Objective:To compare the clinical efficacy of radiofrequency ablation and liver resection in the treatment of gastrointestinal stromal tumor liver metastasis.Methods:A retrospective cohort study was conducted, collecting medical records of 46 patients with gastrointestinal stromal tumor liver metastasis treated at the First Medical Center of the Chinese People′s Liberation Army General Hospital from January 2018 to December 2022. Patients were divided into radiofrequency ablation group ( n=20) and liver resection group ( n=26) based on the treatment method. Short-term efficacy and long-term prognosis between the two groups were compared. Short-term efficacy was evaluated based on intraoperative bleeding volume, operative time, hospital stay, hospitalization costs, while long-term efficacy was assessed by progression-free survival and overall survival. Normally distributed measurement data were expressed as mean±standard deviation ( ± s) and compared using the t-test. Non-normally distributed measurement data were expressed as M( Q1, Q3) and compared using the Wilcoxon rank-sum test. Count data were expressed as frequency (%) and compared using the chi-square test. The long-term prognosis of patients in both groups was compared using the Kaplan-Meier curve. Results:The intraoperative blood loss, operative time, postoperative hospital stay, and hospitalization costs for the radiofrequency ablation group were 5 (3, 5) mL, 60 (55, 60) min, 4.0 (3.0, 4.0) d, and 4.6 (3.8, 5.3) ten thousand yuan, respectively; for the liver resection group, these were 100 (50, 275) mL, 180 (155, 215) min, 7.0 (4.5, 9.5) d, and 8.6 (6.1, 10.8) ten thousand yuan, respectively, with statistically significant differences between the two groups( P<0.05). The median progression-free survival for the liver resection group was 37 months, with 1 and 3-year progression-free survival rates of 96% and 50%, respectively. For the radiofrequency ablation group, the median progression-free survival was 20.5 months, with 1 and 3-year progression-free survival rates of 65% and 20%, respectively, showing statistically significant differences between the two groups ( P<0.05). The 1, 3, and 5-year overall survival rates for the liver resection group were 100%, 100%, and 78.3%, respectively, while for the radiofrequency ablation group, they were 100%, 100%, and 82.2%, respectively, with no statistically significant difference ( P>0.05). Conclusions:Both liver resection and radiofrequency ablation can be considered as treatment options for gastrointestinal stromal tumor liver metastasis, with comparable long-term efficacy. Liver resection has a clear advantage in terms of local tumor control compared to radiofrequency ablation, which has the advantages of fewer complications, faster recovery, and shorter hospital stay.

The stenosis and embolization of internal fistula vessels directly affect the clinical treatment effect of maintenance hemodialysis patients, and the study of the mechanism of internal fistula stenosis has become a research hotspot in recent years. Previous studies mainly focused on the hemodynamics and pathophysiology of blood vessel wall, and there were few studies on molecular biology and its related signaling pathways. This paper reviews the hemodynamics of the vascular pathway of internal arteriovenous fistula (AVF), the pathophysiological mechanism, molecular biology, and changes in various signaling pathways of AVF dysfunction at home and abroad, in order to provide references for the study of AVF dysfunction.

