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Objective
By using the published incidence of Lyme borreliosis in endemic regions of the World, and the sensitivity and specificity data of the best Lyme serological tests, we computed the positive predictive value of Borrelia burgdorferi antibody testing. 相似文献27.
Szekanecz Z Soós L Szabó Z Fekete A Kapitány A Végvári A Sipka S Szücs G Szántó S Lakos G 《Clinical reviews in allergy & immunology》2008,34(1):26-31
Anti-citrullinated protein antibodies (ACPAs) have recently emerged as sensitive and specific serological markers of rheumatoid
arthritis (RA), providing superior alternative of the rheumatoid factor (RF) test in the laboratory diagnostics of RA. The
first members of this autoantibody family were anti-perinuclear factor (APF) and anti-keratin antibodies (AKA). It became
evident that both APF and AKA recognize citrullinated epitopes of filaggrin. Citrullination is a post-translational modification
of arginine by deimination, physiologically occurring during apoptosis, inflammation or keratinization. The presence of several
citrullinated proteins has been demonstrated in the RA synovium. The identification of citrullinated epitopes as targets for
anti-filaggrin antibodies led to the development of the first and later second generation anti-cyclic citrullinated peptide
(anti-CCP) antibody assays. The widely used anti-CCP2 assays have high diagnostic sensitivity and specificity, and they also
show important predictive and prognostic value in RA. The anti-Sa antibody has been identified a decade ago; however, recent
studies confirmed that anti-Sa is directed against citrullinated vimentin, hence it is a new member of the family of ACPAs.
The newly developed anti-mutated citrullinated vimentin (anti-MCV) assay has similar diagnostic performance than the anti-CCP2
ELISA; however, the diagnostic spectrum of the anti-MCV test is somewhat different from that of anti-CCP2. It’s especially
useful in the diagnosis of RA in RF and anti-CCP2 seronegative patients. The combined application of anti-CCP2 and anti-MCV
assays can improve the laboratory diagnostics of RA. The family of ACPAs is expected to expand; there is an increasing need
for developing new diagnostic strategies after careful evaluation of the characteristics of the available assays.
Zoltán Szekanecz and Lilla Soós with equal contribution. 相似文献
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Sustained activation of fibroblast transforming growth factor-beta/Smad signaling in a murine model of scleroderma 总被引:6,自引:0,他引:6
Takagawa S Lakos G Mori Y Yamamoto T Nishioka K Varga J 《The Journal of investigative dermatology》2003,121(1):41-50
Transforming growth factor-beta is responsible for triggering a cascade of events leading to fibrosis in scleroderma. The Smads are intracellular signal transducers recently shown to mediate fibroblast activation and other profibrotic responses elicited by transforming growth factor-betain vitro. To understand better the involvement of Smads in the pathogenesis of fibrosis, we examined Smad expression and activation in situ in a murine model of scleroderma. Bleomycin injections induced striking dermal infiltration with macrophages by 3 d, and progressive fibrosis by 2 wk. Infiltrating macrophages and resident fibroblasts expressed Smad3, the positive mediator for transforming growth factor-beta responses. Importantly, in bleomycin-injected skin, fibroblasts showed predominantly nuclear localization of Smad3 and intense staining for phospho-Smad2/3. Furthermore, phosphorylated Smad2/3 in fibroblasts was detected even after the resolution of inflammation. Expression of Smad7, the endogenous inhibitor of transforming growth factor-beta/Smad signaling, was strongly induced in dermal cells by transforming growth factor-beta, but not by bleomycin injections. Collectively, these results indicate that bleomycin-induced murine scleroderma is associated with rapid and sustained induction of transforming growth factor-beta/Smad signaling in resident dermal fibroblasts. Despite apparent activation of the intracellular transforming growth factor-beta signaling pathway in the lesional dermis, the expression of transforming growth factor-beta-inducible Smad7 was not upregulated. In light of the critical function of Smad7 as an endogenous inhibitor of Smad signaling that restricts the duration and magnitude of transforming growth factor-beta responses, and as a mediator of apoptosis, relative Smad7 deficiency observed in the present studies may account for sustained activation of transforming growth factor-beta/Smad signaling in lesional tissues. These findings raise the possibility that Smads plays an important part in the pathogenesis of fibrosis, and may therefore represent targets for selective anti-fibrotic interventions. 相似文献
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T. Konrad Bernd Markus Carl Allers Paolo Vicini Gianna Toffolo Christos Lakos Katrin Viehmann Ernst Hanisch Albrecht Encke Claudio Cobelli Klaus-Henning Usadel 《Transplant international》2001,14(1):6-11
To examine whether factors controlling glucose tolerance, i. e., insulin sensitivity (SI) and first- (Φ
1) and second-phase insulin secretion (Φ
2), are impaired in after orthotopic liver transplantation (OLT), they were assesssed in patients that had undergone OLT for
cirrhosis (n = 10) with cyclosporin A and low-dose steroid therapy (5 mg prednisone per day) and were compared with those of healthy matched
control subjects (n = 10). These factors were determined by means of computer-based analysis of frequently sampled intravenous glucose tolerance
tests (FSIGTT). Glucose and insulin profiles (posthepatic insulin) did not differ between both groups, whereas C-peptide levels
(prehepatic insulin) were elevated in the transplant group after the FSIGTT, indicating an increased hepatic insulin degradation.
SI and Φ
1 did not differ between both groups. Φ
2, however, was significantly enhanced (23.94 ± 2.63 vs 13.88 ± 1.25 min–1, P < 0.05). These results indicate that cyclosporine and low-dose steroid therapy do not impair SI and Φ
1. However, enhanced Φ
2 compensates the increased hepatic insulin clearance.
Received: 17 November 1998 Revised: 19 June 2000 Accepted: 16 August 2000 相似文献