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AimsMicroRNA-183 ( miR-183) is known to play important roles in osteoarthritis (OA) pain. The aims of this study were to explore the specific functions of miR-183 in OA pain and to investigate the underlying mechanisms.MethodsClinical samples were collected from patients with OA, and a mouse model of OA pain was constructed by surgically induced destabilization of the medial meniscus (DMM). Reverse transcription quantitative polymerase chain reaction was employed to measure the expression of miR-183, transforming growth factor α (TGFα), C-C motif chemokine ligand 2 ( CCL2), proinflammatory cytokines (interleukin (IL)-6, IL-1β, and tumour necrosis factor-α ( TNF-α)), and pain-related factors (transient receptor potential vanilloid subtype-1 ( TRPV1), voltage-gated sodium 1.3, 1.7, and 1.8 ( Nav1.3, Nav1.7, and Nav1.8)). Expression of miR-183 in the dorsal root ganglia (DRG) of mice was evaluated by in situ hybridization. TGFα, CCL2, and C-C chemokine receptor type 2 ( CCR2) levels were examined by immunoblot analysis and interaction between miR-183 and TGFα, determined by luciferase reporter assay. The extent of pain in mice was measured using a behavioural assay, and OA severity assessed by Safranin O and Fast Green staining. Immunofluorescent staining was conducted to examine the infiltration of macrophages in mouse DRG.ResultsmiR-183 was downregulated in tissue samples from patients and mice with OA. In DMM mice, overexpression of miR-183 inhibited the expression of proinflammatory cytokines ( IL-6, IL-1β, TNF-α) and pain-related factors ( TRPV1, Nav1.3, Nav1.7, Nav1.8) in DRG. OA pain was relieved by miR-183-mediated inhibition of macrophage infiltration, and dual luciferase reporter assay demonstrated that miR-183 directly targeted TGFα.ConclusionOur data demonstrate that miR-183 can ameliorate OA pain by inhibiting the TGFα- CCL2/ CCR2 signalling axis, providing an excellent therapeutic target for OA treatment. Cite this article: Bone Joint Res 2021;10(8):548–557.

Infection can hinder the process of wound healing, so it is important to begin antibacterial treatment quickly after a wound forms. Plasma activated water (PAW) can inactivate a variety of common wound infection bacteria. In this study, we compared the effects of PAW prepared with portable surface discharge plasma equipment and medical alcohol on wound healing in a mouse full-thickness skin wound model. The effectiveness of wound healing processes in mice was ranked accordingly: PAW treatment group &gt, medical alcohol treatment group &gt, control group. In order to further understand the mechanism of PAW in promoting wound healing, we tested the expression levels of the pro-inflammatory factors interleukin (IL)-1β and IL-6, the anti-inflammatory factor IL-10, and vascular endothelial growth factor (VEGF). The results showed that PAW promoted the release of pro-inflammatory factors and anti-inflammatory factors from the wounds in mice, which allowed the mice in the treatment group to transition out of the inflammatory period early and enter the next stage of wound healing. The expression level of VEGF in the wounds of mice in the PAW treatment group was higher, which indicates that the microvessels around the wound in the PAW treatment group proliferated faster, and thus the wound healed faster. PAW biosafety experiments showed that PAW did not significantly affect the appearance, morphology, or tissue structure of internal organs, or blood biochemical indicators in mice. In general, PAW prepared via portable devices is expected to become more widely used given its convenience, affordability, and lack of side effects in promoting wound healing.

Qi Qi,* Xuemeng Qian,* Xinfang Zhu, Jiajing Cai, Rong Xia, Qi Zhang Department of Transfusion Medicine, Huashan Hospital, Fudan University, Shanghai, 200040, People’s Republic of China*These authors contributed equally to this workCorrespondence: Qi Zhang; Rong XiaDepartment of Transfusion Medicine, Huashan Hospital, Fudan University, 12 Urumqi Middle Road, Shanghai, 200040, People’s Republic of ChinaEmail friday0451@163.com; xiarongcn@126.comPurpose: Blood loss may be corrected with red blood cell transfusion, but may ultimately contribute to negative impacts. This study was a retrospective analysis to assess the impact of perioperative blood transfusion on hospital stay days in liver cancer patients.Methods: We retrospectively examined data from patients with primary liver cancer who underwent curative resection. Patients were divided into perioperative blood transfusion (PBT) and non-PBT groups. Data were given as means and SDs for continuous variables and as counts and percentage for categorical variables. The correlation between blood transfusion and hospital stay days was analyzed by Fisher’s exact test. Multivariable logistic regression analyses were used to identify independent predictors of length of hospital stays.Results: Totally 206/1031 patients (20.3%) were given perioperative transfusion. The mean length of hospital stay was 17.8 days in PBT and 13.9 days in non-PBT groups. Our multivariable logistic regression showed transfusion, total bilirubin, indirect bilirubin, and the ratio of albumin to bilirubin were all indicators of the length of hospital stay days. Perioperative transfusion was also associated with prolonged length of hospital stays (95% CI: 0.395– 0.811, p = 0.002). Transfusion also affected intrinsic coagulation factors (activated partial thromboplastin time, fibrinogen, platelet), inflammatory index (neutrocyte to lymphocyte ratio, monocyte), albumin and bilirubin levels.Conclusion: Perioperative transfusion of blood was associated with a significantly increased length of hospital stays probably via changing intrinsic coagulation and inflammatory factors and bilirubin levels in plasma.Keywords: primary liver cancer, transfusion, length of hospital stays, bilirubin, coagulation factor, inflammatory factor

To investigate the function and mechanism of Alpinetin on chronic obstructive pulmonary disease (COPD) in rat model. The markers of lung injury (body weight/pulmonary function) were measured, and the protein levels of inflammatory‐, apoptosis‐, and fibrotic‐related were determined by Western blot. HE/TUNEL/Masson staining was performed to investigate the mechanisms involved. The levels of inflammatory factors lung injury were detected by ELISA. The in vivo activities of all molecules were determined using a rat model. Alpinetin suppressed the injury of alveolus pulmonis cells occurred in vivo due to the decrease in inflammatory factors and biochemical markers by reduced the expression of TGF‐β1, α‐SMA, and TNF‐α (p, This work was to evaluate Alpinetin to COPD treatment by vivo study.

Cryptotanshinone (CRY) has been demonstrated to reverse reproductive disorders. However, whether CRY is effective in the treatment of polycystic ovary syndrome (PCOS) remains unknown. The aim of the present study was to evaluate the therapeutic potential of CRY in PCOS. A rat model of PCOS was established by daily injection of human chorionic gonadotropin and insulin for 22 days. Total body weight and ovarian weight, as well as the levels of luteinizing hormone (LH) and the LH to follicle‑stimulating hormone (FSH) ratio (LH/FSH) significantly increased in rats with PCOS, compared with controls. Moreover, the levels of testosterone (T), tumor necrosis factor (TNF)‑α and high‑mobility group box 1 protein (HMGB1) also increased. However, CRY treatment attenuated the increase in body weight, ovarian weight, LH, LH/FSH ratio, T, TNF‑α and HMGB1 levels, compared with the PCOS group. Treatment with CRY also reduced NF‑κB/p65, HMGB1 and toll‑like receptor (TLR)4 mRNA and protein expression levels in the ovarian tissue and granulosa cells, both in vitro and in vivo. Thus, CRY significantly mitigated the changes in body weight, ovary weight, hormone levels and inflammatory factor levels observed in rats with PCOS. Thus, CRY protects against PCOS‑induced damage of ovarian tissue, possibly through a regulatory pathway involving HMGB1, TLR4 and NF‑κB.

Background. Hypothermia is associated with many adverse clinical outcomes in pediatric patients, and thus, it is important to find an effective and safe method for preventing peri-operative hypothermia and its associated adverse outcomes in pediatric patients. This study aimed to investigate the effect of forced-air warming blankets with different temperatures on changes in the transforming growth factor-β (TGF-β), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-10 levels in children undergoing surgical treatment for developmental displacement of the hip (DDH). Methods. The study included 123 children undergoing surgery for DDH under general anesthesia. The patients were randomly assigned to three groups, using a random number table: the 32, 38, and 43°C groups according to the temperature setting of the forced-air warming blankets. For each patient, body temperature was recorded immediately after anesthesia induction and intubation (T0), at initial incision (T1), at 1 h after incision (T2), at 2 h after incision (T3), at the end of surgery (T4), immediately upon return to the ward after surgery (T5), and then at 12 h (T6), 24 h (T7), 36 h (T8), and 48 h (T9) after the surgery. The serum levels of TGF-β, TNF-α, IL-1β, and IL-10 were measured at T0 and T4 for all groups. Results. The number of patients with fever in the 38°C group was significantly less than those in the 32 and 43°C groups (χ2 = 6.630, P = 0.036). At T0, the body temperatures in the 38 and 43°C groups were significantly higher than that in the 32°C group (F = 17.992, P

