Towards the Saturation Throughput Disparity of Flows in Directional CSMA/CA Networks: An Analytical Model

( Jianrui Fan ),( Xinru Zhao ),( Wencan Wang ),( Shengsuo Cai ),( Lijuan Zhang ) 한국인터넷정보학회 2021 KSII Transactions on Internet and Information Syst Vol.15 No.4

Using directional antennas in wireless Ad hoc networks has many superiorities, including reducing interference, extending transmission range, and increasing space division multiplexing. However, directional transmission introduces two problems: deafness and directional hidden terminals problems. We observe that these problems result in saturation throughput disparity among the competing flows in directional CSMA/CA based Ad hoc networks and bring challenges for modeling the saturation throughput of the flows. In this article, we concentrate on how to model and analyze the saturation throughput disparity of different flows in directional CSMA/CA based Ad hoc networks. We first divide the collisions occurring in the transmission process into directional instantaneous collisions and directional persistent collisions. Then we propose a four-dimensional Markov chain to analyze the transmission state for a specific node. Our model has three different kinds of processes, namely back-off process, transmission process and freezing process. Each process contains a certain amount of continuous time slots which is defined as the basic time unit of the directional CSMA/CA protocols and the time length of each slot is fixed. We characterize the collision probabilities of the node by the one-step transition probability matrix in our Markov chain model. Accordingly, we can finally deduce the saturation throughput for each directional data stream and evaluate saturation throughput disparity for a given network topology. Finally, we verify the accuracy of our model by comparing the deviation of analytical results and simulation results.

Influence of thermophilic microorganism on non-volatile metabolites during high-temperature pile-fermentation of Chinese dark tea based on metabolomic analysis

Wen Zhu,Wenfeng Wang,Wencan Xu,Shuang Wu,Wenjun Chen,Youyi Huang,Shengpeng Wang 한국식품과학회 2022 Food Science and Biotechnology Vol.31 No.7

Pile-fermentation is a critical procedure for producing Chinese dark tea, during which thermophilic microorganisms would play an irreplaceable role. However, there have been little researches on the influences of thermophilic microorganism pile-fermentation (TMPF) in high-temperature of Chinese dark tea. Thus, we conducted high-performance liquid chromatography and nontargeted metabolomic to analyze the non-volatile metabolites of TMPF. Our results discovered that the amounts of ( −)-epigallocatechin gallate, ( −)-epigallocatechin, ( −)-epicatechin gallate, and ( −)-epicatechin were decreased significantly (p < 0.05) after TMPF. By using nontargeted metabolomic analysis, a total of 1733 ion features were detected. KEGG pathway enrichment analysis showed that TMPF had a significant impact on caffeine metabolism. Also, theophylline, 3-methylxanthine, and 1,3,7-trimethyluric acid were increased significantly after TMPF, which suggested that demethylation and oxidation reaction might be the main pathways of caffeine metabolism. This study provides a better understanding of the mechanism of TMPF during high-temperature for Chinese dark tea and lays a foundation for further research.

Single-cell characterization of macrophages in uveal melanoma uncovers transcriptionally heterogeneous subsets conferring poor prognosis and aggressive behavior

Li Ke,Sun Lanfang,Wang Yanan,Cen Yixin,Zhao Jingting,Liao Qianling,Wu Wencan,Sun Jie,Zhou Meng 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

Uveal melanoma (UM) is the most frequent primary intraocular malignancy with high metastatic potential and poor prognosis. Macrophages represent one of the most abundant infiltrating immune cells with diverse functions in cancers. However, the cellular heterogeneity and functional diversity of macrophages in UM remain largely unexplored. In this study, we analyzed 63,264 single-cell transcriptomes from 11 UM patients and identified four transcriptionally distinct macrophage subsets (termed MΦ-C1 to MΦ-C4). Among them, we found that MΦ-C4 exhibited relatively low expression of both M1 and M2 signature genes, loss of inflammatory pathways and antigen presentation, instead demonstrating enhanced signaling for proliferation, mitochondrial functions and metabolism. We quantified the infiltration abundance of MΦ-C4 from single-cell and bulk transcriptomes across five cohorts and found that increased MΦ-C4 infiltration was relevant to aggressive behaviors and may serve as an independent prognostic indicator for poor outcomes. We propose a novel subtyping scheme based on macrophages by integrating the transcriptional signatures of MΦ-C4 and machine learning to stratify patients into MΦ-C4-enriched or MΦ-C4-depleted subtypes. These two subtypes showed significantly different clinical outcomes and were validated through bulk RNA sequencing and immunofluorescence assays in both public multicenter cohorts and our in-house cohort. Following further translational investigation, our findings highlight a potential therapeutic strategy of targeting macrophage subsets to control metastatic disease and consistently improve the outcome of patients with UM.

