Jeonbuk National University

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is thatthere is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the completeprocess including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increasedautophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in manycases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as forreviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multipleassays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation, it is imperative to target by gene knockout or RNA interference more than one autophagyrelated protein. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways implying that not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular assays, we hope to encourage technical innovation in the field.

Abstract Turbulent friction and heat transfer behaviors of dispersed fluids (i.e., uttrafine metallic oxide particles suspended in water) in a circular pipe were investigated experimentally. Viscosity measurements were also conducted using a Brookfield rotating viscometer. Two different metallic oxide particles, γ-alumina (Al2O3) and titanium dioxide (TiO2), with mean diameters of 13 and 27 nm, respectively, were used as suspended particles. The Reynolds and Prandtl numbers varied in the ranges l04-I05 and 6.5-12.3, respectively. The viscosities of the dispersed fluids with γ-Al2O3 and TiO2 particles at a 10% volume concentration were approximately 200 and 3 times greater than that of water, respectively. These viscosity results were significantly larger than the predictions from the classical theory of suspension rheology. Darcy friction factors for the dispersed fluids of the volume concentration ranging from 1% to 3% coincided well with Kays' correlation for turbulent flow of a single-phase fluid. The Nusselt number of the dispersed fluids for fully developed turbulent flow increased with increasing volume concentration as well as the Reynolds number. However, it was found that the convective heat transfer coefficient of the dispersed fluid at a volume concentration of 3% was 12% smaller than that of pure water when compared under the condition of constant average velocity. Therefore, better selection of particles having higher thermal conductivity and larger size is recommended in order to utilize dispersed fluids as a working medium to enhance heat transfer performance. A new correlation for the turbulent connective heat transfer for dilute dispersed fluids with submicron metallic oxide particles is given by the following equation: Nu = 0.021 Re0.8Pr0.5.

autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.

The RENO experiment has observed the disappearance of reactor electron antineutrinos, consistent with neutrino oscillations, with a significance of 4.9 standard deviations. Antineutrinos from six $2.8\text{ }\text{ }{\mathrm{GW}}_{\mathrm{th}}$ reactors at the Yonggwang Nuclear Power Plant in Korea, are detected by two identical detectors located at 294 and 1383 m, respectively, from the reactor array center. In the 229 d data-taking period between 11 August 2011 and 26 March 2012, the far (near) detector observed 17102 (154088) electron antineutrino candidate events with a background fraction of 5.5% (2.7%). The ratio of observed to expected numbers of antineutrinos in the far detector is $0.920\ifmmode\pm\else\textpm\fi{}0.009(\mathrm{stat})\ifmmode\pm\else\textpm\fi{}0.014(\mathrm{syst})$. From this deficit, we determine ${sin}^{2}2{\ensuremath{\theta}}_{13}=0.113\ifmmode\pm\else\textpm\fi{}0.013(\mathrm{stat})\ifmmode\pm\else\textpm\fi{}0.019(\mathrm{syst})$ based on a rate-only analysis.

copies/mL). Thus, we have successfully fabricated a promising FET biosensor for SARS-CoV-2; our device is a highly sensitive immunological diagnostic method for COVID-19 that requires no sample pretreatment or labeling.

Plant Diseases and Pests are a major challenge in the agriculture sector. An accurate and a faster detection of diseases and pests in plants could help to develop an early treatment technique while substantially reducing economic losses. Recent developments in Deep Neural Networks have allowed researchers to drastically improve the accuracy of object detection and recognition systems. In this paper, we present a deep-learning-based approach to detect diseases and pests in tomato plants using images captured in-place by camera devices with various resolutions. Our goal is to find the more suitable deep-learning architecture for our task. Therefore, we consider three main families of detectors: Faster Region-based Convolutional Neural Network (Faster R-CNN), Region-based Fully Convolutional Network (R-FCN), and Single Shot Multibox Detector (SSD), which for the purpose of this work are called "deep learning meta-architectures". We combine each of these meta-architectures with "deep feature extractors" such as VGG net and Residual Network (ResNet). We demonstrate the performance of deep meta-architectures and feature extractors, and additionally propose a method for local and global class annotation and data augmentation to increase the accuracy and reduce the number of false positives during training. We train and test our systems end-to-end on our large Tomato Diseases and Pests Dataset, which contains challenging images with diseases and pests, including several inter- and extra-class variations, such as infection status and location in the plant. Experimental results show that our proposed system can effectively recognize nine different types of diseases and pests, with the ability to deal with complex scenarios from a plant's surrounding area.

