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This retrospective study investigated the clinicopathological characteristics of secretory carcinoma of salivary glands (SCSG) in 23 patients with histopathologically confirmed SCSG between January 2010 and December 2020. In total, 13 males and 10 females (ratio, 1.3:1) aged 10 − 69 years (median, 45 years) were enrolled in this study; the average disease duration was 2.44 years (0.25–20 years). Twenty-one patients (91.3%) had SCSG in the parotid gland, and two (8.7%) in the submandibular gland. All patients had single nodules of diameters 0.8–4.8 cm (average 2.6 cm); five with lymph node metastases, and two with distant metastases. Immunohistochemically, tumors stained positive for S-100, mammaglobin, CK7, GATA3 and pan-Trk, and negative for DOG1, P63, and calponin, with Ki-67 positivity from 1 to 50%. ETV6 gene rearrangement was confirmed in 15 patients. All patients underwent oncological resection, four had radioactive particles implanted postoperatively, one received chemotherapy, and seven underwent chemoradiotherapy. Six patients had regional recurrences, two distant metastases, and one died before the last follow-up. SCSGs are typically indolent, with a low locoregional recurrence rate and excellent survival. Prognosis is correlated to clinical stage, pathological grade, and surgical procedures.

Aiming at the engineering requirements of reducing the volume and improving the vibration characteristics of gears in the three-cylinder engine balanced system, a design and optimization method of gear structure is proposed based on the Design of Experiments (DOE) and proxy models. The paper analyzes the structure improvement process based on the gear design model and technical index requirements. By designing the plane characteristics of the weight-increasing module, the weight-reducing module and the elastic module, the calculation model of balance performance indices such as mass, moment of inertia and unbalance of new balanced vibration reduction gear are constructed. Then, a more efficient design method is proposed based on dynamic simulation and multidisciplinary optimization design platform (Isight). The results show that the new design method of gear structure can effectively reduce the structure improvement cycle. At the same time, the improved structure can reduce the thickness of the weight-increasing module by 6.3 mm and the vibration attenuation by more than 90%.

Background (Pro)renin receptor (PRR) is highly expressed in renal tubules, which is involved in physiological and pathological processes. However, the role of PRR, expressed in renal tubular epithelial cells, in diabetic kidney disease (DKD) remain largely unknown. Methods In this study, kidney biopsies, urine samples, and public RNA-seq data from DKD patients were used to assess PRR expression and cell pyroptosis in tubular epithelial cells. The regulation of tubular epithelial cell pyroptosis by PRR was investigated by in situ renal injection of adeno-associated virus9 (AAV9)-shRNA into db/db mice, and knockdown or overexpression of PRR in HK-2 cells. To reveal the underlined mechanism, the interaction of PRR with potential binding proteins was explored by using BioGrid database. Furthermore, the direct binding of PRR to dipeptidyl peptidase 4 (DPP4), a pleiotropic serine peptidase which increases blood glucose by degrading incretins under diabetic conditions, was confirmed by co-immunoprecipitation assay and immunostaining. Results Higher expression of PRR was found in renal tubules and positively correlated with kidney injuries of DKD patients, in parallel with tubular epithelial cells pyroptosis. Knockdown of PRR in kidneys significantly blunted db/db mice to kidney injury by alleviating renal tubular epithelial cells pyroptosis and the resultant interstitial inflammation. Moreover, silencing of PRR blocked high glucose-induced HK-2 pyroptosis, whereas overexpression of PRR enhanced pyroptotic cell death of HK-2 cells. Mechanistically, PRR selectively bound to cysteine-enrich region of C-terminal of DPP4 and augmented the protein abundance of DPP4, leading to the downstream activation of JNK signaling and suppression of SIRT3 signaling and FGFR1 signaling, and then subsequently mediated pyroptotic cell death. Conclusions This study identified the significant role of PRR in the pathogenesis of DKD; specifically, PRR promoted tubular epithelial cell pyroptosis via DPP4 mediated signaling, highlighting that PRR could be a promising therapeutic target in DKD.

Environmental pollution and waste caused by traditional citrus farming has become more serious. As the direct subject of agricultural production, we should pay more attention to the green production behavior of farmers. Numerous studies have fully proven that technology training is the important driving factor of farmers’ production behavior, but the question of which main body or organization should carry out the training is the question that still has no definite conclusion, in order to solve this problem. Based on the perspective of the heterogeneity of agricultural technology training organizations, this study conducts a discussion on the indicators of the difference in training organization and technology adoption behavior, and uses the Oprobit and IV-Oprobit models to conduct an empirical analysis on 782 Chinese farmers’ survey data. Finally, we find: (1) Technical training has a positive impact on farmers’ GPT adoption at the 1% level. For each additional training, the probability of adopting five GPT increased by 2.6%; (2) Different training organizations have different impacts on the farmers’ technology adoption. The training of profit-oriented organizations represented by agricultural enterprises has the most obvious promotion effect on GPT adoption by farmers. The overall effect of the training of government agricultural extension departments is better than that of quasi-public welfare organizations such as scientific research institutions; (3) The above effects also have obvious heterogeneity among farmers of different ages, education levels, family social networks, planting scale, family incomes and structure. Based on this, we put forward policy suggestions such as building a diversified agricultural extension training system.

