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Electrochemical biosensors incorporate a recognition element and an electronic transducer for the highly sensitive detection of analytes in body fluids. Importantly, they can provide rapid readouts and they can be integrated into portable, wearable and implantable devices for point-of-care diagnostics; for example, the personal glucose meter enables at-home assessment of blood glucose levels, greatly improving the management of diabetes. In this Review, we discuss the principles of electrochemical biosensing and the design of electrochemical biosensor devices for health monitoring and disease diagnostics, with a particular focus on device integration into wearable, portable and implantable systems. Finally, we outline the key engineering challenges that need to be addressed to improve sensing accuracy, enable multiplexing and one-step processes, and integrate electrochemical biosensing devices in digital health-care pathways.Electrochemical biosensors can be integrated into wearable, portable and implantable devices for health monitoring and disease diagnosis. This Review discusses the design and integration of different types of electrochemical biosensors for the detection of analytes related to health and disease, and outlines engineering challenges that need to be addressed to enable clinical translation of electrochemical biosensor-based point-of-care devices.

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Recently was been found that pyroptosis is a unique form of proinflammatory programmed death, that is different from apoptosis. A growing number of studies have investigated pyroptosis and its relationship with sepsis, including the mechanisms, role, and relevant targets of pyroptosis in sepsis. While moderate pyroptosis in sepsis can control pathogen infection, excessive pyroptosis can lead to a dysregulated host immune response and even organ dysfunction. This review provides an overview of the mechanisms and potential therapeutic targets underlying pyroptosis in sepsis identified in recent decades, looking forward to the future direction of treatment for sepsis.

The progressive loss of cardiomyocytes caused by cell death leads to cardiac dysfunction and heart failure (HF). Rapamycin has been shown to be cardioprotective in pressure-overloaded and ischemic heart diseases by regulating the mechanistic target of rapamycin (mTOR) signaling network. However, the impact of rapamycin on cardiomyocyte death in chronic HF remains undetermined. Therefore, in the current study we addressed this issue using a rat myocardial infarction (MI)-induced chronic HF model induced by ligating the coronary artery. Following surgery, rats were randomly divided into six groups, including the sham-, vehicle- and rapamycin-operated groups, at 8 or 12 weeks post-MI. A period of 4 weeks after MI induction, the rats were treated with rapamycin (1.4 mg-kg-day) or vehicle for 4 weeks. Cardiac function was determined using echocardiography, the rats were subsequently euthanized and myocardial tissues were harvested for histological and biochemical analyses. In the cell culture experiments with H9c2 rat cardiomyocytes, apoptosis was induced using angiotensin II (100 nM; 24 h). Cardiomyocyte apoptosis and autophagy were assessed via measuring apoptosis- and autophagy-associated proteins. The activities of mTOR complex 1 (mTORC1) and mTORC2 were evaluated using the phosphorylation states of ribosomal S6 protein and Akt, respectively. The activity of the endoplasmic reticulum (ER) stress pathway was determined using the levels of GRP78, caspase-12, phospho-JNK and DDIT3. Echocardiographic and histological measurements indicated that rapamycin treatment improved cardiac function and inhibited cardiac remodeling at 8 weeks post-MI. Additionally, rapamycin prevented cardiomyocyte apoptosis and promoted autophagy at 8 weeks post-MI. Rapamycin treatment for 4 weeks inhibited the mTOR and ER stress pathways. Furthermore, rapamycin prevented angiotensin II-induced H9c2 cell apoptosis and promoted autophagy by inhibiting the mTORC1 and ER stress pathways. These results demonstrated that rapamycin reduced cardiomyocyte apoptosis and promoted cardiomyocyte autophagy, by regulating the crosstalk between the mTOR and ER stress pathways in chronic HF.

