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51.
Julie Seguier Véronique Gelsi-Boyer Mikael Ebbo Zeinab Hamidou Aude Charbonnier Emmanuelle Bernit Jean-Marc Durand Jean-Robert Harlé Norbert Vey Nicolas Schleinitz 《Autoimmunity reviews》2019,18(1):36-42
Background
We conducted a monocentric retrospective study of patients with myelodysplastic syndromes (MDS) and autoimmune or inflammatory disorders (AIMs) and a literature review. We analyzed the association with subgroups of the WHO 2016 MDS classification and patient's survival in a case control study. Risk factors associated with survival were analyzed by uni- and multivariate analysis.Results
From all MDS patients 11% presented with AIMs. These were heterogeneous and the most frequent where polyarthritis (25%) and autoimmune cytopenias (17%). No difference for frequency and type of AIMs was observed for the WHO 2016 MDS subgroups (p?=?.3). In the case control study WHO classification, karyotype abnormalities, IPSS-R and IPSS were similar in both groups. The overall survival from MDS diagnosis was better in the group with AIMs [10.3?±?0.6 (IC95% 6.2–12.9) versus 4.8?±?1.1?years (IC95% 4.2–8.7), p?=?.04]. The better survival was restricted to MDS with low or intermediate-1 IPSS [11.1?±?1.5 (IC95% 9.9-NR) versus 8.7?±?1.3?years (IC95% 4.8–10.3), p?=?.006]. The better survival was only observed when AIMs diagnosis was timely associated or appeared after MDS diagnosis (p?=?.04). Factors associated with a better overall survival and survival without AML were steroid dependence [respectively HR?=?0.042, p?=?.003, (IC95% 0.005–0.33) and HR?=?0.07, p?=?.002, (IC95% 0.013–0.39)], a diagnosis of AIMs and MDS timely associated [respectively HR?=?0.05, p?=?.009, (IC95% 0.006–0.478) and HR?=?0.1, p?=?.008, (IC95% 0.018–0.54)] or a diagnosis of AIMs after MDS [respectively HR?=?0.024, p?=?.009, (IC95% 0.001–0.39) and HR?=?0.04, p?=?.008, (IC95% 0.003–0.43)].Conclusion
Autoimmune and inflammatory diseases associated to MDS are heterogeneous. AIMs diagnosed after or concomitantly to MDS seems associated with a better survival. Prospective studies are necessary to demonstrate that autoimmunity is associated to a better control of the MDS clone. 相似文献52.
J. B. Matthews A. Pitigala-Arachchi I. J. Crane C. Scully S. S. Prime 《Virchows Archiv : an international journal of pathology》1988,413(6):521-528
Summary The development of oral epithelial expression of Ia antigens and its relationship to the presence of IL-2r+ (CD25+) cells was investigated in rats treated with the water soluble carcinogen 4-nitroquinoline-N-oxide (4NQO). Acetone fixed frozen sections of the palate and tongue were stained using an indirect immunoperoxidase technique and monoclonal antibodies to rat Ia (I-A & I-E) and IL-2 receptor. After 4 weeks 4NQO treatment all rats expressed oral epithelial Ia but thereafter (2–9 months) expression was present in only 20–40% of animals. Epithelial expression of Ia by histologically normal, dysplastic and neoplastic epithelium was always associated with the presence of an underlying inflammatory cell infiltrate containing CD25+ cells. Overall there were significantly more CD25+ cells in tissue specimens containing Ia+ epithelium compared with Ia– epithelium. Furthermore, during the first 4 weeks of carcinogen treatment, a significant positive correlation was found between the CD25+ cell density and occurrence of focal epithelial Ia expression. These results, together with analysis of the T cell, NK cell, macrophage and B cell content of the infiltrates induced by 4NQO, suggest that the CD25+ cells represent activated T cells. Thus, our results in this experimental model are consistent with the idea that epithelial expression of Ia is the result of production of IFN- by locally activated T cells. 相似文献
53.
Folwaczny M Glas J Török HP Fricke K Folwaczny C 《Clinical immunology (Orlando, Fla.)》2003,109(3):325-329
A 32-base-pair deletion in the CCR5 gene was previously shown to influence the susceptibility for several infectious diseases. The present study compared the frequency of the CCR5-Delta32 mutation among subjects with periodontal disease and healthy control individuals. The prevalence of the CCR5-Delta32 mutation was determined in 81 patients with generalized periodontitis and 121 healthy controls. Standardized clinical and radiographic criteria were used for the diagnosis of periodontitis for each subject. The CCR5-Delta32 mutation was identified by PCR amplification and subsequent agarose gel electrophoresis. Genotype and allele frequencies among both study groups were compared using Fisher's exact test at a level of significance of 5% (P<0.05). The frequency of the CCR5-Delta32 allele was 9.9% (16/162) for periodontitis patients and 10.7% (26/216) for the healthy controls. The allele frequencies between periodontitis patients and the control group for the CCR5-Delta32 mutation were not significantly different (P=0.801). The present study revealed no association between the CCR5-Delta32 mutation and susceptibility to periodontal disease. 相似文献
54.
