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71.
John R. de Almeida Gordon H. Guyatt Sachin Sud Joanne Dorion Michael D. Hill Michael R. Kolber Jane Lea Sylvia Loong Reg Balvinder K. Somogyi Brian D. Westerberg Chris White Joseph M. Chen Bell Palsy Working Group Canadian Society of Otolaryngology – Head Neck Surgery Canadian Neurological Sciences Federation 《CMAJ》2014,186(12):917-922
72.
Linda Näsvik Öjemyr Amandine Maréchal Henrik Vestin Brigitte Meunier Peter R. Rich Peter Brzezinski 《BBA》2014
We have studied internal electron transfer during the reaction of Saccharomyces cerevisiae mitochondrial cytochrome c oxidase with dioxygen. Similar absorbance changes were observed with this yeast oxidase as with the previously studied Rhodobacter sphaeroides and bovine mitochondrial oxidases, which suggests that the reaction proceeds along the same trajectory. However, notable differences were observed in rates and electron-transfer equilibrium constants of specific reaction steps, for example the ferryl (F) to oxidized (O) reaction was faster with the yeast (0.4 ms) than with the bovine oxidase (~ 1 ms) and a larger fraction CuA was oxidized with the yeast than with the bovine oxidase in the peroxy (PR) to F reaction. Furthermore, upon replacement of Glu243, located at the end of the so-called D proton pathway, by Asp the PR → F and F → O reactions were slowed by factors of ~ 3 and ~ 10, respectively, and electron transfer from CuA to heme a during the PR → F reaction was not observed. These data indicate that during reduction of dioxygen protons are transferred through the D pathway, via Glu243, to the catalytic site in the yeast mitochondrial oxidase. This article is part of a Special Issue entitled: 18th European Bioenergetic Conference. 相似文献
73.
Martina Ferraguti Sergio Magallanes Jéssica Jiménez-Peñuela Josué Martínez-de la Puente Luz Garcia-Longoria Jordi Figuerola Jaime Muriel Tamer Albayrak Staffan Bensch Camille Bonneaud Rohan H. Clarke Gábor Á. Czirják Dimitar Dimitrov Kathya Espinoza John G. Ewen Farah Ishtiaq Wendy Flores-Saavedra László Zsolt Garamszegi Olof Hellgren Dita Horakova Kathryn P. Huyvaert Henrik Jensen Asta Križanauskienė Marcos R. Lima Charlene Lujan-Vega Eyðfinn Magnussen Lynn B. Martin Kevin D. Matson Anders Pape Møller Pavel Munclinger Vaidas Palinauskas Péter L. Pap Javier Pérez-Tris Swen C. Renner Robert Ricklefs Sergio Scebba Ravinder N. M. Sehgal Manuel Soler Eszter Szöllősi Gediminas Valkiūnas Helena Westerdahl Pavel Zehtindjiev Alfonso Marzal 《Global Ecology and Biogeography》2023,32(5):809-823
Aim
The increasing spread of vector-borne diseases has resulted in severe health concerns for humans, domestic animals and wildlife, with changes in land use and the introduction of invasive species being among the main possible causes for this increase. We explored several ecological drivers potentially affecting the local prevalence and richness of avian malaria parasite lineages in native and introduced house sparrows (Passer domesticus) populations.Location
Global.Time period
2002–2019.Major taxa studied
Avian Plasmodium parasites in house sparrows.Methods
We analysed data from 2,220 samples from 69 localities across all continents, except Antarctica. The influence of environment (urbanization index and human density), geography (altitude, latitude, hemisphere) and time (bird breeding season and years since introduction) were analysed using generalized additive mixed models (GAMMs) and random forests.Results
Overall, 670 sparrows (30.2%) were infected with 22 Plasmodium lineages. In native populations, parasite prevalence was positively related to urbanization index, with the highest prevalence values in areas with intermediate urbanization levels. Likewise, in introduced populations, prevalence was positively associated with urbanization index; however, higher infection occurred in areas with either extreme high or low levels of urbanization. In introduced populations, the number of parasite lineages increased with altitude and with the years elapsed since the establishment of sparrows in a new locality. Here, after a decline in the number of parasite lineages in the first 30 years, an increase from 40 years onwards was detected.Main conclusions
Urbanization was related to parasite prevalence in both native and introduced bird populations. In invaded areas, altitude and time since bird introduction were related to the number of Plasmodium lineages found to be infecting sparrows. 相似文献74.
Konyukh M Delorme R Chaste P Leblond C Lemière N Nygren G Anckarsäter H Rastam M Ståhlberg O Amsellem F Gillberg IC Mouren-Simeoni MC Herbrecht E Fauchereau F Toro R Gillberg C Leboyer M Bourgeron T 《PloS one》2011,6(3):e17289
Background
Autism spectrum disorders (ASD) are a group of severe childhood neurodevelopmental disorders with still unknown etiology. One of the most frequently reported associations is the presence of recurrent de novo or inherited microdeletions and microduplications on chromosome 16p11.2. The analysis of rare variations of 8 candidate genes among the 27 genes located in this region suggested SEZ6L2 as a compelling candidate.Methodology/Principal Findings
We further explored the role of SEZ6L2 variations by screening its coding part in a group of 452 individuals, including 170 patients with ASD and 282 individuals from different ethnic backgrounds of the Human Genome Diversity Panel (HGDP), complementing the previously reported screening. We detected 7 previously unidentified non-synonymous variations of SEZ6L2 in ASD patients. We also identified 6 non-synonymous variations present only in HGDP. When we merged our results with the previously published, no enrichment of non-synonymous variation in SEZ6L2 was observed in the ASD group compared with controls.Conclusions/Significance
Our results provide an extensive ascertainment of the genetic variability of SEZ6L2 in human populations and do not support a major role for SEZ6L2 sequence variations in the susceptibility to ASD. 相似文献75.
