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71.
Joo Young Na Ki Young Huh KyungSang Yu Joon Young Hyon Hye Cheong Koo Jong Ho Lee Ji Chang You JaeYong Chung 《CTS Clinical and Translational Science》2022,15(5):1123
For the long‐term efficacy of dry eye disease treatment, relieving underlying inflammation is necessary. Imatinib mesylate is a novel ophthalmic formulation of imatinib mesylate, which is expected to alleviate inflammation by inhibiting the discoidin domain receptor 1 activity. This study aims to evaluate the safety and pharmacokinetics of imatinib mesylate in healthy subjects. A randomized, double‐blind, placebo‐controlled study was conducted. In a single ascending dose, 16 subjects received a single eye drop of imatinib mesylate 0.1%, 0.3%, or matching placebo. In the multiple ascending dose (MAD), subjects received multiple eye drops of imatinib mesylate 0.1%, 0.3%, or matching placebo once daily for 7 days. Safety and tolerability were assessed by ophthalmic examination, including the visual analog scale (VAS) to monitor the burning sensation in the eyes. A total of four treatment‐emergent adverse events (TEAEs) occurred during the study. All TEAEs were mildly severe with no serious cases. VAS results in the 0.1% MAD group exhibited highest score of two points, whereas it was less than one point in others. Insignificant difference between the imatinib mesylate and placebo groups in the VAS results was seen. After a single dose administration of imatinib mesylate 0.1%, all plasma concentrations were below the lower limit of quantification. The peak plasma concentrations of imatinib were less than 0.54 µg/L in all groups. In conclusion, a single and multiple topical ophthalmic administration of imatinib mesylate was well‐tolerated in healthy subjects. Because there was minimal systemic exposure to imatinib, the adverse effect in the body seems to be insignificant. 相似文献
72.
Dae Yun Seo SungRyul Lee Arturo Figueroa Hyoung Kyu Kim Yeong Ho Baek Yi Sub Kwak Nari Kim Tae Hoon Choi Byoung Doo Rhee Kyung Soo Ko Byung Joo Park Song Young Park Jin Han 《The Korean journal of physiology & pharmacology》2012,16(3):175-180
Yoga has been known to have stimulatory or inhibitory effects on the metabolic parameters and to be uncomplicated therapy for obesity. The purpose of the present study was to test the effect of an 8-week of yoga-asana training on body composition, lipid profile, and insulin resistance (IR) in obese adolescent boys. Twenty volunteers with body mass index (BMI) greater than the 95th percentile were randomly assigned to yoga (age 14.7±0.5 years, n=10) and control groups (age 14.6±1.0 years, n=10). The yoga group performed exercises three times per week at 40~60% of heart-rate reserve (HRR) for 8 weeks. IR was determined with the homeostasis model assessment of insulin resistance (HOMA-IR). After yoga training, body weight, BMI, fat mass (FM), and body fat % (BF %) were significantly decreased, and fat-free mass and basal metabolic rate were significantly increased than baseline values. FM and BF % were significantly improved in the yoga group compared with the control group (p<0.05). Total cholesterol (TC) was significantly decreased in the yoga group (p<0.01). HDL-cholesterol was decreased in both groups (p<0.05). No significant changes were observed between or within groups for triglycerides, LDL-cholesterol, glucose, insulin, and HOMA-IR. Our findings show that an 8-week of yoga training improves body composition and TC levels in obese adolescent boys, suggesting that yoga training may be effective in controlling some metabolic syndrome factors in obese adolescent boys. 相似文献
73.
