High Glucose Alters Fetal Rat Islet Transcriptome and Induces Progeny Islet Dysfunction

Offspring of diabetic mothers are susceptible to developing type 2 diabetes due to pancreatic islet dysfunction. However, the initiating molecular pathways leading to offspring pancreatic islet dysfunction are unknown. We hypothesized that maternal hyperglycemia alters offspring pancreatic islet transcriptome and negatively impacts offspring islet function. We employed an infusion model capable of inducing localized hyperglycemia in fetal rats residing in the left uterine horn, thus avoiding other factors involved in programming offspring pancreatic islet health. While maintaining euglycemia in maternal dams and right uterine horn control fetuses, hyperglycemic fetuses in the left uterine horn had higher serum insulin and pancreatic beta cell area. Upon completing infusion from GD20 to 22, RNA sequencing was performed on GD22 islets to identify the hyperglycemia-induced altered gene expression. Ingenuity pathway analysis of the altered transcriptome found that diabetes mellitus and inflammation/cell death pathways were enriched. Interestingly, the downregulated genes modulate more diverse biological processes, which includes responses to stimuli and developmental processes. Next, we performed ex and in vivo studies to evaluate islet cell viability and insulin secretory function in weanling and adult offspring. Pancreatic islets of weanlings exposed to late gestation hyperglycemia had decreased cell viability in basal state and glucose-induced insulin secretion. Lastly, adult offspring exposed to in utero hyperglycemia also exhibited glucose intolerance and insulin secretory dysfunction. Together, our results demonstrate that late gestational hyperglycemia alters the fetal pancreatic islet transcriptome and increases offspring susceptibility to developing pancreatic islet dysfunction

Development of High-Performance Fly-Ash-Based Controlled Low-Strength Materials for Backfilling in Metropolitan Cities

Controlled low-strength materials (CLSMs) have been developed using various byproducts for backfilling or void-filling around pipelines or culvert boxes. However, these CLSMs have encountered issues related to their inadequate placement around underground facilities, despite satisfying the performance requirements, especially flowability, recommended by the American Concrete Institute (ACI) 229 committee. In this study, a new CLSM is developed to ensure a significantly higher flowability, lower segregation, and faster installation compared with previously developed CLSMs. This is achieved through a series of laboratory tests. To enhance the flowability and prevent segregation, a calcium-sulfoaluminate-based binder and fly ash are used in combination with two types of additives. The measured flowability of the new CLSM is 700 mm, while its compressive strength and bleeding satisfy the general criteria specified by the ACI 229R-13. In addition, the performance of the developed CLSM is compared with that of predeveloped CLSMs. The new CLSM was not only shown to exhibit the highest flowability, but also to satisfy the specified requirements for compressive strength and bleeding. Overall, it is anticipated that the developed CLSM can significantly reduce the costs related to the disposal of old pavements, the installation of new pavements, and other construction expenses compared to the costs related to the conventional method, even though the expenses for the backfill materials could increase due to the higher production costs of CLSMs than soil. In addition, there is a need to investigate its field applicability in order to evaluate the precise costs, maintenance, and long-term stabilities after installation

Bis-ureidoquinoline as a Selective Fluoride Anion Sensor through Hydrogen-Bond Interactions

Bis-ureidoquinoline shows a characteristic UV–vis absorbance and turn-on fluorescence changes in the presence of the fluoride anion. Such selective changes probably originate from the hydrogen-bond interactions, as shown by the ¹H NMR titration and DFT calculations. Bis-ureidoquinoline can be used as a fluoride-selective sensor for the detection of fluoride anions under illumination from a laboratory hand-held UV lamp

Genetics and Genomics of Carrot Biotic Stress

International audienceCarrot (Daucus carota ssp. sativus) production can be affected by a wide range of pests and pathogens. At least five diseases of carrot are caused by bacterial pathogens, 36 by fungal and oomycete pathogens, two by phytoplasmas, and 13 by viruses; and seven genera of nematodes and two genera of parasitic plants affect carrot. In addition, numerous insect and mite pests can cause losses. There have been extensive efforts to select carrot cultivars with partial or complete resistance to many of these pathogens and pests, and to identify wild species with resistance to specific biotic stresses for introgression into breeding populations and commercial cultivars. For some pathogens and pests, significant advances have been made at identifying resistance and mapping that resistance to the carrot genome. For others, resistance has been identified, but the genetic basis is yet to be determined. For a majority of these diverse stresses, however, there has been little success at identifying highly effective resistance and understanding the genetic basis of resistance. The diversity of stresses as well as interactions among these pests and pathogens can complicate efforts to develop cultivars with resistance to all key biotic stresses in a region that also meet market and consumer expectations. New approaches to identifying resistant material and speeding traditional breeding are being developed with molecular breeding tools, including simple sequence repeat markers and deep-coverage libraries of the carrot genome. These valuable genomic resources will enhance efforts to identify and breed for resistance to carrot pests and pathogens