Uniportal left middle lobectomy in a patient with situs inversus totalis: a case report.

BACKGROUND: Situs inversus totalis (SIT), a rare recessive autosomal disease, involves the complete transposition of the thoracic and abdominal viscera in the left-right axis. Patients with SIT combined with lung cancer are extremely uncommon. CASE PRESENTATION: We present a case of a 57-year-old woman with SIT who underwent uniportal video-assisted thoracoscopic left middle lobectomy for adenocarcinoma of the lung. The procedure was performed safely with adequate anatomical identification and careful intraoperative manipulation based on the preoperative three-dimensional-computed tomography bronchography and angiography (3D-CTBA). The patient's perioperative period was uneventful, and no recurrence was observed 2 year postoperatively. CONCLUSION: With the preoperative planning of the 3D-CTBA, uniportal video-assisted thoracoscopic lobectomy in lung cancer patients with sit can be performed safely and effectively.

Screening, identification and targeted intervention of necroptotic biomarkers of asthma.

BACKGROUND: As a pivotal pathway of programmed cell death, necroptosis significantly contributes to the pathogenesis of respiratory disorders. However, its role in asthma is not yet fully elucidated. Therefore, this study aimed to identify markers associated with necroptosis, evaluate their functions in asthma, and explore potential therapeutic agents targeting necroptosis for the management of asthma. METHODS: Firstly, machine learning algorithms, including Least Absolute Shrinkage and Selection Operator (LASSO), Random Forest, and Support Vector Machine-Recursive Feature Elimination (SVM-RFE), were utilized to identify necroptosis-related differentially expressed genes (NRDEGs) in asthma patients compared to healthy controls. Concurrently, the expression of NRDEGs was validated using external datasets, Western blot, and quantitative real-time polymerase chain reaction (qPCR). Secondly, the clinical relevance of NRDEGs was assessed through Receiver Operating Characteristic (ROC) curve analysis and correlation with clinical indicators. Thirdly, the relationship between NRDEGs and pulmonary immune cell infiltration, as well as the signaling interactions between different cells types, were analyzed through immune infiltration and single-cell analysis. Fourthly, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA), were conducted to elucidate the functional roles of NRDEGs. Finally, compounds targeting NRDEGs were screened, and their binding affinities were evaluated using molecular docking studies. RESULTS: In asthma, necroptosis is activated, leading to the identification of four NRDEGs: NLRP3, PYCARD, ALOX15, and VDAC3. Among these, NLRP3, PYCARD, and ALOX15 are upregulated, whereas VDAC3 is downregulated in asthma. Comprehensive clinical evaluations indicated that NRDEGs hold diagnostic value for asthma. Specifically, NLRP3 was inversely correlated with forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC), while VDAC3 showed an inverse correlation with sputum neutrophils. Conversely, ALOX15 expression was positively correlated with fractional exhaled nitric oxide (FeNO) levels, as well as sputum eosinophils, blood eosinophils, and blood IgE levels. Subsequent immune infiltration analysis revealed associations between NRDEGs and activated dendritic cells, mast cells, and eosinophils. Single-cell RNA sequencing (scRNA-seq) further confirmed the communication signals between myeloid dendritic cells, fibroblasts, neutrophils, and helper T cells, predominantly related to fibrosis and immune-inflammatory responses. Pathway enrichment analysis demonstrated that NRDEGs are involved in ribosomal function, oxidative phosphorylation, and fatty acid metabolism. Finally, resveratrol and triptonide were identified as potential therapeutic agents targeting the proteins encoded by NRDEGs for asthma treatment. CONCLUSIONS: The necroptosis pathway is activated in asthma, with NRDEGs-namely PYCARD, NLRP3, ALOX15, and VDAC3-correlated with declines in lung function and airway inflammation. These genes serve as reliable predictors of asthma risk and are involved in the regulation of the immune-inflammatory microenvironment. Resveratrol and triptolide have been identified as promising therapeutic candidates due to their potential to target the proteins encoded by these genes.

