Image neural style transfer with global and local optimization fusion

This paper presents a new image synthesis method for image style transfer. For some common methods, the textures and colors in the style image are sometimes applied inappropriately to the content image, which generates artifacts. In order to improve the results, we propose a novel method based on a new strategy that combines both local and global style losses. On the one hand, a style loss function based on a local approach is used to keep the style details. On the other hand, another style loss function based on global measures is used to capture the more global structural information. Results on various images show that the proposed method reduces artifacts while faithfully transferring the style image’s characteristics and preserving the structure and color of the content image

Risk prediction models for incident type 2 diabetes in Chinese people with intermediate hyperglycemia : a systematic literature review and external validation study

Background People with intermediate hyperglycemia (IH), including impaired fasting glucose and/or impaired glucose tolerance, are at higher risk of developing type 2 diabetes (T2D) than those with normoglycemia. We aimed to evaluate the performance of published T2D risk prediction models in Chinese people with IH to inform them about the choice of primary diabetes prevention measures. Methods A systematic literature search was conducted to identify Asian-derived T2D risk prediction models, which were eligible if they were built on a prospective cohort of Asian adults without diabetes at baseline and utilized routinely-available variables to predict future risk of T2D. These Asian-derived and five prespecified non-Asian derived T2D risk prediction models were divided into BASIC (clinical variables only) and EXTENDED (plus laboratory variables) versions, with validation performed on them in three prospective Chinese IH cohorts: ACE (n = 3241), Luzhou (n = 1333), and TCLSIH (n = 1702). Model performance was assessed in terms of discrimination (C-statistic) and calibration (Hosmer-Lemeshow test). Results Forty-four Asian and five non-Asian studies comprising 21 BASIC and 46 EXTENDED T2D risk prediction models for validation were identified. The majority were at high (n = 43, 87.8%) or unclear (n = 3, 6.1%) risk of bias, while only three studies (6.1%) were scored at low risk of bias. BASIC models showed poor-to-moderate discrimination with C-statistics 0.52-0.60, 0.50-0.59, and 0.50-0.64 in the ACE, Luzhou, and TCLSIH cohorts respectively. EXTENDED models showed poor-to-acceptable discrimination with C-statistics 0.54-0.73, 0.52-0.67, and 0.59-0.78 respectively. Fifteen BASIC and 40 EXTENDED models showed poor calibration (P < 0.05), overpredicting or underestimating the observed diabetes risk. Most recalibrated models showed improved calibration but modestly-to-severely overestimated diabetes risk in the three cohorts. The NAVIGATOR model showed the best discrimination in the three cohorts but had poor calibration (P < 0.05). Conclusions In Chinese people with IH, previously published BASIC models to predict T2D did not exhibit good discrimination or calibration. Several EXTENDED models performed better, but a robust Chinese T2D risk prediction tool in people with IH remains a major unmet need.Peer reviewe

Risk prediction models for incident type 2 diabetes in Chinese people with intermediate hyperglycemia: a systematic literature review and external validation study

BACKGROUND: People with intermediate hyperglycemia (IH), including impaired fasting glucose and/or impaired glucose tolerance, are at higher risk of developing type 2 diabetes (T2D) than those with normoglycemia. We aimed to evaluate the performance of published T2D risk prediction models in Chinese people with IH to inform them about the choice of primary diabetes prevention measures. METHODS: A systematic literature search was conducted to identify Asian-derived T2D risk prediction models, which were eligible if they were built on a prospective cohort of Asian adults without diabetes at baseline and utilized routinely-available variables to predict future risk of T2D. These Asian-derived and five prespecified non-Asian derived T2D risk prediction models were divided into BASIC (clinical variables only) and EXTENDED (plus laboratory variables) versions, with validation performed on them in three prospective Chinese IH cohorts: ACE (n = 3241), Luzhou (n = 1333), and TCLSIH (n = 1702). Model performance was assessed in terms of discrimination (C-statistic) and calibration (Hosmer-Lemeshow test). RESULTS: Forty-four Asian and five non-Asian studies comprising 21 BASIC and 46 EXTENDED T2D risk prediction models for validation were identified. The majority were at high (n = 43, 87.8%) or unclear (n = 3, 6.1%) risk of bias, while only three studies (6.1%) were scored at low risk of bias. BASIC models showed poor-to-moderate discrimination with C-statistics 0.52-0.60, 0.50-0.59, and 0.50-0.64 in the ACE, Luzhou, and TCLSIH cohorts respectively. EXTENDED models showed poor-to-acceptable discrimination with C-statistics 0.54-0.73, 0.52-0.67, and 0.59-0.78 respectively. Fifteen BASIC and 40 EXTENDED models showed poor calibration (P < 0.05), overpredicting or underestimating the observed diabetes risk. Most recalibrated models showed improved calibration but modestly-to-severely overestimated diabetes risk in the three cohorts. The NAVIGATOR model showed the best discrimination in the three cohorts but had poor calibration (P < 0.05). CONCLUSIONS: In Chinese people with IH, previously published BASIC models to predict T2D did not exhibit good discrimination or calibration. Several EXTENDED models performed better, but a robust Chinese T2D risk prediction tool in people with IH remains a major unmet need.This work was supported by 1.3.5 Project for Disciplines of Excellence, West China Hospital, Sichuan University (Grant no. ZYGD18017 to NT)

