全文获取类型
收费全文 | 196篇 |
免费 | 22篇 |
专业分类
218篇 |
出版年
2023年 | 1篇 |
2021年 | 3篇 |
2019年 | 5篇 |
2017年 | 2篇 |
2016年 | 5篇 |
2015年 | 13篇 |
2014年 | 13篇 |
2013年 | 6篇 |
2012年 | 10篇 |
2011年 | 12篇 |
2010年 | 10篇 |
2009年 | 8篇 |
2008年 | 5篇 |
2007年 | 6篇 |
2006年 | 3篇 |
2005年 | 10篇 |
2004年 | 11篇 |
2003年 | 6篇 |
2002年 | 4篇 |
2001年 | 11篇 |
2000年 | 9篇 |
1999年 | 8篇 |
1998年 | 7篇 |
1997年 | 2篇 |
1996年 | 3篇 |
1995年 | 2篇 |
1994年 | 1篇 |
1991年 | 5篇 |
1990年 | 3篇 |
1989年 | 3篇 |
1988年 | 2篇 |
1987年 | 4篇 |
1982年 | 3篇 |
1981年 | 3篇 |
1979年 | 3篇 |
1978年 | 2篇 |
1977年 | 3篇 |
1976年 | 1篇 |
1972年 | 3篇 |
1969年 | 1篇 |
1968年 | 1篇 |
1967年 | 1篇 |
1965年 | 1篇 |
1956年 | 1篇 |
1954年 | 1篇 |
1889年 | 1篇 |
排序方式: 共有218条查询结果,搜索用时 11 毫秒
121.
Environmental anaerobic ammonium oxidation (anammox) was demonstrated for the first time in 2002, using 15N labeling, in homogenized sediment from the Skagerrak, where it accounted for up to 67% of N2 production. We returned to some of these original sites in 2010 to make measurements of nitrogen and carbon cycling under conditions more representative of those in situ, quantifying anammox and denitrification, together with oxygen penetration and consumption, in intact sediment cores. Overall, oxygen consumption and N2 production decayed with water depth, as expected, but the drop in N2 production was relatively more pronounced. Whereas we confirmed the dominance of N2 production by anammox (72% and 77%) at the two deepest sites (∼700 m of water), anammox was conspicuously absent from two shallower sites (∼200 m and 400 m). At the shallower sites, we could measure no anammox activity with either intact or homogeneous sediment, and quantitative PCR (16S rRNA) gave a negligible abundance of anammox bacteria in the anoxic layers. Such an absence of anammox, especially at one locale where it was originally demonstrated, is hard to reconcile. Despite the dominance of anammox at the deepest sites, anammox activity could not make up for the drop in denitrification, and assuming Redfield ratios for the organic matter being mineralized, the estimated retention of fixed N actually increased to 90% to 97% of that mineralized, whereas it was 80% to 86% at the shallower sites. 相似文献
122.
123.
Understanding decisions is the fundamental aim of the behavioural sciences. The theory of rational choice is based on axiomatic principles such as transitivity and independence of irrelevant alternatives (IIA). Empirical studies have demonstrated that the behaviour of humans and other animals often seems irrational; there can be a lack of transitivity in choice and seemingly irrelevant alternatives can alter decisions. These violations of transitivity and IIA undermine rational choice theory. However, we show that an individual that is maximizing its rate of food gain can exhibit failure of transitivity and IIA. We show that such violations can be caused because a current option may disappear in the near future or a better option may reappear soon. Current food options can be indicative of food availability in the near future, and this key feature can result in apparently irrational behaviour. 相似文献
124.
Measurement of gluconeogenesis in exercising men by mass isotopomer distribution analysis. 总被引:1,自引:0,他引:1
Jeff K Trimmer Jean-Marc Schwarz Gretchen A Casazza Michael A Horning Nestor Rodriguez George A Brooks 《Journal of applied physiology》2002,93(1):233-241
We evaluated the hypothesis that coordinated adjustments in absolute rates of gluconeogenesis (GNG(ab)) and hepatic glycogenolysis (Gly) would maintain euglycemia and match glucose production (GP) to peripheral utilization during rest and exercise. Specifically, we evaluated the extent to which gradations in exercise power output would affect the contribution of GNG(ab) to GP. For these purposes, we employed mass isotopomer distribution analysis (MIDA) and isotope-dilution techniques on eight postabsorptive (PA) endurance-trained men during 90 min of leg cycle ergometry at 45 and 65% peak O(2) consumption (VO(2 peak); moderate and hard intensities, respectively) and the preceding rest period. GP was constant in resting subjects, whereas the fraction from GNG (f(GNG)) increased over time during rest (22.3 +/- 0.9% at 11.25 h PA vs. 25.6 +/- 0.9% at 12.0 h PA, P < 0.05). In the transition from rest to exercise, GP increased in an intensity-dependent manner (rest, 2.0 +/- 0.1; 45%, 4.0 +/- 0.4; 65%, 5.84 +/- 0.64 mg. kg(-1). min(-1), P < 0.05), although glucose rate of disappearance exceeded rate of appearance during the last 30 min of exercise at 65% VO(2 peak). Compared with rest, increases in GP were sustained by 92 and 135% increments in GNG(ab) during moderate- and hard-intensity exercises, respectively. Correspondingly, Gly (calculated as the difference between GP and MIDA-measured GNG(ab)) increased 100 and 203% over rest during the two exercise intensities. During moderate-intensity exercise, f(GNG) was the same as at rest; however, during the harder exercise f(GNG) decreased significantly to account for only 21% of GP. The highest sustained GNG(ab) observed in these trials on PA men was 1.24 +/- 0.3 mg. kg(-1). min(-1). We conclude that, after an overnight fast, 1) absolute GNG rates increased with intensity of effort despite a reduced f(GNG) at 65% VO(2 peak), 2) during exercise Gly is more responsible than GNG(ab) for maintaining GP, and 3) in 12-h fasted men, neither increased Gly or GNG(ab) nor was their combination able to maintain euglycemia during prolonged hard (65% VO(2 peak)) exercise. 相似文献
125.
