Novel Architecture of OneM2M-Based Convergence Platform for Mixed Reality and IoT

There have been numerous works proposed to merge augmented reality/mixed reality (AR/MR) and Internet of Things (IoT) in various ways. However, they have focused on their specific target applications and have limitations on interoperability or reusability when utilizing them to different domains or adding other devices to the system. This paper proposes a novel architecture of a convergence platform for AR/MR and IoT systems and services. The proposed architecture adopts the oneM2M IoT standard as the basic framework that converges AR/MR and IoT systems and enables the development of application services used in general-purpose environments without being subordinate to specific systems, domains, and device manufacturers. We implement the proposed architecture utilizing the open-source oneM2M-based IoT server and device platforms released by the open alliance for IoT standards (OCEAN) and Microsoft HoloLens as an MR device platform. We also suggest and demonstrate the practical use cases and discuss the advantages of the proposed architecture

Supervised Learning-Based Fast, Stealthy, and Active NAT Device Identification Using Port Response Patterns

Although network address translation (NAT) provides various advantages, it may cause potential threats to network operations. For network administrators to operate networks effectively and securely, it may be necessary to verify whether an assigned IP address is using NAT or not. In this paper, we propose a supervised learning-based active NAT device (NATD) identification using port response patterns. The proposed model utilizes the asymmetric port response patterns between NATD and non-NATD. In addition, to reduce the time and to solve the security issue that supervised learning approaches exhibit, we propose a fast and stealthy NATD identification method. The proposed method can perform the identification remotely, unlike conventional methods that should operate in the same network as the targets. The experimental results demonstrate that the proposed method is effective, exhibiting a F1 score of over 90%. With the efficient features of the proposed methods, we recommend some practical use cases that can contribute to managing networks securely and effectively

Peroxiredoxin 3 deficiency induces cardiac hypertrophy and dysfunction by impaired mitochondrial quality control

Mitochondrial quality control (MQC) consists of multiple processes: the prevention of mitochondrial oxidative damage, the elimination of damaged mitochondria via mitophagy and mitochondrial fusion and fission. Several studies proved that MQC impairment causes a plethora of pathological conditions including cardiovascular diseases. However, the precise molecular mechanism by which MQC reverses mitochondrial dysfunction, especially in the heart, is unclear. The mitochondria-specific peroxidase Peroxiredoxin 3 (Prdx3) plays a protective role against mitochondrial dysfunction by removing mitochondrial reactive oxygen species. Therefore, we investigated whether Prdx3-deficiency directly leads to heart failure via mitochondrial dysfunction. Fifty-two-week-old Prdx3-deficient mice exhibited cardiac hypertrophy and dysfunction with giant and damaged mitochondria. Mitophagy was markedly suppressed in the hearts of Prdx3-deficient mice compared to the findings in wild-type and Pink1-deficient mice despite the increased mitochondrial damage induced by Prdx3 deficiency. Under conditions inducing mitophagy, we identified that the damaged mitochondrial accumulation of PINK1 was completely inhibited by the ablation of Prdx3. We propose that Prdx3 interacts with the N-terminus of PINK1, thereby protecting PINK1 from proteolytic cleavage in damaged mitochondria undergoing mitophagy. Our results provide evidence of a direct association between MQC dysfunction and cardiac function. The dual function of Prdx3 in mitophagy regulation and mitochondrial oxidative stress elimination further clarifies the mechanism of MQC in vivo and thereby provides new insights into developing a therapeutic strategy for mitochondria-related cardiovascular diseases such as heart failure. © 20221

Naa12 compensates for Naa10 in mice in the amino-terminal acetylation pathway.

Amino-terminal acetylation is catalyzed by a set of N-terminal acetyltransferases (NATs). The NatA complex (including X-linked Naa10 and Naa15) is the major acetyltransferase, with 40-50% of all mammalian proteins being potential substrates. However, the overall role of amino-terminal acetylation on a whole-organism level is poorly understood, particularly in mammals. Male mice lacking Naa10 show no globally apparent in vivo amino-terminal acetylation impairment and do not exhibit complete embryonic lethality. Rather Naa10 nulls display increased neonatal lethality, and the majority of surviving undersized mutants exhibit a combination of hydrocephaly, cardiac defects, homeotic anterior transformation, piebaldism and urogenital anomalies. Naa12 is a previously unannotated Naa10-like paralogue with NAT activity that genetically compensates for Naa10. Mice deficient for Naa12 have no apparent phenotype, whereas mice deficient for Naa10 and Naa12 display embryonic lethality. The discovery of Naa12 adds to the currently known machinery involved in amino-terminal acetylation in mice

Naa12 compensates for Naa10 in mice in the amino-terminal acetylation pathway

Amino-terminal acetylation is catalyzed by a set of N-terminal acetyltransferases (NATs). The NatA complex (including X-linked Naa10 and Naa15) is the major acetyltransferase, with 40-50% of all mammalian proteins being potential substrates. However, the overall role of amino-terminal acetylation on a whole-organism level is poorly understood, particularly in mammals. Male mice lacking Naa10 show no globally apparent in vivo amino-terminal acetylation impairment and do not exhibit complete embryonic lethality. Rather Naa10 nulls display increased neonatal lethality, and the majority of surviving undersized mutants exhibit a combination of hydrocephaly, cardiac defects, homeotic anterior transformation, piebaldism, and urogenital anomalies. Naa12 is a previously unannotated Naa10-like paralog with NAT activity that genetically compensates for Naa10. Mice deficient for Naa12 have no apparent phenotype, whereas mice deficient for Naa10 and Naa12 display embryonic lethality. The discovery of Naa12 adds to the currently known machinery involved in amino-terminal acetylation in mice

QoS improvement with an optimum controller selection for software-defined networks.

