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排序方式: 共有818条查询结果,搜索用时 15 毫秒
811.
Makoto Chuma Haruki Uojima Atsushi Hiraoka Satoshi Kobayashi Hidenori Toyoda Toshifumi Tada Hisashi Hidaka Shogo Iwabuchi Kazushi Numata Ei Itobayashi Norio Itokawa Kazuya Kariyama Hideko Ohama Nobuhiro Hattori Shunji Hirose Hiroshi Shibata Joji Tani Michitaka Imai Kazuto Tajiri Satoshi Moriya Naohisa Wada Shuitirou Iwasaki Taito Fukushima Makoto Ueno Satoshi Yasuda Masanori Atsukawa Kazuhiro Nouso Shinya Fukunishi Tsunamasa Watanabe Toru Ishikawa Shinichiro Nakamura Manabu Morimoto Tatehiro Kagawa Michiie Sakamoto Takashi Kumada Shin Maeda 《Hepatology research》2021,51(2):201-215
812.
Kaoru Yagita Naokazu Sasagasako Sachiko Koyama Hideko Noguchi Hiroyuki Honda 《Neuropathology》2023,43(1):117-126
Here we present the autopsy case of an 80-year-old woman with a 9-year history of motor neuron disease and atypical Parkinsonism. Her initial symptom was gait disturbance, and she subsequently developed limb weakness and Parkinsonism without response to levodopa. Her motor symptoms progressed to bulbar palsy, and she died of respiratory failure. Postmortem examination revealed characteristic findings of amyotrophic lateral sclerosis (ALS), including motor neuronal loss with astrogliosis, corticospinal tract degeneration, and TAR DNA-binding protein of 43 kDa abnormalities, including nuclear loss and skein-like inclusions. In contrast, severe tau pathological changes were seen in the frontotemporal lobes and pallido-nigral system. Tau pathologies affected not only neuronal components, such as neurofibrillary tangles and neuropil threads, but also glial cells (astrocytes and oligodendrocytes). Some glial tau pathologies exhibited peculiar round accumulations, reminiscent of globular glial inclusions (GGIs) in globular glial tauopathy. This unique autopsy case demonstrates that ALS with TDP-43 could be comorbid with globular glial tau inclusions and indicates that common pathological mechanisms exist among ALS and GGI formation. 相似文献
813.
Rinko Takashiki Junko Komatsu Mari Nowicki Yuki Moritoki Mieko Okazaki Shigetoshi Ohshima Hitoshi Hasegawa Kyoko Nomura Gen Ouchi Benjamin W. Berg Hideko Shirakawa Katsutoshi Nakayama Naoto Takahashi 《Japan Journal of Nursing Science》2023,20(2):e12519
Aim
Acute chest pain is a commonly encountered symptom in hospital medical/surgical units; however, almost half of nurses in their second year of clinical experience in our facility have reported struggling to care for acute chest pain patients. We developed, implemented, and examined the effectiveness of a simulation-based, mastery learning clinical nursing educational program to improve self-efficacy and performance in caring for patients with acute chest pain.Methods
The study adopted a single-site, single-cohort design using simulation-based performance assessment and self-efficacy surveys on a convenience sample of 37 second-year clinical nurse participants in multi-stage hybrid mastery learning educational intervention using asynchronous e-learning, and hands-on simulation training and assessment with feedback on caring for chest pain patients. Performance assessments and self-efficacy surveys were administered pre-, post-, and 5 months post-intervention.Results
Clinical performance on the post- and 5 months follow-up assessments were significantly higher than those for the pre-test (P < .0001). The self-efficacy scores for the post- and the 5 months follow-up assessments were significantly higher than the pre-course scores (P < .0001). Participants' self-efficacy perceptions were positively correlated with their performances at 5 months post-intervention.Conclusion
Performance and self-efficacy of novice nurses in caring for acute chest pain patients improved significantly with the multi-stage hybrid mastery learning educational intervention, with improvements retained 5 months post-intervention. The results suggest the applicability of simulation-based mastery learning in a clinical setting for novice nurses to attain specific skills, and raise their self-perception of competence to care for patients in acute settings. 相似文献814.
Takeshi Hatanaka Satoru Kakizaki Atsushi Hiraoka Toshifumi Tada Masashi Hirooka Kazuya Kariyama Joji Tani Masanori Atsukawa Koichi Takaguchi Ei Itobayashi Shinya Fukunishi Kunihiko Tsuji Toru Ishikawa Kazuto Tajiri Hironori Ochi Satoshi Yasuda Hidenori Toyoda Chikara Ogawa Takashi Nishimura Noritomo Shimada Kazuhito Kawata Hisashi Kosaka Atsushi Naganuma Yutaka Yata Takaaki Tanaka Hideko Ohama Fujimasa Tada Kazuhiro Nouso Asahiro Morishita Akemi Tsutsui Takuya Nagano Norio Itokawa Tomomi Okubo Taeang Arai Michitaka Imai Yohei Koizumi Shinichiro Nakamura Masaki Kaibori Hiroko Iijima Yoichi Hiasa Takashi Kumada Real-life Practice Experts for HCC Study Group and HCC Group 《Hepatology research》2023,53(8):737-748
815.
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818.
Kazuya Miyashita Takuya Yagi Noritaka Kagaya Azusa Takechi Chihiro Nakata Risa Kanda Hideko Nuriya Kosuke Tanegashima Shota Hoyano Fumiya Seki Chihiro Yoshida Yoshifumi Hachiro Tomoya Higashi Nobuo Kitada Takashi Toya Takeshi Kobayashi Yuho Najima Susumu Goyama Shojiro A. Maki Toshio Kitamura Noriko Doki Kazuo Shin-ya Takahiko Hara 《Cancer science》2023,114(10):4032-4040
T-cell acute lymphoblastic leukemia (T-ALL) is one of the most frequently occurring cancers in children and is associated with a poor prognosis. Here, we performed large-scale screening of natural compound libraries to identify potential drugs against T-ALL. We identified three low-molecular-weight compounds (auxarconjugatin-B, rumbrin, and lavendamycin) that inhibited the proliferation of the T-ALL cell line CCRF-CEM, but not that of the B lymphoma cell line Raji in a low concentration range. Among them, auxarconjugatin-B and rumbrin commonly contained a polyenyl 3-chloropyrrol in their chemical structure, therefore we chose auxarconjugatin-B for further analyses. Auxarconjugatin-B suppressed the in vitro growth of five human T-ALL cell lines and two T-ALL patient-derived cells, but not that of adult T-cell leukemia patient-derived cells. Cultured normal T cells were several-fold resistant to auxarconjugatin-B. Auxarconjugatin-B and its synthetic analogue Ra#37 depolarized the mitochondrial membrane potential of CCRF-CEM cells within 3 h of treatment. These compounds are promising seeds for developing novel anti-T-ALL drugs. 相似文献