Manipulation of Host Microtubule Networks by Viral Microtubule-Associated Proteins

Diverse DNA and RNA viruses utilize cytoskeletal networks to efficiently enter, replicate, and exit the host cell, while evading host immune responses. It is well established that the microtubule (MT) network is commonly hijacked by viruses to traffic to sites of replication after entry and to promote egress from the cell. However, mounting evidence suggests that the MT network is also a key regulator of host immune responses to infection. At the same time, viruses have acquired mechanisms to manipulate and/or usurp MT networks to evade these immune responses. Central to most interactions of viruses with the MT network are virally encoded microtubule-associated proteins (MAPs) that bind to MTs directly or indirectly. These MAPs associate with MTs and other viral or cellular MAPs to regulate various aspects of the MT network, including MT dynamics, MT-dependent transport via motor proteins such as kinesins and dyneins, and MT-dependent regulation of innate immune responses. In this review, we examine how viral MAP interactions with the MT network facilitate viral replication and immune evasion

Noninvasive Brain Stimulation Using a Modulated Microwave Signal

We propose a microwave signal generation system for brain stimulation. The existing brain stimulation system uses a signal of several tens of kHz, and the magnetic field distribution is wide. Microwave is used to locally limit the distribution of the electromagnetic field and to change the action potential of the cell with less power. The switch modulates the microwave signal to obtain a pulse envelope. The action potential of the cell can be controlled to the excitation/inhibition state by adjusting the repetition frequency. These results are confirmed by measuring the cell potential of the mouse brain

Structural and Chemical Evolutions of Li/Electrolyte Interfaces in Li-Metal Batteries: Tracing Compositional Changes of Electrolytes under Practical Conditions

Despite the promises in high-energy-density batteries, Li-metal anodes (LMAs) have suffered from extensive electrolyte decomposition and unlimited volume expansion owing to thick, porous layer buildup during cycling. It mainly originates from a ceaseless reiteration of the formation and collapse of solid-electrolyte interphase (SEI). This study reveals the structural and chemical evolutions of the reacted Li layer after different cycles and investigates its detrimental effects on the cycling stability under practical conditions. Instead of the immediately deactivated top surface of the reacted Li layer, the chemical nature underneath the reacted Li layer can be an important indicator of the electrolyte compositional changes. It is found that cycling of LMAs with a lean electrolyte (approximate to 3 g Ah(-1)) causes fast depletion of salt anions, leading to the dynamic evolution of the reacted Li layer structure and composition. Increasing the salt-solvent complex while reducing the non-solvating diluent retards the rate of depletion in a localized high-concentration electrolyte, thereby demonstrating prolonged cycling of Li||NMC622 cells without compromising the Li Coulombic efficiencies and high-voltage stability. © 2022 The Authors. Advanced Science published by Wiley-VCH GmbH.TRU

Association between Risk Communication Format and Perceived Risk of Adverse Events after COVID-19 Vaccination among US Adults

The format used to communicate probability—verbal versus numerical descriptors—can impact risk perceptions and behaviors. This issue is salient for the Coronavirus disease 2019 (COVID-19), where concerns about vaccine-related risks may reduce uptake and verbal descriptors have been widely used by public health, news organizations and on social media, to convey risk. Because the effect of risk-communication format on perceived COVID-19 vaccine-related risks remains unknown, we conducted an online randomized survey among 939 US adults. Participants were given risk information, using verbal or numerical descriptors and were asked to report their perceived risk of experiencing headache, fever, fatigue or myocarditis from COVID-19 vaccine. Associations between risk communication format and perceived risk were assessed using multivariable regression. Compared to numerical estimates, verbal descriptors were associated with higher perceived risk of headache (β = 5.0 percentage points, 95% CI = 2.0–8.1), fever (β = 27 percentage points, 95% CI = 23–30), fatigue (β = 4.9 percentage points, 95% = CI 1.8–8.0) and myocarditis (β = 4.6 percentage points, 95% CI = 2.1–7.2), as well as greater variability in risk perceptions. Social media influence was associated with differences in risk perceptions for myocarditis, but not side effects. Verbal descriptors may lead to greater, more inaccurate and variable vaccine-related risk perceptions compared to numerical descriptors

