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Roselien Pas Mira Meeus Anneleen Malfliet Isabel Baert Sophie Van Oosterwijck Laurence Leysen Jo Nijs Kelly Ickmans 《Revista brasileira de fisioterapia (S?o Carlos (S?o Paulo, Brazil))》2018,22(3):248-253
Background
Current treatment for adults with chronic pain often includes Pain Neuroscience Education (PNE) to make people understand the nature underlying their pain and thus provides a clear rational for a biopsychosocial approach. Despite recommendations to use Pain Neuroscience Education as well in children with chronic pain, a specific program, tailored to children aged 6–12 years is lacking.Objectives
The aim of this study was to develop a Pain Neuroscience Education program for children with chronic pain and test its feasibility.Methods
First the internet and scientific literature was searched for sources (e.g., books, videos, etc.) that might be supportive in teaching children about the neurophysiology of pain. Based on this content, we developed a Pain Neuroscience Education program for children, ‘PNE4Kids’, which was tested for feasibility in three groups of healthy children (n = 18; 9 girls and 9 boys) aged between 6 and 12 years old.Results and conclusions
This paper provides both scientists and clinicians with a specific program to explain the neurophysiology of pain to children with chronic pain, since it is past high time to use a modern neuroscience approach in this vulnerable population. Further research should examine the effectiveness of this developed PNE4Kids program on pain-related outcomes in children with chronic pain.Registration number: NCT02880332 (https://clinicaltrials.gov/ct2/show/NCT02880332). 相似文献4.
Anneleen Pletinck Griet Glorieux Eva Schepers Gerald Cohen Bertrand Gondouin Maria Van Landschoot Sunny Eloot Angelique Rops Johan Van de Voorde An De Vriese Johan van der Vlag Philippe Brunet Wim Van Biesen Raymond Vanholder 《Journal of the American Society of Nephrology : JASN》2013,24(12):1981-1994
Leukocyte activation and endothelial damage both contribute to cardiovascular disease, a major cause of morbidity and mortality in CKD. Experimental in vitro data link several protein-bound uremic retention solutes to the modulation of inflammatory stimuli, including endothelium and leukocyte responses and cardiovascular damage, corroborating observational in vivo data. However, the impact of these uremic toxins on the crosstalk between endothelium and leukocytes has not been assessed. This study evaluated the effects of acute and continuous exposure to uremic levels of indoxylsulfate (IS), p-cresylsulfate (pCS), and p-cresylglucuronide (pCG) on the recruitment of circulating leukocytes in the rat peritoneal vascular bed using intravital microscopy. Superfusion with IS induced strong leukocyte adhesion, enhanced extravasation, and interrupted blood flow, whereas pCS caused a rapid increase in leukocyte rolling. Superfusion with pCS and pCG combined caused impaired blood flow and vascular leakage but did not further enhance leukocyte rolling over pCS alone. Intravenous infusion with IS confirmed the superfusion results and caused shedding of heparan sulfate, pointing to disruption of the glycocalyx as the mechanism likely mediating IS-induced flow stagnation. These results provide the first clear in vivo evidence that IS, pCS, and pCG exert proinflammatory effects that contribute to vascular damage by stimulating crosstalk between leukocytes and vessels.Cardiovascular disease remains the most important cause of death among patients with CKD,1 and it is associated with a baseline inflammatory status.2,3 Atherosclerosis is highly prevalent and advances more rapidly in individuals with renal dysfunction compared with the general population.4–6 A key role in the development of atherosclerosis is played by leukocyte–endothelial interactions.2CKD is characterized by the progressive retention of a host of solutes. A substantial number of these compounds is protein-bound.7,8 The indole indoxylsulfate (IS) and the phenolic conjugates p-cresylsulfate (pCS) and p-cresylglucuronide (pCG) are prototype members of this group. Observational data associate these solutes with enhanced cardiovascular damage and progression of kidney failure, and in in vitro experiments, several underlying isolated molecular mechanisms support the link with these observational data.8–12 Although for all three compounds, one of two key mechanisms of vascular damage (i.e., leukocyte activation or endothelial dysfunction) have been shown in separate in vitro models, they were, to the best of our knowledge, never directly assessed by evaluating the complicated crosstalk between endothelium and leukocytes in an in vivo situation. Intravital microscopy permits in vivo visualization of leukocyte recruitment in translucent tissues in real time. This technique was already applied successfully by our group to study harmful effects of peritoneal dialysis solutions on peritoneal membrane physiology.13The present study evaluates the effects of an acute peritoneal superfusion of the protein-bound uremic compounds IS, pCS, and pCG and also, continuous intravenous infusion of IS on the recruitment of circulating leukocytes in the rat peritoneal vascular bed using this intravital microscopic method. 相似文献
