Objective:To design a single-line low-temperature plasma ablation electrode, aiming to solve the problem of uniform, continuous and stable microbubbles generated by conventional electrodes, and improve the ablation and cutting effect of low-temperature plasma.Methods:The structures of low temperature plasma three-wire electrode and single-line electrode were modeled in SolidWorks 2021 3D modeling software, and the prototype was made by 3D printing. The finite element analysis of electric field and temperature field of the two kinds of electrode ablation process was carried out by COMSOL Multiphysics 6.1 software, and the validity and correctness of the finite element simulation model were verified by temperature test experiment, and the ablation effect and plasma excitation process of the two kinds of electrode were compared by tissue ablation experiment and low temperature plasma excitation experiment.Results:The results of finite element analysis showed that the maximum surface temperature of three-wire electrode and single-wire electrode were 70.2 and 63.3 ℃, respectively, and the surface temperature of single-wire electrode was more ideal, and the maximum electric field intensity of the two electrodes was more than 1.0 × 10 7 V/m, which met the electric field condition of microbubble breakdown. The electric field intensity of the two ends of the three-wire electrode was much higher than that of the other regions, while the electric field intensity of the single-wire electrode had no obvious sudden change and fluctuation. The experimental values of the temperature at the electrode surface and a distance of 1 cm on the electrode surface were basically consistent with the simulation values, the degree of fit was good, and the relative error was 3.2%. The highest ablation temperature of single linear electrode on pig fat was 46.8 ℃. After ablation, there was no coking area in morphology, and the tissue cutting depth of 0.5 mm could be reached in 1 s. When connected to the energy platform, microbubbles would occur on the working electrode surface of the single-wire electrode; when 6 ms was electrified, the working electrode surface was completely covered by microbubbles; when 9 ms was energized, the low-temperature plasma was excited and the blue-purple plasma could be seen; when 25 ms was energized, the microbubbles were still regular and stable. Conclusions:A kind of single-line low-temperature plasma ablation electrode is designed, which can produce uniform, continuous and stable microbubbles and achieve better ablation and cutting effect than the traditional electrode.

Objective:To design a new type of intelligent power-assisted hip disarticulation prosthesis and to use experiments to verify its kinematic performance.Methods:The main body of the prosthesis was designed using a double parallel four-link configuration based on a remote motion center mechanism. A series elastic actuator was used to provide external power for the prosthesis, and an antagonistic torsion spring structure was used to achieve bidirectional energy storage assistance in hip flexion and extension. A control system based on impedance control was established. By setting up an auxiliary force field to compensate for the difference between the actual angle of the prosthesis and the target angle, the prosthesis assist function was realized. Finally, the traditional hip disarticulation prosthesis was used as a comparison to test the overall performance of the new intelligent power-assisted hip disarticulation prosthesis worn by normal people.Results:For the new smart-assisted hip-disarticulation prosthesis, the goodness-of-fit of its hip joint angle curve to that of a normal person was 86%, which was 14% higher than that of the traditional hip-disarticulation prosthesis (72%). The goodness-of-fit of the healthy-side angle of the new smart-assisted hip disarticulation prosthesis to the normal human was 94%, which was the same as that of the traditional hip disarticulation prosthesis.Conclusions:A new type of intelligent power-assisted hip disarticulation prosthesis is designed to realize the function of prosthesis-assisted movement.

Objective:To design an electronic nose that can detect and identify urinary volatile organic compounds (VOCs) as marker gases for bladder cancer.Methods:Isopropyl alcohol, ethylbenzene, acetic acid, and ammonia were selected as target gases, and 8 metal oxide gas sensors were used to construct sensor arrays for testing and collecting experimental data, and different characteristics were normalized. Recursive feature elimination (RFE) was used to select the best feature subset, and principal component analysis (PCA) and linear discriminant analysis (LDA) were further introduced to reduce the data dimension and facilitate visual analysis. In addition, three machine learning algorithms, including support vector machine (SVM), random forest (RF), and K-nearest neighbor (KNN), were combined to train and verify the model.Results:When the feature number was 12, the accuracy of the model classification had the best performance. The feature subset consisted of 5 differences, 5 sensitivities, and 2 integrals, and the data was reduced to 12 dimensions. Only PCA couldn’t distinguish the four gases. The LDA classification performance was significantly better than that of PCA, except that isopropyl alcohol and acetic acid had a small overlap area. LDA could distinguish ethylbenzene and ammonia from isopropyl alcohol and acetic acid; the sample points were gathered, which means the clustering performance was also better. The prediction accuracy of SVM, RF, and KNN was 0.85, 0.56, and 0.79, respectively. After model verification, the classification accuracy of PCA+SVM, LDA+RF, and LDA+KNN was 0.97, 0.94, and 0.97, respectively.Conclusions:An electronic nose was designed to detect and identify urinary VOCs marker gases for bladder cancer.