Jong-Sun Yoo Yun-Jung Lee Kyeong Eun Hyung Joo Won Yoon Ik Hee Lee So-Young Park Kwang Woo Hwang 《The Korean journal of physiology & pharmacology》2012,16(6):463-468
Type 1 diabetes (T1D) is caused by dysregulation of the immune system in the pancreatic islets, which eventually leads to insulin-producing pancreatic β-cell death and destabilization of glucose homeostasis. One of the major characteristics of T1D pathogenesis is the production of inflammatory mediators by macrophages that result in destruction or damage of pancreatic β-cells. In this study the inflammatory microenvironment of T1D was simulated with RAW264.7 cells and MIN6 cells, acting as macrophages and pancreatic β-cells respectably. In this setting, peroxiredoxin-1, an anti-oxidant enzyme was knocked down to observe its functions in the pathogenesis of T1D. RAW264.7 cells were primed with lipopolysaccharide and co-cultured with MIN6 cells while PRX-1 was knocked down in one or both cell types. Our results suggest that hindrance of PRX-1 activity or the deficiency of this enzyme in inflammatory conditions negatively affects pancreatic β-cell survival. The observed decrease in viability of MIN6 cells seems to be caused by nitric oxide production. Additionally, it seems that PRX-1 affects previously reported protective activity of IL-6 in pancreatic β cells as well. These results signify new, undiscovered roles for PRX-1 in inflammatory conditions and may contribute toward our understanding of autoimmunity. 相似文献
74.
We investigated the effects of β-glucan purified from Paenibacillus polymyxa JB115 on the viability and proliferation of splenocytes. Splenocytes play a critical role in host immunity. MTT assays and trypan blue exclusion tests revealed that β-glucan significantly promoted the viability and proliferation of splenocytes over a range of concentrations. However, there was no specific subset change. β-glucan protected splenocytes from cytokine withdrawal-induced spontaneous cell death. For further mechanistic studies, ELISA assay revealed that β-glucan enhanced the expression of anti-apoptotic molecules and interleukin 7 (IL-7), a cytokine critical for lymphocyte survival. We also investigated the IL-2 dependency of β-glucan-treated splenocytes to determine if treated cells could still undergo clonal expansion. In flow cytometric analysis, β-glucan induced increased levels of the activation marker CD25 on the surface of splenocytes and β-glucan-treated splenocytes showed higher proliferation rates in response to IL-2 treatment. This study demonstrates that β-glucan can enhance the survival of splenocytes and provides valuable information to broaden the use of β-glucan in research fields. 相似文献
75.
Jong-Sun Yoo Yun-Jung Lee Joo Won Yoon Kyeong Eun Hyung Kwang Woo Hwang 《The Korean journal of physiology & pharmacology》2012,16(5):349-353
Activated T cells express inhibitory receptors such as CTLA-4 that can downregulate immune responses. Blockade of or genetic deficiency in CTLA-4 can result in autoimmunity. Therefore, strategies to increase the inhibitory function of CTLA-4 may be attractive in settings of undesirable T cell responses such as autoimmunity or transplant rejection. We have tested the hypothesis that transgenic constitutive expression of CTLA-4 can further attenuate immune responses when compared with normal inducible expression. Our results indicate that transgenic expression of CTLA-4 in mouse T cells (CTLA-4-Tg T cells) results in reduced cell cycle progression and increased apoptosis of TCR-stimulated T cells. CTLA-4-Tg T cells display reduced T cell proliferation in an in vivo model of graft versus host disease (GVHD). These results further our understanding of how CTLA-4 can be manipulated to inhibit immune responses and may help development of new therapeutic strategies for clinical settings of autoimmunity and transplantation. 相似文献
76.
Ju Hwan Park Mee Yeon Lee Min Ju Kang Geon Kim Dae-Duk Kim 《Journal of Pharmaceutical Investigation》2012,42(6):293-307
TNF-?? is an endogenous signaling protein which controls physiological activities and participates in immune response. It is known to interact with TNF receptors (TNFR), of which have two kinds leading to totally different effects. Binding of TNF-?? to TNFR1 can induce either cell proliferation or cell death, i.e., necroptosis, depending on the kinds of protein to which it binds during the signaling cascade. On the contrary, binding of TNF-?? to TNFR2 induces only cell death process. TNF-?? can also cause antiviral effect by inducing interferon, and can inhibit tumor growth. Moreover, TNF-?? helps action of immune cells and it leads to increasement of tumor cell lysis. TNF-?? also makes tumor vessels more permeable and induces coagulation and thrombosis in the tumor vessels, which ultimately contribute to antitumor effect. However, TNF-?? also has several toxic effects, which include the change in redox status of antioxidant factors, induction of excess inflammation response, and action as pro-inflammatory cytokine of itself. These toxicities need to be considered when developing TNF-?? as an anticancer agent. In this review, pharmaceutical approaches to optimize and utilize its antitumor activity of TNF-?? as well as to decrease its adverse effect are discussed. 相似文献
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