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Precise localization of the site of origin of premature ventricular contractions (PVCs) before ablation can facilitate the planning and execution of the electrophysiological procedure.The purpose of this study was to develop a predictive model that can be used to differentiate PVCs between the left ventricular outflow tract and right ventricular outflow tract (RVOT) using surface electrocardiogram characteristics.A total of 851 patients undergoing radiofrequency ablation of premature ventricular beats from January 2015 to March 2022 were enrolled. Ninety-two patients were excluded. The other 759 patients were enrolled into the development (n = 605), external validation (n = 104), or prospective cohort (n = 50). The development cohort consisted of the training group (n = 423) and the internal validation group (n = 182). Machine learning algorithms were used to construct predictive models for the origin of PVCs using body surface electrocardiogram features.In the development cohort, the Random Forest model showed a maximum receiver operating characteristic curve area of 0.96. In the external validation cohort, the Random Forest model surpasses 4 reported algorithms in predicting performance (accuracy 94.23%; sensitivity 97.10%; specificity 88.57%). In the prospective cohort, the Random Forest model showed good performance (accuracy 94.00%; sensitivity 85.71%; specificity 97.22%).Random Forest algorithm has improved the accuracy of distinguishing the origin of PVCs, which surpasses 4 previous standards, and would be used to identify the origin of PVCs before the interventional procedure.

The aim of this study was to analyze the relationship between cerebrospinal fluid variation and hydrocephalus through deep learning-based (DL-based) magnetic resonance imaging (MRI), in order to improve the postoperative recovery of craniocerebral injury (CI) patients and reduce the deterioration after decompressive craniectomy of the patient. 50 patients with CI who received the diagnosis and treatment at the hospital were chosen as the subjects. The retrospective analysis on patients with CI was conducted herein. First, the general clinical data of the patients were analyzed. Next, the MRI images for brain damage of the patients were collected. After that, the DL-based brain image classification and the artificial intelligence technology were utilized to solve the classification problems with classifiers. Finally, the DL-based convolutional neural network (CNN) was adopted to preprocess the image features, and the offline training and online reconstruction were conducted after the construction of the model. Four groups of databases were selected for deep learning and analyzed in terms of data feature analysis, principal component analysis (PCA), and application of 3D scale-invariant feature transformation (SIFT) operators in image data analysis. The results manifested that, the WHGO descriptor and the area under the curve were the largest. SIFI, PCA, and WHGO had the sensitivity of 87.5%, 88.2%, and 90.1%, the specificity of 91.8%, 90.1%, and 94.2%, and the correct rate of 90.6%, 87.5%, and 92.4%, respectively. The volume content of the cerebrospinal fluid in the subarachnoid space was 77.04% higher than that of cerebrospinal fluid in the ventricle. In conclusion, the intelligent deep learning model proposed in this article was able to assume the measurement of clinical cases and auxiliary diagnosis. This model not only can help doctors save the diagnosis time and enhance the medical efficiency, but also can precisely identify the patient’s lesion area. Therefore, it had substantial application potential in mobile-based clinical practice.

As a pathological myocardial remodeling process in a variety of cardiovascular diseases, cardiac hypertrophy still has no effective treatment. Human mesenchymal stem cells (hMSCs) derived extracellular vesicles (EVs) has been recognized as a promising treatment strategy for cardiac disease.In this study, the inhibitory effects on cardiac hypertrophy are compared between normoxia-conditioned hMSC-derived EVs (Nor-EVs) and hypoxia-conditioned hMSC-derived EVs (Hypo-EVs) in neonatal rat cardiomyocytes (NRCMs) after angiotensin II (Ang II) stimulation and in a mouse model of transverse aortic constriction (TAC).We demonstrate that Hypo-EVs exert an increased inhibitory effect on cardiac hypertrophy compared with Nor-EVs. Parkinson disease protein 7 (PARK7/DJ-1) is identify as a differential protein between Nor-EVs and Hypo-EVs by quantitative proteomics analysis. Results show that DJ-1, which is rich in Hypo-EVs, alleviates mitochondrial dysfunction and excessive mitochondrial reactive oxygen species (mtROS) production as an antioxidant. Mechanistic studies demonstrate for the first time that DJ-1 may suppress cardiac hypertrophy by inhibiting the activity of proteasome subunit beta type 10 (PSMB10) through a direct physical interaction. This interaction can inhibit angiotensin II type 1 receptor (AT1R)-mediated signaling pathways resulting in cardiac hypertrophy through alleviating ubiquitination degradation of AT1R-associated protein (ATRAP).When taken together, our study suggests that Hypo-EVs have significant potential as a novel therapeutic agent for the treatment of cardiac hypertrophy.

