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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)
Background
Hypoxia and pressure-overload induce heme oxygenase-1 (HO-1) in cardiomyocytes and vascular smooth muscle cells (VSMCs). HO-1−/− mice exposed to chronic hypoxia develop pulmonary arterial hypertension (PAH) with exaggerated right ventricular (RV) injury consisting of dilation, fibrosis, and mural thrombi. Our objective was to indentify the HO-1 product(s) mediating RV protection from hypoxic injury in HO-1−/− mice.Methodology/Principal Findings
HO-1−/− mice were exposed to seven weeks of hypoxia and treated with inhaled CO or biliverdin injections. CO reduced right ventricular systolic pressure (RVSP) and prevented hypoxic pulmonary arteriolar remodeling in both HO-1−/− and control mice. Biliverdin had no significant effect on arteriolar remodeling or RVSP in either genotype. Despite this, biliverdin prevented RV failure in the hypoxic HO-1−/− mice (0/14 manifested RV wall fibrosis or thrombus), while CO-treated HO-1−/− mice developed RV insults similar to untreated controls. In vitro, CO inhibited hypoxic VSMC proliferation and migration but did not prevent cardiomyocyte death from anoxia-reoxygenation (A-R). In contrast, bilirubin limited A-R-induced cardiomyocyte death but did not inhibit VSMC proliferation and migration.Conclusions/Significance
CO and bilirubin have distinct protective actions in the heart and pulmonary vasculature during chronic hypoxia. Moreover, reducing pulmonary vascular resistance may not prevent RV injury in hypoxia-induced PAH; supporting RV adaptation to hypoxia and preventing RV failure must be a therapeutic goal. 相似文献74.
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Impacts of forestry planting on primary production in upland lakes from north‐west Ireland 下载免费PDF全文
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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JF Yuan SJ Zhang O Jafer RA Furlong OE Chausiaux CA Sargent GH Zhang NA Affara 《BMC microbiology》2009,9(1):246
Background
Pseudorabies virus (PRV) is an alphaherpesviruses whose native host is pig. PRV infection mainly causes signs of central nervous system disorder in young pigs, and respiratory system diseases in the adult. 相似文献77.
Hsin-Chou Yang Mei-Chu Huang Ling-Hui Li Chien-Hsing Lin Alice LT Yu Mitchell B Diccianni Jer-Yuarn Wu Yuan-Tsong Chen Cathy SJ Fann 《BMC bioinformatics》2008,9(1):196
Background
Microarray-based pooled DNA experiments that combine the merits of DNA pooling and gene chip technology constitute a pivotal advance in biotechnology. This new technique uses pooled DNA, thereby reducing costs associated with the typing of DNA from numerous individuals. Moreover, use of an oligonucleotide gene chip reduces costs related to processing various DNA segments (e.g., primers, reagents). Thus, the technique provides an overall cost-effective solution for large-scale genomic/genetic research. However, few publicly shared tools are available to systematically analyze the rapidly accumulating volume of whole-genome pooled DNA data. 相似文献78.
J W McGowan B Borwein J A Medeiros T Beveridge J D Brown E Spiller R Feder J Topalian W Gudat 《The Journal of cell biology》1979,80(3):732-735
High resolution x-ray lithographic studies of cells from chick embryo hearts dried by the CO2 critical point method have been made with soft x-ray radiation of different wavelengths. A marked difference in the relief replica in polymethyl methacrylate (PMMA) resulting from the differential absorption by the dried cells of carbon K alpha radiation at 4.48 nm and broad band synchrotron radiation (SR) with lambda is greater than 1.5 nm demonstrates the potential usefulness of the technique in making high resolution (approximately or equal to 10 nm) chemical identification of the constitutents which make up the various parts of the cell. 相似文献
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McGowan E Pickford F Kim J Onstead L Eriksen J Yu C Skipper L Murphy MP Beard J Das P Jansen K Delucia M Lin WL Dolios G Wang R Eckman CB Dickson DW Hutton M Hardy J Golde T 《Neuron》2005,47(2):191-199
Considerable circumstantial evidence suggests that Abeta42 is the initiating molecule in Alzheimer's disease (AD) pathogenesis. However, the absolute requirement for Abeta42 for amyloid deposition has never been demonstrated in vivo. We have addressed this by developing transgenic models that express Abeta1-40 or Abeta1-42 in the absence of human amyloid beta protein precursor (APP) overexpression. Mice expressing high levels of Abeta1-40 do not develop overt amyloid pathology. In contrast, mice expressing lower levels of Abeta1-42 accumulate insoluble Abeta1-42 and develop compact amyloid plaques, congophilic amyloid angiopathy (CAA), and diffuse Abeta deposits. When mice expressing Abeta1-42 are crossed with mutant APP (Tg2576) mice, there is also a massive increase in amyloid deposition. These data establish that Abeta1-42 is essential for amyloid deposition in the parenchyma and also in vessels. 相似文献
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