Anionic Metal-Organic Framework Derived Cu Catalyst for Selective CO2 Electroreduction to Hydrocarbons.

Metal-organic frameworks (MOFs)-related Cu materials are promising candidates for promoting electrochemical CO2 reduction to produce valuable chemical feedstocks. However, many MOF materials inevitable undergo reconstruction under reduction conditions; therefore, exploiting the restructuring of MOF materials is of importance for the rational design of high-performance catalyst targeting multi-carbon products (C2). Herein, a facile solvent process is choosed to fabricate HKUST-1 with an anionic framework (a-HKUST-1) and utilize it as a pre-catalyst for alkaline CO2RR. The a-HKUST-1 catalyst can be electrochemically reduced into Cu with significant structural reconstruction under operating reaction conditions. The anionic HKUST-1 derived Cu catalyst (aHD-Cu) delivers a FEC2H4 of 56% and FEC2 of ≈80% at -150 mA cm-2 in alkaline electrolyte. The resulting aHD-Cu catalyst has a high electrochemically active surface area and low coordinated sites. In situ Raman spectroscopy indicates that the aHD-Cu surface displays higher coverage of *CO intermediates, which favors the production of hydrocarbons.

Lead Bromide Complex in Tri-n-Octylphosphine Oxide Matrix with Bright Photoluminance and Exceptional Thermoplasticity.

Metal halide materials have recently drawn increasing research interest for their excellent opto-electronic properties and structural diversity, but their resulting rigid structures render them brittle and poor formability during manufacturing. Here we demonstrate a thermoplastic luminant hybrid lead halide solid by integrating lead bromide complex into tri-n-octylphosphine oxide (TOPO) matrix. The construction of the hybrid materials can be achieved by a simple dissolution process, in which TOPO molecules act as the solvents and ligands to yield the monodispersed clusters. The combination of these functional units enables the near-room-temperature melt-processing of the materials into targeted geometry by simple molding or printing techniques, which offer possibilities for fluorescent writing inks with outstanding self-healing capacity to physical damage. The intermarriage between metal halide clusters with functional molecules expands the range of practical applications for hybrid metal halide materials.

Catalytic Hydrolysis-Oxidation of Halogenated Methanes over Phase- and Defect-Engineered CePO4: Halogenated Byproduct-Free and Stable Elimination.

Catalytic elimination of halogenated volatile organic compound (HVOC) emissions was still a huge challenge through conventional catalytic combustion technology, such as the formation of halogenated byproducts and the destruction of the catalyst structure; hence, more efficient catalysts or a new route was eagerly desired. In this work, crystal phase- and defect-engineered CePO4 was rationally designed and presented abundant acid sites, moderate redox ability, and superior thermal/chemical stability; the halogenated byproduct-free and stable elimination of HVOCs was achieved especially in the presence of H2O. Hexagonal and defective CePO4 with more structural H2O and Brønsted/Lewis acid sites was more reactive and durable compared with monoclinic CePO4. Based on the phase and defect engineering of CePO4, in situ diffuse reflectance infrared Fourier transform spectra (DRIFTS), and kinetic isotope effect experiments, a hydrolysis-oxidation pathway characterized by the direct involvement of H2O was proposed. Initiatively, an external electric field (5 mA) significantly accelerated the elimination of HVOCs and even 90% conversion of dichloromethane could be obtained at 170 °C over hexagonal CePO4. The structure-performance-dependent relationships of the engineered CePO4 contributed to the rational design of efficient catalysts for HVOC elimination, and this pioneering work on external electric field-assisted catalytic hydrolysis-oxidation established an innovative HVOC elimination route.

Global, regional, and national burden of non-communicable diseases attributable to occupational asbestos exposure 1990-2019 and prediction to 2035: worsening or improving?