Importance Dexmedetomidine inhibits the inflammatory response associated with cardiopulmonary bypass (CPB) and protects neural function. However, the mechanism of dexmedetomidine’s anti‐inflammatory pathway is unclear. Objective To investigate the effect of dexmedetomidine on the cognitive level and expression of inflammatory factors in children with congenital heart disease undergoing intraoperative CPB. Methods Ninety children with congenital heart disease were recruited and randomly divided into 3 groups of 30 children in each. In Group 1, a 1.0 µg·kg‐1·h‐1 intravenous bolus of dexmedetomidine was administered 10 minutes after induction of anesthesia, followed by a 0.2 µg·kg‐1·h‐1 infusion until the surgical incision. In Group 2, a 0.5 µg/kg intravenous bolus of dexmedetomidine was administered 10 minutes after induction of anesthesia, followed by a 0.1 µg·kg‐1·h‐1 infusion until the surgical incision. The control group was given physiological saline using the same method as in Groups 1 and 2. The serum levels of nuclear factor‐kappa B (NF‐κB), S‐100β protein, neuron‐specific enolase (NSE), tumor necrosis factor‐α (TNF‐α), and interleukin‐6 (IL‐6) were measured before the surgery (T1), at the end of CPB (T2), 2 hours after CPB (T3), 6 hours after CPB (T4), and 24 hours after CPB (T5). The Wechsler Intelligence Scale for children (WISC) was measured before the operation and at 3, 6, and 12 months after the operation to evaluate the neurodevelopmental state of the children. Results The levels of the NF‐κB, S‐100β protein, NSE, TNF‐α, IL‐6 were significantly higher at T2, T3, or T4 than before the surgery (T1) in the control group or the dexmedetomidine groups. However, the increases of NF‐κB, TNF‐α, IL‐6, S‐100β and NSE levels were significantly smaller in the dexmedetomidine groups than those in the control group (P < 0.017). The WISC scores were similar among the three groups before or after the operation. Interpretation The increases in NF‐κB, TNF‐α, and IL‐6 levels indicated aggravation of the inflammatory reaction and the increase S‐100β protein and NSE levels indicated that the nervous system was damaged. Administration of dexmedetomidine to children with congenital heart disease undergoing intraoperative CPB can inhibit the inflammatory response and may ameliorate the neurodevelopmental damage caused by CPB.

This study investigated the expression of inflammatory factors in tumour tissues, monocytes and blood of non-small cell lung cancer (NSCLC) patients taking tetrandrine (Tet) during low-dose radiotherapy. Sixty NSCLC patients underwent surgical resection of lung cancer after low-dose radiotherapy. Thirty patients did not take Tet (control group) and the other thirty patients took Tet during radiotherapy (experimental group). Lung cancer tissues were collected from patients, and tumour-adjacent tissues were collected as controls. Peripheral blood was collected on the morning of radiotherapy for mononuclear cell separation. Quantitative real-time polymerase chain reaction was used to determine mRNA expression, and Western blotting was used to measure protein expression. Enzyme-linked immunosorbent assay was used to determine the inflammatory factor contents in liquid samples. Cell proliferation was determined via MTT assay at 24, 48 and 72 h after transfection in A549 cells. Tet reduced COX-2 mRNA in serum and blood monocytes and decreased COX-2 protein expression in monocytes from patients with radiotherapy. It decreased the release of inflammatory factors to blood after radiotherapy. Combined treatment with low-dose radiotherapy and Tet tablets reduced the expression of Ki-67 protein in tumour tissues, and decreased the release of inflammatory factors from NSCLC tissues after radiotherapy. Combined treatment with low-dose radiotherapy and Tet tablets reduced the proliferation of cancer cells possibly through reducing inflammatory factors released by tumour tissues. The study demonstrates that Tet administration during low-dose radiotherapy reduces the release of inflammatory factors by NSCLC tissues, and decreases tumour proliferation. Tet plays an auxiliary role in NSCLC radiotherapy.

Objective: To explore levels of anti-oxidative molecules and inflammatory factors in patients with vascular dementia (VD) and their clinical significance. Methods: Sixty VD patients admitted in our hospital from January 2016 to January 2019 were classified into an experimental group, while another 60 healthy patients seeking physical examinations in the corresponding period were selected as a control group. Various indexes related to serum inflammatory factors and anti-oxidative molecules were compared among patients in such two groups. For the purpose of comparing anti-oxidative molecular expression levels and inflammatory factor levels in patients with VD of different severities, 60 cases in the experimental group were divided, based on a Mini-mental State Examination (MMSE) scale, into patients with mild symptoms (n=20, score: 21~26), patients with moderate symptoms (n=22, score: 10~20) and patients with severe symptoms (n=18, score: 0~9). Results: By contrast to the control group, levels of inflammatory factors (e.g., TNF-a, CRP and IL-б) in VD patients are all significantly increased and their differences show statistical significance (p

The tryptophan (TRP)-kynurenine (KYN) metabolic pathway is a main player of TRP metabolism through which more than 95% of TRP is catabolized. The pathway is activated by acute and chronic immune responses leading to a wide range of illnesses including cancer, immune diseases, neurodegenerative diseases and psychiatric disorders. The presence of positive feedback loops facilitates amplifying the immune responses vice versa. The TRP-KYN pathway synthesizes multifarious metabolites including oxidants, antioxidants, neurotoxins, neuroprotectants and immunomodulators. The immunomodulators are known to facilitate the immune system towards a tolerogenic state, resulting in chronic low-grade inflammation (LGI) that is commonly present in obesity, poor nutrition, exposer to chemicals or allergens, prodromal stage of various illnesses and chronic diseases. KYN, kynurenic acid, xanthurenic acid and cinnabarinic acid are aryl hydrocarbon receptor ligands that serve as immunomodulators. Furthermore, TRP-KYN pathway enzymes are known to be activated by the stress hormone cortisol and inflammatory cytokines, and genotypic variants were observed to contribute to inflammation and thus various diseases. The tryptophan 2,3-dioxygenase, the indoleamine 2,3-dioxygenases and the kynurenine-3-monooxygenase are main enzymes in the pathway. This review article discusses the TRP-KYN pathway with special emphasis on its interaction with the immune system and the tolerogenic shift towards chronic LGI and overviews the major symptoms, pro- and anti-inflammatory cytokines and toxic and protective KYNs to explore the linkage between chronic LGI, KYNs, and major psychiatric disorders, including depressive disorder, bipolar disorder, substance use disorder, post-traumatic stress disorder, schizophrenia and autism spectrum disorder.

BACKGROUND Osteoarthritis is a chronic degenerative disease with an incidence of 50% in people over 65 years old and 80% in people over 80 years old worldwide. It is the second leading reason of loss of working capacity after cardiovascular diseases and severely affects the society and families. Therefore, finding biological markers related to the diagnosis and treatment of osteoarthritis is of great significance in clinical practice. AIM To observe the changes and clinical value of serum inflammatory factors and miR-145 expression in patients with osteoarthritis before and after treatment. METHODS Eighty-three patients with knee osteoarthritis (observation group) who were admitted to our hospital from April 2013 to June 2015, and 60 healthy people (control group) during the same period were selected. After 4 wk of treatment, the levels of miR-145, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10 were compared between the control group and the observation group before treatment. The correlation of miR-145, TNF-α, IL-6, and IL-10 levels with visual analogue scale (VAS), Lysholm, and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scores was assessed by Pearson correlation analysis. The correlation of the expression of miR-145, TNF-α, IL-6, and IL-10 with Kellgren-Lawrence (K-L) grades was assessed by Spearman correlation analysis. The critical levels of miR-145, TNF-α, IL-6, and IL-10 in distinguishing different K-L grades were determined by receiver operating characteristic (ROC) curve analysis. RESULTS The expression level of miR-145 in the observation group was significantly higher than that in the control group before treatment (P < 0.05). After treatment, the expression level of miR-145 in the observation group was significantly lower than that before treatment (P < 0.05). The levels of TNF-α and IL-6 in the observation group were significantly higher than those in the control group (P < 0.05), and the level of IL-10 was significantly lower than that in the control group (P < 0.05). After treatment, the levels of TNF-α and IL-6 in the observation group were significantly lower than those before treatment (P < 0.05), and IL-I0 level was significantly higher than that before treatment (P < 0.05). VAS and WOMAC scores were both positively correlated with miR-145, TNF-α, and IL-6 (P < 0.05), and negatively correlated with IL-10 (P < 0.05), while Lysholm scores were negatively correlated with miR-145, TNF-α, and IL-6 (P < 0.05), and positively correlated with IL-10 (P < 0.05). K-L grades were positively correlated with miR-145, TNF-α, and IL-6 (P < 0.05), and negatively correlated with IL-10 (P < 0.05). The area under the ROC curve (AUC) and specificity of TNF-α in differentiating K-L grades I-II were the highest, which were 0.785 and 97.45%, respectively, and miR145 had the highest sensitivity of 94.59%; the AUC and sensitivity of IL-6 in differentiating K-L grades II-III were the highest, which were 0.766 and 97.30%, respectively, and TNF-α had the highest specificity of 86.68%. CONCLUSION MiR-145 and inflammatory factors have certain diagnostic value in osteoarthritis, and they are expected to become potential indicators for the diagnosis and evaluation of osteoarthritis in the future.

