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排序方式: 共有1882条查询结果,搜索用时 500 毫秒
991.
Takahiro Nakano Kazuhiko Uchiyama Chihiro Ushiroda Saori Kashiwagi Yuki Toyokawa Katsura Mizushima Ken Inoue Osamu Dohi Tetsuya Okayama Naohisa Yoshida Kazuhiro Katada Kazuhiro Kamada Osamu Handa Takeshi Ishikawa Tomohisa Takagi Hideyuki Konishi Yuji Naito Yoshito Itoh 《Journal of gastroenterology and hepatology》2020,35(7):1171-1179
992.
993.
Nilendra Singh Bo Ma Christopher Charles Leonardo Abdullah Shafique Ahmad Shuh Narumiya Sylvain Doré 《Neurotoxicity research》2013,24(4):549-559
Prostaglandin E2 (PGE2) has been described to exert beneficial and detrimental effects in various neurologic disorders. These conflicting roles of PGE2 could be attributed to its diverse receptor subtypes, EP1–EP4. At present, the precise role of EP1 in intracerebral hemorrhage (ICH) is unknown. Therefore, to elucidate its possible role in ICH, intrastriatal injection of collagenase was given in randomized groups of adult male wildtype (WT) and EP1 receptor knockout (EP1?/?) C57BL/6 mice. Functional outcomes including neurologic deficits, rotarod performance, open field activity, and adhesive removal performance were evaluated at 24, 48, and 72 h post-ICH. Lesion volume, cell survival and death, were assessed using Cresyl Violet, and Fluoro-Jade staining, respectively. Microglial activation and phagocytosis were estimated using Iba1 immunoreactivity and fluorescently-labeled microspheres. Following 72 h post-ICH, EP1?/? mice showed deteriorated outcomes compared to the WT control mice. These outcomes were demonstrated by elevated neurological deficits, exacerbated lesion volume, and significantly worsened sensorimotor functions. Fluoro-Jade staining showed significantly increased numbers of degenerating neurons and reduced neuronal survival in EP1?/? compared to WT mice. To assess in vivo phagocytosis, the number of microspheres phagocytosed by Iba1-positive cells was 145.4 ± 15.4 % greater in WT compared to EP1?/? mice. These data demonstrate that EP1 deletion exacerbates neuro-behavioral impairments following ICH, potentially by slowing down/impairing microglial phagocytosis. A better understanding of this EP1 mechanism could lead to improved intervention strategies for hemorrhagic stroke. 相似文献
994.
Chihiro Imura Azumi Ueyama Yoshikazu Sasaki Masaya Shimizu Yoko Furue Nobuyuki Tai Kenichiro Tsujii Kazufumi Katayama Takayuki Okuno Michitaka Shichijo Kiyoshi Yasui Mina Yamamoto 《Journal of dermatological science》2019,93(3):176-185
Background
Retinoic acid receptor-related orphan receptor gamma t (RORγt) has critical roles in the development, maintenance and function of interleukin (IL)-17-producing cells and is a highly attractive target for the treatment of IL-17-mediated autoimmune disease, particularly psoriasis. On the other hand, RORγt is also critical for controlling apoptosis during thymopoiesis, and genetic RORγt ablation or systematic RORγt inhibition cause progressive thymic aberrations leading to T cell lymphomas.Objective
We investigated whether topical administration of our novel RORγt inhibitor, S18-000003 has therapeutic potential for psoriasis with low risk of thymic aberrations.Methods
We evaluated the effect of topical S18-000003 on psoriasis-like skin inflammation and influence on the thymus in a 12-O-tetradecanoylphorbol-13-acetate-induced K14.Stat3C mouse psoriasis model.Results
S18-000003 markedly inhibited the development of psoriatic skin inflammation via suppression of the IL-17 pathway. In the skin, S18-000003 suppressed all subsets of IL-17-producing cells that we previously identified in this psoriasis model: Th17 cells, Tc17 cells, dermal γδ T cells, TCR? cells that probably included innate lymphoid cells, and CD4?CD8? double-negative αβ T cells. Notably, neither reduction of CD4+CD8+ double-positive thymocytes nor dysregulation of cell cycling was observed in S18-000003-treated mice, even at a high dose.Conclusion
Our topically administered RORγt inhibitor is a potential therapeutic agent for psoriasis with low risk of thymic lymphoma. 相似文献995.
996.
997.
Eun-Kyeong Jo Jin Kyung Kim Dong-Min Shin Chihiro Sasakawa 《Cellular & molecular immunology》2016,13(2):148-159
Inflammasomes are multi-protein signaling complexes that trigger the activation of inflammatory caspases and the maturation of interleukin-1β. Among various inflammasome complexes, the NLRP3 inflammasome is best characterized and has been linked with various human autoinflammatory and autoimmune diseases. Thus, the NLRP3 inflammasome may be a promising target for anti-inflammatory therapies. In this review, we summarize the current understanding of the mechanisms by which the NLRP3 inflammasome is activated in the cytosol. We also describe the binding partners of NLRP3 inflammasome complexes activating or inhibiting the inflammasome assembly. Our knowledge of the mechanisms regulating NLRP3 inflammasome signaling and how these influence inflammatory responses offers further insight into potential therapeutic strategies to treat inflammatory diseases associated with dysregulation of the NLRP3 inflammasome. 相似文献
998.
999.
Takeaki Fukui Chishio Munemura Satoko Maeta Chihiro Ishida Yoshikazu Murawaki 《Yonago acta medica》2011,54(3):49-58
Recently, an angiotensin inhibitor has been shown to upregulate the
klotho mRNA level in chronic renal failure. In addition, the
administration of vitamin D has been reported to improve the mortality of patients with
chronic renal failure. In this study, we examined the effects of an angiotensin inhibitor
and/or vitamin D on the progression of chronic renal failure by using male 5/6
nephrectomized (5/6Nx) spontaneously hypertensive rats. Male 5/6Nx spontaneously
hypertensive rats were assigned to 4 groups as follows: 5/6Nx group, 5/6Nx rats; Alf
group, 5/6Nx rats administered alfacalcidol (0.2 μg/kg/day); Olm group, 5/6Nx rats
administered olmesartan (15 mg/kg/day); Alf + Olm group, 5/6Nx rats administered
alfacalcidol (0.2 μg/kg/day) and olmesartan (15 mg/kg/day). These drugs were administered
for 12 weeks. Systolic blood pressure in the Alf, Olm and Alf + Olm groups were
significantly decreased relative to that in the 5/6Nx group during the 12-week
experimental period. As a result, all treated groups showed renoprotection based on
improvement of the systolic blood pressure, urinary protein excretion and histological
renal fibrosis. Combination therapy of alfacalcidol and olmesartan was more effective than
either alfacalcidol or olmesartan alone. Expression of klotho mRNA was
significantly upregulated in the Alf + Olm group in comparison with in the 5/6Nx group.
Serum levels of fibroblast growth factor 23 in the Alf group and the Alf + Olm group were
significantly higher than those in the 5/6Nx group and the Olm group. In conclusion, the
combination of Olm and Alf inhibited the progression of renal damage in the 5/6Nx group
through the strong antihypertensive effect as well as the upregulation of the
klotho gene. 相似文献