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41.
Lo Monaco A Lanza F Dabusti M Padovan M La Corte R Castoldi G Trotta F 《Reumatismo》2002,54(4):351-356
Systemic Sclerosis (SSc) is a systemic disease of unknown etiology presenting with disseminated skin thickening and fibrotic impairment of various organs including lung and kidney. According to the rate and degree of skin involvement, SSc can be classified in a limited and a diffuse form, the latter showing a severe and progressive lung involvement, which is responsible for its high related morbidity and mortality along with resistance to standard therapeutic protocols. High dose chemotherapy, followed by autologous stem cell transplantation, is a standard therapeutic regimen for haematological diseases: re-infusion of mobilised peripheral blood progenitor cells overcomes the myeloablative effect of super-maximal eradicative doses of chemotherapeutic agents. Recently, this therapeutic approach has been applied in some cases of resistant SSc and, albeit the low number of cases, it has been proven effective in early diagnosed and rapidly progressive forms of the disease showing a clinical improvement and an instrumentally detectable decrease of fibrosis extent. We report the case of a young woman affected by diffuse SSc with a rapid progression of clinical signs and instrumentally detectable lesions who underwent a conditioning regimen with fludarabine, cyclophosphamide and anti-thymoglobulines followed by re-infusion of autologous peripheral blood stem cells. Two years after transplantation a clinical and instrumental evidence of treatment was observed, with good control of disease evolution. The only sign of disease resumption was a slow worsening of skin involvement. 相似文献
42.
Janneke AL van Kempen Henk J Schers Anne Jacobs Sytse U Zuidema Franca Ruikes Sarah HM Robben René JF Melis Marcel GM Olde Rikkert 《The British journal of general practice》2013,63(608):e225-e231
Background
Primary care is increasingly interested in the identification of frailty, as it selects the target population for integrated care. However, instruments for the identification of frailty specifically validated for use in primary care are scarce. This study developed the Easycare Two-step Older persons Screening (Easycare-TOS), which provides a valid, efficient, and pragmatic screening procedure to identify frail older people.Aim
This paper aims to describe the development of the Easycare-TOS and the data from the pilot studies.Design and setting
Observational pilot study in seven academic GP practices in and around Nijmegen, The Netherlands.Method
The Easycare-TOS was developed in a cyclic process with the input of stakeholders. In every cycle, the requirements were first defined, then translated into a prototype that was tested in a pilot study. The Easycare-TOS makes optimal use of prior knowledge of the GP, and the professionals’ appraisal is decisive in the frailty decision, instead of a cut-off score. Further, it considers aspects of frailty, as well as aspects of the care context of the patient.Results
The pilot data have shown that after step 1, two-thirds of the patients do not need further assessment, because they are judged as not frail, based on prior knowledge of the GP. The overall prevalence of frailty in this pilot study is 24%. Most professionals who participated in the pilot studies considered the time investment acceptable and the method to be of added value.Conclusion
The Easycare-TOS instrument meets the predefined efficiency, flexibility, and acceptability requirements for use as an identification instrument for frailty in primary care. 相似文献43.
Roberta Biancheri Camillo Rosano Laura Denegri Eleonora Lamantea Francesca Pinto Federica Lanza Mariasavina Severino Mirella Filocamo 《European journal of human genetics : EJHG》2013,21(1):34-39
Homozygous or compound heterozygous mutations in the GJC2 gene, encoding the gap
junction protein connexin47 (Cx47), cause the autosomal recessive hypomyelinating
Pelizaeus–Merzbacher-like disease (PMLD1, MIM# 608804). Although clinical and
neuroradiological findings resemble those of the classic Pelizaeus–Merzbacher
disease, PMLD patients usually show a greater level of cognitive and motor functions.
Unpredictably a homozygous missense GJC2 mutation (p.Glu260Lys) was found in a
patient presenting with a very severe clinical picture characterised by congenital
nystagmus and severe neurological impairment. Also magnetic resonance imaging was
unusually severe, showing an abnormal supra- and infratentorial white matter involvement
extending to the spinal cord. The novel p.Glu260Lys (c.778G>A) mutation, occurring in a
highly conserved motif (SRPTEK) of the Cx47 extracellular loop-2 domain, was
predicted, by modelling analysis, to break a ‘salt bridge network'', crucial
for a proper connexin–connexin interaction to form a connexon, thus hampering the
correct formation of the connexon pore. The same structural analysis, extended to the
previously reported missense mutations, predicted that most changes were expected to have
less severe impact on protein functions, correlating with the mild PMLD1 form of the
patients. Our study expands the spectrum of PMLD1 and provides evidence that the extremely
severe clinical and neuroradiological PMLD1 form of our patient likely correlates with the
predicted impairment of gap junction channel assembly resulting from the detrimental
effect of the new p.Glu260Lys mutant allele on Cx47 protein. 相似文献
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45.
