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81.
82.
Loss of the p21(Cip1/Waf1) cyclin kinase inhibitor results in propagation of horizontally transferred DNA. 总被引:2,自引:0,他引:2
We have shown previously that phagocytosis of cells dying by apoptosis results in transfer of whole or fragments of chromosomes into the nucleus of the recipient cell. Although DNA transfer was detected in normal cells, stable propagation of the transferred DNA was only observed in cells deficient in p53. Here we show that mouse embryonic fibroblast cells lacking the p21 (Cip1/Waf1) cyclin-kinase inhibitor are able to propagate DNA engulfed by phagocytosis of apoptotic bodies. Feeding mouse embryonic fibroblast p21(-/-) cells with apoptotic bodies derived from a rat fibrosarcoma resulted in focus formation in vitro and tumor formation in vivo. In contrast, cells lacking the p19 alternative reading frame gene did not show any evidence of transformation. These data indicate that p53, via the activation of p21, blocks normal cells from replicating transferred DNA from engulfed apoptotic bodies. This may be one protection level against the propagation of potentially pathological DNA. 相似文献
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Metabolism of low-dose inorganic arsenic in a central European population: influence of sex and genetic polymorphisms 总被引:4,自引:1,他引:3
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Lindberg AL Kumar R Goessler W Thirumaran R Gurzau E Koppova K Rudnai P Leonardi G Fletcher T Vahter M 《Environmental health perspectives》2007,115(7):1081-1086
BACKGROUND: There is a wide variation in susceptibility to health effects of arsenic, which, in part, may be due to differences in arsenic metabolism. Arsenic is metabolized by reduction and methylation reactions, catalyzed by reductases and methyltransferases. OBJECTIVES: Our goal in this study was to elucidate the influence of various demographic and genetic factors on the metabolism of arsenic. METHODS: We studied 415 individuals from Hungary, Romania, and Slovakia by measuring arsenic metabolites in urine using liquid chromatography with hydride generation and inductively coupled plasma mass spectrometry (HPLC-HG-ICPMS). We performed genotyping of arsenic (+III) methyltransferase (AS3MT), glutathione S-transferase omega 1 (GSTO1), and methylene-tetrahydrofolate reductase (MTHFR). RESULTS: The results show that the M287T (T-->C) polymorphism in the AS3MT gene, the A222V (C-->T) polymorphism in the MTHFR gene, body mass index, and sex are major factors that influence arsenic metabolism in this population, with a median of 8.0 microg/L arsenic in urine. Females < 60 years of age had, in general, higher methylation efficiency than males, indicating an influence of sex steroids. That might also explain the observed better methylation in overweight or obese women, compared with normal weight men. The influence of the M287T (T-->C) polymorphism in the AS3MT gene on the methylation capacity was much more pronounced in men than in women. CONCLUSIONS: The factors investigated explained almost 20% of the variation seen in the metabolism of arsenic among men and only around 4% of the variation among women. The rest of the variation is probably explained by other methyltransferases backing up the methylation of arsenic. 相似文献
85.
Autoantibodies against alpha -MSH,ACTH, and LHRH in anorexia and bulimia nervosa patients 总被引:1,自引:0,他引:1
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Fetissov SO Hallman J Oreland L Af Klinteberg B Grenbäck E Hulting AL Hökfelt T 《Proceedings of the National Academy of Sciences of the United States of America》2002,99(26):17155-17160
The hypothalamic arcuate nucleus is involved in the control of energy intake and expenditure and may participate in the pathogenesis of eating disorders such as anorexia nervosa (AN) and bulimia nervosa (BN). Two systems are of particular interest in this respect, synthesizing alpha-melanocyte-stimulating hormone (alpha-MSH) and synthesizing neuropeptide Y, respectively. We report here that 42 of 57 (74%) AN andor BN patients studied had in their plasma Abs that bind to melanotropes andor corticotropes in the rat pituitary. Among these sera, 8 were found to bind selectively to alpha-MSH-positive neurons and their hypothalamic and extrahypothalamic projections as revealed with immunostaining on rat brain sections. Adsorption of these sera with alpha-MSH peptide abolished this immunostaining. In the pituitary, the immunostaining was blocked by adsorption with alpha-MSH or adrenocorticotropic hormone. Additionally, 3 ANBN sera bound to luteinizing hormone-releasing hormone (LHRH)-positive terminals in the rat median eminence, but only 2 of them were adsorbed with LHRH. In the control subjects, 2 of 13 sera (16%) displayed similar to ANBN staining. These data provide evidence that a significant subpopulation of ANBN patients have autoantibodies that bind to alpha-MSH or adrenocorticotropic hormone, a finding pointing also to involvement of the stress axis. It remains to be established whether these Abs interfere with normal signal transduction in the brain melanocortin circuitryLHRH system andor in other central and peripheral sites relevant to food intake regulation, to what extent such effects are related to andor could be involved in the pathophysiology or clinical presentation of ANBN, and to what extent increased stress is an important factor for production of these autoantibodies. 相似文献
86.