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Annick Moens C. Janneke van der Woude Mette Julsgaard Evelien Humblet Juliette Sheridan Daniel C. Baumgart Cyrielle Gilletta De Saint-Joseph Stéphane Nancey Jean-François Rahier Peter Bossuyt Anneline Cremer Sophie Dewit Carl Eriksson Frank Hoentjen Thomas Krause Edouard Louis Elisabeth Macken Zoran Milenkovic Jochen Nijs Annelies Posen Anneleen Van Hootegem Wouter Van Moerkercke Séverine Vermeire Ariella Bar-Gil Shitrit Marc Ferrante 《Alimentary pharmacology & therapeutics》2020,51(1):129-138
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R. Achterbergh L. A. Lammers L. Kuijsten H. J. Klümpen R. A. A. Mathôt J. A. Romijn 《Clinical toxicology (Philadelphia, Pa.)》2019,57(1):42-49
Introduction: Fasting, as well as a high-fat diet, might increase the risk on acetaminophen-induced toxicity after an acute overdose. Therefore, it has been suggested to lower the threshold for acetylcysteine treatment to prevent liver injury in case of fasting. This study aims to investigate the effects of 36?hours of fasting and three days of a hypercaloric high-fat diet on acetaminophen measurement and exposure.Methods: Nine healthy male subjects were enrolled in a randomized crossover intervention study. Subjects received 1000mg oral acetaminophen after an overnight fast following: (1) regular diet,(2) 36h of fasting and (3) three days of a hypercaloric high-fat diet consisting of 500ml of cream (1715?kcal) supplemented to their regular diet. Pharmacokinetic parameters were determined by non-compartmental analysis. Samples were analyzed by an enzymatic colorimetric method used in routine practice and by LC-MS/MS being the gold standard. Agreement between these methods was assessed by the Bland–Altman method.Results: Short-term fasting increased acetaminophen exposure by 20% (ΔAUC0-8?hours, p?=?.04) in comparison with the control diet. Three days of hypercaloric high-fat diet did not affect acetaminophen exposure (ΔAUC0–8 hours= 9%, p?=?.67). The intraclass correlation coefficient between the enzymatic assay and LC-MS/MS methods of the fasting samples was 0.46 (0.28–0.61), compared to 0.87 (0.81–0.92) and 0.87 (0.79–0.91) in the control and high-fat samples respectively.Conclusions: Short-term fasting increases acetaminophen exposure in healthy subjects, whereas no effect is observed after a high-fat diet. Furthermore, short-term fasting decreases the accuracy of the enzymatic colorimetric method when measuring relatively low acetaminophen concentrations. This suggests considering nutritional status when assessing the risk of acetaminophen-induced toxicity, although further research at toxic doses is needed. 相似文献
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Anneleen Malfliet Thomas Bilterys Eveline Van Looveren Mira Meeus Lieven Danneels Kelly Ickmans Barbara Cagnie Olivier Mairesse Daniel Neu Maarten Moens Dorien Goubert Steven J. Kamper Jo Nijs 《Revista brasileira de fisioterapia (S?o Carlos (S?o Paulo, Brazil))》2019,23(1):62-70
Background
Insomnia is a highly prevalent and debilitating comorbidity that is often not addressed in therapy for chronic spinal pain (CSP). Given the close interaction between insomnia and CSP severity and related disability, targeting sleep problems during therapy could improve treatment outcomes in these patients.Objective
Can cognitive behavioral therapy for insomnia (CBT-I) combined with the modern neuroscience approach (i.e. pain neuroscience education and cognition-targeted exercise therapy) reduce pain and improve sleep, physical activity and function in people with CSP and comorbid insomnia?Methods
Participants: One-hundred-twenty participants with chronic spinal pain and comorbid insomnia Intervention: CBT-I combined with the modern neuroscience approach (experimental) compared to the modern neuroscience approach alone (control). Both interventions start with three sessions of pain neuroscience education, followed by six sessions of CBT-I and nine sessions of cognition-targeted exercise therapy in the experimental group, or 15 sessions of cognition-targeted exercise therapy in the control group.Measurements
Primary outcome measure: self-reported pain severity (Brief Pain Inventory). Secondary outcome measures: pain sensitivity (pressure pain thresholds, and online questionnaires), sleep-related outcomes (home-based polysomnography and online questionnaires), physical activity (actigraphy), and function (online questionnaires). Online questionnaires will be completed at baseline, directly post-treatment, and at 3, 6 and 12 months post-treatment. Polysomnography, pressure pain thresholds and actigraphy will be carried out at baseline, post-treatment and at 12 months follow-up.Discussion
Findings may provide (1) a novel therapeutic approach for people with CSP and comorbid insomnia to improve pain, sleep, physical activity and function, and (2) new treatment guidelines for professionals.Trial registration
Clinicaltrials.gov NCT03482856 (https://clinicaltrials.gov/ct2/show/NCT03482856). 相似文献9.
