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131.
Leanne Tamm Jeffery N. Epstein Richard E.A. Loren Stephen P. Becker Sarah B. Brenner Morgan E. Bamberger 《Journal of clinical child and adolescent psychology》2019,48(2):S131-S145
This goal of this study was to assess the initial feasibility and efficacy of a play-based intervention targeting executive functions (EF) and parent–child relationships in preschoolers compared with an active control group. Preschoolers with EF deficits (M age = 3.7 ± 0.47, predominantly White boys) and their parents were randomized to intervention (n = 36) or active control (n = 32) conditions. Child performance on EF tasks, parent and masked teacher ratings of EF and behavior, and masked clinician ratings of severity were collected at baseline and at 3 and 6 months postbaseline. Partial eta-squared effect sizes at .02 or higher comparing performance across the two groups was considered evidence of meaningful, albeit small, intervention effects. Intervention effects were observed for parent ratings of inattention, hyperactivity/impulsivity, and number/severity of problems experienced in various home situations, teacher ratings of severity of problems in various school situations, parent and teacher ratings of overall impairment, and clinician ratings of impairment. Intervention effects for functional improvements were maintained at the 6-month follow-up. No effect of the intervention was observed on the objective EF measures, although parent ratings of emotional control were improved for children in the intervention group. An intervention utilizing play-based activities targeting EF, when administered in a structured way by parents, is a promising approach for improving behavior in preschoolers with self-regulation deficits. More work is needed to investigate potential impact on EF and to disentangle mechanisms of action. It may be that the intervention’s focus on the structure and quality of parent–child interactions is a mediator of outcomes, rather than improved EFs. 相似文献
132.
Analysis of the Virus Population Present in Equine Faeces Indicates the Presence of Hundreds of Uncharacterized Virus Genomes 总被引:7,自引:0,他引:7
Virus DNA was isolated from horse faeces and cloned in a sequence-independent fashion. 268 clones were sequenced and 178140 nucleotides of sequence obtained. Statistical analysis suggests the library contains 17560 distinct clones derived from up to 233 different virus genomes. TBLASTX analysis showed that 32% of the clones had significant identity to GenBank entries. Of these 63% were viral; 20% bacterial; 7% archaeal; 6% eukarya; and 5% were related to mobile genetic elements. Fifty-two percent of the virus identities were with Siphoviridae; 26% unclassified phages; 17% Myoviridae; 4% Podoviridae; and one clone (2%) was a vertebrate Orthopoxvirus. Genes coding for predicted virus structural proteins, proteases, glycosidases and nucleic acid-binding proteins were common. 相似文献
133.
Gail Shor-Posner Christopher Ian Glen Brennan Tamara Cohn Harvey Moy Autumn Ning Sarah F. Leibowitz 《Physiology & behavior》1991,50(6):1187-1195
Analyses of natural feeding behavior in albino male Sprague-Dawley rats demonstrate that, when allowed to self-select from pure macronutrient diets (protein, carbohydrate and fat), these rats of the same genetic strain can be categorized into 3 subpopulations according to either their 24-h or their 12-h nocturnal patterns of nutrient intake. A majority of the animals (HC for high carbohydrate, 50% of the total population) consumed a diet rich in carbohydrate relative to protein or fat, while a smaller population of rats (HF, 30%) preferred the fat diet, and an even smaller population (HP, 20%) chose a high-protein diet. These 3 subpopulations, after a few weeks of maintenance on the diets, differed in their body weight, with the HF rats having a higher body weight than the HP animals, who tended to weigh more than the lightest HC rats. Whereas all subgroups exhibited a similar bimodal distribution of feeding during the nocturnal cycle, with peaks during the early and late dark periods, they were distinguishable on the basis of their nutrient consumption during specific phases of the dark cycle. This difference was most apparent in the early dark phase, when the 3 subgroups exhibited exaggerated preferences for the specific nutrient that was generally preferred over the 24-h cycle. This is in contrast to the middle dark phase, when diet preferences were attenuated or lost, and the late dark phase, when most rats were similar in showing an increased preference for protein and fat and a decreased preference for carbohydrate. The HF group was further distinguished by an unusually strong burst of feeding during the first 2 h of the dark period and an extra peak of feeding in the middle dark period (7th h), both of which were relatively high in fat content. 相似文献
134.