Hydrogen produced from neutral seawater electrolysis faces many challenges including high energy consumption, the corrosion/side reactions caused by Cl - , and the blockage of active sites by Ca 2+ /Mg 2+ precipitates. Herein, we design a pH-asymmetric electrolyzer with a Na + exchange membrane for direct seawater electrolysis, which can simultaneously prevent Cl - corrosion and Ca 2+ /Mg 2+ precipitation and harvest the chemical potentials between the different electrolytes to reduce the required voltage. In-situ Raman spectroscopy and density functional theory calculations reveal that water dissociation can be promoted with a catalyst based on atomically dispersed Pt anchored to Ni-Fe-P nanowires with a reduced energy barrier (by 0.26 eV), thus accelerating the hydrogen evolution kinetics in seawater. Consequently, the asymmetric electrolyzer exhibits current densities of 10 mA cm −2 and 100 mA cm −2 at voltages of 1.31 V and 1.46 V, respectively. It can also reach 400 mA cm −2 at a low voltage of 1.66 V at 80 °C, corresponding to the electricity cost of US$1.36 per kg of H 2 ($0.031/kW h for the electricity bill), lower than the United States Department of Energy 2025 target (US$1.4 per kg of H 2 ). Hydrogen produced directly from neutral seawater is promising but challenging due to seawater’s complex composition. Here, the authors report a Na + -conducted pH-asymmetric electrolyzer that can directly split seawater into hydrogen with low electricity cost and nearly zero chloride interference.

Modern tourism plays an increasingly important economic role in regional development. However, in the practice of regional economic development, there is often a lag in economic development where the tourism industry is prosperous. We explored the potential impact of the development level of informatization on the coupling and coordination relationship between the tourism industry and regional economic development. Using provincial panel data from 2008 to 2017, we constructed a spatial Dubin model for empirical research. We established an evaluation model for the coupling and coordination relationship between tourism and regional economic development based on the establishment of evaluation models and indicator systems for informatization, tourism, and regional economic development. The results show that improvements to informatization generally promoted the coupling and coordination of tourism and regional economic development. Informatization not only improved the coupling and coordination of tourism and economic development in the region but also had significant spatial spillover effects. In addition to the influencing factors at the information level, the advantages of tourism resources and the level of economic development on the whole also helped to improve the degree of coupling and coordination, while the widening of the income gap between urban and rural areas hindered coordinated development. Further discussion shows that informatization will affect the degree of coupling and coordination between the tourism industry and regional economic development by influencing the level of institutional environment. The findings highlight the need to focus on diversified development of the regional tourism industry and economy while improving the level of informatization and strengthening cross-regional cooperation during informatization. The conclusions contribute to improving the coordinated development of regional tourism and regional economy and provide a scientific basis for the development of informatization and the formulation of tourism and economic policies.

Background The importance of mRNA methylation erased by ALKBH5 in mRNA biogenesis, decay, and translation control is an emerging research focus. Ectopically activated YAP is associated with the development of many human cancers. However, the mechanism whereby ALKBH5 regulates YAP expression and activity to inhibit NSCLC tumor growth and metastasis is not clear. Methods Protein and transcript interactions were analyzed in normal lung cell and NSCLC cells. Gene expression was evaluated by qPCR and reporter assays. Protein levels were determined by immunochemical approaches. Nucleic acid interactions and status were analyzed by immunoprecipitation. Cell behavior was analyzed by standard biochemical tests. The m 6 A modification was analyzed by MeRIP. Results Our results show that YAP expression is negatively correlated with ALKBH5 expression and plays an opposite role in the regulation of cellular proliferation, invasion, migration, and EMT of NSCLC cells. ALKBH5 reduced m 6 A modification of YAP . YTHDF3 combined YAP pre-mRNA depending on m 6 A modification. YTHDF1 and YTHDF2 competitively interacted with YTHDF3 in an m 6 A-independent manner to regulate YAP expression. YTHDF2 facilitated YAP mRNA decay via the AGO2 system, whereas YTHDF1 promoted YAP mRNA translation by interacting with eIF3a; both these activities are regulated by m 6 A modification. Furthermore, ALKBH5 decreased YAP activity by regulating miR-107/LATS2 axis in an HuR-dependent manner. Further, ALKBH5 inhibited tumor growth and metastasis in vivo by reducing the expression and activity of YAP. Conclusions The presented findings suggest m 6 A demethylase ALKBH5 inhibits tumor growth and metastasis by reducing YTHDFs-mediated YAP expression and inhibiting miR-107/LATS2–mediated YAP activity in NSCLC. Moreover, effective inhibition of m 6 A modification of ALKBH5 might constitute a potential treatment strategy for lung cancer.

