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1.
Johannes Brettschneider Axel Petzold Sigurd D Süssmuth Georg B Landwehrmeyer Albert C Ludolph Jan Kassubek Hayrettin Tumani 《Movement disorders》2006,21(12):2224-2227
We aimed to evaluate the potential of the cerebrospinal fluid (CSF) axonal damage biomarker NfH(SMI35) in the laboratory-supported differential diagnosis of parkinsonian syndromes. Patients with idiopathic Parkinson's disease (PD; n = 22), multiple-system atrophy (MSA; n = 21), progressive supranuclear palsy (PSP; n = 21), corticobasal degeneration (CBD; n = 6), and age-matched controls (n = 45) were included. CSF levels of NfH(SMI35) were measured using ELISA. Levels of CSF NfH(SMI35) were elevated in PSP compared to PD and controls (P < 0.05 each). They were also significantly higher in MSA than in PD and controls (P < 0.05 each). NfH(SMI35) differentiated PD from PSP with a sensitivity of 76.5% and a specificity of 94.4%. Axonal damage as measured by CSF NfH(SMI35) is most prominent in the more rapidly progressive syndromes PSP and MSA as compared to PD or CBD. CSF NfH(SMI35) may therefore be of some value for the laboratory-supported differential diagnosis of atypical parkinsonian syndromes. 相似文献
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Unfractionated cytokines have been shown to induce in vitro proliferation of neonatal rat Schwann cells but the nature of the mitogen(s) is not known. A mixture of rabbit antibodies specific for recombinant interleukin-1α (IL-1α) and interleukin-1β (IL-1β) inhibited Schwann cell proliferation induced by unfractionated human cytokines whereas antibodies to interleukin-2 (IL-2) and control IgG did not. However, purified human IL-1 and recombinant human IL-1α or β did not induce Schwann cell proliferation on their own. 相似文献
4.
目的探讨血肿局部炎症、假膜新血管生成、局部纤溶状况及其在CSDH发生、发展中的作用。进而探讨CSDH的发病机制,并为CSDH的治疗及预防复发提供理论依据。方法以78例CSDH患者作为病例组,20例健康人作为正常对照组。采用ELISA法测定患者血清及血肿液中VEGF及IL-6的含量。比较患者末梢静脉血及血肿液中四种因子的含量变化并与正常对照组比较。结果病例组血肿液FDP、d-dimer检测均为阳性,血液为阴性;正常对照组血液FDP、d-dimer检测均为阴性;病例组血清VEGF含量与正常对照组比较差异无统计学意义。血肿液中VEGF浓度高于血清中。病例组血清IL-6浓度与正常对照组差异无统计学意义,血肿液中IL-6浓度高于血清中。CSDH患者血肿液VEGF、IL-6水平没有相关性。结论CSDH患者血肿液局部纤溶亢进,局部VEGF分泌旺盛,新血管生成活跃,局部炎症活跃,可导致CSDH不断扩大而参与CSDH发病机制。抗炎治疗、抑制VEGF的生理作用、有选择的对病人施行促凝治疗,可成为部分CSDH病人保守治疗及预防复发的有效手段。 相似文献
5.
The treatment of neoplasia with interleukin-2 (IL-2) can be complicated by neurological deficits resembling transient Ischemic attack and stroke. We investigated whether interleukin-2 contributes to the natural course of cerebrovascular ischemia and particularly to the pathogenesis of infection-associated stroke. Plasma levels of interleukin-2 were below the level of detectability in almost all measurements. Patients with and without previous infection (n = 11, 805 ±445 U/ml vs n = 19, 824 ± 501 U/ml) did not have significantly higher levels of soluble interleukin-2 receptors than control subjects with (n = 14, 667 ± 229 U/ml) or without vascular risk factors (n = 17, 567 ± 176 U/ml). Receptor levels increased in patients during the first week after stroke (n = 15, 1157 ± 1013, p < 0.02). Levels of soluble T8 antigen (sT8) were higher in patients (n – 26, 320 ± 112 U/ml) than in healthy control subjects (n = 15, 246 ± 92 U/ml; p < 0.05) and sT8 levels increased during the first week after stroke (p < 0.05). These results reflect an immunological response to the cerebral infarct; they do not indicate a general role of the IL-2 system in the pathogenesis of ischemic stroke with or without previous infection. 相似文献
6.
J.M. Smith D. Stablein A. Singh W. Harmon R.A. McDonald 《American journal of transplantation》2006,6(3):585-588
Graft thrombosis is the most common cause of first year graft failure in pediatric renal transplantation. The North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) database was analyzed for cases of graft failure due to thrombosis among patients transplanted from 1998 to 2004. The impact of interleukin-2 (IL-2) receptor antagonists as induction therapy was determined. There were a total of 51 graft failures due to thrombosis among the 2750 reported renal transplants (1.85%) (95% CI (1.39%, 2.41%)). This represents the most common cause of graft loss during the first year post-transplant accounting for 35% of first year losses and 18% of all graft losses. The incidence of thrombosis among patients who received IL-2 receptor antibodies was 1.07% (12/1126) compared to 2.40% (39/1624) among patients who did not (OR 0.44, 95% CI 0.23, 0.84, p = 0.014). Use of IL-2 receptor blockade was the only significant prognostic factor in a multivariate model with previously identified risk factors. Analysis of NAPRTCS data found that the use of IL-2 receptor antibodies as induction therapy is associated with a significantly decreased risk of graft failure due to thrombosis. This provocative finding requires further investigation to determine whether thrombotic failure can be decreased by this therapeutic strategy. 相似文献
7.
