全文获取类型
收费全文 | 12158篇 |
免费 | 729篇 |
国内免费 | 447篇 |
专业分类
耳鼻咽喉 | 42篇 |
儿科学 | 55篇 |
妇产科学 | 42篇 |
基础医学 | 1468篇 |
口腔科学 | 305篇 |
临床医学 | 600篇 |
内科学 | 993篇 |
皮肤病学 | 82篇 |
神经病学 | 1381篇 |
特种医学 | 146篇 |
外国民族医学 | 1篇 |
外科学 | 807篇 |
综合类 | 949篇 |
现状与发展 | 1篇 |
预防医学 | 196篇 |
眼科学 | 83篇 |
药学 | 5203篇 |
中国医学 | 847篇 |
肿瘤学 | 133篇 |
出版年
2023年 | 106篇 |
2022年 | 231篇 |
2021年 | 358篇 |
2020年 | 241篇 |
2019年 | 271篇 |
2018年 | 289篇 |
2017年 | 284篇 |
2016年 | 331篇 |
2015年 | 328篇 |
2014年 | 561篇 |
2013年 | 1195篇 |
2012年 | 550篇 |
2011年 | 608篇 |
2010年 | 466篇 |
2009年 | 499篇 |
2008年 | 494篇 |
2007年 | 482篇 |
2006年 | 393篇 |
2005年 | 379篇 |
2004年 | 294篇 |
2003年 | 327篇 |
2002年 | 261篇 |
2001年 | 232篇 |
2000年 | 242篇 |
1999年 | 240篇 |
1998年 | 235篇 |
1997年 | 239篇 |
1996年 | 215篇 |
1995年 | 210篇 |
1994年 | 196篇 |
1993年 | 198篇 |
1992年 | 187篇 |
1991年 | 164篇 |
1990年 | 189篇 |
1989年 | 182篇 |
1988年 | 150篇 |
1987年 | 127篇 |
1986年 | 147篇 |
1985年 | 164篇 |
1984年 | 161篇 |
1983年 | 125篇 |
1982年 | 155篇 |
1981年 | 143篇 |
1980年 | 107篇 |
1979年 | 78篇 |
1978年 | 73篇 |
1977年 | 50篇 |
1976年 | 51篇 |
1975年 | 27篇 |
1974年 | 27篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
121.
新型控释化疗系统的基础研究 总被引:2,自引:0,他引:2
研究一种新型的控释化疗系统聚-二聚酸一葵二酸一阿霉索(P(DA—SA)-阿霉索(在脑组织内的相容性、体内外释药特性及体外抑瘤特性。将空载体P(DA—SA)分别植入实验动物脑内,观察局部反应;用紫外线光谱测定P(DA—SA)-阿霉素在磷酸盐缓冲液及兔脑内的控释特性;流式细胞仪检测P(DA—SA)-阿霉索诱发的胶质瘤细胞株的凋亡。P(DA—SA)在兔脑内引起的反应较轻,与明胶海绵相比无明显差异。P(DA—SA)-阿霉素在体内外释药速率稳定,控释时间达3周。控释剂组的胶质瘤细胞凋亡率达69.9%,与对照组有明显差异。P(DA—SA)具有良好的组织相容性,P(DA—SA)-阿霉索控释剂在体内外的控释效果理想,杀伤效应明显,该控释化疗系统有很好的临床应用价值。 相似文献
122.
