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991.
Yasuhiro Sano Seiichi Kondo Yasunori Isshiki Toshio Shimada Kazuhito Hisatsune 《Microbiology and immunology》1996,40(10):735-741
Chemical and serological studies were performed with the lipopolysaccharide (LPS) from Vibrio cholerae O144 (O144). The LPS of O144 contained D -glucose, D -galactose, L -glycero-D -manno-heptose, D -fructose, D -quinovosamine (2-amino-2,6-dideoxy-D -gluco-pyranose) and L -perosamine (4-amino-4,6-dideoxy-L -manno-pyranose). The perosamine, a major component sugar of the LPS from O144, was in an L -configuration, as is also the case in the LPS from V. cholerae O76 (O76), in contrast to the D -configuration of the perosamine in the LPS of V. cholerae O1. A structural analysis revealed that the O polysaccharide chain of the LPS from O144 is an α(1 → 2)-linked homopolymer of (R)-(-)-2-hydroxypropionyl-L -perosamine. The serological cross-reactivity between O144 and O76 was clearly revealed by cross-agglutination and cross-agglutinin absorption tests with whole cells, as well as by passive hemolysis tests with sheep red-blood cells that had been sensitized with the LPS from O144 and O76. In contrast, in passive hemolysis tests, the LPS of O144 did not cross-react serologically with the LPSs from other strains such as V. cholerae O1 (Ogawa and Inaba), V. cholerae O140, Vibrio bio-serogroup 1875 (Original and Variant) and Yersinia enterocolitica O9. The LPSs from these strains consist of O polysaccharide chains composed of α(1 → 2)-linked homopolymers of D -perosamine with various N-acyl groups, and they share the Inaba antigen factor C of V. cholerae O1 in common. The results obtained in this study demonstrate that the absolute configuration of the perosamine residue in homopolymers plays a very important role in the expression of the serological specificity of the Inaba antigen factor C of V. cholerae O1. 相似文献
992.
The R40H mutation in a late onset type of human ornithine transcarbamylase deficiency in male patients 总被引:2,自引:0,他引:2
Atsushi Nishiyori M. Yoshino Hirohisa Kato Toshinobu Matsuura Ryuuji Hoshide Ichiro Matsuda Tateo Kuno Sumio Miyazaki Shin-ichi Hirose Ryu-ichi Kuromaru Masataka Mori 《Human genetics》1997,99(2):171-176
Ornithine transcarbamylase (OTC) deficiency is an X-linked trait and is one of the most frequent of the inherited urea cycle
enzyme deficiencies. Most male patients with OTC deficiency develop a hyperammonemic crisis and die in the neonatal period
or in early infancy. In contrast to those patients, in some male patients the disease first becomes overt in adolescence or
during the reproductive age period. In the present report, we describe six such male patients who first developed clinical
signs at ages ranging from 6 to 58 years, all of whom came from a limited area of the northern part of Kyushu Island in southern
Japan. The mutation analysis disclosed a R40H mutation in exon 2 of the OTC gene in each of these patients. Transmission of
this mutant gene through paternal lineage as well as through maternal lineage was documented in one family. The levels of
mRNA of the mutant OTC gene expressed in transfected Cos 1 cells and in the liver tissue obtained by biopsy in one patient
were both similar to those of the wild-type gene. The activity of the mutant OTC was, however, decreased to a level of 28%
of the wild-type OTC, and the levels of the mutant OTC protein expressed in Cos 1 cells were decreased, as assessed by western
blot analysis. Apparent K
m values of the mutant enzyme for ornithine (1.1 mM) and carbamylophosphate (2.0 mM) were similar to those of the wild-type
enzyme. Both enzymes gave similar pH-dependency profiles, giving a maximal activity at pH 7.8–7.9. Activity of wild-type OTC
expressed in Cos 1 cells did not change after five cycles of freezing and thawing, whereas that of the mutant OTC decreased
to 17% by this treatment. These results suggest that deficiency is due to inactivation of the mutant OTC under certain conditions.
Received: 15 May 1996 相似文献
993.