Objective:To design a fully integrated multi-channel implantable brain-computer interface electrical stimulation system.Methods:The human-computer interaction interface of the upper computer was set by users, and the data was packaged via a self-built protocol. When parameters were transmitted to the field programmable gate array (FPGA) chip through the Bluetooth module, the stimulation chip was controlled after the parameter analysis was completed. Eventually the user-set current stimulation was output. To verify the system feasibility, the accuracy of the single-channel stimulation waveform, the multi-channel output capability, and the adjustable range of the parameter were tested separately.Results:It realized 16 channels of time-sharing differential stimulation current output, the output stimulation current waveform was dual-phase equal-width pulse, the amplitude ranged within 4~1 000 μA, the pulse single-phase width range was 10~1 000 μs, the cycle time was 1~1 000 ms, thus the current parameters could be accurately adjusted.Conclusions:A fully integrated multi-channel implantable brain-computer interface electrical stimulation system was completed.

Objective:To investigate the effect of inhibitory activity of high mobility group protein B1 (HMGB1), signal transduction and activator of transcription 3 (STAT3) on myocardial ischemia-reperfusion injury in rats.Methods:In vivo and in vitro models of MIRI were established. SD rats were randomly divided into a sham group, a model group, a glycyrrhizic acid group, and a NSC74859 group, with 6 rats in each group. Rats in the sham group were not ligation, and rats in the sham group and model group were not given medication. The rats in the glycyrrhizic acid group and the NSC74859 group were injected with HMGB1 antagonist glycyrrhizic acid or STAT3 inhibitor NSC74859 5 mg/kg in the tail vein at 12 h 30 min before ischemia/reperfusion and 30 min after ischemia, respectively. Left ventricular shortening fraction (FS) and left ventricular ejection fraction (EF) were evaluated by echocardiography, and apoptosis of cardiomyocytes was evaluated by hematoxylin-eosin (HE) and TUNEL staining. The expression levels of HMGB1, STAT3, and phosphorylated STAT3 (p-STAT3) were detected by real-time fluorescence quantitative PCR and Western Blot. The viability of H9C2 cells was determined by the MTS assay, intracellular ATP content was determined, and the mitochondrial membrane potential of H9C2 cells was measured by flow cytometry to evaluate the survival of cardiomyocytes. The action mode of HMGB1/STAT3 was studied by the immunoprecipitation method. The expression and migration of HMGB1/STAT3 in the nucleus and cytoplasm were detected by immunostaining. Results:After inhibiting the expression of HMGB1 or STAT3, EF and FS were increased, and immune infiltration and apoptosis of cardiomyocytes were decreased. Inhibition of HMGB1 expression could decrease the expression of STAT3, but inhibition of STAT3 expression didn’t affect the expression of HMGB1. Hypoxia could lead to increased expression of HMGB1 and p-STAT3, and decreased expression of STAT3. After 8 hours of hypoxia, the expression level of STAT3 suddenly increased. After reoxygenation, the expression of HMGB1 and STAT3 decreased, and the expression of p-STAT3 increased, but p-STAT3 (Ser 727) didn’t participate in this process. After ischemia-reperfusion injury, HMGB1 and STAT3 binded firmly in cardiomyocytes, but inhibition of STAT3 or HMGB1 weakened this binding. Inhibition of HMGB1 or STAT3 expression could reduce myocardial ischemia-reperfusion injury. The expression of HMGB1 in reoxygenated cardiomyocytes increased after hypoxia, and HMGB1 migrated from the nucleus to the cytoplasm.Conclusions:Inhibiting the activity of the HMGB1/STAT3 axis effectively reduces MIRI in rats.

