Abnormal persistence of the chorioallantoic membrane is associated with severe developmental abnormalities in freshwater turtles

Development in oviparous reptiles requires the correct formation and function of extra-embryonic membranes in the egg. In 2017 we incubated 2,583 eggs from five species of freshwater turtle during a long-term ecological study, and opened eggs that failed to hatch. We described a previously unreported developmental anomaly: the retention of an extra-embryonic membrane around seven turtles (1 Apalone spinifera Le Sueur 1827, 1 Chelydra serpentina Linnaeus 1758, and 5 Graptemys geographica Le Sueur 1817) that were alive but unhatched >14 days after their clutch-mates had emerged. We investigated the association between retention of this membrane and the exhibition of other developmental deformities of varying severity, and we tested whether this novel abnormality was associated with reduced fertility or hatching success in affected clutches. Consultation of ~150 years of literature suggests that we observed persistence of the chorioallantoic membrane (CAM, also called the chorio-allantois). Our data suggest that clutches where at least one turtle exhibits a persistent CAM may also exhibit slightly reduced fertility or hatch success in the rest of the clutch, compared to conspecific clutches that do not contain this anomaly. Future research should investigate the factors predicting CAM retention and other developmental abnormalities.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Commentary: Zebrafish as a Model for Osteoporosis—An Approach to Accelerating Progress in Drug and Exercise-Based Treatment

Osteoporosis (OP) is a degenerative disease characterized by reduced bone strength and increased fracture risk. As the global population continues to age, the prevalence and economic burden of osteoporosis can be expected to rise substantially, but there remain various gaps in the field of OP care. For instance, there is a lack of anti-fracture drugs with proven long-term efficacy. Likewise, though exercise remains widely recommended in OP prevention and management, data regarding the safety and efficacy for patients after vertebral fracture remain limited. This lack of evidence may be due to the cost and inherent difficulties associated with exercise-based OP research. Thus, the current research landscape highlights the need for novel research strategies that accelerate OP drug discovery and allow for the low-cost study of exercise interventions. Here, we outline an example of one strategy, the use of zebrafish, which has emerged as a potential model for the discovery of anti-osteoporosis therapeutics and study of exercise interventions. The strengths, limitations, and potential applications of zebrafish in OP research will be outlined

Low Dose Cadmium Inhibits Proliferation of Human Renal Mesangial Cells via Activation of the JNK Pathway

Cadmium (Cd) is a heavy metal and environmental pollutant. The kidney is the principal target organ of Cd exposure. Previously, we found that low concentration of Cd damages the integrity of the glomerular filtration barrier. However, little is known about the effects of Cd on renal mesangial cells, which provide structural support for the glomerular capillary loops and regulate intraglomerular blood flow. In this study, human renal mesangial cells (HRMCs) were cultured in the presence of serum and treated with 4 μM Cd. We found that Cd activates the c-Jun N-terminal kinase (JNK) pathway, and increases the protein levels of c-Jun and c-Fos. Cd treatment also induces a decrease in proliferation and an increase in apoptosis of HRMCs, but only the decrease in HRMC proliferation was reversed by pretreatment with SP600125, an inhibitor of the JNK pathway. In addition, Cd does not change the expression of α-smooth muscle actin and platelet-derived growth factor receptor-β, the markers of mesangial cells, or the alignment of the filamentous actin (F-actin) cytoskeleton of HRMCs. Our data indicate that the JNK pathway mediates the inhibitory effects of Cd on HRMC proliferation

Low-Dose Cadmium Upregulates VEGF Expression in Lung Adenocarcinoma Cells

Cadmium (Cd) is a heavy metal and environmental toxin. Exposure to Cd has been associated with a variety of human cancers. In this study, we performed in vitro assays to examine the effects of cadmium chloride (CdCl2) on A549 cells, a human lung adenocarcinoma cell line. Cd does not affect proliferation, migration, or apoptosis of A549 cells at concentrations of 0.1–10 μM. At 0.5 and 1 μM, Cd increases the expression of vascular endothelial growth factor (VEGF) (p < 0.05, p < 0.01, respectively), but not basic fibroblast growth factor (b-FGF) in A549 cells. The conditioned media were collected from the A549 cells treated with 1 μM Cd and were co-cultured with human umbilical vein endothelial cells (HUVECs). Upon treatment with the conditioned media, the proliferation and migration of HUVECs significantly increased (p < 0.01, p < 0.05, respectively), while apoptosis remained unchanged. In addition, 1 μM Cd increases the level of hypoxia inducible factor 1-α (HIF1-α), which is a positive regulator of VEGF expression. Although low-dose Cd does not directly affect the growth of lung adenocarcinoma cells, it might facilitate the development of tumors through its pro-angiogenic effects