Study of J/ψ→ppˉJ/\psi\to p\bar{p} and J/ψ→nnˉJ/\psi\to n\bar{n}

The decays $J/\psi\to p\bar{p}$ and $J/\psi\to n\bar{n}$ have been investigated with a sample of 225.2 million $J/\psi$ events collected with the BESIII detector at the BEPCII $e^+e^-$ collider. The branching fractions are determined to be $\mathcal{B}(J/\psi\to p\bar{p})=(2.112\pm0.004\pm0.031)\times10^{-3}$ and $\mathcal{B}(J/\psi\to n\bar{n})=(2.07\pm0.01\pm0.17)\times10^{-3}$. Distributions of the angle $\theta$ between the proton or anti-neutron and the beam direction are well described by the form $1+\alpha\cos^2\theta$, and we find $\alpha=0.595\pm0.012\pm0.015$ for $J/\psi\to p\bar{p}$ and $\alpha=0.50\pm0.04\pm0.21$ for $J/\psi\to n\bar{n}$. Our branching-fraction results suggest a large phase angle between the strong and electromagnetic amplitudes describing the $J/\psi\to N\bar{N}$ decay.Comment: 16 pages, 13 figures, the 2nd version, submitted to PR

First observation of the M1 transition ψ(3686)→γηc(2S)\psi(3686)\to \gamma\eta_c(2S)

Using a sample of 106 million \psi(3686) events collected with the BESIII detector at the BEPCII storage ring, we have made the first measurement of the M1 transition between the radially excited charmonium S-wave spin-triplet and the radially excited S-wave spin-singlet states: \psi(3686)\to\gamma\eta_c(2S). Analyses of the processes \psi(2S)\to \gamma\eta_c(2S) with \eta_c(2S)\to \K_S^0 K\pi and K^+K^-\pi^0 gave an \eta_c(2S) signal with a statistical significance of greater than 10 standard deviations under a wide range of assumptions about the signal and background properties. The data are used to obtain measurements of the \eta_c(2S) mass (M(\eta_c(2S))=3637.6\pm 2.9_\mathrm{stat}\pm 1.6_\mathrm{sys} MeV/c^2), width (\Gamma(\eta_c(2S))=16.9\pm 6.4_\mathrm{stat}\pm 4.8_\mathrm{sys} MeV), and the product branching fraction (\BR(\psi(3686)\to \gamma\eta_c(2S))\times \BR(\eta_c(2S)\to K\bar K\pi) = (1.30\pm 0.20_\mathrm{stat}\pm 0.30_\mathrm{sys})\times 10^{-5}). Combining our result with a BaBar measurement of \BR(\eta_c(2S)\to K\bar K \pi), we find the branching fraction of the M1 transition to be \BR(\psi(3686)\to\gamma\eta_c(2S)) = (6.8\pm 1.1_\mathrm{stat}\pm 4.5_\mathrm{sys})\times 10^{-4}.Comment: 7 pages, 1 figure, 1 tabl

Two-photon widths of the χc0,2\chi_{c0, 2} states and helicity analysis for \chi_{c2}\ar\gamma\gamma}

Based on a data sample of 106 M $\psi^{\prime}$ events collected with the BESIII detector, the decays \psi^{\prime}\ar\gamma\chi_{c0, 2},\chi_{c0, 2}\ar\gamma\gamma are studied to determine the two-photon widths of the $\chi_{c0, 2}$ states. The two-photon decay branching fractions are determined to be {\cal B}(\chi_{c0}\ar\gamma\gamma) = (2.24\pm 0.19\pm 0.12\pm 0.08)\times 10^{-4} and {\cal B}(\chi_{c2}\ar\gamma\gamma) = (3.21\pm 0.18\pm 0.17\pm 0.13)\times 10^{-4}. From these, the two-photon widths are determined to be $\Gamma_{\gamma \gamma}(\chi_{c0}) = (2.33\pm0.20\pm0.13\pm0.17)$ keV, $\Gamma_{\gamma \gamma}(\chi_{c2}) = (0.63\pm0.04\pm0.04\pm0.04)$ keV, and $\cal R$ $=\Gamma_{\gamma \gamma}(\chi_{c2})/\Gamma_{\gamma \gamma}(\chi_{c0})=0.271\pm 0.029\pm 0.013\pm 0.027$, where the uncertainties are statistical, systematic, and those from the PDG {\cal B}(\psi^{\prime}\ar\gamma\chi_{c0,2}) and $\Gamma(\chi_{c0,2})$ errors, respectively. The ratio of the two-photon widths for helicity $\lambda=0$ and helicity $\lambda=2$ components in the decay \chi_{c2}\ar\gamma\gamma is measured for the first time to be $f_{0/2} =\Gamma^{\lambda=0}_{\gamma\gamma}(\chi_{c2})/\Gamma^{\lambda=2}_{\gamma\gamma}(\chi_{c2}) = 0.00\pm0.02\pm0.02$.Comment: 10 pages, 4 figure

