Objective To evaluate the efficacy and safety of modified decompressive craniectomy in treatment of traumatic brain injury and its impact on the serum levels of inflammatory mediators and prognosis. Methods According to different surgical methods, 82 patients with traumatic brain injury admitted to the department of neurosurgery of Nanyang Central Hospital from June 2020 to January 2022 were divided into standard group (n=41) and modified group (n=41). The standard group was given standard decompressive craniectomy, and the modified group was given modified decompressive craniectomy. The intraoperative blood loss, operation time and hospital stay, the levels of neuron-specific enolase (NSE), S-100 calcium binding protein B (S-100β), C-reaction protein (CRP), procalcitonin (PCT), and interleukin-6 (IL-6) before operation, 6 hours after operation, and 3 days after operation, Glasgow Outcome Scale (GOS), incidence of complications, and incision healing grade 1 month after operation were compared between two groups. Results Compared with standard group, the hospital stay was significant shorter in modified group (P<0.05), and intraoperative blood loss and operation time were no significant difference in modified group (P>0.05). At 6 hours and 3 days after operation, the levels of NSE, S-100β, CRP, PCT and IL-6 in modified group were lower than those in standard group (P<0.05). Compared with standard group, the good prognosis rate based of GOS was higher in modified group [82.9% (34/41) vs. 63.4% (26/41), P<0.05]; the total incidence of complications was lower in modified group [2.4%(1/41) vs. 19.5%(26/41), P<0.05]; and the grade of incision healing was better in modified group (P<0.05). Conclusions Modified decompressive craniectomy in the treatment of traumatic brain injury could reduce stress of brain injury and surgical trauma, and the incidence of complications, help to speed up the postoperative recovery process, improve the rate of good prognosis and the grade of incision healing. Its efficacy and safety is better than standard decompressive craniectomy.

Objective To explore the association between triglyceride glucose (TyG) index and TyG-body mass index (TyG-BMI) and the prevalence of metabolic associated fatty liver disease (MAFLD) in the elderly men. Methods Totally 2290 elderly men were selected from January to December in 2021 in the Second Medical Center of Chinese PLA General Hospital, and divided into MAFLD group (n=1322) and non-MAFLD group (n=968). Multivariate logistic regression was used to analyze the association between TyG index, TyG-BMI and MAFLD. The receiver operating characteristic (ROC) curve was drawn to explore the predictive value of TyG index and TyG-BMI with MAFLD in the elderly men. Results Two thousand two hundred and ninety elderly men were (74.3±10.1) years old, and an average BMI of (24.63±2.70) kg/m². BMI, γ‑glutamyl transaminase (γ‑GT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), serum creatinine (Scr), thyroid stimulating hormone (TSH), free triiodothyronine (FT₃), the rate of smoking and drinking, and the prevalence of hypertension, diabetes, hyperuricemia, high triglyceride (TG), low high density lipoprotein cholesterol (HDL-C), hyperuricemia, thyroid nodules and cholelithiasis were all significantly higher in non-MAFLD group than those in MAFLD group (P<0.05), while the age of MAFLD group was lower than that of non-MAFLD group (P=0.003). Multivariate logistic regression analysis showed that the risk of MAFLD in patients of TyG quartile groups Q₂, Q₃, Q₄ was 1.667 (95%CI 1.257-2.236, P<0.001), 2.004 (95%CI 1.482-2.710, P<0.001) and 5.420 (95%CI 3.266-8.995, P<0.001) times higher than that of TyG Q₁, respectively. The risk of MAFLD in patients of TyG-BMI Q₂, Q₃, Q₄ was 2.215 (95%CI 1.549-3.167, P<0.001), 2.809 (95%CI 1.723-4.580, P<0.001) and 2.513 (95%CI 1.253-5.040, P=0.009) times higher than that of TyG-BMI Q₁, respectively. The ROC curve showed that areas under the curve (AUC) of MAFLD predicted by TyG index and TyG-BMI were 0.717 (95%CI 0.696-0.738) and 0.840 (95%CI 0.823-0.856), and the best cut-off values were 8.63 and 205.20, respectively. Moreover, the ROC curve showed that AUC of MAFLD in the elderly men without hyperlipidemia or diabetes predicted by TyG index and TyG-BMI were 0.653 (95%CI 0.622-0.684) and 0.840 (95%CI 0.818-0.862), and the best cut-off values were 8.42 and 202.66, respectively. In addition, AUC, accuracy, specificity, sensitivity, positive predictive value and negative predictive value predicted by TyG-BMI were higher than those by TyG index. Conclusions TyG index and TyG-BMI are significantly associated with MAFLD in the elderly men. Both TyG index and TyG-BMI have certain predictive value for the prevalence of MAFLD in the elderly men, and TyG-BMI may be better.

