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Earlier studies have developed models of carrying capacity to predict the number of animals a certain area can support. These models assume that resources are not renewed after consumption ('standing stock' models), and that the initial number of prey and the rate of prey consumption determine the time a population of foragers can live in an area. Within such areas, foragers give up feeding at a sub-site or patch when intake rates no longer cover energy expenditure. To improve the success rate of the models' predictions, we here change the existing rate-maximising models into fitness-maximising models, and include dynamics in the availability of patches. These new (conceptual) models show that the approaches used so far may over- as well as underestimate carrying capacity. We review empirical studies that have aimed to estimate carrying capacity, and discuss how concepts have been confused. We make explicit suggestions on how to proceed in predicting carrying capacities in future studies.  相似文献   
105.

Background  

The Y-chromosomal diversity in the African buffalo (Syncerus caffer) population of Kruger National Park (KNP) is characterized by rainfall-driven haplotype frequency shifts between year cohorts. Stable Y-chromosomal polymorphism is difficult to reconcile with haplotype frequency variations without assuming frequency-dependent selection or specific interactions in the population dynamics of X- and Y-chromosomal genes, since otherwise the fittest haplotype would inevitably sweep to fixation. Stable Y-chromosomal polymorphism due one of these factors only seems possible when there are Y-chromosomal distorters of an equal sex ratio, which act by negatively affecting X-gametes, or Y-chromosomal suppressors of a female-biased sex ratio. These sex-ratio (SR) genes modify (suppress) gamete transmission in their own favour at a fitness cost, allowing for stable polymorphism.  相似文献   
106.

Purpose

We aimed to study the association between lung function decline and quantitative computed tomography (CT) air trapping.

Materials and Methods

Current and former heavy smokers in a lung cancer screening trial underwent volumetric low-dose CT in inspiration and expiration. Spirometry was obtained at baseline and after 3 years. The expiratory to inspiratory ratio of mean lung density (E/I-ratioMLD) was used to quantify air trapping. CT emphysema was defined as voxels in inspiratory CT below −950 Hounsfield Unit. Linear mixed modeling was used to determine the association between CT air trapping and lung function.

Results

We included 985 subjects with a mean age of 61.3 years. Independent of CT emphysema, CT air trapping was significantly associated with a reduction in forced expiratory volume in one second (FEV1) and the ratio of FEV1 over the forced vital capacity (FEV1/FVC); FEV1 declines with 33 mL per percent increase in CT air trapping, while FEV1/FVC declines 0.58% per percent increase (both p<0.001). CT air trapping further elicits accelerated loss of FEV1/FVC (additional 0.24% reduction per percent increase; p = 0.014).

Conclusion

In a lung cancer screening cohort, quantitatively assessed air trapping on low-dose CT is independently associated with reduced lung function and accelerated decline of FEV1/FVC.  相似文献   
107.
The presence of porcine endogenous retroviruses presents a potential risk of transmission of infectious diseases (xenozoonosis) if tissues and organs from genetically modified pigs are to be used in xenotransplantation. Here, we report that intracellular expression of a llama single-domain antibody against p15, the matrix domain protein of the porcine endogenous retrovirus Gag polyprotein, blocks retrovirus production, providing the possibility of eliminating the risk of infection in xenotransplantation.  相似文献   
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Purpose: We assessed the temporal pattern of 29 immune and inflammatory proteins in post-acute coronary syndrome (ACS) patients, prior to the development of recurrent ACS.

Methods: High-frequency blood sampling was performed in 844 patients admitted for ACS during one-year follow-up. We conducted a case-control study on the 45 patients who experienced reACS (cases) and two matched event-free patients (controls) per case. Olink Proteomics’ immunoassay was used to obtain serum levels of the 29 proteins, expressed in an arbitrary unit on the log2-scale (Normalized Protein eXpression, NPX). Linear mixed-effects models were applied to examine the temporal pattern of the proteins, and to illustrate differences between cases and controls.

Results: Mean age was 66?±?12 years and 80% were men. Cases and controls had similar baseline clinical characteristics. During the first 30 days, and after multiple testing correction, cases had significantly higher serum levels of CXCL1 (difference of 1.00 NPX, p?=?0.002), CD84 (difference of 0.64 NPX, p?=?0.002) and TNFRSF10A (difference of 0.41 NPX, p?<?0.001) than controls. After 30 days, serum levels of all 29 proteins were similar in cases and controls. In particular, no increase was observed prior to reACS.

Conclusions: Among 29 immune and inflammatory proteins, CXCL1, CD84 and TNFRSF10A were associated with early reACS after initial ACS-admission.  相似文献   

110.
A common and histologically well defined subtype of glioma are the oligodendroglial brain tumors. Approximately 70% of all oligodendrogliomas have a combined loss of the entire 1p and 19q chromosomal arms. This remarkably high frequency suggests that the remaining arms harbor yet to be identified tumor suppressor genes. Identification of these causal genetic changes in oligodendrogliomas is important because they form direct targets for treatment. In this study we therefore performed targeted resequencing of all exons, microRNAs, splice sites and promoter regions residing on 1p and 19q on 7 oligodendrogliomas and 4 matched controls. Only one missense mutation was identified in a single sample in the ARHGEF16 gene. This mutation lies within- and disrupts the conserved PDZ binding domain. No similar ARHGEF16 mutations or deletions were found in a larger set of oligodendrogliomas. The absence of common somatic changes within genes located on 1p and 19q in three out of four samples indicates that no additional "second hit" is required to drive oncogenic transformation on either chromosomal arm.  相似文献   
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