Rationale: With the widespread development of the interventional technique for cardiovascular diseases and the widespread use of contrast medium (CM), the incidence of contrast-induced nephropathy (CIN) has been increasing, which is associated with poor prognosis for cardiovascular diseases. This study aims to explore the effect of circulating exosomal microRNA from patients with myocardial infarction (MI) on CIN and related molecular mechanism. Methods: A rat MI model was established by ligating the left anterior descending coronary artery. Circulating exosomes were isolated from control (Exo-NC) and MI rats (Exo-MI) using a commercial kit. The in vivo and in vitro models of CIN were created using iodixanol. Reverse transcription quantitative PCR (RT-qPCR) was utilized to detect the expression of miR-1-3p. Western blot (WB) was used to detect the expression of exosomal surface markers, and apoptosis-related and autophagy-related proteins. The apoptosis rate was examined by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining and flow cytometry (FC). Transmission electron microscopy (TEM) was utilized to observe the exosomes and autophagosomes. Rat kidney injury was assessed by hematoxylin and eosin (H&E) staining and kidney injury molecule-1 (KIM-1) immunohistochemical staining. Renal function of rats was assessed by detecting the levels of blood urea nitrogen (BUN) and serum creatinine (Cr). The dual luciferase reporter assay was performed to identify the target gene of miR-1-3p. Results: The treatment of CM induced NRK-52E cell damage, which manifested as enhanced cell autophagy and enhanced apoptosis. The Exo-MI treatment significantly inhibited the CM-induced autophagy and apoptosis of NRK-52E cells. Furthermore, the Exo-MI treatment increased the Bcl-2 expression, but decreased the Bax expression and the ratio of LC3II/LC3I. Furthermore, the results of the TUNEL staining and FC showed that Exo-MI can reduce apoptotic rate. Through TEM, it was found that Exo-MI reduced the number of autophagosomes in NRK-52E cells. The rescue experiments revealed that the function of Exo-MI is to inhibit the CM-induced autophagy and apoptosis of NRK-52E cells, which can be inhibited by the miR-1-3p inhibitor. Furthermore, it was found that the overexpression of miR-1-3p can also inhibit the CM-induced autophagy and apoptosis of NRK-52E cells. Through dual luciferase reporter assay, ATG13 was found to be the target of miR-1-3p. In addition, the overexpression of miR-1-3p significantly reversed the CM-induced decrease in phosphorylation level of AKT. Furthermore, ATG13 silencing can also inhibit the CM-induced autophagy and apoptosis of NRK-52E cells. In vivo, Exo-MI significantly alleviated the renal injury, reduced the renal fibrosis, and improved the renal function of CIN rats. Conclusion: The circulating exosomal miR-1-3p after MI inhibited the CM-induced apoptosis and autophagy of renal tubular epithelial cells, and improved the renal function of rats by targeting ATG13 and activating the AKT signaling pathway.

