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1.
PJ Commerford 《Cardiovascular journal of Africa》2015,26(4):151-Aug;26(4):151
2.
Hans Bosma Martin PJ van Boxtel Gertrudis IJM Kempen Jacques ThM van Eijk Jelle Jolles 《BMC public health》2007,7(1):179
Background
The aims of this study were to examine the extent to which higher intellectual abilities protect higher socio-economic groups from functional decline and to examine whether the contribution of intellectual abilities is independent of childhood deprivation and low birth weight and other socio-economic and developmental factors in early life. 相似文献3.
4.
Myofibroblasts and the progression of diabetic nephropathy 总被引:23,自引:3,他引:20
Essawy M; Soylemezoglu O; Muchaneta-Kubara E; Shortland J; Brown C; El Nahas A 《Nephrology, dialysis, transplantation》1997,12(1):43-50
Background. The cellular mediators of progressive
renal fibrosis in diabetic nephropathy remain unknown. Myofibroblasts have
been implicated in the pathogenesis of experimental and clinical renal
fibrosis. Their role in the progression of diabetic nephropathy is the
subject of this study.Subjects and methods. We have
studied by immunohistochemistry the expression of cytoskeletal proteins
associated with the activation of myofibroblasts; &agr;-smooth-muscle
actin (&agr;-SMA), vimentin (Vi) and desmin (D), in the kidneys of 25
patients with diabetic nephropathy (5 patients with diabetic nephropathy (5
patients had a superimposed glomerulonephritis). Comparisons were made with
normal tissue for three kidneys removed for renal-cell carcinoma.
Correlations were studied between clinical and biochemical parameters with
the expression renal cytoskeletal proteins. Results.
In normal kidneys, cells expressing &agr;-SMA were confined to the
vascular media and adventia while immunoreactive Vi was detected in
glomerular epithelial cells. In diabetic kidneys, cells expressing
&agr;-SMA were detected primarily in the renal interstitium and to a
lesser extent in some glomeruli in association with mesangial
proliferation. Vimentin immunostain decreased in glomeruli displaying
diabetic hyalinosis and sclerosis. By contrast, strong Vi immunoreactivity
was noted in atrophic diabetic tubules and to a lesser extent in the
interstitium. Desmin was not detected in either normal or diabetic kidneys.
Close correlations were observed between the expression of renal
cytoskeletal proteins and the progression of renal insufficiency.
Interstitial &agr;-SMA proved to be a predictor of progressive diabetic
nephropathy (R2 for 1/serum Cr slope=0.608,
P=0.00001). This predictive parameters; tubular atrophy
(R2=0.477, P=0.00004) and interstitial fibrosis
(R2=0.28, P=0.001). Conclusion.
We have demonstrated in this study the neoexpression of cytoskeletal
proteins within diabetic kidneys. This has allowed the identification of
new predicting histological markers for the progression of diabetic
nephropathy. 相似文献
5.
6.
Previous reports in the literature have described correlation of increasing repeat length with severity of the phenotype, in Kennedy syndrome. We describe male siblings with different repeat lengths, with lack of expression of the phenotype in the sibling with the longer repeat length. The phenotype was identical to motor neurone disease. There is variability of expression in Kennedy syndrome and repeat length even in siblings cannot be taken as a conclusive indicator of severity. CAG repeat length cannot be used to predict the natural history of Kennedy disease. The diagnosis of Kennedy syndrome should be considered in male patients presenting with atypical motor neurone disease. 相似文献
7.
PJ Woll PhD MRCP R Pettengell PhD FRACP 《International journal of clinical practice》1997,51(2):111-115
SUMMARY The interferons are natural glycoproteins secreted in response to various stimuli, including viral infection. They have antiviral, antiproliferative and immunomodulatory effects on different target cell populations. Since recombinant human interferons have become available, they have been tested in a wide range of malignancies. They are well established in the treatment of hairy cell leukaemia, chronic myelogenous leukaemia and multiple myeloma. Although they have documented activity against lymphoma, melanoma, renal cell cancer and carcinoid tumours, their role in the treatment of these tumours is less clear. In the common solid tumours, such as lung cancer and colorectal cancer, the use of interferons remains experimental. Here we will summarise their practice applications in oncology, using randomised studies where available to establish their place in multi-modality treatment. We will not discuss their use as antiviral or immunomodulating agents in viral and autoimmune diseases, multiple sclerosis or after organ transplantation. 相似文献
8.
9.
10.
Ming Yang Chang Emma Parker Salwa Ibrahim John R Shortland Meguid El Nahas John L Haylor Albert C M Ong 《Nephrology, dialysis, transplantation》2006,21(8):2078-2084
BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited human kidney disease and is caused by germline mutations in PKD1 (85%) or PKD2 (15%). It has been estimated that around 1% of tubular cells give rise to cysts, and cell hyperproliferation has been noted to be a cardinal feature of cystic epithelium. Nevertheless, it is uncertain whether the increase in proliferative index observed is an early or late feature of the cystic ADPKD kidney. METHODS: Two Pkd2 mouse mutants (WS25 and WS183) have been recently generated as orthologous models of PKD2. To determine the effect of Pkd2 dosage on cell proliferation, cyst formation and renal fibrosis, we studied renal tissue from Pkd2(WS25/WS25) and Pkd2(+/-) mice by histological analysis. We also examined the proliferative index in archival nephrectomy tissue obtained from patients with ADPKD and normal controls. RESULTS: The proliferative index of non-cystic tubules in Pkd2 mutant mice as assessed by proliferating cell nuclear antigen and Ki67-positive nuclei was between 1-2%, values 5-10 times higher than control tissue. Similarly, the proliferative index of non-cystic tubules in human ADPKD kidneys was 40 times higher than corresponding controls. In Pkd2 mutant mice, significant correlations were found between the fibrosis score and the mean cyst area as well as with the proliferative index. Of significance, proliferating tubular cells were uniformly positive for polycystin-2 expression in Pkd2(+/-) kidney. CONCLUSION: These results suggest that an increase in cell proliferation is an early event preceding cyst formation and can result from haploinsufficiency at Pkd2. The possible pathogenic link between tubular cell proliferation, interstitial fibrosis and cyst formation is discussed. 相似文献