Purpose: To study the effect of early restrictive fluid resuscitation (EFR) on inflammatory and immune factors in patients with severe pelvic fracture (SPF ). Methods: A total of 174 SPF patients in the Department of Orthopaedics, the First Affiliated Hospital of Chengdu Medical College from July 2015 to June 2018 were involved in this study and divided into EFR group (n = 87) and control group (n = 87) using the random number table method. Conventional fluid resuscitation (CFR) was performed in control group, and EFR was performed in EFR group. The incidences of acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS) during rescue, successful rescue rate, blood transfusion volume, fluid input, and resuscitation time were compared between the two groups. The parameters including prothrombin time (PT), hematocrit (HCT), platelet (PLT) and blood lactate (BL) at the 4th hour after fluid resuscitation were recorded. The levels of inflammatory factors (TNF-α, IL-6, CRP) and immune factors (CD3＋, CD4＋, CD8＋, CD4＋/CD8＋) were compared between the two groups before treatment and 7 days after treatment. The revised acute physiologic and chronic health evaluation system and the sequential organ failure assessment scores were adopted for evaluation before treatment and 7 days after treatment. Results: The incidences of ARDS and MODS during rescue in EFR group were significantly lower than those in control group (p=0.015 and 0.010 respectively), and the successful rescue rate in EFR group was significantly higher than that in control group (p = 0.011). The blood transfusion volume, fluid input, resuscitation time in EFR group were significantly lower than those in control group (p = 0.016, 0.002 and 0.001 respectively). At the 4th hour after fluid resuscitation, PT and BL in EFR group were significantly lower than those in control group (p = 0.021 and 0.003 respectively), while HCT and PLT in EFR group were significantly higher than those in control group (p = 0.016 and 0.021 respectively). On day 7 after treatment, TNF-α, IL-6, CRP and CD8＋ in EFR group were significantly lower than those in control group (p = 0.003, 0.004, 0.007 and 0.003 respectively), while CD3＋, CD4＋ and CD4＋/CD8＋in EFR group were significantly higher than those in control group (p = 0.004, 0.000, 0.007 respectively). On day 7 after treatment, the revised acute physiologic and chronic health evaluation (APACHE) system and the sequential organ failure assessment (SOFA) scores in EFR group were significantly lower than those in control group. Conclusion: EFR can effectively eliminate inflammatory factors, improve immune function, maintain the stability of blood components, reduce the incidences of ARDS and MODS, and elevate the successful rescue rate in patients with SPF. Key words: Pelvic fracture; Resuscitation; Inflammatory factor; Immune factor

Background Chronic inflammation is crucial in the evolution of hepatocellular carcinoma (HCC). Circulatory and intratumoral inflammatory factors are always increased in these patients. In this study, we determined the value of pretherapy serum concentrations of several inflammatory cytokines for predicting survival among patients with HCC. Methods We retrospectively analyzed data of 85 patients with HCC with known alpha-fetoprotein (AFP) concentrations diagnosed at our institute. Before therapy, serum concentrations of interleukin (IL)-2, -4, -6, -10, interferon gamma, and tumor necrosis factor alpha were measured by flow cytometry. Correlations between these serum factors and clinical parameters were tested. Statistical analysis was made by using non-parametric procedures and survival analysis. The expression of IL-6 and the co-expression of IL-6 and CD11b, marker of myeloid cell in HCC tumor tissues, were evaluated by immunohistochemistry and immunofluorescence, respectively. Results The only independent predictor of overall survival (OS) was IL-6 [hazard ratio (HR), 3.338; 95% CI, 1.671 to 6.666; P=0.001]. OS was shorter among patients with high concentrations of both IL-6 (≥1.435 pg/mL) and AFP (≥400 ng/mL) than it was in those with high concentrations of either IL-6 or AFP; survival was significantly longer in patients with low concentrations of both markers (P

We have previously reported that 8-bromo-7-methoxychrysin (BrMC), a novel synthetic derivative of chrysin, was demonstrated anti-tumor activities against several human cancers, including lung cancer. Interaction between inflammation and cancer stem cell are recently increasingly recognized in tumorigenesis and progression. The purpose of this study was to investigate whether BrMC inhibits lung cancer stemness of H460 cells induced by inflammatory factors (TGF-β combined with TNF-α) and its potential mechanism. Our results showed that BrMC inhibited lung cancer stemness, as validated by enhanced self-renewal ability, higher in vitro tumorigenicity, and increased expression of CD133, CD44, Bmi1 and Oct4 in H460 cells administered TNF-α after prolonged induction by TGF-β, in a concentration-dependent manner. Both NF-κB inhibition by SN50 and FoxM1 suppression by thiostrepton (THI) prompted the inhibition of BrMC on lung CSCs. Conversely, overexpression of NF-κBp65 significantly antagonized the above effects of BrMC. Meanwhile, overexpression of FoxM1 also significantly compromised BrMC function on suppression of FoxM1 and NF-κBp65 as well as stemness of lung CSCs. Our results suggest that activation of NF-κB and FoxM1 by cytokines facilitate the acquisition CSCs phenotype, and compromise the chemical inhibition, which may represent an effective therapeutic target for treatment of human lung cancer. Moreover, BrMC may be a potential promising candidate for targeting NF-κB/ FoxM1 to prevent the tumorigenesis under inflammatory microenvironment.

The aim of this study was to observe dynamic changes in immunological parameters and levels of inflammatory factors from pre-radiotherapy to post-radiotherapy in patients with esophageal cancer, and to evaluate the related clinical prognosis. In all, 110 patients with esophageal cancer who underwent radiotherapy were enrolled. Before radiotherapy, post-radiotherapy, and 3 months after radiotherapy, the percentages of T lymphocyte subsets and natural killer (NK) cells in peripheral blood were detected using flow cytometry. The levels of serum inflammatory factors were measured with the enzyme-linked immunosorbent assay (ELISA). Thirty peripheral blood samples from healthy people were similarly analysed as the control. Before radiotherapy, the percentages of CD4+ and CD8+ T cells and NK cells, and the CD4+/CD8+ rate in esophageal cancer patients were significantly different from those in the healthy control group (P < 0.001); the levels of inflammatory factors were increased significantly (P < 0.001). The percentages of the above cells and the levels of inflammatory factors also differed statistically significantly between pre- and post-radiotherapy (P < 0.001) in the esophageal cancer patients. Three months after radiotherapy, the percentages of CD3+ (P = 0.453), CD4+ (P = 0.108), and CD8+ T cells (P = 0.163) and NK cells (P = 0.103) had recovered to the level before radiotherapy; and the levels of TNF-α (P = 0.101), IL-6 (P = 0.302) and IL-8 (P = 0.250) were also restored. After radiotherapy, alterations in immunological parameters were associated with the irradiation volume and the myelosuppression condition. Patients with recovered immunological parameters showed a longer median survival time than those with poor recovery of immunological parameters. For esophageal cancer patients who were immunosuppressive and had an activated inflammatory response before radiotherapy, radiotherapy aggravated these symptoms, and this aggravation was positively associated with myelosuppression and irradiation volume. In addition, recovery of the immunological parameters indicated better prognosis.

Objective We investigated the effect of the Mendelsohn maneuver and swallowing training in patients with senile vascular dementia complicated with dysphagia. Methods We randomly classified 214 patients with senile vascular dementia and swallowing dysfunction into a control group (CG, n = 106) and observation group (OG, n = 108). Both groups underwent health education, psychological intervention, and training of the oral muscle group. The OG additionally underwent the Mendelsohn maneuver and swallowing training. The Hasegawa Dementia Scale (HDS), China Stroke Scale (CSS), and Neurobehavioral Cognitive Status Examination (NCSE) were used to evaluate dementia, neurological impairment, and cognitive dysfunction, respectively. Results The OG had a higher rate of effective therapy than the CG. After intervention, the OG showed better swallowing function than the CG. At 15 days and 1 month after intervention, the OG had higher video fluoroscopic swallowing exam scores than the CG. The OG had lower serum interleukin (IL)-1, IL-6, and tumor necrosis factor-α levels than the CG. After intervention, the OG had higher HDS and NCSE scores and lower CSS scores than the CG. Conclusions The Mendelsohn maneuver and swallowing training can improve swallowing function in patients with senile vascular dementia complicated with dysphagia and help to ameliorate the inflammatory response.

