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91.
Elizabeth A McCliment Craig E Nelson Craig A Carlson Alice L Alldredge Jan Witting Linda A Amaral-Zettler 《The ISME journal》2012,6(2):309-319
The Moorea Coral Reef Long Term Ecological Research (LTER) Site (17.50°S, 149.83°W) comprises the fringe of coral reefs and lagoons surrounding the volcanic island of Moorea in the Society Islands of French Polynesia. As part of our Microbial Inventory Research Across Diverse Aquatic LTERS biodiversity inventory project, we characterized microbial community composition across all three domains of life using amplicon pyrosequencing of the V6 (bacterial and archaeal) and V9 (eukaryotic) hypervariable regions of small-subunit ribosomal RNA genes. Our survey spanned eight locations along a 130-km transect from the reef lagoon to the open ocean to examine changes in communities along inshore to offshore gradients. Our results illustrate consistent community differentiation between inshore and offshore ecosystems across all three domains, with greater richness in all domains in the reef-associated habitats. Bacterial communities were more homogenous among open ocean sites spanning >100 km than among inshore sites separated by <1 km, whereas eukaryotic communities varied more offshore than inshore, and archaea showed more equal levels of dissimilarity among subhabitats. We identified signature communities representative of specific geographic and geochemical milieu, and characterized co-occurrence patterns of specific microbial taxa within the inshore ecosystem including several bacterial groups that persist in geographical niches across time. Bacterial and archaeal communities were dominated by few abundant taxa but spatial patterning was consistent through time and space in both rare and abundant communities. This is the first in-depth inventory analysis of biogeographic variation of all three microbial domains within a coral reef ecosystem. 相似文献
92.
Witting L 《Biological reviews of the Cambridge Philosophical Society》2008,83(3):259-294
Since neo-Darwinism arose from the work of Darwin and Mendel evolution by natural selection has been seen as contingent and historical being defined by an a posteriori selection process with no a priori laws that explain why evolution on Earth has taken the direction of the major evolutionary trends and transitions instead of any other direction. Recently, however, major life-history trends and transitions have been explained as inevitable because of a deterministic selection that unfolds from the energetic state of the organism and the density-dependent competitive interactions that arise from self-replication in limited environments. I describe differences and similarities between the historical and deterministic selection processes, illustrate concepts using life-history models on large body masses and limited reproductive rates, review life-history evolution with a wider focus on major evolutionary transitions, and propose that biotic evolution is driven by a universal natural selection where the long-term evolution of fitness-related traits is determined mainly by deterministic selection, while contingency is important predominately for neutral traits. Given suitable environmental conditions, it is shown that selection by energetic state and density-dependent competitive interactions unfolds to higher level selection for life-history transitions from simple asexually reproducing self-replicators to large bodied organisms with senescence and sexual reproduction between males and females, and in some cases, to the fully evolved eusocial colony with thousands of offspring workers. This defines an evolutionary arrow of time for open thermodynamic systems with a constant inflow of energy, predicting similar routes for long-term evolution on similar planets. 相似文献
93.
Brande-Lavridsen N Christensen-Dalsgaard J Korsgaard B 《Journal of experimental zoology. Part A, Ecological genetics and physiology》2008,309(7):389-398
A wide range of environmental xenobiotics that mimic hormones (endocrine-disrupting chemicals) may cause alterations in sexual development or reproductive function in aquatic organisms such as amphibians when exposed during early sensitive stages. We exposed tadpoles of the Common frog, Rana temporaria, from hatch to metamorphosis, to two different endocrine disruptors, the synthetic estrogen 17 alpha-ethinylestradiol and the fungicide prochloraz. The object of the study was to assess the effects of these two compounds on the sexual development of the tadpoles by investigating sex ratio, gonadal development, sex steroid concentrations and vitellogenin induction. Histology revealed that a large percentage of all groups were juvenile hermaphrodites at metamorphosis. Tadpoles exposed to 115 and 251 microg/L prochloraz showed a significant increased proportion of males. However, the testosterone concentrations were depressed in those groups. Ethinylestradiol in concentrations of 77 and 159 ng/L EE(2) increased whole-body calcium levels in a dose-dependent manner indicating induction of the egg yolk protein vitellogenin, verified also by gel electrophoresis. The study shows that ethinylestradiol may induce vitellogenesis and prochloraz may affect the sexual development in Common frogs. 相似文献
94.
