Fast Compartment Model Calibration using Annealed and Transformed Variational Inference

Compartment models are widely used in climate science, epidemiology, and physics, among other disciplines. An important example of a compartment model is susceptible-infected-recovered (SIR) model, which can describe disease dynamics. Bayesian inference for SIR models is challenging because likelihood evaluation requires solving expensive ordinary differential equations. Although variational inference (VI) can be a fast alternative to the traditional Bayes approaches, VI has limited applicability due to boundary issues and local optima problems. To address these challenges, we propose flexible VI methods based on deep generative models that do not require parametric assumptions on the variational distribution. We embed a surjective transformation in our framework to avoid posterior truncation at the boundary. We provide theoretical conditions that guarantee the success of the algorithm. Furthermore, our temperature annealing scheme can avoid being trapped in local optima through a series of intermediate posteriors. We apply our method to variants of SIR models, illustrating that the proposed method can provide fast and accurate inference compared to its competitors

Value Discount of Business Groups Surrounding the Asia Financial Crisis: Evidence from Korean Chaebols

Asian Financial Crisis, Business Group, Chaebol, Diversification, Firm Value

Point Mutation of Hoxd12 in Mice

Purpose: Genes of the HoxD cluster play a major role in vertebrate limb development, and changes that modify the Hoxd12 locus affect other genes also, suggesting that HoxD function is coordinated by a control mechanism involving multiple genes during limb morphogenesis. In this study, mutant phenotypes were produced by treatment of mice with chemical mutagen, N-ethyl-N-nitrosourea (ENU). We analyzed mutant mice exhibiting the specific microdactyly phenotype and examined the genes affected. Materials and Methods: We focused on phenotype characteristics including size, bone formation, and digit morphology of ENU-induced microdactyly mice. The expressions of several molecules were analyzed by genome-wide screening and quantitative real-time PCR to define the affected genes. Results: We report on limb phenotypes of an ENU-induced A-to-C mutation in the Hoxd12 gene, resulting in alanine-to-serine conversion. Microdactyly mice exhibited growth defects in the zeugopod and autopod, shortening of digits, a missing tip of digit I, limb growth affected, and dramatic increases in the expressions of Fgf4 and Lmx1b. However, the expression level of Shh was not changed Hoxd12 point mutated mice. Conclusion: These results suggest that point mutation rather than the entire deletion of Hoxd12, such as in knockout and transgenic mice, causes the abnormal limb phenotype in microdactyly mice. The precise nature of the spectrum of differences requires further investigation.link_to_subscribed_fulltex

Role of G{alpha}12 and G{alpha}13 as Novel Switches for the Activity of Nrf2, a Key Antioxidative Transcription Factor

G{alpha}12 and G{alpha}13 function as molecular regulators responding to extracellular stimuli. NF-E2-related factor 2 (Nrf2) is involved in a protective adaptive response to oxidative stress. This study investigated the regulation of Nrf2 by G{alpha}12 and G{alpha}13. A deficiency of G{alpha}12, but not of G{alpha}13, enhanced Nrf2 activity and target gene transactivation in embryo fibroblasts. In mice, G{alpha}12 knockout activated Nrf2 and thereby facilitated heme catabolism to bilirubin and its glucuronosyl conjugations. An oligonucleotide microarray demonstrated the transactivation of Nrf2 target genes by G{alpha}12 gene knockout. G{alpha}12 deficiency reduced Jun N-terminal protein kinase (JNK)-dependent Nrf2 ubiquitination required for proteasomal degradation, and so did G{alpha}13 deficiency. The absence of G{alpha}12, but not of G{alpha}13, increased protein kinase C {delta} (PKC {delta}) activation and the PKC {delta}-mediated serine phosphorylation of Nrf2. G{alpha}13 gene knockout or knockdown abrogated the Nrf2 phosphorylation induced by G{alpha}12 deficiency, suggesting that relief from G{alpha}12 repression leads to the G{alpha}13-mediated activation of Nrf2. Constitutive activation of G{alpha}13 promoted Nrf2 activity and target gene induction via Rho-mediated PKC {delta} activation, corroborating positive regulation by G{alpha}13. In summary, G{alpha}12 and G{alpha}13 transmit a JNK-dependent signal for Nrf2 ubiquitination, whereas G{alpha}13 regulates Rho-PKC {delta}-mediated Nrf2 phosphorylation, which is negatively balanced by G{alpha}12

Effectiveness of the Novel Herbal Medicine, KIOM-MA, and Its Bioconversion Product, KIOM-MA128, on the Treatment of Atopic Dermatitis

This study was conducted to determine if oral administration of the novel herbal medicine, KIOM-MA, and its Lactobacillus acidophilus-fermented product, KIOM-MA128, has therapeutic properties for the treatment of atopic dermatitis (AD). Using AD-induced BALB/c mice by Ovalbumin and aluminum hydroxide, the effectiveness of KIOM-MA and KIOM-MA128 on AD was evaluated. Oral administration of KIOM-MA and KIOM-MA128 reduced major clinical signs of AD including erythema/darkening, edema/papulation, excoriations, lichenification/prurigo, and dryness. Interestingly, KIOM-MA128 more significantly improved AD-related symptoms including decrease of IgE level in the plasma as well as reduction of scratching behavior, skin severity in the AD BALB/c model. HPLC analysis showed the significant changes in the constituent patterns between KIOM-MA and KIOM-MA128. Our results suggest that both KIOM-MA and KIOM-MA128 have potential for therapeutic reagent for the treatment of AD, and further, the efficacy is significantly enhanced by L. acidophilus fermentation via increases in its indicator molecule