Chronic obstructive pulmonary disease (COPD) is a frequent and common disease of the respiratory system. The problem of low early diagnosis rate, low treatment compliance, and low treatment standardization has persisted in the diagnosis and treatment of COPD. Heterogeneity found in clinical practice is one of the reasons why COPD is difficult to treat. In recent years, it has been gradually recognized that the occurrence and development of COPD are closely related to the immune state of the body. At present, it become one of the hot spots in clinical and basic research that searching for specific and sensitive cell and molecular biomarkers to early diagnose acute exacerbation and subtype differentiation of COPD, which ultimately provide individual diagnosis and treatment strategies for COPD patients. This review focuses on the research progress of immunocytes and immunologic factors as biomarkers to different phenotypes and progression of COPD in recent years, providing a reference for the research on diagnosis and treatment of COPD.

Esophagogastric variceal bleeding in cirrhotic patients is associated with high mortality if not adequately managed. Standardized treatment of esophagogastric variceal bleeding includes adequate resuscitation maneuvers, restrictive transfusion policy, antibiotic prophylaxis, pharmacologic therapy, and endoscopic therapy. After this initial treatment, the most appropriate therapy to prevent both early and late rebleeding must be instituted following a risk stratification strategy. Placing a preemptive transjugular intrahepatic portosystemic shunt in high-risk patients, as soon as possible after admission, to achieve early control of bleeding has proved to improve survival. The present review will focus on the initial management of patients with acute esophagogastric variceal bleeding, including general management and assessment, pharmacotherapy, as well as the available endoscopic, interventional and salvage treatments, trying to provide reference for standardizing the treatment process of such patients, in order to improve their survival rate.

Objective To investigate the effect and potential mechanism of angiopoietin 1 (Ang1) on choroidal neovascularization (CNV) of rats. Methods A total of 30 Norwegian (BN) rats aged 6-8 weeks were randomized into three groups (n=10/group): normal group, model group, and Ang1 treatment group. The normal group was not processed, but the other two groups used multi-wavelength krypton laser to model the eyes of BN rats. We then performed fundus fluorescein angiography 14 days post-surgery. After confirming the success of the surgery, on the next day, the Ang1 treatment group received 200 μg/L Ang1 20 μl through vitreous cavity injection, while the other two groups received an equal volume of saline. After another 10-day, we performed Fundus fluorescein angiography examination, measured the CNV area through choroidal patching using FITC-labeled dextran (FITC-dextran) cardiac perfusion, and observed the retinal-choroidal structure changes of rats by Hematoxylin-eosin staining (HE) staining. We also detected the expression of Ang1, Rap1, GAPRap1, and vascular endothelial-cadherin (VE-cadherin) in the retinal-choroidal-sclera complex by Western blotting. Next, we cultured the rat choroidal vascular endothelial cells (RCVECs). When the cells were in the logarithmic growth phase, we stimulated these cells with vascular endothelial growth factor (VEGF) and cultured them for 24 hours, and divided into negative control group (siRNA-NC group), GAPRap1-siRNA group and GAPRap1-siRNA+Ang1 group. We further transfected cells with siRNA-NC (siRNA-NC group) or GAPRap1 small interfering RNA (GAPRap1-siRNA group and GAPRap1-siRNA+Ang1 group). In the GAPGAPRap1 small interfering RNA transfected cells, 6 hours after transfection, we set aside some cells coculture with 200 μg/L Ang1 (GAPRap1-siRNA+Ang1 group). After another 24 hours, we extracted and quantified the expression levels of GAPRap1, Rap1, and VE-cadherin by Western blotting. We detected the expression of VE-cadherin using immunofluorescence. Results Compared with normal group, in model group, the neovascular leakage area and choroidal damage degree significantly increased (P<0.01), the expression of GAPRap1 and VE-cadherin proteins significantly reduced (P<0.05), and the expression of Rap1 had no significant change (P>0.05). Compared with model group, in the Ang1 treatment group the neovascular leakage area and choroidal damage degree were significantly reduced (P<0.01), the expression of GAPRap1 and VE-cadherin proteins in the choroid and cells significantly increased (P<0.01), the expression of Rap1 had no statistical change (P>0.05). In choroidal tissue, the expression of Ang1 protein in Ang1 treatment group was significantly higher than that in the other two groups (P<0.01). In the cell experiment, the expressions of GAPRap1 and VE-cadherin in GAPRap1-siRNA group were significantly lower than those in the GAPRap1-siRNA+Ang1 group and the siRNA-NC group (P<0.01), while the expression of Rap1 had no significant change (P>0.05). The immunofluorescence results showed that the fluorescence of VE-cadherin in the GAPRap1-siRNA group was significantly lower than that in the GAPRap1-siRNA+Ang1 group and siRNA-NC group (P<0.001). Conclusion Ang1 can reduce the leakage of choroidal neovascularization in rats, which has an inhibitory effect on CNV growth, and its mechanism may be related to the enhancement of cell adhesion through the GAPRap1-VE-cadherin pathway.

