ObjectiveTo explore the surgical treatment of deep chest wall infection, improve the cure rate and reduce the recurrence rate.MethodsThe clinical data of 655 patients with deep chest wall infection treated in Yanda Hospital and Beijing Royal Integrative Medicine Hospital from June 2015 to June 2020 were retrospectively analyzed. There were 450 males and 205 females, aged 55.6±12.8 years. There were 8 patients with chest wall infection after tumor necrosis, 15 patients after radiotherapy and 632 patients after thoracotomy (612 patients after cardiovascular surgery and 20 patients after general thoracic surgery). Among them, 649 patients underwent debridement and reconstruction of chest wall defect with muscle flap.ResultsThe average operation time was 95±65 min, the average intraoperative blood loss was 180±100 mL, and the average postoperative hospital stay was 13±6 d. Of the 649 patients who underwent muscle flap reconstruction after debridement, 597 patients recovered within 2 weeks, and the primary wound healing rate was 94.4%. Twenty-three (3.5%) patients died. The median follow-up time was 25 (2-40) months. Among the remaining 632 patients, 20 recurred, with a recurrence rate of 3.1% (20/632).ConclusionPedicled muscle flap after thorough debridement of deep chest wall infection is one of the best methods to repair chest wall defect with pedicled muscle flap.
Human tumor necrosis factor-related apoptosis-inducing ligand (hTRAIL) might be developed as a novel anti-tumor drug due to its selective cytotoxicity in tumor cells. The predicted Macaca mulatta TRAIL (mmTRAIL) is highly homologous to hTRAIL in nucleotide acid as well as amino acid sequence, suggesting that mmTRAIL might induce apoptosis of human cancer cells. However, the cytotoxicity of mmTRAIL in human cancer cells has not been investigated. In this paper, it is reported that the gene encoding mmTRAIL has been cloned by using reverse-transcriptase polymerase chain reaction (RT-PCR) from monkey peripheral blood mononuclear cells (PBMCs) in our laboratory. Subsequently, an expression plasmid was constructed by inserting mmTRAIL gene into pQE30 plasmid. After induction by addition of Isopropylβ-D-1-Thiogalactopyranoside (IPTG), mmTRAIL was expressed. MmTRAIL was recovered from supernatant of sonicated bacteria by Ni-NTA agarose affinity chromatography. SDS-PAGE and gel filtration chromatography demonstrated that mmTRAIL forms trimer in solution. In vitro assays indicated that mmTRAIL was cytotoxic to human COLO205 tumor cells but not to normal cells at low concentration of nanomole. In addition, antitumor effect of mmTRAIL was evaluated in mice bearing human COLO205 tumor xenografts. Intratumorally injected mmTRAIL significantly inhibited growth of tumor grafts. These results suggested that mmTRAIL was valuable as candidate drug for cancer-targeted therapy.
Objective To explore effects of macrophage migration inhibitory factor (MIF) inhibitor ISO-1 on intestinal injury in acute necrotic pancreatitis in pregnancy (ANPIP) rat. Methods Twenty-four pregnant SD rats were randomly averagely divided into three groups: a sham operation (SO) group, an ANP group, and an ANP model plus ISO-1 treatment group (ISO-1 group). A rat model of ANP was induced by the retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. The rats were killed and the inferior vena cava blood and the tissues of pancreas and jejunum were harvested at 12 h after the operation. The serum amylase (AMY), lipase (LIP), diamine oxidase (DAO), interleukin (IL)-1β, and IL-6 levels were measured. The pancreatic and jejunal tissues were taken for the pathological examination scoring. The immunohistochemical method was used to detect the expression of the MIF, nuclear factor (NK)-κB, or tumor necrosis factor (TNF)-α protein. Results ① Compared with the SO group, the serum AMY, LIP, DAO, IL-1β, and IL-6 levels were increased in the ANP group (P<0.050), which in the ISO-1 group were decreased as compared with the ANP group, the DAO, IL-1β, and IL-6 levels had significant differences (P<0.050), but the AMY and LIP levels had no significant differences (P>0.050). ② The pathological points of the pancreas and jejunum tissues were increased in the ANP group as compared with the SO group, which were significantly decreased in the ISO-1 group as compared with the ANP group (P<0.050). ③ The average integrated optical density divide by area of the NF-κB,TNF-α, and MIF were significantly increased in the ANP group as compared with the SO group, which were significantly decreased in the ISO-1 group as compared with the ANPgroup (P<0.050). Conclusions MIF inhibitor ISO-1 could protect intestinal injury in ANPIP rat. It is suggested that MIF is one of mechanisms in ANPIP with intestinal injury and might be correlated with activities of TNF-α and NF-κB.
