A Redescription of Periclimenes yaldwyni Holthuis (Brachycarpus audouini Bate, 1888, Crustacea, Decapoda, Palaemonidae) and Its Occurrence in Australian Waters

The pontoniine shrimp Periclimenes yaldwyni Holthuis is recorded for the first time from Australian waters and is redescribed and figured in detail to augment the original description and illustration provided by Bate (1888) as Brachycarpus audouini. The presently available data on carideans (eight spp.) occurring in both Australian and New Zealand waters are summarized

Rural Cooperatives Magazine, March/April 2003

Features- Hard choices; Turning problems into profits; Bargaining is big for small business; The “closure” dilemma; Network difficulties; Striking oil; A shared harves

Rural Cooperatives Magazine, March/April 2003

Features- Hard choices; Turning problems into profits; Bargaining is big for small business; The “closure” dilemma; Network difficulties; Striking oil; A shared harves

<it>In vitro </it>effects of selenium deficiency on West Nile virus replication and cytopathogenicity

Abstract Background Selenium (Se) deficiency plays an important role in viral pathogenesis. To understand the effects of Se deficiency on West Nile virus (WNV) infection, we analyzed cytopathogenicity, apoptosis and viral replication kinetics, using a newly developed Se-deficient cell culture system. Results Both Vero and SK-N-SH cells grown in Se-deficient media exhibited a gradual loss of glutathione peroxidase (GPx1) activity without any significant effect on cell growth and viability. In SK-N-SH cells, Se deficiency had no effect on the expression of key antioxidant enzymes, including manganese- and copper-zinc superoxide dismutase (MnSOD and CuZnSOD), catalase and inducible nitric oxide synthase, whereas Vero cells demonstrated a significant increase in the expression of MnSOD and an overall increase in oxidative stress (OS) at day 7 post-induction of Se deficiency. At 2 days after infection with WNV, CPE and cell death were significantly higher in WNV-infected Se-deficient Vero cells, compared to WNV-infected control cells. Furthermore, WNV-induced apoptosis was significantly heightened in Se-deficient cells and was contributed by loss of mitochondrial membrane potential and increased caspase activity. However, no significant difference was found in WNV copy numbers between control, Se-adequate and Se-deficient cell cultures. Conclusion Overall results demonstrate that the in vitro Se-deficient model can be used to study responses of WNV to this essential nutrient. Although Se deficiency has no in vitro effect on WNV replication kinetics, adequate Se is presumably critical to protect WNV-infected cells against virus-induced cell death.</p

In vitro effects of selenium deficiency on West Nile virus replication and cytopathogenicity

BACKGROUND: Selenium (Se) deficiency plays an important role in viral pathogenesis. To understand the effects of Se deficiency on West Nile virus (WNV) infection, we analyzed cytopathogenicity, apoptosis and viral replication kinetics, using a newly developed Se-deficient cell culture system. RESULTS: Both Vero and SK-N-SH cells grown in Se-deficient media exhibited a gradual loss of glutathione peroxidase (GPx1) activity without any significant effect on cell growth and viability. In SK-N-SH cells, Se deficiency had no effect on the expression of key antioxidant enzymes, including manganese- and copper-zinc superoxide dismutase (MnSOD and CuZnSOD), catalase and inducible nitric oxide synthase, whereas Vero cells demonstrated a significant increase in the expression of MnSOD and an overall increase in oxidative stress (OS) at day 7 post-induction of Se deficiency. At 2 days after infection with WNV, CPE and cell death were significantly higher in WNV-infected Se-deficient Vero cells, compared to WNV-infected control cells. Furthermore, WNV-induced apoptosis was significantly heightened in Se-deficient cells and was contributed by loss of mitochondrial membrane potential and increased caspase activity. However, no significant difference was found in WNV copy numbers between control, Se-adequate and Se-deficient cell cultures. CONCLUSION: Overall results demonstrate that the in vitro Se-deficient model can be used to study responses of WNV to this essential nutrient. Although Se deficiency has no in vitro effect on WNV replication kinetics, adequate Se is presumably critical to protect WNV-infected cells against virus-induced cell death

Nucleic Acid Amplification Assays for Detection of La Crosse Virus RNA

We report the development of nucleic acid sequence-based amplification (NASBA) and quantitative real-time reverse transcription (RT)-PCR assays for the detection of La Crosse (LAC) virus in field-collected vector mosquito samples and human clinical samples. The sensitivities of these assays were compared to that of a standard plaque assay in Vero cells. The NASBA and quantitative real-time RT-PCR assays demonstrated sensitivities greater than that of the standard plaque assay. The specificities of these assays were determined by testing a battery of reference strain viruses, including representative strains of LAC virus and other arthropod-borne viruses. Additionally, these assays were used to detect LAC viral RNA in mosquito pool samples and human brain tissue samples and yielded results within less than 4 h. The NASBA and quantitative real-time RT-PCR assays detect LAC viral RNA in a sensitive, specific, and rapid manner; these findings support the use of these assays in surveillance and diagnostic laboratory systems

SEROLOGIC EVIDENCE OF WEST NILE VIRUS INFECTION IN BIRDS, TAMAULIPAS STATE, MEXICO

Following the introduction of West Nile virus (WNV) into North America in 1999, surveillance for WNV in migratory and resident birds was established in Tamaulipas State, northern Mexico in December 2001. Overall, 796 birds representing 70 species and 10 orders were captured and assayed for antibodies to WNV. Nine birds had flavivirus-specific antibodies by epitope-blocking enzyme-linked immunosorbent assay; four were confirmed to have antibody to WNV by plaque reduction neutralization test. The WNV-infected birds were a house wren, mourning dove, verdin and Bewick's wren. The house wren is a migratory species; the other WNV-infected birds are presumably residents. The WNV-infected birds were all captured in March 2003. These data provide the first indirect evidence of WNV transmission among birds in northern Mexico

Effects of selenium deficiency on West Nile virus replication and cytopathogenicity-1

E extracted from control, Se- and Se+ Vero and SK-N-SH cells and GPx1 enzyme activity was measured at days 3, 7 and 10 post-induction of Se deficiency by using the cGPx1 assay kit. Data are reported as mean ± SD of triplicate experiments. * p < 0.05, ** p < 0.005 compared to control cells. Analyses of GPx1 protein by Western blot. 50 μg of total protein extracted from Vero and SK-N-SH cells grown in control, Se- and Se+ media were separated on PAGE, followed by immunoblotting with anti-GPx1. Equal loading was confirmed by re-blotting the same membranes with anti-β-actin.<p><b>Copyright information:</b></p><p>Taken from "effects of selenium deficiency on West Nile virus replication and cytopathogenicity"</p><p>http://www.virologyj.com/content/5/1/66</p><p>Virology Journal 2008;5():66-66.</p><p>Published online 31 May 2008</p><p>PMCID:PMC2453119.</p><p></p