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31.
32.
实验性自身免疫性脑脊髓炎巨噬细胞活性MR成像的研究进展 总被引:2,自引:0,他引:2
MR成像是监测多发性硬化(MS)病情及其演变、评价疗效的重要手段,实验性自身免疫性脑脊髓炎(EAE)是公认的研究人类多发性硬化的动物模型。常规MR扫描仅能分析MS和EAE炎症反应的继发性改变。巨噬细胞是MS和EAE炎症反应中重要的效应细胞,超微超顺磁性氧化铁(USPIO)粒子能被巨噬细胞摄取,MR成像能显示MS和EAE病灶内吞噬了USPIO的巨噬细胞,分析其炎症反应自身的信息,是动态观察巨噬细胞浸润过程、进一步探索MS免疫病理机制的有效手段。本文综述超微超顺磁性对比剂的特性及其MR成像在EAE和MS病理机制方面的研究进展,评价其发展前景。 相似文献
33.
Sabrina Benedetto Roberta Pulito Simonetta Geninatti Crich Guido Tarone Silvio Aime Lorenzo Silengo Jrg Hamm 《Magnetic resonance in medicine》2006,56(4):711-716
Targeted imaging requires site-specific accumulation of a contrast agent (CA), and the properties of that agent must be selected according to the abundance of the target to obtain a signal above the detection limit of the instrument. However, numerical estimates of receptors per cell are rarely found in the literature. Integrin receptors would be particularly promising targets because of their accessibility from the blood stream and expression on activated neovascular endothelial cells. We systematically estimated the number of integrin receptors of cell lines and primary cells by flow cytometry analysis. Since integrin receptors are heterodimeric molecules, and alpha(v) forms complexes with various beta subunits, the numbers of alpha(v) and beta(3) subunits are therefore dissimilar. The observed values are 3 . 10(3)-1.4 . 10(4)/cell for alpha(v), and 5.3 . 10(2)-1.1 . 10(4)/cell for beta(3). Despite the low number of exposed receptors, we show that up to single-cell MR visualization can be achieved with the use of iron oxide beads complexed with antibodies as CAs. 相似文献
34.
NOS1 polymorphism is associated with atopy but not exhaled nitric oxide levels in healthy children 总被引:1,自引:0,他引:1
May Ali Siew-Kim Khoo Stephen Turner Stephen Stick Peter Le Souëf Peter Franklin 《Pediatric allergy and immunology》2003,14(4):261-265
Exhaled nitric oxide (FENO ) is raised in atopy. The mechanism for this is unclear. The aim of this study was to investigate whether the number of AAT repeats in intron 20 of the NOS1 gene, recently associated with variations in FENO in adults with asthma and cystic fibrosis, was associated with the raised FENO in healthy atopic children. Eighty-seven healthy children (44 girls, 42 atopic, age range 6–18 years) underwent measurements of FENO , spirometry, airway responsiveness and skin prick testing. Genotyping was carried out to determine the number of AAT repeats. There was no association between the number of AAT repeats and FENO in either the whole sample of healthy children (n = 87) or in the subsample of healthy atopics (n = 42). However, a greater number of atopic children had two high repeat alleles compared with non-atopic children (33.3% vs. 13.6%, respectively, p = 0.03). This suggests that variations in the NOS1 gene may contribute to atopy without this relationship being reflected by FENO . 相似文献
35.
Fumio Nakajima Tomohiko Asano Masamichi Hayakawa Hiroshi Nakamura 《International journal of urology》1996,3(1):s19-s21
We evaluated nitric oxide induction in antitumor therapy consisting of anti–CD3 monoclonal antibody (anti–CD3) and interleukin–2 (IL–2), then determined the effect of nitric oxide reduction with L–NG –monomethyl arginine (LNMA) on the therapeutic methods. Female C57BL/6 mice, MCA102 (a non immunogenic, NK–resistant murine fibrosarcoma cell line), and 145–2C11 (hamster anti–murine–CD3 mAb) were utilized in an experimental hepatic metastasis model developed by injecting a tumor cell suspension into the spleen of mice. A marked increase in serum NO2 – + NO1 was observed at 19 hours after anti–CD3 (10 μ, IV) and additional IL–2 administrations (40times101 U, twice, If) induced a further increase. The NO2 , + NO3- elevation in spot urine in the combination therapy was not suppressed with LNMA at a dose of 100 μg/h but was significantly lowered at 300 μg/h. The efficacy of the anti–CD3 + IL–2 therapy was not diminished by LNMA administration either at 100 μg/h or at 300 μg/h. 相似文献
36.