Contamination of the environment by mercury(II) ions (Hg 2+ ) poses a serious threat to human health and ecosystems. Up to now, many reported Hg 2+ sensors require complex procedures, long measurement times and sophisticated instrumentation. We have developed a simple, rapid, low cost and naked-eye quantitative method for Hg 2+ environmental analysis using a paper-based colorimetric device (PCD). The sample solution to which platinum nanoparticles (PtNPs) have been added is dispensed to the detection zone on the PCD, where the 3,3,5,5-tetramethylbenzidine (TMB) substrate has been pre-loaded. The PtNPs effect a rapid oxidization of TMB, inducing blue colorization on the PCD. However, Hg 2+ in the solution rapidly interact with the PtNPs, suppressing the oxidation capacity and hence causing a decrease in blue intensity, which can be observed directly by the naked eye. Moreover, Hg 2+ at concentrations as low as 0.01 uM, can be successfully monitored using a fiber optic device, which gives a digital readout proportional to the intensity of the blue color change. This paper-based colorimetric device (PCD) shows great potential for field measurement of Hg 2+ .

Hyperlipidemia is increasingly recognized as a significant global health issue, often associated with conditions such as hypertension, diabetes, and obesity. While statins are frequently prescribed to manage lipid levels, recent studies indicate that reliance solely on statin therapy may present certain disadvantages, including prolonged treatment durations, the potential for drug resistance, and various adverse effects. Research indicates that the combination of ezetimibe and statins demonstrates a favorable therapeutic effect in the management of hyperlipidemia. However, existing studies have not consistently confirmed these benefits, and there is no current meta-analysis available. As a result, we will perform a meta-analysis to assess the effectiveness and safety of the combination of ezetimibe and statins in managing hyperlipidemia, aiming to offer evidence-based medical guidance for clinical practice. The systematic review and meta-analysis will adhere to the PRISMA guidelines for systematic reviews and meta-analyses. We will search for randomized controlled trials that investigate the efficacy and safety of the combination of ezetimibe and statins in treating hyperlipidemia, based on specific criteria. The following electronic databases will be searched by two researchers for relevant records published up to October 1, 2024: Cochrane Central Register of Controlled Trials (CENTRAL) in Cochrane Library, Embase.com, Web of Science, MEDLINE (via PubMed), Wanfang China Database, China National Knowledge Infrastructure (CNKI), Chinese Biomedical Literature Database (CBM) and Chinese Scientific Journal Database (VIP). They will also check references and relevant journals manually. Two independent reviewers will handle screening, data extraction, and quality assessment. Subgroup analysis, sensitivity analysis, and publication bias analysis will be performed to assess consistency and reliability. Review Manager 5.4 will be used for data analysis and synthesis, while the GRADE approach will be employed to evaluate the overall study's evidence quality. The findings of this systematic review will be shared with various stakeholders who are interested in the combination of ezetimibe and statins for hyperlipidemia. This will offer valuable insights for researchers undertaking future investigations and for clinical practitioners specializing in the treatment of hyperlipidemia. This study is based on a secondary analysis of the literature, so ethical review approval is not required. The final report will be published in a peer-reviewed journal. The protocol of the systematic review has been registered on Open Science Framework, with a registration DOI https://doi.org/10.17605/OSF.IO/TEVUY.

Although nontumor components play an essential role in colon cancer (CC) progression, the intercellular communication between CC cells and adjacent colonic epithelial cells (CECs) remains poorly understood. Here, we show that intact mitochondrial genome (mitochondrial DNA, mtDNA) is enriched in serum extracellular vesicles (EVs) from CC patients and positively correlated with tumor stage. Intriguingly, circular mtDNA transferred via tumor cell-derived EVs (EV-mtDNA) enhances mitochondrial respiration and reactive oxygen species (ROS) production in CECs. Moreover, the EV-mtDNA increases TGFβ1 expression in CECs, which in turn promotes tumor progression. Mechanistically, the intercellular mtDNA transfer activates the mitochondrial respiratory chain to induce the ROS-driven RelA nuclear translocation in CECs, thereby transcriptionally regulating TGFβ1 expression and promoting tumor progression via the TGFβ/Smad pathway. Hence, this study highlights EV-mtDNA as a major driver of paracrine metabolic crosstalk between CC cells and adjacent CECs, possibly identifying it as a potential biomarker and therapeutic target for CC. The interaction between colon cancer cells and colonic epithelial cells (CECs) is critical yet not well-known. Here, the authors show that tumor extracellular vesicles mediate mitochondrial DNA transfer to CECs, initiating mitochondrial activation and RelA-induced TGFβ1 expression, leading to tumor progression.