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21.
Despite the use of gold complexes in modern medicine for over 100 years and the use of gold complexes in the management of
rheumatoid disease for more than 60 years, the definitive mechanisms of action for efficacy and for toxicity have not been
established.
Gold is a group 1b metal in the periodic table with several oxidation states but it is only Au(I) which is active in the biological
milieu. Gold sodium thiomalate is not only a polymeric structure, but also has the chiral ligand, thiomalic acid. Gold sodium
thiomalate thus can exist in several different physical states which may have different biological activity. In addition the
pharmacokinetic profile of gold complexes has been of little value in the understanding of either the mechanism of action,
efficacy or toxicity for both the injectable and the oral gold complexes. Many authors have misinterpreted research data on
the activities of gold complexes because they compared gold complexes of different structures, and gold complexes which exist
at different pH.
Experimental work in our laboratory has identified that gold sodium thiomalate is a mixture and can exist as either a yellow
or a colourless solution. These have some similar but several different biological activities.
Many factors contribute to the lack of understanding of the action of gold complexes. Some of these factors are related to
the wide variation in physical structure and biological activities exhibited by these compounds. 相似文献
22.
23.
R. Lemmens-Gruber H. Marei P. Heistracher 《Naunyn-Schmiedeberg's archives of pharmacology》1997,355(2):230-238
GE 68 ((Rac.)-1-[3-(Phenylethyl)-2-benzofuryl]-2-(propylamino)-ethanol hydrochloride) is structurally related to propafenone,
and exerts negative inotropic and negative chronotropic effects similar to the parent drug, but lacks any β-adrenoceptor blocking
activity contrary to propafenone. Thus, the electrophysiological effects of GE 68 were studied in papillary muscles, left
atria, Purkinje fibres, sinoatrial nodes and ventricular myocytes of the guinea-pig heart with the intracellular microelectrode
technique and the patch-clamp technique in the cell-attached mode.
The decrease of the maximum upstroke velocity (V˙max) by GE 68 (1 to 10 μM) was use- and frequency-dependent. V˙max recovered from the use-dependent block with a time constant of 4.1 ± 0.6 s. In papillary muscles and Purkinje fibres action
potential duration was shortened, while it was prolonged in left atria and sinoatrial nodes. Half-maximal steady-state inactivation
of the sodium channels was shifted to more negative membrane potentials (control: –91.5 ± 0.8 mV, 10 μM GE 68: –97.9 ± 2.5 mV).
The peak of the current-voltage relationship and the reversal potential were not changed by GE 68. The amplitude of the unitary
current remained unaltered, while open state probability was decreased. The most striking effect of GE 68 was an increase
of the number of sweeps without single channel openings (1 μM: 2 fold, 10 μM: 6 fold). GE 68 also caused a decrease of the
mean open times, and an increase of the mean closed times in unmodified and pronase-modified sodium channels.
Besides the lack of β-adrenoceptor blocking activity, data present a faster recovery from the use-dependent block by GE 68
and a lower affinity to inactivated sodium channels compared to the reference drug propafenone, as well as differences in
the effect on single channel kinetics.
Received: 25 July 1996 / Accepted: 14 October 1996 相似文献
24.
二巯基丙磺酸钠对苯硫丹和多噻烷急性中毒小鼠的保护作用 总被引:1,自引:0,他引:1
用二巯基丙磺酸钠对苯硫丹、多噻烷急性染毒小鼠进行保护解救。结果表明:二巯基丙磺酸钠对该两农药急性染毒小鼠具有显著的保护作用(P<0.05)。本实验填补了以二巯基丙磺酸钠作为首选药物治疗沙蚕毒系现有全部品种急性中毒解毒谱的空白。 相似文献
25.
26.
职业接触氯乙烯对生殖功能影响的调查 总被引:4,自引:0,他引:4
Huang Mei-yuan Institute of Occupational Medicine Chinese Academy of Preventive Medicine Beijing 《中华劳动卫生职业病杂志》1994,12(1):12-15
对全国12个城市中13个聚氯乙烯制造工厂中2736名接触氯乙烯的工人及3442名对照厂工人,进行了生殖功能的流行病学调查研究,结果表明,接触氯乙烯男、女工人的各项生殖结局指标与对照组比较无显著性差异,但女工氯乙烯接触组妊娠合并症的发生率明显高于对照组,表明氯乙烯对女工的妊娠过程有一定影响,因此积极改善劳动条件,不仅对保护工人健康,而且对保护其子代的正常发育成长也有重要意义。 相似文献
27.
