be, quantitatively,
the two major regulatory factors of eNOS gene expression. However, eNOS seems to be mainly regulated by modulation of its
activity. Stimulation of specific receptors to various agonists (e.g., bradykinin, serotonin, adenosine, ADP/ATP, histamine,
thrombin) increases eNOS enzymatic activity at least in part through an increase in intracellular free Ca2+. However, the mechanical stimulus shear stress appears again to be the major stimulus of eNOS activity, although the precise
mechanisms activating the enzyme remain to be elucidated. Phosphorylation and subcellular translocation (from plasmalemmal
caveolae to the cytoskeleton or cytosol) are probably involved in these regulations. Although eNOS plays a major vasodilatory
role in the control of vasomotion, it has not so far been demonstrated that a defect in endothelial NO production could be
responsible for high blood pressure in humans. In contrast, a defect in endothelium-dependent vasodilation is known to be
promoted by several risk factors (e.g., smoking, diabetes, hypercholesterolemia) and is also the consequence of atheroma (fatty
streak infiltration of the neointima). Several mechanisms probably contribute to this decrease in NO bioavailability. Finally,
a defect in NO generation contributes to the pathophysiology of pulmonary hypertension. Elucidation of the mechanisms of eNOS
enzyme activity and NO bioavailability will contribute to our understanding the physiology of vasomotion and the pathophysiology
of endothelial dysfunction, and could provide insights for new therapies, particularly in hypertension and atherosclerosis. 相似文献
368.
B. Thébaud J.-F. Arnal J. C. Mercier A.-T. Dinh-Xuan 《Cellular and molecular life sciences : CMLS》1999,55(8-9):1103-1112
Inhaled nitric oxide (NO) is used to treat various cardiopulmonary disorders associated with pulmonary hypertension. The
rationale is based on the fact that NO, given by inhalation, only dilates those pulmonary vessels that perfuse well-ventilated
lung units. As a result, pulmonary gas exchange is improved while pulmonary vascular resistance is reduced and pulmonary blood
flow is increased. Inhaled NO has been succesfully applied to treat persistent pulmonary hypertension of the newborn, reducing
the need for extracorporeal life support. Although pulmonary hypertension and altered vasoreactivity contribute to profound
hypoxaemia in adult and paediatric acute respiratory distress syndrome (ARDS), the benefit of inhaled NO still remains to
be established in patients with ARDS. ARDS is a complex response of the lung to direct or indirect insults, leading to pulmonary
vasoconstriction and various inflammatory responses. Recent randomized trials suggest that inhaled NO only causes a transient
improvement in oxygenation. Whether this effect is important in the long-term management of ARDS remains to be established.
NO, measured in the exhaled breath, is an elegant and non-invasive means to monitor inflammation of the upper and lower respiratory
tract. In the normal upper airways, the bulk of exhaled NO originates from the paranasal sinuses. Exhaled NO is increased
in nasal allergy and decreased in cystic fibrosis, nasal polyposis and chronic sinusitis. That NO production is increased
in asthmatic airways is also well established. However, several questions still need to be addressed, in particular evaluation
of the sensitivity and specificity of the measurement techniques, and assessment of the bronchodilator action of endogenous
NO. 相似文献
369.
目的 :将修饰电极应用于电位溶出分析 .方法 :采用化学吸附法制备出meso -四 (对 -乙基苯基 )卟啉和meso -四 (对 -甲氧基苯基 )卟啉修饰玻碳电极 .研究Zn(Ⅱ ) ,Cu(Ⅱ ) ,Cd(Ⅱ )和Pb(Ⅱ )金属离子在该电极上的电位溶出行为 ,并与预镀汞膜玻碳电极、玻碳电极的电位溶出行为进行了比较 .结果 :溶出时间 (τ)与金属离子浓度均有良好的线性关系 ,最适宜分析的浓度范围是Zn(Ⅱ ) :1× 10 - 7~ 5× 10 - 5mol/L ;Cd(Ⅱ )和Pb(Ⅱ ) :6× 10 - 7~ 5× 10 - 5mol/L ;Cu(Ⅱ ) :5× 10 - 8~2× 10 - 5mol/L .微分电位溶出分析时灵敏度提高一个数量级 ,相对标准偏差为 0 .90 %~ 2 .3% (n=15) .结论 :使用卟啉修饰电极进行电位溶出分析可获得好的重现性和满意的灵敏度 相似文献
370.