As a new treatment option after conventional corticosteroids and immunomodulatory drugs, biologics have been widely used in the clinical management of non-infectious uveitis in many countries due to their approved efficacy and safety. Anti-tumor necrosis factor-alpha monoclonal antibody is the most commonly used one. However, the guidance on its standardized application is lacking. The Ocular Immunology Group of Immunology and Rheumatology Academy in Cross-Straits Medicine Exchange Association compiled the Chinese expert consensus on treatment of non-infectious uveitis with anti-tumor necrosis factor-alpha monoclonal antibody. This evidence-based consensus is made according to the principle of consensus building and combines the clinical experience of the experts. Twelve recommendations are formatted on the application of Adalimumab and Infliximab. The interpretation of this consensus point will help improve the normative and effective application of anti-tumor necrosis factor-alpha monoclonal antibody in ophthalmologists, rheumatologists and immunologists.
ObjectiveTo explore the serum concentrations of complement C1q tumor necrosis factor related protein 5 (CTRP5) in patients with acute exacerbations and stable stage of chronic obstructive pulmonary disease (COPD), and analyze the correlation of CTRP5 with high sensitivity C-reactive protein (hs-CRP) and FEV1/FVC and FEV1%pred.MethodsThirty hospitalized patients with acute exacerbation of COPD and 30 outpatients with stable COPD according with diagnostic criteria and inclusive criteria were sampled successively. At the same time 30 healthy volunteers were selected as normal control. All subjects were measured the concentrations of CTRP5 and hs-CRP in serum and lung function test was performed.ResultsThe serum CTRP5 and hs-CRP concentrations of the acute exacerbation group was higher than those in the stable group and the control group. The serum CTRP5 and hs-CRP concentrations of the stable group was also higher than those of the control group. The FEV1/FVC of the acute exacerbation group was lower than those of the stable group and the control group; and the FEV1/FVC of the stable group was lower than that of the control group. The FEV1%pred of three groups by analysis indicated the difference was statistically significant. Further pairwise comparisons demonstrated that the FEV1%pred of two COPD groups were lower than that of the control group but the FEV1%pred of the acute exacerbation group and stable group was not significantly different. The correlation analysis of the acute exacerbation group and the stable group demonstrated that the levels of serum CTRP5 and hs-CRP were postively correlated and the level of serum CTRP5 was negatively correlated with FEV1/FVC and FEV1%pred.ConclusionsThe level of CTRP5 in serum of COPD patients is increased. No matter in acute exacerbation or stable phase, the level of serum CTRP5 is positively correlated with hs-CRP and negatively correlated with FEV1/FVC and FEV1%pred, which suggests that CTRP5 is involved in the pathogenesis of COPD but the exact mechanism needs further study.
Objective To investigate effect of different resuscitation liquids and different resuscitation methods on contents of interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) in early resuscitation process of rats with traumatic hemorrhagic shock. Methods Sixty-four healthy SD rats (450–550 g) were chosen and divided into 4 groups randomly and averagely: crystal liquid limited resuscitation group, colloidal liquid limited resuscitation group, 7.5% NaCl limited resuscitation group, and colloidal liquid non-limited resuscitation group. There were 16 rats in each group. All the experimental rats were weighed before intraperitoneal injection of pentobarbital sodium anesthesia. Animal model was established via Chaudry’s method. The rats were killed and the abdominal aorta bloods were drew on hour 2, 6, 12, and 24 after recovering from anesthesia. The contents of IL-8 and TNF-α in plasmas were detected by enzyme linked immunosorbent assay. Results The contents of IL-8 and TNF-α among three kinds of limited resuscitation groups on hour 6 after resuscitation were significantly higher than those on hour 2 after resuscitation (P<0.05) and reached the peaks, then began to decrease. On hour 12 after resuscitation, the contents of IL-8 and TNF-α were decreased continuously among three kinds of limited resuscitation groups (P<0.05). The contents of IL-8 and TNF-α in the colloidal liquid non-limited resuscitation group at each point time were significantly higher than those among three kinds of limited resuscitation groups (P<0.05), which in the crystal liquid resuscitation group were significantly lower than those in the other limited liquid resuscitation groups (P<0.05). Conclusions In process of liquid resuscitation of rats with traumatic hemorrhagic shock, limited resuscitation method is better than that of non-limited resuscitation method. Among three kinds of limited resuscitation methods, crystal resuscitation liquid is more effective than the other two resuscitation liquids in prohibiting releases of IL-8 and TNF-α in rats with traumatic hemorrhagic shock.