Understanding the burden associated with occupational asbestos exposure on a global and regional scale is necessary to implement coordinated prevention and control strategies. By the GBD Study 2019, we conducted a comprehensive assessment of the non-communicable diseases burden attributable to occupational asbestos exposure. In 2019, 239,330 deaths and 4,189,000 disability-adjusted life years (DALYs) worldwide due to occupational asbestos exposure occurred. 1990-2019, deaths and DALYs attributed to occupational asbestos exposure increased by 65.65% and 43.66%, respectively. Age-standardized mortality rate (ASMR) and age-standardized DALYs rate (ASDR) decreased, with the most rapid declines in high Socio-Demographic Index (SDI) regions, with average annual percent change (AAPC) of - 1.05(95%CI: -1.2, -0.89) and -1.53(95%CI: -1.71, -1.36), respectively. Lung cancer, mesothelioma and ovarian cancer were the top three contributors to the increase in deaths and DALYs, accounting for more than 96%. AAPCs of ASMR and ASDR were positively associated with SDI. Global deaths from occupational asbestos exposure were predicted to increase and ASMR to decrease by 2035, mostly in males. Due consideration should be given to the susceptibility of the elderly, the lag of asbestos onset, and the regional differences, and constantly improve the prevention and control measures of occupational asbestos exposure and related diseases.

Rutin mitigates fluoride-induced nephrotoxicity by inhibiting ROS-mediated lysosomal membrane permeabilization and the GSDME-HMGB1 axis involved in pyroptosis and inflammation.

Fluoride is known to induce nephrotoxicity; however, the underlying mechanisms remain incompletely understood. Therefore, this study aims to explore the roles and mechanisms of lysosomal membrane permeabilization (LMP) and the GSDME/HMGB1 axis in fluoride-induced nephrotoxicity and the protective effects of rutin. Rutin, a naturally occurring flavonoid compound known for its antioxidative and anti-inflammatory properties, is primarily mediated by inhibiting oxidative stress and reducing proinflammatory markers. To that end, we established in vivo and in vitro models. In the in vivo study, rats were exposed to sodium fluoride (NaF) throughout pregnancy and up until 2 months after birth. In parallel, we employed in vitro models using HK-2 cells treated with NaF, n-acetyl-L-cysteine (NAC), or rutin. We assessed lysosomal permeability through immunofluorescence and analyzed relevant protein expression via western blotting. Our findings showed that NaF exposure increased ROS levels, resulting in enhanced LMP and increased cathepsin B (CTSB) and D (CTSD) expression. Furthermore, the exposure to NaF resulted in the upregulation of cleaved PARP1, cleaved caspase-3, GSDME-N, and HMGB1 expressions, indicating cell death and inflammation-induced renal damage. Rutin mitigates fluoride-induced nephrotoxicity by suppressing ROS-mediated LMP and the GSDME/HMGB1 axis, ultimately preventing fluoride-induced renal toxicity occurrence and development. In conclusion, our findings suggest that NaF induces renal damage through ROS-mediated activation of LMP and the GSDME/HMGB1 axis, leading to pyroptosis and inflammation. Rutin, a natural antioxidative and anti-inflammatory dietary supplement, offers a novel approach to prevent and treat fluoride-induced nephrotoxicity.

TFEB ameliorates DEHP-induced neurotoxicity by activating GAL3/TRIM16 axis dependent lysophagy and alleviating lysosomal dysfunction.

Di-(2-ethylhexyl) phthalate (DEHP) is a commonly used plasticizer with known neurotoxic effects. However, the specific mechanism underlying this neurotoxicity remains unclear. This study aimed to investigate the role of lysosomal function and lysophagy in DEHP-induced neurotoxicity, with a particular focus on the regulatory role of Transcription factor EB (TFEB). To achieve this, we utilized in vitro models of DEHP-exposed SH-SY5Y cells and HT22 cells. Our findings revealed that DEHP exposure led to lysosomal damage and dysfunction. Moreover, we observed impaired autophagic degradation, characterized by elevated levels of LC3II and p62. DEHP treatment downregulated the expression of TFEB, GAL3, and TRIM16, while upregulating the expression of PARP. This led to the inhibition of GAL3/TRIM16 axis dependent lysophagy and ultimately excessive apoptosis in neuronal cells. Importantly, TFEB overexpression alleviated lysosomal dysfunction, activated lysophagy, and mitigated DEHP-induced apoptosis. Overall, our results suggest that DEHP induces not only lysosomal dysfunction, but also inhibits lysophagy through the suppression of GAL3/TRIM16 axis. Consequently, impaired clearance of damaged lysosomes occurs, culminating in neuronal apoptosis. Taken together, our findings highlight the critical role of TFEB in regulating lysophagy and lysosomal function. Furthermore, TFEB may serve as a potential therapeutic target for mitigating DEHP-induced neuronal toxicity.