The natural selection of metabolism and mass selects lifeforms from viruses to multicellular animals 下载免费PDF全文
Lars Witting 《Ecology and evolution》2017,7(21):9098-9118
I show that the natural selection of metabolism and mass can select for the major life‐history and allometric transitions that define lifeforms from viruses, over prokaryotes and larger unicells, to multicellular animals. The proposed selection is driven by a mass‐specific metabolism that is selected as the pace of the resource handling that generates net energy for self‐replication. An initial selection of mass is given by a dependence of mass‐specific metabolism on mass in replicators that are close to a lower size limit. A sublinear maximum dependence selects for virus‐like replicators, with no intrinsic metabolism, no cell, and practically no mass. A superlinear dependence selects for prokaryote‐like self‐replicating cells, with asexual reproduction and incomplete metabolic pathways. These self‐replicators have selection for increased net energy, and this generates a gradual unfolding of population‐dynamic feed‐back selection from interactive competition. The incomplete feed‐back selects for larger unicells with more developed metabolic pathways, and the completely developed feed‐back for multicellular animals with sexual reproduction. This model unifies the natural selection of lifeforms from viruses to multicellular animals, and it provides a parsimonious explanation where allometries and major life histories evolve from the natural selection of metabolism and mass. 相似文献
95.
96.
Mohammed Freewan Martin D. Rees Tito S. Sempértegui Plaza Elias Glaros Yean J. Lim Xiao Suo Wang Amanda W. S. Yeung Paul K. Witting Andrew C. Terentis Shane R. Thomas 《The Journal of biological chemistry》2013,288(3):1548-1567
The heme enzyme indoleamine 2,3-dioxygenase (IDO) is a key regulator of immune responses
through catalyzing l-tryptophan (l-Trp) oxidation. Here, we show that
hydrogen peroxide (H2O2) activates the peroxidase function of IDO to
induce protein oxidation and inhibit dioxygenase activity. Exposure of IDO-expressing
cells or recombinant human IDO (rIDO) to H2O2 inhibited dioxygenase
activity in a manner abrogated by l-Trp. Dioxygenase inhibition correlated with
IDO-catalyzed H2O2 consumption, compound I-mediated formation of
protein-centered radicals, altered protein secondary structure, and opening of the distal
heme pocket to promote nonproductive substrate binding; these changes were inhibited by
l-Trp, the heme ligand cyanide, or free radical scavengers. Protection by
l-Trp coincided with its oxidation into oxindolylalanine and kynurenine and the
formation of a compound II-type ferryl-oxo heme. Physiological peroxidase substrates,
ascorbate or tyrosine, enhanced rIDO-mediated H2O2 consumption and
attenuated H2O2-induced protein oxidation and dioxygenase
inhibition. In the presence of H2O2, rIDO catalytically consumed
nitric oxide (NO) and utilized nitrite to promote 3-nitrotyrosine formation on IDO. The
promotion of H2O2 consumption by peroxidase substrates, NO
consumption, and IDO nitration was inhibited by l-Trp. This study identifies IDO
as a heme peroxidase that, in the absence of substrates, self-inactivates dioxygenase
activity via compound I-initiated protein oxidation. l-Trp protects against
dioxygenase inactivation by reacting with compound I and retarding compound II reduction
to suppress peroxidase turnover. Peroxidase-mediated dioxygenase inactivation, NO
consumption, or protein nitration may modulate the biological actions of IDO expressed in
inflammatory tissues where the levels of H2O2 and NO are elevated
and l-Trp is low. 相似文献
97.
β- and γ-Hydroxynitrile glucosides are structurally related to cyanogenic glucosides (α-hydroxynitrile glucosides) but do not give rise to hydrogen cyanide release upon hydrolysis. Structural similarities and frequent co-occurrence suggest that the biosynthetic pathways for these compounds share common features. Based on available literature data we propose that oximes produced by CYP79 orthologs are common intermediates and that their conversion into β- and γ-hydroxynitrile glucosides is mediated by evolutionary diversified multifunctional orthologs to CYP71E1. We designate these as CYP71βγ and CYP71αβγ; in combination with the classical CYP71α (CYP71E1 and orthologs) these are able to hydroxylate any of the carbon atoms present in the amino acid and oxime derived nitriles. Subsequent dehydration reactions and hydroxylations and a final glycosylation step afford the unsaturated β- and γ-hydroxynitrile glucosides. This scheme would explain the distribution patterns of α-, β- and γ-hydroxynitrile glucosides found in plants. The possible biological functions of these hydroxynitriles are discussed. 相似文献
98.