126.
Modulation of Second Messengers in the Nervous System of Larval Manduca sexta by Muscarinic Receptors 总被引:1,自引:1,他引:0
Abstract: Measurements were made of the effects of muscarinic agents on endogenous levels of cyclic AMP and cyclic GMP, and the turnover of radiolabeled inositol phosphates in the abdominal nervous system of larval Manduca sexta . Cyclic AMP levels were increased by treatment with 3-isobutyl-1-methylxanthine or tetrodotoxin, but the muscarinic agonist oxotremorine-M and the muscarinic antagonist scopolamine had no consistent effects. In contrast, cyclic GMP levels were significantly increased by oxotremorine-M and by oxotremorine-M in the presence of 3-isobutyl-1-methylxanthine and tetrodotoxin but not in the presence of scopolamine. Using lithium to inhibit the recycling of inositol phospholipid metabolites in isolated nerve cords, we detected a small but consistent increase in inositol phosphate production by oxotremorine-M. The primary inositol metabolite generated during a 5-min exposure to oxotremorine-M co-eluted from ion-exchange columns with inositol-1-monophosphate, although other more polar metabolites were also detected. This agonist-evoked increase in inositol phosphate production was unaffected by tetrodotoxin but inhibited by scopolamine, suggesting that it is directly mediated by muscarinic receptors. Further evidence for coupling between muscarinic receptors and inositol metabolism was obtained using a cell-free preparation of nerve cord membranes labeled with [3 H]inositol. Incubation with oxotremorine-M evoked a significant increase in labeled inositol bisphosphate, consistent with muscarinic receptors coupling to phosphatidylinositol metabolism. The accumulation of inositol bisphosphate in cell-free preparations suggests that the normal breakdown to inositol monophosphate requires cytosolic components. Together, these results indicate that muscarinic acetylcholine receptors in Manduca couple predominantly to the inositol phospholipid signaling system, although some receptors may modulate cyclic GMP. 相似文献
127.
The histone demethylase, lysine (K)-specific demethylase 2A (Kdm2a), is highly conserved and expressed ubiquitously. Kdm2a can regulate cell proliferation and osteo/dentinogenic, adipogenic and chondrogenic differentiation of mesenchymal stem cells (MSCs) derived from dental tissue. We used quantitative real-time RT-PCR analysis and immunohistochemistry to detect Kdm2a expression during development of the murine molar at embryonic days E12, E14, E16 and E17 and postnatal days P3 and P14. Immunohistochemistry results showed no positive staining of Kdm2a at E12. At E14, Kdm2a was expressed weakly in the inner enamel epithelium, stellate reticulum cells and dental sac. At E16, Kdm2a was expressed mainly in the inner and outer enamel epithelium, stratum intermedium and dental sac, but weaker staining was found in cervical loop and dental papilla cells adjacent to the basement membrane. At E17, the strongest Kdm2a staining was detected in the ameloblasts and stronger Kdm2a staining also was detected in the stratum intermedium, outer enamel epithelium and dental papilla cells compared to the expression at E16. Postnatally, we found that Kdm2a was localized in secretory and mature ameloblasts and odontoblasts, and dentin was unstained. Real-time RT-PCR showed that Kdm2a mRNA levels in murine germ cells increased from E12 to E14 and from E14 to E16; no significant change occurred at E16, E17 or P3, then the levels decreased at P14 compared to P3. Kdm2a expression may be closely related to cell proliferation, to ameloblast and odontoblast differentiation and to the secretion of extracellular enamel and dentin during murine tooth development. 相似文献
128.
129.