Objective:To assess the efficacy of different fusion strategies involving the convolutional block attention module (CBAM) and Unet for automatic pancreas segmentation in enhanced CT images of patients with acute pancreatitis.Methods:A retrospective analysis was conducted on 1 158 patients with acute pancreatitis admitted to the Affiliated Hospital of North Sichuan Medical College between January 1st, 2016 and July 30th, 2021. Among them, 141 patients with first-episode acute pancreatitis were randomly categorized into mild, moderate, and severe cases. The test set comprised 5 mild and 15 severe cases, while the remaining 126 cases were used for training. Within the training set, 20% of the data was randomly allocated as the validation set. Different fusion paths of the CBAM and Unet networks were trained, utilizing the Dice similarity coefficient, Hausdorff distance (HD), and pixel accuracy (PA) as evaluation metrics. The model demonstrating the best performance on the validation set was selected and evaluated on the test set. Additionally, the Unet model was combined with the attention gate attention mechanism (AttentionUnet) in the skip connection, and the ResBlock replaced the original convolution module (ResUnet) in the Unet network. Moreover, the skip connection branch module of feature extraction was integrated with CBAM (ResUnet_CBAM) for comparison.Results:Unet_CBAM achieved better results on the test set with a Dice value of 80.06%, a HD value of 3.765 9 and a PA value of 0.992 3, all surpassing other fusion strategies. The segmentation accuracy of the pancreatic region in CT images of acute pancreatitis patients was notably enhanced compared to Unet and its related variant networks.Conclusions:The Unet network integrated into CBAM after skip connection can better perform pancreatic segmentation on enhanced CT images of patients with acute pancreatitis and can effectively improve the efficiency of relevant personnel in pancreatic segmentation on enhanced CT images of patients with acute pancreatitis.

Objective:To identify early diagnostic biomarkers for preeclampsia by analyzing the placental and peripheral circulatory transcriptomic data of patients.Methods:Clinical information and microarray expression profiles of preeclampsia patients were sourced from high-throughput gene expression databases. Multi-omics approaches, including differential gene expression analysis, enrichment analysis, and weighted gene co-expression network analysis (WGCNA), were utilized to identify candidate diagnostic markers and explore potential mechanisms of preeclampsia. Subsequently, a combination of machine learning techniques, including random forest, support vector machine, and least absolute shrinkage and selection operator (LASSO), were employed for further screening of these candidates. Finally, the selected diagnostic markers were validated using a peripheral circulation dataset.Results:Differential gene expression analysis revealed 71 upregulated and 21 downregulated genes in preeclampsia. WGCNA linked the onset of preeclampsia with blue and teal modules. Enrichment analysis of candidate biomarkers suggested changes in cell cycle, cellular senescence, and immune-related pathways as primary drivers of preeclampsia. Further refinement through machine learning identified significant upregulation of COL17A1 and DIO2 genes in the peripheral blood of patients, demonstrating robust diagnostic potential. Conclusions:COL17A1 and DIO2 genes can be used as peripheral circulating diagnostic markers for the early diagnosis of eclampsia.

Objective:To determine the content of the released nickel ion through the 7 extraction media to extract the Ni-Ti wires and to plot the curve of the released nickel ion so as to identify a leaching medium that can be substituted for blood for in vitro Ni release evaluation. Methods:The release of Ni through microwave digestion/inductively coupled plasma mass spectrometry (ICP-MS) in the goat serum was determined. Because of the high content of Ni release, it could be determined by diluting the extraction medium, and other extraction media could be determined directly. Ni release standard curves were plotted by the release amount and different time point variables. Though the different extraction media Ni release curves confirm the specificity of extraction media instead of blood.Results:By analyzing the Ni release curves of seven leaching media, it was found that none of these seven extraction media was suitable for the evaluation of Ni release in in vitro leaching media. Considering the safety of the leaching medium and the simplicity of preparation, hydrochloric acid solution was chosen as the leaching medium, but the concentration needed to be diluted accordingly. Finally, a hydrochloric acid solution was created as an alternative to blood for the in vitro study of Ni release from Ni-Ti alloy cardiovascular products, with a volume fraction of 0.005%. Conclusions:The in vitro leaching medium that can replace blood was found to be hydrochloric acid for the time being, but its concentration was too high, resulting in too much Ni release as well, which deviated from the actual situation. Therefore, the hydrochloric acid solution was diluted step by step, and the Ni release curve was examined until it was close to the clinical release level, and the actual concentration was determined, thus laying a solid foundation for the subsequent evaluation of the safety and risk.

