10 research outputs found
Complete Coverage Path Planning Based on Bioinspired Neural Network and Pedestrian Location Prediction
No full textExperimental Research and Theoretical Analysis of the Coupling Mechanism Between Microstructure and Acoustics in Porous Materials
No full textBased on the three-parameter approximate JCAL analytical model (hereinafter referred to as the three-parameter model), this study conducted an in-depth analysis of the effects of porosity, median pore size, and pore size standard deviation on the acoustic performance of porous materials and developed a composite porous material composed of glass fibers and zeolite particles. Experimental results indicate that the pore size distribution significantly affects the acoustic performance of fibrous porous sound-absorbing materials. Specifically, smaller pores lead to better sound absorption at mid–low frequencies, with the optimal sound absorption performance observed when the median pore size is between 60 and 80 μm. Increasing the material density and decreasing the fiber diameter help reduce the internal pore size, thereby improving the material’s sound absorption performance. Additionally, the appropriate addition of zeolite can further optimize the internal pore size and effective sound-absorbing interface, thus enhancing the material’s sound absorption performance. When the material density is 120 kg/m3 and the zeolite substitution rate is around 10%, the material exhibits the best acoustic performance, with a noise reduction coefficient (NRC) reaching 0.65, which is a 10.17% increase compared to the material without zeolite. Comparing the simulation data from the three-parameter model with the actual measurement data shows that the model has excellent predictive performance for the sound absorption coefficient (SAC) of single-fiber porous materials (with an error of approximately 5%). However, for composite porous materials, due to the complex changes in interfaces, there is a certain prediction error (with the maximum error reaching 12.81%), indicating that the model needs further optimization and correction when applied to composite materials
ProMoHGT: a heterogeneous graph transformer with graph contrastive learning for robust microbial protein function prediction
No full textDetermination of ED90 and ED99 of Oliceridine combined with Propofol in inhibiting responses to gastroscope insertion: a biased coin up-and-down design
No full textAbstract Background Gastroscopy is a common medical procedure, but the insertion of the endoscope often causes significant discomfort and anxiety in patients, necessitating effective sedation strategies. Traditional sedatives, such as propofol, are widely used for procedural sedation but can lead to adverse effects, including respiratory depression and cardiovascular instability at higher doses. Oliceridine, a novel opioid analgesic, has emerged as a potential alternative due to its biased agonist properties, which may provide effective analgesia with a more favorable side effect profile. The potential for its combination with propofol warrants further investigation. Methods The ED90 and ED99 were calculated using a biased coin design and central ordered regression. Measurements: The primary outcome measure was the occurrence of body movements or coughing responses during gastroscopy. Results A total of 49 patients were included in this study, with anesthesia successfully achieved in 45 cases and failed in 4 cases. The calculated ED90 and ED99 for Oliceridine combined with Propofol to suppress the response during gastroscopy were22.5 and 23.8 µg·kg− 1, respectively. Conclusions The combination of 2 mg·kg− 1 Propofol and 23.8 µg·kg− 1 Oliceridine is effective in suppressing the responses during the gastroscopy procedure. Trial registration The study was registered in the Chinese Clinical Trial Registry (ChiCTR2400092318) on November 14, 2024
Novel diagnostic biomarkers regulating macrophages autophagy in ischemic cardiomyopathy: An analysis integrating bulk RNA sequencing with single-cell RNA sequencing
No full textMacrophage autophagy plays a pivotal role in ischemia cardiomyopathy (ICM). However, the underlying mechanisms and macrophage autophagy-related biomarkers in ICM have not been elucidated. Therefore, this study was designed to explore novel macrophage autophagy-related biomarkers for ICM. The autophagy-related genes were downloaded from the Human Autophagy Modulator and intersected with the differentially expressed genes (DEGs) of GSE46224 identified with “limma” package in R to obtain the autophagy-related DEGs. Immune infiltration analysis showed that macrophages were the dominant immune cells in ICM tissue. Then the macrophage autophagy-related DEGs were identified using the weighted gene co-expression network analysis (WGCNA). A total of six hub genes were obtained from the PPI network. All of the hub genes showed specific diagnostic significance with AUCs higher than 0.7, as also validated in the external dataset GSE116250. RT-qPCR was conducted to detect the mRNA expression levels of hub genes in vivo ICM rat model. Single-cell RNA sequencing analysis was also performed to investigate gene expression profiles. Our study explored the macrophage autophagy-related biomarkers and their relative pathways in ICM, provided novel diagnostic biomarkers for ICM, and gave new insight into the progression mechanism of ICM
Developmental Characteristics of Skeletal Muscle during the Embryonic Stage in Chinese Yellow Quail (Coturnix japonica)
No full textThe quail is an important research model, and the demand for quail meat has been increasing in recent years; therefore, it is worthwhile investigating the development of embryonic skeletal muscle and the expression patterns of regulatory genes. In this study, the expression of MyoD and Pax7 in the breast muscle (m. pectoralis major) and leg muscle (m. biceps femoris) of quail embryos on days 10 through 17 were determined using qRT-PCR. Paraffin sections of embryonic muscle were analyzed to characterize changes over time. Results showed that MyoD and Pax7 were expressed in both breast and leg muscles and played a significant role in embryonic muscle development. Compared to breast muscle, leg muscle grew faster and had greater weight and myofiber size. The findings suggested that embryonic day 12 (E12) may be a key point for muscle development. Correlation analysis showed that MyoD expression was significantly negatively correlated with muscle and embryo weight, whereas Pax7 gene expression had no significant correlation with these characteristics. These fundamental results provide a theoretical basis for understanding the characteristics and transition points of skeletal muscle development in quail embryos and an important reference for farmers raising quail from eggs
Evaluation of left ventricular strain in patients with dilated cardiomyopathy
No full textObjective Dilated cardiomyopathy (DCM) can cause structural and functional changes in the left ventricle (LV). In this study, we evaluated whether cardiac magnetic resonance tissue-tracking (MR-TT) can be applied to the detection of LV abnormalities in patients with DCM. Methods We used MR-TT to analyze the global peak radial strain (GPRS), global peak circumferential strain (GPCS), and global peak longitudinal strain (GPLS) in every segment of the LV in 23 patients with DCM and 25 controls. The LV ejection fraction was also measured as a function indicator. Results Compared with the controls, the GPRS, GPCS, and GPLS were significantly reduced in patients with DCM, indicating global LV function impairment in all directions. We also identified a significant linear correlation between the GPRS, GPCS, and GPLS and the LV ejection fraction, indicating that LV function relies on coordinated wall motion from all directions. Moreover, we found that patients with DCM had a significantly reduced magnitude of the PRS, PCS, and PLS in most segments at different levels, indicating impaired myocardial function in most LV regions. Conclusions Our results demonstrate that LV myocardial strain in patients with DCM can be sensitively detected by MR-TT (not only the global LV function changes but also the segmental strain), which can help to identify the injured segment at an early stage and guide clinical treatment. </jats:sec
Image_1_The Potential of Metabolism-Related Gene OGDHL as a Biomarker for Myocardial Remodeling in Dilated Cardiomyopathy.tif
