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The background of pipeline weld surface defect image is complex, and the defect size is small. Aiming at the small defect size in the weld image, which is easy to cause missed detection and false detection, a lightweight target detection algorithm based on improved YOLOv7 is proposed. Firstly, in the feature fusion network of YOLOv7, the detection ability of the algorithm to detect small and medium-sized targets in defect images is enhanced by adding a 160*160 small target detection head. Then, the convolution module in the backbone network and the feature fusion network is replaced by the depthwise separable convolution with less computational overhead, so as to effectively reduce the network calculation, parameter quantity and model volume. Finally, the loss function CIoU of YOLOv7 is optimized to EIoU loss function to accelerate the convergence speed of the model. The experimental results show that the defect detection mAP@0.5 based on the improved YOLOv7 algorithm can reach 72.2%, which is 11% higher than that of YOLOv7, and the model calculation amount and parameter amount are reduced by 75.6% and 60.3%, respectively. It can completely detect the small size defects and has a high degree of confidence, which can be effectively applied to the detection of small size defects on the surface of pipeline weld.

Diabetic nephropathy (DN) is the primary microvascular complication of diabetes mellitus and may result in end-stage renal disease. The overproduction of various inflammatory factors is involved in the pathogenesis of DN. Protein tyrosine phosphatase 1B (PTP1B) modulates the expression of a series of cytokines and nuclear factor kappa B (NF-κB) activity. cAMP response element-binding protein (CREB) and lysine methyltransferase 5A (KMT5A) have been reported to participate in the maintenance of a healthy endothelium. In the present study, we hypothesise that CREB associates with KMT5A to modulate PTP1B expression, thus contributing to high glucose-mediated glomerular endothelial inflammation. Our analyses revealed that plasma inflammatory factor levels, glomerular endothelial p65 phosphorylation and PTP1B expression were increased in DN patients and rats. In vitro, high glucose increased endothelial inflammatory factor levels and p65 phosphorylation by augmenting PTP1B expression in human umbilical vein endothelial cells (HUVECs). Moreover, high glucose decreased CREB and KMT5A expression. CREB overexpression and KMT5A overexpression both inhibited high glucose-induced PTP1B expression, p65 phosphorylation and endothelial inflammatory factor levels. si-CREB- and sh-KMT5A-induced p65 phosphorylation and endothelial inflammatory factor levels were reversed by si-PTP1B. Furthermore, CREB was associated with KMT5A. Mechanistic research indicated that CREB and histone H4 lysine 20 methylation (H4K20me1, a downstream target of KMT5A) occupy the PTP1B promoter region. sh-KMT5A augmented PTP1B promoter activity and activated the positive effect of si-CREB on PTP1B promoter activity. Our in vivo study demonstrated that CREB and KMT5A were downregulated in glomerular endothelial cells of DN patients and rats. In conclusion, CREB associates with KMT5A to promote PTP1B expression in vascular endothelial cells, thus contributing to hyperglycemia-induced inflammatory factor levels in DN patients and rats.

Background Diabetic nephropathy (DN), the most common microvascular complication in patients with diabetes, induces kidney failure. Previous research showed that endothelial-to-mesenchymal transition (EndMT) of human glomerular endothelial cells (HGECs) is involved in the progression of DN. Moreover, SET domain-containing protein 8 (SETD8), ETS-domain containing protein (ELK1) and BTB and CNC homology 1 (bach1) all participate in endothelial injury. In this study, we hypothesize that the SETD8/ELK1/bach1 functional axis is involved in mediating EndMT in diabetic nephropathy. Methods Immunohistochemistry, Western blotting and qPCR were performed to determine the protein and mRNA levels of genes in HGECs and the kidney tissues of participants and rats. Immunofluorescence, Co-IP and GST pulldown assays were performed to verify the direct interaction between SETD8 and ELK1. ChIP and dual-luciferase assays were performed to determine the transcriptional regulation of bach1 and Snail. AVV-SETD8 injection in rat kidney was used to verify the potential protective effect of SETD8 on DN. Results Our current study showed that hyperglycaemia triggered EndMT by increasing Snail expression both in vitro and in vivo. Moreover, high glucose increased bach1 expression in HGECs, positively regulating Snail and EndMT. As a transcription factor, ELK1 was augmented and participated in hyperglycaemia-induced EndMT via modulation of bach1 expression. Moreover, ELK1 was found to associate with SETD8. Furthermore, SETD8 negatively regulated EndMT by cooperating with bach1 to regulate Snail transcription. Furthermore, histone H4-Lys-20 monomethylation (H4K20me1), which is downstream of SETD8, was accompanied by ELK1 localization at the same promoter region of bach1. ELK1 overexpression enhanced bach1 promoter activity, which disappeared after specific binding site deletion. Mutual inhibition between ELK1 and SETD8 was found in HGECs. In vivo, SETD8 overexpression decreased ELK1 and bach1 expression, as well as EndMT. Moreover, SETD8 overexpression improved the renal function of rats with DN. Conclusions SETD8 cooperates with ELK1 to regulate bach1 transcription, thus participating in the progression of DN. In addition, SETD8 interacts with bach1 to modulate Snail transcription, thus inducing EndMT in DN. SETD8 plays a core role in the SETD8/ELK1/bach1 functional axis, which participates in hyperglycaemia-mediated EndMT in DN, and SETD8 may be a potential therapeutic target for DN. Trial registration ChiCTR, ChiCTR2000029425. 2020/1/31, http://www.chictr.org.cn/showproj.aspx?proj=48548

