Did Neoliberalizing West African Forests Produce a New Niche for Ebola?

A recent study introduced a vaccine that controls Ebola Makona, the Zaire ebolavirus variant that has infected 28,000 people in West Africa. We propose that even such successful advances are insufficient for many emergent diseases. We review work hypothesizing that Makona, phenotypically similar to much smaller outbreaks, emerged out of shifts in land use brought about by neoliberal economics. The epidemiological consequences demand a new science that explicitly addresses the foundational processes underlying multispecies health, including the deep-time histories, cultural infrastructure, and global economic geographies driving disease emergence. The approach, for instance, reverses the standard public health practice of segregating emergency responses and the structural context from which outbreaks originate. In Ebola's case, regional neoliberalism may affix the stochastic "friction" of ecological relationships imposed by the forest across populations, which, when above a threshold, keeps the virus from lining up transmission above replacement. Export-led logging, mining, and intensive agriculture may depress such functional noise, permitting novel spillovers larger forces of infection. Mature outbreaks, meanwhile, can continue to circulate even in the face of efficient vaccines. More research on these integral explanations is required, but the narrow albeit welcome success of the vaccine may be used to limit support of such a program.SCOPUS: re.jinfo:eu-repo/semantics/publishe

Toward a unified pathophysiology in COVID-19 acute aortopathies

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Aortoaortic bypass pathophysiology

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Iron and liver diseases.

A mild to moderate iron excess is found in patients with liver diseases apparently unrelated to genetic hemochromatosis. Iron appears to affect the natural history of hepatitis C virus-related chronic liver diseases, alcoholic liver disease and nonalcoholic steatohepatitis by leading to a more severe fibrosis and thus aiding the evolution to cirrhosis.Ahigher frequency of mutations of the HFE gene, the gene responsible for hereditary hemochromatosis, is found in patients with liver diseases and increased liver iron than in normal patients. Patients with excess iron are potentially at a higher risk of developing hepatocellular carcinoma. Iron depletion therapy could interfere with fibrosis development and possibly reduce the risk of liver cancer occurrence

Opposite Hydrogen Behaviors in GaAsN and InAsN Alloys: Band Gap Opening Versus Donor Doping

Experiments suggest that atomic H neutralizes the effects of N (i.e., it recovers the host energy gap) without inducing any band-filling effect (i.e., without behaving as a shallow donor) in the GaAsN alloy, while the vice versa is true in the InAsN one. Moreover, theoretical results on H in GaAsN contradict some experiments. These facts motivated the present study, where the role of N-H complexes has been investigated by performing density functional theory-Heyd-Scuseria-Emzerhof calculations. Present results confirm and explain the H properties; N neutralization is certain only in GaAsN, while H behaves as a shallow donor only in InAsN. They also show that, despite an identical geometry, single-H complexes neutralize the N effects in GaAsN, not in InAsN. This result is accounted for by a simple model showing that: (i) band gap recovery is directly related to a recovery of the atomic charge of the Ga/In cations neighboring the N atom in a N-H complex and (ii) a larger extent of charge recovery is found for the Ga cations with respect to the In ones, consistently with an electronegativity larger for Ga than for In. Remarkably, the same reason is at the ground of the different H behavior, deep versus shallow, in the two GaAsN and InAsN alloys