The software-defined networking (SDN) paradigm has simplified the management of computer networks by decoupling data and control planes. Moreover, the separation of the data and control planes has transitioned network complexity from traditional devices to controllers; therefore, controllers have become indispensable entities in SDN. Controllers have multiple features and direct the network from a central point and respond to updates to topological changes. However, the supportive capability of these features is strong in one controller but weak in another. Due to several controllers and each controller having a set of features, selecting an optimal SDN controller can be considered to be a multi-criteria decision-making (MCDM) problem. Herein, a two-step approach is proposed for SDN controller selection. First, the controllers are ranked with analytical network process (ANP) according to their qualitative features which influence the performance of these controllers and then a performance comparison is performed to check for the QoS improvement. The controller with a high-weight value from the feature-based comparison is quantitatively analysed by experimental analysis. The main contribution of this paper is checking the applicability of the ANP for controller selection in SDN considering its features and performance analysis in real-world Internet and Brite topologies. The simulation results show that the controller computed through the proposed approach outperforms the controller selected with existing approaches. The selection of an optimum controller with ANP results in a reduction of topology discovery time and delay in the normal and traffic load scenario. Similarly, an increase in throughput with a reasonable utilization of the central processing unit (CPU) is observed for the proposed controller

Gamma-aminobutyric acid production using immobilized glutamate decarboxylase followed by downstream processing with cation exchange chromatography

Abstract: We have developed a gamma-aminobutyric acid (GABA) production technique using his-tag mediated immobilization of Escherichia coli-derived glutamate decarboxylase (GAD), an enzyme that catalyzes the conversion of glutamate to GABA. The GAD was obtained at 1.43 g/L from GAD-overexpressed E. coli fermentation and consisted of 59.7 % monomer, 29.2 % dimer and 2.3 % tetramer with a 97.6 % soluble form of the total GAD. The harvested GAD was immobilized to metal affinity gel with an immobilization yield of 92%. Based on an investigation of specific enzyme activity and reaction characteristics, glutamic acid (GA) was chosen over monosodium glutamate (MSG) as a substrate for immobilized GAD, resulting in conversion of 2.17 M GABA in a 1 L reactor within 100 min. The immobilized enzymes retained 58.1 % of their initial activities after ten consecutive uses. By using cation exchange chromatography followed by enzymatic conversion, GABA was separated from the residual substrate and leached GAD. As a consequence, the glutamic acid was mostly removed with no detectable GAD, while 91.2 % of GABA was yielded in the purification step. Int. J. Mol. Sci. 2013, 14 172

Stabilization of Precursor Solution and Perovskite Layer by Addition of Sulfur

Efficient perovskite solar cells (PSCs) are mainly fabricated by a solution coating processes. However, the efficiency of such devices varies significantly with the aging time of the precursor solution used to fabricate them, which includes a mixture of perovskite components, especially methylammonium (MA), and formamidinium (FA) cations. Herein, how the inorganic-organic hybrid perovskite precursor solution of (FAPbI(3))(0.95)(MAPbBr(3))(0.05) degrades over time and how such degradation can be effectively inhibited is reported on, and the associated mechanism of degradation is discussed. Such degradation of the precursor solution is closely related to the loss of MA cations dissolved in the FA solution through the deprotonation of MA to volatile methylamine (CH3NH2). Addition of elemental sulfur (S-8) drastically stabilizes the precursor solution owing to amine-sulfur coordination, without compromising the power conversion efficiency (PCE) of the derived PSCs. Furthermore, sulfur introduced to stabilize the precursor solution results in improved PSC stability

High-level conversion of L-lysine into 5-aminovalerate that can be used for nylon 6,5 synthesis

L-Lysine is a potential feedstock for the production of bio-based precursors for engineering plastics. In this study, we developed a microbial process for high-level conversion of L-lysine into 5-aminovalerate (5AVA) that can be used as a monomer in nylon 6,5 synthesis. Recombinant Escherichia coli WL3110 strain expressing Pseudomonas putida delta-aminovaleramidase (DavA) and lysine 2-monooxygenase (DavB) was grown to high density in fed-batch culture and used as a whole cell catalyst. High-density E. coli WL3110 expressing DavAB, grown to an optical density at 600 nm (OD600) of 30, yielded 36.51 g/L 5AVA from 60 g/L L-lysine in 24 h. Doubling the cell density of E. coli WL3110 improved the conversion yield to 47.96 g/L 5AVA from 60 g/L of L-lysine in 24 h. 5AVA production was further improved by doubling the L-lysine concentration from 60 to 120 g/L. The highest 5AVA titer (90.59 g/L; molar yield 0.942) was obtained from 120 g/L L-lysine by E. coli WL3110 cells grown to OD600 of 60. Finally, nylon 6,5 was synthesized by bulk polymerization of ε{lunate}-caprolactam and δ-valerolactam prepared from microbially synthesized 5AVA. The hybrid system demonstrated here has promising possibilities for application in the development of industrial bio-nylon production processes. L-lysine, a feedstock for the production of bio-nylon precursors, can be converted into 5AVA by whole-cell catalytic reaction of recombinant E. coli expressing the P. putida davAB genes. This 5AVA can be further converted into δ-valerolactam to synthesize bio-nylon 6,5. The hybrid system is expected to be applicable in the development of bio-nylon production processes