Objective The aim of this study was to investigate the effects of morusin on the migration and invasion of human glioblastoma U87 cells,and to explore its mechanism of action.Methods The Cell Counting Kit-8(CCK-8)was used to detect the effect of morusin on proliferation of U87 cells.Wound-healing and Transwell assays were used to detect the effects of morusin on mi-gration and invasion of U87 cells.Western blot was employed to detect the effect of morusin on the expressions of MMP-2 and Vimen-tin in U87 cells.Results The results of CCK-8 assay showed that morusin(1,2,4,and 6μg/mL)could significantly inhibit the pro-liferation of U87 cells compared to the 0 μg/mL morusin(P<0.001).The results of wound-healing assay showed that the migration rates of morusin-treated groups(2,4,and 6 μg/mL)were(20.597±1.225)%,(14.734±1.528)%and(7.811±1.496)%,respec-tively,which were significant lower than that in the 0 μg/mL group(40.566±3.284)%(P<0.001).The results of Transwell assay showed that the invasion number of U87 cells treated with morusin at the concentrations of 2,4,and 6 μg/mL was 85.000±6.557,41.000±6.245,and 13.333±3.215,respectively,which were significant lower than that in the 0 μg/mL group(116.667±14.572)(P<0.001).The results of Western blot showed that the expression of Vimentin in U87 cells increased gradually accompanying with the increase of morusin concentrations,while the expression of MMP-2 decreased gradually accompanying with the increase of morusin concentrations(P<0.001).Conclusion Morusin can effectively inhibit the migration and invasion ability of U87 cells,and its effect is positively correlated with the concentration of morusin within a certain range.

The risk of patient infection inevitably increases with the use of more invasive operations in the intensive care unit(ICU),including endotracheal tubes,indwelling catheter,central venous catheter,etc.The preparation of antibacterial coatings is an effective way to solve such infections.Antibacterial coatings,such as silver nanoparticles coating,zinc oxide coating,methyl blue coating,antimicrobial peptides coating,and nano titanium dioxide(TiO2)coating,can effectively prevent the formation of biofilms on the surface of implant materials.As a photocatalyst,TiO2 has excellent photocatalytic and antibacterial activity,non-toxic and biocompatible properties,strong physical and chemical stability,and long-lasting antibacterial properties,which makes it high value for research.This review summarizes the bactericidal mechanism and clinical application of TiO2,offering valuable reference for clinical practice.

Sepsis is a syndrome of systemic inflammatory response in which the body′s response to infection is dysregulated, and is characterized by persistent infection, excessive inflammation and immunosuppression, etc. It often leads to organ dysfunction and can be life threatening, and also a common complication after trauma. The pathogenesis of post-traumatic sepsis is still unclear at present due to the complexity of its etiology, progression and prognosis. Multi-omics technology is a method to combine two or more single omics for comprehensive analysis, which can reveal the interaction network among the disease-associated molecules from multiple perspectives and aspects and is of great significance for the analysis of the pathogenesis of post-traumatic sepsis. To this end, the authors reviewed the research progress on the role of multi-omics technology in elucidating the pathogenesis of post-traumatic sepsis from the perspectives of genomics, transcriptomics, proteomics, metabolomics, single-cell transcriptomics and combination of multi-omics technologies, etc so as to provide a reference for the researches on post-traumatic sepsis.

