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101.
Fromentin C Azzout-Marniche D Tomé D Even P Luengo C Piedcoq J Fromentin G Gaudichon C 《Amino acids》2011,40(5):1461-1472
The aim of this study was to determine the contribution of dietary amino acids (AA) to energy metabolism under high protein
(HP) diets, using a double tracer method to follow simultaneously the metabolic fate of α-amino groups and carbon skeletons.
Sixty-seven male Wistar rats were fed a normal (NP) or HP diet for 14 days. Fifteen of them were equipped with a permanent
catheter. On day 15, after fasting overnight, they received a 4-g meal extrinsically labeled with a mixture of 20 U-[15N]-[13C] AA. Energy metabolism, dietary AA deamination and oxidation and their transfer to plasma glucose were measured kinetically
for 4 h in the catheterized rats. The transfer of dietary AA to liver glycogen was determined at 4 h. The digestive kinetics
of dietary AA, their transfer into liver AA and proteins and the liver glycogen content were measured in the 52 other rats
that were killed sequentially hourly over a 4-h period. [15N] and [13C] kinetics in the splanchnic protein pools were perfectly similar. Deamination increased fivefold in HP rats compared to
NP rats. In the latter, all deaminated AA were oxidized. In HP rats, the oxidation rate was slower than deamination, so that
half of the deaminated AA was non-oxidized within 4 h. Non-oxidized carbon skeletons were poorly sequestrated in glycogen,
although there was a significant postprandial production of hepatic glycogen. Our results strongly suggest that excess dietary
AA-derived carbon skeletons above the ATP production capacity, are temporarily retained in intermediate metabolic pools until
the oxidative capacities of the liver are no longer overwhelmed by an excess of substrates. 相似文献
102.
Yiying Liu Irene de Bruijn Allison LH Jack Keith Drynan Albert H van den Berg Even Thoen Vladimir Sandoval-Sierra Ida Skaar Pieter van West Javier Diéguez-Uribeondo Menno van der Voort Rodrigo Mendes Mark Mazzola Jos M Raaijmakers 《The ISME journal》2014,8(10):2002-2014
Animals and plants are increasingly suffering from diseases caused by fungi and oomycetes. These emerging pathogens are now recognized as a global threat to biodiversity and food security. Among oomycetes, Saprolegnia species cause significant declines in fish and amphibian populations. Fish eggs have an immature adaptive immune system and depend on nonspecific innate defences to ward off pathogens. Here, meta-taxonomic analyses revealed that Atlantic salmon eggs are home to diverse fungal, oomycete and bacterial communities. Although virulent Saprolegnia isolates were found in all salmon egg samples, a low incidence of Saprolegniosis was strongly correlated with a high richness and abundance of specific commensal Actinobacteria, with the genus Frondihabitans (Microbacteriaceae) effectively inhibiting attachment of Saprolegniato salmon eggs. These results highlight that fundamental insights into microbial landscapes of fish eggs may provide new sustainable means to mitigate emerging diseases. 相似文献
103.
Camilla Krakstad Even Birkeland Danila Seidel Kanthida Kusonmano Kjell Petersen Siv Mj?s Erling A. Hoivik Elisabeth Wik Mari Kylles? Halle Anne M. ?yan Karl-Henning Kalland Henrica Maria Johanna Werner Jone Trovik Helga Salvesen 《PloS one》2012,7(12)
Background
Despite being the most common pelvic gynecologic malignancy in industrialized countries, no targeted therapies are available for patients with metastatic endometrial carcinoma. In order to improve treatment, underlying molecular characteristics of primary and metastatic disease must be explored.Methodology/Principal Findings
We utilized the mass spectrometric-based mutation detection technology OncoMap to define the types and frequency of point somatic mutations in endometrial cancer. 67 primary tumors, 15 metastases corresponding to 7 of the included primary tumors and 11 endometrial cancer cell lines were screened for point mutations in 28 known oncogenes. We found that 27 (40.3%) of 67 primary tumors harbored one or more mutations with no increase in metastatic lesions. FGFR2, KRAS and PIK3CA were consistently the most frequently mutated genes in primary tumors, metastatic lesions and cell lines.Conclusions/Significance
Our results emphasize the potential for targeting FGFR2, KRAS and PIK3CA mutations in endometrial cancer for development of novel therapeutic strategies. 相似文献104.
