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31.
BACKGROUND: Growing interest is nowadays focused on the quality of life of
elderly people who survive with chronic diseases. Coronary heart disease
(CHD) is one of the most common diseases among the elderly and may have an
unfavourable impact on the patient's emotional well-being. OBJECTIVES: We
aimed to describe the prevalence of depression and the occurrence of
depressive symptoms among elderly CHD patients, with a special emphasis on
the relations between depression and the severity of CHD, and to find out
the possible association between CHD and depression. METHODS: The study was
carried out at the health centre of the municipality of Lieto, in
south-west Finland. The study population consisted of 488
community-dwelling men and 708 women, over 64 years old, from among whom
the participants with CHD (89 men and 73 women) were selected, and for whom
178 male and 146 female sex- and age- matched controls (free of CHD) were
drawn from the population. CHD patients were selected on the basis of the
presence of angina pectoris or a past myocardial infarction. Depressive
symptoms were measured with the Zung Self-rating Depression Scale.
Depression was described in relation to the severity of dyspnoea and chest
pain among patients. The associations between depression and age, health,
health behaviour, drugs, functional ability and social, psychosocial and
environmental factors were analysed by logistic regression analyses.
RESULTS: The prevalence of depression was 29% among male patients and 20%
among female patients. Depression was significantly more common among male
CHD patients than among male controls (P = 0.011). Among women, depression
was not associated with CHD. Earlier, depression had gone undiagnosed among
many CHD patients and controls, especially male patients. Among male CHD
patients, depression was associated with more severe dyspnoea, but no
similar association was found among female CHD patients. Among men the
occurrence of CHD, physical disability, widowhood or divorce, and among
women previous clinical depression, physical disability and the use of
angiotensin-converting enzyme (ACE) inhibitors, were associated with
depression. CONCLUSION: Depression is common among patients with CHD. It
seems that CHD is not an independent factor in the aetiology of depression
among the elderly. The association of CHD with depression among men is
explained by the acute or chronic psychic stress caused by CHD. It may be
that the more complicated the patient's CHD, the more probable is the
presence of depression.
相似文献
32.
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
33.
Alves C Silva F Gusmão L Seruca R Soares P Reis RM Amorim A 《European journal of human genetics : EJHG》2000,8(7):540-544
The promoter region of the human GSTP1 gene contains a polymorphic short tandem repeat (STR) locus consisting of pentanucleotide repeat units (ATAAA). In this work we report the existence of a total of 26 alleles in a Caucasian population. While differences in size (ranging from one to five base pairs) were responsible for the major variation, in five size-defined classes, two alternative sequences were found. Automatic fragment sizing and sequencing analysis revealed that this polymorphism is of a highly complex nature in contrast with previous reports. A genetic population study was carried out on a random sample from Portugal showing no deviation from Hardy-Weinberg equilibrium. Somatic instability studies were also performed on gastric and thyroid tumours using this STR: no instability was detected in thyroid tumour tissues when compared with their normal counterpart but in gastric tumour tissues microsatellite instability (MSI) was detected in 9.6% of the cases and loss of heterozygosity (LOH) also in 9.6% of the cases studied. The results obtained with GSTP1 in gastric cancer were compared with previously reported data on MSI using BAT-26 and several dinucleotide repeat markers. 相似文献
34.
Dina Ruano António Macedo Ana Dourado Maria Jo?o Soares José Valente Isabel Coelho Vítor Santos Maria Helena Azevedo Ann Goodman Mara Helena Hutz Clarissa Gama Maria Inês Lobato Paulo Belmonte-de-Abreu Joana Almeida Palha 《American journal of medical genetics. Part B, Neuropsychiatric genetics》2004,(1):41-45
35.
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
36.
Microsatellite instability, mitochondrial DNA large deletions, and mitochondrial DNA mutations in gastric carcinoma 总被引:30,自引:0,他引:30
Máximo V Soares P Seruca R Rocha AS Castro P Sobrinho-Simões M 《Genes, chromosomes & cancer》2001,32(2):136-143
Mitochondrial DNA (mtDNA) large deletions and mtDNA mutations have been demonstrated in various types of human cancer. The relationship between the occurrence of such alterations and the nuclear microsatellite instability (MSI) status of the neoplastic cells remains controversial. In an attempt to clarify the situation in gastric carcinoma, we studied, by PCR/SSCP and sequencing, five mitochondrial genes and two D-loop regions in 32 gastric carcinomas that had been previously screened for MSI and mitochondrial common deletion. MtDNA alterations were detected in 26 carcinomas (81%). All the mtDNA mutations, which occurred mainly in the D-loop and ND1 and ND5 genes, were transitions. D-loop alterations (insertions and/or deletions) were not significantly associated with mutations in the coding regions. There was a trend towards an inverse relationship between the occurrence of mitochondrial common deletion and mtDNA mutations. No significant relationship was observed between MSI status and mtDNA mutations, whereas the mitochondrial common deletion appeared to be almost exclusively restricted to MSI-negative tumors. The latter finding--almost no gastric carcinoma with MSI-positive phenotype has large deletions of mtDNA--needs to be confirmed in a larger series and in tumors from other organs. 相似文献
37.