LincR-PPP2R5C Deficiency Alleviates Airway Remodeling by Inhibiting Epithelial-Mesenchymal Transition Through the PP2A/TGF-ß1 Signaling Pathway in Chronic Experimental Allergic Asthma.

Airway remodeling is a key characteristic of allergic asthma. Epithelial-mesenchymal transition (EMT) induced by various factors, particularly transforming growth factor (TGF)-ß1, orchestrates airway remodeling. Protein phosphatase 2A (PP2A), an important serine-threonine phosphatase, is involved in TGF-ß1 production and EMT. Long noncoding RNAs (lncRNAs) have emerged as novel players in regulating EMT. Here, we aimed to explore the effects and mechanisms of action of lincR-PPP2R5C, a lncRNA that affects PP2A activity, on airway remodeling in a mouse model of chronic allergic asthma. LincR-PPP2R5C knockout (KO) alleviated inflammatory responses in house dust mite (HDM)-induced chronic allergic asthma. Moreover, airway remodeling and EMT were reduced in lung tissues of lincR-PPP2R5C KO mice. HDM extract induced EMT in airway epithelial cells, which was decreased following lincR-PPP2R5C KO. Mechanistically, lincR-PPP2R5C deficiency enhanced PP2A activity, which inhibited TGF-ß1 production in epithelial cells. In conclusion, lincR-PPP2R5C deficiency prevented HDM-induced airway remodeling in mice by reversing EMT, which was mediated by the PP2A/TGF-ß1 signaling pathway. Thus, lncRNAs, i.e., lincR-PPP2R5C, may be potential targets to prevent airway remodeling in allergic asthma.

Increased macrolide resistance rate of Mycoplasma pneumoniae correlated with epidemic in Beijing, China in 2023.

We collected respiratory specimens from 128 pediatric patients diagnosed with pneumonia in Beijing in late 2023. Mycoplasma pneumoniae was detected in 77.3% (99/128) patients, with 36.4% (4/11), 82.9% (34/41), 80.3% (61/76) in children aged less than 3 years, 3-6 years, over 7 years, respectively. Mycoplasma pneumoniae (M. pneumoniae) was characterized using P1 gene typing, MLVA typing and sequencing of domain V of the 23S rRNA gene. P1 gene type 1 (P1-1; 76.1%, 54/71) and MLVA type 4-5-7-2 (73.7%, 73/99) were predominant. MLVA identified a new genotype: 3-4-6-2. Macrolide resistance-associated mutations were detected in 100% of samples, with A2063G accounting for 99% and A2064G for 1%. The positive rate of M. pneumoniae was higher compared to previous reports, especially in children less than 3 years, suggesting a M. pneumoniae epidemic showing a younger age trend occurred in late 2023 in Beijing, China. Higher proportions of macrolide-resistant M. pneumoniae, P1-1 and 4-5-7-2 genotype M. pneumoniae indicated increased macrolide resistance rate and genotyping shift phenomenon, which might be attributable to this epidemic. Additionally, complete clinical information from 73 M. pneumoniae pneumonia inpatients were analyzed. The incidence of severe M. pneumoniae pneumonia was 56.2% (41/73). Mycoplasma pneumoniae pneumonia patients exhibited longer duration of fever, with a median value of 10.0 days (IQR, 8.0-13.0), and higher incidence of complications (74.0%, 54/73). However, in this cohort, we found that the severity of M. pneumoniae pneumonia, co-infection, or complications were not associated with M. pneumoniae P1 gene or MLVA types. Clinicians should be aware that patients infected with macrolide-resistant M. pneumoniae exhibited more severe clinical presentations.

A micropeptide TREMP encoded by lincR-PPP2R5C promotes Th2 cell differentiation by interacting with PYCR1 in allergic airway inflammation.

