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排序方式: 共有622条查询结果,搜索用时 15 毫秒
1.
Kei Kamide Yoshihiro Kokubo Hironori Hanada Junko Nagura Jin Yang Shin Takiuchi Chihiro Tanaka Mariko Banno Yoshikazu Miwa Masayoshi Yoshii Tetsutaro Matayoshi Hisayo Yasuda Takeshi Horio Akira Okayama Hitonobu Tomoike Yuhei Kawano Toshiyuki Miyata 《Hypertension research》2006,29(4):243-252
Mutations in the gene encoding 11beta-hydroxysteroid dehydrogenase type 2, HSD11B2, cause a rare monogenic juvenile hypertensive syndrome called apparent mineralocorticoid excess (AME). In AME, defective HSD11B2 enzyme activity results in overstimulation of the mineralocorticoid receptor (MR) by cortisol, causing sodium retention, hypokalemia, and salt-dependent hypertension. Here, we have studied whether genetic variations in HDS11B2 are implicated in essential hypertension in Japanese hypertensives and the general population. By sequencing the entire coding region and the promoter region of HDS11B2 in 953 Japanese hypertensives, we identified five missense mutations in 11 patients (L14F, n = 5; R74H, n = 1; R147H, n = 3; T156I, n = 1; R335H, n = 1) and one novel frameshift mutation (4884Gdel, n = 1) in a heterozygous state, in addition to 19 genetic variations. All genetic variations identified were rare, with minor allele frequencies less than 0.005. Four of 12 patients with the missense/frameshift mutations showed renal failure. Four missense mutations, L14F, R74H, R147H, and R335H, were successfully genotyped in the general population, with a sample size of 3,655 individuals (2,175 normotensives and 1,480 hypertensives). Mutations L14F, R74H, R147H, and R335H were identified in hypertensives (n = 6, 8, 3, and 0, respectively) and normotensives (n = 8, 12, 5, and 0, respectively) with a similar frequency, suggesting that these missense mutations may not strongly affect the etiology of essential hypertension. Since the allele frequency of all of the genetic variations identified in this study was rare, an association study was not conducted. Taken together, our results indicate that missense mutations in HSD11B2 do not substantially contribute to essential hypertension in Japanese. 相似文献
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H Sasano Y Saito H Nagura R Kudo M Rojas S G Silverberg 《International journal of gynecological pathology》1991,10(3):252-259
The lectin-binding properties of 44 cases of serous and mucinous ovarian cystadenoma, tumor of low malignant potential (LMP), and invasive carcinoma were examined histochemically. Wheat germ agglutinin (WGA), concanavalin A (con A), Ulex europaeus agglutinin I (UEA-I), peanut agglutinin (PNA), Ricinus communis agglutinin I (RCA-I), soybean agglutinin (SBA), and Robina pseudoaccacia (RPA) were employed. All the lectins examined were bound to neoplastic epithelial cells of benign and malignant tumors, but none bound exclusively to ovarian tumor cells. Different lectin-binding patterns between serous and mucinous neoplasms were observed, with the exception of RPA. UEA-I, con A, RPA, and PNA in serous neoplasms and UEA-I, RPA, and WGA in mucinous neoplasms demonstrated lectin-binding properties of LMP tumors intermediate between those of cystadenoma and invasive carcinoma. These findings indicate that serous and mucinous ovarian neoplasms contain different glycoconjugates, that malignant transformation of the neoplasms is associated with alteration of these glycoconjugates, and especially that LMP tumors have a different composition of cellular glycoconjugates from that of invasive ovarian carcinoma. 相似文献
5.
Shinichiro Iwata Yasunori Suda Takeo Nagura Hideo Matsumoto Toshiro Otani Yoshiaki Toyama 《Knee surgery, sports traumatology, arthroscopy》2007,15(4):343-349
The purpose of this study is to evaluate the relationship between the magnitude of knee laxity and posterior instability at
different knee flexion angles and clinical disability in isolated posterior cruciate ligament (PCL) deficient patients. Knee
laxity at 20° and 70° of knee flexion were evaluated using KT-2000 arthrometer, and the posterior instability at 20°, 45°
and 90° of flexion were evaluated using stress radiography. We assessed the differences in the knee laxity and the tibial
translation between isolated PCL deficient knees and normal knees, and between the patients with giving-way during activities
of daily living (ADL) and without giving-way. There were statistical differences in the knee laxity and the tibial translation
at all knee flexion angles between the PCL deficient knees and normal knees. The magnitude of the knee laxity at 20° of flexion
measured with KT-2000 arthrometer was significantly larger in the patients with giving-way than those in the patients without
giving-way although there was no significant difference in the tibial translation at 70° between the two groups. The tibial
translation in both medial and lateral compartments at 20° and 45° measured with stress radiography were significantly larger
in the patients with giving-way than those in the patients without giving-way although there was not significant difference
at 90° between the two groups. These results suggested that the magnitude of the knee laxity and the posterior tibial translation
at shallow knee flexion angles would be related to giving-way during ADL in isolated PCL deficient patients. 相似文献
6.
H Saito K Kishi M Narita T Furukawa E Nagura T Maekawa T Abe A Shibata 《Leukemia research》1992,16(3):217-226
To test the relationship between DMs and drug resistance in newly established AML cell lines, KY821, and its clone KY821A3, the latter had lost DMs during cloning, were cultured in increasing concentrations of MTX. KY821 became resistant against 2 x 10(-4) M MTX, whereas KY821A3 did against 2 x 10(-5) M MTX in a same period. Enhanced enzyme activities of DHFR were correspondent to the increased DMs numbers and DHFR gene amplification in both resistant clones. The amplified DHFR gene was located on DMs by in situ hybridization. These data indicated that the presence of DMs in KY821 would facilitate the acquisition of drug resistance. 相似文献
7.