Polyethyleneimine Modified Two-Dimensional GO/MXene Composite Membranes with Enhanced Mg2+/Li+ Separation Performance for Salt Lake Brine.

As global demand for renewable energy and electric vehicles increases, the need for lithium has surged significantly. Extracting lithium from salt lake brine has become a cutting-edge technology in lithium resource production. In this study, two-dimensional (2D) GO/MXene composite membranes were fabricated using pressure-assisted filtration with a polyethyleneimine (PEI) coating, resulting in positively charged PEI-GO/MXene membranes. These innovative membranes, taking advantage of the synergistic effects of interlayer channel sieving and the Donnan effect, demonstrated excellent performance in Mg2+/Li+ separation with a mass ratio of 20 (Mg2+ rejection = 85.3%, Li+ rejection = 16.7%, SLi,Mg = 5.7) in simulated saline lake brine. Testing on actual salt lake brine in Tibet, China, confirmed the composite membrane's potential for effective Mg2+/Li+ separation. In the actual brine test with high concentration, Mg2+/Li+ after membrane separation is 2.2, which indicates that the membrane can significantly reduce the concentration of Mg2+ in the brine. Additionally, the PEI-GO/MXene composite membrane demonstrated strong anti-swelling properties and effective divalent ion rejection. This research presents an innovative approach to advance the development of 2D membranes for the selective removal of Mg2+ and Li+ from salt lake brine.

Sensitive and Specific Detection of Carcinoembryonic Antigens Using Toroidal Metamaterial Biosensors Integrated with Functionalized Gold Nanoparticles.

Carcinoembryonic antigen (CEA) is a biomarker that is highly expressed in cancer patients. Label-free, highly sensitive, and specific detection of CEA biomarkers can therefore greatly aid in the early detection and screening of cancer. This study presents a toroidal metamaterial biosensor integrated with functionalized gold nanoparticles (AuNPs) that demonstrated highly sensitive and specific detection of CEA using terahertz (THz) time-domain spectroscopy. In the biosensor, a closed-loop magnetic field formed an electrical confinement, resulting in a high sensitivity (287.8 GHz/RIU) and an ultrahigh quality factor (15.04). In addition, the integrated AuNPs with high refractive indices significantly enhanced the sensing performance of the biosensor. To explore the quantitative and qualitative detection of CEA, CEA biomarkers with various concentrations and four types of proteins were measured by the designed biosensor, achieving a limit of detection of 0.17 ng and high specificity. Even more significant, the proposed AuNP-integrated THz toroidal metamaterial biosensor demonstrates exceptional potential for use in technologies for cancer diagnosis and monitoring.

Effective SrWO4 /TiO2 Heterojunction with Enhanced Carriers Separation and Transfer for Photocatalytic Methane Oxidation.

Photocatalytic methane oxidation to oxygenates with promising performance remains as a grand challenge due to the low productivity and severe overoxidation. Herein, SrWO4 /TiO2 heterojunction was developed for photocatalytic methane oxidation with O2 to liquid oxygenates ( Please replace "oxygenates" with "oxygenated")products under mild reaction conditions. The optimized SrWO4 /TiO2 catalyst exhibited high productivity of 13365 µmol/g with high selectivity of 98.7 % for oxygenates. Benefited from the intimate heterojunction interface of SrWO4 /TiO2 , the constructed I-type heterostructure improved the separation and transfer of photogenerated carriers, and a high-speed transfer channel for photogenerated carriers was fabricated. Simultaneously, the special band structure can increase the amount of photogenerated electrons and holes on the TiO2 surface, which promoted the formation of reactive oxygen species to enhance liquid oxygenates productivity.