Colorectal cancer (CRC) is one of the most common malignant tumors with high incidence and mortality. The challenge remains to construct reliable prognostic prediction models and to further elucidate the key molecular mechanisms of tumor progression. To address this, we performed WGCNA based on 120 immune cell expression profiles from GEO sources to obtain a collection of monocytes/macrophages-related genes. The prognostic model was constructed by univariate survival analysis and LASSO regression analysis. Then, the prognostic model was validated by Multivariate Cox regression, Kaplan–Meier survival analysis and ROC analysis. In this prognostic model, we identified that PLIN2 has a potential value for CRC prognosis. PLIN2 expression in monocytes/macrophages was verified by scRNA-seq datasets and spatial transcriptome datasets, and PLIN2 was found to promote macrophage transformation to M2 subtype. Clinical specimens and tissue microarrays confirmed the differential expression and prognostic value of PLIN2 in CRC patients. Functional experiments demonstrated that PLIN2 gene overexpression promoted the proliferation, migration and invasion of CRC cells and significantly facilitated tumor growth in vivo. Mechanistically, we revealed that CD36 is a potential downstream target gene of PLIN2. The CD36 inhibitor Sulfo-N-succinimidyl Oleate significantly reversed PLIN2-induced proliferation, migration, invasion, and EMT activity of CRC cells in vitro and in vivo. Immunoprecipitation and immunofluorescence experiments confirmed that PLIN2 could interact with CD36. PLIN2 stabilized CD36 protein expression by inhibiting the proteasomal degradation pathway, thereby promoting CD36-mediated EMT activity. Overall, our study highlights that the PLIN2/CD36 axis regulates EMT activity and CRC progression, suggesting that interventions in this signaling pathway may offer a promising therapeutic approach to CRC progression. Schematic diagram elucidating the role of PLIN2 in CRC by Figdraw. FA is transported into the cell via CD36-mediated endocytosis. In CRC cells, PLIN2 promotes stability of CD36 and interacts with CD36 to activate the EMT process. However, the CD36 inhibitor SSO inhibits the binding of FAs to CD36 and attenuates its endocytosis, thereby reversing the PLIN2-mediated EMT process. Ultimately, the PLIN2-induced enhancement of CRC cell proliferation, migration, and invasion is attenuated by the CD36 inhibitor SSO.

Centrifugal compressors are widely used in the oil and natural gas industry for gas compression, reinjection, and transportation, To address the challenges of the difficult separation of data anomalies from equipment failures and limited knowledge acquisition from expert knowledge bases, this article proposes a dynamic fault diagnosis method for centrifugal compressor expert systems, combining convolutional neural networks (CNN) and principal component analysis for statistical process monitoring (PCA-SPE). Realize the combination of expert knowledge and instrument data, and break through the weak links in existing petrochemical instrument safety monitoring technology and traditional expert systems. The method has been validated using process data from centrifugal compressors. The results demonstrate that the method achieved 100% classification accuracy for two types of faults: non-starting of the drive machine and excessively low oil pressure. Combined with the expert system, it reached a satisfactory diagnostic performance.