Erlandsen SE Qvigstad G Fossmark R Bakke I Chen D Sandvik AK 《Regulatory peptides》2012,177(1-3):53-59
The regulated endocrine-specific protein 18 (RESP18) has previously been localized to different endocrine cells and neurons, in particular the pituitary gland and hypothalamus. It is found in the lumen of the endoplasmic reticulum and is degraded at the post-ER pre-Golgi compartment, and a role in processing of secreted peptides has been hypothesized. The present study examines localization of RESP18 in the gastrointestinal mucosa of rats by immunohistochemistry, and expression and regulation in response to hypergastrinemia induced by acid inhibition (pantoprazole), gastrin antagonism (YF476), fasting-refeeding and octreotide by mRNA measurements. RESP18 was mainly found in the gastric mucosa, but could also be detected in a few, scattered cells in the lower small intestine and in colon. In the antral mucosa, all RESP18 immunoreactivity was localized to ghrelin-producing A-like cells and gastrin-producing G-cells. In the corpus mucosa, a significant fraction, but not all of the RESP18 immunoreactive cells, were A-like cells. In both antrum and corpus, Resp18 mRNA seemed to vary similarly with the activation of the A-like cells, and in the antrum also with stimulation of the G-cells. This study demonstrates, for the first time, the localization of RESP18 to specific neuroendocrine cells of the gastrointestinal mucosa and that it seems to be regulated synchronously with the peptides secreted from these cells. This suggests that Resp18 may indeed have a functional role in the synthesis or storage of these gastrointestinal peptides. 相似文献
105.
Hao Q Lillefosse HH Fjaere E Myrmel LS Midtbø LK Jarlsby RH Ma T Jia B Petersen RK Sonne SB Chwalibog A Frøyland L Liaset B Kristiansen K Madsen L 《American journal of physiology. Endocrinology and metabolism》2012,302(9):E1097-E1112
Fish oil rich in n-3 polyunsaturated fatty acids is known to attenuate diet-induced obesity and adipose tissue inflammation in rodents. Here we aimed to investigate whether different carbohydrate sources modulated the antiobesity effects of fish oil. By feeding C57BL/6J mice isocaloric high-fat diets enriched with fish oil for 6 wk, we show that increasing amounts of sucrose in the diets dose-dependently increased energy efficiency and white adipose tissue (WAT) mass. Mice receiving fructose had about 50% less WAT mass than mice fed a high fish oil diet supplemented with either glucose or sucrose, indicating that the glucose moiety of sucrose was responsible for the obesity-promoting effect of sucrose. To investigate whether the obesogenic effect of sucrose and glucose was related to stimulation of insulin secretion, we combined fish oil with high and low glycemic index (GI) starches. Mice receiving the fish oil diet containing the low-GI starch had significantly less WAT than mice fed high-GI starch. Moreover, inhibition of insulin secretion by administration of nifedipine significantly reduced WAT mass in mice fed a high-fish oil diet in combination with sucrose. Our data show that the macronutrient composition of the diet modulates the effects of fish oil. Fish oil combined with sucrose, glucose, or high-GI starch promotes obesity, and the reported anti-inflammatory actions of fish oil are abrogated. In conclusion, our data indicate that glycemic control of insulin secretion modulates metabolic effects of fish oil by demonstrating that high-GI carbohydrates attenuate the antiobesity effects of fish oil. 相似文献
106.
Rami Abu-Fanne Emad Maraga Ihab Abd-Elrahman Aviel Hankin Galia Blum Suhair Abdeen Nuha Hijazi Douglas B. Cines Abd Al-Roof Higazi 《The Journal of biological chemistry》2016,291(6):2777-2786
Approximately one-half of the patients who develop clinical atherosclerosis have normal or only modest elevations in plasma lipids, indicating that additional mechanisms contribute to pathogenesis. In view of increasing evidence that inflammation contributes to atherogenesis, we studied the effect of human neutrophil α-defensins on low density lipoprotein (LDL) trafficking, metabolism, vascular deposition, and atherogenesis using transgenic mice expressing human α-defensins in their polymorphonuclear leukocytes (Def+/+). Accelerated Def+/+ mice developed α-defensin·LDL complexes that accelerate the clearance of LDL from the circulation accompanied by enhanced vascular deposition and retention of LDL, induction of endothelial cathepsins, increased endothelial permeability to LDL, and the development of lipid streaks in the aortic roots when fed a regular diet and at normal plasma levels of LDL. Transplantation of bone marrow from Def+/+ to WT mice increased LDL clearance, increased vascular permeability, and increased vascular deposition of LDL, whereas transplantation of WT bone marrow to Def+/+ mice prevented these outcomes. The same outcome was obtained by treating Def+/+ mice with colchicine to inhibit the release of α-defensins. These studies identify a potential new link between inflammation and the development of atherosclerosis. 相似文献
107.
