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21.
Evidence for genetic correlation between human cerebral white matter microstructure and inflammation
Amanda L Rodrigue Emma EM Knowles Josephine Mollon Samuel R Mathias Marinka MG Koenis Juan M Peralta Ana C Leandro Peter T Fox Emma Sprooten Peter Kochunov Rene L Olvera Ravindranath Duggirala Laura Almasy Joanne E Curran John Blangero David C Glahn 《Human brain mapping》2019,40(14):4180-4191
White matter microstructure is affected by immune system activity via the actions of circulating pro‐inflammatory cytokines. Although white matter microstructure and inflammatory measures are significantly heritable, it is unclear if overlapping genetic factors influence these traits in humans. We conducted genetic correlation analyses of these traits using randomly ascertained extended pedigrees from the Genetics of Brain Structure and Function Study (N = 1862, 59% females, ages 18–97 years; 42 ± 15.7). White matter microstructure was assessed using fractional anisotropy (FA) calculated from diffusion tensor imaging (DTI). Circulating levels (pg/mL) of pro‐inflammatory cytokines (IL‐6, IL‐8, and TNFα) phenotypically associated with white matter microstructure were quantified from blood serum. All traits were significantly heritable (h2 ranging from 0.41 to 0.66 for DTI measures and from 0.18 to 0.30 for inflammatory markers). Phenotypically, higher levels of circulating inflammatory markers were associated with lower FA values across the brain (r = ?.03 to r = ?.17). There were significant negative genetic correlations between most DTI measures and IL‐8 and TNFα, although effects for TNFα were no longer significant when covarying for body mass index. Genetic correlations between DTI measures and IL‐6 were not significant. Understanding the genetic correlation between specific inflammatory markers and DTI measures may help researchers focus questions related to inflammatory processes and brain structure. 相似文献
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Marinka M. G. Koenis Joke Durnez Amanda L. Rodrigue Samuel R. Mathias Aaron F. AlexanderBloch Jennifer A. Barrett Gaelle E. Doucet Sophia Frangou Emma E. M. Knowles Josephine Mollon Dominique Denbow Katrina Aberizk Molly Zatony Ronald J. Janssen Joanne E. Curran John Blangero Russell A. Poldrack Godfrey D. Pearlson David C. Glahn 《Human brain mapping》2021,42(6):1727
Although previous studies have highlighted associations of cannabis use with cognition and brain morphometry, critical questions remain with regard to the association between cannabis use and brain structural and functional connectivity. In a cross‐sectional community sample of 205 African Americans (age 18–70) we tested for associations of cannabis use disorder (CUD, n = 57) with multi‐domain cognitive measures and structural, diffusion, and resting state brain‐imaging phenotypes. Post hoc model evidence was computed with Bayes factors (BF) and posterior probabilities of association (PPA) to account for multiple testing. General cognitive functioning, verbal intelligence, verbal memory, working memory, and motor speed were lower in the CUD group compared with non‐users (p < .011; 1.9 < BF < 3,217). CUD was associated with altered functional connectivity in a network comprising the motor‐hand region in the superior parietal gyri and the anterior insula (p < .04). These differences were not explained by alcohol, other drug use, or education. No associations with CUD were observed in cortical thickness, cortical surface area, subcortical or cerebellar volumes (0.12 < BF < 1.5), or graph‐theoretical metrics of resting state connectivity (PPA < 0.01). In a large sample collected irrespective of cannabis used to minimize recruitment bias, we confirm the literature on poorer cognitive functioning in CUD, and an absence of volumetric brain differences between CUD and non‐CUD. We did not find evidence for or against a disruption of structural connectivity, whereas we did find localized resting state functional dysconnectivity in CUD. There was sufficient proof, however, that organization of functional connectivity as determined via graph metrics does not differ between CUD and non‐user group. 相似文献
23.
John M van Ochten Marinka CE Mos Nienke van Putte-Katier Edwin HG Oei Patrick JE Bindels Sita MA Bierma-Zeinstra Marienke van Middelkoop 《The British journal of general practice》2014,64(626):e545-e553
Background
Persistent complaints are very common after a lateral ankle sprain.Aim
To investigate possible associations between structural abnormalities on radiography and MRI, and persistent complaints after a lateral ankle sprain.Design and setting
Observational case control study on primary care patients in general practice.Method
Patients were selected who had visited their GP with an ankle sprain 6–12 months before the study; all received a standardised questionnaire, underwent a physical examination, and radiography and MRI of the ankle. Patients with and without persistent complaints were compared regarding structural abnormalities found on radiography and MRI; analyses were adjusted for age, sex, and body mass index.Results
Of the 206 included patients, 98 had persistent complaints and 108 did not. No significant differences were found in structural abnormalities between patients with and without persistent complaints. In both groups, however, many structural abnormalities were found on radiography in the talocrural joint (47.2% osteophytes and 45.1% osteoarthritis) and the talonavicular joint (36.5% sclerosis). On MRI, a high prevalence was found of bone oedema (33.8%) and osteophytes (39.5) in the talocrural joint; osteophytes (54.4%), sclerosis (47.2%), and osteoarthritis (55.4%, Kellgren and Lawrence grade >1) in the talonavicular joint, as well as ligament damage (16.4%) in the anterior talofibular ligament.Conclusion
The prevalence of structural abnormalities is high on radiography and MRI in patients presenting in general practice with a previous ankle sprain. There is no difference in structural abnormalities, however, between patients with and without persistent complaints. Using imaging only will not lead to diagnosis of the explicit reason for the persistent complaint. 相似文献24.
