Impact of Artificial Sunlight Aging on the Respiratory Effects of Polyethylene Terephthalate Microplastics through Degradation-Mediated Terephthalic Acid Release in Male Mice.

Microplastics are ubiquitous in the atmosphere, leading to human exposure through inhalation. Airborne microplastics undergo degradation due to sunlight irradiation, yet the respiratory risks associated with degraded microplastics remain poorly understood. In this study, we investigated the respiratory effects of polyethylene terephthalate (PET) degraded by artificial sunlight and created a transport and degradation model of PET for risk assessment.

Enhancement of keratinocyte survival and migration elicited by interleukin 24 upregulation in dermal microvascular endothelium upon welding-fume exposure.

Occupational exposure to welding fumes constitutes a serious health concern. Although the effects of fumes on the respiratory tract have been investigated, few apparent reports were published on their effects on the skin. The purpose of this study was to investigate the effects of exposure to welding fumes on skin cells, focusing on interleukin-24 (IL-24), a cytokine involved in the pathophysiology of skin conditions, such as atopic dermatitis and psoriasis.

Cold-induced suspension and resetting of Ca and transcriptional rhythms in the suprachiasmatic nucleus neurons.

Does the circadian clock keep running under such hypothermic states as daily torpor and hibernation? This fundamental question has been a research subject for decades but has remained unsettled. We addressed this subject by monitoring the circadian rhythm of clock gene transcription and intracellular Ca in the neurons of the suprachiasmatic nucleus (SCN), master circadian clock, under a cold environment. We discovered that the transcriptional and Ca rhythms are maintained at 22°C-28°C, but suspended at 15°C, accompanied by a large Ca increase.

Na/Ca exchanger mediates cold Ca signaling conserved for temperature-compensated circadian rhythms.

Circadian rhythms are based on biochemical oscillations generated by clock genes/proteins, which independently evolved in animals, fungi, plants, and cyanobacteria. Temperature compensation of the oscillation speed is a common feature of the circadian clocks, but the evolutionary-conserved mechanism has been unclear. Here, we show that Na/Ca exchanger (NCX) mediates cold-responsive Ca signaling important for the temperature-compensated oscillation in mammalian cells.

Candidate plasticity gene 16 and jun dimerization protein 2 are involved in the suppression of insulin gene expression in rat pancreatic INS-1 β-cells.

Chronic hyperglycemia causes pancreatic β-cell dysfunction, impaired insulin secretion and the suppression of insulin gene expression. This phenomenon is referred to as glucotoxicity, and is a critical component of the pathogenesis of type 2 diabetes. We previously reported that the expression of candidate plasticity gene 16 (CPG16) was higher in rat pancreatic INS-1 β-cells under glucotoxic conditions and CPG16 suppressed insulin promoter activity.

Candidate plasticity gene 16 mediates suppression of insulin gene expression in rat insulinoma INS-1 cells under glucotoxic conditions.

Chronic hyperglycemia causes pancreatic β-cell dysfunction, impaired insulin secretion and suppression of insulin gene expression, referred to as glucotoxicity. Insulin gene expression is regulated by several protein kinases and protein phosphatases. However, the molecular mechanisms of the suppressed insulin gene expression in glucotoxicity are not fully understood.