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1.
Tetsuji Terazawa Takeshi Kato Masahiro Goto Katsuya Ohta Shingo Noura Hironaga Satake Yoshinori Kagawa Hisato Kawakami Hiroko Hasegawa Kazuhiro Yanagihara Tatsushi Shingai Ken Nakata Masahito Kotaka Masayuki Hiraki Ken Konishi Shiro Nakae Daisuke Sakai Yukinori Kurokawa Toshio Shimokawa Taroh Satoh 《The oncologist》2021,26(1):17-e47
Lessons Learned
- Panitumumab monotherapy showed favorable efficacy and feasibility in the treatment of frail or elderly patients with RAS wild‐type unresectable colorectal cancer.
- It is especially effective for left‐sided tumors; therefore, panitumumab as first‐line treatment could be an additional therapeutic option for frail elderly patients, particularly in those who are unsuitable for upfront oxaliplatin‐based or irinotecan‐based combination regimens.
2.
Tetsuji Terazawa Jin Matsuyama Masahiro Goto Ryohei Kawabata Shunji Endo Motohiro Imano Shoichiro Fujita Yusuke Akamaru Hirokazu Taniguchi Mitsutoshi Tatsumi Sang-Woong Lee Yoshitaka Kurisu Hisato Kawakami Yukinori Kurokawa Toshio Shimokawa Daisuke Sakai Takeshi Kato Kazumasa Fujitani Taroh Satoh 《The oncologist》2020,25(2):119-e208
3.
Taroh Satoh Kyung Hee Lee Sun Young Rha Yasutsuna Sasaki Se Hoon Park Yoshito Komatsu Hirofumi Yasui Tae-You Kim Kensei Yamaguchi Nozomu Fuse Yasuhide Yamada Takashi Ura Si-Young Kim Masaki Munakata Soh Saitoh Kazuto Nishio Satoshi Morita Eriko Yamamoto Qingwei Zhang Jung-mi Kim Yeul Hong Kim Yuh Sakata 《Gastric cancer》2015,18(4):824-832
4.
Phenotype–genotype correlations of PIGO deficiency with variable phenotypes from infantile lethality to mild learning difficulties 下载免费PDF全文
Seiji Mizuno Nobuhiko Okamoto Daisuke Fukushi Koji Tominaga Hiroyuki Kidokoro Yukako Muramatsu Eriko Nishi Shota Nakamura Daisuke Motooka Noriko Nomura Kiyoshi Hayasaka Tetsuya Niihori Yoko Aoki Shin Nabatame Masahiro Hayakawa Jun Natsume Keiichi Ozono Taroh Kinoshita Nobuaki Wakamatsu Yoshiko Murakami 《Human mutation》2017,38(7):805-815
Inherited GPI (glycosylphosphatidylinositol) deficiencies (IGDs), a recently defined group of diseases, show a broad spectrum of symptoms. Hyperphosphatasia mental retardation syndrome, also known as Mabry syndrome, is a type of IGDs. There are at least 26 genes involved in the biosynthesis and transport of GPI‐anchored proteins; however, IGDs constitute a rare group of diseases, and correlations between the spectrum of symptoms and affected genes or the type of mutations have not been shown. Here, we report four newly identified and five previously described Japanese families with PIGO (phosphatidylinositol glycan anchor biosynthesis class O) deficiency. We show how the clinical severity of IGDs correlates with flow cytometric analysis of blood, functional analysis using a PIGO‐deficient cell line, and the degree of hyperphosphatasia. The flow cytometric analysis and hyperphosphatasia are useful for IGD diagnosis, but the expression level of GPI‐anchored proteins and the degree of hyperphosphatasia do not correlate, although functional studies do, with clinical severity. Compared with PIGA (phosphatidylinositol glycan anchor biosynthesis class A) deficiency, PIGO deficiency shows characteristic features, such as Hirschsprung disease, brachytelephalangy, and hyperphosphatasia. This report shows the precise spectrum of symptoms according to the severity of mutations and compares symptoms between different types of IGD. 相似文献
5.
Junpei Tanigawa Haruka Mimatsu Seiji Mizuno Nobuhiko Okamoto Daisuke Fukushi Koji Tominaga Hiroyuki Kidokoro Yukako Muramatsu Eriko Nishi Shota Nakamura Daisuke Motooka Noriko Nomura Kiyoshi Hayasaka Tetsuya Niihori Yoko Aoki Shin Nabatame Masahiro Hayakawa Jun Natsume Keiichi Ozono Taroh Kinoshita Nobuaki Wakamatsu Yoshiko Murakami 《Human mutation》2017,38(7):i-i
6.