Lesley Pritchard PT MSc PhD Katherine S. Bright RN PhD Catharine M. Walsh MD MEd PhD Susan Samuel MD Queenie K. W. Li BSc Krista Wollny RN MN PhD Marinka Twilt MD MScE PhD Lianne Tomfohr-Madsen PhD RPsych Linda Pires BSc Gina Dimitropoulos MSW PhD 《Journal of evaluation in clinical practice》2023,29(1):59-68
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Ovrutsky AR Kartalija M Bai X Chan ED 《American journal of respiratory and critical care medicine》2011,184(7):860; author reply 860-860; author reply 861
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Bai X Ovrutsky AR Kartalija M Chmura K Kamali A Honda JR Oberley-Deegan RE Dinarello CA Crapo JD Chang LY Chan ED 《International immunology》2011,23(11):679-691
Lung disease due to Mycobacterium avium complex (MAC) organisms is increasing. A greater understanding of the host immune response to MAC organisms will provide a foundation to develop novel therapies for these recalcitrant infections. IL-32 is a newly described pro-inflammatory cytokine that enhances host immunity against various microbial pathogens. Cytokines that induce IL-32 such as interferon-gamma, IL-18, IL-12 and tumor necrosis factor-alpha are of considerable importance to mycobacterial immunity. We performed immunohistochemistry and morphometric analysis to quantify IL-32 expression in the lungs of 11 patients with MAC lung disease and 10 controls with normal lung tissues. After normalizing for basement membrane length, there was a profound increase in IL-32 expression in the airway epithelial cells of the MAC-infected lungs compared with controls. Following normalization for alveolar surface area, there was a trend toward increased IL-32 expression in type II alveolar cells and alveolar macrophages in the lungs of MAC patients. Human airway epithelial cells (BEAS-2B) infected with M. avium produced IL-32 by a nuclear factor-kappa B-dependent mechanism. In both BEAS-2B cells and human monocyte-derived macrophages, exogenous IL-32γ significantly reduced the growth of intracellular M. avium. This finding was corroborated by an increase in the number of intracellular M. avium recovered from THP-1 monocytes silenced for endogenous IL-32 expression. The anti-mycobacterial effect of IL-32 may be due, in part, to increased apoptosis of infected cells. These findings indicate that IL-32 facilitates host defense against MAC organisms but may also contribute to the airway inflammation associated with MAC pulmonary disease. 相似文献
30.
Association between structural brain network efficiency and intelligence increases during adolescence 下载免费PDF全文
Marinka M.G. Koenis Rachel M. Brouwer Suzanne C. Swagerman Inge L.C. van Soelen Dorret I. Boomsma Hilleke E. Hulshoff Pol 《Human brain mapping》2018,39(2):822-836
Adolescence represents an important period during which considerable changes in the brain take place, including increases in integrity of white matter bundles, and increasing efficiency of the structural brain network. A more efficient structural brain network has been associated with higher intelligence. Whether development of structural network efficiency is related to intelligence, and if so to which extent genetic and environmental influences are implicated in their association, is not known. In a longitudinal study, we mapped FA‐weighted efficiency of the structural brain network in 310 twins and their older siblings at an average age of 10, 13, and 18 years. Age‐trajectories of global and local FA‐weighted efficiency were related to intelligence. Contributions of genes and environment were estimated using structural equation modeling. Efficiency of brain networks changed in a non‐linear fashion from childhood to early adulthood, increasing between 10 and 13 years, and leveling off between 13 and 18 years. Adolescents with higher intelligence had higher global and local network efficiency. The dependency of FA‐weighted global efficiency on IQ increased during adolescence (rph=0.007 at age 10; 0.23 at age 18). Global efficiency was significantly heritable during adolescence (47% at age 18). The genetic correlation between intelligence and global and local efficiency increased with age; genes explained up to 87% of the observed correlation at age 18. In conclusion, the brain's structural network differentiates depending on IQ during adolescence, and is under increasing influence of genes that are also associated with intelligence as it develops from late childhood to adulthood. 相似文献