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排序方式: 共有429条查询结果,搜索用时 31 毫秒
1.
Olle Zetterström Christer Andersson Leif Eriksson ers Fredriksson Johan Friskopp Gunnar Heden Bernt Jansson Tord Lundgren Rolf Nilveus ers Olsson Stefan Renvert Lars Salonen Lars Sjöström ers Winell ers Östgren Stina Gestrelius 《Journal of clinical periodontology》1997,24(9):697-704
Abstract The aim of the present clinical trial was to test tolerability during 2 treatments with EMDOGAIN® in a large number of patients. An open, controlled study design in 10 Swedish specialist clinics was chosen, with a test group of 107 patients treated with EMDOGAIN® in connection with periodontal surgery at 2 surgical test sites per patient. The procedures were performed 2 to 6 weeks apart on one-rooted teeth with at least 4 mm deep intraosseous lesions. A control group of 33 patients underwent flap surgery without EMDOGAIN® at I comparable site. In total 214 test and 33 control surgeries were performed. Serum samples were obtained from test patients for analysis of total and specific antibody levels. 10 of the patients had samples taken before and after the first surgery. 56 other samples were taken after one treatment with EMDOGAIN®, and 63 after 2 treatments. None of the samples, not even from allergy-prone patients after 2 treatments, indicated deviations from established baseline ranges. This indicates that the immunogenic potential of EMDOGAIN® is extremely low when applied in conjunction with periodontal surgery. Comparison between the test and control groups demonstrated the same type and frequency of post-surgical experiences, i.e., reactions caused by the surgical procedure itself. Clinical probing and radiographic evaluation was performed at baseline and 8 months postsurgery. About half of the patients (44 test and 21 control) were also evaluated after 3 years. There was a significant difference between the test and control results at 8 months post surgery. and this difference had increased further at the 3 year follow-up. The 2.5–3 mm increase in attachment and bone level after treatment with EMDOGAIN® was of the same magnitude as seen in the studies with split-mouth design aiming for lest of effectiveness of EMDOGAIN®. 相似文献
2.
Anders Baerheim Per Hjortdahl Are Holen Tor Anvik Ole Bernt Fasmer Hilde Grimstad Tore Gude Terje Risberg Per Vaglum 《BMC medical education》2007,7(1):35
Background
Communication training builds on the assumption that understanding of the concepts related to professional communication facilitates the training. We know little about whether students' knowledge of clinical communication skills is affected by their attendance of communication training courses, or to what degree other elements of the clinical training or curriculum design also play a role. The aim of this study was to determine which elements of the curriculum influence acquisition of knowledge regarding clinical communication skills by medical students. 相似文献3.
A tumor-targeted and conditionally replicating oncolytic adenovirus vector expressing TRAIL for treatment of liver metastases. 总被引:3,自引:0,他引:3
Pavel Sova Xiao-Wei Ren Shaoheng Ni Kathrin M Bernt Jie Mi Nancy Kiviat André Lieber 《Molecular therapy》2004,9(4):496-509
We have constructed a new capsid-modified adenovirus (Ad) vector that specifically replicates in tumor cells and expresses TNF-related apoptosis-inducing ligand (TRAIL). The Ad capsid contains short-shafted fibers derived from Ad serotype 35, which allow for efficient infection of malignant tumor cells, and largely avoids innate toxicity after intravenous application. Replication-dependent homologous recombination in Ad genomes was used to achieve tumor-specific expression of Ad E1a (to mediate viral replication) and TRAIL (to mediate apoptosis and enhance release of progeny virus from infected cells). We demonstrated that our oncolytic vector (Ad5/35.IR-E1A/TRAIL) induced apoptosis in human tumor cell lines derived from colorectal, lung, prostate, and liver cancer. Both in vitro and in vivo tumor models showed efficient intratumoral spread of this vector. In a model for metastatic colon cancer, tail vein infusion of Ad5/35.IR-E1A/TRAIL resulted in elimination of preestablished liver metastases. Intravenous injection of this vector caused a transient elevation of serum glutamic pyruvic transaminase in tumor-bearing mice, which we attributed to factors released from apoptotic tumor cells. Liver histology analyzed at day 14 after virus injection did not show signs of hepatocellular damage. This new oncolytic vector represents a potentially efficient means for gene therapy of metastatic cancer. 相似文献
4.
