Diffusion of False Information During Public Crises: Analysis Based on the Cellular Automaton Method

The progress of false information diffusion in the public crisis is harmful to the society. When the public crisis occurs, the public respond in different ways and the public also want to tell others what they think right. But what they think is right is not recognized by the government. Thus the false information forms and it begins to diffuse. As the false information spreads, the harm to society magnifies gradually. Particularly in network society, false information diffusion can easily cause secondary hazards and accelerate public crises to a devastating degree. Thus intervening and controlling the false information diffusion is an important aspect of the public crisis management. From the perspective of the social network theory, this study analyzes the progress of false information diffusion in terms of different public crisis management strategies and presents the result of false information diffusion through simulation on cellular automaton of different public crisis management strategies. In simulations on cellular automaton, interventions are also carried to control false information diffusion and alternatives are proposed to help reduce public crises. This study also extends the theory of false information management, which is significant for the government to improve the ability to evaluate the false information and carry out interventions effectively to control the false information when it begins to diffuse

Analisis Pajak Penghasilan Pasal 23 Atas Jasa Freight Forwarding Pada PT Armarda Samudera Samarinda

Penelitian ini akan dibahas mengingat kegiatan Jasa Freight Forwarding yang dilakukan oleh PT. Armada Samudera Raya merupakan objek PPh Pasal 23 yang harus dilakukan perhitungan, pemotongan, penyetoran dan pelaporan di kantor pajak yang terdekat. Dalam menjalankan USAha jasa Freight Forwarding pada PT. Armada Samudera menggunakan pihak ketiga atau sistem Reimbursement. Mengetahui perhitungan dan pemotongan PPh pasal 23 atas jasa Freight Forwarding yang termasuk jenis jasa lain, dasar pengenaan objek pemotongan PPh 23 sebesar 2 % dari jumlah bruto (Penghasilan).Rumusan masalah dalam penelitian ini adalah “Apakah pemotongan Pajak Penghasilan (PPh) Pasal 23 atas jasa freight forwarding pada PT. Armada Samudera Raya telah sesuai dengan Peraturan Menteri Keuangan 141/PMK.03/2015 dan Undang-Undang Nomor 36 Tahun 2008?”. Alat analisis yang digunakan adalah perhitungan PPh berdasarkan Peraturan Menteri Keuangan Nomor 141/pmk.03/2015 dan Undang-Undang Nomor 7 Tahun 1983 tentang Pajak Penghasilan yang telah diubah terakhir dengan Undang-Undang Nomor 36 Tahun 2008 mewajibkan setiap Perusahaan sebagai wajib pajak untuk melakukan pemotongan PPh 23 sebesar 2 % dari jumlah bruto (Penghasilan) dan membadingkannya dengan perhitungan Perusahaan. Hasil dari penelitian ini adalah Hipotesis diterima apabila pemotongan Pajak Penghasilan (PPh) Pasal 23 atas jasa freight forwarding pada PT. Armada Samudera Raya belum sesuai dengan Peraturan Menteri Keuangan 141/PMK.03/2015 dan Undang-Undang Nomor 36 Tahun 2008 dan sebaliknya Hipotesis ditolak apabila pemotongan Pajak Penghasilan (PPh) Pasal 23 atas jasa freight forwarding pada PT. Armada Samudera Raya sudah sesuai dengan Peraturan Menteri Keuangan 141/PMK.03/2015 dan Undang-Undang Nomor 36 Tahun 2008

IKKα negatively regulates ASC-dependent inflammasome activation.