Background: Sheep (Ovis aries) exhibit significant diversity in adipose tissue deposition, which influences meat quality, environmental adaptation, and economic value. Tail fat, in particular, varies widely among breeds, yet the transcriptomic basis of this variation remains incompletely understood. This study aims to systematically compare the transcriptional profiles of five adipose depots across five sheep breeds to identify molecular mechanisms underlying fat deposition and tail phenotype divergence. Methods: We analyzed 250 publicly available RNA-seq samples from five adipose tissues (caul, subcutaneous, perirenal, intermuscular, and tail fat) of five sheep breeds (Altay, Tibetan, Merino, Wadi, Small-tailed Han). Data were processed using FastQC, STAR, and featureCounts. Differential expression analysis was performed with DESeq2, followed by GO and KEGG enrichment analyses. Breeds were grouped into three tail phenotypes: fat-tailed, short fat-tailed, and thin-tailed. Cross-tissue and phenotype-specific pathway analyses were conducted to identify key regulatory genes. Results: Transcriptional divergence was most pronounced in subcutaneous and intermuscular fat, while tail fat exhibited both conserved and phenotype-specific pathways. Fat-tailed breeds showed enrichment in mitochondrial oxidative phosphorylation and lipid biosynthesis genes (TAFAZZIN, GPAM, COQ family). Short fat-tailed breeds were characterized by extracellular matrix remodeling genes (MMP9, MMP12, MMP19). Thin-tailed sheep lacked these pro-lipogenic and structural remodeling pathways. A dual-axis model of tail fat development is proposed to explain phenotypic diversity. Conclusions: This study reveals that distinct molecular mechanisms underpin tail fat phenotypes in sheep: fat-tailed breeds prioritize metabolic efficiency, short fat-tailed breeds rely on ECM remodeling, and thin-tailed breeds lack these enhancements. The identified candidate genes may serve as potential targets for molecular breeding strategies aimed at optimizing fat deposition and adaptive traits in sheep.

Gnathodiaphyseal dysplasia (GDD) is a rare autosomal dominant genetic disease, mainly characterized by enlargement of the mandible, osteosclerosis, and frequent fracture of tubular bone. GDD is caused by heterozygous mutations in Anoctamin 5 (ANO5). We have previously generated an Ano5 knockout (KO) mice model and validated the phenotypes consistent with GDD patients, including enhanced bone formation and alkaline phosphatase (ALP) activity. Experiments have identified that Ano5 deficiency elevated the osteogenesis of calvaria-derived osteoblasts (mCOBs). In this study, we found that Ano5 deficiency notably inhibited miR-34c-5p expression. Krüppel-Like Factor 4 (Klf4), a target gene of miR-34c-5p confirmed by dual luciferase reporter assay, was up-regulated in Ano5−/− mCOBs, accompanied by activated downstream canonical Wnt/β-catenin signaling and increased expression of β-catenin. Overexpression of miR-34c-5p in Ano5−/− mCOBs inhibited osteogenic capacity by suppressing proliferative capacity, osteoblast-related factor levels, ALP activity, and matrix calcification through regulating KLF4/β-catenin signaling axis. Furthermore, miR-34c-5p adeno-associated virus (AAV) treatment in vivo rescued the abnormally thickened cortical bone and enhanced biomechanical properties in Ano5−/− mice. Importantly, the serum level of P1NP, a marker of bone formation, was also significantly declined. We conclude that dysregulation of miR-34c-5p contributes to the enhanced osteogenesis in GDD by excessive activation of KLF4/β-catenin signaling axis under Ano5-deficient conditions. This study elucidates the pathogenesis of GDD and provides novel insights into the therapeutic strategies.

Background The inter-scanner reproducibility of brain volumetry is important in multi-site neuroimaging studies, where the reliability of automated brain segmentation (ABS) tools plays an important role. This study aimed to evaluate the influence of ABS tools on the consistency and reproducibility of the quantified brain volumetry from different scanners. Methods We included fifteen healthy volunteers who were scanned with 3D isotropic brain T1-weighted sequence on three different 3.0 Tesla MRI scanners (GE, Siemens and Philips). For each individual, the time span between image acquisitions on different scanners was limited to 1 h. All the T1-weighted images were processed with FreeSurfer v6.0, FSL v5.0 and AccuBrain ® with default settings to obtain volumetry of brain tissues (e.g. gray matter) and substructures (e.g. basal ganglia structures) if available. Coefficient of variation (CV) was calculated to test inter-scanner variability in brain volumetry of various structures as quantified by these ABS tools. Results The mean inter-scanner CV values per brain structure among three MRI scanners ranged from 6.946 to 12.29% (mean, 9.577%) for FreeSurfer, 7.245 to 20.98% (mean, 12.60%) for FSL and 1.348 to 8.800% (mean value, 3.546%) for AccuBrain ® . In addition, AccuBrain ® and FreeSurfer achieved the lowest mean values of region-specific CV between GE and Siemens scanners (from 0.818 to 5.958% for AccuBrain ® , and from 0.903 to 7.977% for FreeSurfer), while FSL-FIRST had the lowest mean values of region-specific CV between GE and Philips scanners (from 2.603 to 16.310%). AccuBrain ® also had the lowest mean values of region-specific CV between Siemens and Philips scanners (from 1.138 to 6.615%). Conclusion There is a large discrepancy in the inter-scanner reproducibility of brain volumetry when using different processing software. Image acquisition protocols and selection of ABS tool for brain volumetry quantification have impact on the robustness of results in multi-site studies.