5.
Marie-Louise Dither-Centerlind Bernt Axelsson Sten Hammarstrom Ulla Hellstrm Peter Perlmann 《European journal of immunology》1980,10(6):434-442
The mode of interaction of twelve lectins with human T lymphocytes was investigated. In order to establish possible differences between mitogenic and nonmitogenic lectins, they were studied for their capacity to induce or inhibit DNA synthesis. Their interaction with intact T cells was studied by immunofluorescence and 51Cr release. Further, lectins conjugated to Sepharose were investigated with regard to their capacity to bind surface glycopeptides from T cell lysates. Operationally, the lectins could be divided into three groups: (a) mitogenic lectins; (b) lectins inhibitory for lymphocyte mitogenesis as induced by leucoagglutinin (La) from Phaseolus vulgaris; and (c) nonmitogenic lectins which were noninhibitory in this La system. Six lectins were nonmitogenic. For two or possibly three of these, lack of mitogenicity was due to complete or partial failure to bind to the lymphocytes. This explanation could not account for lack of mitogenicity of the other three nonmitogenic lectins. Only two of the lectins utilized inhibited La-induced mitogenesis. However, when the lectins were compared with regard to their capacity to bind surface glycopeptides from T cell lysates, important differences between mitogenic and nonmitogenic lectins were seen. As revealed by polyacrylamide gel electrophoresis in sodium dodecyl sulfate and autoradiography, the mitogenic lectins bound a larger number of surface glycopeptides (15–20) than the nonmitogenic lectins (3–10). More importantly, five distinct glycopeptides (gp 135 K, 125 K, 105 K, 95 K and 43 K) were bound by all mitogenic lectins but not by the nonmitogenic lectins. It remains to be established whether these glycopeptides are present on the T cells which are susceptible to the mitogenic action of the lectins and whether it is the interaction of the lectins with one or several of them which triggers mitogenicity. 相似文献
6.
Pernille Mathiesen Tørring Martin Jakob Larsen Charlotte Brasch-Andersen Lotte Nylandsted Krogh Maria Kibæk Lone Laulund Niels Illum Ulrike Dunkhase-Heinl Antje Wiesener Bernt Popp Giuseppe Marangi Tina Duelund Hjortshøj Jakob Ek Ida Vogel Naja Becher Laura Roos Marcella Zollino Christina Ringmann Fagerberg 《European journal of medical genetics》2019,62(2):129-136
Introduction
MED13L-related intellectual disability is characterized by moderate intellectual disability (ID), speech impairment, and dysmorphic facial features. We present 8 patients with MED13L-related intellectual disability and review the literature for phenotypical and genetic aspects of previously described patients.Materials and methods
In the search for genetic aberrations in individuals with ID, two of the patients were identified by chromosomal microarray analysis, and five by exome sequencing. One of the individuals, suspected of MED13L-related intellectual disability, based on clinical features, was identified by Sanger sequencing.Results
All 8 individuals had de novo MED13L aberrations, including two intragenic microdeletions, two frameshift, three nonsense variants, and one missense variant. Phenotypically, they all had intellectual disability, speech and motor delay, and features of the mouth (open mouth appearance, macroglossia, and/or macrostomia). Two individuals were diagnosed with autism, and one had autistic features. One had complex congenital heart defect, and one had persistent foramen ovale. The literature was reviewed with respect to clinical and dysmorphic features, and genetic aberrations.Conclusions
Even if most clinical features of MED13L-related intellectual disability are rather non-specific, the syndrome may be suspected in some individuals based on the association of developmental delay, speech impairment, bulbous nasal tip, and macroglossia, macrostomia, or open mouth appearance. 相似文献7.