Luis Gandía Baldomero Lara Julita S. Imperial Mercedes Villarroya Almudena Albillos Rosario Maroto A. G. García Baldomero M. Olivera 《Pflügers Archiv : European journal of physiology》1997,435(1):55-64
The characteristics of the binding sites for the Conus magus toxins ω-conotoxin MVIIC and ω-conotoxin MVIID, as well as their effects on K+-evoked 45Ca2+ entry and whole-cell Ba2+ currents (I
Ba), and K+-evoked catecholamine secretion have been studied in bovine adrenal chromaffin cells. Binding of [125I] ω-conotoxin GVIA to bovine adrenal medullary membranes was displaced by ω-conotoxins GVIA, MVIIC and MVIID with IC50 values of around 0.1, 4 and 100 nM, respectively. The reverse was true for the binding of [125I] ω-conotoxin MVIIC, which was displaced by ω-conotoxins MVIIC, MVIID and GVIA with IC50 values of around 30, 80 and 1.200 nM, respectively. The sites recognized by ω-conotoxins MVIIC and MVIID in bovine brain
exhibited higher affinities (IC50 values of around 1 nM). Both ω-conotoxin MVIIC and MVIID blocked I
Ba by 70–80%; the higher the [Ba2+]o of the extracellular solution the lower the blockade induced by ω-conotoxin MVIIC. This was not the case for ω-conotoxin
MVIID; high Ba2+ (10 mM) slowed down the development of blockade but the maximum blockade achieved was similar to that obtained in 2 mM Ba2+. A further difference between the two toxins concerns their reversibility; washout of ω-conotoxin MVIIC did not reverse the
blockade of I
Ba while in the case of ω-conotoxin MVIID a partial, quick recovery of current was produced. This component was irreversibly
blocked by ω-conotoxin GVIA, suggesting that it is associated with N-type Ca2+ channels. Blockade of K+-evoked 45Ca2+ entry produced results which paralleled those obtained by measuring I
Ba. Thus, 1 μM of each of ω-conotoxin GVIA and MVIIA inhibited Ca2+ uptake by 25%, while 1 μM of each of ω-conotoxin MVIIC and MVIID caused a 70% blockade. K+-evoked catecholamine secretory responses were not reduced by ω-conotoxin GVIA (1 μM). In contrast, at 1 μM both ω-conotoxin
MVIIC and MVIID reduced the exocytotic response by 70%. These data strengthen the previously established conclusion that Q-type
Ca2+ channels that contribute to the regulation of secretion and are sensitive to ω-conotoxins MVIIC and MVIID are present in
bovine chromaffin cells. These channels, however, seem to possess binding sites for ω-conotoxins MVIIC and MVIID whose characteristics
differ considerably from those described to occur in the brain; they might represent a subset of Q-type Ca2+ channels or an entirely new subtype of voltage-dependent high-threshold Ca2+ channel.
Received: 16 April 1997 / Received after revision: 10 July 1997 / Accepted: 23 July 1997 相似文献
123.
Intracellular pH changes affect excitation-contraction coupling in skeletal, and cardiac muscles. However the proton implication
in modulating the sarcoplasmic reticulum Ca2+ release channel activity has never been visualized at single channel level. A large conducting Ca2+ release pathway has previously been characterized after incorporation of skeletal and cardiac sarcoplasmic reticulum vesicles
into planar lipid bilayers. This channel has been activated by micromolar and millimolar concentrations of Ca2+ and ATP, respectively. The pH was independently varied on each side of the channels. Acidification of the cis-chamber (7.4
to 6.6) induced a modification of the gating behaviour, resulting in a decrease of the open probability. This effect was completely
reversible. On the other hand, acidification of the trans-chamber (7.4 to 6.8) induced a reduction of the unitary conductance
of the sarcoplasmic reticulum Ca2+ release channel. 相似文献
124.
In order to examine temporal changes in enhancement of transmitter release during long-term potentiation (LTP), we examined amplitude fluctuation of excitatory postsynaptic potentials (EPSPs) for longer periods than 2 h after tetanic stimulation (up to 4 h in the longest observation). The relative magnitude of excitatory postsynaptic potentiation (EPSP) fluctuation (coefficient of variation, CV) reduced throughout the observation periods in association with an increase in EPSP amplitude after tetanic stimulation. The reciprocals of squared CVs (= mean2/variance) were almost in proportion to the magnitude of LTP, and the ratio of 1/CV2 and the LTP magnitude did not change significantly for up to 4 h. These findings suggest that a prolonged enhancement of transmitter release from presynaptic terminals underlies LTP, and the relative contribution of this presynaptic enhancement does not change significantly for 2 h (maybe up to 4 h, or longer) after tetanic stimulation. 相似文献
125.