SiC IGBT degradation mechanism investigation under HV‑H3TRB tests

Ziming Wu,Zongbei Dai,Jian Zhou,Huafeng Dong,Wencan Wang,Feiwan Xie,Haoran Wang,Jiahui Yan,Xiyu Chen,Shaohua Yang,Fugen Wu 전력전자학회 2024 JOURNAL OF POWER ELECTRONICS Vol.24 No.2

The high voltage-high humidity-high temperature reverse bias (HV-H3TRB) test was utilized to evaluate the reliability of silicon carbide insulated gate bipolar transistors (SiC IGBTs). Moisture invasion often induces termination/passivation and metal corrosion. Therefore, the HV-H3TRB test is generally used to assess termination / passivation robustness. However, under the HV-H3TRB test conditions, gate quality degradation may occur. In this study, the dominant degradation mechanism of SiC IGBTs was investigated. The changes of the most sensitive static characteristics (e.g., threshold voltage, breakdown voltage, and leakage current) were recorded. The threshold voltage decreased and leakage current increased substantially after > 1000 h of HV-H3TRB tests under 85 ℃/85% RH climate conditions. Capacitance-voltage (C-V) curve measurements indicated that the mobile ions at the SiC/SiO2 interface or in the gate oxide likely caused the threshold-voltage instability in the SiC IGBTs after the HV-H3TRB tests. This instability can be recovered by applying a negative gate bias. Subsequent failure analysis confirmed no corrosion of metals or termination/passivation in the device, which indicates the robustness of the passivation (consisting of phosphor-silicate glass and Si3N4). Therefore, the gate quality appears to be a significant reliability risk for SiC IGBTs under high humidity, high temperature, and high voltage conditions.

Cytosolic escape of mitochondrial DNA triggers cGAS-STING-NLRP3 axis-dependent nucleus pulposus cell pyroptosis

Zhang Weifeng,Li Gaocai,Luo Rongjin,Lei Jie,Song Yu,Wang Bingjin,Ma Liang,Liao Zhiwei,Ke Wencan,Liu Hui,Hua Wenbin,Zhao Kangcheng,Feng Xiaobo,Wu Xinghuo,Zhang Yukun,Wang Kun,Yang Cao 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

Low back pain (LBP) is a major musculoskeletal disorder and the socioeconomic problem with a high prevalence that mainly involves intervertebral disc (IVD) degeneration, characterized by progressive nucleus pulposus (NP) cell death and the development of an inflammatory microenvironment in NP tissue. Excessively accumulated cytosolic DNA acts as a damage-associated molecular pattern (DAMP) that is monitored by the cGAS-STING axis to trigger the immune response in many degenerative diseases. NLRP3 inflammasome-dependent pyroptosis is a type of inflammatory programmed death that promotes a chronic inflammatory response and tissue degeneration. However, the relationship between the cGAS-STING axis and NLRP3 inflammasome-induced pyroptosis in the pathogenesis of IVD degeneration remains unclear. Here, we used magnetic resonance imaging (MRI) and histopathology to demonstrate that cGAS, STING, and NLRP3 are associated with the degree of IVD degeneration. Oxidative stress induced cGAS-STING axis activation and NLRP3 inflammasome-mediated pyroptosis in a STING-dependent manner in human NP cells. Interestingly, the canonical morphological and functional characteristics of mitochondrial permeability transition pore (mPTP) opening with the cytosolic escape of mitochondrial DNA (mtDNA) were observed in human NP cells under oxidative stress. Furthermore, the administration of a specific pharmacological inhibitor of mPTP and self-mtDNA cytosolic leakage effectively reduced NLRP3 inflammasome-mediated pyroptotic NP cell death and microenvironmental inflammation in vitro and degenerative progression in a rat disc needle puncture model. Collectively, these data highlight the critical roles of the cGAS-STING-NLRP3 axis and pyroptosis in the progression of IVD degeneration and provide promising therapeutic approaches for discogenic LBP.

