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121.
The complete mitochondrial DNA sequence of the shark Mustelus manazo: evaluating rooting contradictions to living bony vertebrates 总被引:5,自引:0,他引:5
A remarkable example of a misleading mitochondrial protein tree is
presented, involving ray-finned fishes, coelacanths, lungfishes, and
tetrapods, with sea lampreys as an outgroup. In previous molecular
phylogenetic studies on the origin of tetrapods, ray-finned fishes have
been assumed as an outgroup to the tetrapod/lungfish/coelacanth clade, an
assumption supported by morphological evidence. Standard methods of
molecular phylogenetics applied to the protein-encoding genes of
mitochondria, however, give a bizarre tree in which lamprey groups with
lungfish and, therefore, ray-finned fishes are not the outgroup to a
tetrapod/lungfish/coelacanth clade. All of the dozens of published
phylogenetic methods, including every possible modification to maximum
likelihood known to us (such as inclusion of site heterogeneity and
exclusion of potentially misleading hydrophobic amino acids), fail to place
the ray-finned fishes in a biologically acceptable position. A likely cause
of this failure may be the use of an inappropriate outgroup. Accordingly,
we have determined the complete mitochondrial DNA sequence from the shark,
Mustelus manazo, which we have used as an alternative and more proximal
outgroup than the lamprey. Using sharks as the outgroup, lungfish appear to
be the closest living relative of tetrapods, although the possibility of a
lungfish/coelacanth clade being the sister group of tetrapods cannot be
excluded.
相似文献
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Natalie Saini Camille K. Giacobone Leszek J. Klimczak Brian N. Papas Adam B. Burkholder Jian-Liang Li David C. Fargo Re Bai Kevin Gerrish Cynthia L. Innes Shepherd H. Schurman Dmitry A. Gordenin 《PLoS genetics》2021,17(1)
Human skin is continuously exposed to environmental DNA damage leading to the accumulation of somatic mutations over the lifetime of an individual. Mutagenesis in human skin cells can be also caused by endogenous DNA damage and by DNA replication errors. The contributions of these processes to the somatic mutation load in the skin of healthy humans has so far not been accurately assessed because the low numbers of mutations from current sequencing methodologies preclude the distinction between sequencing errors and true somatic genome changes. In this work, we sequenced genomes of single cell-derived clonal lineages obtained from primary skin cells of a large cohort of healthy individuals across a wide range of ages. We report here the range of mutation load and a comprehensive view of the various somatic genome changes that accumulate in skin cells. We demonstrate that UV-induced base substitutions, insertions and deletions are prominent even in sun-shielded skin. In addition, we detect accumulation of mutations due to spontaneous deamination of methylated cytosines as well as insertions and deletions characteristic of DNA replication errors in these cells. The endogenously induced somatic mutations and indels also demonstrate a linear increase with age, while UV-induced mutation load is age-independent. Finally, we show that DNA replication stalling at common fragile sites are potent sources of gross chromosomal rearrangements in human cells. Thus, somatic mutations in skin of healthy individuals reflect the interplay of environmental and endogenous factors in facilitating genome instability and carcinogenesis. 相似文献
125.
Decomposable graphical Gaussian model determination 总被引:8,自引:0,他引:8
126.
Suppression Subtractive Hybridization (SSH) and its derivative, Pooled Suppression Subtractive hybridization (PSSH), are powerful
tools used to study variances larger than ~100 bp in prokaryotic genome structure. The initial steps involve ligating an oligonucleotide
of known sequence (the “adaptor”) to a fragmented genome to facilitate amplification, subtraction and downstream sequencing.
SSH results in the creation of a library of unique DNA fragments which have been traditionally analyzed via Sanger sequencing.
Numerous next generation sequencing technologies have entered the market yet SSH is incompatible with these platforms. This
is due to the high level of sequence conservation of the oligonucleotide used for SSH. This rigid adherence is partly because
it has yet to be determined if alteration of this oligonucleotide will have a deleterious impact on subtraction efficiency.
The subtraction occurs when non-unique fragments are inhibited by a secondary self-pairing structure which requires exact
nucleotide sequence. We determine if appending custom sequence to the 5′ terminal ends of these oligonucleotides during the
nested PCR stages of PSSH will reduce subtraction efficiency. We compare a pool of ten S. aureus clinical isolates with a standard PSSH and custom tailed-PSSH. We detected no statistically significant difference between
their subtraction efficiencies. Our observations suggest that the adaptor’s terminal ends may be labeled during the nested
PCR step. This produces libraries labeled with custom sequence. This does not lead to loss of subtraction efficiency and would
be invaluable for groups wishing to combine SSH or PSSH with their own downstream applications, such as a high throughput
sequencing platform. 相似文献