Objective To investigate the central mechanism of glial cells of the dorsal reticular nucleus (DRt) in the modulation of chronic orofacial pain after removal of experimental occlusal interference(EOI) in rats. Methods Twenty-four male SD rats (180-200 g) were randomly divided into three groups (8 in each group): sham group, EOI hyperalgesia maintaining group (occlusal interference appliance removed on day 8 after wearing 0.4 mm thick crowns), EOI hyperalgesia maintaining+DRt damage group (EOI hyperalgesia maintaining rats were injected with ibotenic acid to damage DRt). The non-reflexive behaviors of the three groups were evaluated by using orofacial operant test on 7, 10, 14 d after model establishment. Nine male SD rats were randomly divided into three groups (3 in each group): sham group, EOI hyperalgesia maintaining group (day 8 after wearing 0.4 mm thick crowns, before removal of EOI), EOI hyperalgesia maintaining group 6 d (6 days after EOI removed on day 8). DRt sections were obtained and processed for immunofluorescence staining for glai fibrillary acidic protein (GFAP) and OX-42. The levels of expression were hemi-quantitatively analyzed to evaluate the fluorescence area and fluorescence intensity of astrocytes and microglia. Results EOI hyperalgesia maintaining group and EOI hyperalgesia maintaining+DRt damage group exhibited lower feeding time in orofacial operant test, which implied hyperalgesia (P<0.05). The hyperalgesia in EOI hyperalgesia maintaining group persisted after the removal of EOI, and the difference was statistically significant at 10 d and 14 d compared with sham group (P<0.05), while the hyperalgesia in the EOI hyperalgesia maintaining+DRt damage group showed a rebound trend, and the difference was not statistically significant at 10 d and 14 d compared with sham group (P>0.05). The total feeding time at 14 d significant longer compared with the EOI hyperalgesia maintaining group (P<0.05). Semi-quantitative analysis of immunofluorescence staining showed that the fluorescence area and fluorescence intensity of GFAP and OX-42 in EOI hyperalgesia maintaining group did not show any increase compared with that of sham group (P>0.05), whereas the fluorescence area and fluorescence intensity of GFAP as well as the fluorescence area of OX-42 in EOI hyperalgesia maintaining group 6 d were significantly higher (P<0.05). The fluorescence area and fluorescence intensity of GFAP and OX-42 in EOI hyperalgesia maintaining group did not show any increase compared with that of EOI hyperalgesia maintaining group 6 d (P>0.05). Conclusion DRt was involved in the persistent maintenance of hyperalgesia in the EOI model after removal of occlusal interference, in which astrocyte and microglia activation in DRt were the central mechanisms for the maintenance of hyperalgesia.

