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Sphingolipids are an essential subset of bioactive lipids found in most eukaryotic cells that contribute to membrane biophysical properties and are involved in cellular differentiation, recognition, and mediating interactions. The described nanoHPLC-ESI-Q/ToF methodology utilizes known biosynthetic pathways, accurate mass detection, optimized collision-induced disassociation, and a robust nanoflow chromatographic separation for the analysis of intact sphingolipids found in human tissue, cells, and serum. The methodology was developed and validated with an emphasis on addressing the common issues experienced in profiling these amphipathic lipids, which are part of the glycocalyx and lipidome. The high sensitivity obtained using nanorange flow rates with robust chromatographic reproducibility over a wide range of concentrations and injection volumes results in confident identifications for profiling these low-abundant biomolecules.

Renjie Wu,1– 3,* Luchao Lv,1– 3,* Chengzhen Wang,1– 3 Guolong Gao,1– 3 Kaiyang Yu,1– 3 Zhongpeng Cai,1– 3 Yiyun Liu,1– 3 Jun Yang,1– 3 Jian-Hua Liu1– 4 1Key Laboratory of Zoonosis of Ministry of Agricultural and Rural Affairs, College of Veterinary Medicine, South China Agricultural University, Guangzhou, People’s Republic of China; 2Guangdong Provincial Key Laboratory of Veterinary Pharmaceutics Development and Safety Evaluation, College of Veterinary Medicine, South China Agricultural University, Guangzhou, People’s Republic of China; 3National Risk Assessment Laboratory for Antimicrobial Resistance of Microorganisms in Animal, College of Veterinary Medicine, South China Agricultural University, Guangzhou, People’s Republic of China; 4Guangdong Laboratory for Lingnan Modern Agriculture, Guangzhou, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jian-Hua Liu, College of Veterinary Medicine, South China Agricultural University, Wushan Road 483, Guangzhou, 510642, People’s Republic of China, Email jhliu@scau.edu.cnPurpose: The objective of this study was to elucidate the characteristics and mechanism of formation of the fusion plasmid pHNSHP24 carrying mcr-1.1.Materials and Methods: mcr-1.1-bearing Escherichia coli SHP24 and the corresponding transconjugant were subjected to whole-genome sequencing (WGS) combining the Illumina and MinION platforms to obtain the complete sequences of the fusion plasmid and its original plasmids.Results: Complete sequence analysis and S1 nuclease-pulsed field gel electrophoresis (S1-PFGE) results indicated that E. coli SHP24 carried four plasmids: mcr-1.1-harboring phage-like plasmid pHNSHP24-3, F53:A-:B- plasmid pHNSHP24-4, pHNSHP24-1, and pHNSHP24-2. However, the plasmid pHNSHP24 carrying mcr-1.1 presents in the transconjugant differed from the four plasmids in the donor strain SHP24. Further analysis showed that pHNSHP24 may be the fusion pr

With the wide applications of colored point cloud in many fields, point cloud perceptual quality assessment plays a vital role in the visual communication systems owing to the existence of quality degradations introduced in various stages. However, the existing point cloud quality assessments ignore the mechanism of human visual system (HVS) which has an important impact on the accuracy of the perceptual quality assessment. In this paper, a progressive knowledge transfer based on human visual perception mechanism for perceptual quality assessment of point clouds (PKT-PCQA) is proposed. The PKT-PCQA merges local features from neighboring regions and global features extracted from graph spectrum. Taking into account the HVS properties, the spatial and channel attention mechanism is also considered in PKT-PCQA. Besides, inspired by the hierarchical perception system of human brains, PKT-PCQA adopts a progressive knowledge transfer to convert the coarse-grained quality classification knowledge to the fine-grained quality prediction task. Experiments on three large and independent point cloud assessment datasets show that the proposed no reference PKT-PCQA network achieves better of equivalent performance comparing with the state-of-the-art full reference quality assessment methods, outperforming the existed no reference quality assessment network.

