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51.
Lisa Arnetz Mozhgan Dorkhan Michael Alvarsson Kerstin Brismar Neda Rajamand Ekberg 《Acta diabetologica》2014,51(2):185-192
Excess cortisol and GH induce insulin resistance, a central feature of type 2 diabetes (T2D). To study whether the insulin sensitizer pioglitazone affects basal cortisol levels and the GH–IGF-I axis in patients with T2D. Forty-eight patients with T2D (men/women = 28:20, age 61 ± 1 years, BMI 31 ± 0.6 kg/m2) were treated for 26 weeks with pioglitazone 30–45 mg daily in addition to their preexisting therapy. Insulin, proinsulin, HbA1c, IGF-I, IGFBP-1, and basal cortisol were analyzed before and after treatment. Pioglitazone decreased proinsulin/insulin ratio and HbA1c decreased (HbA1c from 7.8 ± 0.2 to 6.6 ± 0.2 % in men and from 7.6 ± 0.2 to 6.1 ± 0.2 % in women, p < 0.001 in both). There was a redistribution of fat but no change in waist circumference. IGF-I and adiponectin increased (p ≤ 0.001) in both genders. IGFBP-1 increased but significantly only for the whole group (p = 0.033). Triglycerides decreased significantly in women only (p = 0.015). Before treatment, women had lower basal cortisol (p = 0.045). Basal cortisol increased in women (from 390 ± 26 to 484 ± 32 nmol/L, p = 0.020) but not in men and did not differ between genders at week 26. ΔIGFBP-1 correlated with Δcortisol (r = 0.458; p = 0.049) and Δadiponectin (r = 0.600; p = 0.005) in women only. In addition to the known effect of improving insulin sensitivity, pioglitazone increased IGF-I regardless of gender and in women also increased basal cortisol. Increased IGF-I may contribute to improved insulin sensitivity after treatment. There seems to be gender differences in treatment responses to pioglitazone on lipid metabolism and basal cortisol, perhaps correcting different mechanisms of insulin resistance between genders. 相似文献
52.
Talia M. Nir Neda Jahanshad Edgar Busovaca Lauren Wendelken Krista Nicolas Paul M. Thompson Victor G. Valcour 《Human brain mapping》2014,35(3):975-992
People with HIV are living longer as combination antiretroviral therapy (cART) becomes more widely available. However, even when plasma viral load is reduced to untraceable levels, chronic HIV infection is associated with neurological deficits and brain atrophy beyond that of normal aging. HIV is often marked by cortical and subcortical atrophy, but the integrity of the brain's white matter (WM) pathways also progressively declines. Few studies focus on older cohorts where normal aging may be compounded with HIV infection to influence deficit patterns. In this relatively large diffusion tensor imaging (DTI) study, we investigated abnormalities in WM fiber integrity in 56 HIV+ adults with access to cART (mean age: 63.9 ± 3.7 years), compared to 31 matched healthy controls (65.4 ± 2.2 years). Statistical 3D maps revealed the independent effects of HIV diagnosis and age on fractional anisotropy (FA) and diffusivity, but we did not find any evidence for an age by diagnosis interaction in our current sample. Compared to healthy controls, HIV patients showed pervasive FA decreases and diffusivity increases throughout WM. We also assessed neuropsychological (NP) summary z‐score associations. In both patients and controls, fiber integrity measures were associated with NP summary scores. The greatest differences were detected in the corpus callosum and in the projection fibers of the corona radiata. These deficits are consistent with published NP deficits and cortical atrophy patterns in elderly people with HIV. Hum Brain Mapp 35:975–992, 2014. © 2013 Wiley Periodicals, Inc. 相似文献
53.