Objective To study the expression profile and possible roles of ferroptosis-related genes in a bleomycin-induced murine model of pulmonary fibrosis. Methods Twelve 6-7-week-old male C57BL/6 mice were randomly divided into model group and control group, 6 in each group. The model group received nasal inhalation of bleomycin, while the control group was given an equal volume of normal saline. Lung tissues were collected 3 weeks after modeling. Pathological changes and collagen deposition in lungs were observed by HE and Masson staining. Prussian blue staining was used to observe the level of iron accumulation in lung tissue. Total RNA was extracted for PCR Array to identify ferroptosis-related differentially expressed genes (DEGs). Functional analysis for DEGs was performed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Expression levels of DEGs were verified by RT-qPCR analysis. Results Compared with control group, fibrosis and obvious iron deposition occured in mouse lung tissue of model group. The PCR array identified five ferroptosis-related genes that expression significantly decreased in model group compared with control group including carbonic anhydrase 9 (CA9), cysteinyl-tRNA synthetase 1 (CARS1), heat shock transcription factor 1 (HSF1), NADPH oxidase 3 (NOX3) and mitochondrial ferritin (FTMT)(P<0.05). GO functional enrichment analysis and KEGG pathway analysis showed that the DEGs were mainly related to temperature homeostasis, NADPH oxidase complex, and carbonate dehydratase activity, and were involved in nitrogen metabolism, aminoacyl-tRNA biosynthesis and legionellosis signaling pathways. RT-qPCR verification confirmed that the expression levels of CA9, CARS1, HSF1 and FTMT were significantly decreased in model group than those in control group (P<0.05). Conclusions Change of the expression of genes related to ferroptosis has been confirmed in a murine model of pulmonary fibrosis induced by bleomycin. The result indicates that ferroptosis is involved in the process of idiopathic pulmonary fibrosis, ferroptosis-associated DEGs might provide potential targets for clinical treatment of it.

Objective To investigate the effect and its mechanism of vitamin A (VA) deficiency (VAD) on regulating alveolar macrophage polarization in neonatal rats with acute respiratory distress syndrome (ARDS). Methods Sixty neonatal SD rats were divided into vitamin A normal control group (VAN ctrl group, n=10), normal vitamin A group (VAN group, n=10), vitamin A deficiency control group (VAD ctrl group, n=10), vitamin A deficiency group (VAD group, n=10), vitamin A rescue control group (VADR ctrl group, n=10) and vitamin A rescue group (VADR group, n=10). The VADR ctrl and VADR groups were injected with 25 µg VA at the second day after birth. All the neonatal rats were given lipopolysaccharide (LPS) to establish the neonatal rat model of ARDS, and serum and lung tissue samples were collected. The weight of newborn rats in each group was recorded before modeling, the May-Grunwald-Giemsa staining was performed to observe the number of main cells in bronchoalveolar lavage fluid (BALF), and HE staining was used to detect the pathological damage of lung tissue. The polarization of alveolar macrophages was evaluated by immunofluorescence. qRT-PCR and ELISA were performed to detected the expression of downstream markers of the polarization of alveolar macrophages inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-10 and arginase-1 (Arg-1). The content of superoxide dismutase (SOD) and malondialdehyde (MDA) in lung tissue were calculated by colorimetric method, and cell apoptosis was detected by TUNEL. Results Compared with the neonatal rats in VAN group, the neonatal rats in VAD group had lower body weight, small physique, and sparse hair, while the body weight and general condition of the newborn rats in the VADR group did not change significantly. Compared with the VAD group, the neonatal rats in VADR group gained weight and shiny hair. Compared with VAN group, the lung damage of ARDS neonatal rats in VAD group was aggravated, the number of major cells in BALF increased, the M1 polarization of alveolar macrophages activated (P<0.05), the expression levels of M1 polarization markers iNOS, IL-6, TNF-α and CD86 increased significantly (P<0.05), the content of oxidative stress marker MDA and cell apoptosis increased (P<0.05), SOD activity decreased (P<0.05), while the levels of IL-10 and Arg-1 were not statistically significant (P>0.05); Compared with VAN group, there were no significant differences in macrophage M1 polarization, TNF-α, IL-6, SOD, MDA, IL-10 and Arg-1 in newborn rats in VADR group (P>0.05). Compared with VAD group, the lung damage of ARDS neonatal rats in VADR group was significantly reduced, the number of alveolar macrophages and the polarization of alveolar macrophages M1 decreased (P<0.05), the expression levels of M1 polarization markers iNOS, IL-6, TNF-α and CD86 decreased (P<0.05), the content of the oxidative stress marker MDA and cell apoptosis decreased (P<0.05), and the SOD activity enhanced (P<0.05). Conclusion VAD could regulate the M1 polarization of alveolar macrophages, up-regulated the expression of inflammatory markers downstream of M1 polarization, increased pulmonary oxidative stress and apoptosis, and aggravated ARDS in neonatal rats.

