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131.
Summary and conclusion Measurements were made of the length growth ofZea mays seedlings in Shive culture solution and the results classified according to initial length.It was found that in general less growth occured the less the initial length.This is apparently not due to less cell proliferation stimulus, but to lesser production of available nutrients for cell size growth. 相似文献
132.
Herman L. Mays Chih-Ming Hung Pei-Jen Shaner James Denvir Megan Justice Shang-Fang Yang Terri L. Roth David A. Oehler Jun Fan Swanthana Rekulapally Donald A. Primerano 《Current biology : CB》2018,28(1):70-76.e4
133.
New alleles of brachyury (Tkt1, Tkt4) were induced in the mouse complete tw5 haplotype by ethylnitrosourea (ENU). Like the original brachyury (T) mutation, the new alleles cause a short-tailed phenotype in heterozygotes, and interact with the t complex tail interaction factor (tct) in trans to cause phenotypically tailless mice. Because ENU is mainly a point mutagen, it is important to determine that the new alleles are homozygous embryonic lethal mutations like the original T allele, and to characterize their embryonic lethal phenotype. Moreover, the Tkt1 mutation maps to an inverted position relative to quaking (qk) in t haplotypes as compared with its position on normal chromosome 17. The Tkt1 allele was separated from the resident tw5 lethal gene, tclw5, by recombination, allowing embryology studies to be performed. Embryological analyses show that the Tkt1 allele is nearly identical to the classic T allele. At 9 and 10 days of development, homozygous Tkt1/Tkt1 embryos are grossly abnormal with properties including 1) irregular, disorganized somite pairs, 2) a shortened posterior end of the embryo, 3) an irregular neural tube, and 4) an abnormal notochord. In addition, 10 day-old abnormal embryos have anterior limb buds that point dorsally rather than ventrally, and are smaller than normal littermates. We conclude that the Tkt1 mutation is a valuable allele for both mapping and molecular characterization of the brachyury locus. 相似文献
134.
A molecular genetic linkage map of mouse chromosome 13 anchored by the beige (bg) and satin (sa) loci 总被引:5,自引:0,他引:5
A molecular genetic linkage map of mouse chromosome 13 was constructed using cloned DNA markers and interspecific backcross mice from two independent crosses. The map locations of Ctla-3, Dhfr, Fim-1, 4/12, Hexb, Hilda, Inhba, Lamb-1.13, Ral, Rrm2-ps3, and Tcrg were determined with respect to the beige (bg) and satin (sa) loci. The map locations of these genes confirm and extend regions of homology between mouse chromosome 13 and human chromosomes 5 and 7, and identify a region of homology between mouse chromosome 13 and human chromosome 6. The molecular genetic linkage map of chromosome 13 provides a framework for establishing linkage relationships between cloned DNA markers and known mouse mutations and for identifying homologous genes in mice and humans that may be involved in disease processes. 相似文献
135.
Many preschool language-focused interventions attempt to boost language and literacy skills in young children at risk in these areas of development, though the long-term effects of such interventions are not well-established. This study investigated kindergarten language and reading skills, specifically the subcomponents of vocabulary, decoding, and reading comprehension, for children exposed to the language-focused intervention Learning Language and Loving It (LLLI; Weitzman &; Greenberg, 2002) during preschool. End of kindergarten skills were examined, comparing children whose teachers implemented LLLI (n = 25) or business-as-usual (BAU) instruction (n = 24). Hierarchical linear modeling results showed the LLLI intervention to have significant effects on children's decoding and reading comprehension in kindergarten for children who had high levels of language skill at preschool, as compared to their counterparts in the BAU condition. Study findings therefore indicate that preschool language-focused interventions may primarily benefit children with higher skill levels. This suggests the need to explore avenues for addressing the needs of children with relatively low language skills during preschool and the eventual transition to reading. 相似文献
136.
