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At Cape Evans on Ross Island, Antarctica, the rhodophyte Phyllophora antarctica is the dominant primary producer in terms of biomass from 10 to >30 m depth. The vast majority of Phyllophora occurs as accumulations of unattached plants. Whilst decomposition and incorporation of macroalgal drift material into the food web is rapid in temperate ecosystems, we predicted these processes to be slow in Antarctica. We address the functional role of macroalgal detritus in fuelling the biodiversity of benthic communities at Cape Evans during the summers of 2001 and 2002. Specifically we (a) describe the distribution and biomass of attached and drift algae, (b) assess the photosynthetic capacity and degradation of drift accumulations using in situ fluorometry, (c) assess the effect of patches of drift Phyllophora on underlying macrofaunal communities, and, (d) use stable isotopes to investigate the possible uptake of Phyllophora by macrofauna. We found drift Phyllophora accumulations throughout the depth range investigated (3–31 m), with peak biomasses of 140±30 g dwt m–2 in the 15–25 m depth strata. At this depth stratum Phyllophora was a conspicuous habitat element with the % cover on the seafloor averaging 30%. While initially the drift algal accumulations appeared in good health we measured significant declines in photosynthetic capacity between years suggesting ongoing, albeit slow, degradation of the drift algal accumulations. Our results demonstrate that Phyllophora drift accumulations have a structuring role on soft-sediment communities, which increases in strength with the gradual degradation of the algae. The longevity of Phyllophora is enhanced by secondary metabolites, which serve as protection against grazers, and their extreme shade adaptation. However, our carbon and nitrogen stable isotope data of polychaetes and amphipods associated with Phyllophora suggest that macroalgal detritus enters the food web, and although this process is slow, Phyllophora accumulations might serve to dampen the seasonality in food supply providing higher trophic levels with a more constant food source.  相似文献   
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A reduction in fatty acid oxidation has been associated with lipid accumulation and insulin resistance in the skeletal muscle of obese individuals. We examined whether this decrease in fatty acid oxidation was attributable to a reduction in muscle mitochondrial content and/or a dysfunction in fatty acid oxidation within mitochondria obtained from skeletal muscle of age-matched, lean [body mass index (BMI) = 23.3 +/- 0.7 kg/m2] and obese women (BMI = 37.6 +/- 2.2 kg/m2). The mitochondrial marker enzymes citrate synthase (-34%), beta-hydroxyacyl-CoA dehydrogenase (-17%), and cytochrome c oxidase (-32%) were reduced (P < 0.05) in obese participants, indicating that mitochondrial content was diminished. Obesity did not alter the ability of isolated mitochondria to oxidize palmitate; however, fatty acid oxidation was reduced at the whole muscle level by 28% (P < 0.05) in the obese. Mitochondrial fatty acid translocase (FAT/CD36) did not differ in lean and obese individuals, but mitochondrial FAT/CD36 was correlated with mitochondrial fatty acid oxidation (r = 0.67, P < 0.05). We conclude that the reduction in fatty acid oxidation in obese individuals is attributable to a decrease in mitochondrial content, not to an intrinsic defect in the mitochondria obtained from skeletal muscle of obese individuals. In addition, it appears that mitochondrial FAT/CD36 may be involved in regulating fatty acid oxidation in human skeletal muscle.  相似文献   
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The process of infection during an epidemic can be envisaged as being transmitted via a network of routes represented by a contact network. Most differential equation models of epidemics are mean-field models. These contain none of the underlying spatial structure of the contact network. By extending the mean-field models to pair-level, some of the spatial structure can be contained in the model. Some networks of transmission such as river or transportation networks are clearly asymmetric, whereas others such as airborne infection can be regarded as symmetric. Pair-level models have been developed to describe symmetric contact networks. Here we report on work to develop a pair-level model that is also applicable to asymmetric contact networks. The procedure for closing the model at the level of pairs is discussed in detail. The model is compared against stochastic simulations of epidemics on asymmetric contact networks and against the predictions of the symmetric model on the same networks. DEFRA funded project FC1153  相似文献   
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The input of terrestrial silt and clay (hereafter mud) into coastal environments can alter sediment grain size distribution affecting the structure and functioning of benthic communities. The relationship between sediment mud content and macrofaunal community structure has been well documented, but not the effects on ecosystem function. In 143 plots from the mid-intertidal sites in 9 estuaries, we measured sediment properties, macrofaunal community composition and fluxes of O2 and NH4 + across the sediment–water interface to derive process-based measures of ecosystem function across the sand–mud gradient. We observed reductions in measures of macrofaunal diversity and decreases in the maximum density of key bioturbating bivalves (Austrovenus stutchburyi and Macomona liliana) with increased mud content. Concurrently, the maximum rates of sediment oxygen consumption (SOC), NH4 + efflux (NH4 +) and biomass standardized gross primary production (GPPChl-a ) also decreased with increasing mud content. Environmental predictors explained 34–39% (P = 0.005–0.01) of the total variation in ecosystem function in distance-based linear models. After partitioning out the effect of mud, A. stutchburyi abundance was positively correlated and explained 25 and 23% (P = 0.0001) of the variation of SOC and NH4 +, respectively. Also, mud content (negatively correlated) and temperature (positively correlated) explained 26% of variability in GPPChl-a (P = 0.0001). Our results highlight the importance of increased mud content and the associated reduction in the abundance of strongly interacting key species on the loss of ecosystem function in intertidal sand flats.  相似文献   
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Dormant tumor cells resistant to ablative cancer therapy represent a significant clinical obstacle due to later relapse. Experimentally, the murine B cell lymphoma (BCL1) is used as a model of tumor dormancy in mice vaccinated with the BCL1 Ig. Here, we used this model to explore the cellular mechanisms underlying dormancy. Our previous studies have demonstrated that T cell-mediated immunity is an important component in the regulation of tumor dormancy because Id-immune T cells adoptively transferred into passively immunized SCID mice challenged with BCL1 cells significantly increased the incidence and duration of the dormant state. We have extended these observations and demonstrate that CD8+, but not CD4+, T cells are required for the maintenance of dormancy in BCL1 Ig-immunized BALB/c mice. In parallel studies, the transfer of Id-immune CD8+ cells, but not Id-immune CD4+ cells, conferred significant protection to SCID mice passively immunized with nonprotective levels of polyclonal anti-Id and then challenged with BCL1 cells. Furthermore, the ability of CD8+ T cells to induce a state of dormancy in passively immunized SCID mice was completely abrogated by treatment with neutralizing alpha-IFN-gamma mAbs in vivo. In vitro studies demonstrated that IFN-gamma alone or in combination with reagents to cross-link the surface Ig induced both cell cycle arrest and apoptosis in a BCL1 cell line. Collectively, these data demonstrate a role for CD8+ T cells via endogenous production of IFN-gamma in collaboration with humoral immunity to both induce and maintain a state of tumor dormancy.  相似文献   
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Intrauterine growth restriction (IUGR) is associated with an increased risk of developing obesity, insulin resistance and cardiovascular disease. However, its effect on energetics in heart remains unknown. In the present study, we examined respiration in cardiac muscle and liver from adult mice that were undernourished in utero. We report that in utero undernutrition is associated with impaired cardiac muscle energetics, including decreased fatty acid oxidative capacity, decreased maximum oxidative phosphorylation rate and decreased proton leak respiration. No differences in oxidative characteristics were detected in liver. We also measured plasma acylcarnitine levels and found that short-chain acylcarnitines are increased with in utero undernutrition. Results reveal the negative impact of suboptimal maternal nutrition on adult offspring cardiac energy metabolism, which may have life-long implications for cardiovascular function and disease risk.  相似文献   
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