A measurement of the Higgs boson mass is presented based on the combined data samples of the ATLAS and CMS experiments at the CERN LHC in the H→γγ and H→ZZ→4ℓ decay channels. The results are obtained from a simultaneous fit to the reconstructed invariant mass peaks in the two channels and for the two experiments. The measured masses from the individual channels and the two experiments are found to be consistent among themselves. The combined measured mass of the Higgs boson is m_{H}=125.09±0.21 (stat)±0.11 (syst) GeV.

This study describes a simple approach to generate relatively pure cultures of cardiomyocytes from differentiating murine embryonic stem (ES) cells. A fusion gene consisting of the alpha-cardiac myosin heavy chain promoter and a cDNA encoding aminoglycoside phosphotransferase was stably transfected into pluripotent ES cells. The resulting cell lines were differentiated in vitro and subjected to G418 selection. Immunocytological and ultrastructural analyses demonstrated that the selected cardiomyocyte cultures (> 99% pure) were highly differentiated. G418 selected cardiomyocytes were tested for their ability to form grafts in the hearts of adult dystrophic mice. The fate of the engrafted cells was monitored by antidystrophin immunohistology, as well as by PCR analysis with primers specific for the myosin heavy chain-aminoglycoside phosphotransferase transgene. Both analyses revealed the presence of ES-derived cardiomyocyte grafts for as long as 7 wk after implantation, the latest time point analyzed. These studies indicate that a simple genetic manipulation can be used to select essentially pure cultures of cardiomyocytes from differentiating ES cells. Moreover, the resulting cardiomyocytes are suitable for the formation of intracardiac grafts. This selection approach should be applicable to all ES-derived cell lineages.

Coronavirus disease 2019 (COVID-19), which causes serious respiratory illness such as pneumonia and lung failure, was first reported in Wuhan, the capital of Hubei, China. The etiological agent of COVID-19 has been confirmed as a novel coronavirus, now known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is most likely originated from zoonotic coronaviruses, like SARS-CoV, which emerged in 2002. Within a few months of the first report, SARS-CoV-2 had spread across China and worldwide, reaching a pandemic level. As COVID-19 has triggered enormous human casualties and serious economic loss posing global threat, an understanding of the ongoing situation and the development of strategies to contain the virus's spread are urgently needed. Currently, various diagnostic kits to test for COVID-19 are available and several repurposing therapeutics for COVID-19 have shown to be clinically effective. In addition, global institutions and companies have begun to develop vaccines for the prevention of COVID-19. Here, we review the current status of epidemiology, diagnosis, treatment, and vaccine development for COVID-19.

Environmental stresses converge on the mitochondria that can trigger or inhibit cell death.Excitable, postmitotic cells, in response to sublethal noxious stress, engage mechanisms that afford protection from subsequent insults.We show that reoxygenation after prolonged hypoxia reduces the reactive oxygen species (ROS) threshold for the mitochondrial permeability transition (MPT) in cardiomyocytes and that cell survival is steeply negatively correlated with the fraction of depolarized mitochondria.Cell protection that exhibits a memory (preconditioning) results from triggered mitochondrial swelling that causes enhanced substrate oxidation and ROS production, leading to redox activation of PKC, which inhibits glycogen synthase kinase-3 (GSK-3).Alternatively, receptor tyrosine kinase or certain G protein-coupled receptor activation elicits cell protection (without mitochondrial swelling or durable memory) by inhibiting GSK-3, via protein kinase B/Akt and mTOR/p70 s6k pathways, PKC pathways, or protein kinase A pathways.The convergence of these pathways via inhibition of GSK-3 on the end effector, the permeability transition pore complex, to limit MPT induction is the general mechanism of cardiomyocyte protection.Nonstandard abbreviations used: bisindolylmaleimide I (BIS); 2-chloro-N6-cyclopentyladenosine (CCPA); diazoxide (Dz); 2,7-dichlorodihydrofluorescein diacetate (DCF); glucagon-like peptide-a (GLP-1); glycogen synthase kinase-3 (GSK-3); 5-hydroxydecanoate (5HD); indanyloxyacetic acid 94 (IAA94); mitochondrial ATPdependent K + channel (mitoKATP); mitochondrial permeability transition (MPT); N-acetyl-L-cysteine (NAC); partial fatty acid oxidation (PFAO); Na/H exchange (NHE); preconditioning (PC); protein kinase A (PKA); protein kinase B (PKB); reactive oxygen species (ROS); receptor for activated C kinase (RACK); Sanglifehrin A (SFA); short interfering RNA (siRNA); S-nitroso-N-acetyl-penicillamine (SNAP); tetramethylrhodamine methyl ester (TMRM); transgenic (TG); transmembrane potential (); trimetazidine (TMZ); Tyr-D-Ala-Gly-Phe-D-Leu (DADLE).

