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41.
高效液相色谱法测定寒痹停片中士的宁含量 总被引:6,自引:0,他引:6
目的:建立用HPLC测定寒痹停片中士的含量的方法。方法:氰基柱;流动相-甲醇-水-三乙胺-乙酸(9800:155:15:30);紫外检测波长254nm。结果:在4~20ug/ml范围内,标准曲线回归方程为:Y=-2803+8967x(r=0.9997),RSD=1.65%?加样回收率的平均值为99.82%。结论:实验表明,这是一个适用于生产控制和产品质量检验的简单、快速、准确的方法。 相似文献
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IS Park H Kiyomoto F Alvarez YC Xu HE Abboud SL Abboud 《American journal of kidney diseases》1998,32(6):1000-1010
The renal insulin-like growth factor-I (IGF-I) system has been implicated in the pathogenesis of renal hypertrophy, altered hemodynamics, and extracellular matrix expansion associated with early diabetes. The relative abundance of IGF binding proteins (IGFBPs) in the renal microenvironment may modulate IGF-I actions. However, the precise IGFBPs expressed in the glomerular and tubulointerstitial compartments during diabetic renal growth have not been characterized. In the present study, in situ hybridization studies were performed to examine the expression of IGFBP-1 to -6 messenger RNAs (mRNAs) 3, 7, and 14 days after streptozotocin (STZ) injection in rats. In control, nondiabetic kidneys, all six IGFBP mRNAs were differentially expressed with a predominance of IGFBP-5. The onset of renal hypertrophy in STZ-induced diabetes was associated with a rapid and site-specific induction of IGFBP-1, -3, and -5 mRNAs. In contrast, basal expression of IGFBP-2, -4, and -6 mRNAs was not altered in diabetic rats. IGFBP-5 mRNA expression increased in diabetic glomeruli, cortical, and inner medullary peritubular interstitial cells at days 3, 7, and 14. Although normal glomeruli failed to express IGFBP-3, it was induced concomitantly with IGFBP-5 in diabetic glomeruli and cortical peritubular interstitial cells. IGFBP-1 mRNA levels also increased in cortical tubular cells at each time point tested. Peak induction of IGFBP-3 and -5 was observed at day 3, whereas IGFBP-1 was delayed until day 7. IGFBP-1, -3, and -5 mRNA levels declined by day 14, but remained persistently elevated above control. By immunoperoxidase staining, similar alterations in the pattern of IGFBP-3 and -5 protein expression were observed at each time point. The preferential and site-specific increase in IGFBP-1, -3, and -5 suggest that these IGFBPs may regulate the local autocrine and/or paracrine actions of IGF-I and contribute to the pathogenesis of the early manifestations of diabetic nephropathy. 相似文献
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Linkage of the MHC to familial multiple sclerosis suggests genetic heterogeneity. The Multiple Sclerosis Genetics Group 总被引:5,自引:0,他引:5
Haines JL; Terwedow HA; Burgess K; Pericak-Vance MA; Rimmler JB; Martin ER; Oksenberg JR; Lincoln R; Zhang DY; Banatao DR; Gatto N; Goodkin DE; Hauser SL 《Human molecular genetics》1998,7(8):1229-1234
Multiple sclerosis (MS) is a demyelinating autoimmune disease of the
central nervous system. While its etiology is not well understood, genetic
factors are clearly involved. Until recently, most genetic studies in MS
have been association studies using the case-control design testing
specific candidate genes and studying only sporadic cases. The only
consistently replicated finding has been an association with the HLA-DR2
allele within the major histocompatibility complex (MHC) on chromosome 6.
Using the genetic linkage design, however, evidence for and against linkage
of the MHC to MS has been found, fostering suggestions that sporadic and
familial MS have different etiologies. Most recently, two of four genomic
screens demonstrated linkage to the MHC, although specific allelic
associations were not tested. Here, a dataset of 98 multiplex families was
studied to test for an association to the HLA-DR2 allele in familial MS and
to determine if genetic linkage to the MHC was due solely to such an
association. Three highly polymorphic markers (HLA-DR, D6S273 and TNFbeta)
in the MHC demonstrated strong genetic linkage (parametric lod scores of
4.60, 2.20 and 1.24, respectively) and a specific association with the
HLA-DR2 allele was confirmed (TDT; P < 0.001). Stratifying the results
by HLA-DR2 status showed that the linkage results were limited to families
segregating HLA-DR2 alleles. These results demonstrate that genetic linkage
to the MHC can be explained by the HLA-DR2 allelic association. They also
indicate that sporadic and familial MS share a common genetic
susceptibility. In addition, preliminary calculations suggest that the MHC
explains between 17 and 62% of the genetic etiology of MS. This
heterogeneity is also supported by the minority of families showing no
linkage or association with loci within the MHC.
相似文献
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Monoclonal antibodies cross‐reactive with four major aflatoxins (AFs) were produced by fusion of P3/NS‐1/1‐AG4–1 murine myeloma cells with spleen cells isolated from a BALB/c mouse that had been immunized with aflatoxin B3‐hemisuccinate conjugated to bovine serum albumin. Six stable clones were obtained. Isotyping by enzyme‐linked immunosorbent assay (ELISA) revealed that the antibodies produced by all but two of the clones were of the IgG1 type. Of the remaining clones, one produced IgG21, and the other IgA. Competitive radioimmunoassay using tritiated AFB1 as the marker ligand revealed that two clones produced antibody that cross‐reacted well with both AFB1 and AFG1; one clone produced an antibody that had good specificity toward AFB1. The relative cross‐reactivities (RCR) of antibody produced by clone 575B8F12 for AFB1, AFB2, AFG1, and AFG2 were 100, 5, 153, and 6, respectively. The RCR of antibody produced by clone 575G4H7 for the above AFs were 100, 40, 153, and 40, respectively. The RCR of antibody produced by clone 585D4D6 for the above AFs were 100, 40, 152, and 23, respectively. Antibodies produced by the other three clones were inadequate for immunoassay because their affinities for the AFs were 100 times less than the three clones described above. 相似文献
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