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81.
Shinzaki Shinichiro Matsuoka Katsuyoshi Tanaka Hiroki Takeshima Fuminao Kato Shingo Torisu Takehiro Ohta Yuki Watanabe Kenji Nakamura Shiro Yoshimura Naoki Kobayashi Taku Shiotani Akiko Hirai Fumihito Hiraoka Sakiko Watanabe Mamoru Matsuura Minoru Nishimoto Shohei Mizuno Shinta Iijima Hideki Takehara Tetsuo Naka Tetsuji Kanai Takanori Matsumoto Takayuki 《Journal of gastroenterology》2021,56(6):560-569
Journal of Gastroenterology - This multicenter prospective study (UMIN000019958) aimed to evaluate the usefulness of serum leucin-rich alpha-2 glycoprotein (LRG) levels in monitoring disease... 相似文献
82.
T. Ohira K. Nishio Y. Ohe H. Arioka M. Nishio Y. Funayama H. Ogasawara M. Fukuda K. Yazawa H. Kato N. Saijo 《Journal of cancer research and clinical oncology》1996,122(12):711-715
Cachexia frequently occurs in the late stages of cancer, and is difficult to manage. We previously reported that interleukin-6 (IL-6) cDNA transfection into Lewis lung carcinoma (LLC-IL6) induced cachexia-like symptoms in C57BL/6 mice. This was thought to be a useful experimental model of cancer cachexia. We have examined the effects of two eicosanoids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), in order to evaluate whether they could relieve cachexia. LLC-IL6-bearing animals were divided into three treatment groups receiving DHA, EPA or water as the control; 80-l samples of these compounds (purity>95%) were administered orally by catheter daily starting 7 days after tumor transplantation. Tumor growth curves were similar in the three groups. There were no differences in water or food intake in the three groups. However, body weight, a marker of cachexia, was significantly higher in treated mice than in the control group. Sixteen days after tumor transplantation, the mean body weight was 17.45 g (P<0.05), 17.2 g and 16.41 g in the groups receiving DHA, EPA and water respectively. The eicosanoids did not affect serum levels of IL-6. Ubiquitination of muscle protein, a marker of proteolysis coupled to cachexia, was compared in LLC-IL6-and LLC-transplanted mice. The eicosanoids prevented the ubiquitination of approximately 180 kDa protein. These results suggest that eicosanoids may prevent the cachexia mediated by IL-6.Abbreviations
DHA
docosahexaenoic acid
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EPA
eicosapentaenoic acid
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LLC
Lewis lung carcinoma
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IL
interleukin 相似文献
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Maegawa H Obata T Shibata T Fujita T Ugi S Morino K Nishio Y Kojima H Hidaka H Haneda M Yasuda H Kikkawa R Kashiwagi A 《Diabetologia》1999,42(2):151-159
Summary A newly synthesized antidiabetic agent, JTT-501 is an isoxazolidinedione rather than a thiazolidinedione. An oral dose of
JTT-501 (100 mg · kg–1· day–1) given to 12-week-old male Zucker fatty rats for 7 days led to the amelioration of both hyperinsulinaemia (40 % of non-treated)
and hypertriglyceridaemia (23 % of non-treated) as well as a 2.4-fold increased insulin sensitivity as determined by a euglycaemic
insulin clamp. In our study, we further evaluated the acute effect of JTT-501 on both the glucose infusion rates (GIR) and
insulin signalling in skeletal muscle. Male Sprague-Dawley (SD) rats aged 10 weeks were injected intravenously with JTT-501
(5 mg/kg) and then a euglycaemic insulin clamp was initiated and glucose infusion rates monitored for 150 min. We found that
this treatment increased the glucose infusion rate by 33 % during the last 30 min in SD rats. After the clamp had been initiated
for 30 min, the insulin-stimulated phosphatidylinositol 3-kinase (PI3-kinase) activities co-immunoprecipitated with insulin
receptor substrate 1 (IRS-1) were also enhanced, resulting in increased glycogen synthase activities in the soleus muscles.
Treatment with JTT-501 also enhanced the phosphorylation of insulin receptors and insulin receptor-substrate 1 rapidly as
well as the phosphatidylinositol 3-kinase activities, which were stimulated by a bolus injection of insulin. Similarly, JTT-501
stimulated the glucose infusion rate by 30 % and enhanced insulin signalling in Zucker fatty rats. In conclusion, a newly
developed isoxazolidinedione, JTT-501, rapidly potentiates the insulin sensitivity of skeletal muscle by enhancing insulin
signalling and could be useful for the treatment of insulin-resistant diabetic subjects. [Diabetologia (1999) 42: 151–159]
Received: 2 June 1998 and in final revised form: 2 October 1998 相似文献
90.
Emma Tabe Eko Niba Hisahide Nishio Yogik Onky Silvana Wijaya Poh San Lai Takenori Tozawa Tomohiro Chiyonobu Misaki Yamadera Kentaro Okamoto Hiroyuki Awano Yasuhiro Takeshima Toshio Saito Masakazu Shinohara 《Brain & development》2021,43(2):294-302
BackgroundSpinal muscular atrophy (SMA) is a neuromuscular disease caused by homozygous deletion of SMN1 exons 7 and 8. However, exon 8 is retained in some cases, where SMN2 exon 7 recombines with SMN1 exon 8, forming a hybrid SMN gene. It remains unknown how the hybrid SMN gene contribute to the SMA phenotype.MethodWe analyzed 515 patients with clinical suspicion for SMA. SMN1 exons 7 and 8 deletion was detected by PCR followed by enzyme digestion. Hybrid SMN genes were further analyzed by nucleotide sequencing. SMN2 copy number was determined by real-time PCR.ResultsSMN1 exon 7 was deleted in 228 out of 515 patients, and SMN1 exon 8 was also deleted in 204 out of the 228 patients. The remaining 24 patients were judged to carry a hybrid SMN gene. In the patients with SMN1 exon 7 deletion, the frequency of the severe phenotype was significantly lower in the patients with hybrid SMN gene than in the patients without hybrid SMN gene. However, as for the distribution of SMN2 exon 7 copy number among the clinical phenotypes, there was no significant difference between both groups of SMA patients with or without hybrid SMN gene.ConclusionHybrid SMN genes are not rare in Japanese SMA patients, and it appears to be associated with a less severe phenotype. The phenotype of patients with hybrid SMN gene was determined by the copy number of SMN2 exon 7, as similarly for the patients without hybrid SMN gene. 相似文献