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991.
Nicolas Papon Vincenzo Savini Arnaud Lanoue Andrew J. Simkin Joël Crèche Nathalie Giglioli-Guivarc’h Marc Clastre Vincent Courdavault Andriy A. Sibirny 《Current genetics》2013,59(3):73-90
Candida guilliermondii (teleomorph Meyerozyma guilliermondii) is an ascomycetous species belonging to the Saccharomycotina CTG clade which has been studied over the last 40 years due to its biotechnological interest, biological control potential and clinical importance. Such a wide range of applications in various areas of fundamental and applied scientific research has progressively made C. guilliermondii an attractive model for exploring the potential of yeast metabolic engineering as well as for elucidating new molecular events supporting pathogenicity and antifungal resistance. All these research fields now take advantage of the establishment of a useful molecular toolbox specifically dedicated to C. guilliermondii genetics including the construction of recipient strains, the development of selectable markers and reporter genes and optimization of transformation protocols. This area of study is further supported by the availability of the complete genome sequence of the reference strain ATCC 6260 and the creation of numerous databases dedicated to gene ontology annotation (metabolic pathways, virulence, and morphogenesis). These genetic tools and genomic resources represent essential prerequisites for further successful development of C. guilliermondii research in medical mycology and in biological control by facilitating the identification of the multiple factors that contribute to its pathogenic potential. These genetic and genomic advances should also expedite future practical uses of C. guilliermondii strains of biotechnological interest by opening a window into a better understanding of the biosynthetic pathways of valuable metabolites. 相似文献
992.
Marie-Josèphe Tainturier Jennifer Roberts E. Charles Leek 《Cognitive neuropsychology》2013,30(8):546-563
In English, the relationship between the written and spoken forms of words is relatively opaque, leading to proposals that skilled reading requires two procedures: (a) a sublexical grapheme/phoneme conversion process allowing the correct reading of regular words (CAT) and new or pseudowords (ZAT); (b) a lexical process necessary to read irregular words accurately (TWO) and assumed to be the dominant process for familiar words. However, it has been argued that the sublexical process may be sufficient in highly transparent languages such as Welsh. If this is the case, damage to the sublexical process may lead to more severe deficits in transparent languages due to the lack of an alternative lexical process. To test this hypothesis, we compared Welsh and English oral reading and written-word recognition and comprehension in seven bilingual stroke participants with comparably impaired pseudoword reading in English and Welsh. Performance was remarkably similar across languages. Irrespective of the language tested, words were read more accurately than pseudowords. Lexical decision and word comprehension were as accurate in Welsh and in English, and when imageability effects were present they were of a similar size in both languages. This study does not support the hypothesis that orthographic transparency determines the nature of cognitive reading processes, but rather suggests that readers develop a sight vocabulary through reading experience irrespective of orthographic transparency. 相似文献
993.
994.
David Hassanein Berro Solène Collet Jean-Sébastien Guillamo Ararat Chakhoyan Jean-Marc Constans Emmanuèle Lechapt-Zalcman Jean-Michel Derlon Mathieu Hatt Dimitris Visvikis Stéphane Guillouet Cécile Perrio Myriam Bernaudin Samuel Valable 《Journal of neuroradiology. Journal de neuroradiologie》2021,48(4):230-231
995.
Emilie Montellier Fay?al Boussouar Sophie Rousseaux Kai Zhang Thierry Buchou Fran?ois Fenaille Hitoshi Shiota Alexandra Debernardi Patrick Héry Sandrine Curtet Mahya Jamshidikia Sophie Barral Hélène Holota Aurélie Bergon Fabrice Lopez Philippe Guardiola Karin Pernet Jean Imbert Carlo Petosa Minjia Tan Yingming Zhao Matthieu Gérard Saadi Khochbin 《Genes & development》2013,27(15):1680-1692
The conversion of male germ cell chromatin to a nucleoprotamine structure is fundamental to the life cycle, yet the underlying molecular details remain obscure. Here we show that an essential step is the genome-wide incorporation of TH2B, a histone H2B variant of hitherto unknown function. Using mouse models in which TH2B is depleted or C-terminally modified, we show that TH2B directs the final transformation of dissociating nucleosomes into protamine-packed structures. Depletion of TH2B induces compensatory mechanisms that permit histone removal by up-regulating H2B and programming nucleosome instability through targeted histone modifications, including lysine crotonylation and arginine methylation. Furthermore, after fertilization, TH2B reassembles onto the male genome during protamine-to-histone exchange. Thus, TH2B is a unique histone variant that plays a key role in the histone-to-protamine packing of the male genome and guides genome-wide chromatin transitions that both precede and follow transmission of the male genome to the egg. 相似文献
996.
