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Nickel (Ni) is ubiquitous in the environment and evidence has suggested that Ni can cause ocular surface inflammation, especially in fine particulate matter and personal products. Continuous daily exposure to Ni-containing dust may adversely impact the human cornea, whereas the underlying mechanism of this phenomenon remains not fully understood. Here, human corneal epithelial cells (HCEC) were employed to analyze the toxicity of Ni via detections of cell morphology, cell viability, reactive oxygen species production, cell apoptosis rate, and apoptotic gene expression levels after exposure for 24 h to uncover the damage of Ni to the cornea. A concentration-dependent inhibition of HCECs' viability and growth was observed. In particular, Ni at 100 μM significantly decreased cell viability to 76%, and many cells displayed an abnormal shape and even induced oxidative damage of HCEC by increasing ROS to 1.2 times, and further led to higher apoptosis (24%), evidenced by up-regulation of apoptotic genes Caspase-8, Caspase-9, NF-κB, IL-1β, and Caspase-3, posing a risk of dry eye. Our study suggested that Ni induces apoptosis of HCEC through oxidative damage. Therefore, Ni pollution should be comprehensively considered in health risks or toxic effects on the ocular surface. [ABSTRACT FROM AUTHOR]

The field of cholecystokinin (CCK) stimulation of exocrine pancreatic secretion has experienced major changes in the recent past. This review attempts to summarize the present status of the field. CCK production in the intestinal I cells, the molecular forms of CCK produced and subsequently circulated in the blood, the presence or absence of CCK receptors on the isolated pancreatic acinar cells and the associated signaling for acinar cell secretion, and the actual circuits and sites of action for CCK regulation of exocrine pancreatic secretion in vivo are reviewed in different animal species with an emphasis on birds, rodents, and humans. Clear differences in the relative importance of neural and direct modes of CCK action on pancreatic acinar cells were identified. Rodents seem to be endowed with both modes of action, whereas in humans the neural mode may predominate. In birds, such as duck, the direct mode needs further assistance from pituitary adenylate cyclaseactivating peptide/VIP receptors. However, much further work needs to be directed to the neural mode to map out all sites of CCK action and details of the full circuits, and we foresee a major revival for this field of research in the near future. pancreatic acinar cells; vagal afferent nerves; plasma cholecystokinin concentration; species specificity

Arsenic (As) is a carcinogen and it is ubiquitous in the environment. Its accumulation in plants can enter the food chain, thereby causing adverse impacts on human health. Based on studies using Xenopus oocytes, engineered microbes, and model plants, aquaporins play key roles in arsenite (AsIII) passage across the cell membrane. Herein, we summarized the roles of aquaporins in AsIII uptake, transport, and accumulation. The coupling action between polar-localized aquaporins and positive transporters probably explains the efficient As transport mediated by bi-directional channels. The expression of aquaporins is regulated at both transcriptional and post-transcriptional levels via microRNAs. However, in response to As, the proteins can be modified through phosphorylation and be degraded via the ubiquitin 26S proteasome system. Further, a proposed model comprising reactive oxygen species, Ca, Ca-dependent kinases, and transcriptional factors is constructed to reveal the signaling pathways and aquaporins' responses to As in model plants. We also provided strategies to identify and investigate putative aquaporins in plants. Identification and modification of aquaporins' residues critical for their substrate selectivity, and optimization of their expression pattern by employing appropriate promoters can be employed to reduce As accumulation in crops. Based on the characteristics of their functions and expression patterns, it is promising to employ aquaporins for genetic-engineering of crops to reduce As content and increase food safety. [ABSTRACT FROM AUTHOR]

The field of cholecystokinin (CC K) stimulation of exocrine pancreatic secretion has experienced major changes in the recent past. This review attempts to summarize the present status of the field. CCK production in the intestinal I cells, the molecular forms of CCK produced and subsequently circulated in the blood, the presence or absence of CCK receptors on the isolated pancreatic acinar cells and the associated signaling for acinar cell secretion, and the actual circuits and sites of action for CCK regulation of exocrine pancreatic secretion in vivo are reviewed in different animal species with an emphasis on birds, rodents, and humans. Clear differences in the relative importance of neural and direct modes of CCK action on pancreatic acinar cells were identified. Rodents seem to be endowed with both modes of action, whereas in humans the neural mode may predominate. In birds, such as duck, the direct mode needs further assistance from pituitary adenylate cyclase-activating peptide/VIP receptors. However, much further work needs to be directed to the neural mode to map out all sites of CCK action and details of the full circuits, and we foresee a major revival for this field of research in the near future. [ABSTRACT FROM AUTHOR]