A commonly carried genetic variant in the delta opioid receptor gene,OPRD1, is associated with smaller regional brain volumes: Replication in elderly and young populations 下载免费PDF全文
Florence F. Roussotte Neda Jahanshad Derrek P. Hibar Elizabeth R. Sowell Omid Kohannim Marina Barysheva Narelle K. Hansell Katie L. McMahon Greig I. de Zubicaray Grant W. Montgomery Nicholas G. Martin Margaret J. Wright Arthur W. Toga Clifford R. Jack Jr Michael W. Weiner Paul M. Thompson the ADNI 《Human brain mapping》2014,35(4):1226-1236
Delta opioid receptors are implicated in a variety of psychiatric and neurological disorders. These receptors play a key role in the reinforcing properties of drugs of abuse, and polymorphisms in OPRD1 (the gene encoding delta opioid receptors) are associated with drug addiction. Delta opioid receptors are also involved in protecting neurons against hypoxic and ischemic stress. Here, we first examined a large sample of 738 elderly participants with neuroimaging and genetic data from the Alzheimer's Disease Neuroimaging Initiative. We hypothesized that common variants in OPRD1 would be associated with differences in brain structure, particularly in regions relevant to addictive and neurodegenerative disorders. One very common variant (rs678849) predicted differences in regional brain volumes. We replicated the association of this single‐nucleotide polymorphism with regional tissue volumes in a large sample of young participants in the Queensland Twin Imaging study. Although the same allele was associated with reduced volumes in both cohorts, the brain regions affected differed between the two samples. In healthy elderly, exploratory analyses suggested that the genotype associated with reduced brain volumes in both cohorts may also predict cerebrospinal fluid levels of neurodegenerative biomarkers, but this requires confirmation. If opiate receptor genetic variants are related to individual differences in brain structure, genotyping of these variants may be helpful when designing clinical trials targeting delta opioid receptors to treat neurological disorders. Hum Brain Mapp 35:1226–1236, 2014. © 2013 Wiley Periodicals, Inc. 相似文献
54.
55.
Bahman Mosallanejad Reza Avizeh Masoud Ghorbanpour Neda Mohammadian 《Comparative clinical pathology》2014,23(5):1233-1236
Canine brucellosis, caused by Brucella canis, is an important cause of abortions, stillbirths, uveitis, epididymitis, orchitis, and sperm abnormalities in dogs. Anterior uveitis is one of the most common ocular diseases in dogs. The aim of this study was to describe the clinical and diagnostic features of anterior uveitis in dogs affected with B. canis in the Ahvaz district, southwestern Iran. A total of 243 blood samples were obtained from urban dogs between 2006 and 2010 and examined by immuno-chromatography assay (Anigen Rapid C. Brucella Ab Test Kit). Prevalence to B. canis antibodies was 6.58 % (16 out of 243) in the studied dogs. B. canis-induced anterior uveitis was seen in two German Shepherd dogs (12.5 %; 2 out of 16), the first was a 3.5-year-old male and the second was a 2.5-year-old female. Clinical ophthalmologic abnormalities included moderate anterior uveitis, mild conjunctival hyperemia, and iris hyperpigmentation. Following routine treatment (a median of 9 weeks from the onset of therapy), ocular inflammation resolved and serological tests were negative. The present study shows that ocular inflammation due to B. canis is present among the urban dog population in the Ahvaz district, Iran. B. canis infection should be included in the differential diagnosis for dogs with intraocular inflammation, regardless of previous history. 相似文献
56.
57.
Seyed Hossein Mohseni Salehi Monfared Gholamreza Shirani Neda Moslemi Faranak Noori Amir Raee 《Clinical Case Reports》2022,10(2)
Shallow lingual vestibule and lack of keratinized attached mucosa are considered risk factors for the long‐term success of dental implants. This article describes a modified surgical approach accompanied by a free gingival graft to correct the shallow lingual/buccal vestibule and to increase the keratinized tissue around dental implants. 相似文献
58.
Salarinasab Sadegh Salimi Leila Alidadiani Neda Shokrollahi Elhameh Arzhanga Pishva Karbasforush Saedeh Marofi Faroogh Nasirzadeh Mahdieh Rahbarghazi Reza Nourazarian Alireza Nikanfar Masoud 《Journal of molecular neuroscience : MN》2020,70(6):819-834
Journal of Molecular Neuroscience - Alzheimer's disease is associated with biochemical and histopathological changes characterized by molecular abnormalities. Due to the lack of effective... 相似文献
59.