Coenzyme Q improves LDL resistance to ex vivo oxidation but does not enhance endothelial function in hypercholesterolemic young adults 总被引:3,自引:0,他引:3
Raitakari OT McCredie RJ Witting P Griffiths KA Letters J Sullivan D Stocker R Celermajer DS 《Free radical biology & medicine》2000,28(7):1100-1105
Oxidative modification of low-density lipoprotein (LDL) may cause arterial endothelial dysfunction in hyperlipidemic subjects. Antioxidants can protect LDL from oxidation and therefore improve endothelial function. Dietary supplementation with coenzyme Q (CoQ(10)) raises its level within LDL, which may subsequently become more resistant to oxidation. Therefore, the aim of this study was to assess whether oral supplementation of CoQ(10) (50 mg three times daily) is effective in reducing ex vivo LDL oxidizability and in improving vascular endothelial function. Twelve nonsmoking healthy adults with hypercholesterolemia (age 34+/-10 years, nine women and three men, total cholesterol 7.4+/-1.1 mmol/l) and endothelial dysfunction (below population mean) at baseline were randomized to receive CoQ(10) or matching placebo in a double-blind crossover study (active/placebo phase 4 weeks, washout 4 weeks). Flow-mediated (FMD, endothelium-dependent) and nitrate-mediated (NMD, smooth muscle-dependent) arterial dilatation were measured by high-resolution ultrasound. CoQ(10) treatment increased plasma CoQ(10) levels from 1.1 +/-0.5 to 5.0+/-2.8 micromol/l (p =.009) but had no significant effect on FMD (4.3+/-2.4 to 5.1+/-3.6 %, p =.99), NMD (21.6+/-6.1 to 20.7+/-7.8 %, p = .38) or serum LDL-cholesterol levels (p = .51). Four subjects were selected randomly for detailed analysis of LDL oxidizability using aqueous peroxyl radicals as the oxidant. In this subgroup, CoQ(10) supplementation significantly increased the time for CoQ(10)H(2) depletion upon oxidant exposure of LDL by 41+/-19 min (p = .04) and decreased the extent of lipid hydroperoxide accumulation after 2 hours by 50+/-37 micromol/l (p =.04). We conclude that dietary supplementation with CoQ(10) decreases ex-vivo LDL oxidizability but has no significant effect on arterial endothelial function in patients with moderate hypercholesterolemia. 相似文献
99.
J M Letters P K Witting J K Christison A W Eriksson K Pettersson R Stocker 《Journal of lipid research》1999,40(6):1104-1112
Oxidation of lipoproteins is thought to be an early event in atherogenesis. To evaluate whether aortic lipoprotein lipid (per)oxidation contributes to atherosclerosis, we investigated the time-dependent changes to lipids and antioxidants in plasma and aortas of apolipoprotein E gene knockout (apoE-/-) mice receiving a high fat diet, and compared these changes with lesion development. Circulating buoyant lipoproteins and associated cholesterol (C), cholesteryl esters (CE), and alpha-tocopherol (alpha-TOH) increased within 1 month then remained largely constant up to 6 months. Coenzyme Q (CoQ) remained unchanged for the first 3 months and increased marginally after 6 months. With increasing duration of the diet, plasma lipids showed an increased propensity to undergo peroxyl radical-induced (per)oxidation. Absolute concentrations of aortic C, hydroperoxides and hydroxides of CE (CE-O(O)H) and alpha-TOH increased gradually while aortic CE increased more markedly with changes to cholesteryl linoleate being most pronounced. Aortic CoQ remained largely unchanged. Overall, the extent of aortic CE (per)oxidation remained low (=1%) and the ratio of incremental changes of alpha-TOH to oxidizable lipid remained unchanged. Aortic biochemistry paralleled lesion formation, particularly that in the descending thoracic aorta.Together, our results show that progressing atherosclerosis in apoE-/- mice is associated with increased aortic lipid (per)oxidation as assessed by the concentrations of CE-O(O)H, measured directly by HPLC. This supports the oxidation theory. Measurement of aortic CE-O(O)H may be useful for mechanistic studies studying the relationship between inhibition of in vivo lipid (per)oxidation and atherosclerosis. 相似文献
100.
P K Witting K Pettersson A M Ostlund-Lindqvist C Westerlund A W Eriksson R Stocker 《FASEB journal》1999,13(6):667-675
Antioxidants can inhibit atherosclerosis in animals, though it is not clear whether this is due to the inhibition of aortic lipoprotein lipid (per)oxidation. Coantioxidants inhibit radical-induced, tocopherol-mediated peroxidation of lipids in lipoproteins through elimination of tocopheroxyl radical. Here we tested the effect of the bisphenolic probucol metabolite and coantioxidant H 212/43 on atherogenesis in apolipoprotein E and low density lipoprotein (LDL) receptor gene double knockout (apoE-/-;LDLr-/-) mice, and how this related to aortic lipid (per)oxidation measured by specific HPLC analyses. Dietary supplementation with H 212/43 resulted in circulating drug levels of approximately 200 microM, increased plasma total cholesterol slightly and decreased plasma and aortic alpha-tocopherol significantly relative to age-matched control mice. Treatment with H 212/43 increased the antioxidant capacity of plasma, as indicated by prolonged inhibition of peroxyl radical-induced, ex vivo lipid peroxidation. Aortic tissue from control apoE-/-;LDLr-/- mice contained lipid hydro(pero)xides and substantial atherosclerotic lesions, both of which were decreased strongly by supplementation of the animals with H 212/43. The results show that a coantioxidant effectively inhibits in vivo lipid peroxidation and atherosclerosis in apoE-/-;LDLr-/- mice, consistent with though not proving a causal relationship between aortic lipoprotein lipid oxidation and atherosclerosis in this model of the disease. 相似文献