BACKGROUND: Allergic asthma is largely dominated by Th2 lymphocytes. Micropeptides in Th2 cells and asthma remain unmasked. Here, we aimed to demonstrate a micropeptide, T-cell regulatory micropeptide (TREMP), in Th2 cell differentiation in asthma. METHODS: TREMP translated from lincR-PPP2R5C was validated using Western blotting and mass spectrometry. TREMP knockout mice were generated using CRISPR/Cas9. Coimmunoprecipitation revealed that TREMP targeted pyrroline-5-carboxylate reductase 1 (PYCR1), which was further explored in vitro and in vivo. The levels of TREMP and PYCR1 in Th2 cells from clinical samples were determined by flow cytometry. RESULTS: TREMP, encoded by lincR-PPP2R5C, was in the mitochondrion. The lentivirus encoding TREMP promoted Th2 cell differentiation. In contrast, Th2 differentiation was suppressed in TREMP-/- CD4+ T cells. In the HDM-induced model of allergic airway inflammation, TREMP was increased in pulmonary tissues. Allergic airway inflammation was relieved in TREMP-/- mice treated with HDM. Mechanistically, TREMP interacted with PYCR1, which regulated Th2 differentiation via glycolysis. Glycolysis was decreased in Th2 cells from TREMP-/- mice and PYCR1-/- mice. Similar to TREMP-/- mice, allergic airway inflammation was mitigated in HDM-challenged PYCR1-/- mice. Moreover, we measured TREMP and PYCR1 in asthma patients. And we found that, compared with those in healthy controls, the levels of TREMP and PYCR1 in Th2 cells were significantly increased in asthmatic patients. CONCLUSIONS: The micropeptide TREMP encoded by lincR-PPP2R5C promoted Th2 differentiation in allergic airway inflammation by interacting with PYCR1 and enhancing glycolysis. Our findings highlight the importance of neglected micropeptides from noncoding RNAs in allergic diseases.

"Adjusting internal organs and dredging channelon" electroacupuncture glycolipid metabolism disorders in NAFLD mice by mediating the AMPK/ACC signaling pathway.

To investigate the effect mechanism of electroacupuncture based on the AMP-activated protein kinase (AMPK) /acetyl-CoA carboxylase (ACC) signaling pathway to improve glycolipid metabolism disorders in db/db mice. 10 db/m mice with normal genotype were used as the normal control group without diabetes (Con), and 30 db/db mice were divided randomly into three groups: Pathological model mice (Mod), Acupuncture + ACC antagonist group (Acu + ACC), and Acupuncture + AMPK antagonist group (Acu + AMPK). Con and Mod did not receive any special treatment, only as a control observation. The latter two groups of mice received electroacupuncture treatment for 4 weeks. Mouse triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol(LDL-C), and cholesterin(CHO) levels were detected by colorimetric assay. Enzyme-linked immunoassay (ELISA) was used to detect insulin(INS) levels. Liver histopathologic changes and hepatic glycogen synthesis were observed by HE and PAS staining. The mRNA and protein expression of insulin receptor substrate-1(IRS1), Phosphatidylinositol 3-kinase(PI3K), protein kinase B (AKT), AMPK, and ACC were detected by Western blot and qRT-PCR.The results show that compared with Mod, TG, LDL, CHO, and INS levels of Acu + AMPK and Acu + ACC mice were significantly reduced (P < 0.05), and the HDL levels were significantly increased (P < 0.05), the steatotic degeneration of mice hepatocytes was reduced to different degrees, and the hepatocyte glycogen particles were increased, and the latter two groups had a decrease in AKT, ACC mRNA expression was reduced (P < 0.05), PI3K protein expression was increased, and AKT and ACC protein expression was reduced (P < 0.05), in addition, protein expression of AMPK was increased and IRS1 protein expression was reduced in Acu + ACC (P < 0.05). The study showed that electroacupuncture improves glucose-lipid metabolism disorders in db/db mice, and this mechanism is related to the AMPK/ACC signaling pathway.

LincR-PPP2R5C regulates IL-1ß ubiquitination in macrophages and promotes airway inflammation and emphysema in a murine model of COPD.