Unmanned Aircraft Systems (UASs) have undergone rapid development over recent years, but have also became vulnerable to security attacks and the volatile external environment. Ensuring that the performance of UASs is safe and secure no matter how the environment changes is challenging. Runtime Verification (RV) is a lightweight formal verification technique that could be used to monitor UAS performance to guarantee safety and security, while reactive synthesis is a methodology for automatically synthesizing a correct-by-construction controller. This paper addresses the problem of the generation and design of a secure UAS controller by introducing a unified monitor and controller synthesis method based on RV and reactive synthesis. First, we introduce a novel methodological framework, in which RV monitors is applied to guarantee various UAS properties, with the reactive controller mainly focusing on the handling of tasks. Then, we propose a specification pattern to represent different UAS properties and generate RV monitors. In addition, a detailed priority-based scheduling method to schedule monitor and controller events is proposed. Furthermore, we design two methods based on specification generation and re-synthesis to solve the problem of task generation using metrics for reactive synthesis. Then, to facilitate users using our method to design secure UAS controllers more efficiently, we develop a domain-specific language (UAS-DL) for modeling UASs. Finally, we use F Prime to implement our method and conduct experiments on a joint simulation platform. The experimental results show that our method can generate secure UAS controllers, guarantee greater UAS safety and security, and require less synthesis time.

Diabetes nephropathy (DN) is the leading cause of end-stage renal disease (ESRD) worldwide, and podocyte injury is the central contributor to the progression of DN. Despite the emerging evidence that has established the importance of podocyte endoplasmic reticulum (ER) stress in the pathogenesis of DN, abnormal protein O-GlcNAcylation is also augmented. Currently, the mechanism associating these two hyperglycemia-induced disorders remains poorly understood. This study intended to elucidate whether ER stress drives hyper-protein O-GlcNAcylation to cause podocyte injury in DN. We used both type 1 and type 2 DN models to confirm the occurrence of ER stress and excessive protein O-GlcNAcylation, and then podocyte purification was also conducted for further investigation. Nephroseq V5 data were mined and in vitro studies were applied to reveal the involvement of ER stress and hyper-O-GlcNAcylation in podocyte injury. Our results indicated that ER stress was induced in both type 1 and type 2 DN, and the human RNA-seq data from Nephroseq V5 showed that O-GlcNAcylation-related genes were significantly upregulated in the DN patients. We further demonstrated that ER stress occurred prior to hyper-O-GlcNAc modification and that pharmacologically inhibited protein O-GlcNAcylation can help decrease the podocyte apoptosis induced by hyperglycemia. Together, these discoveries will aid in uncovering the activation of the ER stress–O-GlcNAcylation axis in podocyte injury under DN, which will help open up new therapeutic approaches for preventing DN progression.

Xenogeneic extracellular matrices (xECM) for cell support have emerged as a potential strategy for addressing the scarcity of donor matrices for allotransplantation. However, the poor survival rate or failure of xECM-based organ transplantation is due to the negative impacts of high-level oxidative stress and inflammation on seed cell viability and stemness. Herein, we constructed xenogeneic bioengineered tooth roots (bio-roots) and used extracellular vesicles from human adipose-derived mesenchymal stem cells (hASC-EVs) to shield bio-roots from oxidative damage. Pretreatment with hASC-EVs reduced cell apoptosis, reactive oxygen species generation, mitochondrial changes, and DNA damage. Furthermore, hASC-EV treatment improved cell proliferation, antioxidant capacity, and odontogenic and osteogenic differentiation, while significantly suppressing oxidative damage by activating the phosphatidylinositol 3-kinase (PI3K)/Akt pathway and nuclear factor erythroid 2 (NFE2)-related factor 2 (NRF2) nuclear translocation via p62-associated Kelch-like ECH-associated protein 1 (KEAP1) degradation. Inhibition of PI3K/Akt and Nrf2 knockdown reduced antioxidant capacity, indicating that the PI3K/Akt/NRF2 pathway partly mediates these effects. In subcutaneous grafting experiments using Sprague–Dawley rats, hASC-EV administration significantly enhanced the antioxidant effect of the bio-root, improved the regeneration efficiency of periodontal ligament-like tissue, and maximized xenograft function. Conclusively, therefore, hASC-EVs have the potential to be used as an immune modulator and antioxidant for treating oxidative stress-induced bio-root resorption and degradation, which may be utilized for the generation and restoration of other intricate tissues and organs. Graphic Abstract