Ficolin-2 Levels and FCN2 Haplotypes Influence Hepatitis B Infection Outcome in Vietnamese Patients

Human Ficolin-2 (L-ficolins) encoded by FCN2 gene is a soluble serum protein that plays an important role in innate immunity and is mainly expressed in the liver. Ficolin-2 serum levels and FCN2 single nucleotide polymorphisms were associated to several infectious diseases. We initially screened the complete FCN2 gene in 48 healthy individuals of Vietnamese ethnicity. We genotyped a Vietnamese cohort comprising of 423 clinically classified hepatitis B virus patients and 303 controls for functional single nucleotide polymorphisms in the promoter region (-986G>A, -602G>A, -4A>G) and in exon 8 (+6424G>T) by real-time PCR and investigated the contribution of FCN2 genotypes and haplotypes to serum Ficolin-2 levels, viral load and liver enzyme levels. Haplotypes differed significantly between patients and controls (P = 0.002) and the haplotype AGGG was found frequently in controls in comparison to patients with hepatitis B virus and hepatocellular carcinoma (P = 0.0002 and P<0.0001) conferring a protective effect. Ficolin-2 levels differed significantly between patients and controls (p<0.0001). Patients with acute hepatitis B had higher serum Ficolin-2 levels compared to other patient groups and controls.The viral load was observed to be significantly distributed among the haplotypes (P = 0.04) and the AAAG haplotype contributed to higher Ficolin-2 levels and to viral load. Four novel single nucleotide polymorphisms in introns (-941G>T, -310G>A, +2363G>A, +4882G>A) and one synonymous mutation in exon 8 (+6485G>T) was observed. Strong linkage was found between the variant -986G>A and -4A>G. The very first study on Vietnamese cohort associates both Ficolin-2 serum levels and FCN2 haplotypes to hepatitis B virus infection and subsequent disease progression

2023 roadmap for potassium-ion batteries

The heavy reliance of lithium-ion batteries (LIBs) has caused rising concerns on the sustainability of lithium and transition metal and the ethic issue around mining practice. Developing alternative energy storage technologies beyond lithium has become a prominent slice of global energy research portfolio. The alternative technologies play a vital role in shaping the future landscape of energy storage, from electrified mobility to the efficient utilization of renewable energies and further to large-scale stationary energy storage. Potassium-ion batteries (PIBs) are a promising alternative given its chemical and economic benefits, making a strong competitor to LIBs and sodium-ion batteries for different applications. However, many are unknown regarding potassium storage processes in materials and how it differs from lithium and sodium and understanding of solid–liquid interfacial chemistry is massively insufficient in PIBs. Therefore, there remain outstanding issues to advance the commercial prospects of the PIB technology. This Roadmap highlights the up-to-date scientific and technological advances and the insights into solving challenging issues to accelerate the development of PIBs. We hope this Roadmap aids the wider PIB research community and provides a cross-referencing to other beyond lithium energy storage technologies in the fast-pacing research landscape

An essential role for the Id1/PI3K/Akt/NFkB/survivin signalling pathway in promoting the proliferation of endothelial progenitor cells in vitro

The enhancement of re-endothelialisation is a critical therapeutic option for repairing injured blood vessels. Endothelial progenitor cells (EPCs) are the major source of cells that participate in endothelium repair and contribute to re-endothelialisation by reducing neointima formation after vascular injury. The over-expression of the inhibitor of differentiation or DNA binding 1 (Id1) significantly improved EPC proliferation. This study aimed to investigate the effects of Id1 on the phosphatidylinositol-3-kinase (PI3K)/Akt/nuclear factor kappa B (NFκB)/survivin signalling pathway and its significance in promoting EPC proliferation in vitro. Spleen-derived EPCs were cultured as previously described. Id1 was presented at low levels in EPCs, and was rapidly up-regulated by stimulation with vascular endothelial growth factor. We demonstrated that transient transfection of Id1 into EPCs activated the PI3K/Akt/NFκB/survivin signalling pathway and promoted EPC proliferation. The proliferation of EPCs was extensively inhibited by silencing of endogenous Id1, and knockdown of Id1 expression led to suppression of PI3K/Akt/NFκB/survivin signalling pathway in EPCs. In addition, blockade by the PI3K-specific inhibitor LY294002, Akt inhibitor, the NFκB inhibitor BAY 11-7082, the survivin inhibitor Curcumin, or the survivin inhibitor YM155 reduced the effects of Id1 transfection. These results suggest that the Id1/PI3K/Akt/NFκB/survivin signalling pathway plays a critical role in EPC proliferation. The Id1/PI3K/Akt/NFκB/survivin signalling pathway may represent a novel therapeutic target in the prevention of restenosis after vascular injury