Chronic obstructive pulmonary disease (COPD) is a common disease with high global morbidity and mortality. Macrophages release IL-1ß and orchestrate airway inflammation in COPD. Previously, we explored the role of a new lncRNA, LincR-PPP2R5C, in regulating Th2 cells in asthma. Here, we established a murine model of COPD and explored the roles and mechanisms by which LincR-PPP2R5C regulates IL-1ß in macrophages. LincR-PPP2R5C was highly expressed in pulmonary macrophages from COPD-like mice. LincR-PPP2R5C deficiency ameliorated emphysema and pulmonary inflammation, as characterized by reduced IL-1ß in macrophages. Unexpectedly, in both lung tissues and macrophages, LincR-PPP2R5C deficiency decreased the expression of the IL-1ß protein but not the IL-1ß mRNA. Furthermore, we found that LincR-PPP2R5C deficiency increased the level of ubiquitinated IL-1ß in macrophages, which was mediated by PP2A activity. Targeting PP2A with FTY720 decreased IL-1ß and improved COPD. In conclusion, LincR-PPP2R5C regulates IL-1ß ubiquitination by affecting PP2A activity in macrophages, contributing to the airway inflammation and emphysema in a murine model of COPD. PP2A and IL-1ß ubiquitination in macrophages might be new therapeutic avenues for COPD therapy.

A randomized controlled clinical trial of concentrated growth factor combined with sodium hyaluronate in the treatment of temporomandibular joint osteoarthritis.

OBJECTIVE: To investigate the effect of concentrated growth factor (CGF) combined with sodium hyaluronate (SH) on temporomandibular joint osteoarthritis (TMJOA). METHODS: Sixty patients with TMJOA who were diagnosed by cone-beam computed tomography (CBCT) between March 2020 and March 2023 at the Stomatological Hospital of Xi'an Jiaotong University were randomly divided into a control group (n = 30) and an experimental group (n = 30). The patients in the experimental group were treated with CGF + SH, and those in the control group were treated with SH only. The visual analogue scale (VAS) score indicating pain in the temporomandibular joint (TMJ) area; the Helkimo Clinical Dysfunction Index (Di); and changes in condylar CBCT at the first visit and 2 weeks, 3 months and 6 months after treatment were recorded. The CBCT data of the patients in the experimental and control groups were collected, and the three-dimensional CBCT image sequences were imported into Mimics Medical 19.0 software in DICOM format for condylar reconstruction. RESULTS: The VAS scores at 2 weeks, 3 months and 6 months after treatment were significantly lower in the experimental group than in the control group (P < 0.05), and the pain in the experimental group was significantly relieved. The Di was significantly lower in the experimental group than in the control group (P < 0.05), and the clinical function of the TMJ improved. After treatment, the CBCT score was significantly lower in the experimental group than in the control group (P < 0.05), and the condylar bone cortex was obviously repaired. Observation of the condylar bone cortex by three-dimensional reconstruction showed the same results as those obtained by CBCT. CONCLUSION: CGF combined with SH is effective in the treatment of TMJOA and can improve muscle pain, TMJ pain, Impaired TMJ function, Impaired range of movement, Pain on movement of the mandible and promote bone repair. THE REGISTRATION NUMBER (TRN): ChiCTR2400082712. THE DATE OF REGISTRATION: April 5, 2024.

A programmable topological photonic chip.

Controlling topological phases of light allows the observation of abundant topological phenomena and the development of robust photonic devices. The prospect of more sophisticated control with topological photonic devices for practical implementations requires high-level programmability. Here we demonstrate a fully programmable topological photonic chip with large-scale integration of silicon photonic nanocircuits and microresonators. Photonic artificial atoms and their interactions in our compound system can be individually addressed and controlled, allowing the arbitrary adjustment of structural parameters and geometrical configurations for the observation of dynamic topological phase transitions and diverse photonic topological insulators. Individual programming of artificial atoms on the generic chip enables the comprehensive statistical characterization of topological robustness against relatively weak disorders, and counterintuitive topological Anderson phase transitions induced by strong disorders. This generic topological photonic chip can be rapidly reprogrammed to implement multifunctionalities, providing a flexible and versatile platform for applications across fundamental science and topological technologies.