Lei Li,1,* Ling Chen,1,* Fang Lin,2 Jinsong Mu,2 Dan Wang,1 Wei Zhang,1 Lai Mi,1 Yuling Qin,1 Yuesu Zhou1 1Department of Emergency, Fifth Medical Center of Chinese PLA Hospital, Beijing, 100039, People’s Republic of China; 2Department of Critical Care Medicine, Fifth Medical Center of Chinese PLA Hospital, Beijing, 100039, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yuesu Zhou; Yuling QinDepartment of Emergency, Fifth Medical Center of Chinese PLA Hospital, No. 100 Middle Road of West 4th Ring Road, Fengtai District, Beijing, 100039, People’s Republic of ChinaTel/Fax +86 10 66933202Email yuesu_zhou@163.com; ylqin90@163.comObjective: The present study aims to investigate the cytokines interleukin (IL)-4, IL-6, IL-10, and IL-17 in the peripheral blood of patients with acute-on-chronic liver failure combined with sepsis, patients with acute-on-chronic liver failure, and patients with liver cirrhosis; to investigate the changes in the levels of inflammatory factors in cases of coagulation dysfunction in liver failure combined with sepsis; and to discover more typical inflammatory factors for further evaluation by functional experiments.Methods: In the present study, 41 patients with acute-on-chronic liver failure and sepsis were enrolled as study subjects. These patients were compared with 20 patients with either acute-on-chronic liver failure and liver cirrhosis during the same period. The changes in IL-4, IL-6, IL-10, and IL-17 were detected in each group by enzyme-linked immunosorbent assay, and SPSS 17.0 software was adopted for data analysis.Results: There were no significant changes in the levels of IL-4 in any of the groups. However, the levels of IL-6, IL-10, and IL-17 were significantly higher in the acute-on-chronic liver failure and sepsis group than in the acute-on-chronic liver failure and the liver cirrhosis groups.Conclusion: The present study shows that when liver failure is accompanied by sepsis, the serum levels of inflammatory factors IL-6, IL-10, and IL-17 are significantly increased. This could be closely correlated with the occurrence and development of coagulation dysfunction and sepsis. These findings provide new ideas for delaying the deterioration of patients with liver failure in clinical practice.Keywords: liver failure, coagulation dysfunction, sepsis, inflammatory factor, expression

Intestinal barrier dysfunction is an important contributor to morbidity caused by sepsis. This study investigates the molecular mechanism by which Ghrelin affects intestinal dysfunction in rat model of sepsis. A rat model of sepsis was established by cecal ligation and puncture (CLP), revealing that Ghrelin was downregulated when sepsis occurs. Increases in the levels of inflammatory factors tumor necrosis factor α (TNF-α), interleukin-1 (IL-1β), IL-6, gastrin, γ-H2AX and 8-OHdG was also detected in this model system, as was an overall increase in oxidative stress. Introduction of exogenous Ghrelin inhibited these increases in inflammatory response and oxidative stress, leading to a reduction of overall sepsis-induced intestinal dysfunction. Ghrelin was then shown to activate SIRT1 expression in vitro, while SIRT1 was found to co-express with KLF4, which in turn was predicted to bind to matrix metalloproteinase 2 (MMP2) promoter. Finally, gain- and loss-of-function experiment demonstrated that SIRT1 upregulated the expression of KLF4 to downregulate MMP2. Collectively, Ghrelin inhibits the oxidative stress and intestinal dysfunction to attenuate sepsis by activating SIRT1 and regulating a KLF4/MMP2 regulatory axis.

Background The purpose of this study was to establish a novel rat model for ligamentum flavum (LF) hypertrophy using increased motion of lumbar and to elucidate the etiology of (LFH). Methods A total number of 30 male rats were used. The increased motion of lumbar was induced by surgical resection of L5/6 posterior elements (n = 15). The other rats underwent a sham operation (n = 15). After 8 weeks, all rats were taken lateral plain X-rays. The LF from L5/6 in both groups were harvested to investigate histological, immunohistological, and real-time PCR analysis. Results According to radiological results, the disc height ratio, flexion ratio, and extension ratio were larger in the rats in the experimental group than that of in the sham group. The HE staining showed that the LF thickness in the experimental group significantly increased in comparison to the sham group. The Masson trichrome staining showed that the ratio of elastic fibers to collagen fibers in experimental group was lower than that in the sham group. The protein and gene expression of TGF-β1, TNF-α, IL-1β, and Col 1 were significantly higher in the experimental group than that in the sham group. Conclusion A relatively safe, simple, and rapid rat model of LFH using increased motion of lumbar was established. The increased motion of lumbar could lead to high expression of inflammatory and fibrotic factors in LF, causing the accumulation of collagen fibers and decreasing of elastic fibers.

BackgroundThe outbreak of coronavirus disease 2019 (COVID-19) has become a global public health concern. Many inpatients with COVID-19 have shown clinical symptoms related to sepsis, which will aggravate the deterioration of patients’ condition. We aim to diagnose Viral Sepsis Caused by SARS-CoV-2 by analyzing laboratory test data of patients with COVID-19 and establish an early predictive model for sepsis risk among patients with COVID-19.MethodsThis study retrospectively investigated laboratory test data of 2,453 patients with COVID-19 from electronic health records. Extreme gradient boosting (XGBoost) was employed to build four models with different feature subsets of a total of 69 collected indicators. Meanwhile, the explainable Shapley Additive ePlanation (SHAP) method was adopted to interpret predictive results and to analyze the feature importance of risk factors.FindingsThe model for classifying COVID-19 viral sepsis with seven coagulation function indicators achieved the area under the receiver operating characteristic curve (AUC) 0.9213 (95% CI, 89.94–94.31%), sensitivity 97.17% (95% CI, 94.97–98.46%), and specificity 82.05% (95% CI, 77.24–86.06%). The model for identifying COVID-19 coagulation disorders with eight features provided an average of 3.68 (±) 4.60 days in advance for early warning prediction with 0.9298 AUC (95% CI, 86.91–99.04%), 82.22% sensitivity (95% CI, 67.41–91.49%), and 84.00% specificity (95% CI, 63.08–94.75%).InterpretationWe found that an abnormality of the coagulation function was related to the occurrence of sepsis and the other routine laboratory test represented by inflammatory factors had a moderate predictive value on coagulopathy, which indicated that early warning of sepsis in COVID-19 patients could be achieved by our established model to improve the patient’s prognosis and to reduce mortality.

Objective: To explore the effect of dexmedetomidine hydrochloride on perioperative inflammation and postoperative lung infection in patients with spinal tuberculosis. Method: A double-blind control observation was conducted in spinal tuberculosis patients with the use of general anesthesia during the operation. A total of 171 spinal tuberculosis patients who received endotracheal intubation for general anesthesia in Henan University of Chinese Medicine from January 2017 to April 2019 were included. The concentration changes in serum TNF-α and IL-6 were recorded at one hour, six hour and one day after the operation. The incidence of postoperative pulmonary complications of patients were also evaluated. Results: The results showed that in the experimental group compared with the control group, serum TNF-α and IL-6 concentrations one hour, six hour and one day after the operation were significantly lower (P

Photodynamic therapy (PDT) is a promising new method to eliminate microbial infection and promote wound healing. Its effectiveness has been confirmed by some studies; however, the mechanisms of PDT in wound healing remain obscure. We used mouse skin wounds infected withPseudomonas aeruginosaas a research object to explore the therapeutic effects and mechanisms of 5-aminolevulinic acid photodynamic therapy (ALA-PDT). ALA-PDT treatment significantly reduced the load ofP. aeruginosain the wound and surrounding tissues and promoted the healing of skin wounds in mice. Hematoxylin-eosin (HE) and Sirius red staining showed that ALA-PDT promoted granulation tissue formation, angiogenesis, and collagen regeneration and remodeling. After ALA-PDT treatment, the expression of inflammatory factors (TNF-α and IL-1β) first increased and then decreased, while the secretion of growth factors (TGF-β-1 and VEGF) increased gradually after treatment. Furthermore, ALA-PDT affected the polarization state of macrophages, activating and promoting macrophages from an M1 to an M2 phenotype. In conclusion, ALA-PDT can not only kill bacteria but also promote wound healing by regulating inflammatory factors, collagen remodeling and macrophages. This study further clarifies the mechanism of PDT in the healing of infectious skin wounds and provides further experimental evidence for its clinical treatment of skin wounds infected byP. aeruginosa.

Tumor angiogenesis is necessary for the continued survival and development of tumor cells, and plays an important role in their growth, invasion, and metastasis. The tumor microenvironment—composed of tumor cells, surrounding cells, and secreted cytokines—provides a conducive environment for the growth and survival of tumors. Different components of the tumor microenvironment can regulate tumor development. In this review, we have discussed the regulatory role of the microenvironment in tumor angiogenesis. High expression of angiogenic factors and inflammatory cytokines in the tumor microenvironment, as well as hypoxia, are presumed to be the reasons for poor therapeutic efficacy of current anti-angiogenic drugs. A combination of anti-angiogenic drugs and antitumor inflammatory drugs or hypoxia inhibitors might improve the therapeutic outcome.

Purpose Behavioral symptoms, including depression, anxiety, and cognitive impairment, are common clinical symptoms of patients with glioma. However, the mechanisms underlying the behavioral symptoms of glioma patients remain unclear. In this study, we explore the correlation between markers of systemic inflammation and preoperational behavioral symptoms in glioma patients. Patients and Methods Patients (n = 71) who had recently undertaken imaging (i.e., CT, MRI) for suspected glioma had a face‐to‐face interview, completed self‐report scales, and provided blood samples. Furthermore, we tested blood samples by a protein chip to select differential inflammatory cytokines and further confirm such differences using liquid‐phase chip technology. Results The prevalence of depression, anxiety, and cognitive impairment in glioma patients prior to surgery in this study was 53.5%, 70.4%, and 32.4%, respectively. The increased levels of IFN‐γ were positively correlated with clinical symptoms of depression in the glioma patients. Moreover, increased IL‐2 levels were negatively associated with anxiety symptoms (p = .00) and positively correlated with cognitive impairment in glioma patients. Conclusion This study suggests that systemic inflammation is associated with behavioral symptoms in glioma patients. This provides further evidence of the contribution of inflammatory markers to psychological symptoms in the context of physical conditions and lays the foundation for the development of further treatments of the behavioral symptoms in glioma patients., The incidence of behavioral symptoms was not described before surgery in glioma patients. The correlation between behavioral symptoms and inflammation has not been studied in glioma patients before surgery.