The CMS apparatus was identified, a few years before the start of the LHC operation at CERN, to feature properties well suited to particle-flow (PF) reconstruction: a highly-segmented tracker, a fine-grained electromagnetic calorimeter, a hermetic hadron calorimeter, a strong magnetic field, and an excellent muon spectrometer. A fully-fledged PF reconstruction algorithm tuned to the CMS detector was therefore developed and has been consistently used in physics analyses for the first time at a hadron collider. For each collision, the comprehensive list of final-state particles identified and reconstructed by the algorithm provides a global event description that leads to unprecedented CMS performance for jet and hadronic decay reconstruction, missing transverse momentum determination, and electron and muon identification. This approach also allows particles from pileup interactions to be identified and enables efficient pileup mitigation methods. The data collected by CMS at a centre-of-mass energy of 8show excellent agreement with the simulation and confirm the superior PF performance at least up to an average of 20 pileup interactions.

This paper reviews the state of the art of composite polymer electrolytes (CPE) in view of their electrochemical and physical properties for the applications in lithium batteries. This review mainly encompasses on composite polymer electrolyte hosts namely poly(ethylene oxide) (PEO), poly(acrylonitrile) (PAN), poly(methyl methacrylate) (PMMA) and poly(vinylidene fluoride) (PVdF) studied so far. Also the ionic conductivity, transference number, compatibility and the cycling behavior of poly(vinylidene fluoride-hexafluoro propylene) (PVdF-HFP)–[AlO(OH)]n–LiPF6/LiClO4 composite electrolytes have been studied and the results are discussed.

Although three-dimensional (3D) bioprinting technology has gained much attention in the field of tissue engineering, there are still several significant engineering challenges to overcome, including lack of bioink with biocompatibility and printability. Here, we show a bioink created from silk fibroin (SF) for digital light processing (DLP) 3D bioprinting in tissue engineering applications. The SF-based bioink (Sil-MA) was produced by a methacrylation process using glycidyl methacrylate (GMA) during the fabrication of SF solution. The mechanical and rheological properties of Sil-MA hydrogel proved to be outstanding in experimental testing and can be modulated by varying the Sil-MA contents. This Sil-MA bioink allowed us to build highly complex organ structures, including the heart, vessel, brain, trachea and ear with excellent structural stability and reliable biocompatibility. Sil-MA bioink is well-suited for use in DLP printing process and could be applied to tissue and organ engineering depending on the specific biological requirements.

This paper proposes a novel hybrid genetic algorithm for feature selection. Local search operations are devised and embedded in hybrid GAs to fine-tune the search. The operations are parameterized in terms of their fine-tuning power, and their effectiveness and timing requirements are analyzed and compared. The hybridization technique produces two desirable effects: a significant improvement in the final performance and the acquisition of subset-size control. The hybrid GAs showed better convergence properties compared to the classical GAs. A method of performing rigorous timing analysis was developed, in order to compare the timing requirement of the conventional and the proposed algorithms. Experiments performed with various standard data sets revealed that the proposed hybrid GA is superior to both a simple GA and sequential search algorithms.

The endoplasmic reticulum (ER) is a fascinating network of tubules through which secretory and transmembrane proteins enter unfolded and exit as either folded or misfolded proteins, after which they are directed either toward other organelles or to degradation, respectively. The ER redox environment dictates the fate of entering proteins, and the level of redox signaling mediators modulates the level of reactive oxygen species (ROS). Accumulating evidence suggests the interrelation of ER stress and ROS with redox signaling mediators such as protein disulfide isomerase (PDI)-endoplasmic reticulum oxidoreductin (ERO)-1, glutathione (GSH)/glutathione disuphide (GSSG), NADPH oxidase 4 (Nox4), NADPH-P450 reductase (NPR), and calcium. Here, we reviewed persistent ER stress and protein misfolding-initiated ROS cascades and their significant roles in the pathogenesis of multiple human disorders, including neurodegenerative diseases, diabetes mellitus, atherosclerosis, inflammation, ischemia, and kidney and liver diseases.