Thoracoscopic resection of paraesophageal ectopic mediastinal parathyroid adenoma in the superior posterior mediastinum: a case report.

BACKGROUND: The ectopic superior parathyroid in the tracheoesophageal groove and paraesophageal region is rare. Hyperparathyroidism results when these glands become hyperfunctioning. That may necessitate surgical intervention in the form of parathyroidectomy, which requires a transsternal or transthoracic approach due to a deeply seated mediastinal parathyroid gland. Minimally invasive strategies have emerged recently as an alternative approach with less morbidity. CASE PRESENTATION: We present a case of the paraesophageal ectopic parathyroid gland in the superior posterior mediastinum, which was successfully treated with thoracoscopic resection. CONCLUSION: The current imaging tools improve the thoracoscopic management of mediastinal parathyroid glands. Video-assisted thoracoscopic surgery (VATS) can provide access and exposure to ectopic parathyroid adenoma with low morbidity and financial burden.

Plasma sCD146 is a potential biomarker for acute exacerbation of chronic obstructive pulmonary disease.

This study examined the levels of soluble CD146 (sCD146) in plasma samples from patients with chronic obstructive pulmonary disease (COPD) and assessed the relationship between sCD146 and the severity of COPD. A total of 97 COPD patients were recruited from 20 medical centers in Jiangsu, China, including 13 stable subjects and 84 exacerbated subjects. The plasma sCD146 level in exacerbated subjects (28.77 ± 10.80 ng/mL) was significantly lower than that in stable subjects (38.84 ± 15.00 ng/mL). In the high sCD146 group, the proportion of subjects with modified Medical Research Council (mMRC) scores of 0-1 was higher, the proportion of subjects with the Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 4 was lower, and the proportion of subjects with ≥1 hospitalizations in the past year was lower. The plasma sCD146 level was negatively correlated with the COPD Assessment Test (CAT) score (r = -0.2664, p = 0.0087). Logistic regression analysis showed that sCD146 was an independent risk factor for acute exacerbation of COPD (AECOPD). Receiver operating characteristic (ROC) analysis suggested that sCD146 combined with sex, age, pulmonary function, and acute exacerbations in the past year had clinical value for the accurate identification of AECOPD, with an area under the ROC curve (AUC) of 0.908 (95% CI: 0.810-1.000, p < 0.001). In addition, there was a significant negative correlation between plasma sCD146 and S100A9 (r = -0.3939, p < 0.001).

Enhancing Fat Graft Survival via Upregulating Autophagy of Adipocytes.

BACKGROUND: Autophagy is a cellular self-protection mechanism. The upregulation of adipose-derived stem cells' (ADSCs) autophagy can promote fat graft survival. However, the effect of interfering with adipocyte autophagy on graft survival is still unknown. In addition, autophagy is involved in adipocyte dedifferentiation. We investigated the effect of autophagy on adipocyte dedifferentiation and fat graft survival. METHODS: The classic autophagy regulatory drugs rapamycin (100 nM) and 3-methyladenine (3-MA; 10 mM) were used to treat adipocytes, adipocyte dedifferentiation was observed, and their effects on ADSCs were detected. In our experiments, 100 nM rapamycin, 10 mM 3-MA and saline were mixed with human adipose tissue and transplanted into nude mice. At 2, 4, 8 and 12 weeks postoperatively, the grafts were harvested for histological and immunohistochemical analysis. RESULTS: Rapamycin and 3-MA can promote and inhibit adipocyte dedifferentiation by regulating autophagy. Both drugs can inhibit ADSC proliferation, and 10 mM 3-MA can inhibit ADSC adipogenesis. At weeks 8 and 12, the volume retention rate of the rapamycin group (8 weeks, 64.77% ± 6.36%; 12 weeks, 56.13% ± 4.73%) was higher than the control group (8 weeks, 52.62% ± 4.04%; P < 0.05; 12 weeks, 43.17% ± 6.02%; P < 0.05) and the rapamycin group had more viable adipocytes and better vascularization. Compared with the control group, the volume retention rate, viable adipocytes and vascularization of the 3-MA group decreased. CONCLUSIONS: Rapamycin can promote adipocyte dedifferentiation by upregulating autophagy to promote fat graft survival. 3-MA can inhibit graft survival, but its mechanism includes the inhibition of adipocyte dedifferentiation and ADSC proliferation and adipogenesis. NO LEVEL ASSIGNED: This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. 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 .