Objective To investigate the effect of Gegen Qinlian Decoction on liver energy metabolism and free fatty acid(FFA)in rats with insulin resistance(IR).Methods IR rat model was established by feeding 60%fat high-fat diet for 13 consecutive weeks.SD rats were randomly divided into normal group,model group,Rosiglitazone(5 mg·kg-1)group and Gegen Qinlian Decoction low-,medium-and high-dose groups(1.65,4.96,14.86 g·kg-1),with 6 rats in each group.Intragastric administration was given once a day,continuous administration intervention lasted for 16 weeks.Determination of IR-related indicators:serum fasting insulin(FINS),fasting blood glucose(FPG),calculate the IR index;HPLC method was established for the determination of adenosine triphosphate(ATP),adenosine diphosphate(ADP)and adenosine monophosphate(AMP)in rat liver tissue;ELISA was used to determine the content of FFA in rat liver tissue.The contents of serum total cholesterol(TC)and triglyceride(TG)were detected by automatic biochemical analyzer.The pathological changes of liver tissue were observed by HE staining.Results(1)After the model replication,compared with the normal group,the FINS,FPG levels and IR index of the model group were significantly increased(P＜0.05).(2)Compared with the normal group,the levels of FINS,FPG and IR index in the model group were significantly increased(P＜0.01),the contents of ATP,ADP and AMP in liver tissue were significantly decreased(P＜0.01),the content of FFA was significantly increased(P＜0.01),and the levels of TC and TG in serum were significantly increased(P＜0.05).Liver cells arranged in disorder,fatty degeneration,and there are a large number of lipid droplets.Compared with the model group,the FINS level and IR index of rats in each administration group were significantly decreased(P＜0.05,P＜0.01),and the FPG level of rats in the Rosiglitazone group was significantly decreased(P＜0.05).The contents of ADP and AMP in liver tissue of rats in each administration group were significantly increased(P＜0.05,P＜0.01),and the contents of ATP in liver tissue of rats in low-,medium-and high dose-groups of Gegen Qinlian Decoction were significantly increased(P＜0.05,P＜0.01).The content of FFA in liver tissue of rats in Rosiglitazone group and Gegen Qinlian Decoction low-and high-dose groups was significantly decreased(P＜0.01).The serum TC level of rats in the low-and high-dose groups of Gegen Qinlian Decoction was significantly decreased(P＜0.05,P＜0.01),and the serum TG level of rats in the Rosiglitazone group and the low-dose group of Gegen Qinlian Decoction was significantly decreased(P＜0.05,P＜0.01).The steatosis of hepatocytes in rats of each administration group was alleviated to varying degrees,and the lipid droplets were reduced,and the pathological damage was improved.Conclusion Gegen Qinlian Decoction may improve liver lipid metabolism disorder and restore lipid and energy balance by regulating energy metabolism and reducing FFA level,thus improving IR.

H 1-antihistamines are widely used in the treatment of various allergic diseases, but there are still many challenges in the safe and rational use of H 1-antihistamines in pediatrics, and there is a lack of guidance on the prescription review of H 1-antihistamines for children.In this paper, suggestions are put forward from the indications, dosage, route of administration, pathophysiological characteristics of children with individual difference and drug interactions, so as to provide reference for clinicians and pharmacists.

Objective: To study the effect of stem cell factor (SCF) on the angiogenic ability of cocultured dental pulp stem cells (DPSCs) and human umbilical vein endothelial cells (HUVECs). Methods : This study has been reviewed and approved by the Ethics Committee. The experiment was split into the HUVECs, SCF+HUVECs, DPSCs+HUVECs, and SCF+DPSCs+HUVECs groups. A mixture of SCF and culture medium was used to prepare a mixed culture medium with an SCF concentration of 100 ng/mL. In vitro coculture of DPSCs and HUVECs was performed at a 1∶5 ratio. CCK-8 proliferation assay was used to observe the proliferative capacity of cells in each group on days 1, 3, 5, and 7. Wound healing and Transwell migration assays were used to detect the effect of SCF on cell migration under either direct or indirect coculture conditions, respectively. In vitro angiogenesis experiments were performed to detect the angiogenic capacity of the cells in each group. The vascular endothelial growth factor A (VEGFA) concentration in the cell culture supernatant was detected using ELISAs, and the protein expression levels of CD31, CD34, and VEGFA were detected using Western blot analysis. Results : Wound healing and Transwell migration experiments showed that SCF significantly promoted the migration of cocultured DPSCs and HUVECs (P<0.05). The in vitro angiogenesis experiment showed that the number of branches and the total length of branches of tubular structures in the SCF+DPSCs+HUVECs group were significantly greater than those of the other groups (P<0.05), and the expression levels of the vascular-related proteins CD31, CD34, and VEGFA in this group were greater (P<0.01). Conclusion SCF can enhance the migration and in vitro angiogenesis of cocultured DPSCs and HUVECs.