The development of gut-associated lymphoid tissue (GALT) in the rat was investigated, with special reference to the behavior and ultrastructure of Ia(+) cells during the development of Peyer's patches (PP). At birth, Ia(+) cells were randomly scattered in the lamina propria. From three days, small aggregates of CD4(+), Ia(+), CD5(−) and IL-1(+) cells were observed in the lamina propria. Immunoelectron microscopically, these appeared as mixed populations of dendritic cells, capillary endothelial cells, flbroblast-like spindle cells and lymphocytes. In addition, CD8(+), CD4(–) and IL-1(−) cells were present in the interepithelial space. By seven days, lymphoid follicles were recognizable in the lamina propria, each with an aggregate of IgM-positive small lymphocytes at its center, surrounded by CD4(+) or CD8(+) lymphocytes. Between the 10th and 14th days, these follicles were covered with single-layered, specially differentiated epithelial cells, and structures resembling PP were formed. IgA plasma cells were identified in the lamina propria between the third and the fourth weeks. We speculate that the PP developed from aggregates of Ia(+), IL-1(+) spindle- or dendritic-shaped cells in the lamina propria. The PP were structurally complete by two weeks, although establishment of the characteristic distribution of GALT components evident in the adult took more than six weeks. 相似文献
8.
Nagura M Nagao Y Takita J Igarashi T LeGuern E Hayashi Y 《International journal of molecular medicine》2003,11(1):45-47
Charcot-Marie-Tooth disease type 4C (CMT4C) is an autosomal recessive peripheral neuropathy reported in several Algerian families. The gene locus of this disease has been narrowed to 5q31-33. Recently, a missense mutation in the gene for the kinesin superfamily KIF1B was reported as the cause of Charcot Marie Tooth disease type 2A (CMT2A). We suspected that Rab6KIFL, one of the kinesin superfamily proteins, might be involved in the pathophysiology of CMT4C, because Rab6KIFL gene is located in 5q31. The coding regions of the Rab6KIFL gene of genomic DNA derived from one Algerian family with CMT4C were analyzed by direct sequencing. No mutation in Rab6KIFL gene was found in this family. Further investigation is necessary to identify the causative gene for CMT4C. 相似文献
9.
Hoshi T Sasano H Kato K Ohara S Shimosegawa T Toyota T Nagura H 《Human pathology》1999,30(12):1412-1417
Helicobacter pylori (HP) is believed to be involved in the transition from normal gastric mucosa to atrophic gastritis and intestinal metaplasia. Infection with the organism is one of the risk factors for development of intestinal-type gastric adenocarcinoma, possibly through altered cell turnover. Medical eradication of HP is widely performed for the treatment of peptic ulcers and other upper gastrointestinal disorders. Eradication of HP may affect altered cell turnover of the gastric mucosa caused by the infection, but there are few reports comparing sterilized mucosa with HP-infected and non-infected mucosa. In this study, we examined cell damage using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL), in situ nick translation (ISNT), and cell proliferation by Ki 67 immunohistochemistry staining in gastric mucosa before and after HP eradication and in non-infected gastric mucosa. We then compared these findings using endoscopic gastric biopsy specimens. Labeling indices of TUNEL (2.46 +/- 1.22), ISNT (1.13 +/- 0.42), and Ki67 (21.8 +/- 6.14) in tissue from which HP had been eradicated were significantly lower than those of HP-infected mucosa (6.36 +/- 2.26, 4.00 +/- 1.62, 45.8 +/- 5.35, for TUNEL, ISNT, and Ki67, respectively). There were no significant differences between formerly infected and non-infected mucosa (TUNEL: 2.26 +/- 0.69, ISNT: 1.29 +/- 0.63, Ki67: 23.5 +/- 8.20). These results indicate that medical HP eradication results in decreased cell proliferation and damage, restoring the condition seen in non-infected mucosa. Thus, HP eradication may be effective, not only in the treatment of gastric ulcers or gastric symptoms, but also in the prevention of gastric carcinoma. 相似文献
10.
IgA plasma cells in biliary mucosa: a likely source of locally synthesized IgA in human hepatic bile 总被引:2,自引:0,他引:2
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H Nagura Y Tsutsumi H Hasegawa K Watanabe P K Nakane W R Brown 《Clinical and experimental immunology》1983,54(3):671-680
IgA synthesized in hepatobiliary tissues accounts for about one-half of the IgA present in human hepatic bile, but the location of the IgA synthesizing cells has been in doubt because few plasma cells are present in normal liver. Therefore, we immunocytochemically localized IgA, J chain and secretory component in bile duct tissues of six patients operated upon for biliary duct obstruction. Numerous plasma cells containing IgA and J chain were found surrounding the accessory glands of the major bile ducts and in the area just beneath the surface epithelium of the ducts. At the ultrastructural level, IgA and SC in the epithelial cells had the features characteristic of secretory component-mediated endocytic translocation of IgA. We conclude that plasma cells in biliary duct mucosa are the likely source of much of the locally synthesized IgA that is secreted into human hepatic bile. The IgA probably reaches the bile by direct transfer across biliary epithelium. 相似文献