Toshio Matsumoto Yumiko Kawanobe Etsuro Ogata 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》1985,845(3):358-365
Regulation of 25-hydroxyvitamin D-3 24-hydroxylase by 1,25-dihydroxyvitamin D-3 and synthetic human parathyroid hormone fragment 1–34 (PTH1–34) was investigated using a cloned monkey kidney cell line, JTC-12. Treatment of the cells with 1,25-dihydroxyvitamin D-3 markedly enhanced the conversion of [3H]-25-hydroxyvitamin D-3 into a more polar metabolite. The metabolite was identified as 24,25-dihydroxyvitamin D-3 by normal phase and reverse phase high-performance liquid chromatography and periodate oxidation. The 24-hydroxylae activity appeared to follow Michaelis-Menten kintics, and 1,25-dihydroxyvitamin D-3 treatment increased the of 24-hydroxylase from 33 to 95 pmol/h per 106 cells without affecting the apparent value of the enzyme (220 nM in control vs. 205 nM in 1,25-dihydroxyvitamin D-3 treated cells). The enzyme activity reached a maximum between 4 and 8 h of treatment with 1,25-dihydroxyvitamin D-3. The dose of 1,25-dihydroxyvitamin D-3 required to cause a half-maximal stimulation was about 3 · 10?10 M. The 1,25-dihydroxyvitamin D-3-induced increase in 24-hydroxylase was almost completely inhibited by the presence of 1 μM cycloheximide. Treatment of the cells with PTH1–34 caused a dose-dependent increase in cyclic AMP production. Half-maximal stimulation of cyclic AMP production was obtained at about 5 · 10?9 M PTH1–34. When 2.4 · 10?9 M PTH1–34 was added after 1,25-dihydroxyvitamin D-3 treatment, the 1,25-dihydroxyvitamin D-3-stimulated 24-hydroxylase was inhibited to of control. Higher concentrations of PTH1–34 caused less inhibition of the enzyme activity. When cyclic AMP was added instead of PTH1–34, the enzyme activity was also suppressed significantly. These results indicate that, in JTC-12 cells, 1,25-dihydroxyvitamin D-3 stimulates 24-hydroxylase in a dose- and time-dependent manner by increasing the of the enzyme through a mechanism dependent upon new protein synthesis, and suggest that PTH1–34 inhibits the 1,25-dihydroxyvitamin D-3-induced stimulation of 24-hydroxylase through its effect on cyclic AMP production. 相似文献
994.
Old hen tendon provides a model suitable for the study of calcification in an extracellular matrix. In the present study, we observed the mineralizing substances of hen tendon by scanning electron microscopy of plasma-osmium-coated specimens and by transmission electron microscopy of those processed by a plasma-polymerization film replica method. The mineralizing front area revealed a number of elliptical particles fused to each other and forming rod-like structures oriented parallel to collagen fibrils. The area of advanced mineralization possessed non-mineralizing cavities, in which tendon cells were likely to exist. At this site, we recognized a second form of mineral structure, one in which the crystals had a scale-like morphology and were deposited onto the major first-form mineral component. This crystal form was similar to hydroxyapatite synthesized under wet reaction conditions. These findings strongly suggest that the second form of mineral formed independent of collagen fibrils existed together with the predominant, collagen-dependent form of mineral. We speculate that cell membranes and an extremely slow mineralization process may contribute to the formation of this form of mineral during the mineralization process in the hen tendon. 相似文献
995.
Takumi Okubo Daiki Hayashi Takayuki Yaguchi Yudai Fujita Motoharu Sakaue Takehito Suzuki Atsushi Tsukamoto Ohoshi Murayama Jonathan Lynch Yoko Miyazaki Kazuaki Tanaka Tatsuya Takizawa 《Experimental Animals》2016,65(1):45-51
Valproic acid (VPA) is a widely used antiepileptic drug, which has recently been reported
to modulate the neuronal differentiation of adipose tissue-derived stem cells (ASCs) in
humans and dogs. However, controversy exists as to whether VPA really acts as an inducer
of neuronal differentiation of ASCs. The present study aimed to elucidate the effect of
VPA in neuronal differentiation of rat ASCs. One or three days of pretreatment with VPA (2
mM) followed by neuronal induction enhanced the ratio of immature neuron marker
βIII-tubulin-positive cells in a time-dependent manner, where the majority of cells also
had a positive signal for neurofilament medium polypeptide (NEFM), a mature neuron marker.
RT-PCR analysis revealed increases in the mRNA expression of microtubule-associated
protein 2 (MAP2) and NEFM mature neuron markers, even
without neuronal induction. Three-days pretreatment of VPA increased acetylation of
histone H3 of ASCs as revealed by immunofluorescence staining. Chromatin
immunoprecipitation assay also showed that the status of histone acetylation at H3K9
correlated with the gene expression of TUBB3 in ASCs by VPA. These
results indicate that VPA significantly promotes the differentiation of rat ASCs into
neuron-like cells through acetylation of histone H3, which suggests that VPA may serve as
a useful tool for producing transplantable cells for future applications in clinical
treatments. 相似文献
996.
997.
998.
