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971.
Application of novel quantitative techniques for fluorodeoxyglucose positron emission tomography/computed tomography in patients with non‐small‐cell lung cancer 下载免费PDF全文
972.
Chul S. Ha Joel E. Michalek Richard Elledge Kevin R. Kelly Suthakar Ganapathy Hang Su Carol A. Jenkins Athanassios Argiris Ronan Swords Tony Y. Eng Anand Karnad Richard L. Crownover Gregory P. Swanson Martin Goros Brad?H. Pollock Zhi-Min Yuan 《Molecular oncology》2016,10(1):148-156
p53 activation is a primary mechanism underlying pathological responses to DNA damaging agents such as chemotherapy and radiotherapy. Our recent animal studies showed that low dose arsenic (LDA)‐induced transient p53 inhibition selectively protected normal tissues from chemotherapy‐induced toxicity.Study objectives were to: 1) define the lowest safe dose of arsenic trioxide that transiently blocks p53 activation in patients and 2) assess the potential of LDA to decrease hematological toxicity from chemotherapy.Patients scheduled to receive minimum 4 cycles of myelosuppressive chemotherapy were eligible. For objective 1, dose escalation of LDA started at 0.005 mg/kg/day for 3 days. This dose satisfied objective 1 and was administered before chemotherapy cycles 2, 4, and 6 for objective 2. p53 level in peripheral lymphocytes was measured on day 1 of each cycle by ELISA assay. Chemotherapy cycles 1, 3, and 5 served as the baseline for the subsequent cycles of 2, 4, and 6 respectively. If p53 level for the subsequent cycle was lower (or higher) than the baseline cycle, p53 was defined as “suppressed” (or “activated”) for the pair of cycles. Repeated measures linear models of CBC in terms of day, cycle, p53 activity and interaction terms were used.Twenty‐six patients treated with 3 week cycle regimens form the base of analyses. The mean white blood cell, hemoglobin and absolute neutrophil counts were significantly higher in the “suppressed” relative to the “activated” group.These data support the proof of principle that suppression of p53 could lead to protection of bone marrow in patients receiving chemotherapy.This trial is registered in ClinicalTrials.gov. Identifier: . NCT01428128相似文献
973.
Terence Ng Shu Mei Teo Hui Ling Yeo Maung Shwe Yan Xiang Gan Yin Ting Cheung Koon Mian Foo Mooi Tai Cham Jung Ah Lee Yee Pin Tan Gilbert Fan Wei Sean Yong Madhukumar Preetha Wei-Jen Kiley Loh Si-Lin Koo Amit Jain Guek Eng Lee Mabel Wong Rebecca Dent Yoon Sim Yap Raymond Ng Chiea Chuen Khor Han Kiat Ho Alexandre Chan 《Neuro-oncology》2016,18(2):244-251
Background
Brain-derived neurotrophic factor (BDNF), a neurotrophin that regulates neuronal function and development, is implicated in several neurodegenerative conditions. Preliminary data suggest that a reduction of BDNF concentrations may lead to postchemotherapy cognitive impairment. We hypothesized that a single nucleotide polymorphism (rs6265) of the BDNF gene may predispose patients to cognitive impairment. This study aimed to evaluate the effect of BDNF gene polymorphism on chemotherapy-associated cognitive impairment.Methods
Overall, 145 patients receiving chemotherapy for early-stage breast cancer (mean age: 50.8 ± 8.8 y; 82.1% Chinese) were recruited. Patients'' cognitive functions were assessed longitudinally using the validated Functional Assessment of Cancer Therapy–Cognitive Function (v.3) and an objective computerized tool, Headminder. Genotyping was performed using Sanger sequencing. Logistic regression was used to evaluate the association between BDNF Val66Met polymorphism and cognition after adjusting for ethnicity and clinically important covariates.Results
Of the 145 patients, 54 (37%) reported cognitive impairment postchemotherapy. The Met/Met genotype was associated with statistically significant lower odds of developing cognitive impairment (odds ratio [OR] = 0.26; 95% CI: 0.08–0.92; P = .036). The Met carriers were less likely to experience impairment in the domains of verbal fluency (OR = 0.34; 95% CI: 0.12–0.90; P = .031) and multitasking ability (OR = 0.37; 95% CI: 0.15–0.91; P = .030) compared with the Val/Val homozygote. No associations were observed between Headminder and the BDNF Val66Met polymorphism.Conclusions
This is the first study to provide evidence that carriers of the BDNF Met allele are protected against chemotherapy-associated cognitive impairment. Further studies are required to validate the findings. 相似文献974.