L. C. Pele S. J. Thompson B. Kirkham R. P. H. Thompson J. J. Powell 《Inflammation research》2007,56(4):143-148
Objectives: The aims of this study were to determine, in peripheral blood mononuclear cells (PBMC), whether particulate antigen triggers
(i) an amplified cell proliferative response compared to soluble antigen and (ii) a dysfunctional response in cells derived
from patients with chronic inflammation and specifically in those with inflammatory bowel disease (IBD).
Subjects: Healthy volunteers (n = 17), inflammatory controls (n = 8) and patients with IBD (n = 17) were recruited from St Thomas’ and
Guys’ Hospital, London, UK.
Methods: Following optimisation of experimental conditions (0.1–10.0 μg/ml antigen), PBMC were stimulated with (i) 10.0 μg/ml recombinant
soluble heat shock protein 65 (hsp 65) and (ii) 1.0 and 10.0 μg/ml hsp 65 conjugated to microparticles (0.5 μm diameter).
PBMC proliferative responses were measured by 3H-Thymidine incorporation at day 5 and results compared between groups using unpaired t-test.
Results: Conjugation to microparticles of low dose hsp 65 significantly increased overall proliferative responses by 2–11 fold compared
to soluble antigen alone (p < 0.05). However, no specific PBMC proliferative dysregulation was noted in cells from subjects
with IBD.
Conclusions: Low dose antigen, in microparticulate form, leads to amplified cell proliferation in primary human cells, as showed previously
in cell lines and animal studies. However there is no abnormal proliferative response in cells from subjects with IBD.
Received 8 February 2006; returned for revision 7 March 2006; accepted by G. Wallace 25 October 2006 相似文献
55.
Immunomodulation of autoimmune and inflammatory diseases with intravenous immunoglobulin 总被引:2,自引:0,他引:2
Ephrem A Misra N Hassan G Dasgupta S Delignat S Duong Van Huyen JP Chamat S Prost F Lacroix-Desmazes S Kavery SV Kazatchkine MD 《Clinical and experimental medicine》2005,5(4):135-140
Abstract Intravenous immunoglobulin (IVIg) has been used in the treatment of primary and secondary antibody deficiencies for over two
decades. Since the early 1980s, the therapeutic efficacy of IVIg has been established in idiopathic thrombocytopenic purpura,
Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, myasthenia gravis, dermatomyositis and Kawasaki
syndrome, and the prevention of graft versus host disease in recipients of allogeneic bone marrow transplants. Its use has
also been reported in a large number of other autoimmune and systemic inflammatory conditions. In this review, we discuss
the mechanisms by which IVIg exerts immunomodulatory effects in immune pathologies. 相似文献
56.
Jeong HJ Sung SH Hong SW Moon JI Kim SI Kim YS Park K 《Virchows Archiv : an international journal of pathology》2000,437(1):69-73
The distribution pattern of extracellular matrix (ECM) components in transplant glomerulopathy was studied in relation to
light microscopic features, actin expression of mesangial cells, and intraglomerular inflammatory cells. Nine cases of mild
(group I) and nine cases of severe (group II) transplant glomerulopathy were stained with antisera against fibronectin (FN),
tenascin (TN), collagen types III and IV, smooth muscle actin, CD45RO, CD68, and Ki-67 antigen. The composition of ECM was
similar in the two groups. The expanded mesangium was diffusely stained by type-IV collagen, FN and TN, and focally and weakly
stained by type-III collagen and smooth muscle actin. Type-IV collagen was linearly stained along the capillary walls, imparting
a double-contour feature, whereas FN and TN showed granular staining along the capillary walls. CD68 positive cells were increased
in severe transplant glomerulopathy, but this increase was not related to ECM deposition. These findings suggest that increased
glomerular deposition of normal and abnormal ECM components participate in the evolution of transplant glomerulopathy.
Received: 5 October 1999 / Accepted: 17 January 2000 相似文献
57.
We report on a case of a 40-year-old male patient who underwent a gastrectomy because of a biopsy-proven large B-cell lymphoma of the stomach. On surgery, a nodule in the spleen also was noted. Grossly and microscopically, the two lesions were different: the tumor of the stomach appeared white-gray on the cut surface and was a centroblastic variant of diffuse large B-cell lymphoma. Histologically, one perigastric lymph node was involved. Grossly, the splenic nodule was gray-yellow and had a histological appearance of an inflammatory myofibroblastic tumor (IMT). The association between malignant tumor and IMT is rare. In such an association, the latter lesion most often has been reported in the spleen. As EBV may be involved in the genesis of both lymphoma and IMT, we tested both lesions for its presence using in situ hybridization, but the tests were negative. It remains to be verified whether the association between lymphoma and IMT is more than fortuitous. 相似文献
58.