The inflammasomes are multiprotein complexes that activate caspase-1 in response to infections and stress, resulting in the secretion of pro-inflammatory cytokines. Here we report that IκB kinase α (IKKα) is a critical negative regulator of apoptosis-associated specklike protein containing a C-terminal caspase-activation-andrecruitment (CARD) domain (ASC)-dependent inflammasomes. IKKα controls the inflammasome at the level of the adaptor ASC, which interacts with IKKα in the nucleus of resting macrophages in an IKKα kinase-dependent manner. Loss of IKKα kinase activity results in inflammasome hyperactivation. Mechanistically, the downstream nuclear effector IKK-related kinase (IKKi) facilitates translocation of ASC from the nucleus to the perinuclear area during inflammasome activation. ASC remains under the control of IKKα in the perinuclear area following translocation of the ASC/IKKα complex. Signal 2 of NLRP3 activation leads to inhibition of IKKα kinase activity through the recruitment of PP2A, allowing ASC to participate in NLRP3 inflammasome assembly. Taken together, these findings reveal a IKKi-IKKα-ASC axis that serves as a common regulatory mechanism for ASC-dependent inflammasomes

MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases.

Low-grade systemic inflammation is often associated with metabolic syndrome, which plays a critical role in the development of the obesity-associated inflammatory diseases, including insulin resistance and atherosclerosis. Here, we investigate how Toll-like receptor-MyD88 signaling in myeloid and endothelial cells coordinately participates in the initiation and progression of high fat diet-induced systemic inflammation and metabolic inflammatory diseases. MyD88 deficiency in myeloid cells inhibits macrophage recruitment to adipose tissue and their switch to an M1-like phenotype. This is accompanied by substantially reduced diet-induced systemic inflammation, insulin resistance, and atherosclerosis. MyD88 deficiency in endothelial cells results in a moderate reduction in diet-induced adipose macrophage infiltration and M1 polarization, selective insulin sensitivity in adipose tissue, and amelioration of spontaneous atherosclerosis. Both in vivo and ex vivo studies suggest that MyD88-dependent GM-CSF production from the endothelial cells might play a critical role in the initiation of obesity-associated inflammation and development of atherosclerosis by priming the monocytes in the adipose and arterial tissues to differentiate into M1-like inflammatory macrophages. Collectively, these results implicate a critical MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases

Plant biomass allocation and driving factors of grassland revegetation in a Qinghai-Tibetan Plateau chronosequence

Biomass allocation is a key factor in understanding how ecosystems respond to changing environmental conditions. The role of soil chemistry in the above- and belowground plant biomass allocation in restoring grassland is still incompletely characterized. Consequently, it has led to two competing hypotheses for biomass allocation: optimal partitioning, where the plants allocate biomass preferentially to optimize resource use; and the isometric hypothesis, which postulates that biomass allocation between roots and shoots is fixed. Here we tested these hypotheses over a chronosequence of alpine grasslandsion undergoing restoration in the Qinghai-Tibetan Plateau, these range from severely degraded to those with 18 years of revegetation with an intact grassland (as a reference). A high proportion of biomass was allocated to the roots in the revegetated grasslands, and more biomass to shoots in the degraded and intact grasslands. The grasslands gradually decreased their root to shoot ratio as revegetation continued, with the lowest value in year 18 of revegetation. Our results showed that aboveground biomass (AGB) was increased by available phosphorus (P), soil moisture, and negatively related to bulk density, while belowground biomass (BGB) was positively impacted by total P and negatively by nitrate nitrogen (N). The trade-off between them was positively associated with available P and nitrate-N, and soil nutrient availability is more linked to increased AGB relative to BGB. Our study indicates that biomass allocation is highly variable during the revegetation period from degraded grassland, and is linked with soil properties, thus supporting the optimal partitioning hypothesis.</p

GmDAD1, a Conserved Defender Against Cell Death 1 (DAD1) From Soybean, Positively Regulates Plant Resistance Against Phytophthora Pathogens