ObjectiveBased on ultra performance liquid chromatography-quadrupole time-of-flight mass spectrometry （UPLC-Q-TOF/MS）， the changes of endogenous markers in rat plasma at the different stage， namely modeling and administration of Shenling Baizhusan （SLBZS）， and the mechanism of SLBZS in the treatment of ulcerative colitis （UC） were studied. MethodIn the modeling stage， rats were randomly divided into normal group， spleen deficiency with dampness retention-UC （SDDR-UC） and pure-UC （P-UC） model group. In the administration stage， SLBZS was given to the above two different model groups. After modeling and administration， rat plasma was collected and determined by UPLC-Q-TOF/MS. The mobile phase was 0.1% formic acid aqueous solution （A）-acetonitrile （B） for gradient elution （in positive ion mode：0-2 min， 99%A； 2-9 min， 99%-73%A； 9-10 min， 73%-44%A； 10-13 min， 44%-38%A； 13-19 min， 38%-28%A； 19-21 min， 28%-2%A； 21-23 min， 2%A； 23-25 min， 2%-10%A； 25-27 min， 10%-99%A； in negative ion mode：0-2 min， 85%A； 2-3 min， 85%-65%A； 3-5.5 min， 65%-44%A； 5.5-8 min， 44%-25%A； 8-10 min， 25%-2%A； 10-16 min， 2%-85%A）. The electrospray ionization （ESI） temperature was 120 ℃ under the positive and negative ion modes， and the acquisition range was 50-1 000. Partial least squares-discriminant analysis （PLS-DA） was used to analyze the changes of endogenous metabolites in the above two different model rats from the different stage. MetaboAnalyst 5.0 was used to analyze the metabolic pathways of these identified metabolites. ResultSixteen potential biomarkers were screened and identified in the modeling stage， among which 11 potential biomarkers were common in the two model rats， which mainly affected the primary bile acid biosynthesis pathway. Twenty-three potential biomarkers were screened and identified during the administration stage， among which 3 potential biomarkers were shared by the two model rats， and SDDR-UC and P-UC model rats had 11 and 9 potential biomarkers， respectively. It mainly affected 6 pathways such as purine metabolism， pentose phosphate pathway， pyrimidine metabolism， retinol metabolism， primary bile acid biosynthesis and steroid hormone synthesis. ConclusionThe primary bile acid biosynthesis pathway appears in the different stage of modeling and administration of UC， showing a dynamic change process. The therapeutic effect of SLBZS on SDDR-UC rats may be related to inhibiting the expression of nuclear transcription factor -κB （NF-κB） signaling pathway， activating farnesoid X receptor （FXR） and enhancing the expression of cytochrome P450.

Objective:To explore the effects of necroptosis specific inhibitor-1 (Nec-1) on brain injury in rats after cardiac arrest and its mechanism.Methods:A total of 24 Sprague-Dawley (SD) rats were divided into Sham group, model group and Nec-1 group ( n = 8 per group) according to random number table method. In the Sham group, only general surgical procedures were underdone without inducing cardiac arrest. In the model group, the rats were subjected to asphyxial cardiac arrest followed by cardiopulmonary resuscitation (CPR) at 6 minutes after cardiac arrest. In the Nec-1 group, Nec-1 of 1 mg/kg was administered after cardiac arrest, and CPR was performed at 6 minutes after cardiac arrest. At 72 hours after CPR, neurological deficit scores (NDS) were assessed, serum S100B levels were measured by enzyme linked immunosorbent assay (ELISA), receptor-interacting protein 3 (RIP3) expression in cerebral cortex and hippocampus was observed under immunofluorescence and positive rate was calculated, and the levels of RIP3 protein expression in brain were analyzed by Western blotting. Results:At 72 hours after CPR, the rats in the model group showed obvious necroptosis and injury in brain. Compared with the Sham group, the NDS scores in the model group were significantly decreased [57.0 (52.7, 60.0) vs. 80.0 (80.0, 80.0), P < 0.05], the serum S100B was significantly increased (ng/L: 44.9±4.5 vs. 18.6±1.5, P < 0.05), the percentages of RIP3 positive cells in cerebral cortex and hippocampus were significantly elevated [cerebral cortex: (31.7±4.8)% vs. (11.6±3.2)%, hippocampus: (28.4±0.8)% vs. (10.9±0.6)%, both P < 0.05], and the levels of RIP3 protein expression in brain were significantly increased [RIP3 protein (RIP3/GAPDH): 0.708 (0.642, 0.722) vs. 0.408 (0.253, 0.504), P < 0.05]. After Nec-1 intervention, necroptosis and injury in brain were obviously improved. Compared with the model group, the NDS scores at 72 hours after CPR in the Nec-1 group were significantly increased [70.5 (68.5, 71.7) vs. 57.0 (52.7, 60.0), P < 0.05), the serum S100B was significantly decreased (ng/L: 31.9±2.7 vs. 44.9±4.5, P < 0.05), the percentages of RIP3 positive cells in cerebral cortex and hippocampus were significantly lowered [cerebral cortex: (23.7±4.1)% vs. (31.7±4.8)%, hippocampus: (20.4±0.4)% vs. (28.4±0.8)%, both P < 0.05], and the levels of RIP3 protein expression in brain were significantly declined [RIP3 protein (RIP3/GAPDH): 0.437 (0.379, 0.507) vs. 0.708 (0.642, 0.722), P < 0.05]. Conclusion:Nec-1 attenuated necroptosis of brain cells by inhibiting the expression of RIP3 protein, so as to reduce brain injury after cardiac arrest in rats.

