Discourse Analysis of Public Debates Using Corpus Linguistic Methodologies

The aim of this study is to develop a computational method of discourse analysis based on corpus semantics. The objective is to achieve an accurate understanding of the debate content and structure through hypotheses generation. As for verifying the hypotheses, the topic extraction and semantic similarity evaluation from the public debate minute corpus is examined by using a multimethod which includes TFIDF, T-VSM, and MDS. The main issue of public debate and the inconsistency level between participants’ utterance could be described by using the method. The methodology presented in this study is applied to a case example. Finally, the applicability of the proposed methodology to practical debates is discussed

Public reviews and trust formation in disaster risk management

This paper investigated two roles of public reviews in disaster risk management: 1) providing information to a policy maker about the desirability of a disaster risk management plan and 2) promoting stakeholders' trust in policy maker's decision. Our analysis was conducted by formulating two linked communication games, which described, respectively, information transmission from public reviewers to a policy maker and trust formation between the policy maker and an individual. It was shown that there exists an externality between the two games, and the policy maker accordingly faces a trade-off between the two roles of public reviews. Due to this trade-off, trust formation between the policy maker and the individual might be prevented. Finally, alternative institutional design for realizing trust formation between the policy maker and the individual through public reviews was discussed. It was pointed out that a communication protocol that disciplines the way in which reviewers express their opinions has to be designed in order to realize the two roles of public reviews

A System-Level Mechanism of Anmyungambi Decoction for Obesity: A Network Pharmacological Approach

Obesity is a low-grade systemic inflammatory disease involving adipocytokines. As though Anmyungambi decoction (AMGB) showed significant improvement on obesity in a clinical trial, the molecular mechanism of AMGB in obesity remains unknown. Therefore, we explored the potential mechanisms of action of AMGB on obesity through network pharmacological approaches. We revealed that targets of AMGB are significantly associated with obesity-related and adipocyte-elevated genes. Evodiamine, berberine, genipin, palmitic acid, genistein, and quercetin were shown to regulate adipocytokine signaling pathway proteins which mainly involved tumor necrosis factor receptor 1, leptin receptor. In terms of the regulatory pathway of lipolysis in adipocytes, norephedrine, pseudoephedrine, quercetin, and limonin were shown to affect adrenergic receptor-beta, protein kinase A, etc. We also found that AMGB has the potentials to enhance the insulin signaling pathway thereby preventing type II diabetes mellitus. Additionally, AMGB was discovered to be able to control not only insulin-related proteins but also inflammatory mediators and apoptotic regulators and caspases, hence reducing hepatocyte injury in nonalcoholic fatty liver disease. Our findings help develop a better understanding of how AMGB controls obesity

Fatty acylated caveolin-2 is a substrate of insulin receptor tyrosine kinase for insulin receptor substrate-1-directed signaling activation

AbstractHere, we demonstrate that insulin receptor (IR) tyrosine kinase catalyzes Tyr-19 and Tyr-27 phosphorylation of caveolin-2 (cav-2), leading to stimulation of signaling proteins downstream of IR, and that the catalysis is dependent on fatty acylation status of cav-2, promoting its interaction with IR. Cav-2 is myristoylated at Gly-2 and palmitoylated at Cys-109, Cys-122, and Cys-145. The fatty acylation deficient mutants are unable to localize in the plasma membrane and not phosphorylated by IR tyrosine kinase. IR interacts with the C-terminal domain of cav-2 containing the cysteines for palmitoylation. IR mutants, Y999F and K1057A, but not W1220S, fail interaction with cav-2. Insulin receptor substrate-1 (IRS-1) is recruited to interact with the IR-catalyzed phospho-tyrosine cav-2, which facilitates IRS-1 association with and activation by IR to initiate IRS-1-mediated downstream signaling. Cav-2 fatty acylation and tyrosine phosphorylation are necessary for the IRS-1-dependent PI3K-Akt and ERK activations responsible for glucose uptake and cell survival and proliferation. In conclusion, fatty acylated cav-2 is a new substrate of IR tyrosine kinase, and the fatty acylation and phosphorylation of cav-2 present novel mechanisms by which insulin signaling is activated

Effect of Roasting Time and Cryogenic Milling on the Physicochemical Characteristics of Dried Ginseng Powder

This study aimed to evaluate the effect of reduced particle size of ginseng by roasting and cryogenic milling on increasing its water solubility and physiological activity. The samples were roasted for different times (9–21 min) and generated in different sizes (10–50, and >50 μm). All roasted samples revealed significantly smaller particle sizes than did non-roasted samples, based on Sauter mean diameter (D [3,2], p < 0.05). Furthermore, the particle sizes of roasted samples decreased until roasting up to 15 min. In terms of the water solubility index (WSI), antioxidant activity, total polyphenol content (TPC), and total polysaccharides according to particle size, 10–20 μm-sized samples showed the highest values when compared with >50 μm-sized samples. Based on roasting time, WSI values of all samples roasted for up to 15 min were higher than those of the control (not roasted) (p < 0.05). Antioxidant activity and TPC also increased with increasing roasting time. Total polysaccharide content was the highest upon roasting for 15 min, except for the 10–20 μm sample. Ginsenoside content of roasted samples >20 μm size was higher than that of the control (not roasted) except after 15 min of roasting. Therefore, roasting and cryogenic milling are effective in producing ginseng root powder