Henrik Gustafsson Abdullahi Afrah Ernst Brodin & Carl-Olav Stiller 《Journal of neurochemistry》1999,73(3):1145-1154
Previous studies indicate that an increased release of cholecystokinin (CCK) in response to morphine administration may counteract opioid-induced analgesia at the spinal level. In the present study we used in vivo microdialysis to demonstrate that systemic administration of antinociceptive doses of morphine (1-5 mg/kg, s.c.) induces a dose-dependent and naloxone-reversible release of CCK-like immunoreactivity (CCK-LI) in the dorsal horn of the spinal cord. A similar response could also be observed following perfusion of the dialysis probe for 60 min with 100 microM but not with 1 microM morphine. The CCK-LI release induced by morphine (5 mg/kg, s.c.) was found to be calcium-dependent and tetrodotoxin-sensitive (1 microM in the perfusion medium). Topical application of either the L-type calcium channel blocker verapamil (50 microg) or the N-type calcium channel blocker omega-conotoxin GVIA (0.4 microg) onto the dorsal spinal cord completely prevented the CCK-LI release induced by morphine (5 mg/kg, s.c.). Our data indicate that activation of L- and N-type calcium channels is of importance for morphine-induced CCK release, even though the precise site of action of morphine in the dorsal horn remains unclear. The present findings also suggest a mechanism for the potentiation of opioid analgesia by L- and N-type calcium channel blocking agents. 相似文献
76.
Zhang Yang Catharina Steentoft Camilla Hauge Lars Hansen Allan Lind Thomsen Francesco Niola Malene B. Vester-Christensen Morten Fr?din Henrik Clausen Hans H. Wandall Eric P. Bennett 《Nucleic acids research》2015,43(9):e59
The nuclease-based gene editing tools are rapidly transforming capabilities for altering the genome of cells and organisms with great precision and in high throughput studies. A major limitation in application of precise gene editing lies in lack of sensitive and fast methods to detect and characterize the induced DNA changes. Precise gene editing induces double-stranded DNA breaks that are repaired by error-prone non-homologous end joining leading to introduction of insertions and deletions (indels) at the target site. These indels are often small and difficult and laborious to detect by traditional methods. Here we present a method for fast, sensitive and simple indel detection that accurately defines indel sizes down to ±1 bp. The method coined IDAA for Indel Detection by Amplicon Analysis is based on tri-primer amplicon labelling and DNA capillary electrophoresis detection, and IDAA is amenable for high throughput analysis. 相似文献
77.
Background
Diabetic retinopathy and retinopathy of prematurity are diseases caused by pathological angiogenesis in the retina as a consequence of local hypoxia. The underlying mechanism for epiretinal neovascularization (tuft formation), which contributes to blindness, has yet to be identified. Neural cell adhesion molecule (N-CAM) is expressed by Müller cells and astrocytes, which are in close contact with the retinal vasculature, during normal developmental angiogenesis.Methodology/Principal Findings
Notably, during oxygen induced retinopathy (OIR) N-CAM accumulated on astrocytes surrounding the epiretinal tufts. Here, we show that N-CAM ablation results in reduced vascular tuft formation due to reduced endothelial cell proliferation despite an elevation in VEGFA mRNA expression, whereas retinal developmental angiogenesis was unaffected.Conclusion/Significance
We conclude that N-CAM exhibits a regulatory function in pathological angiogenesis in OIR. This is a novel finding that can be of clinical relevance in diseases associated with proliferative vasculopathy. 相似文献78.
Henrik Ærenlund Pedersen 《Nordic Journal of Botany》1992,12(4):387-388
A new name (Pteroceras semiteretifolium H. Æ. Peders.) and two new combinations (P. cladostachyum (Hook.f.) H. Æ. Peders., P. unguiculatum (Lindley) H. Æ. Peders.) are presented. The correct application of the name P. pallidum (Blume) Holttum is discussed. 相似文献
79.
Jannik E. Jakobsen Juan Li Peter M. Kragh Brian Moldt Lin Lin Ying Liu Mette Schmidt Kjeld Dahl Winther Brian Dall Schyth Ida E. Holm G��bor Vajta Lars Bolund Henrik Callesen Arne Lund J?rgensen Anders Lade Nielsen Jacob Giehm Mikkelsen 《Transgenic research》2011,20(3):533-545
Modelling of human disease in genetically engineered pigs provides unique possibilities in biomedical research and in studies of disease intervention. Establishment of methodologies that allow efficient gene insertion by non-viral gene carriers is an important step towards development of new disease models. In this report, we present transgenic pigs created by Sleeping Beauty DNA transposition in primary porcine fibroblasts in combination with somatic cell nuclear transfer by handmade cloning. Göttingen minipigs expressing green fluorescent protein are produced by transgenesis with DNA transposon vectors carrying the transgene driven by the human ubiquitin C promoter. These animals carry multiple copies (from 8 to 13) of the transgene and show systemic transgene expression. Transgene-expressing pigs carry both transposase-catalyzed insertions and at least one copy of randomly inserted plasmid DNA. Our findings illustrate critical issues related to DNA transposon-directed transgenesis, including coincidental plasmid insertion and relatively low Sleeping Beauty transposition activity in porcine fibroblasts, but also provide a platform for future development of porcine disease models using the Sleeping Beauty gene insertion technology. 相似文献