Objective Diabetic nephropathy (DN) is regarded as the main vascular complication of diabetes mellitus, directly affecting the outcome of diabetic patients. Inflammatory factors were reported to participate in the progress of DN. Wingless-type family member 5 (WNT5A), myeloid zinc finger 1 (MZF1), and lysine methyltransferase 8 (SETD8) have also been reported to elevate inflammatory factor levels and activate the nuclear factor kappa B (NF-κB) pathway to induce endothelial dysfunction. In the current study, it was assumed that MZF1 associates with SETD8 to regulate WNT5A transcription, thus resulting in hyperglycemia-induced glomerular endothelial inflammation in DN. Methods The present study recruited 25 diagnosed DN patients (type 2 diabetes) and 25 control participants (nondiabetic renal cancer patients with normal renal function, stage I–II) consecutively. Moreover, a DN rat and cellular model was constructed in the present study. Immunohistochemistry, Western blot, and quantitative polymerase chain reaction (qPCR) were implemented to determine protein and messenger RNA (mRNA) levels. Coimmunoprecipitation (CoIP) and immunofluorescence were implemented in human glomerular endothelial cells (HGECs). Chromatin immunoprecipitation assays and dual luciferase assays were implemented to determine transcriptional activity. Results The results of this study indicated that levels of WNT5A expression, p65 phosphorylation (p-p65), and inflammatory factors were all elevated in DN patients and rats. In vitro, levels of p-p65 and inflammatory factors increased along with the increase of WNT5A expression in hyperglycemic HGECs. Moreover, high glucose increased MZF1 expression and decreased SETD8 expression. MZF1 and SETD8 inhibit each other under the stimulus of high glucose, but cooperate to regulate WNT5A expression, thus influencing p-p65 and endothelial inflammatory factors levels. Overexpression of MZF1 and silencing of SETD8 induced endothelial p-p65 and inflammatory factors levels, which can be reversed by si-WNT5A. Mechanistic research indicated that MZF1, SETD8, and its downstream target histone H4 lysine 20 methylation (H4K20me1) all occupied the WNT5A promoter region. sh-SETD8 expanded the enrichment of MZF1 on WNT5A promoter. Our in vivo study proved that SETD8 overexpression inhibited levels of WNT5A, p-p65 expression, and inflammatory factors in DN rats. Conclusions MZF1 links with SETD8 to regulate WNT5A expression in HGECs, thus elevating levels of hyperglycemia-mediated inflammatory factors in glomerular endothelium of DN patients and rats. Trial registration ChiCTR, ChiCTR2000029425. 2020/1/31, http://www.chictr.org.cn/showproj.aspx?proj=48548

We herein report two cases of paradoxical carbon dioxide (CO2) embolism during laparoscopic nephrectomy and hepatic left lateral lobectomy without evidence of a right-to-left shunt or obvious rupture of blood vessels. Transesophageal echocardiography detected paradoxical CO2 embolism before the end-tidal CO2 partial pressure (PETCO2) dropped from baseline. The pneumoperitoneum was reduced or stopped immediately after detection of the embolism. One patient developed a postoperative epileptiform seizure. In the other patient, many gas bubbles were drawn out from the central venous line. We speculate that rapid introduction of pneumoperitoneum pushed a large amount of CO2 into the abdominal blood vessels, exceeding the gas exchange capacity of the lung and causing CO2 bubble formation in the left-side cardiac system. These two cases indicate that intraoperative transesophageal echocardiography can reduce the influence of CO2 embolism during laparoscopic tumor surgery by early diagnosis of the embolism and provide helpful information to establish a list of differential diagnoses of postoperative complications.

Background Hemodynamic instability is common during hepatectomy under general anesthesia combined with thoracic epidural anesthesia, along with intraoperative low central venous pressure (LCVP). We hypothesized that remimazolam-based anesthesia would improve hemodynamic instability compared to propofol-based anesthesia. Methods The patients undergoing elective hepatectomy under general anesthesia combined with thoracic epidural anesthesia were enrolled and randomly allocated to either group R (remimazolam anesthesia) or group P (propofol anesthesia). The hemodynamic instability was evaluated by the hemodynamic instability scores (HI-score) at induction period, during hepatectomy and hemostasis. The advanced hemodynamic parameters (cardiac index CI, system vascular resistance index SVRI) were recorded. The secondary outcomes including length of PACU stay, changes in hemoglobin level, major cardiovascular events within postoperative 3 days, length of hospital stay, postoperative ambulation time, and time to first flatus were also documented. Results A total of 72 subjects were randomized, and 33 ones under minor hepatectomy surgery in each group were analyzed finally. There was significant hemodynamics instability in both groups, however, the total HI-score was significantly lower in group R (22.8 ± 2.1) than group P (33.0 ± 4.1, P  = 0.029). Further analysis demonstrated that the HI-scores were also lower in group R than group P during induction period (11.9 ± 1.0 vs. 22.6 ± 4.2, P  = 0.017), hepatectomy period (23.2 ± 3.2 vs. 38.5 ± 6.0, P  = 0.027) and hemostasis period (22.2 ± 2.8 vs. 33.5 ± 3.8, P  = 0.019). Nevertheless, compared with propofol-based anesthesia, remimazolam-based anesthesia did not reduce incidence of major cardiovascular events and length of hospital stay ( P  > 0.05). Conclusions When compared with propofol-based anesthesia, remimazolam-based anesthesia has better intraoperative hemodynamic stability during minor hepatectomy surgery under combined general-epidural anesthesia. However, this improved hemodynamics may not necessarily translate into better perioperative outcomes. Trial registration Registered at ClinicalTrials.gov (Registration No. NCT06565715 Principal investigator Jun Zhang Date of registration 08/21/2024 https://clinicaltrials.gov/study/NCT06565715?term=NCT06565715&rank=1 ).