Purpose: This study aimed to elucidate whether lncRNA ZFAS1 is involved in neuronal apoptosis and inflammation in temporal lobe epilepsy (TLE). Materials and Methods: Ninety-six TLE patients were recruited, and their peripheral venous blood was gathered to determine Zfas1 expression with polymerase chain reaction. Neurons were separated from hippocampal tissue of newborn SD rats, and siZfas1 or pcDNA3.1-Zfas1 was transfected into the neurons. Inflammatory cytokines released by neurons were determined, and neuronal activities were evaluated through MTT assay, colony formation assay, and flow cytometry. Results: Serum levels of Zfas1 were higher in TLE patients than in healthy controls (p<0.05). Furthermore, Zfas1 expression in neurons was raised by pcDNA3.1-Zfas1 and declined after silencing of Zfas1 (p<0.05). Transfection of pcDNA-Zfas1 weakened the viability and proliferation of neurons and increased neuronal apoptosis (p<0.05). Meanwhile, pcDNA3.1-Zfas1 transfection promoted lipopolysaccharide-induced release of cytokines, including tumor necrosis factor-α, interleukin (IL)-1, IL-6, and intercellular adhesion molecule-1 (p<0.05), and boosted NF-κB activation by elevating the expression of NF-κB p65, pIκBα, and IKKβ in neurons (p<0.05). Conclusion Our results indicated that lncRNA ZFAS1 exacerbates epilepsy development by promoting neuronal apoptosis and inflammation, implying ZFAS1 as a promising treatment target for epilepsy.

Objective: To evaluate the endothelial function in obstructive sleep apnea syndrome(OSAS) children and to identify related factors of endothelial dysfunction. Methods: This was a cross-sectional study. Children with habitual snoring (snoring ≥3 nights per week) admitted to the ward of otolaryngology, head and neck surgery, Beijing Children′s Hospital were recruited to this study between 1^st June 2015 and 1^st March 2016. All children aged 3 to 11 years and of them 245 were boys and 110 were girls. All subjects underwent an overnight polysomnography (PSG), as well as endothelial function testing. All subjects were grouped into primary snoring (PS) and OSAS group according to the obstructive apnea hypopnea index (OAHI). T test or Wilcoxon test were used to compare the differences in PSG results between the two groups, and univariate and multivariate correlation analyses were used to explore the relevant factors affecting the endothelial function. Results: A total of 355 subjects were enrolled and 248 had OSAS, and 107 had PS. There were no significant differences in age, gender and body mass index (BMI) Z-score between the two groups (all P>0.05). OSAS group had higher OAHI, oxgen desaturation index and respiratory related arousal index (5.2 (2.2, 13.2) vs. 0.4 (0.1, 0.7), 4.1 (2.0, 13.1) vs. 0.5 (0.1, 1.0), 2.5 (1.0, 4.8) vs. 0.4 (0.1, 0.9), Z=-14.957, -11.790, -10.378, all P<0.01), and lower minimum oxygen saturation and reactive hyperemia index (RHI) than those of PS (0.89 (0.85, 0.92) vs. 0.94 (0.91, 0.95), 1.2±0.2 vs. 1.1±0.1, Z=-9.337, t=5.354, P<0.01). Univariate regression analysis showed that RHI was linearly correlated with age (parameter estimate=0.017, P<0.01), gender (parameter estimate=0.065, P<0.01), OAHI (parameter estimate=-0.023, P<0.01), oxygen desaturation index (parameter estimate=-0.019, P<0.01), respiratory related arousal index (parameter estimate=-0.031, P<0.01), and oxygen saturation nadir (parameter estimate=0.067, P=0.045). The relationship between BMI Z-score and RHI was quadratic. Multivariate regression analysis showed that age (parameter estimate=0.015, P<0.01), BMI Z-score (parameter estimate=0.040, P<0.01), BMI Z-score quadratic form (parameter estimate=-0.010, P<0.01), respiratory related arousal index (parameter estimate=-0.020, P<0.01) were independently correlated with RHI. Conclusions Children with OSAS have significant endothelial dysfunction compared with PS. Frequent arousals due to obstructive respiratory events during sleep may be a candidate risk factor for endothelial dysfunction in children with OSAS.