Summary— To investigate if the functional alterations observed in resistance arteries of spontaneously hypertensive rats (SHRs) were also present at the coronary level, in vitro experiments were performed in mesenteric resistance arteries (MRA) and in right (RIC) and left interventricular coronary (LIC) arteries taken from 15–25-week-old SHR and age-matched Wistar Kyoto rats WKYs. Using a passive extension protocol, internal diameters corresponding to 100 mmHg intraluminal pressure (D100) were determined and vessels were set up to a normalized internal diameter (0.9 D100). SHR mesenteric resistance arteries had a significantly smaller diameter compared to WKY arteries, whereas both types of SHR coronary arteries had a greater diameter compared to those of WKY rats. In arteries in the absence of contracting agonist, nitro-L-arginine (NOLA, 100 μM) induced a progressive rise in basal tone, which could be reversed by subsequent addition of L-arginine (100 μM) but not D-arginine (100 μM). When expressed as percent of maximal contractions induced by agonists (noradrenaline, NA [10 μM] in MRA; serotonin, 5-HT [10 μM], in RIC and LIC), these contractions were significantly stronger in WKY compared to SHR coronary and mesenteric resistance arteries. In NA-precontracted MRA and 5HT-precontracted coronary arteries in the presence of indomethacin (10 μM), the magnitude of acetylcholine-induced maximal relaxations (expressed as percent of maximal contractions induced by agonists) was greater in WKY compared to SHR arteries. After a 30-min incubation period, NOLA (100 μM) completely inhibited relaxations induced by acetylcholine (0.01–10 μM) in all types of precontracted arteries. Subsequent additions of sodium nitroprusside, (SNP, 10 μM) induced complete relaxations in all preparations. These results show that a basal release of NO or NO-like compound by endothelial cells is present in isolated mesenteric resistance and coronary arteries of WKY rats and SHRs. The contribution of endothelium-derived relaxing factor-nitric oxide (EDRF-NO) to arterial tone was lower in MRA compared to coronary arteries in both strains and in SHR compared to WKY arteries. In the SHR preparations, the impaired relaxation induced by acetylcholine appeared to be due to a functional alteration of the endothelium in the presence of normal reactivity of the smooth muscle cells. 相似文献
37.
H. Ekroos J. Tuominen A. R. A. Sovijrvi 《Clinical physiology and functional imaging》2000,20(6):434-439
Exhaled nitric oxide (NOexp) is an indicator of inflammation in the airways. Reference values obtained from healthy adults or information on long‐term variation of NOexp are not yet available. The aims of this pilot study were to collect values of NOexp from a selected group of healthy adults and to assess their long‐term variation. We studied 26 healthy subjects (age 21–48, 16 male, 10 female) with normal findings in flow‐volume spirometry, pulmonary diffusing capacity, relative amount of blood eosinophils, chest X‐ray and ECG at rest. NOexp was determined according to the European Respiratory Society guidelines during slow expiration against an airflow resistance. The measurements were repeated after 7 (n=13) and 23 days (n=17). The mean value of NOexp (n=26) was 6·9 ng g–1 (95% confidence interval, 6·0–7·9 ng g–1). The upper limit of intra‐individual variation (+2 SD) was 11·9 ng g–1 and the lower limit (–2 SD) 1·9 ng g–1, respectively. The mean (SD) value of NO production (NO output) was 39·1 pmol s–1 (20 pmol s–1). We found no correlation between NOexp and age (r=–0·06, P=0·78) and no association of NOexp with the gender (male vs. female, P=0·40). The intraindividual coefficient of variation (CoV) was 15·8% of NOexp and 20·7% of NO output within the interval of 7 days. CoV was 16·8% of NOexp and 18% of NO output within the interval 23 days. The results suggest that NOexp values over 12 ng g–1 are abnormally high in healthy subjects. According to the results the change of NOexp by 30–35% or more within the interval of 1–3 weeks would be abnormal. 相似文献
38.
