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"Zoppo, David"
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Is the EPA's proposed clean power plan legal?
Last June 18, the US EPA released what is undoubtedly its most significant proposed rule ever: its Clean Power Plan. If finalized, the rule would reduce carbon dioxide emissions from America's power plants by 30% from 2005 levels by 2030. Within hours of the release of the proposed rule, four attorneys from the national law firm Squire Patton Boggs filed a 46-page petition in the US Court of Appeals for the District of Columbia Circuit on behalf of Murray Energy, the largest underground coal mining company in America. The petition asks the court to issue an extraordinary writ because the text of the Clean Air Act (CAA) \"unambiguously prohibits\" the EPA's proposal. Amid all the rhetoric and political posturing, the question raised in this case is a good one, and one that everyone (including the EPA and supporters of climate regulation) should want the courts to decide now: does the EPA actually have the statutory authority to issue its Clean Power Plan?
Journal Article
Let's Find Out How Much 'Clean Power' the Feds Really Have
The EPA already regulates mercury emissions from existing power plants under the toxics program, so -- as the EPA has acknowledged -- a \"literal reading\" of the act would prohibit the agency from issuing its climate rule, in any form. Under the Clean Air Act, carbon dioxide isn't a \"toxic pollutant,\" so the Senate version gives the EPA the authority it wants.
Newspaper Article
Let's Find Out How Much 'Clean Power' the Feds Really Have
The Environmental Protection Agency's proposed Clean Power Plan is unquestionably the most controversial rule the agency has ever proposed. If it goes into effect, the plan would require that total carbon emissions from the power sector in the U.S. be reduced by 30% (from 2005 levels)...
Newspaper Article
Let's Find Out How Much 'Clean Power' the Feds Really Have; The EPA should ask for a court ruling before states and utilities spend billions in compliance costs
Within hours of the proposal's June 2 release, Murray Energy Corp., the largest underground coal-mining company in the country, filed a lawsuit asking the court to invoke an \"extraordinary writ\" to halt the rule-making process in its tracks. The EPA already regulates mercury emissions from existing power plants under the toxics program, so--as the EPA has acknowledged--a \"literal reading\" of the act would prohibit the agency from issuing its climate rule, in any form.
Newspaper Article
TbD1 deletion as a driver of the evolutionary success of modern epidemic Mycobacterium tuberculosis lineages
Mycobacterium tuberculosis
(Mtb) strains are classified into different phylogenetic lineages (L), three of which (L2/L3/L4) emerged from a common progenitor after the loss of the MmpS6/MmpL6-encoding Mtb-specific deletion 1 region (TbD1). These TbD1-deleted “modern” lineages are responsible for globally-spread tuberculosis epidemics, whereas TbD1-intact “ancestral” lineages tend to be restricted to specific geographical areas, such as South India and South East Asia (L1) or East Africa (L7). By constructing and characterizing a panel of recombinant TbD1-knock-in and knock-out strains and comparison with clinical isolates, here we show that deletion of TbD1 confers to Mtb a significant increase in resistance to oxidative stress and hypoxia, which correlates with enhanced virulence in selected cellular, guinea pig and C3HeB/FeJ mouse infection models, the latter two mirroring in part the development of hypoxic granulomas in human disease progression. Our results suggest that loss of TbD1 at the origin of the L2/L3/L4 Mtb lineages was a key driver for their global epidemic spread and outstanding evolutionary success.
Mycobacterium tuberculosis
(Mtb) modern strains emerged from a common progenitor after the loss of Mtb-specific deletion 1 region (TbD1). Here, the authors show that deletion of TbD1 correlates with enhanced Mtb virulence in animal models, mirroring the development of hypoxic granulomas in human disease progression.
Journal Article
Immunologic Privilege in the Central Nervous System and the Blood–Brain Barrier
The brain is in many ways an immunologically and pharmacologically privileged site. The blood–brain barrier (BBB) of the cerebrovascular endothelium and its participation in the complex structure of the neurovascular unit (NVU) restrict access of immune cells and immune mediators to the central nervous system (CNS). In pathologic conditions, very well-organized immunologic responses can develop within the CNS, raising important questions about the real nature and the intrinsic and extrinsic regulation of this immune privilege. We assess the interactions of immune cells and immune mediators with the BBB and NVU in neurologic disease, cerebrovascular disease, and intracerebral tumors. The goals of this review are to outline key scientific advances and the status of the science central to both the neuroinflammation and CNS barriers fields, and highlight the opportunities and priorities in advancing brain barriers research in the context of the larger immunology and neuroscience disciplines. This review article was developed from reports presented at the 2011 Annual Blood-Brain Barrier Consortium Meeting.
Journal Article
Fibrinogen Chains Intrinsic to the Brain
We observed fine fibrin deposition along the paravascular spaces in naive animals, which increased dramatically following subarachnoid hemorrhage (SAH). Following SAH, fibrin deposits in the areas remote from the hemorrhage. Traditionally it is thought that fibrinogen enters subarachnoid space through damaged blood brain barrier. However, deposition of fibrin remotely from hemorrhage suggests that fibrinogen chains Aα, Bβ, and γ can originate in the brain. Here we demonstrate
and
that astroglia and neurons are capable of expression of fibrinogen chains. SAH in mice was induced by the filament perforation of the circle of Willis. Four days after SAH animals were anesthetized, transcardially perfused and fixed. Whole brain was processed for immunofluorescent (IF) analysis of fibrin deposition on the brain surface or in brains slices processed for fibrinogen chains Aα, Bβ, γ immunohistochemical detection. Normal human astrocytes were grown media to confluency and stimulated with NOC-18 (100 μM), TNF-α (100 nM), ATP-γ-S (100 μM) for 24 h. Culture was fixed and washed/permeabilized with 0.1% Triton and processed for IF. Four days following SAH fibrinogen chains Aα IF associated with glia limitans and superficial brain layers increased 3.2 and 2.5 times (
< 0.05 and
< 0.01) on the ventral and dorsal brain surfaces respectively; fibrinogen chains Bβ increased by 3 times (
< 0.01) on the dorsal surface and fibrinogen chain γ increased by 3 times (
< 0.01) on the ventral surface compared to sham animals. Human cultured astrocytes and neurons constitutively expressed all three fibrinogen chains. Their expression changed differentially when exposed for 24 h to biologically significant stimuli: TNFα, NO or ATP. Western blot and RT-qPCR confirmed presence of the products of the appropriate molecular weight and respective mRNA. We demonstrate for the first time that mouse and human astrocytes and neurons express fibrinogen chains suggesting potential presence of endogenous to the brain fibrinogen chains differentially changing to biologically significant stimuli. SAH is followed by increased expression of fibrinogen chains associated with glia limitans remote from the hemorrhage. We conclude that brain astrocytes and neurons are capable of production of fibrinogen chains, which may be involved in various normal and pathological processes.
Journal Article
Food chain information systems in medium- and smallsized slaughterhouses of central Italy and organ and carcass condemnations: A five-year survey
The flow of information between farms and slaughterhouses about animal health, is a fundamental process for modern meat inspection. The information provided by Food Chain Information (FCI) systems in medium-small sized slaughterhouses in central Italy, focusing on the data provided on the animal’s health status, was performed through a five-year survey together with the number of organ and carcass condemnation for bovine, swine and ovine. The annual prevalence of condemnation was higher in bovine (from 10.49% in 2015 to 17.16% in 2019) than swine (from 6.39% in 2015 to 12.64% in 2019) and ovine (from 8.05% in 2019 to 8.98% in 2017), and an overall prevalence increase was observed in bovine and swine, throughout the years. The frequent lack of Food Chain Information (FCI) from farms to slaughterhouses should be emphasised, taking into consideration that a poor implementation of the system by farmers, could lead to a persistent risk of disease at farm level for these two species.
Journal Article