Background Previous studies have shown that chronic inflammation and oxidative stress may play an important role in the pathophysiology of polycystic ovary syndrome (PCOS), and glutamine (Gln) have showed the anti-inflammatory and antioxidant properties. So the aim of this study is to investigate the effect of glutamine supplementation on PCOS rats. Methods Female Sprague–Dawley rats were randomly assigned into four groups (n = 10 /group), control group, PCOS group, PCOS+ 0.5 g/kg Gln group and PCOS+ 1.0 g/kg Gln group. All the PCOS rats were administrated with 6 mg/100 g dehydroepiandrosterone (DHEA) for 20 consecutive days, all the PCOS+Gln groups were intraperitoneal injected glutamine twice in the next morning after the last DHEA injection. All the samples were collected 12 h after the last administration. Ovarian histological examinations were analyzed and the concentration of serum hormone, inflammatory and oxidative stress factors were measured. Results There was no obvious ovarian histological change among the PCOS group and PCOS+Gln groups. All the detected inflammation factors [C-reactive protein, interleukin (IL)-6, IL-18, tumor necrosis factor] showed significantly higher in all the PCOS groups compared to the control group (P P P P P P Conclusion There is low-grade inflammation and oxidative stress in DHEA-induced PCOS rats. The supplementation of 0.5 g/kg glutamine could effectively ameliorate the inflammation and oxidative stress conditions of PCOS.

Objective We investigated the effect of untransplantable bone marrow-derived mesenchymal stem cells (BMSCs) in acute lung injury (ALI) and whether BMSCs attenuate damage of lipopolysaccharide (LPS) to alveolar type II epithelial cells (AECIIs). Methods ALI models were prepared by nebulizing LPS and then BMSCs were infused 1 hour later. We observed histopathological changes of lung tissue and evaluated inflammatory exudation by the wet/dry weight ratio, bronchiolar lavage fluid cell count, and protein concentration determination. Inflammatory and vascular factors were detected by immunohistochemistry and western blotting. For in vitro experiments, AECIIs were stimulated with 10 μg/mL LPS for 4 hours and then BMSCs were seeded in transit inserts to co-culture for 24 hours. The activity of AECIIs was detected. Results In the LPS + BMSCs group, histopathological examination showed that the degree of lung injury was significantly reduced compared with the LPS group. Protein expression of inflammatory and vascular factors was significantly lower with treatment. Optical density values and cell viability of the LPS + BMSCs group were significantly higher than those of the LPS group. Conclusions Untransplanted-BMSCs can inhibit the inflammatory response in ALI and promote repair of AECIIs. This might be due to substances secreted by BMSCs and interaction between these substances.

Purpose: The present paper investigated the expression of TLR2 in serum of patients with pulmonary tuberculosis and lung cancer, and verifiedthe effect of TLR2 on the biological characteristics of lung cancer cells. Methods: The common differentially expressed genes in tuberculosis and lung cancer samples were analyzed by edgeR. The intersection of genes was taken and the enrichment analysis and string interaction analysis were performed. The expression of TLR2, inflammatory factors IL6, IL17 and IL22 in serum of patients with pulmonary tuberculosis or lung cancer and lung cell were detected by ELISA. The mRNA and protein expression levels of TLR2, caspase-3, Bax and Bcl-2 were detected by qRT-PCR and Western blot. CCK-8, colony formation assay, transwell assay and flow cytometry were performed to detect the proliferation, invasion, migration and cells apoptosis of lung cancer cells. Results: Bioinformatics analysis found that high expression of TLR2 is a core regulator in lung cancer and tuberculosis. TLR2 and inflammatory factors IL6, IL17, IL22 are highly expressed in the serum of patients with tuberculosis and lung cancer by ELISA.TLR2 is also highly expressed in lung cancer cells. Silencing TLR2 inhibited the growth, invasion and migration ability of cells, and the expression of IL6, IL17 and IL22. It also promoted the expression of caspase-3 and Baxwith the decreased expression of Bcl-2. Conclusion: TLR2 and inflammatory factors IL6, IL17 and IL22 were highly expressed in the serum of patients with pulmonary tuberculosis and lung cancer. Silencing TLR2 could inhibit the growth, invasion and migration ability of lung cancer cells, and promote apoptosis.

Background Study on the expression of miRNA‐22 in serum of Alzheimer's disease (AD) patients and the mechanism of neuroinflammation regulation. Methods ELISA assay was used to detect the serum level of inflammatory factors, including interleukin‐1β (IL‐1β), interleukin‐18 (IL‐18), and tumor necrosis factor‐α in AD patients. TargetScan database and luciferase reporter gene assay indicated that gasdermin D (GSDMD) was the target gene of miRNA‐22. miRNA‐22 mimic was transfected into microglia, followed by administration of LPS and Nigericin to induce pyroptosis. Results In this study, we found that the expression level of miRNA‐22 in peripheral blood was lower in AD patients than that in healthy population. The expression of inflammatory factors was higher in AD patients than that in healthy people, which was negatively correlated with miRNA‐22. miRNA‐22 mimic could significantly inhibit pyroptosis, the expression of GSDMD and p30‐GSDMD was down‐regulated, the release of inflammatory factor was decreased, and the expression of NLRP3 inflammasome was down‐regulated as feedback. In the APP/PS1 double transgenic mouse model, the injection of miRNA‐22 mimic significantly improved the memory ability and behavior of mice. In addition, the expression of the vital protein of pyroptosis in mouse brain tissue, including GSDMD and p30‐GSDMD, was down‐regulated, and the expression of inflammatory factors was also decreased. Conclusion miRNA‐22 was negatively correlated with the expression of inflammatory factors in AD patients, and miRNA‐22 could inhibit the release of inflammatory cytokines by regulating the inflammatory pyroptosis of glial cells via targeting GSDMD, thereby improving cognitive ability in AD mice. miRNA‐22 and pyroptosis are potential novel therapeutic targets in the treatment of AD., miRNA‐22 was negatively correlated with the expression of inflammatory factors in Alzheimer's disease (AD) patients, and miRNA‐22 could inhibit the release of inflammatory cytokines by regulating the inflammatory pyroptosis of glial cells via targeting GSDMD, thereby improving cognitive ability in AD mice. miRNA‐22 and pyroptosis are potential novel therapeutic targets in the treatment of AD.

Objective: The objective of this study was to investigate the roles and mechanisms of inflammatory mediators NLRP3 and IL-1β in refractory temporal epilepsy brain injury.Method: First, the brain tissue and the peripheral blood of children undergoing intractable temporal lobe epilepsy surgery were analyzed as research objects. The expression levels of NLRP3 in brain tissue and IL-1β in blood were measured. A model of temporal lobe epilepsy was established using wild-type and NLRP3 knockout 129 mice. Pilocarpine was injected intraperitoneally into the experimental group, and isovolumetric saline was injected intraperitoneally into the control group (n = 8 in each group). The expression of IL-1β in the peripheral blood, cerebral cortex, and hippocampus of mice was measured by ELISA at 3 h, 24 h, 3 days, and 7 days after modeling. Fluoro-Jade B (FJB) and TUNEL methods were used to determine necrosis and apoptosis in hippocampal neurons, respectively, and the expression of NLRP3 in the cortex was measured by immunofluorescence methods.Result: (1) The IL-1β levels in the peripheral blood of children with intractable temporal lobe epilepsy were higher than those in the control group (t = 2.813, P = 0.01). There was also a positive correlation between IL-1β expression levels and the onset time of a single convulsion in patients with refractory epilepsy (r = 0.9735, P < 0.05). The expression level of NLRP3 in the cerebral cortex of patients with refractory temporal lobe epilepsy was higher than that in the control group. (2) The expression level of NLRP3 in the hippocampus of wild-type mice increased 3 days after modeling and decreased slightly at 7 days but remained higher than that of the control group. IL-1β levels in peripheral blood were significantly higher than those in the control group at 3 days (t = 8.259, P < 0.0001). The IL-1β levels in the peripheral blood of NLRP3 knockout mice were lower than those in the wild-type group at 3 days (t = 3.481, P = 0.004). At day 7, the neuronal necrosis and apoptosis levels in the CA3 region of the hippocampus decreased.Conclusion: NLRP3 may be involved in the development of refractory temporal lobe epilepsy. Inhibiting NLRP3 may alleviate local brain injury by downregulating the IL-1β expression. The IL-1β levels in the peripheral blood of patients with refractory temporal lobe epilepsy may reflect the severity of convulsions.

Objective To investigate the safety and efficacy of chimeric antigen receptor T (CAR-T) cell infusion in patients with refractory multiple myeloma (MM). Methods Sixteen patients diagnosed with refractory MM were included in this study. Patients received initial infusions of T-derived CD19/B-cell maturation antigen (BCMA) CAR-T cells with 100% CD19, followed by second infusions with 40% BCMA and third infusions with 60% BCMA. The total doses were 0.5–1 × 10 7 /kg CD19 and 1.2 − 6.2 × 10 7 /kg BCMA. Patients were monitored after infusion. Levels of interleukin (IL)-2, IL-6, IL-10, tumor necrosis factor-α, and C-reactive protein were determined by enzyme-linked immunosorbent assay. Results Cytokine release syndrome (CRS) was observed in all 16 patients. Thirteen patients with CRS stage II−IV had persistent hyperthermia from 5−14 days after infusion, while most patients developed hyperthermia from 1 day after infusion and their temperatures returned to normal within 2−10 days. Levels of all factors were significantly elevated 2 days after infusion, peaked at 5 days, and then gradually decreased to normal levels. All inflammatory factors showed normal levels by 10 days after infusion. Conclusion Body temperature and levels of inflammatory factors all increased dramatically after infusion of CD19/BCMA CAR-T cells, but recovered to normal levels after appropriate treatment and nursing.