Effect of interlayer interactions on exciton luminescence in atomic-layered MoS2 crystals

The atomic-layered semiconducting materials of transition metal dichalcogenides are considered effective light sources with both potential applications in thin and flexible optoelectronics and novel functionalities. In spite of the great interest in optoelectronic properties of two-dimensional transition metal dichalcogenides, the excitonic properties still need to be addressed, specifically in terms of the interlayer interactions. Here, we report the distinct behavior of the A and B excitons in the presence of interlayer interactions of layered MoS 2 crystals. Micro-photoluminescence spectroscopic studies reveal that on the interlayer interactions in double layer MoS 2 crystals, the emission quantum yield of the A exciton is drastically changed, whereas that of the B exciton remains nearly constant for both single and double layer MoS 2 crystals. First-principles density functional theory calculations confirm that a significant charge redistribution occurs in the double layer MoS 2 due to the interlayer interactions producing a local electric field at the interfacial region. Analogous to the quantum-confined Stark effect, we suggest that the distinct behavior of the A and B excitons can be explained by a simplified band-bending model.1

Room-temperature polariton lasing in quantum heterostructure nanocavities

Controlling light-matter interactions in solid-state systems has motivated intense research to produce bosonic quasi-particles known as exciton-polaritons, which requires strong coupling between excitons and cavity photons. Ultra-low threshold coherent light emitters can be achieved through lasing from exciton-polariton condensates, but this generally requires sophisticated device structures and cryogenic temperatures. Polaritonic nanolasers operating at room temperature lie on the crucial path of related research, not only for the exploration of polariton physics at the nanoscale but also for potential applications in quantum information systems, all-optical logic gates, and ultra-low threshold lasers. However, at present, progress toward room-temperature polariton nanolasers has been limited by the thermal instability of excitons and the inherently low quality factors of nanocavities. Here, we demonstrate room-temperature polaritonic nanolasers by designing wide-gap semiconductor heterostructure nanocavities to produce thermally stable excitons coupled with nanocavity photons. The resulting mixed states of exciton-polaritons with Rabi frequencies of approximately 370 meV enable persistent polariton lasing up to room temperature, facilitating the realization of miniaturized and integrated polariton systems

Discriminating Pathological and Non-pathological Internet Gamers Using Sparse Neuroanatomical Features

Internet gaming disorder (IGD) is often diagnosed on the basis of nine underlying criteria from the latest version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Here, we examined whether such symptom-based categorization could be translated into computation-based classification. Structural MRI (sMRI) and diffusion-weighted MRI (dMRI) data were acquired in 38 gamers diagnosed with IGD, 68 normal gamers diagnosed as not having IGD, and 37 healthy non-gamers. We generated 108 features of gray matter (GM) and white matter (WM) structure from the MRI data. When regularized logistic regression was applied to the 108 neuroanatomical features to select important ones for the distinction between the groups, the disordered and normal gamers were represented in terms of 43 and 21 features, respectively, in relation to the healthy non-gamers, whereas the disordered gamers were represented in terms of 11 features in relation to the normal gamers. In support vector machines (SVM) using the sparse neuroanatomical features as predictors, the disordered and normal gamers were discriminated successfully, with accuracy exceeding 98%, from the healthy non-gamers, but the classification between the disordered and normal gamers was relatively challenging. These findings suggest that pathological and non-pathological gamers as categorized with the criteria from the DSM-5 could be represented by sparse neuroanatomical features, especially in the context of discriminating those from non-gaming healthy individuals

Development of an easy-to-handle murine model for the characterization of radiation-induced gross and molecular changes in skin

Background Radiation-induced skin injury is a dose-limiting complication of radiotherapy. To investigate this problem and to develop a framework for making decisions on treatment and dose prescription, a murine model of radiation-induced skin injury was developed. Methods The dorsal skin of the mice was isolated, and irradiation was applied at single doses of 15, 30, and 50 Gy. The mice were followed for 12 weeks with serial photography and laser Doppler analysis. Sequential skin biopsy samples were obtained and subjected to a histological analysis, immunostaining against transforming growth factor beta (TGF-β), and Western blotting with Wnt-3 and β-catenin. Increases in the levels of TGF-β, Wnt, and β-catenin were detected after irradiation. Results All tested radiation doses caused progressive dermal thickening and fibrosis. The cause of this process, however, may not be radiation alone, as the natural course of wound healing may elicit a similar response. The latent appearance of molecular and histological markers that induce fibrosis in the 15 Gy group without causing apparent gross skin injuries indicates that 15 Gy is an appropriate dose for characterizing the effects of chronic irradiation alone. Thus, this model best mimics the patterns of injury that occur in human subjects. Conclusions This animal model can be used to elucidate the gross and molecular changes that occur in radiation-induced skin injury and provides an effective platform for studying this adverse effect without complicating the process of wound healing