S.?Mori N.?Muroi S.?Ono H.?K.?Takahashi M.?NishiboriEmail author 《Inflammation research》2004,53(4):164-169
Objective and Design: Carboxymethylcellulose (CMC) has been considered to be inert and is commonly used as an additive in medicines, foods and cosmetics. However, we experienced a patient who developed an anaphylactic reaction to CMC after an upper gastrointestinal examination using a barium meal containing CMC. Therefore, we examined the incidence of sensitization by CMC in healthy subjects, and categorized the high risk group prone to developing anaphylactic response to CMC.Methods: An ELISA for detecting CMC-specific IgE antibody was developed using serum from the patient as a positive control. In the ten subjects exhibiting high anti-CMC IgE among 387 normal populations, histamine release from isolated leukocytes was performed.Results: Five of ten subjects with a high IgE titer showed a significant CMC-induced histamine release from leukocyte preparations in vitro as observed in the patient, and were classified as high risk group. There was a correlation between sensitization by CMC and that by Japanese cedar pollen. The incidence of sensitization in females was 2.4 fold higher than that in males.Conclusions: The combination of ELISA and histamine release experiment made it possible to identify the high risk group for developing anaphylactic response. The administration of high dose CMC as a suspending agent in barium sulfate or injectable corticosteroids to this group should be avoided to prevent anaphylactic reactions in the clinic.Received 18 August 2003; returned for revision 29 September 2003; accepted by M. J. Parnham 10 December 2003 相似文献
126.
Masayuki Ishihara PhD Kiyohaya Obara MD Singo Nakamura PhD Masanori Fujita MD PhD Kazunori Masuoka MD Yasuhiro Kanatani MD PhD Bonpei Takase MD PhD Hidemi Hattori PhD Yuji Morimoto MD PhD Miya Ishihara PhD Tadaaki Maehara MD PhD Makoto Kikuchi PhD 《Journal of artificial organs》2006,9(1):8-16
An aqueous solution of photocrosslinkable chitosan containing azide groups and lactose moieties (Az-CH-LA) incorporating paclitaxel
formed an insoluble hydrogel within 30 s of ultraviolet light (UV) irradiation. The chitosan hydrogel showed strong potential
for use as a new tissue adhesive in surgical applications and wound dressing. The fibroblast growth factor (FGF)-2 molecules
retained in the chitosan hydrogel and in an injectable chitosan/IO4-heparin hydrogel remain biologically active, and were gradually released from the hydrogels as they biodegraded in vivo.
The controlled release of biologically active FGF-2 molecules from the hydrogels caused induction of angiogenesis and collateral
circulation occurred in healing-impaired diabetic (db/db) mice and in the ischemic limbs of rats. Paclitaxel, which is an antitumor reagent, was also retained in the chitosan hydrogel
and remained biologically active as it was released on degradation of the hydrogel in vivo. The chitosan hydrogels incorporating
paclitaxel effectively inhibited tumor growth and angiogenesis in mice. The purpose of this review is to describe the effectiveness
of chitosan hydrogel as a local drug delivery carrier for agents (e.g., FGF-2 and paclitaxel) to control angiogenesis. It
is thus proposed that chitosan hydrogel may be a promising new local carrier for drugs such as FGF-2 and paclitaxel to control
vascularization. 相似文献
127.
Glucagon-induced somatostatin release from perifused rat hypothalamus: calcium dependency and effect of cysteamine treatment 总被引:1,自引:0,他引:1
Somatostatin (SRIF) release from rat hypothalamus was investigated in vitro with a perifusion system. Glucagon (1 microM) and high potassium concentrations (56 mM) stimulated SRIF release in a calcium-dependent manner. Pretreatment of the rat with cysteamine (30 mg/100 g body weight, 7 h earlier) significantly reduced SRIF release from the hypothalamus in glucagon- and high potassium-stimulated states as well as in the basal state. SRIF release from rat hypothalamus was also stimulated by both dibutyryl cyclic AMP (1 mM) and theophylline (3 mM). These results suggest that glucagon, acting in a calcium-dependent manner and possibly through the adenylate cyclase-cyclic AMP system, stimulates SRIF release from rat hypothalamus and that cysteamine treatment reduces releasable SRIF in the hypothalamus. 相似文献
128.