Objective:To investigate the underlying molecular mechanisms of brain injury in rats after cardiac arrest and cardiopulmonary resuscitation (CPR) by observing necroptosis of brain cells and changes of 90 cytokines in brain tissue.Methods:Sprague-Dawley (SD) rats were divided into Sham group ( n = 10) and cardiac arrest group ( n = 10) according to random number table method. The model of asphyxia cardiac arrest for 6 minutes followed by CPR model was established. Tracheal intubation in Sham rats were routinely performed without inducing cardiac arrest. Neurological deficit score (NDS) was evaluated, blood samples were collected and rats were sacrificed, then serum S100B level was measured by enzyme linked immunosorbent assay (ELISA) on the third day after CPR. Necroptotic cells in brain were detected by immunofluorescence staining. The levels of 90 cytokines expression in brain were measured by antibody array. The relative ratio of the two groups of protein expression ≥ 1.5 or ≤ 0.5 and P < 0.05 represented the differential expression protein. Results:There were 8 rats successfully resuscitated and 2 died in cardiac arrest group. There were 8 rats selected in Sham group to match the sample size. Compared with Sham group, the NDS score of cardiac arrest group was significantly lower [63.0 (62.5, 64.3) vs. 80.0 (80.0, 80.0), P < 0.01], and the level of serum S100B was significantly higher (ng/L: 47.96±10.16 vs. 16.56±5.60, P < 0.01). More necroptotic cells in cerebral cortex and hippocampus were found in cardiac arrest group [proportion of cells positive for TdT-mediated nick end labeling (TUNEL) and negative for caspase-3: (15.70±0.32)% vs. (8.00±0.28)% in cortex, (20.80±1.35)% vs. (9.00±4.00)% in hippocampus, both P < 0.05]. The levels of inflammatory cytokines [cytokine-induced neutrophil chemoattractant (CINC-2α/β, CINC-3), interferon-γ (IFN-γ)] and signal protein c-Src kinase (CSK) in brain significantly increased after cardiac arrest as compared to Sham group levels (ratio of cardiac arrest group to Sham group: CINC-2 α/β was 2.503±0.428, P = 0.024; CINC-3 was 2.369±0.142, P = 0.005; IFN-γwas 3.149±1.362, P = 0.044; CSK was 1.887±0.105, P = 0.001). However, the levels of neuroprotective cytokines ciliary neurotrophic factor (CNTF), glial cell-derived neurotrophic factor receptor (GFR α-1, GFR α-2), growth hormone (GH), growth hormone receptor (GHR), granulocyte-macrophage colony-stimulating factor (GM-CSF) and anti-inflammatory protein interleukin-10 (IL-10) significantly decreased after cardiac arrest (ratio of cardiac arrest group to Sham group: CNTF was 0.341±0.137, P = 0.036; GFRα-1 was 0.461±0.164, P = 0.044; GFRα-2 was 0.447±0.017, P = 0.033; GH was 0.450±0.136, P = 0.024; GHR was 0.508±0.128, P = 0.022; GM-CSF was 0.446±0.130, P = 0.035; IL-10 was 0.502±0.211, P = 0.017). Conclusions:Necroptosis is involved in brain injury after cardiac arrest. The molecular mechanisms of brain injury may be related to inflammatory response, neurogenesis disorder and impaired survival of nerve cells.