Apolipoprotein B Is Related to Metabolic Syndrome Independently of Low Density Lipoprotein Cholesterol in Patients with Type 2 Diabetes

BackgroundIncreased low density lipoprotein cholesterol (LDL-C) level and the presence of metabolic syndrome (MetS) are important risk factors for cardiovascular disease (CVD) in type 2 diabetes mellitus (T2DM). Recent studies demonstrated apolipoprotein B (apoB), a protein mainly located in LDL-C, was an independent predictor of the development of CVD especially in patients with T2DM. The aim of this study was to investigate the relationship between apoB and MetS in T2DM patients.MethodsWe analyzed 912 patients with T2DM. Fasting blood samples were taken for glycated hemoglobin, high-sensitivity C-reactive protein, total cholesterol, triglyceride (TG), high density lipoprotein cholesterol, LDL-C, and apoB. MetS was defined by the modified National Cholesterol Education Program Adult Treatment Panel III criteria. We performed a hierarchical regression analysis with apoB as the dependent variable. Age, sex, the number of components of MetS and LDL-C were entered at model 1, the use of lipid-lowering medications at model 2, and the individual components of MetS were added at model 3.ResultsSeventy percent of total subjects had MetS. ApoB level was higher in subjects with than those without MetS (104.5±53.3 mg/dL vs. 87.7±33.7 mg/dL, P<0.01) even after adjusting for LDL-C. ApoB and LDL-C were positively correlated to the number of MetS components. The hierarchical regression analysis showed that the increasing number of MetS components was associated with higher level of apoB at step 1 and step 2 (β=0.120, P<0.001 and β=0.110, P<0.001, respectively). At step 3, TG (β=0.116, P<0.001) and systolic blood pressure (β=0.099, P<0.05) were found to significantly contribute to apoB.ConclusionIn patients with T2DM, apoB is significantly related to MetS independently of LDL-C level. Of the components of MetS, TG, and systolic blood pressure appeared to be determinants of apoB

Peli3 ablation ameliorates acetaminophen-induced liver injury through inhibition of GSK3β phosphorylation and mitochondrial translocation

Abstract The signaling pathways governing acetaminophen (APAP)-induced liver injury have been extensively studied. However, little is known about the ubiquitin-modifying enzymes needed for the regulation of APAP-induced liver injury. Here, we examined whether the Pellino3 protein, which has E3 ligase activity, is needed for APAP-induced liver injury and subsequently explored its molecular mechanism. Whole-body Peli3 −/− knockout (KO) and adenovirus-mediated Peli3 knockdown (KD) mice showed reduced levels of centrilobular cell death, infiltration of immune cells, and biomarkers of liver injury, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), upon APAP treatment compared to wild-type (WT) mice. Peli3 deficiency in primary hepatocytes decreased mitochondrial and lysosomal damage and reduced the mitochondrial reactive oxygen species (ROS) levels. In addition, the levels of phosphorylation at serine 9 in the cytoplasm and mitochondrial translocation of GSK3β were decreased in primary hepatocytes obtained from Peli3 −/− KO mice, and these reductions were accompanied by decreases in JNK phosphorylation and mitochondrial translocation. Pellino3 bound more strongly to GSK3β compared with JNK1 and JNK2 and induced the lysine 63 (K63)-mediated polyubiquitination of GSK3β. In rescue experiments, the ectopic expression of wild-type Pellino3 in Peli3 −/− KO hepatocytes restored the mitochondrial translocation of GSK3β, but this restoration was not obtained with expression of a catalytically inactive mutant of Pellino3. These findings are the first to suggest a mechanistic link between Pellino3 and APAP-induced liver injury through the modulation of GSK3β polyubiquitination