Matthew S. Freiberg Ionut Bebu Russell Tracy Kaku So-Armah Jason Okulicz Anuradha Ganesan Adam Armstrong Thomas O’Bryan David Rimland Amy C. Justice Brian K. Agan Infectious Disease Clinical Research Program HIV Working Group 《PloS one》2016,11(4)
The mechanism underlying the excess risk of non-AIDS diseases among HIV infected people is unclear. HIV associated inflammation/hypercoagulability likely plays a role. While antiretroviral therapy (ART) may return this process to pre-HIV levels, this has not been directly demonstrated. We analyzed data/specimens on 249 HIV+ participants from the US Military HIV Natural History Study, a prospective, multicenter observational cohort of >5600 active duty military personnel and beneficiaries living with HIV. We used stored blood specimens to measure D-dimer and Interleukin-6 (IL-6) at three time points: pre-HIV seroconversion, ≥6 months post-HIV seroconversion but prior to ART initiation, and ≥6 months post-ART with documented HIV viral suppression on two successive evaluations. We evaluated the changes in biomarker levels between time points, and the association between these biomarker changes and future non-AIDS events. During a median follow-up of 3.7 years, there were 28 incident non-AIDS diseases. At ART initiation, the median CD4 count was 361cells/mm3; median duration of documented HIV infection 392 days; median time on ART was 354 days. Adjusted mean percent increase in D-dimer levels from pre-seroconversion to post-ART was 75.1% (95% confidence interval 24.6–148.0, p = 0.002). This increase in D-dimer was associated with a significant 22% increase risk of future non-AIDS events (p = 0.03). Changes in IL-6 levels across time points were small and not associated with future non-AIDS events. In conclusion, ART initiation and HIV viral suppression does not eliminate HIV associated elevation in D-dimer levels. This residual pathology is associated with an increased risk of future non-AIDS diseases. 相似文献
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139.
Bum Jun Kim Hitisha P. Zaveri Oleg A. Shchelochkov Zhiyin Yu Andrés Hernández-García Michelle L. Seymour John S. Oghalai Fred A. Pereira David W. Stockton Monica J. Justice Brendan Lee Daryl A. Scott 《PloS one》2013,8(2)
Individuals with terminal and interstitial deletions of chromosome 1p36 have a spectrum of defects that includes eye anomalies, postnatal growth deficiency, structural brain anomalies, seizures, cognitive impairment, delayed motor development, behavior problems, hearing loss, cardiovascular malformations, cardiomyopathy, and renal anomalies. The proximal 1p36 genes that contribute to these defects have not been clearly delineated. The arginine-glutamic acid dipeptide (RE) repeats gene (RERE) is located in this region and encodes a nuclear receptor coregulator that plays a critical role in embryonic development as a positive regulator of retinoic acid signaling. Rere-null mice die of cardiac failure between E9.5 and E11.5. This limits their usefulness in studying the role of RERE in the latter stages of development and into adulthood. To overcome this limitation, we created an allelic series of RERE-deficient mice using an Rere-null allele, om, and a novel hypomorphic Rere allele, eyes3 (c.578T>C, p.Val193Ala), which we identified in an N-ethyl-N-nitrosourea (ENU)-based screen for autosomal recessive phenotypes. Analyses of these mice revealed microphthalmia, postnatal growth deficiency, brain hypoplasia, decreased numbers of neuronal nuclear antigen (NeuN)-positive hippocampal neurons, hearing loss, cardiovascular malformations–aortic arch anomalies, double outlet right ventricle, and transposition of the great arteries, and perimembranous ventricular septal defects–spontaneous development of cardiac fibrosis and renal agenesis. These findings suggest that RERE plays a critical role in the development and function of multiple organs including the eye, brain, inner ear, heart and kidney. It follows that haploinsufficiency of RERE may contribute–alone or in conjunction with other genetic, environmental, or stochastic factors–to the development of many of the phenotypes seen in individuals with terminal and interstitial deletions that include the proximal region of chromosome 1p36. 相似文献
140.