Modeling of some nonstationary processes in tokamak plasmas

The results of modeling of shots from two series of experiments in two tokamaks with rather different geometric parameters are presented. The first one includes two shots from the spherical tokamak MAST with current ramp up, and the second one, a number of T-10 shots with periodic gas puffing. The modeling was performed with the ASTRA code in the framework of Canonical Profiles Transport Model (CPTM).Представлены результаты моделирования импульсов из двух серий экспериментов на двух разных токамаках, существенно отличающихся геометрическими параметрами. Первая серия включает два импульса с нарастанием тока сферического токамака MAST, а вторая – несколько импульсов Т-10 с периодическим газонапуском. Моделирование осуществлялось с помощью кода ASTRA в рамках транспортной модели канонических профилей (ТМКП).Представлені результати моделювання імпульсів з двох серій експериментів на двох різних токамаках, що істотно відрізняються геометричними параметрами. Перша серія включає два імпульси з наростанням струму сферичного токамака МАST, а друга – декілька імпульсів Т-10 з періодичним газонапуском. Моделювання здійснювалося за допомогою коду ASTRA в рамках транспортної моделі канонічних профілів (ТМКП)

Gut as a target for cadmium toxicity

The primary objective of the present study was to review the impact of Cd exposure on gut microbiota and intestinal physiology, as well as to estimate whether gut may be considered as the target for Cd toxicity. The review is based on literature search in available databases. The existing data demonstrate that the impact of Cd on gut physiology is two-sided. First, Cd exposure induces a significant alteration of bacterial populations and their relative abundance in gut (increased Bacteroidetes-to-Firmicutes ratio), accompanied by increased lipopolysaccharide (LPS) production, reflecting changed metabolic activity of the intestinal microbiome. Second, in intestinal wall Cd exposure induces inflammatory response and cell damage including disruption of tight junctions, ultimately leading to increased gut permeability. Together with increased LPS production, impaired barrier function causes endotoxinemia and systemic inflammation. Hypothetically, Cd-induced increase gut permeability may also result in increased bacterial translocation. On the one hand, bacteriolysis may be associated with aggravation of endotoxemia. At the same time, together with Cd-induced impairment of macrophage inflammatory response, increased bacterial translocation may result in increased susceptibility to infections. Such a supposition is generally in agreement with the finding of higher susceptibility of Cd-exposed mice to infections. The changed microbiome metabolic activity and LPS-induced systemic inflammation may have a significant impact on target organs. The efficiency of probiotics in at least partial prevention of the local (intestinal) and systemic toxic effects of cadmium confirms the role of altered gut physiology in Cd toxicity. Therefore, probiotic treatment may be considered as the one of the strategies for prevention of Cd toxicity in parallel with chelation, antioxidant, and anti-inflammatory therapy. It is hypothesized that increased gut permeability, altered gut microbiota, endotoxinemia, and impaired inflammatory response may at least partially mediate the toxic effects of Cd exposure. © 2018 Elsevier Lt

Gut as a target for cadmium toxicity

The primary objective of the present study was to review the impact of Cd exposure on gut microbiota and intestinal physiology, as well as to estimate whether gut may be considered as the target for Cd toxicity. The review is based on literature search in available databases. The existing data demonstrate that the impact of Cd on gut physiology is two-sided. First, Cd exposure induces a significant alteration of bacterial populations and their relative abundance in gut (increased Bacteroidetes-to-Firmicutes ratio), accompanied by increased lipopolysaccharide (LPS) production, reflecting changed metabolic activity of the intestinal microbiome. Second, in intestinal wall Cd exposure induces inflammatory response and cell damage including disruption of tight junctions, ultimately leading to increased gut permeability. Together with increased LPS production, impaired barrier function causes endotoxinemia and systemic inflammation. Hypothetically, Cd-induced increase gut permeability may also result in increased bacterial translocation. On the one hand, bacteriolysis may be associated with aggravation of endotoxemia. At the same time, together with Cd-induced impairment of macrophage inflammatory response, increased bacterial translocation may result in increased susceptibility to infections. Such a supposition is generally in agreement with the finding of higher susceptibility of Cd-exposed mice to infections. The changed microbiome metabolic activity and LPS-induced systemic inflammation may have a significant impact on target organs. The efficiency of probiotics in at least partial prevention of the local (intestinal) and systemic toxic effects of cadmium confirms the role of altered gut physiology in Cd toxicity. Therefore, probiotic treatment may be considered as the one of the strategies for prevention of Cd toxicity in parallel with chelation, antioxidant, and anti-inflammatory therapy. It is hypothesized that increased gut permeability, altered gut microbiota, endotoxinemia, and impaired inflammatory response may at least partially mediate the toxic effects of Cd exposure. © 2018 Elsevier Lt