No full textThe development of dilated cardiomyopathy (DCM) is accompanied by a series of metabolic disorders, resulting in myocardial remodeling or exacerbation, while the mechanism remains not completely clear. This study was to find out the key metabolism-related genes involved in the onset of DCM, providing new insight into the pathogenesis of this disease. The datasets of GSE57338, GSE116250, and GSE5406 associated with hearts of patients with DCM were downloaded from the Gene Expression Omnibus database. GSE57338 was analyzed to screen out metabolism-related differentially expressed genes (DEGs), while GSE116250 and GSE5406 were utilized to verify the optimal genes through R software. Support vector machine recursive feature elimination algorithm and least absolute shrinkage and selection operator algorithm were used to determine key genes. Finally, 6 of 39 metabolism-related DEGs were screened out and identified as the optimal genes. After quantitative reverse-transcription polymerase chain reaction (qRT-PCR) validation performed on the samples drawn from the left ventricles of human hearts, it showed that only the expression of oxoglutarate dehydrogenase-like (OGDHL) increased while PLA2G2 decreased significantly in patients with DCM compared with non-failing donors, respectively. Furthermore, the higher OGDHL protein expression, except the change of PLA2G2, was also found in DCM hearts, and its mRNA expression was negatively correlated with myocardial Masson’s scores (r = –0.84, P = 0.009) and left ventricular end-diastolic diameter (LVEDd; r = –0.82, P = 0.014), which might be regulated by miR-3925-5p through further bioinformatics prediction and qRT-PCR verification. The data then suggested that the metabolism-related gene OGDHL was associated with myocardial fibrosis of DCM and probably a biomarker for myocardial remodeling in patients with DCM.</p
Integrated weighted gene co-expression network analysis uncovers STAT1(signal transducer and activator of transcription 1) and IFI44L (interferon-induced protein 44-like) as key genes in pulmonary arterial hypertension
No full textDespite the multiple diagnostic and therapeutic strategies implemented in clinical practice, the mortality rate of patients with pulmonary arterial hypertension (PAH) remains high. Understanding the mechanisms and key genes involved could provide insight into the drivers of the pathogenesis of PAH. In this research, we aimed to examine the mechanisms underlying PAH and identify key genes with potential usefulness as clinical biomarkers of PAH and thereby establish therapeutic targets for PAH. The datasets GSE117261, GSE113439, and GSE53408 were downloaded from the Gene Expression Omnibus (GEOs) database. We used weighted gene coexpression network analysis (WGCNA) to identify networks and the most relevant modules in PAH. Functional enrichment analysis was performed for the selected clinically relevant modules. The least absolute shrinkage and selection operator (LASSO) was applied to identify key genes in lung samples from patients with PAH. The genes were validated in a monocrotaline-induced PAH rat model. Three clinically relevant modules were identified through average linkage hierarchical clustering. The genes in the clinically relevant modules were related to endothelial cell differentiation, inflammation, and autoimmunity. Seven genes were screened as key genes significantly associated with PAH. Interferon-induced protein 44-like (IFI44L) and signal transducer and activator of transcription 1 (STAT1) were expressed at higher levels in the lung tissues of the PAH rat model than in those of the controls. Our findings reveal the novel pathological mechanisms underlying PAH and indicate that STAT1 and IFI44L may represent potential therapeutic targets in PAH.</p
NDP52 deficiency accelerates chondrocyte degeneration through promoting pathogenic mitochondrial ROS via reverse electron transport
No full textNDP52, a constituent of the selective autophagy receptors (SARs), was recognized for its involvement in facilitating substrate degradation via autophagic bridging. However, its autonomous function apart from autophagy remained largely unexplored. Here, we reported that NDP52 was down-regulated in degenerated chondrocytes. Besides, NDP52 deficiency promoted the extracellular matrix (ECM) degradation, inflammation, cell apoptosis and senescence via its autophagy-independent functions. The absence of NDP52 disrupted the flow of electron respiration chains and led to the production of intracellular mitochondrial reactive oxygen species (mtROS). Subsequent mechanistic investigations revealed that the downregulation of NDP52 upregulated the expression levels of mitochondrial complex Ⅰ by modulating MTIF3 expression, leading to reverse electron transport (RET) and mtROS production. Our research highlights the significance of NDP52 in facilitating chondrocyte degeneration and osteoarthritis, and provides insights into the distinctive mechanism by which autophagy receptors NDP52 induce intracellular mitochondrial ROS dysregulation via non-canonical pathways