Felicitas Thol Michaela Scherr Aylin Kirchner Rabia Shahswar Karin Battmer Sofia Kade Anuhar Chaturvedi Christian Koenecke Michael Stadler Uwe Platzbecker Christian Thiede Thomas Schroeder Guido Kobbe Gesine Bug Oliver Ottmann Wolf-Karsten Hofmann Nicolaus Kr?ger Walter Fiedler Richard Schlenk Konstanze D?hner Hartmut D?hner Jürgen Krauter Matthias Eder Arnold Ganser Michael Heuser 《Haematologica》2015,100(4):e122-e124
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Judith Montag Mandy Syring Julia Rose Anna-Lena Weber Pia Ernstberger Anne-Kathrin Mayer Edgar Becker Britta Keyser Cristobal dos Remedios Andreas Perrot Jolanda van der Velden Antonio Francino Francesco Navarro-Lopez Carolyn Yung Ho Bernhard Brenner Theresia Kraft 《Journal of muscle research and cell motility》2017,38(3-4):291-302
HCM, the most common inherited cardiac disease, is mainly caused by mutations in sarcomeric genes. More than a third of the patients are heterozygous for mutations in the MYH7 gene encoding for the β-myosin heavy chain. In HCM-patients, expression of the mutant and the wildtype allele can be unequal, thus leading to fractions of mutant and wildtype mRNA and protein which deviate from 1:1. This so-called allelic imbalance was detected in whole tissue samples but also in individual cells. There is evidence that the severity of HCM not only depends on the functional effect of the mutation itself, but also on the fraction of mutant protein in the myocardial tissue. Allelic imbalance has been shown to occur in a broad range of genes. Therefore, we aimed to examine whether the MYH7-alleles are intrinsically expressed imbalanced or whether the allelic imbalance is solely associated with the disease. We compared the expression of MYH7-alleles in non-HCM donors and in HCM-patients with different MYH7-missense mutations. In the HCM-patients, we identified imbalanced as well as equal expression of both alleles. Also at the protein level, allelic imbalance was determined. Most interestingly, we also discovered allelic imbalance and balance in non-HCM donors. Our findings therefore strongly indicate that apart from mutation-specific mechanisms, also non-HCM associated allelic-mRNA expression regulation may account for the allelic imbalance of the MYH7 gene in HCM-patients. Since the relative amount of mutant mRNA and protein or the extent of allelic imbalance has been associated with the severity of HCM, individual analysis of the MYH7-allelic expression may provide valuable information for the prognosis of each patient. 相似文献
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90.
Michael Rink MD Daniel Sjoberg Evi Comploj MD Vitaly Margulis MD Evanguelos Xylinas MD Richard K. Lee MD Jens Hansen MD Eugene K. Cha MD Jay D. Raman MD Mesut Remzi MD Karim Bensalah MD Giacomo Novara MD Surena F. Matin MD Felix K. Chun MD Eiji Kikuchi MD Wassim Kassouf MD Juan I. Martinez-Salamanca MD Yair Lotan MD Christian Seitz MD Armin Pycha MD Richard Zigeuner MD Pierre I. Karakiewicz MD Douglas S. Scherr MD Andrew J. Vickers MD Shahrokh F. Shariat MD 《Annals of surgical oncology》2012,19(13):4337-4344