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101.
Thompson HJ; McGinley JN; Wolfe P; Singh M; Steele VE; Kelloff GJ 《Carcinogenesis》1998,19(12):2181-2185
An experimental model for mammary carcinogenesis has been described in
which intraductal proliferations, ductal carcinomas in situ and
adenocarcinomas can be readily detected and the frequency of their
occurrence quantified. The objective of the experiment reported in this
study was to determine the latency period between carcinogen administration
and the occurrence of each of these types of lesion. A total of 150 female
Sprague-Dawley rats were injected i.p. with 50 mg 1- methyl-1-nitrosourea
(MNU)/kg body wt at 21 days of age. Groups of 30 rats each were killed at
7, 14, 21, 28 and 35 days post-carcinogen. Mammary intraductal
proliferations were the first detected lesions and were observed in 20% of
the animals at 14 days following carcinogen administration. At 21 days
post-carcinogen ductal carcinomas in situ and adenocarcinomas were
observed. The number of each type of lesion increased with time
post-carcinogen, but the temporal pattern of occurrence was different among
lesion types. The pattern of lesion occurrence was consistent with
intraductal proliferations being a precursor lesion for ductal carcinomas
in situ and adenocarcinomas. Furthermore, the data imply that ductal
carcinomas in situ represent one pathway of morphological progression by
which intraductal proliferations evolve into invasive carcinomas, but that
this lesion type, as currently defined histologically, may not be an
obligatory intermediate in morphologic progression. These findings are
consistent with emerging evidence of multiple but distinct pathogenetic
pathways leading to mammary carcinomas that display different morphological
patterns and biological activities.
相似文献
102.
G. Viot-Szoboszlai J. Amiel F. Doz M. Prieur J. Couturier JN Zucker I. Henry A. Munnich M. Vekemans S. Lyonnet 《Clinical genetics》1998,53(4):278-280
Here we report Wilms' tumor, gonadal dysgenesis and a bifid uterus in an 18-month-old female with a terminal deletion of the long arm of chromosome 2 [46, XX, del(2)(q37.1)]. Since Wilms' tumor has been previously reported in the 2q37 deletion syndrome, the present observation raises the question of whether a tumor susceptibility gene maps to chromosome 2q37 and suggests giving consideration to the possible occurrence of Wilms' tumor in the course of disease. 相似文献
103.
104.
Purified interleukin-3 and erythropoietin support the terminal differentiation of hemopoietic progenitors in serum-free culture 总被引:4,自引:0,他引:4
We studied the effect of purified interleukin-3 (IL-3) and erythropoietin on colony formation by hemopoietic progenitors in serum- free cultures of spleen cells from 5-fluorouracil (5-FU)-treated mice. In the presence of IL-3 alone, most of the multilineage (three or more lineages) colonies did not contain erythroid cells. However, in the presence of IL-3 and erythropoietin, most of the multilineage colonies contained various numbers of erythroid cells. Replating experiments suggest that IL-3 maintains the growth of the progenitor cells, which could differentiate into erythroid cells. Erythropoietin facilitated the terminal differentiation and amplification of erythroid cells, although it did not sustain the growth of multipotential stem cells. Single-cell transfer experiments demonstrate that IL-3 supported the late stages of differentiation of neutrophils, macrophages, eosinophils, and megakaryocytes in the absence of lineage-specific factors. Therefore, IL-3 supports the differentiation of multilineage hemopoietic progenitors, and the terminal differentiation of most hemopoietic lineages, with the exception of the erythroid lineage. 相似文献
105.
Tinidazole as a single drug therapy given in a single dose daily for 5 or 3 days was put to rigorous test in malnourished children. Of 25 children with amoebic liver abscess, 23 were cured. The 2 remaining cases required surgical drainage followed by other amoebicides, one subsequently dying from complicating bronchopneumonia. 相似文献
106.
The conformation of myelin encephalitogenic or basic protein (BP) was investigated with a double-antibody radioimmunoassay by studying the reaction of BP or its fragments with antibodies produced in two rabbits against peptide 43-88 linked to rabbit serum albumin. Both antisera reacted well with peptide 43-88 but showed little or no reaction with BP. Absorption of these antisera with a BP-immunoadsorbent did not remove the antibody activity against peptide 43-88. Within the region of peptide 43- 88 it was shown that peptides 68-88 and 79-88 gave an equivalent or better reaction than peptide 43-88, whereas peptides 43-67 and 64-73 had very little reactivity. In the BP fragments containing region 43-88, peptide 1-88 showed the best reactivity, peptide 20-166 showed minimal reactivity, while peptide 1-115 showed none. These data document the internal position of at least a portion of peptide 43-88 and all of residues 79-88 in the BP molecule. The much greater reactivity of peptide 1-88 as compared to peptide 1-115 suggests that the region or a portion of the region of BP containing residues 89- 115 participates in the conformational alignment of BP restricting access to peptide 79-88. After absorption with BP, neither of the antisera prepared to peptide 43-88 reacted with PNS myelin in fixed tissue sections but continued to react with CNS myelin in similarly treated sections. The present findings demonstrate the need to consider the role of shielded antigenic determinants in the investigation of antigens or of immune responses. 相似文献
107.
Erythropoietin (Epo) binding to its receptor (EpoR) induces tyrosine phosphorylation in responsive cells and this ability is required for a mitogenic response. One of the substrates of tyrosine phosphorylation is the Epo receptor (EpoR). The carboxyl region of EpoR cytoplasmic domain is required for EpoR phosphorylation and has been shown to negatively affect the response to Epo both in vivo and in cell lines. Hematopoietic cell phosphatase (HCP) has also been hypothesized to negatively regulate erythropoiesis, based on the hypersensitivity to Epo of erythroid lineage cells in moth-eaten mice that genetically lack HCP. In the studies presented here, we show that HCP binds the tyrosine phosphorylated Epo receptor through the amino-terminal src-homology 2 (SH2) domain of HCP. Using a series of phosphotyrosine-containing peptides, potential HCP binding sites in the cytoplasmic domain of the EpoR are identified. The results support the concept that, after Epo stimulation, phosphorylation of EpoR provides a docking site for HCP in the receptor complex. Recruitment of HCP to the complex and its subsequent dephosphorylation of substrates and/or associated kinases may be important to mitigate the ligand-induced mitogenic response. 相似文献
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