Cigarette smoke exposure is a major cause of chronic obstructive pulmonary disease. Cadmium is a leading toxic component of cigarette smoke. Cadmium and zinc are highly related metals.  https://www.selleckchem.com/products/iwr-1-endo.html  Whereas, zinc is an essential metal required for normal health, cadmium is highly toxic. Zrt- and Irt-like protein 8 (ZIP8) is an avid transporter of both zinc and cadmium into cells and is abundantly expressed in the lung of smokers compared to nonsmokers. Our objective was to determine whether disturbed zinc homeostasis through diet or the zinc transporter ZIP8 increase susceptibility to lung damage following prolonged cigarette smoke exposure. METHODS Cigarette smoke exposure was evaluated in the lungs of mice subject to insufficient and sufficient zinc intakes, in transgenic ZIP8 overexpressing mice, and a novel myeloid-specific ZIP8 knockout strain. RESULTS Moderate depletion of zinc intakes in adult mice resulted in a significant increase in lung cadmium burden and permanent lung tissue loss following prolonged smoke exposure. Overexpression of ZIP8 resulted in increased lung cadmium burden and more extensive lung damage, whereas cigarette smoke exposure in ZIP8 knockout mice resulted in increased lung tissue loss without a change in lung cadmium content, but a decrease in zinc. CONCLUSIONS Overall, findings were consistent with past human studies. Imbalance in Zn homeostasis increases susceptibility to permanent lung injury following prolonged cigarette smoke exposure. Based on animal studies, both increased and decreased ZIP8 expression enhanced irreversible tissue damage in response to prolonged tobacco smoke exposure. We believe these findings represent an important advancement in our understanding of how imbalance in zinc homeostasis and cadmium exposure via tobacco smoke may increase susceptibility to smoking-induced lung disease. Physical activity is considered an effective method to improve sleep quality in adolescents and adults. However, there is mixed evidence among children. Our objectives were to investigate this association in children and to examine potential moderating variables. Eight databases were systematically searched, and we included all study designs with a sample of healthy children ages 3-13 years-old. We identified 47 studies for meta-analysis. Overall, we found little association between physical activity and sleep (r = 0.02, 95% confidence interval = -0.03 to 0.07). There was a high amount of heterogeneity in the overall model (I2 = 93%). However, none of the examined variables significantly moderated the overall effect, including age, gender, risk of bias, study quality, measurement methodology, study direction, and publication year. Exploratory analyses showed some weak, but statistically significant associations for vigorous physical activity with sleep (r = 0.09, 95% CI = 0.01 to 0.17, I2 = 66.3%), specifically sleep duration (r = 0.07, 95% CI = 0.00 to 0.14, I2 = 41.1%). High heterogeneity and the lack of experimental research suggest our findings should be interpreted with caution. The current evidence, however, shows little support for an association between physical activity and sleep in children. Imaging strain fields at the nanoscale is crucial for understanding the physical properties as well as the performance of oxide heterostructures and electronic devices. Based on scanning transmission electron microscopy (STEM) techniques, we successfully imaged the random strain field at the interface of core-shell ZnO nanowires. Combining experimental observations and image simulations, we find that the strain contrast originates from dechanneling of electrons and increased diffuse scattering induced by static atomic displacements. For a thin sample with a random strain field, a positive strain contrast appears in the low-angle annular dark-field (LAADF) image and a negative contrast in the high-angle annular dark-field (HAADF) image, but for a thick sample (> 120 nm), the positive contrast always occurs in both the LAADF and HAADF images. Through the analysis of the relationship between strain contrast and various parameters, we also discuss the optimum experimental condition for imaging random strain fields. The discovery that rare POT1 variants are associated with extremely long telomeres and increased cancer predisposition has provided a framework to revisit the relationship between telomere length and cancer development. Telomere shortening is linked with increased risk for cancer. However, over the past decade, there is increasing evidence to show that extremely long telomeres caused by mutations in shelterin components (POT1, TPP1, and RAP1) also display an increased risk of cancer. Here, we will review current knowledge on germline mutations of POT1 identified from cancer-prone families. In particular, we will discuss some common features presented by the mutations through structure-function studies. We will further provide an overview of how POT1 mutations affect telomere length regulation and tumorigenesis. Published by Elsevier Ltd.Terpenoids are a vast and diverse class of molecules with industrial and medicinal importance. The majority of these molecules are produced across kingdom Plantae via specialized metabolism. Microorganisms, mainly Escherichia coli and Saccharomyces cerevisiae, have become choice platforms for the biosynthesis of terpenoids due to recent advances in synthetic biology and metabolic engineering. New techniques for gene discovery have expanded our search space for novel terpene synthesis pathways and unlocked unrealized potential for the microbial production of more complex derivatives. Additionally, numerous advances in host and pathway engineering have allowed for the production of terpenoids requiring oxidation and glycosylation, effectively expanding the potential target space. These advances will lay the foundation for the microbial biosynthesis of a seemingly infinite domain of terpenoids with varying applications. Prostaglandin E2 (PGE2) exhibits hepatoprotective effects against various types of liver injury. However, there is little information on the disposition of endogenous PGE2 during liver injury. In the present study, we attempted to elucidate the mechanism involved in regulating PGE2 distribution during liver injury. Carbon tetrachloride (CCl4) was used to establish a liver injury mouse model. PGE2 was measured by LC-MS/MS. The plasma and hepatic PGE2 levels were significantly increased at 6 to 48 h after CCl4 treatment. The ratio of plasma levels of 13,14-dihydro-15-ketoPGE2 (PGEM), a major PGE2 metabolite, to PGE2 decreased significantly after CCl4 treatment. PGE2 synthesis and expression of enzymes related to PGE2 production were not induced, while the activity and mRNA expression of 15-prostaglandin dehydrogenase (15-PGDH/Hpgd), a major enzyme for PGE2 inactivation, decreased significantly in the liver of CCl4-treated mice compared to that of vehicle-treated control. The plasma and hepatic PGE2 levels were negatively correlated with the hepatic mRNA expression levels of Hpgd.