Initially identified as a mammalian apoptosis suppressor, defender against apoptotic death 1 (DAD1) protein has conserved plant orthologs acting as negative regulators of cell death. The potential roles and action mechanisms of plant DADs in resistance against Phytophthora pathogens are still unknown. Here, we cloned GmDAD1 from soybean and performed functional dissection. GmDAD1 expression can be induced by Phytophthora sojae infection in both compatible and incompatible soybean varieties. By manipulating GmDAD1 expression in soybean hairy roots, we showed that GmDAD1 transcript accumulations are positively correlated with plant resistance levels against P. sojae. Heterologous expression of GmDAD1 in Nicotiana benthamiana enhanced its resistance to Phytophthora parasitica. NbDAD1 from N. benthamiana was shown to have similar role in conferring Phytophthora resistance. As an endoplasmic reticulum (ER)-localized protein, GmDAD1 was demonstrated to be involved in ER stress signaling and to affect the expression of multiple defense-related genes. Taken together, our findings reveal that GmDAD1 plays a critical role in defense against Phytophthora pathogens and might participate in the ER stress signaling pathway. The defense-associated characteristic of GmDAD1 makes it a valuable working target for breeding Phytophthora resistant soybean varieties

Integrated glycomic analysis of ovarian cancer side population cells

Additional file 2. The category of representative lectins for glycan profiling

Battery Production Systems: State of the Art and Future Developments

This paper discusses the state of the art in battery production research, focusing on high-importance topics to address industrial needs and sustainability goals in this rapidly growing field. We first present current research around three themes: human-centred production, smart production management, and sustainable manufacturing value chains. For each theme, key subtopics are explored to potentially transform battery value chains and shift to more sustainable production models. Such systemic transformations are supported by technological advances to enable superior manufacturing performance through: skills and competence development, improved production ergonomics and human factors, automation and human-robot collaboration, smart production planning and control, smart maintenance, data-driven solutions for production quality and its impact on battery performance (operational efficiency and durability), circular battery systems supported by service-based business models, more integrated and digitalized value chains, and increased industrial resilience. Each subtopic is discussed to suggest directions for further research to realise the full potential of digitalization for sustainable battery production

Dephosphorylated Polymerase I and Transcript Release Factor Prevents Allergic Asthma Exacerbations by Limiting IL-33 Release

BackgroundAsthma is a chronic inflammatory disease characterized by airway inflammation and airway hyperresponsiveness (AHR). IL-33 is considered as one of the most critical molecules in asthma pathogenesis. IL-33 is stored in nucleus and passively released during necrosis. But little is known about whether living cells can release IL-33 and how this process is regulated.ObjectiveWe sought to investigate the role of polymerase I and transcript release factor (PTRF) in IL-33 release and asthma pathogenesis.MethodsOvalbumin (OVA)-induced asthma model in PTRF+/− mice were employed to dissect the role of PTRF in vivo. Then, further in vitro experiments were carried out to unwind the potential mechanism involved.ResultsIn OVA asthma model with challenge phase, PTRF+/− mice showed a greater airway hyper-reaction, with an intense airway inflammation and more eosinophils in bronchoalveolar lavage fluid (BALF). Consistently, more acute type 2 immune response in lung and a higher IL-33 level in BALF were found in PTRF+/− mice. In OVA asthma model without challenge phase, airway inflammation and local type 2 immune responses were comparable between control mice and PTRF+/− mice. Knockdown of PTRF in 16HBE led to a significantly increased level of IL-33 in cell culture supernatants in response to LPS or HDM. Immunoprecipitation assay clarified Y158 as the major phosphorylation site of PTRF, which was also critical for the interaction of IL-33 and PTRF. Overexpression of dephosphorylated mutant Y158F of PTRF sequestered IL-33 in nucleus together with PTRF and limited IL-33 extracellular secretion.ConclusionPartial loss of PTRF led to a greater AHR and potent type 2 immune responses during challenge phase of asthma model, without influencing the sensitization phase. PTRF phosphorylation status determined subcellular location of PTRF and, therefore, regulated IL-33 release

RPS23RG1 modulates tau phosphorylation and axon outgrowth through regulating p35 proteasomal degradation