Isolation of the chicken Lmbr1 coding sequence and characterization of its role during chick limb development. 总被引:2,自引:0,他引:2
In the developing amniote limb, anteroposterior (A/P) patterning is controlled through secretion of the Sonic Hedgehog (SHH) protein by cells in the zone of polarizing activity (ZPA) located in the posterior mesoderm. In the chicken mutant oligozeugodactyly (ozd), Shh is expressed normally in the entire embryo with the exception that it is undetectable in the developing limbs; this results in the loss of specific bones in wings and legs. The ozd phenotype is similar to that of humans affected with acheiropodia (ACHR), and the ACHR mutation has been mapped to a deletion of exon 4 and portions of introns 3 and 4 in the LMBR1 gene. We have cloned the chick ortholog of LMBR1, Lmbr1, and report that, in chick, Lmbr1 is expressed within the ZPA. Although the ozd phenotype is similar to ACHR, the open reading frame of Lmbr1 is normal in ozd. Sequence analysis of Lmbr1 intron 3 demonstrated that this particular genomic region segregates with the ozd phenotype. In addition, overexpression of Lmbr1 throughout the developing limb mesoderm resulted in morphologically normal limbs. Collectively, these data suggest that the Lmbr1 coding sequence is not required for normal chick limb development. We propose that the ozd mutation is linked to the genomic region containing Shh and Lmbr1. 相似文献
135.
William S Stone Stephen V Faraone Jessica Su Sarah I Tarbox Paul Van Eerdewegh Ming T Tsuang 《American journal of medical genetics. Part B, Neuropsychiatric genetics》2004,(1):5-10
Observations of impaired glucose regulation in schizophrenia are long-standing, although their pathological and etiological significance is uncertain. One approach to the issue that minimizes environmental variables (e.g., medication and diet) is to determine whether genes related to glucose regulation show genetic linkage to schizophrenia. We examined the potential role of glucose metabolism in schizophrenia through a genome scan of affection status in schizophrenia and an empirical method for deriving P-values. Data were utilized from the NIMH Genetics Initiative for Schizophrenia dataset, which comprises a total sample consisting of 71 pedigrees containing 218 nuclear families and 987 individuals. A genome scan with 459 markers spaced at an average of 10 cM intervals was conducted using the linkage analysis program Genehunter separately for European- and African-American groups. Enzymes that regulate glycolysis were identified and the genes regulating these enzymes were located through the Online Mendelian Inheritance in Man (OMIM) website. The focus in this study was on genes located near previously reported schizophrenia susceptibility regions. The genome-wide significance of these genes to schizophrenia was assessed using permutation testing. When results were adjusted for multiple testing within and across ethnic groups, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 (PFKFB2; chromosome 1q32.2) achieved genome-wide significance (P = 0.04). In addition, hexokinase 3 (HK3; chromosome 5q35.3) was also suggestive of linkage (P = 0.09). For the European-American sample, PFKFB2 (1q32.2), hexokinase 3 (HK3; 5q35.3), and pyruvate kinase 3 (PK3; chromosome 15q23) achieved significance at the 0.05 level. None of the genes showed significance in the African-American sample. Our results provide further support for the view that genes that regulate glucose metabolism may also influence susceptibility to schizophrenia. More generally, they support the view that relationships between glucose dysregulation and schizophrenia are inherent to the disorder, and are not merely epiphenomena related to medication or other treatment factors. 相似文献
136.
Casey Graham; Plummer Sarah; Hoeltge Gerald; Scanlon David; Fasching Clare; Stanbridge Eric J. 《Human molecular genetics》1993,2(11):1921-1927
Rearrangements or deletions of chromosome 17 are the most frequentlyobserved genetic changes identified in breast tumors. Molecularanalyses suggest that in addition to the p53 gene on 17p13.1there may be at least three other tumor suppressor genes onchromosome 17 involved in breast cancer. Regions of loss ofheterozygosity (LOH) identified on 17p13.3 and 17q12-qter occurfrequently in breast tumors, and the BRCA-1 gene has been mappedto 17q21 by genetic linkage analysis. Here we provide biologicalevidence for the presence of a growth suppressor gene(s) onchromosome 17 that results In the In vitro growth suppressionof the p53 wild-type MCF 7 breast cancer cell line. We haveIntroduced a normal chromosome 17 into MCF 7 cells by microcellmediatedchromosome transfer (MMCT), and demonstrate that cells growtharrest before 10 to 12 population doublings. In contrast, theintroduction of a normal chromosome 13 had no effect upon growthof these cells either In vitro or In vivo. These data providedirect functional evidence for the presence of a growth suppressorgene(s) on chromosome 17, which is not p53, and which may representone of several gene(s) that play a critical role in the developmentof breast cancer. 相似文献
137.
