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21.
大气中不同粒径颗粒物诱导人羊膜FL细胞UDS的研究 总被引:3,自引:0,他引:3
本研究以诱导人羊膜细胞UDS为指标,对太原市大气不同粒径的颗粒物提取液进行了致突变性检验,结果表明,不同粒径颗粒物的提取液均可产生一定的遗传毒性,尤以3.3μm以下的颗粒物的遗传毒性较强。 相似文献
22.
In human Y-79 retinoblastoma cells corticotropin-releasing hormone (CRH) produces a marked and rapid increase of adenylate cyclase activity. The concentration of the peptide producing half-maximal stimulation is 60 nM. The effect of CRH is significantly antagonized by the specific CRH receptor antagonist alpha-helical CHR 9-41 and is mimicked by sauvagine and urotensin I, two peptides displaying sequence homology with CRH. These results demonstrate the presence of functional CRH receptors in human Y-79 retinoblastoma cells and suggest that this cell line may be a suitable model in which to study the action of CRH on human retinal cell function. 相似文献
23.
Evidence for the presence of substance P-like immunoreactivity in the human cerebellum 总被引:1,自引:0,他引:1
M. Del Fiacco M. T. Perra M. Quartu M. D. Rosa G. Zucca M. C. Levanti 《Brain research》1988,446(1):173-177
Preliminary results on the localization of substance P-like immunoreactivity in the human cerebellum are presented. Cerebella from newborn and adult subjects were examined. While only sporadic positive fibres were detected in the adult tissue, the immunoreactive material appeared more abundant in the cerebella from newborn subjects. Varicose and non-varicose fibres and dot-like nerve terminals were present with different density in various regions. The paucity of immunoreactive perikarya suggests that most of the cerebellar substance P-like immunoreactive material has an extrinsic origin. 相似文献
24.
Peter Van Gelder Sergey Lebedev Wai Hon Tsui 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1997,116(2):201-215
Smooth pursuit typically includes corrective catch-up saccades, but may also include such intrusive saccades away from the
target as anticipatory or large overshooting saccades. We sought to differentiate catch-up from anticipatory and overshooting
saccades by their peak velocities, to see whether the higher velocities of visually rather than nonvisually guided saccades
in saccadic tasks may be found also in saccades in pursuit. In experiment 1, 12 subjects showed catch-up, anticipatory, and
overshooting saccades to comprise 70.4% of all saccades in pursuit of periodic, 30°/s constant-velocity targets. Catch-up
saccades were faster than the others. Saccadic tasks were run as well, on 19 subjects, including the 12 whose pursuit data
were analyzed, with target-onset, target-remaining (saccade to the remaining target when the other three extinguish), and
antisaccade tasks. For 17 of the 19 subjects, antisaccade velocities were lower than for either target-onset or target-remaining
tasks. Velocities for the target-remaining task were near those for target onset, indicating that target presence, not its
onset, defines visually guided saccades. Error and reaction-time data suggest greater cognitive difficulty for target remaining
than for target onset, so that the cognitive difficulty of typical nonvisually guided saccade tasks is not sufficient to produce
their lowered velocity. To produce reliably, in each subject, catch-up and anticipatory saccades with comparable amplitude
distributions, nine new subjects were asked in experiment 2 to make intentional catch-up and anticipatory saccades in pursuit,
and were presented with embedded target jumps to elicit catch-up saccades, all with periodic target trajectories of 15°/s
and 30°/s. Velocities of intentional anticipatory saccades were lower than velocities of intentional catch-up saccades, while
velocities of intentional and embedded catch-up saccades were similar. Target-onset and remembered-target saccadic tasks were
run, showing the expected higher velocity for the target-onset task in each subject. Both experiments demonstrate higher peak
velocities for catch-up saccades than for anticipatory saccades, suggesting that cortical structures preferentially involved
in nonvisually guided saccades may initiate the anticipatory and overshooting saccades in pursuit.
Received: 1 December 1995 / Accepted: 25 February 1997 相似文献
25.
骨髓间质干细胞体外预构组织工程化肌腱的实验研究 总被引:2,自引:1,他引:1
目的探讨骨髓间质干细胞与胶原-聚羟基乙酸的细胞相容性,为构建组织工程化肌腱寻求理想方法.方法以贴壁法分离、培养骨髓间质干细胞,并检测CD44.在实验组中将骨髓间质干细胞置入含胶原-聚羟基乙酸的DMEM培基中培养:在对照组中将骨髓间质干细胞置入DMEM培基中培养.通过MTT方法比较两组的细胞活性和生长情况,并对实验组进行超微观察.以骨髓间质干细胞为种子细胞,以胶原-聚羟基乙酸为支架在体外预构组织工程化肌腱.结果以贴壁法原代培养骨髓间质干细胞,11天细胞即汇合成片,检测CD44示阳性.骨髓间质干细胞接种于胶原-聚羟基乙酸中混合培养后14天生长良好,始终保持89%以上的细胞活力,与对照组比较无显著差别;实验组细胞数未发生明显改变,而对照组从第4天开始即发生增殖.透射电镜示实验组细胞培养14天后仍保持旺盛的分泌功能.体外预构的组织工程化肌腱具有良好的形态,细胞伸展成梭形,沿聚羟基乙酸缝线大致平行排列.结论骨髓间质干细胞与胶原-聚羟基乙酸的细胞相容性好.以骨髓间质干细胞为种子细胞,以胶原-聚羟基乙酸为支架可在体外初步预构组织工程化肌腱. 相似文献
26.