Recent experimental and human studies have shown that hyperuricemia is associated with hypertension, systemic inflammation, and cardiovascular disease mediated by endothelial dysfunction and pathologic vascular remodeling. Elevated levels of C-reactive protein (CRP) have emerged as one of the most powerful independent predictors of cardiovascular disease. In addition to being a marker of inflammation, recent evidence suggests that CRP may participate directly in the development of atherosclerotic vascular disease. For investigating whether uric acid (UA)-induced inflammatory reaction and vascular remodeling is related to CRP, the UA-induced expression of CRP in human vascular smooth muscle cells (HVSMC) and human umbilical vein endothelial cells (HUVEC) was examined, as well as the pathogenetic role of CRP in vascular remodeling. It is interesting that HVSMC and HUVEC expressed CRP mRNA and protein constitutively, revealing that vascular cells are another source of CRP production. UA (6 to 12 mg/dl) upregulated CRP mRNA expression in HVSMC and HUVEC with a concomitant increase in CRP release into cell culture media. Inhibition of p38 or extracellular signal-regulated kinase 44/42 significantly suppressed UA-induced CRP expression, implicating these pathways in the response to UA. UA stimulated HVSMC proliferation whereas UA inhibited serum-induced proliferation of HUVEC assessed by 3H-thymidine uptake and cell counting, which was attenuated by co-incubation with probenecid, the organic anion transport inhibitor, suggesting that entry of UA into cells is responsible for CRP expression. UA also increased HVSMC migration and inhibited HUVEC migration. In HUVEC, UA reduced nitric oxide (NO) release. Treatment of vascular cells with anti-CRP antibody revealed a reversal of the effect of UA on cell proliferation and migration in HVSMC and NO release in HUVEC, which suggests that CRP expression may be responsible for UA-induced vascular remodeling. This is the first study to show that soluble UA, at physiologic concentrations, has profound effects on human vascular cells. The observation that UA alters the proliferation/migration and NO release of human vascular cells, mediated by the expression of CRP, calls for careful reconsideration of the role of UA in hypertension and vascular disease.

We have investigated the key factors determining the performance of supercapacitors constructed using single-walled carbon nanotube (SWNT) electrodes. Several parameters, such as composition of the binder, annealing temperature, type of current collector, charging time, and discharging current density have been optimized for the best performance of the supercapacitor with respect to energy density and power density. We find a maximum specific capacitance of 180 F/g and a measured power density of 20 kW/kg at energy densities in the range from 7 to 6.5 Wh/kg at 0.9 V in a solution of 7.5 N KOH (the currently available supercapacitors have energy densities in the range 6–7 Wh/kg and power density in the range 0.2–5 kW/kg at 2.3 V in non-aqueous solvents).

In recent years, nanobiotechnology has emerged as an elementary division of modern science and a noval epoch in the fields of material science and is receiving global attention due to its ample applications. Various physical, chemical, and biological methods have been employed to synthesize nanomaterials. Biological systems such as bacteria, fungi, actinomycetes, yeasts, viruses, and plants have been reported to synthesize various metal and metal oxide nanoparticles. Among these, biosynthesis of nanoparticles from plants seems to be a very effective method in developing a rapid, clean, nontoxic, and eco-friendly technology. The use of plant biomass or extracts for the biosynthesis of novel metal nanoparticles (silver, gold, platinum, and palladium) would be more significant if the nanoparticles are synthesized extracellularly and in a controlled manner according to their dispersity of shape and size. Owing to the rich biodiversity of plants, their potential use toward the synthesis of these nobel metal nanoparticles is yet to be explored. The aim of this review is to provide the recent trends involved in the phytosynthesis of nobel metal nanoparticles in the past decade.

Produced via electrospinning, polyurethane membrane, which has a unique property, has been of interest in medical fields. Electrospinning is a process by which nanofibers can be produced by an electrostatically driven jet of polymer solution. Electrospun fibers are collected in the form of membranes. The porous structured electrospun membrane is particularly important for its favorable properties: it exudates fluid from the wound, does not build up under the covering, and does not cause wound desiccation. The electrospun nanofibrous membrane shows controlled evaporative water loss, excellent oxygen permeability, and promoted fluid drainage ability, but still it can inhibit exogenous microorganism invasion because its pores are ultra-fine. Histological examination indicates that the rate of epithelialization is increased and the dermis becomes well organized if wounds are covered with electrospun nanofibrous membrane. This electrospun membrane has potential applications for wound dressing based upon its unique properties.

Abstract About twenty years ago, in the autumn of 1996, the first white light‐emitting diodes (LEDs) were offered for sale. These then‐new devices ushered in a new era in lighting by displacing lower‐efficiency conventional light sources including Edison's venerable incandescent lamp as well as the Hg‐discharge‐based fluorescent lamp. We review the history of the conception, improvement, and commercialization of the white LED. Early models of white LEDs already exceeded the efficiency of low‐wattage incandescent lamps, and extraordinary progress has been made during the last 20 years. The review also includes a discussion of advances in blue LED chips, device architecture, light extraction, and phosphors. Finally, we offer a brief outlook on opportunities provided by smart LED technology. image