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41.
3-mercapto-5-(3,4-dihydroxyphenylazo-1')-1,2,4-triazole (METRIAP), 3-mercapto-5-(2,4-dihydroxy-3-carboxyphenylazo-1)-1,2,4-triazole (METRIAREZ-gamma) and 2-mercapto-5-(2,4-dihydroxy-5-carboxyphenylazol-)-1,3,4-thiadiazole (METIDAREZ-beta), reagents synthesized in the Department of Medicinal Chemistry of Medical University in Lublin, have been used to determine Fe(II) and Zn(II) in Materna, Centrum, H-Pantoten pharmaceutical multivitamin preparations, containing other trace elements. Zn (II) with METRIAREZ-gamma at pH=7.35, and Fe(II) with METRIAP and METIDAREZ-beta at pH=10.30 or 7.40 constitute soluble in H2O colourful chelate compound at a mole ratio of 1:2 and 1:3, respectively. Volume stability constant of Fe(II) and Zn(II) complexes is equal to log K(METRIAP-Fe(II)) = 16.46; log K(METRIAREZ-beta-Fe(II)) = 14.253; log K(METRIAREZ-gammaZn(II)) = 11.47. Fe(III) and Zn(II) solutions were obtained by wet mineralisation of Materna, Centrum and H-Pantoten preparations with concentrated H2SO4 and 30% H2O2 added. Spectrophotometric determination was carried out in an aqueous-methanolic solution environment. Statistically evaluated results were compared with the results of the AAS (atomic absorption spectrophotometry) determination method. Advantages of the Fe(II) and Zn(II) determination method are its precision RSD = 0.23%-2.09% and repeatability as well as the possibility of Fe(II) determination without the necessity of masking or separating other trace elements. 相似文献
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Nowosad H Derkacz A Staniszewska-Marszałek E Nowicki P Stupiński W Kustrzycki W 《Kardiologia polska》2003,58(5):380-4; discussion: 384
A 55-year-old man was admitted to our Department four weeks after anterior myocardial infarction. A large, mobile thrombus was diagnosed on echocardiography. On the third day of hospitalization systemic arterial embolism with left femoral artery localization occurred. The embolus was removed surgically. During 3-month follow-up the patient received anticoagulant therapy with complete resolution of ventricular thrombus. Therapeutic options in this case are discussed. 相似文献
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Józef Kładny Gabriela Möslein Torben Myrhøj Grzegorz Kurzawski Anna Jakubowska Tadeusz Dębniak Wojciech Petriczko Michał Kozłowski Tariq Al-Amawi Marek Brzosko Jacek Fliciński Arkadiusz Jawień Zbigniew Banaszkiewicz Piotr Rychter Jan Lubiński 《Hereditary cancer in clinical practice》2003,1(1):34-38
Abstract
The criteria for the diagnosis of HNPCC established by the ICG-HNPCC are very restrictive as they do not allow for the diagnosis of a large number of "suspected HNPCC" cases - these are families which do no fulfill the strict diagnostic "Amsterdam criteria", but do present with several pedigree and clinical features characteristic for HNPCC. Several series of families suspected of harboring germline mutations in DNA mismatch repair genes have been studied for germline changes in DNA mismatch repair genes and a mutation rate of somewhere between 8-60% was found. Therefore a subgroup of members of the ICG-HNPCC has been working on pedigree/clinical diagnostic criteria for suspected HNPCC.Materials and methods
Part I
The study was based on two series of colorectal cancer (CRC) cases: 1) HNPCC - this group comprised 190 patients affected by CRC from randomly selected families which fulfilled the Amsterdam II criteria registered in Düsseldorf, Germany (102 cases of CRC), Denmark (18 CRCs), Leiden, Holland (23 CRCs) and Szczecin, Poland (47 CRCs). 2) Consecutive CRCs - this group comprised 629 (78.0%) of 806 individuals with CRC diagnosed in 1991-1997 in the city of Szczecin (ca. 400,000 of inhabitants), Poland. Nuclear pedigrees in both groups were compared for frequency of occurrence of clinical features, that have been shown to be associated with HNPCC.Part II
52 consecutive CRC cases from Szczecin, matching the criteria recognized in part I as appropriate for diagnosis of cases "suspected of HNPCC" were studied for the occurrence of germline hMSH2/hMLH1 constitutional mutations using "exon by exon" sequencing.Results
The combination of features - i.e. the occurrence of an HNPCC associated cancer (CRC or cancer of the endometrium, small bowel or urinary tract) in a 1st degree relative of a CRC patient; at least one of the patients being diagnosed under age of 50 - appeared to be strongly associated to HNPCC with an OR - 161. Constitutional mutations were identified in 18 (10 MLH1 and 8 MSH2 mutations) of 52 (34%) cases matching the above features.Conclusions
The results of our studies strongly suggest that it is possible to diagnose HNPCC with a high degree of accuracy on the basis of nuclear pedigree data and clinical features.46.
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Katarzyna Skonieczna Boris Malyarchuk Arkadiusz Jawień Andrzej Marszałek Zbigniew Banaszkiewicz Paweł Jarmocik Tomasz Grzybowski 《Human mutation》2018,39(5):691-701
So far, a reliable spectrum of mitochondrial DNA mutations in colorectal cancer cells is still unknown, and neither is their significance in carcinogenesis. Indeed, it remains debatable whether mtDNA mutations are “drivers” or “passengers” of colorectal carcinogenesis. Thus, we analyzed 200 mitogenomes from normal and cancer tissues of 100 colorectal cancer patients. Minority variant mutations were detected at the 1% level. We showed that somatic mutations frequently occur in colorectal cancer cells (75%) and are randomly distributed across the mitochondrial genome. Mutational signatures of somatic mitogenome mutations suggest that they might arise through nucleotide deamination due to oxidative stress. The majority of somatic mutations localized within the coding region (in positions not known from the human phylogeny) and was potentially pathogenic to cell metabolism. Further analysis suggested that the relaxation of negative selection in the mitogenomes of colorectal cancer cells may allow accumulation of somatic mutations. Thus, a shift in glucose metabolism from oxidative phosphorylation to glycolysis may create advantageous conditions for accumulation of mtDNA mutations. Considering the fact that the presence of somatic mtDNA mutations was not associated with any clinicopathological features, we suggested that mtDNA somatic mutations are “passengers” rather than the cause of colorectal carcinogenesis. 相似文献
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