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排序方式: 共有416条查询结果,搜索用时 15 毫秒
71.
Mitsuko Nakashima MD PhD Mitsuhiro Kato MD PhD Kazushi Aoto DDS PhD Masaaki Shiina MD PhD Hazrat Belal MS Souichi Mukaida MD PhD Satoko Kumada MD PhD Atsushi Sato MD PhD Ayelet Zerem MD PhD Tally Lerman‐Sagie MD Dorit Lev MD PhD Huey Yin Leong MD Yoshinori Tsurusaki PhD Takeshi Mizuguchi MD PhD Satoko Miyatake MD PhD Noriko Miyake MD PhD Kazuhiro Ogata MD PhD Hirotomo Saitsu MD PhD Naomichi Matsumoto MD PhD 《Annals of neurology》2018,83(4):794-806
72.
Watanabe G Nanjo H Nagai H Wang J Koyota S Yamamoto Y Sugiyama T 《Medical molecular morphology》2011,44(2):103-110
Both liver epithelial and oval cells are believed to be liver stem cells. We investigated the identification by producing
monoclonal antibodies against liver epithelial cells. Monoclonal antibodies against hepatic stem-like cells (HSL cells) have
been selected to follow the hepatic stem cells during hepatic regeneration and developmental changes in the liver. Monoclonal
antibodies were induced by immunization of BALB/c mice with HSL cells established from the epithelial cells of the adult rat
liver. The hybridomas were screened by indirect immunofluorescence staining of HSL cells. We produced a unique monoclonal
antibody against HSL cells, MabH, which specifically recognizes liver epithelial cells. MabH did not react with liver parenchymal
cells but did react with bile ductule cells under normal conditions in the adult liver. This antibody also reacted with oval
cell lines and with the oval cells that appeared during liver regeneration. In addition, fetal liver cells showed immunoreactivity
with MabH. Although the level of staining decreased after birth, some cells in the portal area remained highly reactive. These
results suggested that liver epithelial cells, oval cells, and fetal liver cells possess a common cell marker of liver stem
cells. 相似文献
73.
74.
Sakata Y Iwamoto Y Inata J Matsumoto S Miyamori S Nakashima K Sakamoto S Kanehara M Kitaguchi S Hiraki K 《Gan to kagaku ryoho. Cancer & chemotherapy》2012,39(6):927-932
Pemetrexed, a folate metabolic antagonist, is considered to be effective against plural mesotheliomas, non-small cell lung cancer, and especially for non-squamous cell cancer. However, it has been reported to have adverse interactions with nonsteroid anti-inflammatory drugs(NSAIDs). In the present study, we compared the incidence of adverse events between patients receiving pemetrexed therapy with and without concomitant NSAID administration. No significant difference in the incidence of hematotoxic events of Grade 3 or worse was observed. As for the incidence of non-hematotoxic events, the increase in the amount of creatinine, namely a severe adverse effect of Grade 2 or more, was significantly higher in the combined therapy group (p=0.018). No other significant differences were noted for other adverse events. A creatinine increase to Grade 2 or greater developed significantly earlier in the combined group(median value, 12.7 courses; p=0.0063). Our results suggest that renal dysfunction may easily develop as a result of continued pemetrexed administration combined with NSAID therapy. Therefore, it is necessary to take precautions against adverse side effects such as renal dysfunction when combining pemetrexed with NSAID therapy, by conducting periodic examinations. 相似文献
75.
Kazutoshi Kamiyama Akihiko Wada Masaki Sugihara Souichi Kurioka Kumi Hayashi Takafumi Hayashi Takeshi Yoshisako Nobuko Yamamoto Youji Tsuchie Syuhei Yamaguchi Toshitsugu Sugimoto Hajime Kitagaki 《Japanese journal of radiology》2010,28(4):266-272
Purpose
Among diabetes mellitus type 2 (DM2) patients, the frequency of cognitive dysfunction is higher and the relative risk of Alzheimer’s disease (AD) is approximately twice that of nondiabetics. Cognitive impairment symptoms of AD are induced by limbic system dysfunction, and an early-stage AD brain without dementia has the potential for atrophy in the hippocampal region. In this study, we estimated potential hippocampal region atrophy in DM2 and pursued the association between DM2 and cognitive impairment/AD.Materials and methods
Voxel-based morphometry analysis was performed in 28 diabetics (14 men, 14 women; ages 59–79 years, mean 70.7 years) and 28 sex- and agematched (±1 year) nondiabetics. Severity of gray matter loss in the hippocampal region and whole brain were investigated. Group analysis was performed using twotailed unpaired t-test; significance was assumed with less than 1% (P < 0.01) of the critical rate.Results
There was a significant difference between diabetics and nondiabetics regarding the severity of hippocampal region atrophy and whole-brain atrophy. Only diabetics showed a positive correlation for severity of hippocampal region atrophy and whole-brain atrophy (rs = 0.69, P < 0.0001).Conclusion
Aged DM2 patients have the potential for hippocampal region atrophy, and its dysfunction can be related to the expression of a cognitive impairment that resembles AD. 相似文献76.
