Annual cycle of activity of the neurons of the anterior preoptic area in the brain of Rana esculenta L.

Abstract

Sexually mature male and female Rana esculenta L. were captured in their natural habitat in six phases of the annual cycle. Nuclear volumes in APOA cells were found to fluctuate distinctly in the course of the year. In both sexes nuclear volumes were maximal in the phases preceding the breeding season (IIIrd decade of January, and 1st decade of April), and minimal throughout the phases of active life (IIIrd decade of May, IInd decade of July, and 1st decade of September). No aldehydefuchsin or Gomori‐positive material was found in the APOA perikaryons.     

Lysosomal membrane permeabilization is involved in oxidative stress-induced apoptotic cell death in LAMP2-deficient iPSCs-derived cerebral cortical neurons

Patients with Danon disease may suffer from severe cardiomyopathy, skeletal muscle dysfunction as well as varying degrees of mental retardation, in which the primary deficiency of lysosomal membrane-associated protein-2 (LAMP2) is considerably associated. Owing to the scarcity of human neurons, the pathological role of LAMP2 deficiency in neural injury of humans remains largely elusive. However, the application of induced pluripotent stem cells (iPSCs) may shed light on overcoming such scarcity.In this study, we obtained iPSCs derived from a patient carrying a mutated LAMP2 gene that is associated with Danon disease. By differentiating such LAMP2-deficient iPSCs into cerebral cortical neurons and with the aid of various biochemical assays, we demonstrated that the LAMP2-deficient neurons are more susceptible to mild oxidative stress-induced injury.The data from MTT assay and apoptotic analysis demonstrated that there was no notable difference in cellular viability between the normal and LAMP2-deficient neurons under non-stressed condition. When exposed to mild oxidative stress (10 μM H₂O₂), the LAMP2-deficient neurons exhibited a significant increase in apoptosis. Surprisingly, we did not observe any aberrant accumulation of autophagic materials in the LAMP2-deficient neurons under such stress condition.Our results from cellular fractionation and inhibitor blockade experiments further revealed that oxidative stress-induced apoptosis in the LAMP2-deficient cortical neurons was caused by increased abundance of cytosolic cathepsin L. These results suggest the involvement of lysosomal membrane permeabilization in the LAMP2 deficiency associated neural injury.     

椎体静脉稀疏区注入骨水泥对PVP术中骨水泥渗漏的影响

目的:探讨椎体静脉稀疏区注入骨水泥对骨质疏松椎体压缩性骨折患者行经皮穿刺椎体成形术(percutaneous vertebroplasty,PVP)术中骨水泥渗漏的影响。方法:选择西安交通大学第二附属医院2014年1月至2018年6月收治的61例骨质疏松椎体压缩性骨折患者,根据骨水泥注入区域的不同,将所有患者分为A组(30例)及B组(31例),A组骨水泥注入区域为椎体静脉密集区(椎体中1/3平面处),B组骨水泥注入区域为椎体静脉稀疏区(椎体上1/3及下1/3平面处),对比两组的骨水泥渗漏率,术前、术后6个月时的视觉模拟评分(Visual analogue scale,VAS),治疗中的骨水泥用量、椎体高度恢复率及cobb角恢复度数。结果:B组的骨水泥渗漏率及骨水泥用量均明显低于A组(P0.05)。两组的VAS评分、椎体高度恢复率、cobb角恢复情况对比差异无统计学意义(P0.05)。结论:与椎体静脉密集区相比,在椎体静脉稀疏区注入骨水泥可显著降低骨质疏松椎体压缩性骨折患者PVP术中骨水泥渗漏率,椎体静脉稀疏区可作为PVP术中骨水泥注射的一个相对安全区域。     

MicroRNAs as regulators of cell death mechanisms in amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder affecting upper and lower motor neurons (MNs), resulting in paralysis and precocious death from respiratory failure. Although the causes of ALS are incompletely understood, the role of alterations in RNA metabolism seems central. MicroRNAs (miRNAs) are noncoding RNAs implicated in the regulation of gene expression of many relevant physiological processes, including cell death. The recent model of programmed cell death (PCD) encompasses different mechanisms, from apoptosis to regulated necrosis (RN), in particular necroptosis. Both apoptosis and necroptosis play a significant role in the progressive death of MNs in ALS. In this review, we present key research related to miRNAs that modulate apoptosis and RN pathways in ALS. We also discuss whether these miRNAs represent potential targets for therapeutic development in patients.     

Spinal cord tissue affects sprouting from aortic fragments in ex vivo co‐culture

It is a well‐known fact, that there is a close interconnection between vascular and neural structures in both embryonic development and postnatal life. Different models have been employed to dissect the mechanisms of these interactions, ranging from in vitro systems (e.g., co‐culture of neural and endothelial cells) to in vivo imaging of central neural system recovery in laboratory animals after artificially induced trauma. Nevertheless, most of these models have serious limitations. Here, we describe an ex vivo model, representing an organotypic co‐culture of aortic fragments (AF) with longitudinal slices of mouse neonatal spinal cord (SC) or dorsal root ganglia (DRG). The samples were co‐cultured in a medium adapted for SC tissue and lacking any pro‐angiogenic or neurotrophic growth factors. It was found, that cultivation of AFs in the SC injury zone (transversal dissection of a SC slice) resulted in the initiation of active aortic sprouting. Remarkably, the endothelial cells exiting the AFs never invaded the SC tissue, concentrating in a nearby area (negative taxis). In contrast, the DRGs, while also promoting the sprouting, were a target of active endothelial CD31⁺ cell invasion (positive taxis). Thus, the tissues of both central and peripheral nervous systems have a prominent positive effect on aortic sprouting, while the vector of endothelial cell expansion is strictly nervous‐tissue‐type dependent. The ex vivo AF co‐culture with SC or DRG appeared to be a useful and promising model for a further endeavor into the mechanisms driving the complex interactions between neural and endothelial tissues.     

Acute Complexin Knockout Abates Spontaneous and Evoked Transmitter Release

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Functional Access to Neuron Subclasses in Rodent and Primate Forebrain

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Cortical State Fluctuations across Layers of V1 during Visual Spatial Perception

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Elevated Prolactin during Pregnancy Drives a Phenotypic Switch in Mouse Hypothalamic Dopaminergic Neurons

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