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171.
Koji Muroya Tsutomu Ogata Gudrun Rappold Albrecht Klink Yutaka Nakahori Yoshimitsu Fukushima Katsuya Aizu Nobutake Matsuo 《Human genetics》1995,95(5):577-580
Although the locus for X-linked recessive chondrodysplasia punctata (CDPX1) has been mapped to the region between PABX and DXS31 (the critical region is about 3 Mb long), the precise location within the critical region has not been determined. In this paper, we describe a boy with a 46,Y,der(X)t(X;Y)(p22.3;q11)mat karyotype and review the genotype-phenotype correlations in three male patients with the combination of apparent lack of clinical features of CDPX1 and a partial deletion of the critical region. The results suggest that the region defined by the two BssHII sites at 3180 and 3570 kb from the Xp telomere may be the target region for the CDPX1 locus. 相似文献
172.
A 570-kb DNA Sequence of the Escherichia coli K-12 Genome Corresponding to the 28.0-40.1 min Region on the Linkage Map 总被引:1,自引:0,他引:1
Aiba Hiroji; Baba Tomoya; Hayashi Kouji; Inada Toshifumi; Isono Katumi; Itoh Takeshi; Kasai Hiroaki; Kashimoto Kaoru; Kimura Shigenobu; Kitakawa Madoka; Kitagawa Masanari; Makino Kozo; Miki Takeyoshi; Mizobuchi Kiyoshi; Mori Hirotada; Mori Tomoko; Motomura Kouji; Nakade Shinsuke; Nakamura Yoshikazu; Nashimoto Hiroko; Nishio Yoshitaka; Oshima Taku; Saito Noriko; Sampei Gen-ichi; Seki Yasushi; Sivasundaram Suharnan; Tagami Hideaki; Takeda Jun-ichi; Takemoto Keiko; Takeuchi Yasushi; Wada Chieko; Yamamoto Yoshihiro; Horiuchi Takashi 《DNA research》1996,3(6):363-377
The 569,750 base pair sequence corresponding to the 28.040.1min region on the genetic map of Escherichia coli K-12 (W3110)was determined. This region includes the replication terminusregion and contained at least 549 potential open reading frames.Among them, 160 (29%) were previously reported, 174 (32%) werehomologous to other known genes, 102 (18%) were identical orsimilar to hypothetical genes registered in databases, and theremaining 113 (21%) did not show a significant similarity toany other gene. Of interest was the finding of a large numberof genes and gene clusters in andnear the replication terminationregion which had been thought to be genetically silent. Thoseincludeda cluster of genes for fatty acid ß-oxidation,the third copy of the pot (spermidine/putrescine transport system)gene cluster, the second dpp (dipeptide transport system) operon,the second dsm (anaerobic dimethyl sulfoxide reductase) operon,a cluster of fim (fimbrial) genes anda DNA helicase-like genewith a high molecular weight. In addition, we found the dnaC-and dnaT-like genes in the cryptic prophage, Rac, anda numberof genes originated probably from plasmids. 相似文献
173.
Matthias Schmitz Elisabeth Ebert Katharina Stoeck André Karch Steven Collins Miguel Calero Theodor Sklaviadis Jean-Louis Laplanche Ewa Golanska Ines Baldeiras Katsuya Satoh Raquel Sanchez-Valle Anna Ladogana Anders Skinningsrud Anna-Lena Hammarin Eva Mitrova Franc Llorens Yong Sun Kim Alison Green Inga Zerr 《Molecular neurobiology》2016,53(4):2189-2199
174.
Hiroshi Yokoyama Ayako Sasaki Tadashi Yoshizawa Hiroshi Kijima Kenichi Hakamada Katsuya Yamada 《Human cell》2016,29(3):111-121
Extrahepatic bile duct cancer (cholangiocarcinoma) has a poor prognosis. Since surgical resection is the only way to prolong the patient’s life, it is of critical importance to correctly determine the extent of lesions. However, conventional pre-operative assessments have insufficient spatial resolution for determining the surgical margin. A fluorescent contrast agent might provide a more precise measure to identify anomalies in biliary surface, when combined with probe-based confocal laser endomicroscopy (pCLE). We have previously shown that 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-l-glucose (2-NBDLG), a fluorescent derivative of l-glucose (fLG), is specifically taken up into spheroids consisting of cells showing heterogeneous nuclear-cytoplasm ratio, a feature of malignant cells in clinical settings. In addition, a combined use of 2-TRLG, a membrane-impermeable fLG, with 2-NBDLG visualized membrane integrity as well. We therefore explored in the present study the availability of the fLGs in vivo as a contrast agent for pCLE by using a hamster model of cholangiocarcinoma. Extrahepatic cholangiocarcinoma developed in mid common duct in ~20 % of the animals subjected to cholecystoduodenostomy with the ligation at the distal end of the common duct followed by injection of a carcinogen N-nitrosobis(2-oxopropyl)amine. After infusing bile duct with a solution containing 2-NBDLG and 2-TRLG, the lumen was surgically exposed and examined by pCLE. Fluorescence pattern characterized by bright spots and dark clumps was detected in the areas diagnosed with cholangiocarcinoma in later histopathology, whereas no such pattern was detected in control animals. These findings may form a basis for elucidating a potential availability of fLGs in imaging cholangiocarcinoma by pCLE. 相似文献
175.