To evaluate and analyze the therapeutic effect of stereotactic soft channel puncture and drainage on hypertensive cerebral hemorrhage.Sixty patients with hypertensive cerebral hemorrhage admitted to our hospital from September 2014 to September 2019 were selected for study and randomly divided into study group (n=30) and routine group (n=30) according to admission number. Two groups of patients were given basic treatment after admission, while routine group patients were given small bone window hematoma removal, study group patients were given stereotactic soft channel puncture and drainage, and the clinical effects of the two groups were analyzed.The total effective rate of the study group was 96.67%, which was significantly higher than that of the routine group (80.00%), and the difference was statistically significant (P0.05). The level of independent living in the study group was significantly higher than that in the conventional group, and the level of neurological deficit was lower than that in the conventional group, with statistically significant difference (P0.05). Before treatment, there was no significant difference in the hematoma volume between the two groups (P0.05). after treatment for 1, 2 and 4 weeks, the hematoma volume of the two groups decreased, and the hematoma volume of the study group was significantly less than that of the conventional group, with significant difference (P0.05). There was no difference in CD3+ positive cell rate and CD8+ positive cell rate between the two groups before treatment (P0.05). After treatment, the CD8+ positive cell rate in the study group was lower than that in the conventional group, and the CD3+ positive cell rate was higher than that in the conventional group, with statistically significant difference (P0.05). The incidence of postoperative complications such as pulmonary infection, urinary tract infection, liver and kidney dysfunction in the study group was lower than that in the conventional group, and the difference was statistically significant (P0.05).Stereotactic soft-channel puncture and drainage has the advantages of less trauma, less bleeding, fewer complications and rapid postoperative recovery. It can be used for the treatment of hypertensive cerebral hemorrhage, promote the recovery of neurological function of patients, improve independent living standard and effectively improve prognosis.

Background: Mesenchymal stem cells (MSCs) activated with IFN-γ elicit more powerful physical effects. Exosomes (Exos) secreted from MSCs have protective against myocardial injury. The aim of this study was to investigate whether Exsos derived from IFN-γ-pretreated MSCs exhibit more potent cardioprotective function and the underlying mechanisms. Methods: Exos were isolated from MSCs (Ctrl-Exo) and IFN-γ-primed MSCs (IFN-γ-Exo) and were then delivered to H9c2 cells or human umbilical vein endothelial cells (HUVECs) in vitro under oxygen and glucose deprivation (OGD) condition or in vivo in an infarcted rat heart. RNA sequencing was to identify the different expressed functional transcription factor (TF). Quantitative reverse transcription-PCR (qPCR) was to confirm the upregulated TF and miRNA in IFN-γ-primed MSCs. Dual-luciferase reporter gene assay were to analyze the transcriptional regulation of miRNAs by STAT1. The target of miR-21-5p (miR-21) was disclosed by luciferase reporter assays and qPCR. The function of BTG2 was verified in vitro under OGD condition.Result: IFN-γ-Exo accelerated migration, tube-like structure formation, and prevented H9c2 from OGD-induced apoptosis. Similarly, IFN-γ-Exo leaded to further reduction in fibrosis size, reduced cardiomyocyte apoptosis and improved cardiac function compared to Ctrl-Exo. miR-21 was significantly upregulated in both IFN-γ-primed MSCs and IFN-γ-Exo. STAT1 transcriptionally induced miR-21 expression. Up-regulated miR-21 can inhibit the expression of BTG2. BTG2 promoted H9c2 cells apoptosis and reversed the protective effect of miR-21 under OGD environment.Conclusion: IFN-γ-Exo have enhanced therapeutic efficacy against acute MI possibly through promoting angiogenesis and anti-apoptotic effect through increasing the level of miR-21, which directly targeted on BTG2.

Background Mesenchymal stromal cells (MSCs) activated with IFN-γ elicit stronger physical effects. Exosomes (Exos) secreted from MSCs show protective effects against myocardial injury. This study aimed to determine whether Exos derived from IFN-γ-treated MSCs exhibit more potent cardioprotective function and the underlying mechanisms. Methods H9c2 cells or human umbilical vein endothelial cells (HUVECs) were treated with Exos isolated from MSCs (Ctrl-Exo) or IFN-γ-primed MSCs (IFN-γ-Exo) under oxygen and glucose deprivation (OGD) conditions in vitro and in vivo in an infarcted rat heart. RNA sequencing was used to identify differentially expressed functional transcription factors (TFs). Quantitative reverse transcription-PCR (qPCR) was used to confirm the upregulated TFs and miRNA in IFN-γ-primed MSCs. Dual-luciferase reporter gene assay was used to analyze the transcriptional regulation of miRNAs by STAT1. The target of miR-21-5p (miR-21) was determined by luciferase reporter assays and qPCR. The function of BTG2 was verified in vitro under OGD conditions. Result IFN-γ-Exo accelerated migration and tube-like structure formation and prevented OGD-induced apoptosis in H9c2. Similarly, IFN-γ-Exo treatment caused a decrease in fibrosis, reduced cardiomyocyte apoptosis, and improved cardiac function compared to Ctrl-Exo treatment. MiR-21 was significantly upregulated in IFN-γ-primed MSCs and IFN-γ-Exo. STAT1 transcriptionally induced miR-21 expression. Up-regulated miR-21 could inhibit BTG anti-proliferation factor 2 (BTG2) expressions. BTG2 promoted H9c2 cell apoptosis and reversed the protective effects of miR-21 under OGD conditions. Conclusion IFN-γ-Exo showed enhanced therapeutic efficacy against acute MI, possibly by promoting angiogenesis and reducing apoptosis by upregulating miR-21, which directly targeted BTG2.