Genome Sequence of Staphylococcus aureus Newbould 305, a Strain Associated with Mild Bovine Mastitis
Damien Bouchard Vincent Peton Sintia Almeida Caroline Le Maréchal Anderson Miyoshi Vasco Azevedo Nadia Berkova Lucie Rault Patrice Fran?ois Jacques Schrenzel Sergine Even David Hernandez Yves Le Loir 《Journal of bacteriology》2012,194(22):6292-6293
Staphylococcus aureus is a major etiological agent of mastitis in ruminants. We report here the genome sequence of bovine strain Newbould 305, isolated in the 1950s in a case of bovine mastitis and now used as a model strain able to reproducibly induce chronic mastitis in cows. 相似文献
108.
Ben Zakour NL Sturdevant DE Even S Guinane CM Barbey C Alves PD Cochet MF Gautier M Otto M Fitzgerald JR Le Loir Y 《Journal of bacteriology》2008,190(19):6302-6317
Staphylococcus aureus causes disease in humans and a wide array of animals. Of note, S. aureus mastitis of ruminants, including cows, sheep, and goats, results in major economic losses worldwide. Extensive variation in genome content exists among S. aureus pathogenic clones. However, the genomic variation among S. aureus strains infecting different animal species has not been well examined. To investigate variation in the genome content of human and ruminant S. aureus, we carried out whole-genome PCR scanning (WGPS), comparative genomic hybridizations (CGH), and the directed DNA sequence analysis of strains of human, bovine, ovine, and caprine origin. Extensive variation in genome content was discovered, including host- and ruminant-specific genetic loci. Ovine and caprine strains were genetically allied, whereas bovine strains were heterogeneous in gene content. As expected, mobile genetic elements such as pathogenicity islands and bacteriophages contributed to the variation in genome content between strains. However, differences specific for ruminant strains were restricted to regions of the conserved core genome, which contained allelic variation in genes encoding proteins of known and unknown function. Many of these proteins are predicted to be exported and could play a role in host-pathogen interactions. The genomic regions of difference identified by the whole-genome approaches adopted in the current study represent excellent targets for studies of the molecular basis of S. aureus host adaptation. 相似文献
109.
Major histocompatibility complex (MHC) class II molecules (MHC-II) function by binding antigenic peptides and displaying these peptides on the surface of antigen presenting cells (APCs) for recognition by peptide-MHC-II (pMHC-II)-specific CD4 T cells. It is known that cell surface MHC-II can internalize, exchange antigenic peptides in endosomes, and rapidly recycle back to the plasma membrane; however, the molecular machinery and trafficking pathways utilized by internalizing/recycling MHC-II have not been identified. We now demonstrate that unlike newly synthesized invariant chain-associated MHC-II, mature cell surface pMHC-II complexes internalize following clathrin-, AP-2-, and dynamin-independent endocytosis pathways. Immunofluorescence microscopy of MHC-II expressing HeLa-CIITA cells, human B cells, and human DCs revealed that pMHC enters Arf6(+)Rab35(+)EHD1(+) tubular endosomes following endocytosis. These data contrast the internalization pathways followed by newly synthesized and peptide-loaded MHC-II molecules and demonstrates that cell surface pMHC-II internalize and rapidly recycle from early endocytic compartments in tubular endosomes. 相似文献
110.
How to allow SAR collapse across local and continental scales: a resolution of the controversy between Storch et al. (2012) and Lazarina et al. (2013)
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Arnošt Leoš Šizling Eva Šizlingová Even Tjørve Kathleen M. C. Tjørve William E. Kunin 《Ecography》2017,40(8):971-981
Up‐scaling species richness from local to continental scales is an unsolved problem of macroecology. Macroecologists hope that proper up‐scaling can uncover the hidden rules that underlie spatial patterns in species richness, but a machinery to up‐scale species richness also has a purely practical side at the scales and for the habitats where direct observations cannot be performed. The species–area relationship (SAR) could provide a tool for up‐scaling, but no valid method has yet been put forward. Such a method would have resulted from Storch et al.'s (2012) suggestion that there is a universal curve to which each rescaled SAR collapses, if Lazarina et al. (2013) had not shown that it does not: both arguments were supported by data analyses. Here we present an analytical model for mainland SAR and argue in favour of the latter authors. We identify 1) the variation in mean species‐range size, 2) the variation in forces that drive SAR at various scales, and 3) the finite‐area effect, as the reasons for the absence of collapse. Finally, we suggest a rescaling that might fix the problem. We conclude, however, that ecologists are still far from finding a practical, robust and easy‐to‐use solution for up‐scaling species richness from SARs. 相似文献