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Increasing contamination of urban soil by persistent organic pollutants is a major environmental issue. The purpose of the present study was to investigate the distribution, source and human health risk of polycyclic aromatic hydrocarbons (PAHs) in different functional areas in Zhengzhou City, China. Total 130 soil samples were collected from surface layer (0-10 cm) in urban road, overpass, residential area and park in the city during January 2019. Concentrations of ∑PAH16 in the urban soil ranged from 49.90 to 11,565 µg kg-1 and seven carcinogenic PAHs accounted for 69% of the total PAHs. selleckchem The mean concentrations of PAHs decreased in the following order urban road > overpass > residential area > park. Analysis based on diagnostic rate demonstrated that PAHs mainly originated from pyrolysis sources including traffic emissions and combustion of coal and biomass. Health risk assessment indicated that PAHs in urban road in the city have potential carcinogenic risks to residents. The present study suggested that the control of urban PAHs pollution in Zhengzhou City should be strengthened.
A high-density linkage map of an intraspecific RIL population was constructed using 6187 bins to identify QTLs for fibre quality- and yield-related traits in upland cotton by whole-genome resequencing. Good fibre quality and high yield are important production goals in cotton (Gossypium hirsutum L.), which is a leading natural fibre crop worldwide. However, a greater understanding of the genetic variants underlying fibre quality- and yield-related traits is still required. In this study, a large-scale population including 588 F
recombinant inbred lines, derived from an intraspecific cross between the upland cotton cv. Nongdamian13, which exhibits high quality, and Nongda601, which exhibits a high yield, was genotyped by using 232,946 polymorphic single-nucleotide polymorphisms obtained via a whole-genome resequencing strategy with 4.3-fold genome coverage. We constructed a high-density bin linkage map containing 6187 bin markers spanning 4478.98cM with an average distance of 0.72cM. We identified 58 indiv QTL counts for fibre quality in the Dt subgenome were more than two times that in the At subgenome, and chromosome D02 harboured the greatest number of QTLs and clusters. Furthermore, we discovered 24 stable QTLs for fibre quality and 12 stable QTLs for yield traits. Four novel major stable QTLs related to fibre length, fibre strength and lint percentage, and seven previously unreported candidate genes with significantly differential expression between the two parents were identified and validated by RNA-seq. Our research provides valuable information for improving the fibre quality and yield in cotton breeding.Efforts to phenotype pancreatic islets have contributed tremendously to our present understanding of endocrine function and diabetes. A continued evolution in approaches to study islet physiology is important given the need to establish reference points for mature islet functionality, understanding biological variation amongst individuals and cells, and the ongoing appreciation of the role for islets in diabetes susceptibility. Recent efforts in islet biology have focused on technological improvements in imaging, molecular profiling and data analysis, along with a push for enhanced transparency and reporting. The integration of these approaches within a classical islet physiology framework, and approaches to link these data with in vivo human phenotypes, will be critical as we move towards a better understanding of islet function in health and disease. Here we discuss what we feel are important issues and useful approaches to consider as we move forward as a field in islet and beta cell phenotyping. Graphical abstract.Increasing evidence suggests that, although pancreatic islets can function autonomously to detect and respond to changes in the circulating glucose level, the brain cooperates with the islet to maintain glycaemic control. Here, we review the role of the central and autonomic nervous systems in the control of the endocrine pancreas, including mechanisms whereby the brain senses circulating blood glucose levels. We also examine whether dysfunction in these systems might contribute to complications of type 1 diabetes and the pathogenesis of type 2 diabetes. Graphical abstract.Cells in different tissues, including endocrine cells in the pancreas, live in complex microenvironments that are rich in cellular and acellular components. Intricate interactions with their microenvironment dictate most cellular properties, such as their function, structure and size, and maintain tissue homeostasis. Pancreatic islets are populated by endocrine, vascular and immune cells that are immersed in the extracellular matrix. While the intrinsic properties of beta cells have been vastly investigated, our understanding of their interactions with their surroundings has only recently begun to unveil. Here, we review current research on the interplay between the islet cellular and acellular components, and the role these components play in beta cell physiology and pathophysiology. Although beta cell failure is a key pathomechanism in diabetes, its causes are far from being fully elucidated. We, thus, propose deleterious alterations of the islet niche as potential underlying mechanisms contributing to beta cell failure. In sum, this review emphasises that the function of the pancreatic islet depends on all of its components. Graphical abstract.The islet of Langerhans is a complex endocrine micro-organ consisting of a multitude of endocrine and non-endocrine cell types. The two most abundant and prominent endocrine cell types, the beta and the alpha cells, are essential for the maintenance of blood glucose homeostasis. While the beta cell produces insulin, the only blood glucose-lowering hormone of the body, the alpha cell releases glucagon, which elevates blood glucose. Under physiological conditions, these two cell types affect each other in a paracrine manner. While the release products of the beta cell inhibit alpha cell function, the alpha cell releases factors that are stimulatory for beta cell function and increase glucose-stimulated insulin secretion. The aim of this review is to provide a comprehensive overview of recent research into the regulation of beta cell function by alpha cells, focusing on the effect of alpha cell-secreted factors, such as glucagon and acetylcholine. The consequences of differences in islet architecture between species on the interplay between alpha and beta cells is also discussed.
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