Jordi Llorens Cristina Su ol Josep M. Tusell Eduard Rodrí guez-Farr 《Neurotoxicology and teratology》1990,12(6):607-610
The inhibition of [35S]t-butylbicyclophosphorothionate ([35S]TBPS) binding to the GABAA receptor by the insecticide γ-hexachlorocyclohexane, lindane, was studied in several brain regions and using different membrane preparation methods, both in vitro and after dosing the animals with the chemical. In the latter studies, the amount of lindane remaining in the membrane suspensions used for binding assays was determined. In vitro data showed values of IC50 from 150 to 1675 nM, varying in function of the membrane preparation method used. This may account for the discrepancies in IC50 values found in the literature. IC50 values within the range of 150–250 nM were determined using extensively washed membranes from several brain regions, so no evidence arose for brain regional differences in the affinity of lindane for the TBPS binding site. After different schedules of acute treatment with lindane, we found a manifest relationship between the extent of the observable inhibition of [35S]TBPS binding and the lindane amount remaining in the membrane suspensions used for binding assays. This relationship was in good agreement with the in vitro data, so no support for an in vivo acute regulation of the binding site was obtained. 相似文献
8.
9.
Dr. David M. Euhus MD Lucille Kimura PhD Bruce Arnold MD 《Annals of surgical oncology》1997,4(5):432-439
Background: Mice immunized with murine mammary carcinoma cells genetically engineered to secrete interleukin-2 (IL-2) are rendered resistant
to subsequent challenge with unmodified tumor cells, and in the case of mice bearing established tumors, the rate of development
of pulmonary metastases is reduced. Despite these encouraging animal results, little is known about the induction of antitumor
immunity by IL-2 gene transfer in human breast cancer.
Methods: Adenovirally mediated IL-2 gene transfer was performed in 12 tumor fragment cultures established from seven primary breast
cancers. Autologous tumor infiltrating lymphocytes (TILs) or peripheral blood mononuclear cells (PBMCs) were cocultured with
transduced tumor fragments, and changes in phenotype and cytotoxicity were measured.
Results: IL-2 was never detectable in the untransduced cultures, but it peaked at 5.0—1,324.8 ng/ml in the transduced cultures. Lymphocyte
counts declined in all untransduced cultures, but they increased two- to sevenfold in four transduced cultures. CD4:CD8 ratios
decreased from a mean of 2.11 at baseline to 1.27 after stimulation in coculture (p=0.03). Expansion of lymphocytes expressing
the natural killer cell phenotype (CD3−CD56+) occurred in only one culture, but the CD3+CD56+ population increased in four of six cultures. Lymphocytes from four of 10 cocultures generated significant cytotoxicity against
allogeneic breast cancer cells. Induction of cytotoxicity correlated with expansion of the CD3+CD56+ phenotype (R2=0.805, p=0.02).
Conclusions: IL-2 gene expression by human breast cancer causes expansion of CD3+CD56+ cytotoxic lymphocytes. This phenotype is consistent with that of a non-major histocompatibility complex (MHC)-restricted
cytokine induced killer cell population previously described.
Opinions, interpretations, conclusions and recommendations are those of the author and are not necessarily endorsed by the
U.S. Army.
Presented at the 49th Annual Cancer Symposium of The Society of Surgical Oncology, Atlanta, Georgia, March 21–24, 1996. 相似文献
10.
白细胞介素—2新的功能位点及其中枢镇痛作用 总被引:2,自引:0,他引:2
白细胞介素-2(IL-2)不仅是重要的免疫调节因子,而且还具有重要的中枢调节作用。本实验以钾离子透入引起大鼠甩尾反应为指标,发现侧脑室注射IL—2能显著提高动物痛阈,并能被纳洛酮所阻断,表示IL-2的中枢镇痛作用可能与阿片受体有关。利用基因定位突变技术获得的无免疫活性IL-2实查体仍具有中枢镇痛作用,表明IL—2分子上发挥镇痛和免疫调节作用的功能位点是相互独立的。纳洛酮能够阻断IL—2的中枢镇痛作用,而不能影响IL—2增殖CTLL-2细胞的作用,提示IL-2发挥镇痛和免疫调节作用可能通过不同的受体途径。IL-2分子中第45位Tyr残基突变为Val后,虽仍保留了免疫活性,但丧失了镇痛功能,表示45位Tyr残基是IL—2发挥中枢镇痛功能的关键残基之一。我们推测IL—2的镇痛功能位点可能在IL—2分子中第45位Tyr残基附近区域。 相似文献