The aim of this article is to study the effect of tumor necrosis factor alpha (TNF-α) on the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) in keratoconus fibroblasts in vitro. Normal cornea and keratoconus fibroblasts were extracted using enzyme digestion method and were cultured in the medium containing TNF-α (0, 10 and 100 ng/mL). The expression of MMPs proteins in the supernatant of corneal fibroblasts and the expression of TIMPs in the normal cornea and keratoconus fibroblasts were detected by Western blot and real-time quantitative polymerase chain reaction respectively. The active form of MMP1 could be detected in the supernatant of keratoconus fibroblasts and upregulated by TNF-α. TNF-α could increase the protein expression of MMP2, MMP3, MMP9 in the supernatant of keratoconus fibroblasts and decrease the gene expression of TIMP1, TIMP2 in keratoconus fibroblasts. The increased MMPs and the decreased TIMPs can increase the degradation of the extracellular matrix. TNF-α may play an important role in the occurrence and development of keratoconus by regulating the expression of MMPs/TIMPs.
摘要:目的: 研究蛻皮甾酮對非酒精性脂肪性肝病大鼠模型腫瘤壞死因子α(TNFα)與核因子κB(NFκB)表達的影響，并探索其可能的作用機制。 方法 :健康成年SD大鼠36只,隨機分為正常對照組12只與實驗組24只;正常對照組喂以普通基礎飼料,實驗組應用高脂飼料喂養。實驗12周末時將造模成功的實驗組大鼠隨機分為模型組與蛻皮甾酮治療組2個亞組,每組12只;正常對照組喂以普通基礎飼料至16周,模型組繼續應用改良高脂飼料喂養至16周,蛻皮甾酮治療組大鼠在高脂飲食同時加用蛻皮甾酮灌胃。實驗16周末時處死3組所有大鼠;檢測肝臟指數,血清與肝組織生化指標及肝組織病理改變;ELISA法檢測肝臟TNFα水平;免疫組化檢測各組大鼠肝組織中核因子κB蛋白表達情況。 結果 :蛻皮甾酮治療組血清膽固醇(TC)、丙氨酸氨基轉移酶(ALT)和天門冬氨酸氨基轉移酶(AST)明顯低于模型組(212±058比263±024,Plt;005;5336±1848比8460±3627,P＜005;14020±3595比24359±3638,P＜001);蛻皮甾酮治療組與模型組相比肝組織丙二醛(MDA)水平降低明顯(18454±1645比23928±2376,P＜001),超氧化物歧化酶(SOD)活力增加顯著(942±052比518±043,P＜001),肝臟指數顯著降低(435±037比504±046,P＜001)，肝組織脂肪變性程度和炎癥活動度明顯減輕(546±037比630±049,P＜001)。蛻皮甾酮治療組與模型組相比TNFα與核因子κB水平明顯減輕(4304±748比6156±727,2465±539比4504±746,P值均＜001)。 結論 :蛻皮甾酮具有改善高脂飲食誘發的非酒精性脂肪性肝病大鼠肝臟酶學功能,通過增加肝組織SOD的含量和減少MDA的含量來減輕肝組織氧化應激水平,減輕肝組織TNFα和核因子κB來減輕肝臟炎癥,發揮防治非酒精性脂肪性肝病的作用。Abstract: Objective: To investigate the effect and possible mechanism of ecdysterone on the expression of tumor necrosis factoralpha (TNFα) and nuclear factor κ B (NFκB) in rats with nonalcoholic fatty liver disease of rats. Methods : A total of 36 male Sprague Dawley rats were randomly divided into two groups, who were fed with highfat diet (experimental group, n=24) and normal basic food (normal control, n=12) respectively. At the end of the 12th week, the experimental group was randomly divided into two subgroups: model group and ecdysterone group, each group contained 12 rats. From the 13th week, the rats in the normal control group and model group were lavaged with normal sodium, and the rats in the ecdysterone group were lavaged with ecdysterone at 10 mg·kg-1·d-1. At the end of the 16th week, all rats were weighed, narcotized, sacrificed, and the liver index, biochemical indicators in serum and liver tissues and the hepatic pathological changes were observed. The expression of TNFα was detected by ELISA and the expression of NFκB was measured by immunohistochemical staining. Results : At the end 16th week in ecdysterone group, the serum levels of cholesterol (TC), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were reduced markedly (212±058 vs 263±024 and 5336±1848 vs 8460±3627, both P＜005; 14020±3595 vs 24359±3638, P＜001); the tissue content of malondialdehyde (MDA) was decreased evidently (18454±1645 vs 23928±2376, P＜001), while the activity of superoxide dismutase (SOD) was enhanced notably (942±052 vs 518±043, P＜001); the liver index was decreased significantly in comparison with that inmodel group (435±037 vs 504±046, P＜001); the degree of fatty degeneration and inflammation were relieved dramatically (546±037 vs 630±049, P＜001). The expression of TNFα and the levels of NFκB were significantly lower (4304±748 vs 6156±727 and 2465±539 vs 4504±746, both P＜001) in ecdysterone group compared with model group. Conclusion : The effects of ecdysterone in preventing NAFLD in rats could be related to the increase of SOD content in hepatic tissue and the decrease of MDA content, tumor necrosis factorα and NFκB.
