A picornavirus-like pathogen of Cotylogaster occidentalis (Trematoda: Aspidogastrea), an intestinal parasite of freshwater mollusks

Nonoccluded, icosahedral picornavirus-like (PVL) particles, 23 nm in diameter, forming paracrystalline arrays were seen in the cytoplasm of various cells in Cotylogaster occidentalis. Viral inclusions were visible in live specimens and in sections prepared for light and electron microscopy. All worms examined over a 2-year period were found to be infected. Infections were naturally acquired and susceptibility was not associated with any particular developmental stages. Development of viral inclusions involved an increase in the inclusion volume, progressive accumulation and condensation of materials into the interior of the inclusions, and formation of multilamellar membrane networks. Virus particles were observed in the stroma of the inclusions in association with multilamellar spherical bodies. Mature PVL particles aggregated into polygonally shaped paracrystalline arrays. When such arrays occurred in the surface tegument, local disruption of the tegumentary membrane may liberate these particles into the environment. PVL particle production did not exhaust glycogen content of infected cells and did not appear to affect short-term survival of the parasite outside the molluscan host.     

Recombinant soluble human complement receptor type 1 inhibits inflammation in the reversed passive arthus reaction in rats.

The human CR1 was genetically engineered by site directed mutagenesis into a truncated form which was secreted from transfected Chinese hamster ovary cells. This soluble recombinant CR1 (sCR1) was purified from the supernatants of the Chinese hamster ovary cells cultured in a hollow fiber bioreactor. sCR1 inhibits the C3 and C5 convertases of the classical and the alternative pathways in vitro. The ability of sCR1 to inhibit the immune complex-mediated inflammation in vivo was tested in a rat reversed passive Arthus reaction model. Administration of sCR1 at the dermal sites reduced the Arthus vasculitis in a dose-dependent manner as judged by both gross and microscopic examination, as well as by immunohistologic localization of C3 and C5b-9 neoantigen deposits. These data suggest that sCR1 inhibits the Arthus reaction by interrupting the activation of the C cascade, hence limiting the detrimental immune complex-induced tissue damage in vivo.     

Interaction of selenium deficiency and fat intake in the regulation of enzymes associated with peroxide metabolism

The present study was designed to examine the effect of selenium deficiency on the activities of heme hydroperoxidase and glutathione peroxidases in the liver of male rats maintained on either a 5% or a 25% corn oil diet and treated with phenobarbital. Our results showed that although the basal levels of cytochrome P-450 and heme hydroperoxidase were unaffected by selenium deficiency, the magnitude of phenobarbital induction was impaired because of the depletion of this trace element. This effect was accentuated especially in rats with a high-fat intake. Selenium deprivation resulted in a virtual disappearance of glutathione peroxidase activity when assayed with hydrogen peroxide, because of depletion of the selenium-dependent enzyme. In contrast, only a 60% reduction in glutathione peroxidase activity was observed when assayed with cumene hydroperoxide. Phenobarbital administration was found to increase the activity of the latter only. Unlike the situation with the hemoprotein, dietary fat had no influence on either the basal or stimulated glutathione peroxidase activities, regardless of the selenium status of the animals.     

Shell formation in the giant clam,Tridacna squamosa,may involve an apical Na+/Ca2+ exchanger 3 homolog in the shell-facing epithelium of the whitish inner mantle,which displays light-enhanced gene and protein expression

Coral Reefs - Na+/Ca2+ exchangers (NCXs) transport one Ca2+ in exchange for three Na+ and may participate in the calcification processes of mammalian osteoblasts and invertebrate calcifying cells....     

Intercontinental Spread of Asian-Origin H5N8 to North America through Beringia by Migratory Birds

Phylogenetic network analysis and understanding of waterfowl migration patterns suggest that the Eurasian H5N8 clade 2.3.4.4 avian influenza virus emerged in late 2013 in China, spread in early 2014 to South Korea and Japan, and reached Siberia and Beringia by summer 2014 via migratory birds. Three genetically distinct subgroups emerged and subsequently spread along different flyways during fall 2014 into Europe, North America, and East Asia, respectively. All three subgroups reappeared in Japan, a wintering site for waterfowl from Eurasia and parts of North America.