176.
177.
Eijiro Watanabe Susumu Inamoto Mi-Hion Lee Song Uk Kim Teru Ogua Hirotada Mori Sota Hiraga Makari Yamasaki Kazuo Nagai 《Molecular & general genetics : MGG》1989,218(3):431-436
Summary The mini-F plasmid has the trans-acting sopA, sopB genes and the cis-acting sopC DNA which are essential for plasmid partitioning. In this paper, we report the purification of the sopB gene product from extracts of cells harboring a pBR322 derivative carrying the sopB gene. The purity of the final preparation was more than 95%, as determined by densitometry. The amino acid sequence of the amino-terminal region of the protein for the 17 residues identified was identical to that predicted from the DNA sequence of the sopB gene. Therefore, it was concluded that the protein was the sopB gene product. Using anti-SopB serum, the SopB protein was detected in the cell lysates of F+, F, and Hfr strains. The SopB protein bound to the plasmid DNA of a pBR322 derivative carrying the sopC DNA segment, but not to the vector plasmid pBR322. 相似文献
178.
Bunichi Ezaki Teru Ogura Hirotada Mori Hironori Niki Sota Hiraga 《Molecular & general genetics : MGG》1989,218(2):183-189
Summary The seg mutants (seg-1 and seg-2) of Escherichia coli cannot support the replication of the F factor and mini-F plasmids at 42°C. We cloned the wild-type E. coli chromosomal DNA fragment complementing the seg-1 and seg-2 mutations and found that both mutations were complemented by the wild-type dnaK gene coding for a heat shock protein. Transduction with phage P1 indicated that the seg-2 mutation is located at about 0.3 min in the region containing the dnaK gene in the order trpR-thrA-seg-2-leuB, consistent with the locus of the dnaK gene. Cloning and sequencing of the dnaK gene of the seg mutants showed that there was one base substitution within the dnaK gene in each mutant causing an amino acid substitution. These results indicate that the seg gene in which the seg-1 and seg-2 mutations occurred is identical to the dnaK gene. The mini-F plasmid pXX325 did not transform a dnaK null mutant to ampicillin resistance at 30°C in contrast to plasmids pBR322, pACYC184 and pSC101, which did. The active dnaK (seg) gene product is therefore essential for replication of the mini-F plasmid at both 30° and 42°C. 相似文献
179.
180.
Jaiswal JK Marlow G Summerill G Mahjneh I Mueller S Hill M Miyake K Haase H Anderson LV Richard I Kiuru-Enari S McNeil PL Simon SM Bashir R 《Traffic (Copenhagen, Denmark)》2007,8(1):77-88
Two autosomal recessive muscle diseases, limb girdle muscular dystrophy type 2B (LGMD2B) and Miyoshi myopathy (MM), are caused by mutations in the dysferlin gene. These mutations result in poor ability to repair cell membrane damage, which is suggested to be the cause for this disease. However, many patients who share clinical features with MM-type muscular dystrophy do not carry mutations in dysferlin gene. To understand the basis of MM that is not due to mutations in dysferlin gene, we analyzed cells from patients in one such family. In these patients, we found no defects in several potential candidates - annexin A2, caveolin-3, myoferlin and the MMD2 locus on chromosome 10p. Similar to dysferlinopathy, these cells also exhibit membrane repair defects and the severity of the defect correlated with severity of their disease. However, unlike dysferlinopathy, none of the conventional membrane repair pathways are defective in these patient cells. These results add to the existing evidence that cell membrane repair defect may be responsible for MM-type muscular dystrophy and indicate that a previously unsuspected genetic lesion that affects cell membrane repair pathway is responsible for the disease in the non-dysferlin MM patients. 相似文献