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71.
Impacts of forestry planting on primary production in upland lakes from north‐west Ireland
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Mark A. Stevenson Suzanne McGowan N. John Anderson Robert H. Foy Peter R. Leavitt Yvonne R. McElarney Daniel R. Engstrom Sergi Pla‐Rabés 《Global Change Biology》2016,22(4):1490-1504
Planted forests are increasing in many upland regions worldwide, but knowledge about their potential effects on algal communities of catchment lakes is relatively unknown. Here, the effects of afforestation were investigated using palaeolimnology at six upland lake sites in the north‐west of Ireland subject to different extents of forest plantation cover (4–64% of catchment area). 210Pb‐dated sediment cores were analysed for carotenoid pigments from algae, stable isotopes of bulk carbon (δ13C) and nitrogen (δ15N), and C/N ratios. In lakes with >50% of their catchment area covered by plantations, there were two‐ to sixfold increases in pigments from cryptophytes (alloxanthin) and significant but lower increases (39–116%) in those from colonial cyanobacteria (canthaxanthin), but no response from biomarkers of total algal abundance (β‐carotene). In contrast, lakes in catchments with <20% afforestation exhibited no consistent response to forestry practices, although all lakes exhibited fluctuations in pigments and geochemical variables due to peat cutting and upland grazing prior to forest plantation. Taken together, patterns suggest that increases in cyanobacteria and cryptophyte abundance reflect a combination of mineral and nutrient enrichment associated with forest fertilization and organic matter influx which may have facilitated growth of mixotrophic taxa. This study demonstrates that planted forests can alter the abundance and community structure of algae in upland humic lakes of Ireland and Northern Ireland, despite long histories of prior catchment disturbance. 相似文献
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Juhee Kim Aviva Must Garrett M. Fitzmaurice Matthew W. Gillman Virginia Chomitz Ellen Kramer Robert McGowan Karen E. Peterson 《Obesity (Silver Spring, Md.)》2005,13(7):1246-1254
Objectives: We examined the relationship between comprehensive fitness tests and overweight using a school surveillance system in a racially diverse city in the United States. Research Methods and Procedures: Trained physical education teachers measured weight, height, and fitness annually from 2001 to 2003. We compiled data for a cross‐sectional analysis (11, 845 measurements on 6297 students, 5 to14 years of age) and a 1‐year prospective analysis (4215 measurements on 2927 students not overweight at baseline, 5 to 13 years of age). Overweight was defined as a BMI ≥95th percentile (Centers for Disease Control and Prevention 2000 growth charts), and underfit was defined as failing at least one of five fitness tests: endurance run, abdominal strength, flexibility, upper body strength, and agility (Amateur Athletic Union and Fitnessgram). Associations between fitness and overweight were examined using multivariate logistic regression models, adjusting for sociodemographic status and repeated measurements over time. Results: The mean number of fitness tests passed was lower among students with a BMI above the 80th percentile. Overweight incidence over 1 year was 7% and 2% for underfit and fit girls, respectively (odds ratio, 3.3; 95% confidence interval, 2.0 to 5.6). Not passing either the endurance run or upper body strength test was associated with overweight incidence in both boys and girls. After adjusting for baseline BMI, the endurance run remained a significant predictor of incident overweight among girls (odds ratio, 2.0; 95% confidence interval, 1.1 to 3.5). Discussion: Findings support a cross‐sectional inverse relationship between physical fitness and overweight among school‐aged children. The direction of causation between fitness and overweight is not clearly established and merits further study. 相似文献
74.
C P McGowan R V Baudinette A A Biewener 《Comparative biochemistry and physiology. Part A, Molecular & integrative physiology》2008,150(2):151-158
Hindlimb musculoskeletal anatomy and steady speed over ground hopping mechanics were compared in two species of macropod marsupials, tammar wallabies and yellow-footed rock wallabies (YFRW). These two species are relatively closely related and are of similar size and general body plan, yet they inhabit different environments with presumably different musculoskeletal demands. Tammar wallabies live in relatively flat, open habitat whereas yellow-footed rock wallabies inhabit steep cliff faces. The goal of this study was to explore musculoskeletal differences between tammar wallabies and yellow-footed rock wallabies and determine how these differences influence each species' hopping mechanics. We found the cross-sectional area of the combined ankle extensor tendons of yellow-footed rock wallabies was 13% greater than that of tammar wallabies. Both species experienced similar ankle joint moments during steady-speed hopping, however due to a lower mechanical advantage at this joint, tammar wallabies produced 26% more muscle force. Thus, during moderate speed hopping, yellow-footed rock wallabies operated with 38% higher tendon safety factors, while tammar wallabies were able to store 73% more elastic strain energy (2.18 J per leg vs. 1.26 J in YFRW). This likely reflects the differing demands of the environments inhabited by these two species, where selection for non-steady locomotor performance in rocky terrain likely requires trade-offs in locomotor economy. 相似文献
75.