Molecular Genetics of Paroxysmal Nocturnal Hemoglobinuria 总被引:4,自引:0,他引:4
Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hematopoietic stem cell disorder characterized by the clonal expansion of glycosylphosphatidylinositol (GPI)-deficient cells that leads to complement-mediated hemolysis. A somatic mutation in the PIG-A gene involved in GPI biosynthesis causes a deficiency of GPI-anchored proteins. However, it is evident that the clonal expansion of GPI-deficient cells is not caused by only the PIG-A mutation and that other changes should be involved in the development of PNH. Some patients with aplastic anemia (AA) develop PNH. Furthermore, it has been reported that most patients with AA and refractory anemia (RA) who carry HLA-DRB1*15 and show a good response to immunosuppressive therapies have an expanded population of GPI-deficient clones. This finding, together with recent data showing resistance of GPI-deficient cells to cytotoxic cells, suggests that GPI-deficient cells escape immunologic attack and are positively selected in the autoimmune environment. However, GPI-deficient clones found in AA and RA are generally small and do not increase to near-complete dominance. Therefore, 1 or more additional genetic abnormalities that confer the growth phenotype on GPI-deficient cells are probably required for fully developed PNH or so-called florid PNH. The next 10 years should witness the discovery of the molecular mechanisms of immunologic selection and the identification of abnormalities involved in the further clonal expansion of PNH cells. 相似文献
7.
8.
Tissue-specific knockout of the mouse Pig-a gene reveals important roles for GPI-anchored proteins in skin development 下载免费PDF全文
Masahito Tarutani Satoshi Itami Masaru Okabe Masahito Ikawa Tadashi Tezuka Kunihiko Yoshikawa Taroh Kinoshita Junji Takeda 《Proceedings of the National Academy of Sciences of the United States of America》1997,94(14):7400-7405
Glycosylphosphatidylinositol (GPI)-anchored proteins are widely distributed on plasma membranes of eukaryotes. More than 50 GPI-anchored proteins have been shown to be spatiotemporally expressed in mice with a deficiency of GPI-anchor biosynthesis that causes embryonic lethality. Here, we examine the functional roles of GPI-anchored proteins in mouse skin using the Cre-loxP recombination system. We disrupted the Pig-a gene, an X-linked gene essential for GPI-anchor biosynthesis, in skin. The Cre-mediated Pig-a disruption occurred in skin at almost 100% efficiency in male mice bearing two identically orientated loxP sites within the Pig-a gene. Expression of GPI-anchored proteins was completely absent in the skin of these mice. The skin of such mutants looked wrinkled and more scaly than that of wild-type mice. Furthermore, histological examination of mutant mice showed that the epidermal horny layer was tightly packed and thickened. Electron microscopy showed that the intercellular space was narrow and there were many small vesicles embedded in the intercellular space that were not observed in equivalent wild-type mouse skin preparations. Mutant mice died within a few days after birth, suggesting that Pig-a function is essential for proper skin differentiation and maintenance. 相似文献
9.
Tang C Yamada H Shibata K Maeda N Yoshida S Wajjwalku W Ohara N Yamada T Kinoshita T Yoshikai Y 《The Journal of infectious diseases》2008,197(9):1263-1274
Protection against Mycobacterium tuberculosis not only depends on CD4+ T helper type 1 (Th1) cells but, also, on CD8+ T cells. Interleukin (IL)-15 has an important function in the maintenance of memory CD8+ T cells. In the present study, we examined the efficacy of recombinant Mycobacterium bovis bacille Calmette-Guérin (rBCG) secreting fusion protein antigen (Ag) 85B murine IL-15 (rBCG-Ag85B-IL15) in providing protection against M. tuberculosis infection. The levels of major histocompatibility (MHC) class Ib (H2-M3)-binding TB2- or MHC class Ia (H-2Db)-binding MPT64-specific CD8+ T cells producing interferon (IFN)-gamma were significantly higher after immunization with rBCG-Ag85B-IL15 than after immunization with rBCG secreting Ag85B (rBCG-Ag85B). The levels of purified protein derivative- or Ag85B-specific CD4+ T cells producing IFN-gamma were also higher in mice immunized with rBCG-Ag85B-IL15 than in mice immunized with rBCG-Ag85B. Mice immunized with rBCG-Ag85B-IL15 exhibited CD8+ and CD4+ T cells responses that were stronger than those in mice immunized with rBCG-Ag85B, as well as robust protection in the lung against intratracheal challenge of M. tuberculosis. Thus, rBCG-Ag85B-IL15 vaccination capable of inducing efficient cell-mediated immunity might be used as an effective vaccine for tuberculosis. 相似文献
10.
Mitsuko Nakashima Hirofumi Kashii Yoshiko Murakami Mitsuhiro Kato Yoshinori Tsurusaki Noriko Miyake Masaya Kubota Taroh Kinoshita Hirotomo Saitsu Naomichi Matsumoto 《Neurogenetics》2014,15(3):193-200
Recessive mutations in genes of the glycosylphosphatidylinositol (GPI)-anchor synthesis pathway have been demonstrated as causative of GPI deficiency disorders associated with intellectual disability, seizures, and diverse congenital anomalies. We performed whole exome sequencing in a patient with progressive encephalopathies and multiple dysmorphism with hypophosphatasia and identified novel compound heterozygous mutations, c.250G>T (p. Glu84*) and c.1342C>T (p. Arg488Trp), in PIGT encoding a subunit of the GPI transamidase complex. The surface expression of GPI-anchored proteins (GPI-APs) on patient granulocytes was lower than that of healthy controls. Transfection of the Arg488Trp mutant PIGT construct, but not the Glu84* mutant, into PIGT-deficient cells partially restored the expression of GPI-APs DAF and CD59. These results indicate that PIGT mutations caused neurological impairment and multiple congenital anomalies in this patient. 相似文献