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Rapid screening of fecal samples for Vibrio cholerae by a coagglutination technique. 总被引:4,自引:1,他引:4 下载免费PDF全文
A coagglutination procedure for detecting Vibrio cholerae was applied directly to 125 watery fecal samples received in the laboratory for bacteriological culture: many of these were from suspected cases of cholera. Of 47 bacteriologically proved cases of cholera, 44 (93.6%) gave positive results by the coagglutination method. There was a good correlation between the coagglutination method, dark-field microscopy, and culture. 相似文献
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Rajendran Sanalkumar Sasidharan Vidyanand Chandrasekharan Lalitha Indulekha Jackson James 《Journal of molecular neuroscience : MN》2010,42(1):17-27
Fate-specific differentiation of neural progenitors attracts keen interest in modern medicine due to its application in cell
replacement therapy. Though various signaling pathways are involved in maintenance and differentiation of neural progenitors,
the mechanism of development of lineage-restricted progenitors from embryonic stem (ES) cells is not clearly understood. Here,
we have demonstrated that neuronal vs. glial differentiation potential of ES cell-derived neural progenitors (ES-NPs) are
governed by the growth factors, exposed during their proliferation/expansion phase and cannot be significantly altered during
differentiation phase. Exposure of ES-NPs to fibroblast growth factor-2 (FGF2) during proliferation triggered the expression
of pro-neural genes that are required for neuronal lineage commitment, and upon differentiation, predominantly generated neurons.
On the other hand, epidermal growth factor (EGF)-exposed ES-NPs are not committed to neuronal fate due to decreased expression
of pro-neural genes. These ES-NPs further generate more glial cells due to expression of glial-restricted factors. Exposure
of ES-NPs to the same growth factors during proliferation/expansion and differentiation phase augments the robust differentiation
of neurons or glial subtypes. We also demonstrate that, during differentiation, exposure to growth factors other than that
in which the ES-NPs were expanded does not significantly alter the fate of ES-NPs. Thus, we conclude that FGF2 and EGF determine
the neural vs. glial fate of ES-NPs during proliferation and augment it during differentiation. Further modification of these
protocols would help in generating fate-specified neurons for various regenerative therapies. 相似文献
36.
Background: The spinal cord is a common site of involvement in multiple sclerosis (MS) where pathology contributes substantially to locomotor
disability. Previous studies have demonstrated significant correlations between clinical disability and cervical cord atrophy,
but not with cord T2 lesion load. We evaluate cervical cord pathology using, for the first time, quantitative T1 relaxation time (T1), which shows histopathological specificity for tissue damage in the cerebral white matter. Method: Cervical cord T1 was compared in 15 MS patients [8 relapsing-remitting (RR), 7 secondary progressive (SP)] and 6 healthy controls, and related
to normalised upper cervical cord area (UCCa), cerebral white matter T1, T2 lesion load and disability measures including the Expanded Disability Status Scale (EDSS), Ambulation index (AI) and timed
25-foot walk. T1 maps of the brain and cervical cord were acquired using a high-resolution, 3-dimensional fast low-angle shot
sequence. Dual-echo sequences were also obtained. Results: Median cervical cord T1 [mean (standard deviation)] was significantly greater in RR [854 [28] ms] (p = 0.0006) and SP patients [927 [67] ms] (p <
0.0001) compared with controls [888 [61] ms], and in SP vs. RR patients (p = 0.002). In the overall patient cohort, it correlated
significantly with median cerebral white matter T1 (r = 0.7, p = 0.0046), UCCa (r = −0.87, p < 0.0001), but not T2 lesion
loads. Both median cervical cord T1 and UCCa (respectively) correlated significantly with the EDSS (r = 0.55, p = 0.03; r
= −0.54, p = 0.04), AI (r = 0.77, p = 0.001; r = −0.60, p = 0.02) and timed 25-foot walk (r = 0.56, p = 0.03; r = −0.55, p
= 0.04). Conclusion: Cervical cord T1 distinguishes between MS subgroups and could also prove a useful surrogate outcome measure in MS. The relation of cervical
cord T1 to cerebral white matter T1 suggests that cord pathology may be influenced by tissue damage upstream.
Received: 13 June 2002, Received in revised form: 9 October 2002, Accepted: 18 October 2002
Supported by a research grant from The University of Nottingham.
Correspondence to Lalitha Vaithianathar 相似文献
37.
The "early-labeled" peak (ELP) of 14CO excretion following injection of glycine-2-14C was used to study erythropoiesis in a patient with sideroblastic anemia and in four subjects with myeloproliferative disorders. The ELP was greatly enlarged in all patients, as compared with a normal volunteer. The contour of the peaks from the hematologically abnormal subjects suggested the presence of increased erythroid heme degradation. In the patient with sideroblastic anemia, all hours of the early peak were significantly reduced after transfusion. This was interpreted to mean that even the earliest or "nonerythroid" phase of the peak is influenced by erythropoietic activity, at least under conditions of erythropoietic stress. 相似文献
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Mahabeleshwar GH Kawanami D Sharma N Takami Y Zhou G Shi H Nayak L Jeyaraj D Grealy R White M McManus R Ryan T Leahy P Lin Z Haldar SM Atkins GB Wong HR Lingrel JB Jain MK 《Immunity》2011,34(5):715-728
Highlights? KLF2 deficiency confers a proinflammatory phenotype to myeloid cells ? Myeloid KLF2 deficiency renders animals resistant to polymicrobial infection ? Myeloid KLF2 deficiency renders animals susceptible to endotoxic shock ? KLF2 negatively regulates the NF-κB-HIF-1α axis in macrophages 相似文献
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Microglandular adenosis (MGA) and atypical MGA (AMGA) are unusual lesions of the breast. They were once regarded as benign proliferative lesions and innocent bystanders. Several lines of evidence suggested that they could be neoplastic, clonal lesions and a non‐obligate precursor for triple‐negative breast cancers (TNBC). Recent work published in The Journal of Pathology by Guerini‐Rocco and colleagues provided further evidence regarding the precursor–product relationship between MGA/AMGA and TNBC. Using a massively parallel sequencing approach, they demonstrated that MGA/AMGA, particularly those associated with TNBC, could be clonal neoplastic lesions showing clonal non‐synonymous mutations, but none in pure MGA. Importantly, those alterations were observed in the associated TNBC. They were also able to identify recurrent alterations in TP53 in those MGA/AMGA cases as well as their associated TNBC. The findings, in conjunction with others, underscore the significance for MGA in clinical diagnosis. The potential of a benign lesion to progress into an aggressive malignant tumour implies that modification of the current management approach may be necessary. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. 相似文献