Markus F. Neurath Ivan Fuss Manolis Pasparakis Lena Alexopoulou Sylva Haralambous Karl-Hermann Meyer zum Büschenfelde Warren Strober George Kollias 《European journal of immunology》1997,27(7):1743-1750
Antibodies to tumor necrosis factor (TNF)-α have been recently proposed as effective treatment for patients with Crohn's disease. Here, we analyze the functional role of TNF-α in a mouse model of chronic intestinal inflammation induced by the hapten reagent 2,4,6,-trinitrobenzene sulfonic acid (TNBS) that mimics some characteristics of Crohn's disease in humans. Macrophage-enriched lamina propria (LP) mononuclear cells from mice with TNBS-induced colitis produced 10–30-fold higher levels of TNF-α mRNA and protein than cells from control mice. When mice with chronic colitis were treated by intraperitoneal injection of antibodies to TNF-α, an improvement of both the clinical and histopathologic signs of disease was found. Isolated macrophage-enriched LP cells from anti-TNF-α-treated mice produced strikingly less pro-inflammatory cytokines such as interleukin (IL)-1 and IL-6 in cell culture. The predominant role of TNF-α in the mouse TNBS-induced colitis model was further underlined by the finding that striking colonic inflammation and lethal pancolitis was induced in TNF-α-transgenic mice upon TNBS treatment. Conversely, no significant TNBS-induced colitis could be induced in mice in which the TNF-α gene had been inactivated by homologous recombination. Complementation of TNF-α function in TNF?/? mice by the expression of a mouse TNF-α transgene was sufficient to reverse this effect. Taken together, the data provide direct evidence for a predominant role of TNF-α in a mouse model of chronic intestinal inflammation and encourage further clinical trials with antibodies to TNF-α for the treatment of patients with Crohn's disease. 相似文献
59.
F. J. Martinez-Tello J. J. Navas-Palacios J. R. Ricoy R. Gil-Martín J. M. Conde-Zurita F. Colina-Ruiz Delgado I. Tellez A. Cabello S. Madero-García 《Virchows Archiv : an international journal of pathology》1982,397(3):261-285
Summary The Toxic Syndrome (TS) caused by ingestion of adulterated rapeseed oil in Spain is a new disease of multisystemic character whose aetiology and pathogenesis remains unknown. The most prominent pathological feature is a peculiar non-necrotizing vasculitis, that affects mainly the intima and involves vessels of every type and size in practically every organ. The TS begins with an acute clinical picture with pleuropneumopathy, fever, headaches, exanthems and eosinophilia. In these early clinical phases the main pathological findings were observed in the lungs and consisted of intense pulmonary interstitial oedema with scanty inflammatory mononuclear infiltrates. Ultrastructural study revealed hydropic degeneration of pneumocytes types I and II with desquamation of type I. The patients in this phase died of respiratory failure, later deaths were due to thromboembolic complications. Later still the patients developped a neuromuscular syndrome, sclerodermiform skin lesions and severe weight loss and died predominantly of infectious complications and respiratory failure. The anatomopathological picture in the peripheral nerves was that of inflammatory neuropathy with a lymphocytic perineuritis that led to perineural fibrosis with secondary axonal degeneration. The muscle presented an interstitial inflammatory myopathy at first followed by a neurogenic muscular atrophy. The skin lesions in the late phases consisted in dermal or dermal and subdermal fibrosclerosis, with vasculitis of the small arteries in the lower dermis. The salivary glands and pancreas showed vasculitis and interstitial inflammation which progressed to interstitial fibrosis and parenchymal atrophy. 相似文献
60.
IL-10 Secretion and Sensitivity in Normal Human Intestine and Inflammatory Bowel Disease 总被引:13,自引:0,他引:13
Gasche C Bakos S Dejaco C Tillinger W Zakeri S Reinisch W 《Journal of clinical immunology》2000,20(5):362-370
Interleukin-10 (IL-10) deficiency in gene knockout mice causes chronic enterocolitis. We hypothesized that inflammation in human inflammatory bowel disease might result from innate alterations in the IL-10 pathway. Serum, supernatants, and mRNA of peripheral blood mononuclear cells (PBMC) and lamina propria mononuclear cells (LPMC) derived from inflamed (LPMC-i) and noninflamed colonic mucosa (LPMC-ni) were collected from patients with Crohn's colitis, ulcerative colitis, and controls. IL-10 protein concentrations and IL-10 mRNA were examined in response to PMA/CD3 or PHA stimulation. The response to rhIL-10 was assessed by inhibition of tumor necrosis factor-alpha (TNF-), IL-6, and interferon-gamma (IFN-) production. Serum IL-10 levels of inflammatory bowel disease (IBD) patients were within the normal range. IL-10 concentrations in supernatants from LPMC-i were significantly lower than from LPMC-ni or PBMC. No difference was seen between samples from ulcerative colitis and Crohn's disease. IL-10 mRNA was detected in 0/4 LPMC-i samples compared to 1/6 LPMC-ni and 6/6 PBMC. RhIL-10 inhibited TNF-, IL-6, and IFN- synthesis in PBMC. This effect was strongly diminished in LPMC. Disease-specific alterations were not detected. Our data suggest that LPMC derived from inflamed colonic mucosa have a reduced ability to produce and to respond to rhIL-10. A disease-specific alteration in the IL-10 pathway, however, was not found. 相似文献