Phasically firing neurons in the supraoptic nucleus of the rat hypothalamus: immunocytochemical and electrophysiological studies 总被引:3,自引:0,他引:3
Relations between firing patterns and peptides in supraoptic neurons of rat hypothalamic slice preparations were studied by electrophysiology, intracellular fluorescent dye-marking and immunocytochemistry. Seven out of 10 magnocellular neurons which showed phasically firing patterns were identified by injections of Lucifer Yellow-CH (LY); these were also stained with an anti-vasopressin serum. This report presents direct evidence that most of the phasically firing neurosecretory neurons in the supraoptic nucleus contain vasopressin. This study demonstrates the feasibility of combining immunocytochemical and electrophysiological techniques to study the peptides contents of single mammalian neurons. 相似文献
129.
Mechanisms of peptide YY release induced by an intraduodenal meal in rats: neural regulation by proximal gut 总被引:5,自引:0,他引:5
Fu-Cheng Xiaomei Anini Younes Chariot Jacques Castex Nathalie Galmiche Jean-Paul Rozé C. 《Pflügers Archiv : European journal of physiology》1997,433(5):571-579
Peptide YY (PYY) release in anaesthetized rats was studied during the 2 h following the intraduodenal administration of a
semi-liquid meal of 21 kJ. Surgical and pharmacological manipulations were performed in order to analyse the mechanisms of
PYY release. Postprandial PYY release was suppressed or strongly decreased by caecocolonectomy, truncal vagotomy, tetrodotoxin,
hexamethonium, sensory denervation by perivagal capsaicin, and by the NO-synthase inhibitor L-N-arginine methyl ester, while atropine, adrenergic blockers, antagonists of type-A or type-B cholecystokinin (CCK) receptors
or bombesin receptors had no effect. Comparing the digestive transit of the semi-liquid meal with the amount of PYY contained
in the small bowel wall showed that nutrients had not reached the area rich in cells containing PYY by 30 min, the time at
which there was a large PYY release in plasma. By 120 min, the meal front had travelled 72% of the small intestine length,
just beginning to reach the PYY-rich part of the ileum. We conclude that the main postprandial PYY release studied in this
model comes from ileal and colonic L-cells indirectly stimulated through a neural mechanism originating in the proximal gut
and involving sensory vagal fibres, nicotinic synapses and NO release, while CCK and bombesin do not seem to be physiologically
involved.
Received: 17 July 1996 / Received after revision: 11 October 1996 / Accepted: 18 October 1996 相似文献
130.
Miniature end-plate currents (m.e.p.c.s) were recorded from frog neuromuscular junctions using a two-electrode voltage clamp. The m.e.p.c. frequency was temporarily elevated following 10 s iontophoretic applications of acetylcholine (ACh) when the junctions were clamped at 100 mV. This post-ACh burst of quanta was also observed at unclamped junctions. At –100 mV, the intensity of the burst was proportional to the amount of current flowing across the end-plate during ACh iontophoresis, but usually did not reach its peak until the end-plate receptor channels were almost completely closed. Addition of 0.5 M TTX to the Ringer's solution, or total replacement of sodium with quanidine, lithium, or methylamine did not inhibit the burst. No burst was observed in Ca2+-free, EGTA solutions, or in Ca2+-free solutions containing 2 mM Mn2+. Sr2+ effectively substituted for Ca2+. Addition of 2 mM Co2+ or Mn2+ to normal Ringer's did not inhibit the burst. Presynaptic muscarinic receptors did not obviously contribute to the burst, since it was not blocked by atropine, nor produced by oxotremorine or pilocarpine. The ACh analogs carbachol and acetyl--methylcholine also produced the burst. The burst was highly dependent on the muscle membrane potential during the period of ACh iontophoresis, becoming more intense at potentials negative to –100 mV and disappearing at –60 mV. The critical importance of the post-synaptic membrane potential suggests that the burst may be due to an action of the muscle end-plate on the motor nerve terminal, possibly by the movement of an anionic substance through open end-plate receptor channels, but this hypothesis does not account for the delay of the burst until near the end of the ACh-induced end-plate current. 相似文献