Nicholas Beazley-Long Jing Hua Thomas Jehle Richard P. Hulse Rick Dersch Christina Lehrling Heather Bevan Yan Qiu Wolf A. Lagrèze David Wynick Amanda J. Churchill Patrick Kehoe Steven J. Harper David O. Bates Lucy F. Donaldson 《The American journal of pathology》2013,183(3):918-929
Vascular endothelial growth factor (VEGF) A is generated as two isoform families by alternative RNA splicing, represented by VEGF-A165a and VEGF-A165b. These isoforms have opposing actions on vascular permeability, angiogenesis, and vasodilatation. The proangiogenic VEGF-A165a isoform is neuroprotective in hippocampal, dorsal root ganglia, and retinal neurons, but its propermeability, vasodilatatory, and angiogenic properties limit its therapeutic usefulness. In contrast, a neuroprotective effect of endogenous VEGF-A165b on neurons would be advantageous for neurodegenerative pathologies. Endogenous expression of human and rat VEGF-A165b was detected in hippocampal and cortical neurons. VEGF-A165b formed a significant proportion of total VEGF-A in rat brain. Recombinant human VEGF-A165b exerted neuroprotective effects in response to multiple insults, including glutamatergic excitotoxicity in hippocampal neurons, chemotherapy-induced cytotoxicity of dorsal root ganglion neurons, and retinal ganglion cells (RGCs) in rat retinal ischemia-reperfusion injury in vivo. Neuroprotection was dependent on VEGFR2 and MEK1/2 activation but not on p38 or phosphatidylinositol 3–kinase activation. Recombinant human VEGF-A165b is a neuroprotective agent that effectively protects both peripheral and central neurons in vivo and in vitro through VEGFR2, MEK1/2, and inhibition of caspase-3 induction. VEGF-A165b may be therapeutically useful for pathologies that involve neuronal damage, including hippocampal neurodegeneration, glaucoma diabetic retinopathy, and peripheral neuropathy. The endogenous nature of VEGF-A165b expression suggests that non–isoform-specific inhibition of VEGF-A (for antiangiogenic reasons) may be damaging to retinal and sensory neurons.Vascular endothelial growth factor (VEGF) A, originally described as a potent vascular permeability and growth factor for endothelial cells, is up-regulated in the brain during stroke and ischemic episodes1 and has been linked with many neuronal diseases. The most widely studied isoform of VEGF-A, VEGF-A165a, is up-regulated in hypoxia, induces increased vascular permeability in neuronal vasculature, and can stimulate angiogenesis after ischemic episodes. The resulting edema and hyperemia can be damaging, but VEGF-A165a has also been found to have direct anticytotoxic effects on neurons, raising the possibility that it may act as an endogenous neuroprotective agent in neurodegenerative pathologies. VEGF-A exerts neurotrophic (survival) and neurotropic (neurogenesis and axon outgrowth) actions, which, although initially thought to be a function of increased angiogenesis and perfusion after neuronal injury,2 are now appreciated as direct effects of VEGF-A on neurons.The vegfa gene encodes numerous products by differential splicing, but not all isoforms exert the same effects.3 Alternative splicing of exon 8 leads to two functionally distinct families: the proangiogenic VEGF-Axxxa family and the counteracting VEGF-Axxxb family.4,5 VEGF-A165b prevents the VEGF-A165a effects on increased vascular permeability, blood vessel growth, and vasodilatation.4–7The therapeutic potential of VEGF-A and anti–VEGF-A treatments are now widely recognized, and effective anti–VEGF-A treatments are available in ophthalmology8 and oncology.9 The finding that VEGF-A is implicated in neuronal disorders (eg, Alzheimer disease, Parkinson disease, Huntington disease, diabetic neuropathy, and amyotrophic lateral sclerosis10) provides a rationale for the use of VEGF-A as a therapeutic agent in neurodegenerative conditions. Although this rationale is supported by preclinical evidence,11 the identification of the VEGF-Axxxb family requires reexamination of VEGF-A isoforms in these contexts to allow for the clear evidence that VEGF-A splicing variants are not functionally equivalent3 and to determine whether augmentation of the proangiogenic isoform family (VEGF-Axxxa) alone may have deleterious effects (eg, in occult malignancy and carcinoma in situ).The neuroprotective profile of the exon 8 alternatively spliced isoforms VEGF-Axxxb remains unexplored. Interestingly, VEGF-Axxxb isoforms do not exhibit the vascular effects seen with VEGF-Axxxa isoforms, such as a sustained increase in capillary permeability or hypotension.5,12 The lack of these potential adverse effects may make VEGF-Axxxb isoforms more amenable as therapeutic agents in neurodegenerative diseases.We therefore tested the hypothesis that VEGF-A165b is neuroprotective for central and peripheral neurons. We found that VEGF-A165b is expressed in central neurons and is neuroprotective in vitro and in vivo. This finding indicates that VEGF-A165b may prove to be a suitable therapeutic agent in neurodegenerative disorders, exhibiting fewer adverse effects than VEGF-A165a. 相似文献
997.
