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2.
Objective: To further explore the mechanism of congenital pyrimidine 5'-nucleotidase I deficiency. Methods; The samples were collected from the family members of a patient with P5'N- I deficiency. The enzyme activities were measured by UMP method and the enzyme proteins were quantified by ELISA while the morphology of peripheral blood cells was observed. Results: The enzyme contents reduced as their enzyme activities decreased in the family especially in four members. There was a significant positive correlation(r =0. 955) between the activity and the content of P 5'N- I . The count of the stippling cell was varied in the family. Conclusion.- One of the reasons for congenital P5' N- I deficiency might be the deficiency in the enzyme content. The morphology of peripheral blood erythrocyte may be an assistant diagnotic index. The P5'N- I activities and contents were measured simultaneously may be a effective method in clinic diagnosis. 相似文献
3.
石刻雕塑作业劳动卫生学调查及实验研究 总被引:1,自引:0,他引:1
测定了石雕作业粉尘浓度,几何平均浓度为82.35~3.67mg/m3。工人职业性健康检查结果,接尘工人的咽部充血、咳嗽、咯痰检出率高于对照组;肺功能低下的检出率也高于对照组。该厂自1972年以来发生尘肺患者17例,其病情发展和晋期缓慢,发病工龄长。动物实验研究表明,石雕粉尘有轻微的致纤维化作用。 相似文献
4.
Bayrak S; Holmdahl R; Travers P; Lauster R; Hesse M; Dolling R; Mitchison NA 《International immunology》1997,9(11):1687-1699
Type II collagen (CII) is of immunological interest because of its
repetitive structure and properties as an autoantigen. The mouse gene has
recently been cloned, thus enabling T cell-defined epitopes to be
identified. Multiple novel epitopes on mouse CII are here detected in the
autoreactive T cell response. The major response is directed to an epitope
with residues 707-721 located on the CB10 fragment. Some 25 other epitopes
are also recognized, including the autologous homologue of the 256-270
epitope which dominates in the response to foreign collagen. The cells
reactive with mouse collagen peptides were of Th1 type, as judged by
release of IFN-gamma. No significant reactivity was detected to mouse CII
peptides during ongoing disease. Alignment of the mouse epitopes revealed a
sequence motif with characteristic side chains at residues P1, P4 and P7,
and to a lesser extent at P5, within a nonamer core sequence. Binding of
these epitopes was simulated in a computer model of the I-Aq molecule,
where peptides with anchor residues at P1, P4 and P7 were indeed found to
fit the binding groove best. The spacing of pockets and the fine structure
of the binding surface of the I-Aq molecule meshes with the repetitive
structure of the collagen (X-Y-Gly), thus providing a likely explanation
for the occurrence of multiple epitopes. Comparison with human DR binding
motifs showed that the I-Aq motif resembles most closely that of the DR4
subtypes which predispose for rheumatoid arthritis.
相似文献
5.
6.
7.
Dal Zotto L; Quaderi NA; Elliott R; Lingerfelter PA; Carrel L; Valsecchi V; Montini E; Yen CH; Chapman V; Kalcheva I; Arrigo G; Zuffardi O; Thomas S; Willard HF; Ballabio A; Disteche CM; Rugarli EI 《Human molecular genetics》1998,7(3):489-499
We have recently reported isolation of the gene responsible for X- linked
Opitz G/BBB syndrome, a defect of midline development. MID1 is located on
the distal short arm of the human X chromosome (Xp22. 3) and encodes a
novel member of the B box family of zinc finger proteins. We have now
cloned the murine homolog of MID1 and performed preliminary expression
studies during development. Mid1 expression in undifferentiated cells in
the central nervous, gastrointestinal and urogenital systems suggests that
abnormal cell proliferation may underlie the defect in midline development
characteristic of Opitz syndrome. We have also found that Mid1 is located
within the mouse pseudoautosomal region (PAR) in Mus musculus , while it
seems to be X- specific in Mus spretus. Therefore, Mid1 is likely to be a
recent acquisition of the M. musculus PAR. Genetic and FISH analyses also
demonstrated a high frequency of unequal crossovers in the murine PAR,
creating spontaneous deletion/duplication events involving Mid1. These data
provide evidence for the first time that genetic instability of the PAR may
affect functionally important genes. In addition, we show that MID1 is the
first example of a gene subject to X-inactivation in man while escaping it
in mouse. These data contribute to a better understanding of the molecular
content and evolution of the rodent PAR.
相似文献
8.
Interchromosomal duplications of the adrenoleukodystrophy locus: a phenomenon of pericentromeric plasticity 总被引:13,自引:5,他引:13
Eichler EE; Budarf ML; Rocchi M; Deaven LL; Doggett NA; Baldini A; Nelson DL; Mohrenweiser HW 《Human molecular genetics》1997,6(7):991-1002
A 9.7 kb segment encompassing exons 7-10 of the adrenoleukodystrophy (ALD)
locus of the X chromosome has duplicated to specific locations near the
pericentromeric regions of human chromosomes 2p11,10p11, 16p11 and 22q11.
Comparative sequence analysis reveals 92-96% nucleotide identity,
indicating that the autosomal ALD paralogs arose relatively recently during
the course of higher primate evolution (5-10 million years ago). Analysis
of sequences flanking the duplication region identifies the presence of an
unusual GCTTTTTGC repeat which may be a sequence-specific integration site
for the process of pericentromeric- directed transposition. The breakpoint
sequence and phylogenetic analysis predict a two-step transposition model,
in which a duplication from Xq28 to pericentromeric 2p11 occurred once,
followed by a rapid distribution of a larger duplicon cassette among the
pericentromeric regions. In addition to facilitating more effective
mutation detection among ALD patients, these findings provide further
insight into the molecular basis underlying a pericentromeric-directed
mechanism for non- homologous interchromosomal exchange.
相似文献
9.
p53 immunoreactivity in hepatocellular adenoma, focal nodular hyperplasia, cirrhosis and hepatocellular carcinoma 总被引:2,自引:0,他引:2
I. OJANGUREN A. ARIZA E.M. CASTELLÀ A. FERNÁNDEZ-VASALO J.L. MATE J.J. NA VAS-PALACIOS 《Histopathology》1995,26(1):63-68
The prolonged half-life of mutant p53 makes feasible its immunocytochemical detection. In order to assess the pathogenetic role of mutant p53 in regenerative and neoplastc liver disease we studied its immunohistochemical expression in cases of hepatic cirrhosis, hepatocellular carcinoma (HCC), cirrhosis with areas of HCC, hepatocellular adenoma and focal nodular hyperplasia. The study included needle and wedge biopsies of 50 cirrhotic livers, 59 HCCs (36 of them with associated cirrhosis), six adenomas and two focal nodular hyperplasias. Sixty-five HCC fineneedle cytology specimens were also included in the study. There was no immunohistochemical evidence of mutant p53 expression in any of the cases of cirrhotic liver (except for one instance associated with HCC) adenoma or focal nodular hyperplasia. In contrast p53 was detected in 8.5% of HCC cases in the biopsy series and 24% of HCC cases in the fine needle aspiration series. In addition, mutant p53 expression in HCC was positively correlated with tumour grade. According to grade, the distribution of p53 positive immunoreactivity among HCCs was as follows: Grade I-II, 0% of cases in the biopsy series and 9% in the fine needle aspirates; Grade III, 18% in the biopsy series and 55% in the fine needle aspirates; and Grade IV, 40% in the biopsy series. Therefore, mutant p53 expression does not seem to be associated with benign liver lesions but seems to correlate with the progression of HCC through various grades of increasing malignancy. 相似文献
10.