Decreased expression of DMPK: correlation with CTG repeat expansion and fibre type composition in myotonic dystrophy type 1 总被引:2,自引:0,他引:2
S. Salvatori M. Fanin C. P. Trevisan S. Furlan S. Reddy J. I. Nagy C. Angelini 《Neurological sciences》2005,26(4):235-242
Abstract Myotonic dystrophy type 1 (DM1) is an autosomal dominant disease caused by a trinucleotide repeatexpansion, cytosine-thymine-guanine
(CTG)n, in the 3′ untranslated region of a gene encoding the myotonic dystrophy protein kinase (DMPK). To correlate CTG expansion
and protein expression, we studied muscle specimens from 16 adult DM1 patients using three anti-DMPK antibodies for immunoblotting.
We estimated the amount of the full-length DMPK (85 kDa) in muscle biopsies from normal controls and from DM1 patients carrying
different (CTG)n expansions. We found that DMPK concentration was decreased to about 50% in DM patients’ muscles; the protein decrease did
not seem correlated with the CTG repeat length. However, the fibre type composition in skeletal muscle seemed somehow to affect
DMPK decrease, as the lowest level of the enzyme was found in patients with the lowest content of type 1 fibre. 相似文献
27.
The thymus in seronegative myasthenia gravis patients 总被引:1,自引:0,他引:1
Summary In 5–10% of all patients with typical generalised myasthenia gravis (MG), serum antibody to the acetylcholine receptor (AChR) is undetectable. To determine whether these represent a distinct subgroup, we have compared the thymuses of 14 seronegatives, 70 seropositives and 12 non-myasthenic controls. By quantitative immunohistology on coded sections, the 7 seronegative samples were clearly distinguishable from the controls by the pronounced lymph node-type T-cell areas in the medulla. While these closely resembled those in the seropositive cases, germinal centres were significantly sparser, and total in vitro IgG production was disproportionately low (per B cell) in the 12 cases tested. Furthermore, specific anti-AChR production was never detected in any of these cultures. The data support the view that the medullary T-cell areas are the most consistent abnormalitiy in the MG thymus (though it may not be primary), and they strongly imply that seronegative and seropositive MG are distinct entities. 相似文献
28.
29.
Objective. To provide national estimates of the effect of out-of-pocket premiums and benefits on Medicare beneficiaries' choice among managed care health plans.
Data Sources/Study Setting. The data represent the population of all Medicare+Choice (M+C) plans offered to Medicare beneficiaries in the United States in 1999.
Study Design. The dependent variable is the log of the ratio of the market share of the j th health plan to the lowest cost plan in the beneficiary's county of residence. The explanatory variables are measures of premiums and benefits in the j th health plan relative to the premiums and benefits in the lowest cost plan.
Data Collection Methods. The data are from the 1999 Medicare Compare database, and M+C enrollment data from the Centers for Medicare and Medicaid Services (CMS).
Principal Findings. A $10 increase in an M+C plan's out-of-pocket premium, relative to its competitors, is associated with a decrease of four percentage points in the j th plan's market share (i.e., from 25 to 21 percent), holding the premiums of competing plans constant.
Conclusions. Although our price elasticity estimates are low, the market share losses associated with small changes in a health plan's premium, relative to its competitors, may be sufficient to discipline premiums in a competitive market. Bidding behavior by plans in the Medicare Competitive Pricing Demonstration supports this conclusion. 相似文献
Data Sources/Study Setting. The data represent the population of all Medicare+Choice (M+C) plans offered to Medicare beneficiaries in the United States in 1999.
Study Design. The dependent variable is the log of the ratio of the market share of the j th health plan to the lowest cost plan in the beneficiary's county of residence. The explanatory variables are measures of premiums and benefits in the j th health plan relative to the premiums and benefits in the lowest cost plan.
Data Collection Methods. The data are from the 1999 Medicare Compare database, and M+C enrollment data from the Centers for Medicare and Medicaid Services (CMS).
Principal Findings. A $10 increase in an M+C plan's out-of-pocket premium, relative to its competitors, is associated with a decrease of four percentage points in the j th plan's market share (i.e., from 25 to 21 percent), holding the premiums of competing plans constant.
Conclusions. Although our price elasticity estimates are low, the market share losses associated with small changes in a health plan's premium, relative to its competitors, may be sufficient to discipline premiums in a competitive market. Bidding behavior by plans in the Medicare Competitive Pricing Demonstration supports this conclusion. 相似文献
30.
T J Molloy Y Wang A Horner T M Skerry G A C Murrell 《Journal of orthopaedic research》2006,24(4):842-855
Tendon healing is a complex process consisting of a large number of intricate pathways roughly divided into the phases of inflammation, proliferation, and remodeling. Although these processes have been extensively studied at a variety of levels in recent years, there is still much that remains unknown. This study used microarray analyses to investigate the process at a genetic level in healing rat Achilles tendon at 1, 7, and 21 days postinjury, roughly representing the inflammation, proliferation, and remodeling phases. An interesting temporal expression profile was demonstrated, identifying both known and novel genes and pathways involved in the progression of tendon healing. Both inflammatory response and pro-proliferative genes were shown to be significantly upregulated from 24 h postinjury through to 21 days. Day 7 showed the largest increase in genetic activity, particularly with the expression of collagens and other extracellular matrix genes. Interestingly, there was also evidence of central nervous system-like glutamate-based signaling machinery present in tendon cells, as has recently been shown in bone. This type of signaling mechanism has not previously been shown to exist in tendon. Another novel finding from these analyses is that there appears to be several genes upregulated during healing which have exclusively or primarily been characterized as key modulators of proliferation and patterning during embryonic development. This may suggest that similar pathways are employed in wound healing as in the tightly regulated progression of growth and development in the embryo. These results could be of use in designing novel gene-based therapies to increase the efficacy and efficiency of tendon healing. 相似文献