Humans ; Asthma/drug therapy* ; Biological Therapy

Objective:To explore the expression pattern of aryl hydrocarbon receptor (AhR) in mice peritoneal macrophages (PMs) after major trauma and analyze the effects of enhanced AhR expression on the inflammatory cytokine level and bactericidal ability after trauma.Methods:The experimental study method was used. Forty 6-8-week-old male C57BL/6J mice (the same mouse age, sex, and strain below) were divided into control group, post trauma hour (PTH) 2 group, PTH 6 group, and PTH 12 group according to the random number table (the same grouping method below), with 10 mice in each group. Mice in the latter 3 groups were constructed as severe trauma model with fracture+blood loss, while mice in control group were left untreated. The primary PMs (the same cells below) were extracted from the mice in control group, PTH 2 group, PTH 6 group, and PTH 12 group when uninjured or at PTH 2, 6, and 12, respectively. Then the protein and mRNA expressions of AhR were detected by Western blotting and real-time fluorescence quantitative reverse transcription polymerase chain reaction, respectively, and the gene expressions of AhR signaling pathway related molecules were analyzed by transcriptome sequencing. Twenty mice were divided into control group and PTH 6 group, with 10 mice in each group, and the PMs were extracted. The level of ubiquitin of AhR was detected by immunoprecipitation. Twelve mice were divided into dimethyl sulfoxide (DMSO) alone group, PTH 6+DMSO group, MG-132 alone group, and PTH 6+MG-132 group, with 3 mice in each group. After the corresponding treatment, PMs were extracted, and the protein expression of AhR was detected by Western blotting. Twenty mice were constructed as PTH 6 model. Then, the PMs were extracted and divided into empty negative control adenovirus (Ad-NC) group and AhR overexpression adenovirus (Ad-AhR) group. The protein expression of AhR was detected by Western blotting at 36 h after some PMs were transfected with the corresponding adenovirus. The rest cells in Ad-NC group were divided into Ad-NC alone group and Ad-NC+endotoxin/lipopolysaccharide (LPS) group, and the rest cells in Ad-AhR group were divided into Ad-AhR alone group and Ad-AhR+LPS group. The expressions of interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) in the cell supernatant were detected by enzyme-linked immunosorbent assay at 12 h after the corresponding treatment ( n=6). Twenty mice were obtained to extract PMs. The cells were divided into control+Ad-NC group, PTH 6+Ad-NC group, control+Ad-AhR group, and PTH 6+Ad-AhR group, and the intracellular bacterial load was detected by plate spread method after the corresponding treatment ( n=6). Data were statistically analyzed with one-way analysis of variance, least significant difference test, analysis of variance for factorial design, and independent sample t test. Results:Compared with 1.16±0.28 of control group, the protein expressions of AhR in PMs in PTH 2 group (0.59±0.14), PTH 6 group (0.72±0.16), and PTH 12 group (0.71±0.17) were all significantly decreased ( P<0.05). The overall comparison of the difference of AhR mRNA expression in PMs among control group, PTH 2 group, PTH 6 group, and PTH 12 group showed no statistical significance ( P>0.05). The AhR signaling pathway related molecules included AhR, AhR inhibitor, cytochrome P450 family member 1b1, cytochrome P450 family member 11a1, heat shock protein 90, aryl hydrocarbon receptor-interaction protein, and heat shock protein 70 interaction protein. The heat shock protein 90 expression of PMs in PTH 2 group was higher than that in control group, while the expressions of other molecules did not change significantly after trauma. Compared with that in control group, the level of ubiquitin of AhR in PMs in PTH 6 group was increased. Compared with that in DMSO alone group, the protein expression of AhR in PMs in PTH 6+DMSO group was decreased, while that in PMs in MG-132 alone group had no significant change. Compared with that in PTH 6+DMSO group, the protein expression of AhR in PMs in PTH 6+MG-132 group was up-regulated. At transfection hour 36, compared with that in Ad-NC group, the protein expression of AhR in PMs in Ad-AhR group was increased. At treatment hour 12, compared with those in Ad-NC+LPS group, the expressions of IL-6 and TNF-α in PM supernatant of Ad-AhR+LPS group were significantly decreased (with t values of 4.80 and 3.82, respectively, P<0.05). The number of intracellular bacteria of 1×10 6 PMs in control+Ad-NC group, PTH 6+Ad-NC group, control+Ad-AhR group, and PTH 6+Ad-AhR group was (3.0±1.8), (41.8±10.2), (1.8±1.2), and (24.2±6.3) colony forming unit, respectively. Compared with that in PTH 6+Ad-NC group, the number of intracellular bacteria of PMs in PTH 6+Ad-AhR group was significantly decreased ( t=3.61, P<0.05). Conclusions:Ubiquitin degradation of AhR in PMs of mice after major trauma results in decreased protein expression of AhR. Increasing the expression of AhR in post-traumatic macrophages can reduce the expressions of LPS-induced inflammatory cytokines IL-6 and TNF-α, and improve the bactericidal ability of macrophages after trauma.