MD2 blockade prevents modified LDL-induced retinal injury in diabetes by suppressing NADPH oxidase-4 interaction with Toll-like receptor-4

Chen Huaicheng,Yan Tao,Song Zongming,Ying Shilong,Wu Beibei,Ju Xin,Yang Xi,Qu Jia,Wu Wencan,Zhang Zongduan,Wang Yi 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-

Modified LDL-induced inflammation and oxidative stress are involved in the pathogenesis of diabetic retinopathy. Recent studies have also shown that modified LDL activates Toll-like receptor 4 (TLR4) to mediate retinal injury. However, the mechanism by which modified LDL activates TLR4 and the potential role of the TLR4 coreceptor myeloid differentiation protein 2 (MD2) are not known. In this study, we inhibited MD2 with the chalcone derivatives L2H17 and L6H21 and showed that MD2 blockade protected retinal Müller cells against highly oxidized glycated-LDL (HOG-LDL)-induced oxidative stress, inflammation, and apoptosis. MD2 inhibition reduced oxidative stress by suppressing NADPH oxidase-4 (NOX4). Importantly, HOG-LDL activated TLR4 and increased the interaction between NOX4 and TLR4. MD2 was required for the activation of these pathways, as inhibiting MD2 prevented the association of NOX4 with TLR4 and reduced NOX4-mediated reactive oxygen species production and TLR4-mediated inflammatory factor production. Furthermore, treatment of diabetic mice with L2H17 significantly reduced LDL extravasation in the retina and prevented retinal dysfunction and apoptosis by suppressing the TLR4/MD2 pathway. Our findings provide evidence that MD2 plays a critical role in mediating modified LDL-induced cell injury in the retina and suggest that targeting MD2 may be a potential therapeutic strategy.

O-GlcNAc transferase regulates intervertebral disc degeneration by targeting FAM134B-mediated ER-phagy

Luo Rongjin,Li Gaocai,Zhang Weifei,Liang Huaizhen,Lu Saideng,Cheung Jason Pui Yin,Zhang Teng,Tu Ji,Liu Hui,Liao Zhiwei,Ke Wencan,Wang Bingjin,Song Yu,Yang Cao 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

Both O-linked β-N-acetylglucosaminylation (O-GlcNAcylation) and endoplasmic reticulum-phagy (ER-phagy) are well-characterized conserved adaptive regulatory mechanisms that maintain cellular homeostasis and function in response to various stress conditions. Abnormalities in O-GlcNAcylation and ER-phagy have been documented in a wide variety of human pathologies. However, whether O-GlcNAcylation or ER-phagy is involved in the pathogenesis of intervertebral disc degeneration (IDD) is largely unknown. In this study, we investigated the function of O-GlcNAcylation and ER-phagy and the related underlying mechanisms in IDD. We found that the expression profiles of O-GlcNAcylation and O-GlcNAc transferase (OGT) were notably increased in degenerated NP tissues and nutrient-deprived nucleus pulposus (NP) cells. By modulating the O-GlcNAc level through genetic manipulation and specific pharmacological intervention, we revealed that increasing O-GlcNAcylation abundance substantially enhanced cell function and facilitated cell survival under nutrient deprivation (ND) conditions. Moreover, FAM134B-mediated ER-phagy activation was regulated by O-GlcNAcylation, and suppression of ER-phagy by FAM134B knockdown considerably counteracted the protective effects of amplified O-GlcNAcylation. Mechanistically, FAM134B was determined to be a potential target of OGT, and O-GlcNAcylation of FAM134B notably reduced FAM134B ubiquitination-mediated degradation. Correspondingly, the protection conferred by modulating O-GlcNAcylation homeostasis was verified in a rat IDD model. Our data demonstrated that OGT directly associates with and stabilizes FAM134B and subsequently enhances FAM134B-mediated ER-phagy to enhance the adaptive capability of cells in response to nutrient deficiency. These findings may provide a new option for O-GlcNAcylation-based therapeutics in IDD prevention.