39.
Chronic vitamin E treatment prevents defective endothelium-dependent relaxation in diabetic rat aorta 总被引:2,自引:2,他引:0
Summary We examined the effect in rats of 2 months of streptozotocin-induced diabetes mellitus on relaxation and contraction of aortas in vitro. A further diabetic group was treated from time of diabetes induction with a 1% dietary supplement of vitamin E. Diabetes caused a 26.5% deficit (p<0.001) in maximum endothelium-dependent relaxation to acetylcholine in phenylephrine-precontracted aortas. This was 64.3% attenuated (p<0.01) by vitamin E treatment; maximum relaxation was not significantly altered compared to non-diabetic rats. Vitamin E treatment of non-diabetic rats did not significantly affect acetylcholine-induced relaxation. Diabetes or treatment did not significantly alter acetylcholine sensitivity. Endothelium-independent relaxation response to glyceryl trinitrate was not affected by diabetes or vitamin E treatment, indicating that vascular smooth muscle responses to nitric oxide remained unaltered. There was a 35.4% reduction in the maximum contractile response to phenylephrine with diabetes (p<0.05) which was unaffected by vitamin E treatment. The data suggest that the chronic deficit in nitric oxide-mediated endothelium-dependent relaxation in diabetes depends largely upon excess activity of reactive oxygen species. Treatment with vitamin E to increase free radical scavenging specifically protected vascular endothelium although it had no effect on deficits in vascular smooth muscle contractile responses.Abbreviations NO
Nitric oxide
- ARI
aldose reductase inhibitor
- ACH
acetylcholine
- GTN
glyceryl trinitrate
- GSH
reduced form of glutathione
- EC50
effective concentration for 50% of the maximal response 相似文献
40.
Andrea Bernatowicz Uwe Kdel Karl Frei Adriano Fontana Hans-walter Pfister 《Journal of neuroimmunology》1995,60(1-2):53-61
Recent studies using a rat model of pneumococcal meningitis have shown that nitric oxide synthase (NOS) inhibitors greatly attenuated microvascular changes and brain edema formation. The site of NO production during bacterial meningitis is unknown. In this study we tested whether primary astrocyte cultures from neonatal rat cortex can be induced to release NO upon stimulation with pneumococci. NO production was assessed by measuring nitrite in the cell culture supernatant using the Griess reaction. Stimulation with heat-killed unencapsulated pneumococci (HKP) increased nitrite concentrations in astrocyte culture supernatants in a dose-dependent fashion. Administration of AT-nitro-L-arginine (L-NA), aminoguanidine, L-canavanine, cycloheximide, and dexamethasone prevented the increase in nitrite concentrations. Addition of L-arginine, but not of o-arginine, partially reversed the inhibitory effect of L-NA. Administration of SOD increased nitrite accumulation. Moreover, at 72 h after stimulation with heat-killed pneumococci (107 cfu/ml) astrocytes showed an inducible NOS-like immunoreactivity. Accumulation of nitrite was also observed when rat cerebellar neurons and microglia were stimulated with HKP, whereas there was only a slight increase of nitrite in media of rat C6 glioma cells, but no increase of nitrite when the human glioblastoma cell line LN-229 was stimulated with HKP. There was a stronger increase in nitrite levels when astrocytes from Lewis rats were used compared to that from Wistar rats. In conclusion, our study indicates that astrocytes, neurons and microglia are inducible for NO production upon stimulation with pneumococci. 相似文献