Deals with perspectives on healthcare in the context of Chinese culture. Social structure and values of the Chinese; Influence of religion on public health; Health beliefs and practices.

Tris(1,3-dichloro-2-propyl) phosphate (TDCPP), a widely used organophosphorus flame retardant, has been frequently detected in the environment including indoor dust. Long-term exposure to TDCPP-containing dust may adversely affect human skin, however, little is known about its potential cytotoxicity. In this study, human skin keratinocytes (HaCaT) were employed to study TDCPP-induced cytotoxicity and associated mechanisms. The effects of TDCPP on cell morphology, viability, apoptosis, and cycle, and the mRNA levels of apoptosis (Bcl-2 , Bax and Caspase-3) and cell cycle (cyclin D1 , CDK2 , CDK4 and CDK6) regulatory genes were investigated. The results showed that TDCPP caused a concentration-dependent decrease in cell viability after exposing to TDCPP ≥100 μg/mL for 48 h, with a median lethal concentration of 163 μg/mL (LC 50). In addition, TDCPP induced cell apoptosis and arrested cell cycle in the G0/G1 phase at 16 and 160 μg/mL by enhancing Bax and Caspase-3 expression besides inhibiting cyclin D1 , CDK2 , CDK6 and Bcl-2 expression. Our results showed that TDCPP-induced toxicity in HaCaT cells was probably through cell apoptosis and cell cycle arrest. This study provides information on the toxicity of TDCPP to human skin cells, which may help to reduce its toxicity to human skin. Unlabelled Image • Human skin is exposed to TDCPP-containing dust on a daily basis; • We examined effects of TDCPP on normal human skin keratinocytes (HaCaT); • TDCPP decreased cell viability, and induced cell cycle arrest and apoptosis; • TDCPP enhanced the expression of apoptosis related genes Bax and Caspase3 ; • TDCPP decreased the expression of cell cycle related genes cyclin D1 , CDK2 , and CDK6. [ABSTRACT FROM AUTHOR]

Indoor dust often contains organic contaminants, which adversely impacts human health. In this study, the organic contaminants in the indoor dust from commercial offices and residential houses in Nanjing, China were extracted and their effects on human breast cancer cells (MCF-7) were investigated. Both dust extracts promoted proliferation of MCF-7 cells at ≤24 μg/100 μL, with cell viability being decreased with increasing dust concentrations. Based on LC 50 , house dust was less toxic than office dust. At 8 μg/100 μL, both extracts caused more MCF-7 cells into active cycling (G2/M + S) and increased intracellular Ca2+ influx, with house dust inducing stronger effects than office dust. Further, the expression of estrogen-responsive genes for TFF1 and EGR3 was enhanced by 3-9 and 4-9 folds, while the expression of cell cycle regulatory genes for cyclin D was enhanced by 2-5 folds. The results suggested that organic dust extract influenced cell viability, altered cell cycle, increased intracellular Ca2+ levels, and activated cell cycle regulatory and estrogen-responsive gene expressions, with house dust showing lower cytotoxicity but higher estrogenic potential on MCF-7 cells. The results indicate the importance of reducing organic contaminants in indoor dust to mitigate their adverse impacts on human health. Unlabelled Image • Effects of organic dust extract on human breast cancer cells (MCF-7) were examined. • Both extracts stimulated proliferation of MCF-7 cells at ≤24 μg/100 μL. • Extracts reduced cell viability, altered cell cycle and enhanced intracellular Ca2+. • Extracts increased expression of estrogen-responsive & cell cycle regulatory genes. • House dust induced lower toxicity but higher estrogenic potential on MCF-7 cells. [ABSTRACT FROM AUTHOR]