Objective To summarize and evaluate the significance of tumor necrosis factor (TNF) tolerance, and to understand the general characteristics and known molecular mechanisms of different forms of tolerance, including the roles of transcription factors, signaling systems and receptors. Method The relevant literatures at home and abroad in recent years were collected and readed, and the content related to TNF tolerance was summarized. ResultsTNF tolerance could be produced after TNF pretreatment, and be divided into absolute tolerance and induced tolerance. TNF tolerance was related to a variety of interrelated and interdependent intracellular signal transduction. There was cross tolerance between TNF and lipopolysaccharide. Conclusions TNF tolerance may represent a protective mechanism, participating in the termination of inflammation and preventing excessive or persistent inflammation. TNF tolerance may also trigger immune paralysis, leading to severe inflammatory diseases, such as sepsis. The understanding of TNF tolerance can promote the diagnosis of inflammation related diseases or the implementation of treatment methods, so as to achieve more accurate evaluation and treatment.
ObjectiveTo construct a predictive model for acute kidney injury (AKI) after coronary artery bypass grafting (CABG) based on uromodulin (UMOD) and tumor necrosis factor receptor-associated factor 6 (TRAF6). MethodsPatients undergoing CABG treatment at Tianjin Chest Hospital from 2022 to 2024 were prospectively enrolled. Based on whether they developed AKI post-surgery, patients were divided into the an AKI group and a non-AKI group. Differences in UMOD, TRAF6, blood urea nitrogen (BUN), serum creatinine (SCr), β-N-acetylglucosaminidase (NAG), and SCr clearance rate at different time points were compared between the two groups. Predictive models for AKI after CABG were constructed at various time points, and the predictive efficacy of the models for AKI was analyzed. ResultsA total of 70 patients were included, with 22 in the AKI group [13 males and 9 females, aged 55-72 (67.91±4.91) years] and 48 in the non-AKI group [32 males and 16 females, aged 56-72 (68.07±4.67) years]. The UMOD levels in the AKI group were lower than those in the non-AKI group at various time points including before surgery (t=34.283, P<0.001), postoperative 2 h (t=29.590, P<0.001), 4 h (t=30.705, P<0.001), 8 h (t=26.620, P<0.001), 12 h (t=29.671, P<0.001), and 24 h (t=31.397, P<0.001). The TRAF6 levels in the AKI group were higher than those in the non-AKI group at all these time points (P<0.001). Multivariate analysis showed that higher levels of TRAF6, BUN, SCr, NAG, and lower levels of UMOD and SCr clearance rate were risk factors for AKI after CABG (P<0.05). The receiver operating characteristic curve analysis showed that the area under the curve of the predictive model at postoperative 12 h was significantly higher than that of the remaining models. The risk of AKI after CABG was: log (Y)=12.333?1.582×UMOD+1.270×TRAF6+1.356×BUN+1.356×SCr+1.355×NAG?1.254×SCr clearance rate. ConclusionIn the occurrence process of AKI after CABG, TRAF6 exacerbates renal injury by activating inflammatory signals and promoting cell apoptosis, while UMOD alleviates renal injury by regulating renal tubular function and protecting renal tubular epithelial cells. Through the simulation analysis of the two biomarkers combined with renal injury indicators at postoperative 12 h, the occurrence of AKI after CABG can be effectively predicted.