GrapheneBased Multi purpose Textile for Detecting and also Actuating

The epidemiological correlation between copper exposure and higher risk of Parkinson disease (PD) has been recognized for a long time, and microglia-mediated neuroinflammation has reported to be an important component of the pathogenesis of PD. The present study aimed to investigate the role of microglial activation and neuroinflammation in copper neurotoxicity and the underlying mechanism of copper-induced activation of microglia. Based on the inflammatory changes in mouse brain tissues, the activation of microglia, the loss of dopaminergic neurons and the aggregation of α-syn were found in the substantia nigra. In this study we found that copper significantly caused inflammatory activation of BV2 cells. Importantly, copper increased the level of reactive oxygen species (ROS) in BV2 cells, and then activated the NF-κB pathway which acted as an early survival signal. Further study indicated that sustained copper accumulation in BV2 cells led to the decrease of mitochondrial membrane potential, reduction of Parkin and PINK1 expression, increase of P62 expression and LC3BⅡ/I ratio, as well as upregulation of NLRP3/caspase1/GSDMD axis proteins. In addition, the increased release of inflammatory factors was rescued by redox agent, NF-κB pathway inhibitor and mitophagy inducer. This work illustrated that copper exposure activates microglia to secrete inflammatory products, resulting in the pyroptosis of dopaminergic neurons, which was related to the early activation of ROS/NF-κB pathway and subsequent mitophagy disorder in BV2 cells.Heterocyclic aromatic amines (HAAs) are a class of hazardous compounds produced in food thermal processing. These compounds raise concerns because they have mutagenic and carcinogenic properties. However, the neurotoxicity of these compounds has received limited attention. Here, the toxic effects of three HAAs, i.e. 9H-pyrido[3,4-b]indole (Norharman), 1-methyl-9H-pyrido[3,4-b]indole (Harman), and 2-amino-3-methylimidazole[4,5-f]quinoline (IQ) were investigated in Neuro-2a cells model. The results showed that the survival rate of cells decreased in a dose-dependent manner and apoptosis occurred after exposure to the three HAAs for 24 h and 48 h. Their neurotoxicity was ranked as Harman > Norharman > IQ. Further, treatment of Harman, Norharman, or IQ at 50 and 100 μM for 48 h led to intracellular REDOX imbalance, which was manifested as increased ROS and malondialdehyde (MDA) levels, decreased GSH/GSSG ratio, and reduced SOD and CAT activities. Moreover, Norharman and Harman up-regulated the expression level of nuclear factor erythroid 2-related factor 2 (Nrf2), as well as the mRNA levels of Heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoredutase1 (NQO1), while IQ had no significant effect on the levels of Nrf2, HO-1, and NQO1. Additionally, Harman, Norharman, or IQ exposure significantly reduced mitochondrial membrane potential and intracellular ATP levels and up-regulated the levels of apoptosis-related genes and proteins. Collectively, our finding suggested that HAAs were neurotoxic, with mechanisms related to induction of oxidative stress and mitochondrial dysfunction.In this work, europium ion was doped into boron phosphate nanoparticles (BPO4) using an ultrasonic method followed by the calcination process. The nanoparticles were characterized by various techniques such as X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), photoluminescence spectroscopy, transmission electron microscopy (TEM), and Fourier-transform infrared spectroscopy (FT-IR), Raman spectroscopy, and scanning electron microscopy (SEM). Doping of europium ion into the BPO4 host crystal was proved by cell volume calculation from XRD patterns, the shift in Raman spectra, and photoluminescence properties. In addition, the europium doped boron phosphate (BPE) as a fluorescence sensor for the quantification of Zn2+ cation was studied. tetrathiomolybdate mouse The obtained results showed the enhancement and shift of the photoluminescence peak from 292 to 340 nm. The sensor's selectivity toward this ion was verified in the presence of a variety of common interfering cations. Surprisingly, BPE revealed excellent selectivity and sensitivity towards Zn2+ in the presence of Pb2+, Na+, Fe2+, Al3+, Ca2+, Mg2+, Cu2+, Co2+, Ni2+, Mn2+, Cd2+, Hg2+, Ba2+ and Fe3+ cations. The fluorescence response was linearly proportional to the Zn2+concentration. After the addition of trace amounts of Zn2+ ions into the aqueous solution, a significant enhancement of fluorescence emission occurred with the detection limit of 0.3 μM.The present study was designed to examine if dietary fat sources that have shown differences in lifespan and if some aging-related aspects can modulate the range of histopathologic changes in central nervous and endocrine systems that occur during the lifespan of Wistar rats. Moreover, it was attempted to gain insight into the relationship between longevity and the development of the different pathological changes, as well as possible interaction with diet. In order to achieve this, male Wistar rats were randomly assigned to three experimental groups fed semisynthetic and isoenergetic diets from weaning until death with different dietary fat sources, namely virgin olive, sunflower, or fish oil. An individual follow-up until death of each animal was performed. Incidence, severity, and burden of specific or group (i.e., neoplastic or non-neoplastic proliferative and non-proliferative) of lesions was calculated along with individual's disease and individual organ lesion burden. Most of the histopathological lesions found have been described in previous studies. Neoplasms, and in particular pituitary adenomas followed by brain tumors, were the most prevalent lesions found in the rats and the main cause of death involving both systems. Incidence of brain lesions was associated with age-at-death. Assayed dietary fats did not present differential effects on pathological changes occurring in endocrine and central nervous systems throughout rat lifespan.