Cross-talk between autophagy and ferroptosis contributes to the liver injury induced by fluoride via the mtROS-dependent pathway.

Fluoride can induce hepatotoxicity, but the mechanisms responsible are yet to be investigated. This study sought to investigate the role and mechanism of mitochondrial reactive oxygen species (mtROS), autophagy, and ferroptosis in fluoride-induced hepatic injury with a focus on the role of mtROS-mediated cross-talk between autophagy and ferroptosis. To this end, an in vivo Sprague-Dawley rat model and in vitro BRL3A cells were exposed to sodium fluoride (NaF). The results revealed that NaF exposure diminished the mitochondrial membrane potential, increased mtROS production and TOMM20 expression, and induced autophagic flux blockage and ferroptosis in vivo and in vitro. Furthermore, the autophagy activator (RAPA) enhanced GPX4 expression while inhibiting ACSL4 expression, reduced the accumulation of ferrous ions in BRL3A cells, and restored lipid peroxidation levels, thus inhibiting ferroptosis. Fer-1, a ferritinase inhibitor, downregulated the expression of LC3-II and p62, increased the number of autolysosomes while decreasing the number of autophagosomes, and alleviated the blockage of autophagic flux by improving autophagic degradation. These results suggest the occurrence of a cross-talk between autophagy and ferroptosis. The mtROS inhibitor (Mito-TEMPO) could alleviate autophagic flux blockage and inhibit ferroptosis in NaF-induced liver injury. In addition, the cross-talk between NaF-induced autophagy and ferroptosis was dependent on the mtROS pathway.

TFE3-mediated impairment of lysosomal biogenesis and defective autophagy contribute to fluoride-induced hepatotoxicity.

Excessive fluoride exposure can cause liver injury, but the specific mechanisms need further investigation. We aimed to explore the role of impaired lysosomal biogenesis and defective autophagy in fluoride-induced hepatotoxicity and its potential mechanisms, focusing on the role of transcription factor E3 (TFE3) in regulating hepatocyte lysosomal biogenesis. To this end, we established a Sprague-Dawley (SD) rat model exposed to sodium fluoride (NaF) and a rat liver cell line (BRL3A) model exposed to NaF. The results showed that NaF exposure diminished liver function and led to apoptosis as well as autophagosome accumulation and impaired autophagic degradation. In addition, NaF exposure caused compromised lysosome biogenesis and decreased lysosomal degradation, and inhibited TFE3 nuclear translocation. Notably, the mTOR inhibitors rapamycin (RAPA) and Ad-TFE3 promoted lysosomal biogenesis and enhanced lysosomal degradation function. Furthermore, RAPA and Ad-TFE3 reduced NaF-induced apoptosis by alleviating impaired autophagic degradation. In conclusion, NaF impairs lysosomal biogenesis by inhibiting TFE3 nuclear translocation, decreasing lysosomal degradation function, resulting in impaired autophagic degradation, and ultimately inducing apoptosis. Therefore, TFE3 may be a promising therapeutic target for fluoride-induced hepatotoxicity.

The inhibition of TRPML1/TFEB leads to lysosomal biogenesis disorder, contributes to developmental fluoride neurotoxicity.

Fluoride is capable of inducing developmental neurotoxicity; regrettably, the mechanism is obscure. We aimed to probe the role of lysosomal biogenesis disorder in developmental fluoride neurotoxicity-specifically, the regulating effect of the transient receptor potential mucolipin 1 (TRPML1)/transcription factor EB (TFEB) signaling pathway on lysosomal biogenesis. Sprague-Dawley rats were given fluoridated water freely, during pregnancy to the parental rats to 2 months after delivery to the offspring. In addition, neuroblastoma SH-SY5Y cells were treated with sodium fluoride (NaF), with or without mucolipin synthetic agonist 1 (ML-SA1) or adenovirus TFEB (Ad-TFEB) intervention. Our findings revealed that NaF impaired learning and memory as well as memory retention capacities in rat offspring, induced lysosomal biogenesis disorder, and decreased lysosomal degradation capacity, autophagosome accumulation, autophagic flux blockade, apoptosis, and pyroptosis. These changes were evidenced by the decreased expression of TRPML1, nuclear TFEB, LAMP2, CTSB, and CTSD, as well as increased expression of LC3-II, p62, cleaved PARP, NLRP3, Caspase1, and IL-1ß. Furthermore, TRPML1 activation and TFEB overexpression both restored TFEB nuclear protein expression and promoted lysosomal biogenesis while enhancing lysosomal degradation capacity, recovering autophagic flux, and attenuating NaF-induced apoptosis and pyroptosis. Taken together, these results show that NaF promotes the progression of developmental fluoride neurotoxicity by inhibiting TRPML1/TFEB expression and impeding lysosomal biogenesis. Notably, the activation of TRPML1/TFEB alleviated NaF-induced developmental neurotoxicity. Therefore, TRPML1/TFEB may be promising markers of developmental fluoride neurotoxicity.

PRKAA1 induces aberrant mitophagy in a PINK1/Parkin-dependent manner, contributing to fluoride-induced developmental neurotoxicity.

Chronic fluoride exposure can cause developmental neurotoxicity, however the precise mechanisms remain unclear. To explore the mechanism of mitophagy in fluoride-induced developmental neurotoxicity, specifically focusing on PRKAA1 in regulating the PINK1/Parkin pathway, we established a Sprage Dawley rat model with continuous sodium fluoride (NaF) exposure and an NaF-treated SH-SY5Y cell model. We found that NaF exposure increased the levels of LC3-Ⅱ and p62, impaired autophagic degradation, and subsequently blocked autophagic flux. Additionally, NaF exposure increased the expression of PINK1, Parkin, TOMM-20, and Cyt C and cleaved PARP in vivo and in vitro, indicating NaF promotes mitophagy and neuronal apoptosis. Meanwhile, phosphoproteomics and western blot analysis showed that NaF treatment enhanced PRKAA1 phosphorylation. Remarkably, the application of both 3-methyladenosine (3-MA; autophagy inhibitor) and dorsomorphin (DM; AMPK inhibitor) suppressed NaF-induced neuronal apoptosis by restoring aberrant mitophagy. In addition, 3-MA attenuated an increase in p62 protein levels and NaF-induced autophagic degradation. Collectively, our findings indicated that NaF causes aberrant mitophagy via PRKAA1 in a PINK1/Parkin-dependent manner, which triggers neuronal apoptosis. Thus, regulating PRKAA1-activated PINK1/Parkin-dependent mitophagy may be a potential treatment for NaF-induced developmental neurotoxicity.

Comprehensive risk assessments and anesthetic management for children with osteogenesis imperfecta: A retrospective review of 252 orthopedic procedures over 5 years.

BACKGROUND: Major anesthetic risks arise in orthopedic surgeries for children with osteogenesis imperfecta, a rare genetically inherited condition presenting diverse skeletal issues. AIM: We aimed to investigate anesthetic risks, including difficult airway, hypo- and hyperthermia, blood loss, and pain, in connection with patient, anesthetic, and surgical factors. METHODS: Both descriptive and inferential statistics were employed to study the anesthetic risks and their predictors. Data of 252 surgeries for 132 Chinese osteogenesis imperfecta patients aged 18 or below were retrieved from the authors' hospital between 2015 and 2019. RESULTS: Two thirds of the cohort were Sillence type IV patients, with types I, III, and V accounting for 7.6%, 14.4%, and 11.4%, respectively. Video and direct laryngoscopy were used. No case of difficult airway was identified. Due to a careful management strategy, intraoperative temperature varied on average between -0.38°C and +0.89°C from the initial temperature. Fifty-two and 18 cases of hyper- and hypothermia were encountered, respectively. The use of sevoflurane for maintenance resulted in a mean increase of +0.24°C [95% CI 0.05 ~ 0.42] in the maximum temperature. Massive blood losses (>20% of estimated total blood volume) were observed in 18.3% of the cases. Neither intraoperative temperature changes nor blood loss was found to be related to Sillence classification. Regional anesthesia techniques were applied to 72.6% of the cases. Ultrasound guidance was used per the judgment of anesthesiologists or when in case of difficult landmarks. The incidence of difficult regional anesthesia was low (4 out of 252). For postoperative analgesia, 154 neuraxial blocks (including 77 caudal and 77 lumbar epidural) and 29 peripheral nerve blocks were performed. CONCLUSION: Anesthesia for children with osteogenesis imperfecta undergoing complex orthopedic procedures was challenging. Proper anesthesia planning was essential for both intraoperative management and postoperative analgesia. Age, surgical duration, and use of sevoflurane for maintenance impacted the intraoperative temperature most, and massive blood loss was not uncommon. The risks for airway or regional anesthesia difficulties were low. Pain scores could be controlled to be ≤3 via multiple techniques.

Genome-wide analysis of cell-Free DNA methylation profiling with MeDIP-seq identified potential biomarkers for colorectal cancer.

BACKGROUND: Colorectal cancer is the most common malignancy and the third leading cause of cancer-related death worldwide. This study aimed to identify potential diagnostic biomarkers for colorectal cancer by genome-wide plasma cell-free DNA (cfDNA) methylation analysis. METHODS: Peripheral blood from colorectal cancer patients and healthy controls was collected for cfDNA extraction. Genome-wide cfDNA methylation profiling, especially differential methylation profiling between colorectal cancer patients and healthy controls, was performed by methylated DNA immunoprecipitation coupled with high-throughput sequencing (MeDIP-seq). Logistic regression models were established, and the accuracy of this diagnostic model for colorectal cancer was verified using tissue-sourced data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) due to the lack of cfDNA methylation data in public datasets. RESULTS: Compared with the control group, 939 differentially methylated regions (DMRs) located in promoter regions were found in colorectal cancer patients; 16 of these DMRs were hypermethylated, and the remaining 923 were hypomethylated. In addition, these hypermethylated genes, mainly PRDM14, RALYL, ELMOD1, and TMEM132E, were validated and confirmed in colorectal cancer by using publicly available DNA methylation data. CONCLUSIONS: MeDIP-seq can be used as an optimal approach for analyzing cfDNA methylomes, and 12 probes of four differentially methylated genes identified by MeDIP-seq (PRDM14, RALYL, ELMOD1, and TMEM132E) could serve as potential biomarkers for clinical application in patients with colorectal cancer.

Impaired V-ATPase leads to increased lysosomal pH, results in disrupted lysosomal degradation and autophagic flux blockage, contributes to fluoride-induced developmental neurotoxicity.

Fluoride is capable of inducing developmental neurotoxicity, yet its mechanisms remain elusive. We aimed to explore the possible role and mechanism of autophagic flux blockage caused by abnormal lysosomal pH in fluoride-induced developmental neurotoxicity, focusing on the role of V-ATPase in regulating the neuronal lysosomal pH. Using Sprague-Dawley rats exposed to sodium fluoride (NaF) from gestation through delivery until the neonatal offspring reached six months of age as an in vivo model. The results showed that NaF impaired the cognitive abilities of the offspring rats. In addition, NaF reduced V-ATPase expression, diminished lysosomal degradation capacity and blocked autophagic flux, and increased apoptosis in the hippocampus of offspring. Consistently, these results were validated in SH-SY5Y cells incubated with NaF. Moreover, NaF increased the SH-SY5Y lysosomal pH. Mechanistically, V-ATPase B2 overexpression and ATP effectively restored V-ATPase expression, reducing NaF-induced lysosomal alkalinization while increasing lysosomal degradation capacity. Notably, those above pharmacological and molecular interventions diminished NaF-induced apoptosis by restoring autophagic flux. Collectively, the present findings suggested that NaF impairs the lysosomal pH raised by V-ATPase. This leads to reduced lysosomal degradation capacity and triggers autophagic flux blockage and apoptosis, thus contributing to neuronal death. Therefore, V-ATPase might be a promising indicator of developmental fluoride neurotoxicity.

Weakened interaction of ATG14 and the SNARE complex blocks autophagosome-lysosome fusion contributes to fluoride-induced developmental neurotoxicity.

Fluoride is capable of inducing developmental neurotoxicity, but the mechanisms involved remain unclear. We aimed to explore the role of autophagosome-lysosome fusion in developmental fluoride neurotoxicity, particularly focusing on the interaction between ATG14 and the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex. We developed in vivo models of Sprague-Dawley rats exposed to sodium fluoride (NaF) from the pregnancy of parental rats until the offspring were two months old and in vitro models of NaF and/or Ad-ATG14-treated SH-SY5Y cells. We assessed neurobehavioral changes in offspring and further investigated the effects of NaF exposure on autophagic flux, apoptosis, autophagosome-lysosome fusion, and the interaction between ATG14 and the SNARE complex. NaF exposure impaired offspring learning and memory capabilities and induced the accumulation of autophagosomes and autophagic flux blockage and apoptosis, as indicated by increased LC3-II, p62, and cleaved-caspase-3 expression in vivo and in vitro. In addition, NaF treatment downregulated the protein expression of ATG14 and the SNARE complex and induced autophagosome-lysosome fusion blockage as evidenced by decreased ATG14, STX17, SNAP29, and VAMP8 expression and diminished colocalization of autophagosomes and lysosomes in vivo and in vitro. Furthermore, ATG14 upregulation enhanced the interaction of ATG14 and the SNARE complex to facilitate autophagosome-lysosome fusion, thereby restoring autophagic flux and alleviating NaF-induced apoptosis. In conclusion, NaF exhibited developmental neurotoxicity by restraining the interaction of ATG14 with the SNARE complex and hindering autophagosome-lysosome fusion, thereby participating in the occurrence and development of fluoride neurotoxicity. Notably, ATG14 upregulation protects against developmental fluoride neurotoxicity, and ATG14 may serve as a promising biomarker for further epidemiological investigation.

An RFID-Based Method for Multi-Person Respiratory Monitoring.

Respiratory monitoring is widely used in the field of health care. Traditional respiratory monitoring methods bring much inconvenience to users. In recent years, a great number of respiratory monitoring methods based on wireless technology have emerged, but multi-person respiratory monitoring is still very challenging; therefore, this paper explores multi-person respiratory monitoring. Firstly, the characteristics of human respiratory movement have been analyzed, and a suitable tag deployment method for respiratory monitoring is proposed. Secondly, aiming at the ambiguity and entanglement of radio frequency identification (RFID) phase data, a method of removal of phase ambiguity and phase wrapping is given. Then, in order to monitor multi-person respiration in a noisy environment, the frequency extraction method and waveform reconstruction method of multi-person respiration are proposed. Finally, the feasibility of the method is verified by experiments.

Toward COVID-19 Contact Tracing though Wi-Fi Probes.

COVID-19 is currently the biggest threat that challenges all of humankind's health and property. One promising and effective way to control the rapid spreading of this infection is searching for primary close contacts of the confirmed cases. In response, we propose COVID-19 Tracer, a low-cost passive searching system to find COVID-19 patients' close contacts. The main idea is utilizing ubiquitous WiFi probe requests to describe the location similarity, which is then achieved by two designed range-free judgment indicators: location similarity coefficient and close contact distance. We have carried out extensive experiments in a school office building, and the experimental results show an average accuracy of more than 98%, demonstrating our system's effectiveness in judging close contacts. Last but not least, we have developed a prototype system for a school building to find potential close contacts.

Oral and Maxillofacial Autologous Fat Transplantation: History, Clinical Application Status and Research Progress.

After more than a century of development, autologous fat transplantation (AFT), a repair method for soft tissue defects and deformities, has the advantages of being simple, rapid, effective and safe, and it is increasingly favoured by plastic surgeons. This article reviews the developmental history of AFT, analyses its clinical application status in the oral and maxillofacial regions, and provides a preliminary summary and discussion of the research progress related to AFT. The hope is that that this technique could be widely applied for oral and maxillofacial diseases as well as facial rejuvenation indications. LEVEL OF EVIDENCE III: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .