全文获取类型
收费全文 | 6554篇 |
免费 | 313篇 |
国内免费 | 35篇 |
专业分类
耳鼻咽喉 | 129篇 |
儿科学 | 280篇 |
妇产科学 | 162篇 |
基础医学 | 590篇 |
口腔科学 | 253篇 |
临床医学 | 573篇 |
内科学 | 1597篇 |
皮肤病学 | 111篇 |
神经病学 | 322篇 |
特种医学 | 141篇 |
外国民族医学 | 2篇 |
外科学 | 1045篇 |
综合类 | 362篇 |
一般理论 | 4篇 |
预防医学 | 396篇 |
眼科学 | 235篇 |
药学 | 411篇 |
中国医学 | 32篇 |
肿瘤学 | 257篇 |
出版年
2023年 | 95篇 |
2022年 | 313篇 |
2021年 | 440篇 |
2020年 | 209篇 |
2019年 | 230篇 |
2018年 | 282篇 |
2017年 | 177篇 |
2016年 | 197篇 |
2015年 | 263篇 |
2014年 | 329篇 |
2013年 | 333篇 |
2012年 | 500篇 |
2011年 | 462篇 |
2010年 | 267篇 |
2009年 | 228篇 |
2008年 | 343篇 |
2007年 | 332篇 |
2006年 | 346篇 |
2005年 | 304篇 |
2004年 | 263篇 |
2003年 | 247篇 |
2002年 | 184篇 |
2001年 | 55篇 |
2000年 | 58篇 |
1999年 | 49篇 |
1998年 | 34篇 |
1997年 | 27篇 |
1996年 | 28篇 |
1995年 | 17篇 |
1994年 | 21篇 |
1993年 | 9篇 |
1992年 | 27篇 |
1991年 | 24篇 |
1990年 | 23篇 |
1989年 | 20篇 |
1988年 | 21篇 |
1987年 | 18篇 |
1986年 | 10篇 |
1985年 | 15篇 |
1984年 | 10篇 |
1983年 | 12篇 |
1981年 | 5篇 |
1980年 | 5篇 |
1979年 | 5篇 |
1977年 | 7篇 |
1974年 | 8篇 |
1972年 | 5篇 |
1970年 | 5篇 |
1969年 | 5篇 |
1963年 | 6篇 |
排序方式: 共有6902条查询结果,搜索用时 15 毫秒
311.
312.
Masha Y. Ivanova Thomas M. Achenbach Leslie A. Rescorla Lori V. Turner Julie A. Dumas Vera Almeida Meltem Anafarta-Sendag Ieva Bite Dorret I. Boomsma J. Carlos Caldas John W. Capps Yi-Chuen Chen Paola Colombo Margareth da Silva Oliveira Anca Dobrean Nese Erol Alessandra Frigerio Yasuko Funabiki Reda Gedutienė Halldór S. Guðmundsson Min Quan Heo Young Ah Kim Tih-Shih Lee Manuela Leite Jianghong Liu Jasminka Markovic Monika Misiec Marcus Müller Kyung Ja Oh Verónica Portillo-Reyes Wolfgang Retz Sandra B. Sebre Shupeng Shi Sigurveig H. Sigurðardóttir Roma Šimulionienė Elvisa Sokoli Tanja Tomasevic Jacqueline M. Vink Ewa Zasępa 《International journal of geriatric psychiatry》2020,35(5):525-536
313.
314.
315.
Alzheimer’s disease is characterized by the extracellular accumulation of the amyloidβin the form of amyloid plaques and the intracellular deposition of the microtubule-associated protein tau in the form of neurofibrillary tangles.Most of the Alzheimer’s drugs targeting amyloidβhave been failed in clinical trials.Particularly,tau pathology connects greatly in the pathogenesis of Alzheimer’s disease.Tau protein enhances the stabilization of microtubules that leads to the appropriate function of the neuron.Changes in the quantity or the conformation of tau protein could affect its function as a microtubules stabilizer and some of the processes wherein it is involved.The molecular mechanisms leading to the accumulation of tau are principally signified by numerous posttranslational modifications that change its conformation and structural state.Therefore,aberrant phosphorylation,as well as truncation of tau protein,has come into focus as significant mechanisms that make tau protein in a pathological entity.Furthermore,the shape-shifting nature of tau advocates to comprehend the progression of Alzheimer’s disease precisely.In this review,we emphasize the recent studies about the toxic and shape-shifting nature of tau in the pathogenesis of Alzheimer’s disease. 相似文献
316.
Hsin-Yi Tseng Jan Dreyer Abdullah Al Emran Dilini Gunatilake Mehdi Pirozyan Carleen Cullinane Ken Dutton-Regester Helen Rizos Nicholas K. Hayward Grant McArthur Peter Hersey Jessamy Tiffen Stuart Gallagher 《International journal of cancer. Journal international du cancer》2020,147(8):2176-2189
The treatment of melanoma has been markedly improved by the introduction of targeted therapies and checkpoint blockade immunotherapy. Unfortunately, resistance to these therapies remains a limitation. Novel anticancer therapeutics targeting the MCL1 anti-apoptotic protein have shown impressive responses in haematological cancers but are yet to be evaluated in melanoma. To assess the sensitivity of melanoma to new MCL1 inhibitors, we measured the response of 51 melanoma cell lines to the novel MCL1 inhibitor, S63845. Additionally, we assessed combination of this drug with inhibitors of the bromodomain and extra-terminal (BET) protein family of epigenetic readers, which we postulated would assist MCL1 inhibition by downregulating anti-apoptotic targets regulated by NF-kB such as BCLXL, BCL2A1 and XIAP, and by upregulating pro-apoptotic proteins including BIM and NOXA. Only 14% of melanoma cell lines showed sensitivity to S63845, however, combination of S63845 and I-BET151 induced highly synergistic apoptotic cell death in all melanoma lines tested and in an in vivo xenograft model. Cell death was dependent on caspases and BAX/BAK. Although the combination of drugs increased the BH3-only protein, BIM, and downregulated anti-apoptotic proteins such as BCL2A1, the importance of these proteins in inducing cell death varied between cell lines. ABT-199 or ABT-263 inhibitors against BCL2 or BCL2 and BCLXL, respectively, induced further cell death when combined with S63845 and I-BET151. The combination of MCL1 and BET inhibition appears to be a promising therapeutic approach for metastatic melanoma, and presents opportunities to add further BCL2 family inhibitors to overcome treatment resistance. 相似文献
317.
Cytotoxic Effects of Betel Quid and Areca Nut Aqueous Extracts on Mouse Fibroblast,Human Mouth-Ordinary-Epithelium 1 and Human Oral Squamous Cell Carcinoma Cell Lines 下载免费PDF全文
Badr Abdullah Al-TayarAzlina AhmadMohamad Ezany YusoffSiti Fadilah AbdullahNoor Khairiena MohamadSiti Nurnasihah Md HashimShosei KishidaMichiko KishidaNorifumi NakamuraToshiro KibeMasitah Hayati Harun 《Asian Pacific journal of cancer prevention》2020,21(4):1005-1009
Background: Betel quid chewing is more common among the older generation in rural areas of Malaysia. Oral cancer in Asia has been associated with the habit of chewing betel quid and areca nut. Objective: This study aims to investigate the cytotoxic effects of betel quid and areca nut extracts on the fibroblast (L929), mouth-ordinary-epithelium 1 (MOE1) and oral squamous cell carcinoma (HSC-2) cell lines. Methods: L929, MOE1 and HSC-2 cells were treated with 0.1, 0.2 and 0.4 g/ml of betel quid and areca nut extracts for 24, 48 and 72 h. MTT assay was performed to assess the cell viability. Results: Both extracts, regardless of concentration, significantly reduced the cell viability of L929 compared with the control (P<0.05). Cell viability of MOE1 was significantly enhanced by all betel quid concentrations compared with the control (P<0.05). By contrast, 0.4 g/ml of areca nut extract significantly reduced the cell viability of MOE1 at 48 and 72 h of incubation. Cell viability of HSC-2 was significantly lowered by all areca nut extracts, but 0.4 g/ml of betel quid significantly increased the cell viability of HSC-2 (P<0.05). Conclusion: Areca nut extract is cytotoxic to L929 and HSC-2, whereas the lower concentrations of areca nut extract significantly increased the cell viability of MOE1 compared to the higher concentration and control group. Although betel quid extract is cytotoxic to L929, the same effect is not observed in MOE1 and HSC-2 cell lines. Further investigations are needed to clarify the mechanism of action. 相似文献
318.
We aimed to compare the recent practical method of capillary β-hydroxy butyrate (βOHB) measurement with the widely used urinary
ketone measurement in monitoring metabolic status of the patient during treatment of diabetic ketoacidosis (DKA) and diabetic
ketosis (DK). Patients with DKA and DK admitted to the hospital were followed with simultaneous measurements of capillary
βOHB by electrochemical method (Medisense Optium, Abbott), and urinary ketone by semi-quantitative method. Blood gases were
measured in 2–4 h intervals. Fourteen patients with DKA/DK (7 males and 7 females, age: 9.2 ± 4.2 years) were included with
50 simultaneous measurements of capillary and urinary ketone. No correlation was detected between urinary ketone and blood
pH (P = 0.06) and HCO3 (P = 0.79), whereas a significant negative correlation was found between capillary βOHB and blood pH (r = −0.41, P < 0.05) and HCO3 (r = −0.35, P < 0.05). Capillary βOHB and urinary ketone levels did not correlate at the beginning and 3.3 ± 1.4 h after treatment, but
did correlate in the third samples taken 7.8 ± 2.0 h after treatment (r = 0.8, P < 0.05). Capillary βOHB levels show good correlation with the degree of acidosis (pH and HCO3). Capillary βOHB measurement is more sensitive than urinary ketone measurement in reflecting the patient’s metabolic status
and improvement during treatment. 相似文献
319.
Immunity in young adult survivors of childhood leukemia is similar to the elderly rather than age‐matched controls: Role of cytomegalovirus 下载免费PDF全文
Mohamad Shafiq Azanan Noor Kamila Abdullah Ling Ling Chua Su Han Lum Sayyidatul Syahirah Abdul Ghafar Adeeba Kamarulzaman Shahrul Kamaruzzaman Sharon R. Lewin Yin Ling Woo Hany Ariffin Reena Rajasuriar 《European journal of immunology》2016,46(7):1715-1726
Many treatment complications that occur late in childhood cancer survivors resemble age‐related comorbidities observed in the elderly. An immune phenotype characterized by increased immune activation, systemic inflammation, and accumulation of late‐differentiated memory CD57+CD28? T cells has been associated with comorbidities in the elderly. Here, we explored if this phenotype was present in young adult leukemia survivors following an average of 19 years from chemotherapy and/or radiotherapy completion, and compared this with that in age‐matched controls. We found that markers of systemic inflammation—IL‐6 and human C‐reactive protein and immune activation—CD38 and HLA‐DR on T cells, soluble CD (sCD)163 from monocytes and macrophages—were increased in survivors compared to controls. T‐cell responses specific to cytomegalovirus (CMV) were also increased in survivors compared to controls while CMV IgG levels in survivors were comparable to levels measured in the elderly (>50years) and correlated with IL‐6, human C‐reactive protein, sCD163, and CD57+CD28? memory T cells. Immune activation and inflammation markers correlated poorly with prior chemotherapy and radiotherapy exposure. These data suggest that CMV infection/reactivation is strongly correlated with the immunological phenotype seen in young childhood leukemia survivors and these changes may be associated with the early onset of age‐related comorbidities in this group. 相似文献
320.
Hanan E. Shamseldin Ranad Shaheen Nour Ewida Dalal K. Bubshait Hisham Alkuraya Elham Almardawi Ali Howaidi Yasser Sabr Ebtesam M. Abdalla Abdullah Y. Alfaifi Jameel Mohammed Alghamdi Afaf Alsagheir Ahmed Alfares Heba Morsy Maged H. Hussein Mohammad A. Al-Muhaizea Mohammad Shagrani Essam Al Sabban Fowzan S. Alkuraya 《Genetics in medicine》2022,24(4):966