Bhim M. Adhikari Juergen Dukart Joerg F. Hipp Anna Forsyth Rebecca McMillan Suresh D. Muthukumaraswamy Meghann C. Ryan L. Elliot Hong Simon B. Eickhoff Neda Jahandshad Paul M. Thompson Laura M. Rowland Peter Kochunov 《Human brain mapping》2020,41(3):767-778
Subanesthetic administration of ketamine is a pharmacological model to elicit positive and negative symptoms of psychosis in healthy volunteers. We used resting‐state pharmacological functional MRI (rsPhfMRI) to identify cerebral networks affected by ketamine and compared them to the functional connectivity (FC) in schizophrenia. Ketamine can produce sedation and we contrasted its effects with the effects of the anxiolytic drug midazolam. Thirty healthy male volunteers (age = 19–37 years) underwent a randomized, three‐way, cross‐over study consisting of three imaging sessions, with 48 hr between sessions. A session consisted of a control period followed by infusion of placebo or ketamine or midazolam. The ENIGMA rsfMRI pipeline was used to derive two long‐distance (seed‐based and dual‐regression) and one local (regional homogeneity, ReHo) FC measures. Ketamine induced significant reductions in the connectivity of the salience network (Cohen's d: 1.13 ± 0.28, p = 4.0 × 10?3), auditory network (d: 0.67 ± 0.26, p = .04) and default mode network (DMN, d: 0.63 ± 0.26, p = .05). Midazolam significantly reduced connectivity in the DMN (d: 0.77 ± 0.27, p = .03). The effect sizes for ketamine for resting networks showed a positive correlation (r = .59, p = .07) with the effect sizes for schizophrenia‐related deficits derived from ENIGMA's study of 261 patients and 327 controls. Effect sizes for midazolam were not correlated with the schizophrenia pattern (r = ?.17, p = .65). The subtraction of ketamine and midazolam patterns showed a significant positive correlation with the pattern of schizophrenia deficits (r = .68, p = .03). RsPhfMRI reliably detected the shared and divergent pharmacological actions of ketamine and midazolam on cerebral networks. The pattern of disconnectivity produced by ketamine was positively correlated with the pattern of connectivity deficits observed in schizophrenia, suggesting a brain functional basis for previously poorly understood effects of the drug. 相似文献
60.
Peter Kochunov L. Elliot Hong Emily L. Dennis Rajendra A. Morey David F. Tate Elisabeth A. Wilde Mark Logue Sinead Kelly Gary Donohoe Pauline Favre Josselin Houenou Christopher R. K. Ching Laurena Holleran Ole A. Andreassen Laura S. van Velzen Lianne Schmaal Julio E. Villaln-Reina Carrie E. Bearden Fabrizio Piras Gianfranco Spalletta Odile A. van den Heuvel Dick J. Veltman Dan J. Stein Meghann C. Ryan Yunlong Tan Theo G. M. van Erp Jessica A. Turner Liz Haddad Talia M. Nir David C. Glahn Paul M. Thompson Neda Jahanshad 《Human brain mapping》2022,43(1):194-206
The ENIGMA-DTI (diffusion tensor imaging) workgroup supports analyses that examine the effects of psychiatric, neurological, and developmental disorders on the white matter pathways of the human brain, as well as the effects of normal variation and its genetic associations. The seven ENIGMA disorder-oriented working groups used the ENIGMA-DTI workflow to derive patterns of deficits using coherent and coordinated analyses that model the disease effects across cohorts worldwide. This yielded the largest studies detailing patterns of white matter deficits in schizophrenia spectrum disorder (SSD), bipolar disorder (BD), major depressive disorder (MDD), obsessive–compulsive disorder (OCD), posttraumatic stress disorder (PTSD), traumatic brain injury (TBI), and 22q11 deletion syndrome. These deficit patterns are informative of the underlying neurobiology and reproducible in independent cohorts. We reviewed these findings, demonstrated their reproducibility in independent cohorts, and compared the deficit patterns across illnesses. We discussed translating ENIGMA-defined deficit patterns on the level of individual subjects using a metric called the regional vulnerability index (RVI), a correlation of an individual's brain metrics with the expected pattern for a disorder. We discussed the similarity in white matter deficit patterns among SSD, BD, MDD, and OCD and provided a rationale for using this index in cross-diagnostic neuropsychiatric research. We also discussed the difference in deficit patterns between idiopathic schizophrenia and 22q11 deletion syndrome, which is used as a developmental and genetic model of schizophrenia. Together, these findings highlight the importance of collaborative large-scale research to provide robust and reproducible effects that offer insights into individual vulnerability and cross-diagnosis features. 相似文献