Isabela J. Wastowski Renata T. Simões Layale Yaghi Eduardo A. Donadi João T. Pancoto Isabelle Poras Emmanuèle Lechapt-Zalcman Myriam Bernaudin Samuel Valable Carlos G. Carlotti Sébastien Flajollet Stine S. Jensen Soldano Ferrone Edgardo D. Carosella Bjarne W. Kristensen Philippe Moreau 《The American journal of pathology》2013,182(2):540-552
998.
Philippe Halfon Maria Luisa Mateos Lindemann Audrey Raimondo Sophie Ravet Claire Camus Hacène Khiri Guillaume Pénaranda Mario Sideri Maria Teresa Sandri 《Archives of virology》2013,158(6):1143-1149
A new genotyping-based DNA assay (Digene LQ®) was developed recently. The primary aim was to assess the distribution of HPV types using this new assay in atypical squamous cells of undeterminate significance (ASCUS). The secondary aim was to correlate the HPV types with the severity of the disease. The study population comprised 376 ASCUS women. The women were all Hybrid Capture II (HCII) positive and were admitted in three European referral gynecology clinics between 2007 and 2010. A colposcopy with histological examination was performed in all these patients. HPV 16 was typed in 40 % of patients, HPV 18 in 7 %, and HPV 31 in 17 %, and 18 % of patients had mixed genotypes. Patients aged over 30 more often had the HPV 16 genotype than patients aged under 30 (29 % vs. 11 %, chi-square test p < 0.001). The risk of cervical intra-epithelial neoplasia of grade 2 or more (CIN2 +) when HPV 18 positive is lower than the probability associated with HPV 16 or HPV 31: 28 % vs. 58 % and 52 %, respectively (chi-square test, p = 0.005 and p = 0.05, respectively). The Digene LQ®, a new sequence-specific hybrid capture sample preparation, is fast and efficient and allows high-throughput genotyping of 18 HR HPV types by PCR compared to traditional non-sequence-specific sample preparation methods. 相似文献
999.
De Wel Bram Goosens Veerle Sobota Atka Van Camp Elke Geukens Ellen Van Kerschaver Griet Jagut Marlène Claes Kathleen Claeys Kristl G. 《Journal of neurology》2021,268(3):923-935
Journal of Neurology - Nusinersen recently became available as the first treatment for Spinal Muscular Atrophy (SMA) and data on its effectiveness and safety in adult SMA patients are still scarce.... 相似文献
1000.
Ravel Jean-Marie Benkirane Mehdi Calmels Nadège Marelli Cecilia Ory-Magne Fabienne Ewenczyk Claire Halleb Yosra Tison François Lecocq Claire Pische Guillaume Casenave Philippe Chaussenot Annabelle Frismand Solène Tyvaert Louise Larrieu Lise Pointaux Morgane Drouot Nathalie Bossenmeyer-Pourié Carine Oussalah Abderrahim Guéant Jean-Louis Leheup Bruno Bonnet Céline Anheim Mathieu Tranchant Christine Lambert Laëtitia Chelly Jamel Koenig Michel Renaud Mathilde 《Journal of neurology》2021,268(5):1927-1937
Journal of Neurology - STUB1 has been first associated with autosomal recessive (SCAR16, MIM# 615768) and later with dominant forms of ataxia (SCA48, MIM# 618093). Pathogenic variations in STUB1... 相似文献