Fish are the primary source of protein and docosahexaenoic acid (DHA) for pregnant women and children, but methylmercury (MeHg) pollution is the potential hazard of fish consumption. In risk assessments, the bio-accessibility of MeHg is usually assumed to be 100%, which could lead to overestimation of dietary exposure.
An existing PBTK model was adapted to estimate parameters of the bio-accessibility based on MeHg exposure data from a cohort of 397 Chinese pregnant women. The posterior distributions of parameters were determined by using the ABC - MCMC. RMSEP and Spearman's rank correlation coefficients (Rho) were calculated to determine the goodness of model fitting. The Monte Carlo analysis was performed for the parameter distributions to estimate the model variability.
The median of daily MeHg intake and maternal MeHg levels were 0.018μg/kg bw and 3.01μg/kg in the early and middle terms of pregnancy. The estimated bio-accessibility of freshwater fish, marine fish and others were 46.1, 17.3 and 58.2%, separately. The RMSEP improved from 11.18 to 2.54 and the Rho improved from 0.19 to 0.22 after bio-accessibility optimization. The model variability was estimated to be 2.6.
The bio-accessibility estimated in this study was comparable to that determined in previous in vitro studies. The optimized model could improve the prediction performance on the MeHg body burden by dietary exposure.
The bio-accessibility estimated in this study was comparable to that determined in previous in vitro studies. The optimized model could improve the prediction performance on the MeHg body burden by dietary exposure.The determination of food additives is one of the major points in the food industry that directly is relative to human health. This research work focused on sensing and monitoring sunset yellow as azo additive dyes in fruit juices using an electrochemical sensor amplified with Ni doped Pt decorated carbon nanotubes (NiO/Pt/CNTs) as nano-catalyst and 1-hexyl-3-methylimidazolium chloride ([HMIM][Cl]) as an ionic liquid binder. Carbon paste electrode (CPE) amplified with NiO/Pt/CNTs and [HMIM][Cl] (CPE/([HMIM][Cl])/NiO/Pt/CNTs) improved the sensitivity of sunset yellow sensing in aqueous solution in acidic condition and successfully monitored this azo dye in concentration range 1.0 nM-280 μM with detection limit 0.4 nM. On the other hand, the CPE/([HMIM][Cl])/NiO/Pt/CNTs was used for sensing and analysis of sunset yellow in different fruit juices, and recovery data between 98.65% and 103.66% confirmed the powerful ability of sensor for monitoring of sunset yellow in food samples.Pendimethalin is globally registered for control of a wide range of weeds in agriculture and home landscaping. Human exposure to pendimethalin can occur by the oral route through food and other sources. Endothelial function is vital to numerous biological processes, and endothelial dysfunction and poor vascular health is associated with increased atherosclerotic events; however, no study has yet investigated the potential effect of pendimethalin on endothelial function and vasculature formation. The objective of the current study is to investigate if pendimethalin may affect the viability and function of vascular endothelial cells. We observed that pendimethalin significantly repressed viability of human endothelial cells, inducing G1 cell cycle arrest and apoptotic/necrotic cell death. Pendimethalin treatment also activated ER stress and autophagy, leading to loss of mitochondrial membrane potential. In addition, pendimethalin impaired the tube forming and migratory abilities of endothelial cells. This study provides previously unrecognized adverse effects of pendimethalin in vascular endothelial cells, mediated by ER stress-induced mitochondrial dysfunction.Autism spectrum disorder (ASD) is a neurodevelopmental disorder that includes several key neuropathological changes and behavioral impairments. In utero exposure to the anti-epileptic valproic acid (VPA) increases risk of an ASD diagnosis in human subjects and timed in utero exposure to VPA is a clinically relevant animal model of ASD. Many human subjects with ASD have cerebellar hypoplasia, fewer Purkinje cells, difficulties with balance, ophthalmic dysfunction and abnormal responses to vestibular stimulation and such vestibular difficulties are likely under reported in ASD. We have recently shown that animals exposed to VPA in utero have fewer neurons in their auditory brainstem, reduced axonal projections to the auditory midbrain and thalamus, reduced expression of the calcium binding protein calbindin (CB) in the brainstem and cerebellum, smaller and occasionally ectopic cerebellar Purkinje cells and ataxia on several motor tasks. Based on these findings, we hypothesized that in utero VPA exposure similarly impacts structure and function of the vestibular brainstem. We investigated this hypothesis using quantitative morphometric analyses, immunohistochemistry for CB, a battery of vestibular challenges, recording of vestibular-evoked myogenic potentials and spontaneous eye movements. Our results indicate that VPA exposure results in fewer neurons in the vestibular nuclei, fewer CB-positive puncta, difficulty on certain motor tasks, longer latency VEMPs and significantly more horizontal eye movements. These findings indicate that the vestibular nuclei are impacted by in utero VPA exposure and provide a basis for further study of vestibular circuits in human cases of ASD.