J. Kim Holloway James Booth Winfried Edelmann Clare H. McGowan Paula E. Cohen 《PLoS genetics》2008,4(9)
Two eukaryotic pathways for processing double-strand breaks (DSBs) as crossovers have been described, one dependent on the MutL homologs Mlh1 and Mlh3, and the other on the structure-specific endonuclease Mus81. Mammalian MUS81 has been implicated in maintenance of genomic stability in somatic cells; however, little is known about its role during meiosis. Mus81-deficient mice were originally reported as being viable and fertile, with normal meiotic progression; however, a more detailed examination of meiotic progression in Mus81-null animals and WT controls reveals significant meiotic defects in the mutants. These include smaller testis size, a depletion of mature epididymal sperm, significantly upregulated accumulation of MLH1 on chromosomes from pachytene meiocytes in an interference-independent fashion, and a subset of meiotic DSBs that fail to be repaired. Interestingly, chiasmata numbers in spermatocytes from Mus81−/− animals are normal, suggesting additional integrated mechanisms controlling the two distinct crossover pathways. This study is the first in-depth analysis of meiotic progression in Mus81-nullizygous mice, and our results implicate the MUS81 pathway as a regulator of crossover frequency and placement in mammals. 相似文献
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Andrea K. Townsend Anne B. Clark Kevin J. McGowan Elizabeth L. Buckles Andrew D. Miller Irby J. Lovette 《Proceedings. Biological sciences / The Royal Society》2009,276(1664):2057-2064
Disease-mediated inbreeding depression is a potential cost of living in groups with kin, but its general magnitude in wild populations is unclear. We examined the relationships between inbreeding, survival and disease for 312 offspring, produced by 35 parental pairs, in a large, open population of cooperatively breeding American crows (Corvus brachyrhynchos). Genetic analyses of parentage, parental relatedness coefficients and pedigree information suggested that 23 per cent of parental dyads were first- or second-order kin. Heterozygosity–heterozygosity correlations suggested that a microsatellite-based index of individual heterozygosity predicted individual genome-wide heterozygosity in this population. After excluding birds that died traumatically, survival probability was lower for relatively inbred birds during the 2–50 months after banding: the hazard rate for the most inbred birds was 170 per cent higher than that for the least inbred birds across the range of inbreeding index values. Birds that died with disease symptoms had higher inbreeding indices than birds with other fates. Our results suggest that avoidance of close inbreeding and the absence of inbreeding depression in large, open populations should not be assumed in taxa with kin-based social systems, and that microsatellite-based indices of individual heterozygosity can be an appropriate tool for examining the inbreeding depression in populations where incest and close inbreeding occur. 相似文献
78.