Tau蛋白病（Tauopathies）是由过度磷酸化的tau蛋白聚集形成神经纤维缠结为特征的一类神经退行性疾病，包括阿尔茨海默病（Alzheimer’s disease, AD）、进行性核上性麻痹（Progressive superanuclear palsy, PSP）、额颞叶痴呆（Frontotemporal dementia, FTD）等。随着全球社会结构的老龄化，tau蛋白病患者比率迅速增加，给个人和社会带来巨大的经济及精神负担。厦门大学神经科学研究所张云武教授团队最新发现RPS23RG1（RR1）的胞内羧基端区域能够与Cdk5激酶的激活蛋白p35的氨基端相互作用，介导p35的膜定位并影响其泛素化降解，从而调控在tau蛋白异常磷酸化过程中发挥重要作用的Cdk5激酶的活性。团队研究表明RPS23RG1通过其胞内羧基端与p35相互作用，介导p35膜结合和降解，从而抑制Cdk5活性，平衡tau磷酸化水平，促进轴突生长。此外，RPS23RG1的跨膜区与腺苷酸环化酶AC相互作用，抑制GSK3-β活性，同样控制tau过度磷酸化。提示RPS23RG1是改善tau过度磷酸化水平及治疗tau蛋白病的潜在靶点。 厦门大学医学院神经科学研究所博士后赵东栋为该研究第一作者，张云武教授为通讯作者。【Abstract】Tauopathies are a group of neurodegenerative diseases characterized by hyperphosphorylation of the microtubule-binding protein, tau, and typically feature axon impairment and synaptic dysfunction. Cyclin-dependent kinase5 (Cdk5) is a major tau kinase and its activity requires p35 or p25 regulatory subunits. P35 is subjected to rapid proteasomal degradation in its membrane-bound form and is cleaved by calpain under stress to a stable p25 form, leading to aberrant Cdk5 activation and tau hyperphosphorylation. The type Ib transmembrane protein RPS23RG1 has been implicated in Alzheimer’s disease (AD). However, physiological and pathological roles for RPS23RG1 in AD and other tauopathies are largely unclear. Herein, we observed retarded axon outgrowth, elevated p35 and p25 protein levels, and increased tau phosphorylation at major Cdk5 phosphorylation sites in Rps23rg1 knockout (KO) mice. Both downregulation of p35 and the Cdk5 inhibitor roscovitine attenuated tau hyperphosphorylation and axon outgrowth impairment in Rps23rg1 KO neurons. Interestingly, interactions between the RPS23RG1 carboxyl-terminus and p35 amino-terminus promoted p35 membrane distribution and proteasomal degradation. Moreover, P301L tau transgenic (Tg) mice showed increased tau hyperphosphorylation with reduced RPS23RG1 levels and impaired axon outgrowth. Overexpression of RPS23RG1 markedly attenuated tau hyperphosphorylation and axon outgrowth defects in P301L tau Tg neurons. Our results demonstrate the involvement of RPS23RG1 in tauopathy disorders, and implicate a role for RPS23RG1 in inhibiting tau hyperphosphorylation through homeostatic p35 degradation and suppression of Cdk5 activation. Reduced RPS23RG1 levels in tauopathy trigger aberrant Cdk5-p35 activation, consequent tau hyperphosphorylation, and axon outgrowth impairment, suggesting that RPS23RG1 may be a potential therapeutic target in tauopathy disorders.This work was supported by grants from National Key Research and Development Program of China (2016YFC1305903 and 2018YFC2000400 to Y-wZ), National Natural Science Foundation of China (81771377, U1705285, 91332112, and 81225008 to Y-wZ), Fundamental Research Funds for the Central Universities (20720180049 to Y-wZ), the Fujian Provincial Health Commission-Education Department Joint Tackling Plan (WKJ2016-2-18 to F-rL), and Postdoctoral Science Foundation of China (2020M671948 to DZ)