Gabriel Yvon-Durocher J. Iwan Jones Mark Trimmer Guy Woodward Jose M. Montoya 《Philosophical transactions of the Royal Society of London. Series B, Biological sciences》2010,365(1549):2117-2126
The carbon cycle modulates climate change, via the regulation of atmospheric CO2, and it represents one of the most important services provided by ecosystems. However, considerable uncertainties remain concerning potential feedback between the biota and the climate. In particular, it is unclear how global warming will affect the metabolic balance between the photosynthetic fixation and respiratory release of CO2 at the ecosystem scale. Here, we present a combination of experimental field data from freshwater mesocosms, and theoretical predictions derived from the metabolic theory of ecology to investigate whether warming will alter the capacity of ecosystems to absorb CO2. Our manipulative experiment simulated the temperature increases predicted for the end of the century and revealed that ecosystem respiration increased at a faster rate than primary production, reducing carbon sequestration by 13 per cent. These results confirmed our theoretical predictions based on the differential activation energies of these two processes. Using only the activation energies for whole ecosystem photosynthesis and respiration we provide a theoretical prediction that accurately quantified the precise magnitude of the reduction in carbon sequestration observed experimentally. We suggest the combination of whole-ecosystem manipulative experiments and ecological theory is one of the most promising and fruitful research areas to predict the impacts of climate change on key ecosystem services. 相似文献
130.
Ubaldo E Martinez-Outschoorn Diana Whitaker-Menezes Stephanos Pavlides Barbara Chiavarina Gloria Bonuccelli Casey Trimmer Aristotelis Tsirigos Gemma Migneco Agnieszka K Witkiewicz Renee Balliet Isabelle Mercier Chengwang Wang Neal Flomenberg Anthony Howell Zhao Lin Jaime Caro Richard G Pestell Federica Sotgia Michael P Lisanti 《Cell cycle (Georgetown, Tex.)》2010,9(21):4297-4306
The role of autophagy in tumorigenesis is controversial. Both autophagy inhibitors (chloroquine) and autophagy promoters (rapamycin) block tumorigenesis by unknown mechanism(s). This is called the “Autophagy Paradox.” We have recently reported a simple solution to this paradox. We demonstrated that epithelial cancer cells use oxidative stress to induce autophagy in the tumor microenvironment. As a consequence, the autophagic tumor stroma generates recycled nutrients that can then be used as chemical building blocks by anabolic epithelial cancer cells. This model results in a net energy transfer from the tumor stroma to epithelial cancer cells (an energy imbalance), thereby promoting tumor growth. This net energy transfer is both unilateral and vectorial, from the tumor stroma to the epithelial cancer cells, representing a true host-parasite relationship. We have termed this new paradigm “The Autophagic Tumor Stroma Model of Cancer Cell Metabolism” or “Battery-Operated Tumor Growth.” In this sense, autophagy in the tumor stroma serves as a “battery” to fuel tumor growth, progression and metastasis, independently of angiogenesis. Using this model, the systemic induction of autophagy will prevent epithelial cancer cells from using recycled nutrients, while the systemic inhibiton of autophagy will prevent stromal cells from producing recycled nutrients—both effectively “starving” cancer cells. We discuss the idea that tumor cells could become resistant to the systemic induction of autophagy by the upregulation of natural, endogenous autophagy inhibitors in cancer cells. Alternatively, tumor cells could also become resistant to the systemic induction of autophagy by the genetic silencing/deletion of pro-autophagic molecules, such as Beclin1. If autophagy resistance develops in cancer cells, then the systemic inhibition of autophagy would provide a therapeutic solution to this type of drug resistance, as it would still target autophagy in the tumor stroma. As such, an anti-cancer therapy that combines the alternating use of both autophagy promoters and autophagy inhibitors would be expected to prevent the onset of drug resistance. We also discuss why anti-angiogenic therapy has been found to promote tumor recurrence, progression and metastasis. More specifically, anti-angiogenic therapy would induce autophagy in the tumor stroma via the induction of stromal hypoxia, thereby converting a non-aggressive tumor type to a “lethal” aggressive tumor phenotype. Thus, uncoupling the metabolic parasitic relationship between cancer cells and an autophagic tumor stroma may hold great promise for anti-cancer therapy. Finally, we believe that autophagy in the tumor stroma is the local microscopic counterpart of systemic wasting (cancer-associated cachexia), which is associated with advanced and metastatic cancers. Cachexia in cancer patients is not due to decreased energy intake, but instead involves an increased basal metabolic rate and increased energy expenditures, resulting in a negative energy balance. Importantly, when tumors were surgically excised, this increased metabolic rate returned to normal levels. This view of cachexia, resulting in energy transfer to the tumor, is consistent with our hypothesis. So, cancer-associated cachexia may start locally as stromal autophagy and then spread systemically. As such, stromal autophagy may be the requisite precursor of systemic cancer-associated cachexia.Key words: caveolin-1, autophagy, cancer associated fibroblasts, hypoxia, mitophagy, oxidative stress, DNA damage, genomic instability, tumor stroma, wasting (cancer cachexia), Warburg effect 相似文献