Substantial research attention has been directed at exploring the mechanisms and treatment of renal cell carcinoma (RCC). Indeed, the association between inflammation and tumor phenotypes has been at the center of cancer research. Concomitant with research on the inflammation response and inflammatory molecules involved in RCC, new breakthroughs have emerged. A large body of knowledge now shows that treatments targeting inflammation and immunity in RCC provide substantial clinical benefits. Adequate analysis and a better understanding of the mechanisms of inflammatory factors in the occurrence and progression of RCC are highly desirable. Currently, numerous RCC treatments targeted at inflammation and immunotherapy are available. The current review describes in detail the link between inflammation and RCC.

Objective To investigate the effects of inverse ratio ventilation combined with lung-protective ventilation on pulmonary function and inflammatory factors in severe burn patients undergoing surgery. Populations and Methods: Eighty patients with severe burns undergoing elective surgery were divided randomly into two groups: control (CG, n = 40) and experiment (EG, n = 40). The CG had conventional ventilation, whereas the EG were ventilated with tidal volume (TV) of 6–8 ml/kg, I (inspiration): E (expiration) of 2:1, and positive end-expiratory pressure (PEEP) 5 cm H2O. The following variables were evaluated before (T0), 1 h after start of surgery (T1) and after surgery (T2): oxygenation index (OI), partial pressure of carbon dioxide (PaCO2), TV, peak airway pressure (Ppeak), mean airway pressure (Pmean), PEEP, pulmonary dynamic compliance (Cdyn), alveolar–arterial difference of oxygen partial pressure D(A-a)O2, lactic acid (Lac), interleukin (IL)-6 and IL-10, and lung complications. Results: At T1 and T2 time points, the OI, Pmean and Cdyn were significantly greater in the EG than in the CG while the TV, Ppeak, D(A-a)O2, IL-6 and IL-10 were significantly smaller in the EG than in the CG. At the end of the surgery, the Lac was significantly smaller in the EG than in the CG (1.28 ± 0.19 vs. 1.40 ± 0.23 mmol/L). Twenty-four hours after the surgery, significantly more patients had hypoxemia (27.5 vs. 10.0%), increased expectoration (45.0 vs. 22.5%), increased lung texture or exudation (37.5 vs. 17.5%) in the CG than in the EG. Conclusions: Inverse ratio ventilation combined with lung-protective ventilation can reduce Ppeak, increase Pmean and Cdyn, improve the pulmonary oxygenation function, and decrease ILs in severe burn surgery patients.

Objective: The surgical technique, safety, efficacy, and clinical application value of the intra-neuroendoscopic technique (INET) for the treatment of subacute-chronic and chronic septal subdural hematoma was investigated based on the structure and pathological features of the hematoma wall, and the critical factors of hematoma growth and recurrence were determined, in order to provide reference for clinical drug treatment. Methods: This was non-randomized concurrent control study. A total of 94 patients who met the inclusion criteria were recruited between May 2015 and February 2019 and were divided into the INET treatment group (INET group, 45 cases) and the burr hole drainage (BHD) treatment group (control group, 49 cases). The hematoma fluid components and the morphological structure and pathological characteristics of the hematoma wall were analyzed, and the surgical duration, subdural drainage tube (SDT) placement duration, intracranial infection rate, Bender grade at the 1 month post-operative follow-up and hematoma recurrence rate within the 6 months of post-operative follow-up were compared between the two groups. A multiple logistic regression model was established to analyze the risk factors associated with recurrence within 6 months. Results: Intraoperative endoscopy showed that the adhesion bands that formed early in the hematoma cavity were strip-like and that those that formed late were lock-column-like. The hematoma cavity was divided into different-sized chambers with by these strips/columns. Pathological sections of cyst wall reveled angiogenesis inside the cyst and mucus-like changes, rupture and hemorrhage in the vascular wall. Obvious inflammatory cell infiltration and fibrous connective tissue hyperplasia were observed in the cyst wall. The osmotic pressure of the hematoma fluid was not significantly different from that of the peripheral venous blood [(296.7 ± 10.3) mOsm/kg vs. (291.5 ± 12.4) mOsm/kg, p = 0.68]. However, the D-dimer contents which reflect the severity of fibrinolysis in the hematoma and the proinflammatory cytokine interleukin 6 (IL-6) were significantly higher in the hematoma fluid than in the peripheral venous blood. The surgery duration for the INET group was significantly longer than that for the control group [(60.4 ± 10.6) min vs. (44.1 ± 9.8) min, p = 0.00], but both the hematoma recurrence rate within 6 months of post-operative follow-up (4.4 vs. 24.5%, p = 0.00) and the SDT placement duration [(2.1 ± 0.6) d vs. (3.9 ± 0.7) d, p = 0.00] for the INET group were both lower than those for the control group. The intracranial infection rate did not differ significantly between the two groups (4.4 vs. 10.2%, p = 0.50). The overall effective rate of the Bender grade at 1 month of follow-up did not differ significantly between the two groups (95.6 vs. 87.8%, p = 0.32), but the proportion of patients who recovered to Bender grade 0 with no symptoms was significantly higher in the INET group than in the control group (86.7 vs. 67.3%, p = 0.03). Multiple logistic regression analysis showed that INET surgery [odds ratio (OR) 3.71, 95% confidence interval (CI) 1.31–9.62, p = 0.02], age of 65 years or younger (OR 1.51, 95% CI 1.05–2.87, p = 0.03) and unilateral subdural hematoma (OR 1.76, 95% CI 1.05–3.41, p = 0.02) were independent factors that reduced the post-operative recurrence rate. Conclusion: The INET surgical plan based on the structure and pathological features of the subacute-chronic and chronic subdural hematoma wall can reduce the recurrence rate and improve the clinical prognosis. Trial registration: ClinicalTrials.gov, {"type":"clinical-trial","attrs":{"text":"NCT02515903","term_id":"NCT02515903"}}NCT02515903. Registered 5 August, 2015.

Previous studies have shown that vagus nerve stimulation can improve patients’ locomotor function. The stimulation of the auricular vagus nerve, which is the only superficial branch of the vagus nerve, may have similar effects to vagus nerve stimulation. However, the precise mechanisms remain poorly understood. In this study, rat models of cerebral ischemia/reperfusion injury were established by modified Longa ligation. Twenty-four hours later, 7-day auricular vagus nerve stimulation was performed. The results showed that auricular vagus nerve stimulation promoted the secretion of acetylcholine, inhibited the secretion of interleukin-1β, interleukin-6, and tumor necrosis factor-α, and reduced connexin 43 phosphorylation in the ischemic penumbra and motor cortex, promoting locomotor function recovery in rats with cerebral ischemia/reperfusion injury. These findings suggested that auricular vagus nerve stimulation promotes the recovery of locomotor function in rats with cerebral ischemia/reperfusion injury by altering the secretion of acetylcholine and inflammatory factors and the phosphorylation of connexin 43. This study was approved by the Animal Use and Management Committee of Shanghai University of Traditional Chinese Medicine on November 8, 2019 (approval No. PZSHUTCM191108014).

Objective This study aimed to study the effects of laparoscopic-assisted radical gastrectomy (LAG) and open radical gastrectomy (OG) on immune function and inflammatory factors in patients with early gastric cancer. Methods Seventy-five patients with pT1N0M0 gastric cancer in Ren Ji Hospital from August 2017 to January 2018 were studied. Lymphocytes subsets and interleukins were compared preoperatively and on the third postoperative day (POD3) and seventh postoperative day (POD7). Results There were no significant differences in age, sex, body mass index, duration of the operation, estimated blood loss, total gastrectomy rate, postoperative first fluid diet, and the levels of preoperative lymphocytes subsets and interleukins between the two groups. The number of CD4+ T cells and the CD4+/CD8+ ratio in the LAG group were significantly higher than those in the OG group on POD3. However, the number of CD8+ T cells, and interleukin-6 and interleukin-8 levels in the LAG group were significantly lower than those in the OG group on POD3. Conclusions Laparoscopy can effectively reduce the levels of inflammatory factors and has less effect on the immune system than OG.

Objective To investigate the effects of probiotics combined with early enteral nutrition on levels of endothelin-1 (ET-1), C-reactive protein (CRP), and inflammatory factors, and on the prognosis of patients with severe traumatic brain injury (TBI). Methods We enrolled 76 adults with severe TBI. The patients were divided randomly into two equal groups administered enteral nutrition with and without probiotics, respectively. Demographic and clinical data including age, sex, Glasgow Coma Scale score, Sequential Organ Failure Score, Acute Physiology, Chronic Health Score, hospitalization, mortality, and infections were recorded. Results Serum levels of inflammatory factors gradually decreased with increasing treatment time in both groups. However, ET-1 at 15 days, and interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α, and CRP at 7 and 15 days decreased significantly more in the combined treatment group. Hospitalization duration and pulmonary infection rates were also significantly reduced in the combined compared with the enteral nutrition alone group. GCS scores at 15 days were significantly lower in the combined compared with the enteral nutrition group. Conclusion Probiotics combined with early enteral nutrition could reduce serum levels of ET-1, CRP, and IL-6, IL-10, and TNF-α, and could thus improve the recovery of patients with severe TBI.