We present a formal model of Checked C, a dialect of C that aims to enforce spatial memory safety. Our model pays particular attention to the semantics of dynamically sized, potentially null-terminated arrays. We formalize this model in Coq, and prove that any spatial memory safety errors can be blamed on portions of the program labeled unchecked; this is a Checked C feature that supports incremental porting and backward compatibility. While our model's operational semantics uses annotated ("fat") pointers to enforce spatial safety, we show that such annotations can be safely erased: Using PLT Redex we formalize an executable version of our model and a compilation procedure from it to an untyped C-like language, and use randomized testing to validate that generated code faithfully simulates the original. Finally, we develop a custom random generator for well-typed and almost-well-typed terms in our Redex model, and use it to search for inconsistencies between our model and the Clang Checked C implementation. We find these steps to be a useful way to co-develop a language (Checked C is still in development) and a core model of it., Comment: This is an extended version of a paper that appears at the 2022 Computer Security Foundations Symposium

Acetylcholinesterase (AChE, EC 3.1.1.7) plays important roles in cholinergic neurotransmission and has been widely recognized as a biomarker for monitoring pollution by organophosphate (OP) and carbamate pesticides. Dioxin is an emerging environmental AChE disruptor and is a typical persistent organic pollutant with multiple toxic effects on the nervous system. Growing evidence has shown that there is a significant link between dioxin exposure and neurodegenerative diseases and neurodevelopmental disorders, most of which involve AChE and cholinergic dysfunctions. Therefore, an in-depth understanding of the effects of dioxin on AChE and the related mechanisms of action might help to shed light on the molecular bases of dioxin impacts on the nervous system. In the past decade, the effects of dioxins on AChE have been revealed in cultured cells of different origins and in rodent animal models. Unlike OP and carbamate pesticides, dioxin-induced AChE disturbance is not due to direct inhibition of enzymatic activity; instead, dioxin causes alterations of AChE expression in certain models. As a widely accepted mechanism for most dioxin effects, the aryl hydrocarbon receptor (AhR)-dependent pathway has become a research focus in studies on the mechanism of action of dioxin-induced AChE dysregulation. In this mini-review, the effects of dioxin on AChE and the diverse roles of the AhR pathway in AChE regulation are summarized. Additionally, the involvement of AhR in AChE regulation during different neurodevelopmental processes is discussed. These AhR-related findings might also provide new insight into AChE regulation triggered by diverse xenobiotics capable of interacting with AhR. (Figure presented.). © 2020 International Society for Neurochemistry

Acetylcholinesterase (AChE, EC 3.1.1.7) plays important roles in cholinergic neurotransmission and has been widely recognized as a biomarker for monitoring pollution by organophosphate (OP) and carbamate pesticides. Dioxin is an emerging environmental AChE disruptor and is a typical persistent organic pollutant with multiple toxic effects on the nervous system. Growing evidence has shown that there is a significant link between dioxin exposure and neurodegenerative diseases and neurodevelopmental disorders, most of which involve AChE and cholinergic dysfunctions. Therefore, an in-depth understanding of the effects of dioxin on AChE and the related mechanisms of action might help to shed light on the molecular bases of dioxin impacts on the nervous system. In the past decade, the effects of dioxins on AChE have been revealed in cultured cells of different origins and in rodent animal models. Unlike OP and carbamate pesticides, dioxin-induced AChE disturbance is not due to direct inhibition of enzymatic activity; instead, dioxin causes alterations of AChE expression in certain models. As a widely accepted mechanism for most dioxin effects, the aryl hydrocarbon receptor (AhR)-dependent pathway has become a research focus in studies on the mechanism of action of dioxin-induced AChE dysregulation. In this mini-review, the effects of dioxin on AChE and the diverse roles of the AhR pathway in AChE regulation are summarized. Additionally, the involvement of AhR in AChE regulation during different neurodevelopmental processes is discussed. These AhR-related findings might also provide new insight into AChE regulation triggered by diverse xenobiotics capable of interacting with AhR. (Figure presented.). © 2020 International Society for Neurochemistry