Human gestational diabetes mellitus-derived exosomes impair glucose homeostasis in pregnant mice and stimulate functional maturation of offspring-islets.

AIMS: Pancreatic islets undergo critical development and functional maturation during the perinatal period when they are highly sensitive to microenvironment. We aim to determine the effects and mechanisms of gestational diabetes mellitus (GDM) hypermetabolic stress on glucose homeostasis in pregnant mice and functional maturation of the islets of their offspring. MAIN METHODS: Exosomes were extracted from the umbilical vein blood of individuals with or without GDM for administration to pregnant mice. The blood glucose, serum insulin, glycosylated hemoglobin, and lipopolysaccharide levels were measured in pregnant mice. The expression and localization of insulin, glucagon, PC1/3, PDX1, and p-S6 in the islets of neonatal rats were continuously monitored using immunofluorescence to evaluate their functional status. Primary islet cells were cultured and treated with GDM exosomes and exendin to determine the expression of GLP-1R, AKT, p-AKT, and p-S6 via western blotting. KEY FINDINGS: GDM exosomes induced remarkable oral glucose intolerance, hyperinsulinemia, and metabolic inflammation in pregnant mice. The islets of GDM offspring exhibited high insulin, glucagon, PC1/3, PDX1, and p-S6 expression at and after birth, and activation of the local GLP-1/GLP-1R axis. The functional maturation of normal-offspring islets did not commence until after birth, while it was activated prior to birth in GDM offspring, seriously disrupting the whole process. GDM exosomes activated the GLP-1/GLP-1R axis between α and ß cells, and stimulated functional maturation of ß cells via the Akt-mTORC1-pS6 pathway. SIGNIFICANCE: These findings provide preliminary insights into the mechanisms underlying the high incidence of diabetes in the offspring of mothers with GDM.

Conductive interpenetrating network organohydrogels of gellan gum/polypyrrole with weather-tolerance, piezoresistive sensing and shape-memory capability.

To develop ecofriendly multifunctional gel materials for sustainable flexible electronic devices, composite organohydrogels of gellan gum (GG) and polypyrrole (PPy) with an interpenetrating network structure (IPN-GG/PPy organohydrogels) were developed first time, through fabrication of GG organohydrogels followed by in-situ oxidation polymerization of pyrrole inside. Combination of water with glycerol can not only impart environment-stability to GG hydrogels but promote the mechanics remarkably, with the compressive strength amplified by 1250 % from 0.02 to 0.27 MPa. Incorporation of PPy confers electrical conductivity to the GG organohydrogel as well as promoting the mechanical performance further. The maximum conductivity of the IPN-GG/PPy organohydrogels reached 1.2 mS/cm at 25 °C, and retained at 0.6 mS/cm under -20 °C and 0.56 mS/cm after 7 days' exposure in 25 °C and 60 % RH. The compression strength of that with the maximum conductivity increases by 170 % from 0.27 to 0.73 MPa. The excellent conductivity and mechanical properties endow the IPN-GG/PPy organohydrogels good piezoresistive strain/pressure sensing behavior. Moreover, the thermo-reversible GG network bestows them shape-memory capability. The multifunctionality and intrinsic eco-friendliness is favorable for sustainable application in fields such as flexible electronics, soft robotics and artificial intelligence, competent in motion recognition, physiological signal monitoring, intelligent actuation.