Objective:To explore the prognostic value of tumor deposits (TD) by number and anatomical distribution in gastric cancer (GC) patients without lymph node metastasis.Methods:From Aug 2012 to Aug 2018 all 91 GC patients undergoing radical gastrectomy and without nodal metastasis at Yijishan Hospital of Wannan Medical College were enrolled in this study. Patients were divided into L1, L2, and L3 groups according to the number of TD and into Q1 and Q2 groups according to the anatomical regions of the TD.Results:The 3-year overall survival (OS) rates of groups L1, L2, and L3 were 58.9%, 52.1%, and 31.5%, respectively ( χ2=9.769, P=0.008). The 3-year OS rates of groups Q1 and Q2 were 58.9% and 7.1% ( χ2=46.310, P<0.001). The number of TD, their distribution, neural invasion, vascular invasion, tumor size, and pT stage were all related to prognosis by univariate analysis (all P<0.05). Tumor size>4 cm ( HR=2.460, 95% CI:1.307-4.629, P=0.005), distribution of TD (non-perigastric)( HR=3.959, 95% CI:2.077-7.545, P<0.001), neural invasion ( HR=4.299,95% CI:1.953-9.461, P<0.001), and pT 4 stage ( HR=2.283, 95% CI:1.250-4.171, P=0.007) were independent risk factors for prognosis by multivariate analysis. Conclusion:The distribution of TD (non-perigastric) is an independent risk factor for poor prognosis in gastric cancer patients after radical gastrectomy and with negative lymph node metastasis.

BACKGROUND: The presence of fibrosis is a criterion for subtype classification in the newly updated hypersensitivity pneumonitis (HP) guidelines. The present study aimed to summarize differences in clinical characteristics and prognosis of non-fibrotic hypersensitivity pneumonitis (NFHP) and fibrotic hypersensitivity pneumonitis (FHP) and explore factors associated with the presence of fibrosis. METHODS: In this prospective cohort study, patients diagnosed with HP through a multidisciplinary discussion were enrolled. Collected data included demographic and clinical characteristics, laboratory findings, and radiologic and histopathological features. Logistic regression analyses were performed to explore factors related to the presence of fibrosis. RESULTS: A total of 202 patients with HP were enrolled, including 87 (43.1%) NFHP patients and 115 (56.9%) FHP patients. Patients with FHP were older and more frequently presented with dyspnea, crackles, and digital clubbing than patients with NFHP. Serum levels of carcinoembryonic antigen, carbohydrate antigen 125, carbohydrate antigen 153, gastrin-releasing peptide precursor, squamous cell carcinoma antigen, and antigen cytokeratin 21-1, and count of bronchoalveolar lavage (BAL) eosinophils were higher in the FHP group than in the NFHP group. BAL lymphocytosis was present in both groups, but less pronounced in the FHP group. Multivariable regression analyses revealed that older age, <20% of lymphocyte in BAL, and ≥1.75% of eosinophil in BAL were risk factors for the development of FHP. Twelve patients developed adverse outcomes, with a median survival time of 12.5 months, all of whom had FHP. CONCLUSIONS Older age, <20% of lymphocyte in BAL, and ≥1.75% of eosinophil in BAL were risk factors associated with the development of FHP. Prognosis of patients with NFHP was better than that of patients with FHP. These results may provide insights into the mechanisms of fibrosis in HP.
Humans ; Bronchoalveolar Lavage Fluid ; Prospective Studies ; Alveolitis, Extrinsic Allergic/diagnosis* ; Fibrosis ; Carbohydrates

