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51.
Irmgard Schmidt 《Virchows Archiv : an international journal of pathology》1933,291(1-2):491-506
Ohne ZusammenfassungMit 9 Abbildungen im Text. 相似文献
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Markus M. Lerch M.D. Jochen Riehl Helmut Mann Irmgard Nolte Heinz -Günter Sieberth Siegfried Matern 《Abdominal imaging》1989,14(1):311-314
Several abnormalities regarding pancreatic morphology and function have been reported in patients with chronic renal failure (CRF) with an incidence as high as 72%. In a prospective study we investigated 96 outpatients from our chronic ambulatory hemodialysis program by abdominal ultrasound. Of the patients with CRF, 20.6% were found to have morphologic alterations of the pancreas compared to 4.7% of controls. Although pathologic sonograms of the pancreas correlated with biliary disease, hyperparathyroidism and years of hemodialysis, the most obvious etiologic factor appeared to be the duration of CRF. Possible pathogenetic mechanisms are discussed and screening abdominal ultrasound examinations in patients with long-standing CRF are recommended. 相似文献
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Pierre R Burkhard Roxane Fournier Bernadette Mermillod Karl-Heinz Krause Constantin Bouras Irmgard Irminger 《Clinical chemistry and laboratory medicine》2004,42(4):396-407
Many limitations and conflicting results have cast serious doubts on the validity of cerebrospinal fluid tau and Abeta42 levels for the biological diagnosis of Alzheimer's disease, particularly extreme variations of the reference limits found by unrelated groups as a consequence of different reference populations used. In this study, we addressed the issue of defining reference limits for cerebrospinal fluid tau and Abeta42 in healthy adult individuals. One hundred and five neurologically intact subjects were enrolled according to strict inclusion criteria, 10 of them with autopsy confirmation of brain integrity. All cerebrospinal fluid samples were similarly and optimally processed as were the dosage methods used and the statistical analyses performed. A robust correlation with age was demonstrated for Abeta42 but not for tau. For tau, we found that an upper cut-off value of 443 ng/l allowed 95% of the subjects to be correctly classified as normal. For Abeta42, a lower cut-off value of 90 ng/l allowed a correct classification of 90% of the subjects. However, a large variance of the reference values, partly explained by the potential contamination of the reference population with presymptomatic dementia patients, may limit the use of reference limits based on living subjects. We propose that the issue of defining reference limits for both cerebrospinal fluid tau and Abeta42 may ultimately be settled by studying large numbers of autopsy-proven neurologically intact individuals only. 相似文献
57.
Julia Wilflingseder Alexander Kainz Irmgard Mühlberger Paul Perco Robert Langer Ivan Kristo Bernd Mayer Rainer Oberbauer 《Transplant international》2010,23(8):796-804
We recently showed in a randomized control trial that steroid pretreatment of the deceased organ donor suppressed inflammation in the transplant organ but did not reduce the rate or duration of delayed graft function (DGF). This study sought to elucidate such of those factors that caused DGF in the steroid‐treated subjects. Genome‐wide gene expression profiles were used from 20 steroid‐pretreated donor‐organs and were analyzed on the level of regulatory protein–protein interaction networks. Significance analysis of microarrays (SAM) yielded 63 significantly down‐regulated sequences associated with DGF that could be functionally categorized according to Protein ANalysis THrough Evolutionary Relationships ontologies into two main biologic processes: transport (P < 0.001) and metabolism (P < 0.001). The identified genes suggest hypoxia as the cause of DGF, which cannot be counterbalanced by steroid treatment. Our data showed that molecular pathways affected by ischemia such as transport and metabolism are associated with DGF. Potential interventional targeted therapy based on these findings includes peroxisome proliferator‐activated receptor agonists or caspase inhibitors. 相似文献
58.
Paris I Cardenas S Lozano J Perez-Pastene C Graumann R Riveros A Caviedes P Segura-Aguilar J 《Neurotoxicity research》2007,12(2):125-134
Four decades after L-dopa introduction to PD therapy, the cause of Parkinson's disease (PD) remains unknown despite the intensive research and the discovery of a number of gene mutations and deletions in the pathogenesis of familial PD. Different model neurotoxins have been used as preclinical experimental models to study the neurodegenerative process in PD, such as 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and rotenone. The lack of success in identifying the molecular mechanism for the degenerative process in PD opens the question whether the current preclinical experimental models are suitable to understand the degeneration of neuromelanin-containing dopaminergic neurons in PD. We propose aminochrome as a model neurotoxin to study the neurodegenerative processes occurring in neuromelanin-containing dopaminergic neurons in PD. Aminochrome is an endogenous compound formed during dopamine oxidation and it is the precursor of neuromelanin, a substance whose formation is a normal process in mesencephalic dopaminergic neurons. However, aminochrome itself can induce neurotoxicity under certain aberrant conditions such as (i) one-electron reduction of aminochrome catalyzed by flavoenzymes to leukoaminochrome o-semiquinone radical, which is a highly reactive neurotoxin; or (ii) the formation of aminochrome adducts with alpha-synuclein, enhancing and stabilizing the formation of neurotoxic protofibrils. These two neurotoxic pathways of aminochrome are prevented by DT-diaphorase, an enzyme that effectively reduces aminochrome with two-electrons preventing both aminochrome one-electron reduction or formation alpha synuclein protofibrils. We propose to use aminochrome as a preclinical experimental model to study the neurodegenerative process of neuromelanin containing dopaminergic neurons in PD. 相似文献
59.
Bauer I 《Journal of travel medicine》2011,18(4):292; author reply 292-292;3, discussion 293
60.
Steiner H Bergmeister M Verdorfer I Granig T Mikuz G Bartsch G Stoehr B Brunner A 《BJU international》2008,102(3):291-296