Stretchable N-Type High-Performance Polymers Based on Asymmetric Thienylvinyl-1,1-Dicyanomethylene-3-Indanone for Plastic Electronics

The development of new electron-accepting building blocks to construct high-performance n-type semiconducting polymers is essential for various organic optoelectronic devices. Herein, we have incorporated a newly formulated thienylvinyl-1,1-dicyanomethylene-3-indanone (TIC) electron-accepting monomer into a series of n-type low-band gap polymers alongside cyclopentadithiophene (CDT) and indacenodithiophene (IDT) comonomers. Controlling the regioregularity of the asymmetric TIC has produced regioisomeric polymer structures [semi-regioregular (s-PCDT-TIC and s-PIDT-TIC) and regiorandom (r-PCDT-TIC and r-PIDT-TIC)]. We conducted comparative studies for the regiochemistry control and CDT versus IDT repeating units: (i) The CDT-containing polymers have red-shifted absorption and higher absorptivity compared to the IDT-containing analogues. (ii) The varied regioregularity affects the optical features rather than the energy levels. (iii) All the polymers show excellent n-channel field-effect transistors, with electron mobility higher than 1.0 x 10(-2) cm(2) V-1 s(-1), despite their low-ordered crystallinity. (iv) Stretchable transistors with polymers can achieve high retention of electron mobilities under the external strain; specially, r-PCDT-TIC maintains 95% initial mobility at 100% strain. In addition, an n-type near-infrared organic phototransistor based on s-PCDT-TIC exhibits an excellent photoresponsivity, photodetectivity, and external quantum efficiency of 203 A W-1 , 8.1 x 10(12) Jones, and 2.42 x 10(4)%, respectively, at a wavelength of 838 nm

Targeted Deletion of Thymosin Beta 4 in Hepatic Stellate Cells Ameliorates Liver Fibrosis in a Transgenic Mouse Model

Liver fibrosis is the most common feature of liver disease, and activated hepatic stellate cells (HSCs) are the main contributors to liver fibrosis. Thus, finding key targets that modulate HSC activation is important to prevent liver fibrosis. Previously, we showed that thymosin β4 (Tβ4) influenced HSC activation by interacting with the Hedgehog pathway in vitro. Herein, we generated Tβ4 conditional knockout (Tβ4-flox) mice to investigate in vivo functions of Tβ4 in liver fibrosis. To selectively delete Tβ4 in activated HSCs, double-transgenic (DTG) mice were generated by mating Tβ4-flox mice with α-smooth muscle actin (α-Sma)-Cre-ERT2 mice, and these mice were administered carbon tetrachloride (CCl4) or underwent bile duct ligation to induce liver fibrosis. Tβ4 was selectively suppressed in the activated HSCs of DTG mouse liver, and this reduction attenuated liver injury, including fibrosis, in both fibrotic models by repressing Hedgehog (Hh) signaling. In addition, the re-expression of Tβ4 by an adeno-associated virus reversed the effect of HSC-specific Tβ4 deletion and led to liver fibrosis with Hh activation in CCl4-exposed mice treated with tamoxifen. In conclusion, our results demonstrate that Tβ4 is a crucial regulator of HSC activation, suggesting it as a novel therapeutic target for curing liver fibrosis

Tumor necrosis factor-inducible gene 6 protein and its derived peptide ameliorate liver fibrosis by repressing CD44 activation in mice with alcohol-related liver disease

Abstract Background Alcohol-related liver disease (ALD) is a major health concern worldwide, but effective therapeutics for ALD are still lacking. Tumor necrosis factor-inducible gene 6 protein (TSG-6), a cytokine released from mesenchymal stem cells, was shown to reduce liver fibrosis and promote successful liver repair in mice with chronically damaged livers. However, the effect of TSG-6 and the mechanism underlying its activity in ALD remain poorly understood. Methods To investigate its function in ALD mice with fibrosis, male mice chronically fed an ethanol (EtOH)-containing diet for 9 weeks were treated with TSG-6 (EtOH + TSG-6) or PBS (EtOH + Veh) for an additional 3 weeks. Results Severe hepatic injury in EtOH-treated mice was markedly decreased in TSG-6-treated mice fed EtOH. The EtOH + TSG-6 group had less fibrosis than the EtOH + Veh group. Activation of cluster of differentiation 44 (CD44) was reported to promote HSC activation. CD44 and nuclear CD44 intracellular domain (ICD), a CD44 activator which were upregulated in activated HSCs and ALD mice were significantly downregulated in TSG-6-exposed mice fed EtOH. TSG-6 interacted directly with the catalytic site of MMP14, a proteolytic enzyme that cleaves CD44, inhibited CD44 cleavage to CD44ICD, and reduced HSC activation and liver fibrosis in ALD mice. In addition, a novel peptide designed to include a region that binds to the catalytic site of MMP14 suppressed CD44 activation and attenuated alcohol-induced liver injury, including fibrosis, in mice. Conclusions These results demonstrate that TSG-6 attenuates alcohol-induced liver damage and fibrosis by blocking CD44 cleavage to CD44ICD and suggest that TSG-6 and TSG-6-mimicking peptide could be used as therapeutics for ALD with fibrosis