Adam R. Konopka Albert Asante Ian R. Lanza Matthew M. Robinson Matthew L. Johnson Chiara Dalla Man Claudio Cobelli Mark H. Amols Brian A. Irving K.S. Nair 《Diabetes》2015,64(6):2104-2115
The notion that mitochondria contribute to obesity-induced insulin resistance is highly debated. Therefore, we determined whether obese (BMI 33 kg/m2), insulin-resistant women with polycystic ovary syndrome had aberrant skeletal muscle mitochondrial physiology compared with lean, insulin-sensitive women (BMI 23 kg/m2). Maximal whole-body and mitochondrial oxygen consumption were not different between obese and lean women. However, obese women exhibited lower mitochondrial coupling and phosphorylation efficiency and elevated mitochondrial H2O2 (mtH2O2) emissions compared with lean women. We further evaluated the impact of 12 weeks of aerobic exercise on obesity-related impairments in insulin sensitivity and mitochondrial energetics in the fasted state and after a high-fat mixed meal. Exercise training reversed obesity-related mitochondrial derangements as evidenced by enhanced mitochondrial bioenergetics efficiency and decreased mtH2O2 production. A concomitant increase in catalase antioxidant activity and decreased DNA oxidative damage indicate improved cellular redox status and a potential mechanism contributing to improved insulin sensitivity. mtH2O2 emissions were refractory to a high-fat meal at baseline, but after exercise, mtH2O2 emissions increased after the meal, which resembles previous findings in lean individuals. We demonstrate that obese women exhibit impaired mitochondrial bioenergetics in the form of decreased efficiency and impaired mtH2O2 emissions, while exercise effectively restores mitochondrial physiology toward that of lean, insulin-sensitive individuals. 相似文献
46.
Lanza Castoldi Castagnar Todd III Moretti Spisani Latorraca Focarile Roberti & Traniello 《British journal of haematology》1998,103(1):110-123
Urokinase-type plasminogen activator receptor (UPA-R-CD87) is a GPI-anchored membrane protein which promotes the generation of plasmin on the surface of many cell types, probably facilitating cellular extravasation and tissue invasion. A flow cytometric quantitative analysis of expression levels for UPA-R was performed on fresh blast cells from patients with acute myeloid leukaemia (AML, n = 74), acute lymphoblastic leukaemia (ALL, n = 24), and biphenotypic leukaemia (BAL, n = 3) using two CD87 monoclonal antibodies (McAbs) (3B10 and VIM5). Peripheral blood and bone marrow (BM) cells from 15 healthy adults served as controls. Using 3B10 McAb, UPA-R was expressed (>99%) by blood monocytes, neutrophils, and BM myelomonocytic precursors in controls, whereas resting T and B lymphocytes, and CD34+ cells were UPA-R negative. We also attempted to clarify whether UPA-R has a role in mediating neutrophil functions. Oriented locomotion induced by different chemotaxins and lysozyme release by granules stimulated with fMLP or PMA were significantly decreased when UPA-R was neutralized by CD87 McAb. In contrast, the anti-UPA-R McAb had no effect on superoxide anion generation of normal neutrophils. Blasts from AML showed a heterogenous pattern of expression for the UPA-R McAbs, with reactivity strictly dependent on FAB subtype. The highest UPA-R expression was seen in the M5 group: all patients tested (n = 20) showed strong positivity for the UPA-R McAb whereas only 12% (3/24) of ALL patients were CD87 positive, and 2/3 of BAL patients showed a dim expression for CD87. The number of receptors expressed by blast cells in 6/74 (8.1%) AML patients was higher than those of normal samples; in addition, since co-expression of UPA-R and CD34 was not found in normal haemopoietic cells, it may be postulated that CD87 can be used alone (when overexpressed) or in combination with CD34 for the detection of minimal residual disease. Results also indicated that patients with UPA-receptors >12 × 103 ABC/cell, irrespective of FAB subtype, had a greater tendency for cutaneous and tissue infiltration and a higher frequency of chromosome abnormalities, thus suggesting the concept that cellular UPA-R content positively correlates with the invasive potential of AML cells. The combination of higher UPA-R positivity, abnormalities of chromosome 11, and M5 FAB morphology may identify a peculiar subset of AML, characterized by a more aggressive clinical course. 相似文献
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50.
Giorgio Zauli Claudio Celeghini Elisabetta Melloni Rebecca Voltan Manuele Ongari Mario Tiribelli Maria Grazia di Iasio Francesco Lanza Paola Secchiero 《Haematologica》2012,97(11):1722-1730