77.
We report two male siblings presenting with severe hypotonia, generalized muscle atrophy, multiple joint contractures and respiratory failure. The serum creatine kinase levels were within normal limits, 75 IU/l in the younger boy and 123 IU/l in the older one. Muscle biopsies at the age of 28 days in the younger boy and 48 days in the older one revealed dystrophic pathology with increased interstitial fibrous tissue, scattered basophilic fibers and an increased number of undeveloped type-2C fibers. Although the elder brother died from respiratory failure at 4 months of age, the younger child has been sustained with mechanical ventilation, and has been exhibiting non-progressive muscle symptoms. Upon re-biopsy of the younger sibling at the age of 3 years, neither basophilic regenerating fibers nor degenerating fibers were found. All muscle fibers were found to be extremely atrophic and behaved mostly like type-1 fibers, displaying the features of congenital neuromuscular disease with uniform type-1 fibers. Since early biopsies in congenital myopathies reveal numerous undifferentiated immature muscle fibers, it is difficult to make a definite diagnosis, unless we recognize disease-specific cytoplastic abnormalities of nemaline body formation and abnormalities of core structure. 相似文献
78.
79.
Catechin, green tea component, causes caspase-independent necrosis-like cell death in chronic myelogenous leukemia 总被引:1,自引:0,他引:1
Reo Iwasaki Kinji Ito Takaomi Ishida Makoto Hamanoue Souichi Adachi Toshiki Watanabe Yuko Sato 《Cancer science》2009,100(2):349-356
Management strategies of chronic phase chronic myelogenous leukemia (CML) have been revolutionized due to the discovery of a selective tyrosine kinase inhibitor, imatinib (Gleevec, STI571), which is substantially improving median survival. However, emergence of imatinib-resistance has put up a serious problem that requires novel treatment methods. Catechins, polyphenolic compounds in green tea, are gathering much attention due to their potential antitumor effects. So far (–)-epigallocatechin-3-gallate (EGCG), the most abundant component of catechin, has been shown to cause typical apoptosis in several tumor cell lines in most cases through activation of caspases. In this study, we showed that EGCG predominantly caused necrosis-like cell death via a caspase-independent mechanism in CML cells, K562 and C2F8, whereas imatinib induced the typical apoptotic cell death. Moreover, this caspase-independent cell death partially mediated the release of apoptosis-inducing factor, AIF, and serine protease, HtrA2/Omi, from the mitochondria to cytosol. In addition, EGCG enhanced the imatinib-induced cell death ( P < 0.01) resulting in additive cell death in K562 cells and EGCG alone, effectively reduced the viability of imatinib-resistant K562 cells ( P < 0.01). Catechin is a possible candidate for an antitumor agent that causes cell death in CML cells via a caspase-independent mechanism. ( Cancer Sci 2009; 100: 349–356) 相似文献
80.
Koto K Horie N Kimura S Murata H Sakabe T Matsui T Watanabe M Adachi S Maekawa T Fushiki S Kubo T 《Cancer letters》2009,274(2):271-278
Clinically obtainable concentrations of zoledronic acid (ZOL) inhibited the production of vascular endothelial growth factor and reduced the migration, adhesion, and invasiveness of osteosarcoma (OS) cells in vitro. The in vivo effects of ZOL were investigated by using a murine model of spontaneous lung metastasis. The higher dose of ZOL (80 microg/kg three times/week) inhibited the growth of OS at the primary site, accompanied by inhibition of neovascularization in the tumor. Interestingly, while the lower dose of ZOL (80 microg/kg once a week) could not inhibit the growth of OS at the primary site, it significantly prevented lung metastasis. 相似文献