Objective To observe the changes of motor function and brain tissue transcriptomic profiles in mice with traumatic brain inury (TBI) by seawater immersion, and to explore its potential mechanism. Methods A total of 51 male C57/BL adult mice were randomly divided into sham surgery group, TBI group and TBI+seawater group (17 mice in each group). Behavior tests (rotating bar and balance beam tests) were performed at 1 d, 3 d and 7 d after injury to detect the changes of endurance and motor coordination ability in mice. Blood-brain barrier permeability (Evans blue staining) and brain tissue pathological changes (HE staining) were detected at 12 h and 24 h after injury. The expression levels of apoptosis-related proteins BCL-2 and Bax in brain tissues were detected with Western blotting 24 h after injury, and carry out brain tissue transcriptomics detection and analyze the related differentially expressed genes and signal pathways. Results Behavior tests showed that compared with the sham surgery group and TBI group, mice in TBI+seawater group had a significantly shortened time on the rotating bar (P<0.001) and spend a significantly prolonged time to pass through the balance beam (P<0.001) on 1 d, 3 d, and 7 d after injury. Evans blue staining showed that the EB permeation area of TBI+seawater group was significantly larger than that of the TBI group (P<0.05), and the EB permeation area at 24 h after injury was significantly smaller than that at 12 h after injury in both groups (P<0.05). HE staining results showed that the pathological damage in TBI+seawater group was worsened compared with TBI group. Western blotting results showed that 24 h after injury, the expression of Bax in TBI+seawater group was significantly increased (P<0.05) while the expression of Bcl-2 was significantly decreased (P<0.05) in injured brain tissue compared with TBI group. Transcriptomic analysis showed that there were 625 differentially expressed genes in the injured brain tissue of TBI+seawater group compared with TBI group (P<0.05), and the expression levels of p53-related genes and natural killer cell-related genes were significantly increased (P<0.05). Pathway enrichment analysis showed that natural killer cell immune regulation, lymphocyte immune regulation, and cytokine-cytokine receptor binding pathways were significantly enriched (P<0.05). Conclusions Seawater immersion can promote apoptosis of damaged neural cells in TBI mice, leading to impaired motor coordination and endurance in mice. Endogenous apoptosis mediated by p53 and immune regulation mediated by natural killer cells may be associated with this phenomenon.

Objective To explore the effect and mechanism of acid-sensitive ion channel 3 (ASIC3) expression on visceral sensitivity in irritable bowel syndrome (IBS) rats and the possible regulatory mechanisms of signalling pathways. Methods From the 2nd day postpartum, 6 neonatal rats and their mother were kept in their original cages as control group; the rest of the neonatal rats were separated from their mother to make IBS models. After the neonatal rats grow into rats, use abdominal withdrawal reflex (AWR) score to screen 16 rats that were successful in IBS modeling, and they were randomly divided into neonatal maternal separation (NMS) group and NMS+APETx2 group, with 8 rats in each group. NMS+APETx2 group was given the ASIC3-specific blocker APETx2 100 μg/kg intraperitoneally for 1 week while NMS group and control group were intraperitoneally injected with same amount of normal saline. Visceral pain response was measured by abdominal withdraw reflex (AWR) score, the intestinal transmission rate was measured by ink staining, the 5-hydroxytrgptamine (5-HT) level in colonic tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the expression levels of 5-HT4 receptor and ASIC3 in colonic tissue were measured by immunohistochemistry. Results Compared with control group, rats in NMS group showed significantly increased AWR scores at colorectal pressures of 40, 60, 80 mmHg, decreased intestinal transmission rate, intestinal 5-HT, ASIC3 and 5-HT4 receptor expression increased, all with statistically significant differences (P<0.01). There was no significant difference in AWR score and intestinal propulsion rate in NMS+APETx2 group compared with control group (P>0.05), but the expression levels of 5-HT, ASIC3 and 5-HT4 receptors increased compared with control group with significant difference (P<0.01). Compared with NMS group, the application of ASIC3-specific blocker APETx2 in NMS+APETx2 group resulted in lower AWR scores, enhanced intestinal transmission rate, and the expression levels of 5-HT, ASIC3 and 5-HT4 receptor decreased, and the differences were statistically significant (P<0.05 or P<0.01). Conclusion ASIC3 expression takes part in the generation of high sensitivity in viscera of IBS rat, which may be related to the enhance of 5-HT pathway activation.