The aim of the present study was to investigate the effects of telmisartan on vascular endothelial functions, inflammatory factors and insulin resistance of coronary heart disease patients complicated with diabetes mellitus. In total, 80 coronary heart disease patients complicated with type 2 diabetes mellitus, admitted and treated in the Zhangqiu Hospital from January 2016 to March 2017 were enrolled in the study. Each patient was randomly assigned to an observation (n=40) or a control group (n=40) using a random number table. Conventional symptomatic and supporting therapies were administered to all the patients in the two groups for 12 consecutive weeks, while additional telmisartan was given only to patients in the observation group. Markers of glucose metabolism, vascular endothelial function and inflammation were determined before and after intervention, to compare averages between groups. Results showed the levels of fasting blood glucose and blood glucose in the observation group were significantly lower than those in the control group (p

Objective: To study the expression quantity of serum miR-146a and miR-146b in patients with acute cerebral infarction before and after the intervention of rosuvastatin and its correlation with toll-like receptor 2 (TLR2) and TLR4 signaling pathways. Methods: A total of 65 patients with acute cerebral infarction treated in our hospital from December 2015 to August 2016 were selected for prospective study. They were treated with lipid-lowering rosuvastatin, and peripheral blood samples were collected at 8th week before and after treatment, respectively. Serum was separated and expression quantity of miR-146a and miR-146b and contents of TNF-α, interleukin (IL)-1β, IL-6 and IL-17 were determined. Peripheral blood mononuclear cells were isolated and fluorescence intensities of TLR2, TLR4, myeloid differentiation primary response gene 88 (MyD88), interleukin-1 receptor-associated kinase 1 (IRAK-1) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) were measured. >Results: At 8th week of intervention of rosuvastatin, expression quantity of serum miR-146a [(0.762 ± 0.092) vs. (0.346 ± 0.053)] and miR-146b [(0.714 ± 0.088) vs. (0.317 ± 0.047)] in patients with acute cerebral infarction was significantly higher than those before the intervention. Fluorescence intensities of peripheral blood mononuclear cells such as TLR2 [(10.34 ± 1.27) vs. (16.94 ± 1.94)], TLR4 [(11.37 ± 1.54) vs. (24.35 ± 3.26)], IRAK [(9.34 ± 0.92) vs. (15.32 ± 1.82)], MyD88 [(4.42 ± 0.56) vs. (9.41 ± 1.03)] and NF-kB [(6.65 ± 0.78) vs. (13.49 ± 1.76)] and contents of inflammatory factors such as TNF-α [(64.26 ± 8.29) μg/L vs. (106.39 ± 13.84) μg/L], IL-1β [(37.91 ± 5.24) μg/L vs. (64.23 ± 8.33) μg/L], IL-6 [(34.28 ± 4.85) ng/L vs. (82.46 ± 11.97) ng/L] and IL-17 [(56.75 ± 7.49) ng/L vs. (98.31 ± 11.36) ng/ L] of serum were all significantly lower than those before the intervention. Expression quantity of serum miR-146a and miR-146b had a negative correlation with fluorescence intensities of TLR2, TLR4, IRAK, MyD88 and NF-kB. Fluorescence intensities of TLR2 and TLR4 in peripheral blood mononuclear cells had a positive correlation with contents of TNF-α, IL-1β, IL-6 and IL-17 in serum. >Conclusions: Treatment with rosuvastatin can up-regulate the expression quantity of serum miR-146a and miR-146b in patients with acute cerebral infarction and further inhibit the secretion of IRAK, MyD88, NF-kB, TNF-α, IL-1β, IL-6 and IL-17 mediated by TLR2 and TLR4.

Background: Zhuoduqing formula (ZDQ) is a Chinese herbal decoction and used to treat type 2 diabetes in clinical practice, but the potential evidence needs to be provided.Materials and Methods: Type 2 diabetic model rats were induced by feeding high fat diet (HFD) and intraperitoneal injection of streptozotocin (STZ). The model rats were given ZDQ for 4 weeks. Insulin sensitivity was evaluated by homeostasis model assessment of basal insulin resistance (HOMA-IR) and intraperitoneal glucose tolerance test (IPGTT). Blood insulin and tumour necrosis factor-α (TNF-α) levels as well as SOCS-3 levels in skeletal muscles were analyzed by ELISA.Results: ZDQ significantly decreased fasting blood glucose, ameliorated HOMA-IR and IPGTT, and reduced triglyceride and total cholesterol in type 2 diabetic rats. Moreover, ZDQ remarkably lowered blood TNF-α levels and inhibited SOCS-3 levels in skeletal muscles.Conclusion: The results display that ZDQ performs anti-diabetic functions in type 2 diabetic rats induced by feeding HFD and intraperitoneal injection of STZ.Keywords: Insulin sensitivity, Chinese medicine, anti-diabetic effect, inflammatory factor, SOCS-3Abbreviations: ZDQ, zhuoduqing formula; ROS, rosiglitazone; HOMA-IR, homeostasis model assessment of basal insulin resistance; IPGTT, intraperitoneal glucose tolerance test; HFD, high fat diet; SOCS-3, suppressor of cytokine signaling-3; TNF-α, tumour necrosis factor-α.

The effect of etomidate on the oxidative stress response and levels of inflammatory factors resulting from ischemia-reperfusion injury of the lower extremities during tibial fracture surgery were investigated. From December 2013 to June 2015, 60 tibial fracture patients with surgical indications for open reduction and internal fixation were selected. Patients were randomly divided into the observation group and the control group. All patients were stanched by tourniquet hemostasis. Patients in the observation group were anesthetized with etomidate (3–6 mg/kg·h) + remifentanil (0.1–0.25 µg/kg/min) administered with an injection pump to maintain intraoperative sedation and analgesia anesthesia. Patients in the control group received propofol (3–6 mg/kg·h) + remifentanil (0.1–0.25 µg/kg/min). Before surgery (T0), before surgery was completed and anesthesia was stopped (T1), 24 h after surgery (T3), 48 h after surgery (T4), and 1 week after surgery (T5), serum superoxide dismutase (SOD) activity was determined with a kit, and ELISA was used to measure the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6 in peripheral blood from both groups of patients. Surgery in both groups was completed smoothly. We found that serum SOD levels of patients in the observation group were significantly higher than those of the control group, while the levels of TNF-α, IL-1, and IL-6 released by neutrophils were significantly decreased after ischemia-reperfusion injury (P

Changes in serum neuron-specific enolase (NSE) level, S100β protein concentration and inflammatory factor levels and their correlations with cognitive impairment Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores in intracranial tumor patients with cognitive impairment were explored. Seventy patients diagnosed with intracranial tumor based on clinical symptoms and computed tomography (CT) images were selected and divided into non-cognitive impairment group (MoCA score ≥26 points, n=44) and cognitive impairment group (MoCA score

Inflammation serves a key role in chronic obstructive pulmonary disease (COPD). However, changes in the immune profiles of patients with COPD remain unclear. The present prospective observational study aimed to determine the expression profiles of immune cells and inflammatory factors of patients with COPD and healthy controls, and to analyze the relationship between immune profiles and smoking history. A total of 140 subjects were enrolled in the present study between September 2018 and April 2019 at West China Hospital of Sichuan University (Chengdu, China). These included 87 patients with stable COPD and 24 patients with acute exacerbated COPD, as well as 29 healthy controls. Baseline characteristics were recorded during the screening period, and levels of immune cells were examined using flow cytometry. In addition, levels of inflammatory factors were measured using ELISAs. The results revealed increased expression of the CD64+/CD14+ mononuclear phagocyte system (MPS) and CD16+CD66+ neutrophils, and decreased expression of CD3+CD4+ T cells and CD3+ CD8+ T cells (all P

Background The mechanism of the pathological change of polycystic ovary syndrome (PCOS) is still unclear. Previous studies have shown that PCOS is a chronic nonspecific low-grade inflammatory condition, and that heat shock protein (HSP)70 has a potent anti-inflammatory property. So the aim of this study is to investigate the correlation between HSP70 and the hormones and inflammatory factors and to find out the role of HSP70 in the pathogenesis of PCOS. Methods Twenty female Sprague–Dawley (SD) rats (aged 23 days and weighted 80-90 g) were randomly divided into two groups (n = 10 per group), PCOS group and control group. PCOS group were subcutaneously injected with 6 mg/100 g dehydro-epiandrosterone (DHEA) for 20 consecutive days, the control group were subcutaneously injected with a solvent of equivalent amount. All the samples were collected in the morning fasting state, 12 h after the last administration. Histological examinations of ovarian tissues were analyzed. Hormone levels and inflammatory factors levels were measured by enzyme-linked immunosorbent assay (ELISA) kits. Results Serum concentrations of testosterone (T) and luteinizing hormone (LH) were significantly higher in the PCOS group than the control group (P