Objebtive:To investigate the effect of baicalin on cell apoptosis and related cytokines in diabetic retinopathy.Methods:Sixty SD rats were randomly divided into a control group, a model group, and a baicalin group, with 20 rats in each group. The diabetic retinopathy model was established after fed by a high-sugar, high-fat diet for 4 weeks by intraperitoneal injection of 50 mg/kg streptozotocin. Rats in the control group weren’t done any treatment, only with normal diet. Rats in the model group was not given drug treatment,While rats in the baicalin group 50 mg/kg intrabitoneal injection of baicalin. The results of HE staining, TUNEL cell apoptosis, retinal cell apoptosis index, and the expression of cleaved-cysteinyl aspartate-specific proteinase-3 (cleaved-Caspase-3), B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated X (Bax) protein in the retina of the three groups were observed.Results:The internal limiting membrane of the retina in the control group was smooth. Compared with the control group, the loss of ganglion cells in the model group was significantly increased, the retinal thickness was thinner, and the thickness of the inner nuclear layer and the outer nuclear layer was thinner. Compared with the model group, the number of ganglion cells in the baicalin group was significantly increased, the retinal thickness was thickened, and the thickness of the inner nuclear layer and the outer nuclear layer was thickened. Apoptotic cells were brown after TUNEL labeling. A large number of apoptotic cells were observed in the model group, and the cell arrangement was disordered. Only a few apoptotic cells were observed in the control group, and the cells were arranged neatly. Compared with the model group, the apoptotic cells in the baicalin group were significantly reduced ( P < 0.05), and the cells were arranged neatly. The apoptosis index of retinal cells in the sham group was lower than that in the model group and the baicalin group, and the baicalin group was lower than that in the model group ( P < 0.05). Compared with the control group, the expression of cleaved-Caspase-3 and Bax protein in the retina of the model group was significantly increased, and Bcl-2 was significantly decreased; the difference was statistically significant ( P < 0.05). Compared with the model group, the expression of cleaved-Caspase-3 and Bax protein in the baicalin group was down-regulated, and Bcl-2 was significantly up-regulated; the difference was statistically significant ( P < 0.05). Conclusions:Baicalin can improve diabetic retinopathy by inhibiting the apoptosis rate of DR rats, down-regulating the expression of cleaved-Caspase-3 and Bax, and up-regulating the expression of Bcl-2.

Objective:To explore the effects of MiR-199a-3p on promoting the development of mycoplasma pneumonia via the silent information regulator 1(SIRT1)/nuclear factor-κB (NF-κB) pathway.Methods:Totally 80 SPF-grade BALB/c mice were randomly divided into a control group, a model group, a miR-199a-3p group, and a inhibitory group, with 20 rats in each group. Excep the control group, the model group was established as a mouse model of mycoplasma pneumoniae through a continuous nasal drip of a high-load mycoplasma pneumoniae bacterial solution for 3 days. After modeling, mice in each group had tail vein injections. The miR-199a-3p group and the inhibitory group mice were injected with agomir solution and antagonir solution, respectively. And the model group and control group mice were injected with the same amount of physiological saline through the tail vein. After the experiment, mice of all groups were killed and their blood was collected from the eyeballs, and interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) levels were detected by the enzyme-linked immunosorbent assay method. Subsequently, the lung tissues of the mice were taken for HE staining to observe pathological changes in the lung tissue. Real-time fluorescence quantitative PCR was used to detect miR-199a-3p gene expression levels in lung tissue, and Western Blot was used to detect SIRT1/NF-κB signaling pathway protein expression in lung tissue. Results:Compared with the model group, IL-4, IL-6, IL-1β, and TNF-α levels in the serum of the miR-199a-3p group were decreased, with a significant difference ( P < 0.05). The HE staining results showed that the lung tissue structure of the control group mice was nearly normal and there was no alveolar exudation or inflammatory response. The other three groups all had varying degrees of alveolar interstitial widening, alveolar exudation, and inflammatory cell infiltration. Compared with the model group, miR-199a-3p gene and SIRT1 protein expression levels in the miR-199a-3p group increased, with a significant difference (all P < 0.05). While NF-κB protein expression levels in the miR-199a-3p group decreased, there was a significant difference ( P < 0.05). Conclusions:The expression of miR-199a-3p gene is reduced in the lung tissue of mycoplasma pneumoniae mice. Increasing the level of miR-199a-3p gene has a protective effect on lung tissue damage in mycoplasma pneumoniae mice through anti-inflammatory effects, and its mechanism may be related to its regulatory effect on the SIRT1/NF-κB pathway.