Constructing Built-in-Electric Field for Boosting Electrocatalytic Water Splitting.

Electrocatalytic water splitting shows great potential for producing clean and green hydrogen, but it is hindered by slow reaction kinetics. Advanced electrocatalysts are needed to lower the energy barriers. The establishment of built-in electric fields (BIEF) in heterointerfaces has been found to be beneficial for speeding up electron transfer, increasing electrical conductivity, adjusting the local reaction environment, and optimizing the chemisorption energy with intermediates. Engineering and modifying the BIEF in heterojunctions offer significant opportunities to enhance the electronic properties of catalysts, thus improving the reaction kinetics. This comprehensive review focuses on the latest advances in BIEF engineering in heterojunction catalysts for efficient water electrolysis. It highlights the fundamentals, engineering, modification, characterization, and application of BIEF in electrocatalytic water splitting. The review also discusses the challenges and future prospects of BIEF engineering. Overall, this review provides a thorough examination of BIEF engineering for the next generation of water electrolysis devices.

Effectiveness and Safety of Low-Dose Radiotherapy in Eosinophilic Lymphoid Granuloma.

Objective: To investigate the efficacy and safety of low-dose radiotherapy in treating eosinophilic lymphoid granuloma. Method: This study included a total of 20 patients diagnosed with eosinophilic lymphoid granuloma. All patients underwent low-dose three-dimensional conformal intensity-modulated radiotherapy for their lesions. We analyzed the control status of the lesions and any adverse reactions related to radiotherapy. Results: The overall effectiveness of low-dose radiotherapy in treating eosinophilic lymphoid granuloma was 90%. The incidence of grade I and grade II adverse reactions induced by radiotherapy was 70% and 30%, respectively. Over a median follow-up period of 23.6 months, all patients showed controlled lesions within the target delineation of radiotherapy. After radiotherapy, four patients experienced occasional pruritus, and one patient had a recurrence outside the target area three years later. No long-term severe adverse reactions related to radiotherapy were observed during the follow-up period. Conclusions: Low-dose radiotherapy demonstrates an apparent therapeutic effect on eosinophilic lymphoid granuloma with acceptable adverse reactions.

The Analysis of Sharing Economy on New Business Model Based on BP Neural Network.

The development of social economy and Internet information technology has made the development of the sharing economy relatively rapid. This article aims to study how to promote the sharing economy based on neural networks to play a role in new business models. This article proposes that the sharing economy and the new business model are inseparable. It also discusses how to analyze the relationship between the sharing economy and the new business model based on the BP neural network. With the development of the economy and society, new economic development models have developed, and the sharing economy model has risen. The sharing economy model has brought an impact to the traditional economic development model, affecting the business model. The results show that with the development of society and enterprises, the development of the sharing economy is getting faster and faster. Today, some sharing economy companies are bound to face various obstacles in the process of copying other business models and development. Sharing economy enterprises have made various adjustments and responses to various problems, but they have not found a better model to adapt to the modern social market and environment. Therefore, the business model of the sharing economy requires further analysis and investigation.

TFEC contributes to cardiac hypertrophy by inhibiting AMPK/mTOR signaling.

The underlying mechanism of cardiac hypertrophy has not yet been fully elucidated. The present study aimed to explore the function of transcription factor EC (TFEC) in mouse models of cardiac hypertrophy and to determine the underlying mechanism. Pressure-overload cardiac hypertrophy and angiotensin II (AngII) infusion-induced animal models of cardiac hypertrophy were established in vivo. The expression of TFEC was explored via western blotting. The results demonstrated that TFEC expression was significantly increased in the hearts of mice with pressure overload- and AngII-induced hypertrophy. Injection of rAd-short hairpin (sh)-TFEC significantly decreased the expression of TFEC in heart tissues compared with group injected with rAd-negative control (NC). Furthermore, the expression levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and ß-myosin heavy chain (ß-MHC) were increased in the hearts of AngII-treated mice; however, compared with rAd-NC transfection, transfection with rAd-sh-TFEC decreased the expression levels of ANP, BNP and ß-MHC. The results from echocardiographic analysis indicated that transfection with rAd-sh-TFEC improved the cardiac function of AngII-treated mice compared with transfection with rAd-NC. In addition, the AngII-induced increase in cardiomyocyte size could be reversed by TFEC knockdown in primary cardiomyocytes. The elevated expression levels of ANP, BNP and ß-MHC induced by AngII could be partially abolished following TFEC knockdown. The results from western blotting demonstrated that TFEC overexpression decreased the expression of phosphorylated AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) but increased the expression of phosphorylated mechanistic target of rapamycin (mTOR). Furthermore, Compound C significantly suppressed the activation of AMPK/ACC but increased the activation of mTOR, even in primary cardiomyocytes transfected with rAd-sh-TFEC. In conclusion, the findings from this study demonstrated that TFEC was overexpressed in the hearts of mice with cardiac hypertrophy and that silencing TFEC may improve AngII-induced cardiac hypertrophy and dysfunction by activating AMPK/mTOR signaling.