Potential Candidate Molecule of Photosystem II Inhibitor Herbicide-Brassicanate A Sulfoxide.

Brassicanate A sulfoxide, a secondary metabolite of broccoli, exhibited the inhibition of weed growth, but its mechanism of action on weeds remains unclear. To elucidate the mechanism by which brassicanate A sulfoxide suppresses weeds, this study explores the interaction between brassicanate A sulfoxide and the photosystem II D1 protein through molecular docking and molecular dynamics simulations. This research demonstrates that brassicanate A sulfoxide interacts with the photosystem II D1 protein by forming hydrogen bonds with Phe-261 and His-214. The successful expression of the photosystem II D1 protein in an insect cell/baculovirus system validated the molecular docking and dynamics simulations. Biolayer interferometry experiments elucidated that the affinity constant of brassicanate A sulfoxide with photosystem II was 2.69 × 10-3 M, suggesting that brassicanate A sulfoxide can stably bind to the photosystem II D1 protein. The findings of this study contribute to the understanding of the mode of action of brassicanate A sulfoxide and also aid in the development of natural-product-based photosynthesis-inhibiting herbicides.

Tunable underwater sound absorption characteristics of 0-3 piezoelectric anechoic coating.

Piezoelectric composite materials (PCMs) with shunt damping circuits are used widely in hydroacoustics because of the flexible adjustability of their parameters. PCMs offer good underwater sound absorption, but shortcomings remain, such as poor low-frequency sound absorption, narrow bandwidth, and a single dissipation mechanism. In this paper, the tunable underwater sound absorption of a 0-3 PCM combined with a cavity structure and shunt circuit (PCMC) is studied systematically. First, the equivalent material parameters of 0-3 PCM are derived based on the Yamada model, and then a theoretical electroacoustic model is established for solving the absorption coefficient and is mutually verified with the numerical simulation method. On this basis, the tunable absorption characteristics of the structure are analyzed. The results show that coupling the energy dissipation mechanism of 0-3 PCM with the acoustic mechanism of the cavity structure not only achieves strong absorption at lower frequencies but also enriches the absorption mode in the mid-high frequencies by connecting the shunt circuits. Moreover, the influence of piezoelectric control variables and acoustic cavity morphology characteristics on structural sound absorption performance is further explored. Finally, the acoustic performance of PCMC is improved further via shape optimization and parameter optimization.

A novel dual-pooling attention module for UAV vehicle re-identification.

Vehicle re-identification (Re-ID) involves identifying the same vehicle captured by other cameras, given a vehicle image. It plays a crucial role in the development of safe cities and smart cities. With the rapid growth and implementation of unmanned aerial vehicles (UAVs) technology, vehicle Re-ID in UAV aerial photography scenes has garnered significant attention from researchers. However, due to the high altitude of UAVs, the shooting angle of vehicle images sometimes approximates vertical, resulting in fewer local features for Re-ID. Therefore, this paper proposes a novel dual-pooling attention (DpA) module, which achieves the extraction and enhancement of locally important information about vehicles from both channel and spatial dimensions by constructing two branches of channel-pooling attention (CpA) and spatial-pooling attention (SpA), and employing multiple pooling operations to enhance the attention to fine-grained information of vehicles. Specifically, the CpA module operates between the channels of the feature map and splices features by combining four pooling operations so that vehicle regions containing discriminative information are given greater attention. The SpA module uses the same pooling operations strategy to identify discriminative representations and merge vehicle features in image regions in a weighted manner. The feature information of both dimensions is finally fused and trained jointly using label smoothing cross-entropy loss and hard mining triplet loss, thus solving the problem of missing detail information due to the high height of UAV shots. The proposed method's effectiveness is demonstrated through extensive experiments on the UAV-based vehicle datasets VeRi-UAV and VRU.