Michael CW Chan Renee WY Chan Wendy CL Yu Carol CC Ho WH Chui CK Lo Kit M Yuen Yi Guan John M Nicholls JS Malik Peiris 《Respiratory research》2009,10(1):102
Background
Highly pathogenic avian influenza (HPAI) H5N1 virus is entrenched in poultry in Asia and Africa and continues to infect humans zoonotically causing acute respiratory disease syndrome and death. There is evidence that the virus may sometimes spread beyond respiratory tract to cause disseminated infection. The primary target cell for HPAI H5N1 virus in human lung is the alveolar epithelial cell. Alveolar epithelium and its adjacent lung microvascular endothelium form host barriers to the initiation of infection and dissemination of influenza H5N1 infection in humans. These are polarized cells and the polarity of influenza virus entry and egress as well as the secretion of cytokines and chemokines from the virus infected cells are likely to be central to the pathogenesis of human H5N1 disease.Aim
To study influenza A (H5N1) virus replication and host innate immune responses in polarized primary human alveolar epithelial cells and lung microvascular endothelial cells and its relevance to the pathogenesis of human H5N1 disease.Methods
We use an in vitro model of polarized primary human alveolar epithelial cells and lung microvascular endothelial cells grown in transwell culture inserts to compare infection with influenza A subtype H1N1 and H5N1 viruses via the apical or basolateral surfaces.Results
We demonstrate that both influenza H1N1 and H5N1 viruses efficiently infect alveolar epithelial cells from both apical and basolateral surface of the epithelium but release of newly formed virus is mainly from the apical side of the epithelium. In contrast, influenza H5N1 virus, but not H1N1 virus, efficiently infected polarized microvascular endothelial cells from both apical and basolateral aspects. This provides a mechanistic explanation for how H5N1 virus may infect the lung from systemic circulation. Epidemiological evidence has implicated ingestion of virus-contaminated foods as the source of infection in some instances and our data suggests that viremia, secondary to, for example, gastro-intestinal infection, can potentially lead to infection of the lung. HPAI H5N1 virus was a more potent inducer of cytokines (e.g. IP-10, RANTES, IL-6) in comparison to H1N1 virus in alveolar epithelial cells, and these virus-induced chemokines were secreted onto both the apical and basolateral aspects of the polarized alveolar epithelium.Conclusion
The predilection of viruses for different routes of entry and egress from the infected cell is important in understanding the pathogenesis of influenza H5N1 infection and may help unravel the pathogenesis of human H5N1 disease. 相似文献79.
Patricia W Kimani Amey J Holmes Ruth E Grossmann Stephen E McGowan 《Respiratory research》2009,10(1):119
Background
Platelet-derived growth factor A (PDGF-A) signals solely through PDGF-Rα, and is required for fibroblast proliferation and transdifferentiation (fibroblast to myofibroblast conversion) during alveolar development, because pdgfa-null mice lack both myofibroblasts and alveoli. However, these PDGF-A-mediated mechanisms remain incompletely defined. At postnatal days 4 and 12 (P4 and P12), using mouse lung fibroblasts, we examined (a) how PDGF-Rα correlates with ki67 (proliferation marker) or alpha-smooth muscle actin (αSMA, myofibroblast marker) expression, and (b) whether PDGF-A directly affects αSMA or modifies stimulation by transforming growth factor beta (TGFβ).Methods
Using flow cytometry we examined PDGF-Rα, αSMA and Ki67 in mice which express green fluorescent protein (GFP) as a marker for PDGF-Rα expression. Using real-time RT-PCR we quantified αSMA mRNA in cultured Mlg neonatal mouse lung fibroblasts after treatment with PDGF-A, and/or TGFβ.Results
The intensity of GFP-fluorescence enabled us to distinguish three groups of fibroblasts which exhibited absent, lower, or higher levels of PDGF-Rα. At P4, more of the higher than lower PDGF-Rα + fibroblasts contained Ki67 (Ki67+), and Ki67+ fibroblasts predominated in the αSMA + but not the αSMA- population. By P12, Ki67+ fibroblasts comprised a minority in both the PDGF-Rα + and αSMA+ populations. At P4, most Ki67+ fibroblasts were PDGF-Rα + and αSMA- whereas at P12, most Ki67+ fibroblasts were PDGF-Rα- and αSMA-. More of the PDGF-Rα + than - fibroblasts contained αSMA at both P4 and P12. In the lung, proximate αSMA was more abundant around nuclei in cells expressing high than low levels of PDGF-Rα at both P4 and P12. Nuclear SMAD 2/3 declined from P4 to P12 in PDGF-Rα-, but not in PDGF-Rα + cells. In Mlg fibroblasts, αSMA mRNA increased after exposure to TGFβ, but declined after treatment with PDGF-A.Conclusion
During both septal eruption (P4) and elongation (P12), alveolar PDGF-Rα may enhance the propensity of fibroblasts to transdifferentiate rather than directly stimulate αSMA, which preferentially localizes to non-proliferating fibroblasts. In accordance, PDGF-Rα more dominantly influences fibroblast proliferation at P4 than at P12. In the lung, TGFβ may overshadow the antagonistic effects of PDGF-A/PDGF-Rα signaling, enhancing αSMA-abundance in PDGF-Rα-expressing fibroblasts. 相似文献80.
Sally H. Vitali S. Alex Mitsialis Olin D. Liang Xiaoli Liu Angeles Fernandez-Gonzalez Helen Christou Xinqi Wu Francis X. McGowan Stella Kourembanas 《PloS one》2009,4(6)