The effect of nitric oxide on the pressure of the acutely obstructed ureter

Acute ureteral obstruction leads to changes in pressure inside the ureter, interrupting ureter function. The aim of our study is to explore the relationship between nitric oxide (NO) concentration and pressure in the ureter and to observe the effects of nitric oxide on the revival of renal function. We created the animal models by embedding balloons in the lower ureters of anesthetized dogs and expanding them to simulate acute ureteral obstruction. First, the test animals were pre-treated intravenously with different doses of L-NAME (non-selective nitric oxide synthase inhibitor) to inhibit nitric oxide synthase (NOS), and 10 min later, each subject was administered an intravenous dose of isoproterenol (10 μg/kg). We measured ureter pressure (UP), total and peak concentrations of NO (using an NO monitor, model inNO-T) in ureteral urine, and the volume of the urine (UFV) leaking from the balloon edge. After a certain amount of time had elapsed, it became clear that the dose of L-NAME was inversely related to the total and peak concentrations of NO, the rate of change in UP, and the volume of urine produced. We conclude that L-NAME prevents the NOS from inhibiting the release of NO, then inhibits the effect of isoproterenol reducing the pressure of the acute obstructive ureter. Inversely, we think that NO can reduce the pressure of the acute obstructive ureter and make the obstructive ureter recanalization. And when more the concentration of nitric oxide, the more the pressure will be reduced, and more urine will be collected

The evolution of amniote gastrulation: the blastopore-primitive streak transition

In the animal kingdom, gastrulation, the process by which the primary germ layers are formed involves a dramatic transformation in the topology of the cells that give rise to all of the tissues of the adult. Initially formed as a mono-layer, this tissue, the epiblast, becomes subdivided through the internalization of cells, thereby forming a two (bi-laminar) or three (tri-laminar) layered embryo. This morphogenetic process coordinates the development of the fundamental body plan and the three-body axes (antero-posterior, dorso-ventral, and left-right) and begins a fundamental segregation of cells toward divergent developmental fates. In humans and other mammals, as well as in avians, gastrulating cells internalize along a structure, called the primitive streak, which builds from the periphery toward the center of the embryo. How these morphogenetic movements are orchestrated and evolved has been a question for developmental biologists for many years. Is the primitive streak a feature shared by the whole amniote clade? Insights from reptiles suggest that the primitive streak arose independently in mammals and avians, while the reptilian internalization site is a structure half-way between an amphibian blastopore and a primitive streak. The molecular machinery driving primitive streak formation has been partially dissected using mainly the avian embryo, revealing a paramount role of the planar cell polarity (PCP) pathway in streak formation. How did the employment of this machinery evolve? The reptilian branch of the amniote clade might provide us with useful tools to investigate the evolution of the amniote internalization site up to the formation of the primitive streak. WIREs Dev Biol 2017, 6:e262. doi: 10.1002/wdev.262 For further resources related to this article, please visit the WIREs website

The evolution of amniote gastrulation: the blastopore-primitive streak transition

In the animal kingdom, gastrulation, the process by which the primary germ layers are formed involves a dramatic transformation in the topology of the cells that give rise to all of the tissues of the adult. Initially formed as a mono-layer, this tissue, the epiblast, becomes subdivided through the internalization of cells, thereby forming a two (bi-laminar) or three (tri-laminar) layered embryo. This morphogenetic process coordinates the development of the fundamental body plan and the three-body axes (antero-posterior, dorso-ventral, and left-right) and begins a fundamental segregation of cells toward divergent developmental fates. In humans and other mammals, as well as in avians, gastrulating cells internalize along a structure, called the primitive streak, which builds from the periphery toward the center of the embryo. How these morphogenetic movements are orchestrated and evolved has been a question for developmental biologists for many years. Is the primitive streak a feature shared by the whole amniote clade? Insights from reptiles suggest that the primitive streak arose independently in mammals and avians, while the reptilian internalization site is a structure half-way between an amphibian blastopore and a primitive streak. The molecular machinery driving primitive streak formation has been partially dissected using mainly the avian embryo, revealing a paramount role of the planar cell polarity (PCP) pathway in streak formation. How did the employment of this machinery evolve? The reptilian branch of the amniote clade might provide us with useful tools to investigate the evolution of the amniote internalization site up to the formation of the primitive streak. WIREs Dev Biol 2017, 6:e262. doi: 10.1002/wdev.262 For further resources related to this article, please visit the WIREs website

The head's tale: Anterior-posterior axis formation in the mouse embryo.

The establishment of the anterior-posterior (A-P) axis is a fundamental event during early development and marks the start of the process by which the basic body plan is laid down. This axial information determines where gastrulation, that generates and positions cells of the three-germ layers, occurs. A-P patterning requires coordinated interactions between multiple tissues, tight spatiotemporal control of signaling pathways, and the coordination of tissue growth with morphogenetic movements. In the mouse, a specialized population of cells, the anterior visceral endoderm (AVE) undergoes a migration event critical for correct A-P pattern. In this review, we summarize our understanding of the generation of anterior pattern, focusing on the role of the AVE. We will also outline some of the many questions that remain regarding the mechanism by which the first axial asymmetry is established, how the AVE is induced, and how it moves within the visceral endoderm epithelium