LincR-PPP2R5C Promotes Th2 Cell Differentiation Through PPP2R5C/PP2A by Forming an RNA-DNA Triplex in Allergic Asthma.

PURPOSE: The roles and mechanisms of long noncoding RNAs (lncRNAs) in T helper 2 (Th2) differentiation from allergic asthma are poorly understood. We aimed to explore a novel lncRNA, LincR-protein phosphatase 2 regulatory subunit B' gamma (PPP2R5C), in Th2 differentiation in a mouse model of asthma. METHODS: LincR-PPP2R5C from RNA-seq data of CD4+ T cells of asthma-like mice were validated and confirmed by quantitative reverse transcription polymerase chain reaction, northern blotting, nuclear and cytoplasmic separation, and fluorescence in situ hybridization (FISH). Lentiviruses encoding LincR-PPP2R5C or shRNA were used to overexpress or silence LincR-PPP2R5C in CD4+ T cells. The interactions between LincR-PPP2R5C and PPP2R5C were explored with western blotting, chromatin isolation by RNA purification assay, and fluorescence resonance energy transfer. An ovalbumin-induced acute asthma model in knockout (KO) mice (LincR-PPP2R5C KO, CD4 conditional LincR-PPP2R5C KO) was established to explore the roles of LincR-PPP2R5C in Th2 differentiation. RESULTS: LncR-PPP2R5C was significantly higher in CD4+ T cells from asthmatic mice ex vivo and Th2 cells in vitro. The lentivirus encoding LincR-PPP2R5C suppressed Th1 differentiation; in contrast, the short hairpin RNA (shRNA) lentivirus decreased LincR-PPP2R5C and Th2 differentiation. Mechanistically, LincR-PPP2R5C deficiency suppressed the phosphatase activity of the protein phosphatase 2A (PP2A) holocomplex, resulting in a decline in Th2 differentiation. The formation of an RNA-DNA triplex between LincR-PPP2R5C and the PPP2R5C promoter enhanced PPP2R5C expression and activated PP2A. LincR-PPP2R5C KO and CD4 conditional KO decreased Th2 differentiation, airway hyperresponsiveness and inflammatory responses. CONCLUSIONS: LincR-PPP2R5C regulated PPP2R5C expression and PP2A activity by forming an RNA-DNA triplex with the PPP2R5C promoter, leading to Th2 polarization in a mouse model of acute asthma. Our data presented the first definitive evidence of lncRNAs in the regulation of Th2 cells in asthma.

Efficient degradation of ciprofloxacin in wastewater by CuFe2O4/CuS photocatalyst activated peroxynomosulfate.

In this study, CuFe2O4/CuS composite photocatalysts were successfully synthesized for the activation of peroxynomosulfate to remove ciprofloxacin from wastewater. The structural composition and morphology of the materials were analyzed by XRD, SEM, TEM, and Raman spectroscopy. The electrochemical properties of the samples were tested by an electrochemical workstation. The band gap of the samples was calculated by DFT and compared with the experimental values. The effects of different catalysts, oxidant PMS concentrations, and coexisting ions on the experiments were investigated. The reusability and stability of the photocatalysts were also investigated. The mechanism of the photocatalytic degradation process was proposed based on the free radical trapping experiment. The results show that the p-p heterojunction formed between the two contact surfaces of the CuFe2O4 nanoparticle and CuS promoted the charge transfer between the interfaces and inhibited the recombination of electrons and holes. CuFe2O4-5/CuS photocatalyst has the best catalytic activity, and the removal rate of ciprofloxacin is 93.7%. The intermediates in the degradation process were tested by liquid chromatography-mass spectrometry (LC-MS), and the molecular structure characteristics of ciprofloxacin were analyzed by combining with DFT calculations. The possible degradation pathways of pollutants were proposed. This study reveals the great potential of the photocatalyst CuFe2O4/CuS in the activation of PMS for the degradation of ciprofloxacin wastewater.