Detection of Anticholinesterase Agents in Drinking Water by use of Tandem Packed Bed Reactors with Human Red Blood Cell Acetylcholinesterase and Choline Oxidase in a Switching Flow System

It has been reported that the repeated topical, nonoccluded application of acetone may modulate antibody production in mice, thus producing humoral immunosuppression. However, the evaporative loss expected following nonoccluded dermal application of acetone makes the systemic effect seem unlikely. This study was designed to investigate the immunotoxicity potential of acetone in mice following a more direct systemic route of dosing via drinking water for 28 days. CD-1 male mice consumed average daily acetone doses of 121, 621 or 1144 mg/kg/day. The antibody, plaque-forming cell (AFC) assay was performed to measure the T cell–dependent, anti-sheep red blood cell immunoglobulin M (IgM) response, and hematology and thymus weights were evaluated to provide additional insight into the potential effects to the immune system. Body weights, white blood cell (WBC), numbers, red blood cell (RBC) counts, and hemoglobin and hematocrit levels showed no treatment-related effects at any dose of acetone. Eosinophil percentages were variable but also showed no dose-related trends. Spleen and thymus weights were not statistically different from controls and there were no effects on spleen cellularity or AFC response as a result of acetone administration. The AFC responses ranged from 1088 to 1401 AFCs/106 splenocytes and were not statistically different from controls (1277 AFCs/106 cells). Mice treated with cyclophosphamide (20 mg/kg) on days 25 to 28 demonstrated a 94% reduction in AFC/106 cells. Thus, the direct systemic administration of acetone did not produce evidence for immunotoxicity in CD-1 mice and the no observed adverse effect level (NOAEL) in this study was determined to be 1144 mg/kg/day.

Download Full-text

Experimental and modelling study of drinking water hydrogenotrophic denitrification in packed-bed reactors

Journal of Hazardous Materials ◽

10.1016/j.jhazmat.2008.10.067 ◽

2009 ◽

Vol 165 (1-3) ◽

pp. 812-824 ◽

Cited By ~ 23

Author(s):

I.A. Vasiliadou ◽

K.A. Karanasios ◽

S. Pavlou ◽

D.V. Vayenas

Keyword(s):

Drinking Water ◽

Packed Bed ◽

Packed Bed Reactors ◽

Modelling Study

Download Full-text

Impaired Hemostasis Caused By Deficit of Tissue Factor-Triggered Blood Coagulation Leads to Alveolar Hemorrhages and Increased Mortality in Influenza A Infection

Blood ◽

10.1182/blood.v124.21.2805.2805 ◽

2014 ◽

Vol 124 (21) ◽

pp. 2805-2805

Author(s):

Kohei Tatsumi ◽

Silvio Antoniak ◽

Justin Milner ◽

Melinda Beck ◽

Nigel Mackman

Keyword(s):

Drinking Water ◽

Blood Cell ◽

Red Blood Cell ◽

Influenza A ◽

Influenza Infection ◽

Coagulation Cascade ◽

Wild Type ◽

Body Weights ◽

Deficient Mice

Abstract Objective: Viral infections lead to activation of coagulation which enhances inflammatory responses. For instance, influenza A is associated with activation of coagulation and the increased risk for thrombotic events, such as myocardial infarction. Here we investigated the role of the coagulation cascade and platelets in influenza A virus (IAV) infection in mice. Methods: To investigate the role of the coagulation cascade in influenza infection, we examined the effect of either low levels of tissue factor or wild-type mice that were administered with 4 μg/mL of warfarin via drinking water. To study the role of platelets in influenza infection, we examined protease-activated receptor 4 (PAR-4, the main functional receptor on mouse platelets) deficient mice or wild-type mice treated with 0.15 mg/mL of clopidogrel or 0.4 mg/mL of aspirin via drinking water. All mice were infected intranasally with mouse adapted influenza A H1N1/PR8 (IAV). Changes in body weights and survival were analyzed up to 14 days after infection. In addition, bronchoalveolar lavage fluid (BALF) or lungs were collected and analyzed 7 or 14 days after virus challenge. Results: LowTF mice exhibited higher mortality rate and increased loss of body weights compared to littermate control mice after IAV infection (P<0.01). At day 7, BALF of LowTF was red and had increased red blood cell numbers and hemoglobin levels compared to infected control mice (P<0.001). Thrombin-antithrombin complex (TAT) levels in the BALF of infected LowTF mice were lower than that of control mice. In addition, lung histology revealed that LowTF mice had extensive hemorrhages. Similarly, mice treated with warfarin and infected with IAV showed higher mortality compared with the warfarin-treated mice without infection or IAV-infected mice without drugs. Warfarin treated mice also had red BALF, higher red blood cell number and hemoglobin levels in the BALF, and lung bleeding. PAR-4 deficient mice exhibited visible lung hemorrhages with increased hemoglobin levels in the BAL (P<0.01) and increased mortality compared to controls (P<0.05), although the bleeding was less than LowTF mice. Treatment of mice with clopidogrel or aspirin did not increased lung bleeding or mortality. Conclusion: Pulmonary hemostasis requires both TF-mediated activation of blood coagulation and thrombin activation of platelets during IAVinfection. Use of antithrombotics during IAV infection may increase the risk of lung bleeding. Disclosures No relevant conflicts of interest to declare.

Download Full-text