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931.
932.
Gabrielle J. Halpern Eliahu G. Stoupel Gad Barkai Rina Chaki Cyril Legum Moshe D. Fejgin Mordechai Shohat 《International journal of biometeorology》1995,39(2):59-63
We studied 2001 foetuses during the period of minimal solar activity of solar cycle 21 and 2265 foetuses during the period of maximal solar activity of solar cycle 22, in all women aged 37 years and over who underwent free prenatal diagnosis in four hospitals in the greater Tel Aviv area. There were no significant differences in the total incidence of chromosomal abnormalities or of trisomy between the two periods (2.15% and 1.8% versus 2.34% and 2.12%, respectively). However, the trend of excessive incidence of chromosomal abnormalities in the period of maximal solar activity suggests that a prospective study in a large population would be required to rule out any possible effect of extreme solar activity. 相似文献
933.
《生物化学与生物物理学报:癌评论》2022,1877(5):188782
During the course of pancreatic neuroendocrine tumors (NETs), they generally become more heterogeneous with individual cells exhibiting distinct molecular fingerprints. This heterogeneity manifests itself through an unequal distribution of genetically-variant, tumor cell subpopulations within disease locations (i.e., spatial heterogeneity) or changes in the genomic landscape over time (i.e., temporal heterogeneity); these characteristics complicate clinical diagnosis and treatment. Effective, feasible tumor heterogeneity detection and eradication methods are essential to overcome the clinical challenges of pancreatic NETs. This review explores the molecular fingerprints of pancreatic NETs and the spectrum of tumoral heterogeneity. We then describe the challenges of assessing heterogeneity by liquid biopsies and imaging modalities and the therapeutic challenges for pancreatic NETs. In general, navigating these challenges, refining approaches for translational research, and ultimately improving patient care are available once we have a better understanding of intratumoral spatiotemporal heterogeneity. 相似文献
934.
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935.
《American journal of human genetics》2023,110(8):1356-1376
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936.
Renato Cavasini Marcos Roberto Dias Batista Louis Bernard Klaczko 《Genetics and molecular biology》2015,38(1):55-58
Drosophila mediopunctata has been used as a model organism for
genetics and evolutionary studies in the last three decades. A linkage map with 48
microsatellite loci recently published for this species showed five syntenic groups,
which had their homology determined to Drosophila melanogaster
chromosomes. Then, by inference, each of the groups was associated with one of the
five major chromosomes of D. mediopunctata. Our objective was to
carry out a genetic (chromosomal) analysis to increase the number of available loci
with known chromosomal location. We made a simultaneous analysis of visible mutant
phenotypes and microsatellite genotypes in a backcross of a standard strain and a
mutant strain, which had each major autosome marked. Hence, we could establish the
chromosomal location of seventeen loci; including one from each of the five major
linkage groups previously published, and twelve new loci. Our results were congruent
with the previous location and they open new possibilities to future work integrating
microsatellites, chromosomal inversions, and genetic determinants of physiological
and morphological variation. 相似文献
937.
Essential trace elements such as iron (Fe) are known to interact with nonessential metals like lead (Pb), influencing its
metabolism. Ferric chloride and lead nitrate were administered intraperitoneally to Swiss albino miceMus musculus singly and successively, with or without a time gap of 1 h, to study the degree of protection, if any, afforded by iron against
the clastogenic effects induced by Pb in bone marrow cells. A decrease in the frequency of lead-induced chromosomal aberrations
was observed when Fe was given together with or prior to Pb administration. 相似文献
938.
Ploidy tug‐of‐war: Evolutionary and genetic environments influence the rate of ploidy drive in a human fungal pathogen
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Aleeza C. Gerstein Heekyung Lim Judith Berman Meleah A. Hickman 《Evolution; international journal of organic evolution》2017,71(4):1025-1038
Variation in baseline ploidy is seen throughout the tree of life, yet the factors that determine why one ploidy level is maintained over another remain poorly understood. Experimental evolution studies using asexual fungal microbes with manipulated ploidy levels intriguingly reveals a propensity to return to the historical baseline ploidy, a phenomenon that we term “ploidy drive.” We evolved haploid, diploid, and polyploid strains of the human fungal pathogen Candida albicans under three different nutrient limitation environments to test whether these conditions, hypothesized to select for low ploidy levels, could counteract ploidy drive. Strains generally maintained or acquired smaller genome sizes (measured as total nuclear DNA through flow cytometry) in minimal medium and under phosphorus depletion compared to in a complete medium, while mostly maintained or acquired increased genome sizes under nitrogen depletion. Improvements in fitness often ran counter to changes in genome size; in a number of scenarios lines that maintained their original genome size often increased in fitness more than lines that converged toward diploidy (the baseline ploidy of C. albicans). Combined, this work demonstrates a role for both the environment and genotype in determination of the rate of ploidy drive, and highlights questions that remain about the force(s) that cause genome size variation. 相似文献
939.
Micronuclei from misaligned chromosomes that satisfy the spindle assembly checkpoint in cancer cells
《Current biology : CB》2022,32(19):4240-4254.e5
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940.
S Bhattacharjya S Nath J Ghose G P Maiti N Biswas S Bandyopadhyay C K Panda N P Bhattacharyya S Roychoudhury 《Cell death and differentiation》2013,20(3):430-442
The spindle assembly checkpoint (SAC) is a ‘wait-anaphase'' mechanism that has evolved in eukaryotic cells in response to the stochastic nature of chromosome–spindle attachments. In the recent past, different aspects of the SAC regulation have been described. However, the role of microRNAs in the SAC is vaguely understood. We report here that Mad1, a core SAC protein, is repressed by human miR-125b. Mad1 serves as an adaptor protein for Mad2 – which functions to inhibit anaphase entry till the chromosomal defects in metaphase are corrected. We show that exogenous expression of miR-125b, through downregulation of Mad1, delays cells at metaphase. As a result of this delay, cells proceed towards apoptotic death, which follows from elevated chromosomal abnormalities upon ectopic expression of miR-125b. Moreover, expressions of Mad1 and miR-125b are inversely correlated in a variety of cancer cell lines, as well as in primary head and neck tumour tissues. We conclude that increased expression of miR-125b inhibits cell proliferation by suppressing Mad1 and activating the SAC transiently. We hypothesize an optimum Mad1 level and thus, a properly scheduled SAC is maintained partly by miR-125b. 相似文献