Overactive bladder (OAB) remains challenging to treat due to drug intolerance and limited efficacy of behavioral therapies. The mechanistic basis by which exercise improves bladder function is poorly understood. Here, we established a clinically translatable resistance exercise model using graded treadmill loading (5–15% body weight [BW], 10–30 min/day) in a cyclophosphamide (CYP)-induced OAB rat model to identify the optimal therapeutic intensity and delineate redox-related mechanisms. Functional (urodynamics, urine spot test), MRI imaging, histological, immunofluorescence, and untargeted metabolomic analyses were integrated to assess detrusor remodeling and oxidative stress modulation across 11 experimental groups. ModeratSTREe resistance exercise (10% BW, 20 min/day) significantly increased bladder capacity (0.45 ± 0.17 mL–1.28 ± 0.44 mL) and prolonged voiding interval (2.13 ± 0.64 min–6.35 ± 0.93 min; p  < 0.001). MRI and histology confirmed reversal of detrusor hypertrophy. Immunofluorescence demonstrated reduced 3-nitrotyrosine accumulation, indicating decreased peroxynitrite (ONOO⁻)-mediated nitrative stress. Metabolomic profiling revealed extensive reprogramming of glutathione metabolism, arginine biosynthesis, and glycine–serine pathways, restoring redox balance and antioxidant capacity. Integration of metabolic and histological data defined a mechanistic framework, “resistance exercise–peroxynitrite reduction–oxidative stress attenuation–detrusor remodeling.” In conclusion, our findings identify peroxynitrite reduction and detrusor remodeling as key mechano-redox pathways through which resistance training improves bladder compliance and detrusor relaxation. These results highlight resistance exercise as a clinically feasible, non-pharmacological strategy with translational potential for improving outcomes in patients with OAB.

Backgroud Recurrent laryngeal nerve (RLN) injury is one of the serious complications of thyroid tumour surgery, surgical treatment of thyroid cancer requires careful consideration of the RLN and its impact on glottis function. There has been no unified standard for precise neuromuscular block monitoring to guide the monitoring of RLN in thyroid surgery. This study aimed to investigate the correlation between Train-of-four stabilization ratio (TOFr) and neural signal values of intraoperative neurophysiological monitoring (INOM) during thyroid operation, and further to determine the optimal timing for INOM during thyroid operation. Methods Patients scheduled for thyroid tumour resection with INOM and RLN monitoring from April 2018 to July 2018 in our center were recruited. Electromyography (EMG) signals and corresponding TOFr were collected. All nerve stimulation data were included in group VR. Vagus nerve stimulation data were included in Subgroup V. RLN stimulation data were included in Subgroup R. The timing of recording was as follows: Vagus nerve EMG amplitude after opening the lateral space between the thyroid and carotid sheath and before the initiation of thyroid dissection, RLN EMG amplitude at first recognition, RLN EMG amplitude after complete thyroid dissection (Repeat three times), and Vagus nerve EMG amplitude after resection of the thyroid (Repeat three times). Correlation analysis of continuous variables was described by a scatter diagram. Pearson correlation analysis or Spearman correlation analysis was used for the two groups of variables. Results Finally, 134 vagus nerve signals and 143 RLN signals were analysed after matching with TOFr. The EMG amplitude in the VR group and subgroups after nerve stimulation was positively correlated with TOFr (p < 0.05). In the VR, V and R group, the incidence of EMG ≥ 500 µV in the 0.75 < TOFr ≤ 0.85 interval was significantly higher than the 0 < TOFr ≤ 0.75 interval (P = 0.002, P = 0.013 and P = 0.029), and has no statistical difference compared to 0.85 < TOFr ≤ 0.95 interval (P > 0.05). Conclusions The EMG signals of the RLN and vagus nerve stimulation during thyroid surgery were positively correlated with TOFr. TOFr > 0.75 could reflect more than 50% of the effective nerve electrophysiological signals, 0.75 < TOFr ≤ 0.85 interval was the optimal timing for IONM during thyroid surgery. Trial registration Chinese Clinical Trial Registry (ChiCTR1800015797) Registered on 20/04/2018. https://www.chictr.org.cn .