Proposing prognostic thresholds for lymph node yield in clinically lymph node‐negative and lymph node‐positive cancers of the oral cavity 下载免费PDF全文
975.
The role of the gastrointestinal microbiome in infectious complications during induction chemotherapy for acute myeloid leukemia 下载免费PDF全文
Jessica R. Galloway‐Peña PhD Daniel P. Smith PhD Pranoti Sahasrabhojane MS Nadim J. Ajami PhD W. Duncan Wadsworth MS Naval G. Daver MD Roy F. Chemaly MD Lisa Marsh MSN Shashank S. Ghantoji PhD Naveen Pemmaraju MD Guillermo Garcia‐Manero MD Katayoun Rezvani MD PhD Amin M. Alousi MD Jennifer A. Wargo MD Elizabeth J. Shpall MD Phillip A. Futreal PhD Michele Guindani PhD Joseph F. Petrosino PhD Dimitrios P. Kontoyiannis MD ScD Samuel A. Shelburne MD PhD 《Cancer》2016,122(14):2186-2196
976.
977.
Jawan B Kao YH Goto S Pan MC Lin YC Hsu LW Nakano T Lai CY Sun CK Cheng YF Tai MH Eng HL Wang CS Huang CJ Lin CR Chen CL 《Toxicology and applied pharmacology》2008,229(3):362-373
Propofol (PPF), a widely used intravenous anesthetic for induction and maintenance of anesthesia during surgeries, was found to possess suppressive effect on host immunity. This study aimed at investigating whether PPF plays a modulatory role in the lipopolysaccharide (LPS)-induced inflammatory cytokine expression in a cell line of rat hepatocytes. Morphological observation and viability assay showed that PPF exhibits no cytotoxicity at concentrations up to 300 microM after 48 h incubation. Pretreatment with 100 microM PPF for 24 h prior to LPS stimulation was performed to investigate the modulatory effect on LPS-induced inflammatory gene production. The results of semi-quantitative RT-PCR demonstrated that PPF pretreatment significantly suppressed the LPS-induced toll-like receptor (TLR)-4, CD14, tumor necrosis factor (TNF)-alpha, and granulocyte-macrophage colony-stimulating factor (GM-CSF) gene expression. Western blotting analysis showed that PPF pretreatment potentiated the LPS-induced TLR-4 downregulation. Flow cytometrical analysis revealed that PPF pretreatment showed no modulatory effect on the LPS-upregulated CD14 expression on hepatocytes. In addition, PPF pretreatment attenuated the phosphorylation of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) and IkappaBalpha, as well as the nuclear translocation of NF-kappaB primed by LPS. Moreover, addition of PD98059, a MAPK kinase inhibitor, significantly suppressed the LPS-induced NF-kappaB nuclear translocation and GM-CSF production, suggesting that the PPF-attenuated GM-CSF production in hepatocytes may be attributed to its suppressive effect on MAPK/ERK signaling pathway. In conclusion, PPF as an anesthetic may clinically benefit those patients who are vulnerable to sepsis by alleviating sepsis-related inflammatory response in livers. 相似文献
978.
979.
Aroma Agape Gopalai Azlina Ahmad‐Annuar Hui‐Hua Li Yi Zhao Shen‐Yang Lim Ai Huey Tan Thien Thein Lim Gaik Bee Eow Puvanarajah Santhi Viswanathan Shanthi Mohamed Ibrahim Norlinah Zariah Abdul Aziz Soo Kun Lim Chong Tin Tan Eng‐King Tan 《American journal of medical genetics. Part B, Neuropsychiatric genetics》2016,171(6):839-847