An in vitro model for infection with Leishmania major that mimics the immune response in mice. 总被引:1,自引:0,他引:1
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By using a primary in vitro response specific for Leishmania major, normal T cells from resistant CBA/CaH-T6J and susceptible BALB/c mice commit to a Th1 and a Th2 response, respectively. Since commitment occurred, we measured the production of gamma interferon (IFN-gamma), interleukin-1 (IL-1), IL-2, IL-4, IL-5, IL-10, and IL-12, prostaglandin E2 (PGE2), transforming growth factor beta (TGF-beta), and nitric oxide in the first 7 days of the response to identify factors that are critical for Th1 and Th2 development. While cells from resistant CBA mice produced more IFN-gamma, IL-10, and nitric oxide, cells from susceptible BALB/c mice produced more IL-1alpha, IL-5, PGE2, and TGF-beta. Although substantial amounts of IL-12 were detected, IL-12 did not associate with either Th1 or Th2 development. We did not anticipate that cells from resistant CBA mice would make more IL-10 in vitro. However, this also occurred in vivo since CBA mice produced substantial amounts of IL-10 following infection with L. major. Moreover, adding anti-IL-10 to primary in vitro responses enhanced production of IFN-gamma and nitric oxide by cells from CBA and BALB/c mice. Therefore, IL-10 cannot be regarded as a cytokine that associates with susceptibility to infection with L. major. Finally, the data presented here suggest that a collection of factors that can be produced by accessory cells influence Th commitment (e.g., IL-1, PGE2, and TGF-beta favor Th2 development). 相似文献
38.
Increased numbers of pulmonary megakaryocytes in patients with arterial pulmonary tumour embolism and with lung metastases seen at necropsy.
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![点击此处可从《Journal of clinical pathology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
F. A. Soares 《Journal of clinical pathology》1992,45(2):140-142
AIMS: To compare the number of pulmonary megakaryocytes in patients with local malignant disease without metastases with the numbers in patients with pulmonary tumour emboli without lung metastases and with those with pulmonary metastases. METHODS: The prevalence of pulmonary megakaryocytes was studied in 40 necropsies divided into four groups of 10 cases each: normal lungs (I); localised malignancies (II); pulmonary tumour embolism without lung metastases (III); pulmonary tumour embolism and lung metastases (IV). Five fragments (one of each pulmonary lobe) of tissue lung were collected, embedded in paraffin wax, sectioned, and stained by an immunohistochemical method to detect factor VIII related antigen. The number of megakaryocytes was evaluated in 500 high power fields/case. RESULTS: No differences were observed between groups I and II or between groups III and IV, but there was a 3.5-fold increase in the number of megakaryocytes in the groups with pulmonary tumour embolism or lung metastases compared with those with local neoplasms or normal lungs. CONCLUSIONS: An increased number of pulmonary megakaryocytes correlated with the presence of tumour cells in the microcirculation of the lungs or parenchymal metastases, but not with local malignancies without lung disease. The permanent siting of tumour emboli may stimulate megakaryocytes to migrate to the lungs, and may increase the release of platelets into the pulmonary circulation. 相似文献
39.
Characterization of Paracoccidioides brasiliensis isolates by random amplified polymorphic DNA analysis.
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C M Soares E E Madlun S P da Silva M Pereira M S Felipe 《Journal of clinical microbiology》1995,33(2):505-507
We initially used 25 different random primers in order to test their ability to generate random amplified polymorphic DNA fragments from the dimorphic human pathogenic fungus Paracoccidioides brasiliensis. From the tested primers we chose five to distinguish between seven isolates of this microorganism. The DNA amplification patterns allowed clear differentiation of the seven isolates into two distinct groups with only 35% genomic identity. One of these groups contained two subgroups with 81% genetic similarity. The random amplified polymorphic DNA analysis method proved to be a good tool for analyzing and comparing different genomes of P. brasiliensis isolates. 相似文献
40.
Sobrinho-Simões M Preto A Rocha AS Castro P Máximo V Fonseca E Soares P 《Virchows Archiv : an international journal of pathology》2005,447(5):787-793
The newly discovered molecular features of well-differentiated thyroid carcinomas derived from follicular cells are reviewed,
within the frame of the 2004 WHO classification of thyroid tumours, under the following headings: “Follicular carcinoma”,
“Papillary carcinoma”, “Follicular variant of papillary carcinoma” and “Hürthle cell tumours”. A particular emphasis is put
on the meaning of PAX8–PPARγ rearrangements, RAS and BRAF mutations, and deletions and mutations of mitochondrial genes and of nuclear genes encoding for mitochondrial enzymes, for
thyroid tumorigenesis. 相似文献