Acetylcholinesterase (AChE, EC 3.1.1.7) plays important roles in cholinergic neurotransmission and has been widely recognized as a biomarker for monitoring pollution by organophosphate (OP) and carbamate pesticides. Dioxin is an emerging environmental AChE disruptor and is a typical persistent organic pollutant with multiple toxic effects on the nervous system. Growing evidence has shown that there is a significant link between dioxin exposure and neurodegenerative diseases and neurodevelopmental disorders, most of which involve AChE and cholinergic dysfunctions. Therefore, an in-depth understanding of the effects of dioxin on AChE and the related mechanisms of action might help to shed light on the molecular bases of dioxin impacts on the nervous system. In the past decade, the effects of dioxins on AChE have been revealed in cultured cells of different origins and in rodent animal models. Unlike OP and carbamate pesticides, dioxin-induced AChE disturbance is not due to direct inhibition of enzymatic activity; instead, dioxin causes alterations of AChE expression in certain models. As a widely accepted mechanism for most dioxin effects, the aryl hydrocarbon receptor (AhR)-dependent pathway has become a research focus in studies on the mechanism of action of dioxin-induced AChE dysregulation. In this mini-review, the effects of dioxin on AChE and the diverse roles of the AhR pathway in AChE regulation are summarized. Additionally, the involvement of AhR in AChE regulation during different neurodevelopmental processes is discussed. These AhR-related findings might also provide new insight into AChE regulation triggered by diverse xenobiotics capable of interacting with AhR. (Figure presented.). © 2020 International Society for Neurochemistry

Shaohua Xu, 1–3,* Yiyun Liu, 2, 3,* Juncai Pu, 2, 3,* Siwen Gui, 2–4,* Xiaogang Zhong, 2, 3 Lu Tian, 2, 3 Xuemian Song, 2–4 Xunzhong Qi, 2, 3 Haiyang Wang, 2, 3 Peng Xie 1–3, 5 1Department of Neurology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, People’s Republic of China; 2NHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, People’s Republic of China; 3Chongqing Key Laboratory of Neurobiology, Chongqing 400016, People’s Republic of China; 4College of Biomedical Engineering, Chongqing Medical University, Chongqing 400016, People’s Republic of China; 5Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Peng XieNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, People’s Republic of ChinaTel +86-023-68485490Fax +86-023-68485111Email xiepeng@cqmu.edu.cnBackground: Major depressive disorder (MDD) is a complex psychiatric illness involving multiple brain regions. Increasing evidence indicates that the striatum is involved in depression, but the molecular mechanisms remain unclear.Methods: In this study, we performed a gas chromatography–mass spectrometer (GC/MS)-based metabolomic analysis in the striatum of depressed rats induced by chronic unpredictable mild stress (CUMS). We then compared striatal data with our previous data from the hippocampus and cerebellum to systematically investigate the potential pathogenesis of depression.Results: We identified 22 differential metabolites in the striatum between the CUMS and control groups; these altered metabolites were mainly involved in amino acid, carb

Yu Han,1–3 Jianjun Chen,2–4 Dezhi Zou,1–3 Peng Zheng,1–3 Qi Li,1–3 Haiyang Wang,1–3 Pengfei Li,1–3 Xinyu Zhou,1–3 Yuqing Zhang,1–3 Yiyun Liu,1–3 Peng Xie1–3 1Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, 2Institute of Neuroscience and the Collaborative Innovation Center for Brain Science, 3Chongqing Key Laboratory of Neurobiology, 4Institute of Life Sciences, Chongqing Medical University, Chongqing, People’s Republic of China Background: An increasing number of studies are reporting that ketamine could be treated as a novel antidepressant for major depressive disorder (MDD). Therefore, we performed this meta-analysis to comprehensively and systematically assess the efficacy of ketamine for treating patients with MDD. Method: Randomized, double-blind, placebo-controlled studies on ketamine versus placebo for treating MDD were searched up to April 2016 in medical databases (PubMed, CCTR, Web of Science, Embase, CBM-disc, and CNKI). Three treatment time points (24 and 72 h, and day 7) were chosen. Response and remission rates were the main outcomes. The random effects model was used. An intention-to-treat analysis was conducted. Results: Nine high-quality studies that included 368 patients were selected to compare the efficacy of ketamine to placebo. The therapeutic effects of ketamine at 24 and 72 h, and day 7 were found to be significantly better than placebo. Response and remission rates in the ketamine group at 24 and 72 h, and day 7 were 52.2% and 20.6%; 47.9% and 23.8%; and 39.8% and 26.2%, respectively. No significant heterogeneity existed, and the Egger’s test showed no publication bias. Conclusion: These results indicated that ketamine could yield a good efficacy in the rapid treatment of MDD. Future large-scale clinical studies are needed to confirm our results and investigate the