Anti-Inflammatory Actions of Soluble Ninjurin-1 Ameliorate Atherosclerosis

Background: Macrophages produce many inflammation-associated molecules, released by matrix metalloproteinases, such as adhesion molecules, and cytokines, as well, which play a crucial role in atherosclerosis. In this context, we investigated the relationship between Ninjurin-1 (Ninj1 [nerve injury-induced protein]), a novel matrix metalloproteinase 9 substrate, expression, and atherosclerosis progression. Methods: Ninj1 expression and atherosclerosis progression were assessed in atherosclerotic aortic tissue and serum samples from patients with coronary artery disease and healthy controls, and atheroprone apolipoprotein e-deficient (Apoe(-/-)) and wild-type mice, as well. Apoe(-/-) mice lacking systemic Ninj1 expression (Ninj1(-/-)Apoe(-/-)) were generated to assess the functional effects of Ninj1. Bone marrow transplantation was also used to generate low-density lipoprotein receptor-deficient (Ldlr(-/-)) mice that lack Ninj1 specifically in bone marrow-derived cells. Mice were fed a Western diet for 5 to 23 weeks, and atherosclerotic lesions were investigated. The anti-inflammatory role of Ninj1 was verified by treating macrophages and mice with the peptides Ninj1(1)(-56) (ML56) and Ninj1(26)(-37) (PN12), which mimic the soluble form of Ninj1 (sNinj1). Results: Our in vivo results conclusively showed a correlation between Ninj1 expression in aortic macrophages and the extent of human and mouse atherosclerotic lesions. Ninj1-deficient macrophages promoted proinflammatory gene expression by activating mitogen-activated protein kinase and inhibiting the phosphoinositide 3-kinase/Akt signaling pathway. Whole-body and bone marrow-specific Ninj1 deficiencies significantly increased monocyte recruitment and macrophage accumulation in atherosclerotic lesions through elevated macrophage-mediated inflammation. Macrophage Ninj1 was directly cleaved by matrix metalloproteinase 9 to generate a soluble form that exhibited antiatherosclerotic effects, as assessed in vitro and in vivo. Treatment with the sNinj1-mimetic peptides, ML56 and PN12, reduced proinflammatory gene expression in human and mouse classically activated macrophages, thereby attenuating monocyte transendothelial migration. Moreover, continuous administration of mPN12 alleviated atherosclerosis by inhibiting the enhanced monocyte recruitment and inflammation characteristics of this disorder in mice, regardless of the presence of Ninj1. Conclusions: Ninj1 is a novel matrix metalloproteinase 9 substrate in macrophages, and sNinj1 is a secreted atheroprotective protein that regulates macrophage inflammation and monocyte recruitment in atherosclerosis. Moreover, sNinj1-mediated anti-inflammatory effects are conserved in human macrophages and likely contribute to human atherosclerosis

Abstracts of 2nd International Symposium on Plastic Pollution

This book presents the abstracts of the selected contributions to the Second International Symposium on Plastic Pollution, hosted from 3rd to 4th of November 2022 in hybrid mode by the “Plastic Free” Specialized Graduate School, University of Seoul. The symposium covers “Challenges and Possible Solutions of Plastic Pollution” and “Toxicity Assessment of Plastics”. The symposium was special as it brought together researchers from multidisciplinary fields, bringing new research ideas and creating collaboration in the field of plastic pollution. With 20 experts from 7 countries and two special sessions with different themes, the symposium offered a perfect platform for attendees to share their research ideas. Symposium Title: 2nd International Symposium on Plastic PollutionTheme: SYM-1~2: Challenges and Possible Solutions of Plastic Pollution. SYM-3: Toxicity Assessment of PlasticsSymposium Date: 3-4 November 2022Symposium Location: Hybrid (online and offline – Jeju-Island Pacific, South Korea)Symposium Organizer: Plastic-Free Specialized Graduate School, University of Seoul, South KoreaSymposium Sponsors: Ministry of Environment &amp; KEITI, South Korea Previous Year Abstract Book: Abstracts of 1st International Symposium on Plastic Pollutio