Remote ischemia preconditioning (RIPC) is a convenient and effective method for alleviating cerebral ischemia-reperfusion injury (CIRI). However, to date, the underlying mechanism has not been fully elucidated. The aim of this research was to explore the protective mechanism of RIPC on the brain after CIRI. Four groups of rats were included in this experiment: the sham group, the middle cerebral artery occlusion (MCAO) group, the RIPC group, and the AG490 group. As an inhibitor of Janus kinase 2 (JAK2), AG490 was used after MCAO in the AG490 group to explore the role of JAK2/signal transducers and activators of transcription 3 (STAT3) after CIRI. Brain tissue was collected for evaluation after 2 h of ischemia and 24 h of reperfusion. ELISA for interleukin (IL)-6, IL-1β and tumor necrosis factor-α, western blot for phosphorylated-JAK2 and phosphorylated-STAT3, the neurological severity score and Longa scoring system for neurological deficit evaluation, triphenyltetrazolium chloride staining for cerebral infarction, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining for apoptotic cells in the brain tissue were performed. Neurological function in the RIPC group was notably better than that in the MCAO group. There were smaller infarction sizes and fewer apoptotic cells in the ischemic area in the RIPC group than in the MCAO group. In the RIPC group, the expression levels of IL-1β, tumor necrosis factor-α, IL-6, and phosphorylated-JAK2 and phosphorylated-STAT3 were significantly lower than those in the MCAO group. The findings in the RIPC and AG490 groups were similar. The inflammatory response and apoptosis are two important processes involved in brain dysfunction after CIRI. The JAK2/STAT3 signaling pathway has an underlying relationship with these two processes. These findings suggest that RIPC can alleviate the damage to brain tissue by CIRI by regulating the JAK2/STAT3 signaling pathway negatively.

The occurrence of hyperpigmentation or hypopigmentation after inflammation is a common condition in dermatology and cosmetology. Since the exact mechanism of its occurrence is not yet known, prevention and treatment are troublesome. Previous studies have confirmed that α‑melanocyte‑stimulating hormone, stem cell factor and other factors can promote melanogenesis‑related gene expression through the activation of signaling pathways. Recent studies have revealed that a variety of inflammatory mediators can also participate in the regulation of melanogenesis in melanocytes. In this review, we summarized that interleukin‑18, interleukin‑33, granulocyte‑macrophage colony stimulating factor, interferon‑γ, prostaglandin E2 have the effect of promoting melanogenesis, while interleukin‑1, interleukin‑4, interleukin‑6, interleukin‑17 and tumor necrosis factor can inhibit melanogenesis. Further studies have found that these inflammatory factors may activate or inhibit melanogenesis‑related signaling pathways (such as protein kinase A and mitogen activated protein kinase) by binding to corresponding receptors, thereby promoting or inhibiting the expression of melanogenesis‑related genes and regulating skin pigmentation processes. This suggests that the development of drugs or treatment methods from the perspective of regulating inflammation can provide new ideas and new targets for the treatment of pigmented dermatosis. This review outlines the current understanding of the inflammation factors' roles in melanogenesis.

Background This study aims to investigate the chlamydia pneumoniae infection (PC) in patients with coronary heart disease. Methods A total of 92 patients with coronary heart disease, who were treated with percutaneous coronary intervention (PCI), were selected as the case group. In addition, 50 healthy people were enrolled as the control group. The incidences of CP infection and serum Chlamydia pneumoniae IgA antibody (CP-IgA), high sensitive C-reactive protein (hs-CRP), and interleukin-6 (IL-6) were compared in these two groups. The classification of coronary artery lesion, the incidence of perioperative cardiovascular events, and adverse prognosis events within six months after procedure were compared. Results The incidence of CP infection in the case group was higher (42.4% vs. 0%, P

Context: Huoxin formula is a Traditional Chinese Medicine for coronary heart disease (CHD) treatment. Objective: To explore the therapeutic mechanism of the Huoxin formula on arterial functions in CHD patients. Materials and methods: Fifty-eight CHD patients receiving cardiovascular drugs including β-receptor blocker, statins, and antiplatelet medications or others were randomized into intervention [additionally 13.5 g Huoxin formula granules dissolved in 150 mL warm water per time, twice a day (n = 30)] and control [only cardiovascular drugs (n = 28)] groups. Serum biomarkers (hs-CRP, IL-18, IL-17, TNF-α, MMP-9), and cardiovascular indicators of the common and internal carotid arteries (ICAs) were monitored before and after the treatments. Results: After 3 months of treatment, the increases of intima-media thicknesses (IMT) of the left and right common carotid arteries (CCAs) as well as of the left and right ICAs and the increases of the left and right cardio-ankle vascular index were all significantly (all p

Treatment with direct-acting antivirals (DAAs) cures most patients infected with hepatitis C virus (HCV) in the real world. However, some patients, especially those with the underlying advanced liver disease, have a limited reduction of liver injury after achieving a sustained viral response (SVR). Bicyclol was widely used in clinics for the treatment of a variety of liver injuries but with an unknown mechanism for the treatment of hepatitis C. We investigated the anti-inflammatory effects and mechanisms of bicyclol in HCV-infected hepatocytes and further confirmed the putative results in a mouse hepatitis model induced by the coinjection of polyinosinic-polycytidylic acid [poly (I:C)] and D-galactosamine (D-GalN). The results showed that the activation of nuclear factor kappa B (NF-κB) and the subsequent increase of inflammatory factors were directly induced by HCV infection and were persistent after clearance of the virus in Huh7.5 cells. Bicyclol decreased the activation of NF-κB and the levels of inflammatory factors in HCV-infected hepatocytes by inhibiting the activation of the ROS-MAPK-NF-κB pathway, and the effect was synergistic with DAAs in HCV-infected hepatocytes. Bicyclol attenuated the ROS-MAPK-NF-κB axis via recovering mitochondrial function without a dependence on dihydronicotinamide adenine dinucleotide phosphate oxidase and superoxide dismutases. The anti-inflammatory effects and mechanism of bicyclol were verified in mouse hepatitis induced by the coinjection of poly(I:C)/D-GalN. Bicyclol directly ameliorates the chronic inflammation caused by HCV infection and might be used with DAAs or after DAA therapy for ultimately curing chronic hepatitis C.

Objective To analyze the serum levels of miR-126, miR-146a and its relationship with infarction area, severity of disease and inflammatory reaction degree in patients with acute cerebral infarction (ACI). Methods A total of 75 cases with ACI treated in our hospital from April 2014 to October 2015 and 80 healthy cases were respectively selected as ACI group and control group for retrospective study. Patients' clinical data were collected, and the serum levels of miR-126, miR-146a, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 were detected. Results Serum contents of miR-126 (0.286 ± 0.078 vs . 1.000 ± 0.169) and miR-146a (0.337 ± 0.084 vs . 1.000 ± 0.158) in patients of ACI group were significantly lower than those of control group. Contents of IL-1β [(68.4 ± 10.3) vs . (22.7 ± 5.8) ng/L], TNF-α [(126.9 ± 22.4) vs . (49.6 ± 8.4) ng/L] and IL-6 [(89.3 ± 14.7) vs . (34.8 ± 5.9) ng/L] were obviously higher than those of control group. The bigger the infarction area was, the more severer the degree of nerve defect could be. The lower the serum levels of miR-126, miR-146a were, the higher the levels of TNF-α, IL-1β, IL-6 could be. Levels of miR-126 and miR-146a were negative correlation with levels of TNF-α, IL-1β and IL-6. Conclusions An abnormal decrease in serum levels of miR-126 and miR-146a in patients with ACI was closely related to the severity of disease. Through regulating the generation of inflammatory factors TNF-α, IL-1β and IL-6, miR-126 and miR-146a may get involved in the changes of cerebral infarction condition.

Objective To observe the correlation between the condition of patients with acute cerebral infarction and serum β2-microglobulin (β2-MG) levels. Methods Patients with acute cerebral infarction and healthy physical examinees selected for the prospective study were included into the cerebral infarction group and control group, respectively. Clinical data were collected and the patients' condition were evaluated, and then the contents of the β2-MG, high sensitivity C reactive protein (hsCRP), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), intercellular cell adhesion molecule-1 (ICAM-1) and soluble CD40 Ligand (sCD40L) in serum were tested. Results The contents of serum β2-MG, hsCRP, IL-6, IL-8, TNF-α, ICAM-1, sCD40L in patients with acute cerebral infarction were obviously higher than those in cases of the control group. The severer the condition of the disease was, the higher contents of serum β2-MG, hsCRP, IL-6, IL-8, TNF-α, ICAM-1 and sCD40L became. The greater the volume of cerebral infarction was, the higher the contents of serum β2-MG, hsCRP, IL-6, IL-8, TNF-α, ICAM-1 and sCD40L were. The content of serum β2-MG was positively associated with the contents of hsCRP, IL-6, IL-8, TNF-α, ICAM-1 and sCD40L. Conclusions The level of serum β2-MG was abnormally elevated in the patients with acute cerebral infarction. The level of serum β2-MG can evaluate the severity of disease, infarction size and the degree of inflammation reaction in patients with acute cerebral infarction.