Pulmonary blast injury has become the main type of trauma in modern warfare, characterized by externally mild injuries but internally severe injuries, rapid disease progression, and a high rate of early death. The injury is complicated in clinical practice, often with multiple and compound injuries. Currently, there is a lack of effective protective materials, accurate injury detection instrument and portable monitoring and transportation equipment, standardized clinical treatment guidelines in various medical centers, and evidence-based guidelines at home and abroad, resulting in a high mortality in clinlcal practice. Therefore, the Trauma Branch of Chinese Medical Association and the Editorial Committee of Chinese Journal of Trauma organized military and civilian experts in related fields such as thoracic surgery and traumatic surgery to jointly develop the Clinical treatment guideline for pulmonary blast injury ( version 2023) by combining evidence for effectiveness and clinical first-line treatment experience. This guideline provided 16 recommended opinions surrounding definition, characteristics, pre-hospital diagnosis and treatment, and in-hospital treatment of pulmonary blast injury, hoping to provide a basis for the clinical treatment in hospitals at different levels.

Photohardening therapy, also known as photodesensitization therapy, refers to the phototherapy and photochemotherapy of idiopathic actinic dermatoses, and its goal is to improve the patients′ tolerance to sunlight and prevent disease flares. Its mechanisms of action involve a variety of cellular and inflammatory factors. This therapy is suitable for all idiopathic actinic dermatoses, with definite efficacy and good safety. However, the treatment specificity usually leads to poor compliance. The development of UVA1 rush hardening and home phototherapy is expected to solve this problem.

Objective:To investigate serum lipidomic profiles in patients with chronic actinic dermatitis (CAD), and to search for biomarkers of CAD.Methods:A retrospective analysis was conducted. Serum samples were collected from 46 patients with CAD and 16 age- and gender-matched healthy controls in the Guangzhou Institute of Dermatology from April 2011 to December 2021. Changes in serum lipid composition and expression were assessed by liquid chromatography-mass spectrometry. Principal component analysis, partial least squares discriminant analysis, and orthogonal partial least squares discriminant analysis were performed to screen differential biomarkers, and receiver operating characteristic (ROC) curve analysis was conducted to screen diagnostic markers. Comparisons of the age and gender distribution between groups were performed using t test and chi-square test, respectively. Results:The 46 CAD patients were aged from 30 to 84 (60.39 ± 10.52) years, including 41 males and 5 females; the 16 healthy controls were aged from 50 to 89 (59.81 ± 10.72) years, including 14 males and 2 females; there were no significant differences in the age or gender distribution between the two groups (age: t = 0.19, P = 0.853; gender: χ2 = 0.03, P = 0.859). Totally, 4 136 lipid molecules belonging to 40 subclasses were identified in the serum samples from CAD patients as well as healthy controls. Twenty-two differential lipid molecules were identified between the CAD patients and healthy controls, belonging to 9 subclasses (triglycerides, sphingomyelin, phosphatidylserine, phosphatidylethanolamine, monofatty acid glycerides, lysophosphatidylcholine, hexose ceramide, diglycerides, and cardiolipin). When the combinations of triglycerides (37.7e) and Na, those of monoglycerides (22.3) and NH 4, or those of phosphatidylserine (18.0_18.1) and H served as diagnostic markers separately, the areas under the ROC curve (AUCs) were all > 0.8, and the AUCs of 16 differential lipid molecules were all > 0.7. Conclusion:The serum lipid composition differed between healthy controls and CAD patients, and the combinations of triglycerides (37.7e) and Na, those of monoglycerides (22.3) and NH 4, and those of phosphatidylserine (18.0_18.1) and H may be promising biomarkers for the diagnosis of CAD.