PC12细胞化学缺氧复氧损伤与缺氧诱导因子1表达的关系 总被引:3,自引:0,他引:3
目的 研究缺氧诱导因子1(HIF1)在PC12细胞化学缺氧复氧损伤中的作用。方法 在培养液中加入和去除氯化钴模拟化学缺氧和复氧,以乳酸脱氢酶(LDH)漏出和细胞超微结构改变作为细胞损伤指标,观察化学缺氧和复氧后不同时间细胞损伤和HIF1 α蛋白变化。结果 在氯化钴模拟化学缺氧实验中,LDH漏出明显增加,8h达高峰,随后逐渐下降,电镜结果与LDH改变相一致,HIF1 α蛋白表达在化学缺氧后2,4,8和12h均明显增加,8h达高峰,提示化学缺氧8h后细胞损伤逐渐减轻可能与HIF1 α蛋白水平升高有关。在模拟复氧实验中,LDH和细胞形态学改变都显示化学复氧8h细胞损伤最为严重,而HIF1 α蛋白表达在化学复氧4和8h均明显下降,提示细胞化学复氧损伤可能与HIF1 α蛋白水平下降有关。结论 HIF1对神经细胞化学缺氧复氧损伤具有保护作用。 相似文献
28.
29.
目的:观察高渗氯化钠高氧液对失血性休克家兔动脉血气和血乳酸值的影响,评价其对失血性休克的早期救治效果。方法:制备高渗氯化钠溶液(HS)、生理盐水高氧液(NSO)和高渗氯化钠高氧液(HSO)。30只雄性家兔制备失血性休克模型[于10min内使平均动脉压(MAP)降至40mmHg(1mmHg=0.133kPa),维持60min],随机分为NSO,HS,HSO组3个治疗组。分别按6mL/kg剂量5min内静脉输入NSO,HS和HSO。记录休克前后及给药后心率(HR)、呼吸(RR)、MAP及尿滴(UD),测定休克前、休克60min,给药后30,60,120min时血乳酸(BL)和动脉血气值。最后观察尸肺,测定肺系数。结果:HS和HSO组均显著地改善MAP,HR和UD,降低BL,改善代谢性酸中毒,肺系数明显低于NSO组。HSO与NSO及HS比较,能更显著地降低血BL,提高动脉血氧饱和度(SaO2)和动脉血氧分压(PaO2)。结论:HSO较HS和NSO能更显著地降低血BL,提高SaO2和PaO2,对失血性休克的早期救治具有较高的使用价值。 相似文献
30.
Four novel mutations in the thiazide-sensitive Na-Cl co-transporter gene in Japanese patients with Gitelman's syndrome. 总被引:3,自引:1,他引:2
Nobuki Maki Atsushi Komatsuda Hideki Wakui Hiroshi Ohtani Akihiko Kigawa Namiko Aiba Keiko Hamai Mutsuhito Motegi Akihiko Yamaguchi Hirokazu Imai Ken-ichi Sawada 《Nephrology, dialysis, transplantation》2004,19(7):1761-1766
BACKGROUND: Gitelman's syndrome (GS) is an autosomal recessive disorder resulting from inactivating mutations in the thiazide-sensitive Na-Cl co-transporter (NCCT) gene. To date, almost 90 mutations have been identified. It is possible that there is a population-specific distribution of mutations. In this study, we analysed mutations in the NCCT gene of seven Japanese patients with GS. METHODS: Peripheral blood mononuclear cells were isolated from patients with GS, their family members and healthy control subjects. A mutation analysis of the NCCT gene was performed completely by direct automated sequencing of polymerase chain reaction-amplified DNA products. In patients with a deletion or splice site mutation, we undertook cDNA sequence analysis. RESULTS: We identified nine mutations. Five of them [c.185C>T (Thr60Met), c.1712C>T (Ala569Val), c.1930C>T (Arg642Cys), c.2552T>A (Leu849His) and c.1932delC] have been reported in Japanese patients, but not in GS patients from other ethnic groups. The remaining four mutations [c.7A>T (Met1Leu), c.1181_1186+20del26, c.1811_1812delAT and IVS16+1G>A] were novel. In cDNA derived from a patient with c.1181_1186+20del26, a deletion of exon 9 and a frameshift at the start of exon 10 were observed. In cDNA derived from patients with IVS16+1G>A, an additional 96 bp insertion between exons 16 and 17 was observed. Six out of seven patients were compound heterozygotes, and the remaining one carried a single heterozygous mutation. CONCLUSIONS: We found four novel mutations in the NCCT gene in seven Japanese patients with GS. Moreover, our study suggests that the distribution of mutations in the NCCT gene in Japanese GS patients potentially differs from that in other populations. 相似文献