Hans Hallez Bart Vanrumste Roberta Grech Joseph Muscat Wim De Clercq Anneleen Vergult Yves D'Asseler Kenneth P Camilleri Simon G Fabri Sabine Van Huffel Ignace Lemahieu 《Journal of neuroengineering and rehabilitation》2007,4(1):1-29
Background
The aim of electroencephalogram (EEG) source localization is to find the brain areas responsible for EEG waves of interest. It consists of solving forward and inverse problems. The forward problem is solved by starting from a given electrical source and calculating the potentials at the electrodes. These evaluations are necessary to solve the inverse problem which is defined as finding brain sources which are responsible for the measured potentials at the EEG electrodes.Methods
While other reviews give an extensive summary of the both forward and inverse problem, this review article focuses on different aspects of solving the forward problem and it is intended for newcomers in this research field.Results
It starts with focusing on the generators of the EEG: the post-synaptic potentials in the apical dendrites of pyramidal neurons. These cells generate an extracellular current which can be modeled by Poisson's differential equation, and Neumann and Dirichlet boundary conditions. The compartments in which these currents flow can be anisotropic (e.g. skull and white matter). In a three-shell spherical head model an analytical expression exists to solve the forward problem. During the last two decades researchers have tried to solve Poisson's equation in a realistically shaped head model obtained from 3D medical images, which requires numerical methods. The following methods are compared with each other: the boundary element method (BEM), the finite element method (FEM) and the finite difference method (FDM). In the last two methods anisotropic conducting compartments can conveniently be introduced. Then the focus will be set on the use of reciprocity in EEG source localization. It is introduced to speed up the forward calculations which are here performed for each electrode position rather than for each dipole position. Solving Poisson's equation utilizing FEM and FDM corresponds to solving a large sparse linear system. Iterative methods are required to solve these sparse linear systems. The following iterative methods are discussed: successive over-relaxation, conjugate gradients method and algebraic multigrid method.Conclusion
Solving the forward problem has been well documented in the past decades. In the past simplified spherical head models are used, whereas nowadays a combination of imaging modalities are used to accurately describe the geometry of the head model. Efforts have been done on realistically describing the shape of the head model, as well as the heterogenity of the tissue types and realistically determining the conductivity. However, the determination and validation of the in vivo conductivity values is still an important topic in this field. In addition, more studies have to be done on the influence of all the parameters of the head model and of the numerical techniques on the solution of the forward problem. 相似文献10.
Karin Leunen Olivier Gevaert Anneleen Daemen Vanessa Vanspauwen Geneviève Michils Bart De Moor Philippe Moerman Ignace Vergote Eric Legius 《Human mutation》2009,30(12):1693-1702
Array CGH was used to identify recurrent copy number alterations (RCNA) characteristic of either BRCA1-related or sporadic ovarian cancer. After preprocessing, both groups of patients were modeled using a recurrent Hidden Markov Model to detect RCNA. RCNA with a probability higher than 80% were called. After removing RCNA present in both groups, the genes present in the remaining RCNA were investigated for enrichment of pathways from external databases. More RCNA were observed in the BRCA1 group, and they display more losses than gains compared to the sporadic group. When focusing on the type of RCNA, no significant difference in length was seen for the gains, but there was a statistically significant difference for the losses. In the sporadic group, a great proportion of the altered regions contain genes known to have a function in cell adhesion and complement activation, whereas the BRCA1 samples are characterized by alterations in the HOX genes, metalloproteinases, tumor suppressor genes, and the estrogen-signaling pathways. We conclude that BRCA1 ovarian tumors present a different type, number, and length of RCNA; a huge amount of the genome is lost, resulting in important genomic instability. Moreover, important biological pathways are altered differentially when compared to the sporadic group. Hum Mutat 30:1–10, 2009. © 2009 Wiley-Liss, Inc. 相似文献