We confirmed the binding ability of GPER1 with G1 and G15 in primary macrophages of C. carpio by testing the related gene expression levels after 6 h exposure, and similar to G1, bisphenol A (BPA), a typical environmental estrogen, could interact with GPER1 to increase the Ca2+ concentration in macrophages treated for 30 min. Furthermore, inhibition of GPER1 with GPER1 antagonist G36 rescued the cellular immunotoxicity caused by BPA, which further suggested that carp GPER1 could mediate the estrogen effect. Our findings contribute to better understanding of the role of carp GPER1.Nitrite can cause fishes poisoning. This study evaluated the effects of nitrite exposure on haematological status, ion concentration, antioxidant enzyme activity, immune response, cytokine release and apoptosis in yellow catfish. https://www.selleckchem.com/products/apx2009.html In this study, yellow catfish were exposed to three levels of nitrite (0, 3.00 and 30.00 mg L-1) for 96 h. The results showed that nitrite poisoning could lead to blood deterioration (red blood cell and hemoglobin reduced; white blood cell and methemoglobin elevated), ion imbalance (Na+ and Cl- declined; K+ elevated), oxidative stress (total antioxidant capacity, superoxide dismutase, catalase and glutathione peroxidase activities declined; malondialdehyde accumulation), immunosuppression (lysozyme activity, 50% hemolytic complement, immunoglobulin M, respiratory burst and phagocytic index declined) and cytokines release (TNF, IL 1 and IL 8 elevated). In addition, nitrite poisoning could induce up-regulation of antioxidant enzymes (Cu/Zn-SOD, Mn-SOD, CAT and GPx), cytokines (TNF, IL 1 and IL 8) and apoptosis (P53, Bax, Cytochrome c, Caspase 3, Caspase 9, ERK and JNK) genes transcription. This study suggesting that the nitrite exposure triggers blood deterioration, disrupts the ionic homeostasis, induces oxidative stress, immunosuppression, inflammation and apoptosis in yellow catfish.
Deficits in child growth are associated with poor cognitive outcomes and an increased risk for infection and mortality globally. One hundred forty million people are chronically exposed to arsenic from contaminated drinking water worldwide. While arsenic exposure has been associated with cognitive developmental delays in children, there is limited research on the association between arsenic exposure and growth deficits in young children.

The objective of this study was to assess the association between chronic arsenic exposure and deficits in growth among children under 5 years in a rural setting in Bangladesh.

Urinary arsenic measurements were collected from 465 children between the ages of 28 days-59 months in rural Matlab, Bangladesh, and analyzed by graphite furnace atomic absorption. Height and weight measurements were collected from children according to World Health Organization child growth standards. A z-score cutoff2 standard deviations below the mean was used to define stunting (height-for-agg young children in rural Bangladesh.
Lead (Pb) is widespread and exposure to this non-essential heavy metal can cause multiple negative health effects; however the mechanisms underlying these effects remain incompletely understood.

To identify plasma metabolomic signatures of Pb exposure, as measured in blood and toenails.

In a subset of men from the VA Normative Aging Study, mass-spectrometry based plasma metabolomic profiling was performed. Pb levels were measured in blood samples and toenail clippings collected concurrently. Multivariable linear regression models, smoothing splines and Pathway analyses were employed to identify metabolites associated with Pb exposure.

In 399 men, 858 metabolites were measured and passed QC, of which 154 (17.9%) were significantly associated with blood Pb (p<0.05). Eleven of these passed stringent correction for multiple testing, including pro-hydroxy-pro (β(95%CI) 1.52 (0.93,2.12), p=7.18x10
), N-acetylglycine (β(95%CI) 1.44 (0.85,2.02), p=1.12x10
), tartarate (β(95%CI) 0.68 (0.35,1.00), p=4.84x1se findings help us to better understand the biology of this important public health burden.
Pb exposure is responsible for 0.6% of the global burden of disease and metabolomics is particularly well-suited to explore its pathogenic mechanisms. In this study, we identified metabolites and metabolomic pathways associated with Pb exposure that suggest that Pb exposure acts through oxidative stress and immune dysfunction. These findings help us to better understand the biology of this important public health burden.
Asthma is a heterogeneous disease with multiple phenotypes; however, the relevance of phenotype overlap remains largely unexplored.

To examine the relationship between phenotype overlap and clinical and inflammatory profiles of asthma.

In this cross-sectional study, adult participants with stable asthma (n= 522) underwent multidimensional assessments. The 10 most common phenotypes of asthma were defined and then classified into those commonly associated with Type (T) 2 or non-T2 inflammation. Furthermore, phenotype overlap scores (POS), representing the cumulative concomitant phenotypes, were used to analyze its association with clinical and inflammatory asthmatic profiles.

Among the 522 participants, 73.4% (n= 383) had phenotype overlap, and mixed T2 and non-T2 inflammation coexisted in 47.5% (n= 248). T2 POS was positively associated with eosinophils, IgE, and fractional exhaled nitric oxide (FeNO), and negatively with Asthma Quality of Life Questionnaire (AQLQ), sputum neutrophils, IL-17A, IL-8, anhenotypes associated with mixed T2 and non-T2 inflammation might be unresponsive to medications owing to increased non-T2 inflammation. Multidimensional asthma assessment identifies clinically relevant phenotype overlap.
There is limited information regarding the impact of dose and gestational timing of oral corticosteroid (OCS) use on preterm birth (PTB), especially among women with asthma.

To evaluate OCS dose and timing on PTB for asthma and, as a comparison, systemic lupus erythematosus (SLE).

We used health care data from California Medicaid enrollees linked to birth certificates (2007-2013), identifying women with asthma (n= 22,084) and SLE (n= 1174). We estimated risk ratios (RR) for OCS cumulative dose trajectories and other disease-related medications before gestational day 140and hazard ratios (HR) for time-varying exposures after day139.

For asthma, PTB risk was 14.0% for no OCS exposure and 14.3%, 16.8%, 20.5%, and 32.7% in low, medium, medium-high, and high cumulative dose trajectory groups, respectively, during the first 139 days. The high-dose group remained associated with PTB after adjustment (adjusted RR [aRR] 1.46; 95% confidence interval [CI] 1.00, 2.15). OCS dose after day 139 was not clearly associated with PTB, nor were controller medications.