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Hassona Shahd M. Saad Entsar A. Kiwan Hala A. Hassanien Mohamed M. 《Investigational new drugs》2022,40(4):681-689
Investigational New Drugs - Although many cancer drugs are clinically approved, they still suffer from no adequate efficiency or drug resistance, or bad side effects. Therefore, developing safer... 相似文献
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Marco Bandini Sebastiano Nazzani Michele Marchioni Felix Preisser Zhe Tian Marco Moschini Firas Abdollah Nazareno Suardi Markus Graefen Francesco Montorsi Shahrokh F. Shariat Fred Saad Alberto Briganti Pierre I. Karakiewicz 《Clinical genitourinary cancer》2019,17(1):72-78.e4
Background
The rate of noninterventional treatment (NIT) in prostate cancer (PCa) active surveillance (AS) candidates is on the rise. However, contemporary data are unavailable. We described community-based NIT rates within 16 Surveillance Epidemiology and End Results (SEER) registries between 2010 and 2014.Patients and Methods
We identified 23,360 PCa patients who fulfilled the University of California San Francisco AS criteria (prostate-specific antigen [PSA] < 10 ng/mL, clinical T stage ≤ T2a, Gleason score ≤ 6, and positive cores < 33%). Annual NIT rates as well as patient distribution according to PSA, age, number of positive cores, and clinical T stage were studied. Multivariable logistic regression analysis tested NIT predictors.Results
Between 2010 and 2014, the NIT rate increased from 30.2% to 57.5% (P = .004). Within 16 SEER registries, NIT rates ranged from 25.9% to 62%. NIT rate increased uniformly within all examined registries. Of patient and tumor characteristics (PSA > 4 ng/mL, cT2a and > 1 positive core) only the proportion of NIT patients aged < 65 years increased over time from 47.3% to 53.2% (P = .03). By multivariable logistic regression analysis predicting NIT rate, older age (odd ratio [OR] = 1.05), more contemporary year of diagnosis (OR = 1.41), and being unmarried (OR = 1.45) and uninsured (OR = 2.41) were independent predictors.Conclusion
The NIT rate has markedly increased across all examined SEER registries. Nonetheless, important differences distinguish those who received high-end NIT from low-end NIT. PCa characteristics of NIT patients remained unchanged over time. However, in addition to geographical differences in NIT rates, patient characteristics such as age, marital status, and insurance status represent potential NIT access barriers. 相似文献5.
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Rebecca Robillard Karianne Dion Marie‐Helene Pennestri Elizaveta Solomonova Elliott Lee Mysa Saad Anthony Murkar Roger Godbout Jodi D. Edwards Lena Quilty Alexander R. Daros Raj Bhatla Tetyana Kendzerska 《Journal of sleep research》2021,30(1):e13231
This study aimed to evaluate changes in sleep during the COVID‐19 outbreak, and used data‐driven approaches to identify distinct profiles of changes in sleep‐related behaviours. Demographic, behavioural and psychological factors associated with sleep changes were also investigated. An online population survey assessing sleep and mental health was distributed between 3 April and 24 June 2020. Retrospective questions were used to estimate temporal changes from before to during the outbreak. In 5,525 Canadian respondents (67.1% females, 16–95 years old: Mean ± SD = 55.6 ± 16.3 years), wake‐up times were significantly delayed relative to pre‐outbreak estimates (p < .001, = 0.04). Occurrences of clinically meaningful sleep difficulties significantly increased from 36.0% before the outbreak to 50.5% during the outbreak (all p < .001, g ≥ 0.27). Three subgroups with distinct profiles of changes in sleep behaviours were identified: “Reduced Time in Bed”, “Delayed Sleep” and “Extended Time in Bed”. The “Reduced Time in Bed” and “Delayed Sleep” subgroups had more adverse sleep outcomes and psychological changes during the outbreak. The emergence of new sleep difficulties was independently associated with female sex, chronic illnesses, being employed, family responsibilities, earlier wake‐up times, higher stress levels, as well as heavier alcohol use and television exposure. The heterogeneity of sleep changes in response to the pandemic highlights the need for tailored interventions to address sleep problems. 相似文献
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Ziad Saad Derrek Hibar Maggie Fedgchin Vanina Popova Maura L Furey Jaskaran B Singh Hartmuth Kolb Wayne C Drevets Guang Chen 《The international journal of neuropsychopharmacology / official scientific journal of the Collegium Internationale Neuropsychopharmacologicum (CINP)》2020,23(9):549
BackgroundAt ketamine and esketamine doses at which antidepressant doses are achieved, these agents are relatively selective, noncompetitive, N-methyl-D-aspartate receptor antagonists. However, at substantially higher doses, ketamine has shown mu-opioid receptor (MOR–gene symbol: OPRM1) agonist effects. Preliminary clinical studies showed conflicting results on whether naltrexone, a MOR antagonist, blocks the antidepressant action of ketamine. We examined drug-induced or endogenous MOR involvement in the antidepressant and dissociative responses to esketamine by assessing the effects of a functional single nucleotide polymorphism rs1799971 (A118G) of OPRM1, which is known to alter MOR agonist-mediated responses.MethodsParticipants with treatment-resistant depression from 2 phase III, double-blind, controlled trials of esketamine (or placebo) nasal spray plus an oral antidepressant were genotyped for rs1799971. Participants received the experimental agents twice weekly for 4 weeks. Antidepressant responses were rated using the change in Montgomery–Åsberg Depression Rating Scale (MADRS) score on days 2 and 28 post-dose initiation, and dissociative side effects were assessed using the Clinician-Administered Dissociative-States Scale at 40 minutes post-dose on days 1 and 25.ResultsIn the esketamine + antidepressant arm, no significant genotype effect of single nucleotide polymorphism rs1799971 (A118G) on MADRS score reductions was detected on either day 2 or 28. By contrast, in the antidepressant + placebo arm, there was a significant genotype effect on MADRS score reductions on day 2 and a nonsignificant trend on day 28 towards an improvement in depression symptoms in G-allele carriers. No significant genotype effects on dissociative responses were detected.ConclusionsVariation in rs1799971 (A118G) did not affect the antidepressant response to esketamine + antidepressant. Antidepressant response to antidepressant + placebo was increased in G-allele carriers, compatible with previous reports that release of endorphins/enkephalins may play a role in mediating placebo effect.Trial Registration and NCT02417064; NCT02418585www.clinicaltrials.gov 相似文献
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Gain of chromosome 1q (+1q) is one of the most common recurrent cytogenetic abnormalities in multiple myeloma (MM), occurring in approximately 40% of newly diagnosed cases. Although it is often considered a poor prognostic marker in MM, +1q has not been uniformly adopted as a high-risk cytogenetic abnormality in guidelines. Controversy exists regarding the importance of copy number, as well as whether +1q is itself a driver of poor outcomes or merely a common passenger genetic abnormality in biologically unstable disease. Although the identification of a clear pathogenic mechanism from +1q remains elusive, many genes at the 1q21 locus have been proposed to cause early progression and resistance to anti-myeloma therapy. The plethora of potential drivers suggests that +1q is not only a causative factor or poor outcomes in MM but may be targetable and/or predictive of response to novel therapies. This review will summarize our current understanding of the pathogenesis of +1q in plasma cell neoplasms, the impact of 1q copy number, identify potential genetic drivers of poor outcomes within this subset, and attempt to clarify its clinical significance and implications for the management of patients with multiple myeloma.Subject terms: Cancer genomics, Myeloma, Myeloma 相似文献