Powerful enzyme that tamps down inflammation holds promise for protecting the eyes in diabetes, premature birth MCG_AUG
This work was supported by grants from the National Institute of Health , the Department of Veterans Affairs, Veterans Health Administration , Office of Research and Development, Biomedical Laboratory Research and Development , R00 award and the Culver Vision Discovery Institute at Augusta University. The research reported in this publication was also supported by the NIH core grant number P30EY031631.
Jing Wang and Haiyan Xiao for their help with the fluorescein angiography and ERG as well as the vessel tortuosity measurement.Authors and AffiliationsAbdelrahman Y. Fouda & Esraa ShoshaAbdelrahman Y. Fouda & Esraa ShoshaZhimin Xu, Jutamas Suwanpradid, Modesto Rojas, Tahira Lemtalsi, Chintan Patel, Syed A. Zaidi, Brain K. Stansfield, S. Priya Narayanan & Ruth B. CaldwellZhimin Xu, Jutamas Suwanpradid, Modesto Rojas, Tahira Lemtalsi, Chintan Patel, Ji Xing, Syed A. Zaidi, Brain K.
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Distinct translatome changes in specific neural populations precede electroencephalographic changes in prion-infected miceAuthor summary Prions are infectious agents composed of a misfolded protein. When isolated from a mammalian brain and transferred to the same host species, prions will cause the same neurodegenerative disease affecting the same brain regions and cell types. This concept of selective vulnerability is also a feature of more common types of neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s. To better understand the mechanisms behind selective vulnerability, we studied disease responses of five cell types with different vulnerabilities in prion-infected mice at two different disease stages. Responses were measured as changes to mRNAs undergoing translation, referred to as the translatome. Before prion-infected mice demonstrated typical disease signs, electroencephalography (a method used clinically to characterize neurodegeneration in humans) revealed brain changes resembling those in human prion diseases, and surprisingly, the translatomes of all cells were drastically changed. Furthermore, before electroencephalography changes emerged, three cell types made unique responses while the most vulnerable cell type did not. These results suggests that mechanisms causing selective vulnerability will be difficult to dissect and that therapies will likely need to be provided before clinical signs emerge and individually engage multiple cell types and their distinct molecular pathways.
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Dad caused son's death while driving 13 times over limitLeon Clarke had taken cocaine 'in the hours leading up' to collecting his children Blake, eight, and Mason, six, from their grandmother’s
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Diacetyl Inhalation Impairs Airway Epithelial Repair in Mice Infected with Influenza A Virus | American Journal of Physiology-Lung Cellular and Molecular PhysiologyBronchiolitis obliterans (BO) is a debilitating disease of the small airways that can develop following exposure to toxic chemicals as well as respiratory tract infections. BO development is strongly associated with diacetyl (DA) inhalation exposures at occupationally relevant concentrations or severe influenza A viral (IAV) infections. However, it remains unclear whether lower dose exposures or more mild IAV infections can result in similar pathology. In the current work, we combined these two common environmental exposures, DA and IAV, to test whether shorter DA exposures followed by sublethal IAV infection would result in similar airways disease. Adult mice exposed to DA vapors 1 hr/day for 5 consecutive days followed by infection with the airway-tropic IAV H3N2 (HKx31) resulted in increased mortality, increased bronchoalveolar lavage (BAL) neutrophil percentage, mixed obstruction and restriction by lung function, and subsequent airway remodeling. Exposure to DA or IAV alone failed to result in significant pathology while mice exposed to DA+IAV showed increased alpha-smooth muscle actin (αSMA) and epithelial cells co-expressing the basal cell marker keratin 5 (KRT5) with the club cell marker SCGB1A1. To test whether DA exposure impairs epithelial repair after IAV infection, mice were infected first with IAV and then exposed to DA during airway epithelial repair. Mice exposed to IAV+DA developed similar airway remodeling with increased sub-epithelial αSMA and epithelial cells co-expressing KRT5 and SCGB1A1. Our findings reveal an underappreciated concept that common environmental insults while seemingly harmless by themselves can have catastrophic implications on lung function and long-term respiratory health when combined.
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Scot who stabbed best pal to death after PlayStation session loses court appealDale Gardiner was seeking to reduce the eight-year prison term he received for killing William Wardrop in Lanarkshire.
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