In situ characterization of oxalate transport across the basolateral membrane of the proximal tubule
E. Brändle U. Bernt Richard E. Hautmann 《Pflügers Archiv : European journal of physiology》1998,435(6):840-849
Oxalate transport across the contraluminal membrane of the proximal tubule was studied in vivo using the ”capillary stopped
flow microperfusion method” (Pflügers Arch 400:250–256, 1984). Cellular uptake of oxalate was characteristic of a carrier-mediated
transport process (J
max = 1.6 ± 0.6 pmol/s per cm proximal tubular length, K
m = 2.03 ± 0.77 mmol/l). Sulphate inhibited oxalate transport in a dose-dependent manner (K
i-value = 1.53 ± 0.38 mmol/l). Sulphate transport across the basolateral membrane was also characteristic of a carrier- mediated
transport process (Jmax = 1.83 ± 0.56 pmol/s per cm proximal tubular length, K
m = 1.37 ± 0.57 mmol/l). Oxalate inhibited the sulphate transport in a dose-dependent manner (K
i = 2.06 ± 0.82 mmol/l). No significant differences were found between the K
i values and the K
m values of the two substances, indicating that oxalate and sulphate are transported by the same carrier across the basolateral
membrane of the proximal tubule. Oxalate transport was not dependent on the extracellular sodium or potassium concentration.
Bicarbonate competitively inhibited the oxalate transport. Chloride significantly inhibited the oxalate transport, but not
dose dependently. It is, therefore, suggested that oxalate is transported into the cell of the proximal tubule in exchange
for sulphate or bicarbonate. The dose-independent inhibition by chloride is suggested to be mediated by the coupling of the
sulphate (bicarbonate)/oxalate exchanger with the chloride/bicarbonate exchanger at the basolateral membrane of the proximal
tubule. This, furthermore, suggests that the transport of oxalate or sulphate across the basolateral membrane might be indirectly
coupled with the reabsorption of chloride at this membrane side.
Received: 5 August 1997 / Accepted: 8 January 1998 相似文献
8.
The constitutional gain-of-function variant p.Glu1099Lys in NSD2 is associated with a novel syndrome
Bernt Popp Melanie Brugger Sibylle Poschmann Tobias Bartolomaeus Maximilian Radtke Julia Hentschel Nataliya Di Donato Andreas Rump Janina Gburek-Augustat Elisabeth Graf Matias Wagner Ina Sorge Johannes R Lemke Thomas Meitinger Rami Abou Jamra Vincent Strehlow Theresa Brunet 《Clinical genetics》2023,103(2):226-230
9.
Inhibition of coagulation,fibrinolysis, and endothelial cell activation by a p38 mitogen-activated protein kinase inhibitor during human endotoxemia 总被引:7,自引:2,他引:7
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Branger J van den Blink B Weijer S Gupta A van Deventer SJ Hack CE Peppelenbosch MP van der Poll T 《Blood》2003,101(11):4446-4448
P38 mitogen-activated protein kinase (MAPK) is an important component of intracellular signaling cascades that initiate various inflammatory cellular responses. To determine the role of p38 MAPK in the procoagulant response to lipopolysaccharide (LPS), 24 healthy subjects were exposed to an intravenous dose of LPS (4 ng/kg), preceded 3 hours earlier by orally administered 600 or 50 mg BIRB 796 BS (a specific p38 MAPK inhibitor), or placebo. The 600-mg dose of BIRB 796 BS strongly inhibited LPS-induced coagulation activation, as measured by plasma concentrations of the prothrombin fragment F1 + 2. BIRB 796 BS also dose dependently attenuated the activation and subsequent inhibition of the fibrinolytic system (plasma tissue-type plasminogen activator, plasmin-alpha2-antiplasmin complexes, and plasminogen activator inhibitor type 1) and endothelial cell activation (plasma soluble E-selectin and von Willebrand factor). Activation of p38 MAPK plays an important role in the procoagulant and endothelial cell response after in vivo exposure to LPS. 相似文献
10.