Olaf Brouwers Liang Yu Petra Niessen Jos Slenter Karolien Jaspers Allard Wagenaar Mark Post Toshio Miyata Walter Backes Coen Stehouwer Maya Huijberts Casper Schalkwijk 《Glycoconjugate journal》2016,33(4):627-630
We hypothesize that diabetes-induced impaired collateral formation after a hindlimb ligation in rats is in part caused by intracellular glycation and that overexpression of glyoxalase-I (GLO-I), i.e. the major detoxifying enzyme for advanced-glycation-endproduct (AGE) precursors, can prevent this. Wild-type and GLO-I transgenic rats with or without diabetes (induced by 55 mg/kg streptozotocin) were subjected to ligation of the right femoral artery. Laser Doppler perfusion imaging showed a significantly decreased blood perfusion recovery after 6 days in the diabetic animals compared with control animals, without any effect of Glo1 overexpression. In vivo time-of-flight magnetic resonance angiography at 7-Tesla showed a significant decrease in the number and volume of collaterals in the wild-type diabetic animals compared with the control animals. Glo1 overexpression partially prevented this decrease in the diabetic animals. Diabetes-induced impairment of arteriogenic adaptation can be partially rescued by overexpressing of GLO-I, indicating a role of AGEs in diabetes-induced impaired collateral formation. 相似文献
999.
Aya Yamada Masaharu Futagi Emiko Fukumoto Kan Saito Keigo Yoshizaki Masaki Ishikawa Makiko Arakaki Ryoko Hino Yu Sugawara Momoko Ishikawa Masahiro Naruse Kanako Miyazaki Takashi Nakamura Satoshi Fukumoto 《The Journal of biological chemistry》2016,291(2):904-912
Cell-cell interaction via the gap junction regulates cell growth and differentiation, leading to formation of organs of appropriate size and quality. To determine the role of connexin43 in salivary gland development, we analyzed its expression in developing submandibular glands (SMGs). Connexin43 (Cx43) was found to be expressed in salivary gland epithelium. In ex vivo organ cultures of SMGs, addition of the gap junctional inhibitors 18α-glycyrrhetinic acid (18α-GA) and oleamide inhibited SMG branching morphogenesis, suggesting that gap junctional communication contributes to salivary gland development. In Cx43−/− salivary glands, submandibular and sublingual gland size was reduced as compared with those from heterozygotes. The expression of Pdgfa, Pdgfb, Fgf7, and Fgf10, which induced branching of SMGs in Cx43−/− samples, were not changed as compared with those from heterozygotes. Furthermore, the blocking peptide for the hemichannel and gap junction channel showed inhibition of terminal bud branching. FGF10 induced branching morphogenesis, while it did not rescue the Cx43−/− phenotype, thus Cx43 may regulate FGF10 signaling during salivary gland development. FGF10 is expressed in salivary gland mesenchyme and regulates epithelial proliferation, and was shown to induce ERK1/2 phosphorylation in salivary epithelial cells, while ERK1/2 phosphorylation in HSY cells was dramatically inhibited by 18α-GA, a Cx43 peptide or siRNA. On the other hand, PDGF-AA and PDGF-BB separately induced ERK1/2 phosphorylation in primary cultured salivary mesenchymal cells regardless of the presence of 18α-GA. Together, our results suggest that Cx43 regulates FGF10-induced ERK1/2 phosphorylation in salivary epithelium but not in mesenchyme during the process of SMG branching morphogenesis. 相似文献
1000.
An insight into the thermodynamic characteristics of human thrombopoietin complexation with TN1 antibody 下载免费PDF全文
Shigeki Arai Chie Shibazaki Motoyasu Adachi Eijiro Honjo Taro Tamada Yoshitake Maeda Tomoyuki Tahara Takashi Kato Hiroshi Miyazaki Michael Blaber Ryota Kuroki 《Protein science : a publication of the Protein Society》2016,25(10):1786-1796
Human thrombopoietin (hTPO) primarily stimulates megakaryocytopoiesis and platelet production and is neutralized by the mouse TN1 antibody. The thermodynamic characteristics of TN1 antibody–hTPO complexation were analyzed by isothermal titration calorimetry (ITC) using an antigen‐binding fragment (Fab) derived from the TN1 antibody (TN1‐Fab). To clarify the mechanism by which hTPO is recognized by TN1‐Fab the conformation of free TN1‐Fab was determined to a resolution of 2.0 Å using X‐ray crystallography and compared with the hTPO‐bound form of TN1‐Fab determined by a previous study. This structural comparison revealed that the conformation of TN1‐Fab does not substantially change after hTPO binding and a set of 15 water molecules is released from the antigen‐binding site (paratope) of TN1‐Fab upon hTPO complexation. Interestingly, the heat capacity change (ΔCp) measured by ITC (?1.52 ± 0.05 kJ mol?1 K?1) differed significantly from calculations based upon the X‐ray structure data of the hTPO‐bound and unbound forms of TN1‐Fab (?1.02 ~ 0.25 kJ mol?1 K?1) suggesting that hTPO undergoes an induced‐fit conformational change combined with significant desolvation upon TN1‐Fab binding. The results shed light on the structural biology associated with neutralizing antibody recognition. 相似文献