Report on the 2014 Proficiency Test of the European Union Reference Laboratory for Mycotoxins, for the Network of National Reference Laboratories - Determination of Aflatoxin B1 in Copra (Coconut powder)

This report presents the results of the PT of the EURL for Mycotoxins which focused on the determination of aflatoxin B1 (Afla B1) in coconut powder samples. Sixty-one participants from 31 countries registered for the exercise and fifty-eight sets of results were reported. Only z-scores were used for an evaluation of performance. In total 91 % of the attributed z scores were below an absolute value of two, which indicated that most of the participants performed satisfactorily.JRC.D.5-Standards for Food Bioscienc

Bacteroides fragilis polysaccharide A induces IL-10 secreting B and T cells that prevent viral encephalitis

The gut commensal Bacteroides fragilis or its capsular polysaccharide A (PSA) can prevent various peripheral and CNS sterile inflammatory disorders. Fatal herpes simplex encephalitis (HSE) results from immune pathology caused by uncontrolled invasion of the brainstem by inflammatory monocytes and neutrophils. Here we assess the immunomodulatory potential of PSA in HSE by infecting PSA or PBS treated 129S6 mice with HSV1, followed by delayed Acyclovir (ACV) treatment as often occurs in the clinical setting. Only PSA-treated mice survived, with dramatically reduced brainstem inflammation and altered cytokine and chemokine profiles. Importantly, PSA binding by B cells is essential for induction of regulatory CD4+ and CD8+ T cells secreting IL-10 to control innate inflammatory responses, consistent with the lack of PSA mediated protection in Rag−/−, B cell- and IL-10-deficient mice. Our data reveal the translational potential of PSA as an immunomodulatory symbiosis factor to orchestrate robust protective anti-inflammatory responses during viral infections

Bacteroides fragilis polysaccharide A induces IL-10 secreting B and T cells that prevent viral encephalitis

The gut commensal Bacteroides fragilis or its capsular polysaccharide A (PSA) can prevent various peripheral and CNS sterile inflammatory disorders. Fatal herpes simplex encephalitis (HSE) results from immune pathology caused by uncontrolled invasion of the brainstem by inflammatory monocytes and neutrophils. Here we assess the immunomodulatory potential of PSA in HSE by infecting PSA or PBS treated 129S6 mice with HSV1, followed by delayed Acyclovir (ACV) treatment as often occurs in the clinical setting. Only PSA-treated mice survived, with dramatically reduced brainstem inflammation and altered cytokine and chemokine profiles. Importantly, PSA binding by B cells is essential for induction of regulatory CD4+ and CD8+ T cells secreting IL-10 to control innate inflammatory responses, consistent with the lack of PSA mediated protection in Rag−/−, B cell- and IL-10-deficient mice. Our data reveal the translational potential of PSA as an immunomodulatory symbiosis factor to orchestrate robust protective anti-inflammatory responses during viral infections

Carbamates: a study on genotoxic, cytotoxic, and apoptotic effects induced in Chinese hamster ovary (CHO-K1) cells

In vitro effects of the carbamates pirimicarb and zineb and their formulations Aficida® (50% pirimicarb) and Azzurro® (70% zineb), respectively, were evaluated in Chinese hamster ovary (CHO-K1) cells. Whereas the cytokinesis-blocked micronucleus cytome assay was employed to test for genotoxicity, MTT, neutral red (NR), and apoptosis evaluation were used as tests for estimating cell viability and succinic dehydrogenase activity, respectively. Concentrations tested were 10–300 μg/ml for pirimicarb and Aficida®, and 1–50 μg/ml for zineb and Azzurro®. All compounds were able to increase the frequency of micronuclei. A marked reduction in the nuclear division index was observed after treatment with 5 μg/ml of zineb and Azzurro® and 10 μg/ml of Azzurro®. Alterations in the cellular morphology not allowing the recognition of binucleated cells exposed to 300 μg/ml pirimicarb and Aficida® as well as 10–50 μg/ml zineb and Azzurro®. All four compounds induced inhibition of both cell viability and succinic dehydrogenase activity and trigger apoptosis in CHO-K1 cells, at least when exposed for 24 h. The data herein demonstrate the genotoxic and cytotoxic effects exerted by these carbamates and reveal the potential risk factor of these pesticides, still extensively used worldwide, for both human health and the environment.Fil: Soloneski, Sonia Maria Elsa. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo. Catedra de Citologia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Kujawski, Maciej. City of Hope Comprehensive Cancer Center; Estados UnidosFil: Scuto, Anna. City of Hope Comprehensive Cancer Center; Estados UnidosFil: Larramendy, Marcelo Luis. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo. Catedra de Citologia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Effects of ibuprofen and venlafaxine on behavioural parameters in freshwater bivalve

The pollution of aquatic ecosystems by pharmaceuticals is presently recognized as a serious threat. The drug residues may contaminate surface waters via sewage discharges as well as improper disposal of industrial waste. Very few studies focused on the effects of drug pollutants on behaviour of invertebrates. In this study the effects of ibuprofen and venlafaxine on activity of the Unio tumidus were studied. Changes in behaviours were analysed at concentrations corresponding to wastewater discharges (3.4, 6.8 and 13.6 μgL−1). At dosage of 3.4 μgL−1, ibuprofen affected the activity time and shell opening level. The reduction in activity was particularly evident during the first few days. The same dose of venlafaxine caused hyperactivity of bivalves during the first few days of exposition. The highest doses (13.6 μgL−1) same drugs promoted reduction of activity and shell opening level. Moreover, exposure to these drugs resulted in the reduced water filtering time and hence its purification. The Unio tumidus reaction may indicate negative reaction of other aquatic species to the tested drugs

DNA damage kinetics and apoptosis in ivermectin-treated chinese hamster ovary cells

A comet assay was used to analyze DNA damage kinetics in Chinese hamster ovary (CHO-K1) cells induced by antiparasitic ivermectin (IVM) and the IVM-containing technical formulation IvomecW (IVO; 1% IVM). Cells were treated with 50 mg ml–1 IVM and IVO for 80 min, washed and re-incubated in antiparasiticide-free medium for 0–24 h until assayed using the single-cell gel electrophoresis assay (SCGE). Cell viability remained unchanged up to 3 h of incubation. After 6 h of treatment, cell survival decreased up to 75% and 79% in IVM- and IVO-treated cultures, respectively, remaining unchanged within 12–24 h after treatment. For both anthelmintics, biphasic behavior in DNA damage occurred during the incubation time. A time-dependent increase of IVM- and IVO-induced DNA damage was observed within 0 to 3 h after pulse treatment, revealed by a progressive decrease of undamaged cells and an increase in slightly damaged and damaged cells. Finally, a time-dependent decrease in IVM- and IVO-induced DNA damage was revealed by a progressive decrease of slightly damaged cells and the absence of damaged cells simultaneously with an increase in the frequency of undamaged cells during the final 18 h of incubation. Flow cytometry analysis revealed that both compounds are able to induce a marked increase in early and late apoptosis. Based on our observations, we could conclude that the decrease in DNA lesions is mostly related to IVMinduced cytotoxicity rather than attributable to a repair process. Copyright © 2012 John Wiley & Sons, Ltd.Fil: Molinari, Gabriela Beatriz. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Kujawski, Maciej. City of Hope Comprehensive Cancer Center; Estados UnidosFil: Scuto, Anna. City of Hope Comprehensive Cancer Center; Estados UnidosFil: Soloneski, Sonia Maria Elsa. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Larramendy, Marcelo Luis. Universidad Nacional de La Plata. Facultad de Ciencias Naturales y Museo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin