DFedADMM: Dual Constraints Controlled Model Inconsistency for Decentralized Federated Learning

To address the communication burden issues associated with federated learning (FL), decentralized federated learning (DFL) discards the central server and establishes a decentralized communication network, where each client communicates only with neighboring clients. However, existing DFL methods still suffer from two major challenges: local inconsistency and local heterogeneous overfitting, which have not been fundamentally addressed by existing DFL methods. To tackle these issues, we propose novel DFL algorithms, DFedADMM and its enhanced version DFedADMM-SAM, to enhance the performance of DFL. The DFedADMM algorithm employs primal-dual optimization (ADMM) by utilizing dual variables to control the model inconsistency raised from the decentralized heterogeneous data distributions. The DFedADMM-SAM algorithm further improves on DFedADMM by employing a Sharpness-Aware Minimization (SAM) optimizer, which uses gradient perturbations to generate locally flat models and searches for models with uniformly low loss values to mitigate local heterogeneous overfitting. Theoretically, we derive convergence rates of $\small \mathcal{O}\Big(\frac{1}{\sqrt{KT}}+\frac{1}{KT(1-\psi)^2}\Big)$ and $\small \mathcal{O}\Big(\frac{1}{\sqrt{KT}}+\frac{1}{KT(1-\psi)^2}+ \frac{1}{T^{3/2}K^{1/2}}\Big)$ in the non-convex setting for DFedADMM and DFedADMM-SAM, respectively, where $1 - \psi$ represents the spectral gap of the gossip matrix. Empirically, extensive experiments on MNIST, CIFAR10 and CIFAR100 datesets demonstrate that our algorithms exhibit superior performance in terms of both generalization and convergence speed compared to existing state-of-the-art (SOTA) optimizers in DFL.Comment: 24 page

Evolutionary Game Dynamics for Financial Risk Decision-Making in Global Supply Chain

This paper focuses on the game evolution process and its influencing factors of financial risk cooperation behavior between suppliers and manufacturers in global supply chain system. Using two-population evolutionary game theory, the performance of supply chain members under financial risk environment is modeled. Further, the proposed financial risk game model is applied to simulation cases of global supply chain. Based on the theory analysis and simulation results, it is shown that the cooperation strategy is the optimal evolutionarily stable strategy (ESS) for all supply chain members, when facing the high financial risk. The financial risk-sharing coefficient can be regarded as an adjuster that affects risk ESS of both suppliers and manufacturers under the low financial risk setting. By reducing the financial risk-sharing ratio of one supply chain player, his intention of adopting cooperation strategy would be enhanced. Finally, it is observed that financial risk sharing approach may lead to the alignment among supply chain members. Therefore, setting up an effective financial risk-sharing mechanism is beneficial to realize sustainable development of global supply chain

The Hydrothermal Stability and the Properties of Non- and Strongly-Interacting Rh Species over Rh/γ, θ-Al2O3 Catalysts

The present work reports the effects of γ-, θ-phase of alumina on the hydrothermal stability and the properties of non- and strongly-interacting Rh species of the Rh/Al2O3 catalysts. Comparing to γ-Al2O3, θ-Al2O3 can not only reduce the amount of occluded Rh but also better stabilize Rh during hydrothermal aging treatment. When the aging time was prolonged to 70 h, all the non-interacting Rh was transformed into strongly-interacting Rh and occluded Rh. The XPS results indicated that non- and strongly-interacting Rh might exist in the form of Rh/Rh3+ and Rh4+, respectively. CO-NO reaction was chosen as a probe reaction to research more information about non- and strongly-interacting Rh. The two Rh species had similar apparent activation energy (Eapp) of 170 kJ/mol, which indicated that non- and strongly-interacting Rh follow the same reaction path. The non-interacting Rh was removed from aged samples by the acid-treated method, and obtained results showed that only 2.5% and 4.0% non-interacting Rh was maintained in aged Rh/γ-Al2O3 and Rh/θ-Al2O3

AN IMPROVED ALGORITHM FOR TIME DOMAIN AVERAGING BASED ON FRACTIONAL DELAY FILTERING

For reducing the influence of truncation error on the accuracy of time domain averaging（ TDA） induced by noninteger-period sampling,an improved algorithm of TDA based on fractional delay filtering（ FDF） is presented.On the basis of analyzing the disadvantages of current methods of TDA and the characteristics of FDF,a presently improved method of signal truncation was used in the method to avoid the accumulation of truncation error and obtain a delay factor on each of the truncated signals,the reconstruction and resample for the truncated signals were implemented with FDF,and finally the arithmetic mean were computed after all of the truncated signals were added.The theoretical analysis and experimental results demonstrate that the method which fully makes using of the advantages of FDF on the change of delay factor,apparently reduces the truncation error of signals with non-integer-period sampling,and could obviously improve the accuracy of TDA without key-phase signal

MicroRNA-497 Inhibits Cardiac Hypertrophy by Targeting Sirt4

<div><p>Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to overload pressure of heart. From abundant studies, a conclusion is drawn that many microRNAs (miRNAs) are associated with cardiac hypertrophy and heart failure. To investigate the role of microRNA-497 (miR-497) in myocardial hypertrophy, two models were established in this study from cell level to integral level. Cardiac hypertrophy was induced by using angiotensin Ⅱ (Ang Ⅱ) in vitro and was created by transverse abdominal aortic constriction (TAC) in vivo. There was a significant decrease expression of miR-497 in cardiac hypertrophy models. Moreover, overexpression of miR-497 inhibited myocardial hypertrophy both in vitro and in vivo without heart function variation. In addition, luciferase reporter assays demonstrated that Sirt4 was a direct target gene of miR-497. Taking together, our study indicates that miR-497 modulates cardiac hypertrophy by targeting Sirt4 and may serve as a potential therapeutic substance in the course.</p></div

Improving Charge Injection at Gold/Conjugated Polymer Contacts by Polymer Insulator‐Assisted Annealing for Transistors

The poor chemical miscibility between metal and organic materials usually leads to both structural and energetic mismatches at gold/organic interfaces, and thereby, high contact resistance of organic electronic devices. This study shows that the contact resistance of organic field-effect transistors is significantly reduced by one order of magnitude, by reforming the contact interface between gold electrodes and conjugated polymers upon a polymer insulator-assisted thermal annealing. Upon an optimized solution process, the conjugated polymer is homogenously distributed within the amorphous polymer insulator matrix with relatively low glass transition temperature, and thus, even a moderate annealing temperature can induce sufficient motion of conjugated polymer chains to simultaneously adjust the polymer orientation and improve the packing of gold atoms. Consequently, gold/conjugated polymer contact is reorganized after annealing, which improves both charge transport from bulk gold to interface and charge injection from gold into conjugated polymers. This method, with appropriate insulator matrix, is effective for improving the injection of both holes and electrons, and widely applicable for many unipolar and ambipolar conjugated polymers to optimize the device performance and simultaneously increase the optical transparency (over 80%). A frequency doubler and a phase modulator are demonstrated, respectively, using the ambipolar transistors with optimized charge injection properties

miR-497 suppresses cardiac hypertrophy in vitro.

<p><b>Ang II-induced hypertrophic cardiomyocytes were infected with Leti-miR-497 or Leti-NC (MOI = 50) for 48 h.</b> a: Representative image of GFP in cardiomyocytes under a fluorescence microscope. b: miR-497 determined by qRT-PCR. c: Representative immunofluorescence image of α-actin staining. d: Relative cell area in Ang II-induced hypertrophic cardiomyocytes after infection. e: ANP and β-MHC mRNA expressions measured by qRT-PCR. f: Tritium-leucine incorporations detected by liquid scintillation counting. Data are presented as the mean ± SD; *, P < 0.05, n = 5.</p

miR-497 is down-regulated in hypertrophic cardiomyocytes.

<p><b>Establishment of hypertrophic cardiomyocytes treated with Ang II for 48h.</b> a: Immunofluorescence assay of α-actin was performed to identify cells. b: Relative cell area of cardiomyocytes detected by randomly measuring 10 cells from each section. c: ANP and β-MHC mRNA expression measured by qRT-PCR. d: miR-497 determined by qRT-PCR. e: Establishment of a mouse model of TAC-induced hypertrophy and histological analysis of hearts from different groups using H&E staining. f: The ratio of heart weight to tibial length. g: Relative cell area of cardiomyocytes detected by randomly measuring 10 cells from each section. h: ANP and β-MHC mRNA expression measured by qRT-PCR assay. i: miR-497 determined by qRT-PCR. Data are presented as the mean ± SD; *, P < 0.05, n = 5.</p

Cardiac structure and systolic function.

<p>Cardiac structure and systolic function.</p

miR-497 suppresses cardiac hypertrophy in vivo.

<p><b>Mice were subject to chest reopening injection with Leti-miR-497 or Leti-NC (3.5×10</b>^<b>7</b><b>viral particles per mice).</b> a: Representative image of GFP in myocardium under a fluorescence microscope. b: miR-497 determined by qRT-PCR. c: Morphologic and histological analysis of hearts from different groups using H&E staining. d: The ratio of heart weight to tibial length. e: Relative cell area of cardiomyocytes detected by randomly measuring 10 cells from each section. f: ANP and β-MHC mRNA expression measured by qRT-PCR. Data are shown as the mean ± SD; *, P < 0.05, n = 5.</p