Ischemic cardiomyopathy seriously endangers human health leading to a poor prognosis. Acute myocardial infarction (AMI) is the primary etiology, and the pathophysiological process concludes with the death of cardiomyocytes caused by acute and persistent ischemia and hypoxia in the coronary arteries. We identified a circRNA (circSNRK) which was downregulated in rats with myocardial infarction (MI), however, the role it plays in the MI environment is still unclear. This study contained experiments to investigate the role of circSNRK in the regulation of cardiac survival and explore the mechanisms underlying circSNRK functions. Quantitative real-time PCR (qRT-PCR) was performed to determine the circSNRK expression patterns in hearts. Gain-of-function assays were also conducted in vitro and in vivo to determine the role of circSNRK in cardiac repair. qRT-PCR, western blot, and luciferase reporter assays were used to study circRNA interactions with micro RNAs (miRNAs). Overexpression of circSNRK in cardiomyocytes reduced apoptosis and increased proliferation. Adeno associated virus 9 (AAV9) mediated myocardium overexpression of circSNRK in post MI hearts reduced cardiomyocyte apoptosis, promoted cardiomyocyte proliferation, enhanced angiogenesis, and improved cardiac functions. Overall, upregulation of circSNRK promotes cardiac survival and functional recovery after MI. Mechanistically, circSNRK regulates cardiomyocyte apoptosis and proliferation by acting as a miR-103-3p sponge and inducing increased expression of SNRK which can bind GSK3β to regulate its phosphorylated activity. And thus circSNRK may be a promising therapeutic target for improving clinical prognosis after MI.

The aim of this study is to investigate the efficacy of expanded endonasal approaches (EEAs) in the treatment of pituitary adenoma, and the effects of serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-12 (IL-12) in patients were further analyzed. A total of 80 cases of patients with pituitary adenoma admitted to our hospital from January 2013 to May 2015 were randomly divided into the observation group and control group, with 40 cases in each group. The observation group was treated with EEA technique, while the control group was treated with transcranial microsurgery. The prolactin (PRL), growth hormone (GH) and other endocrine hormone indexes, as well as inflammatory factors such as TNF-α, IL-6, and IL-12 were compared before and 1 week after the operation between the two groups. Moreover, the scores of Karnofsky performance status (KPS) and Mini-Mental State Examination (MMSE) at preoperative and postoperative 1 week were also compared between the two groups. The operation time, hospitalization time, and postoperative complications were compared between the two groups. And the patients were followed up for 2 years to observe the recurrence rate. The operation time and hospital stay in the observation group were 62.8 ± 9.3 min and 12.5 ± 2.1 days, respectively, while the operation time and length of stay in the control group were 105.6 ± 15.7 min and 18.2 ± 3.4 days, respectively. The operation time and hospitalization time were shorter than those in the control group, and the differences were statistically significant ( P 0.05). At 1 week after surgery, the levels of PRL and GH in the two groups were significantly lower than those before surgery ( P 0.05). At 1 week after operation, the scores of KPS and MMSE in both groups were significantly higher than those before the operation ( P 0.05). At 1 week after surgery, the serum levels of IL-6, IL-12, and TNF-α in the two groups were significantly lower than those before surgery ( P