138.
Grimstone SK Hodges PW 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》2003,151(2):218-224
This study evaluated the degree to which the disturbance to posture from respiration is compensated for in healthy normals
and whether this is different in people with recurrent low back pain (LBP), and to compare the changes when respiratory demand
is increased. Angular displacement of the lumbar spine and hips, and motion of the centre of pressure (COP), were recorded
with high resolution and respiratory phase was recorded from ribcage motion. With subjects standing in a relaxed posture,
recordings were made during quiet breathing, while breathing with increased dead-space to induce hypercapnoea, and while subjects
voluntarily increased their respiration to match ribcage expansion that was induced in the hypercapnoea condition. The relationship
between respiration and the movement parameters was measured from the coherence between breathing and COP and angular motion
at the frequency of respiration, and from averages triggered from the respiratory data. Small angular changes in the lumbopelvic
and hip angles were evident at the frequency of respiration in both groups. However, in quiet standing, the LBP subjects had
a greater displacement of their COP that was associated with respiration than the control subjects. The LBP group had a trend
for less hip motion. There were no changes in the movement parameters when respiratory demand increased involuntarily via
hypercapnoea, but when respiration increased voluntarily, the amplitude of motion and the displacement of the COP increased
in both groups. The present data suggest that the postural compensation to respiration counteracts at least part of the disturbance
to posture caused by respiration and that this compensation may be less effective in people with LBP. 相似文献
139.
Margaret O''Dougherty Gary G. Berntson Sarah T. Boysen Francis S. Wright Douglas Teske 《Psychophysiology》1988,25(3):305-315
Cardiac responses to non-signal stimuli and to signal stimuli in a vigilance task were examined in children born with congenital heart defects (CHD), and in normal and attention deficit disordered (ADD) subjects. Overall task performance was lower in subjects with heart defects and in the ADD group. Cardiac measures revealed that normal children displayed significantly larger heart rate deceleration to the target stimuli than did either of the clinical groups. Moreover, although no group differences were observed in the cardiac response to non-signal auditory stimuli, exaggerated heart rate deceleration was observed to vibrotactile stimuli in both the clinical groups. Regression analyses revealed that the magnitude of the cardiac response to somatosensory stimuli was predictive of task performance (both within and between subject groups), with larger responses associated with higher error rates and lower perceptual sensitivity. Results were suggestive of a predictive relationship between somatosensory reactivity and neuropsychological maturation. 相似文献
140.
Sarah L. Rowland-Jones Stephen H. Powis Julian Sutton Ian Mockridge Frances M. Gotch Nick Murray Ann B. Hill William M. Rosenberg John Trowsdale Andrew J. McMichael 《European journal of immunology》1993,23(8):1999-2004
In previous studies of antigen presentation through HLA-B27, we identified a healthy person whose lymphoblastoid cells do not present three B27-restricted viral epitopes to specific cytotoxic T lymphocytes (CTL), despite adequate cell surface expression of HLA-B2702 of normal sequence. Similar findings were observed in all members of his family sharing the HLA-A3-B2702 haplotype. The original donor, NW, carries HLA-B8 on his other class I haplotype, which his daughter, HW, has inherited. We now report a failure to present an HLA-B8-restricted epitope from influenza nucleoprotein following viral infection of NW cells, although exogenous added peptide is still presented normally. However, cells from HW, which do not carry the A3-B2702 haplotype, present the expected epitope after viral infection. Another B8-restricted epitope, from human immunodeficiency virus-gag, is presented equally well by both cell lines when infected with gag-vaccinia. This antigen processing phenotype does not correlate with any of the known human TAP-1 and TAP-2 polymorphisms. 相似文献