ObjectiveTo observe the influence of lipopolysaccharide (LPS) on collagen metabolism of normal human skin fibroblasts and its biological role in the formation of hypertrophic scar.Methods Fibroblasts were isolated and cultured in vitro,and then exposed to different doses of LPS (0.005,0.01,0.05,0.1,0.5,1.0 μg/ml) from E.coli.055:B5 respectively.The expression of proccllagen type Ⅰ,Ⅲand collagenase mRNAs was tested by RT -PCR.Fibroblasts from hypertrophic scar tissue obtained from the same patients in the same culture passage were used as control.ResultsCompared with control group,the expression of procollagen typeⅠ,Ⅲ mRNAs in normal skin fibroblasts increased (0.323 ± 0.041,0.303 ± 0.063,0.391 ± 0.071,0.344 ± 0.086,0.488 ± 0.059,0.401 ± 0.087,0.616 ± 0.107,0.434 ±0.084,0.823 ±0.092,0.542 ± 0.082),while the expression of collagenase mRNAs of normal skin fibroblasts depressed(0.598 ± 0.068,0.556 ± 0.049,0.441 ± 0.043,0.372 ± 0.083,0.260 ± 0.027 ).When LPS was set to the concentration of 0.005 μg/ml,it showed a concentration dependent manner.However,when the concentration of LPS was set to 0.5 μg/ml,the expression of procollagen type Ⅰ,Ⅲ and collagenase mRNAs of normal skin fibroblasts began to decrease (0.451 ± 0.063,0.374 ± 0.072,0.360 ± 0.062).When the concentration of LPS was set to 1.0 μg/ml,the expression of procollagen type Ⅰ,Ⅲ mRNAs (0.162 ± 0.025,0.171 ± 0.061 )were inhibited and the expression of collagenase mRNAs began to increase (0.444 ±0.114).When the concentration of LPS was set to 0.1 μg/ml,the expression of procollagen type Ⅰ,Ⅲ and collagenase mRNAs of normal skin fibroblasts(0.823 ±0.092,0.542 ±0.082,0.260 ±0.027)was similar to that of hypertrophic scar tissue fibroblasts(0.829 ±0.049,0.569 ±0.038,0.277 ±0.059).ConclusionsThis result supported that LPS may be an important factor in collagen metabolism of normal skin fibroblasts and it plays an important role in hypertrophic scar formation.

Objective To explore the relationships among pulmonary function,DVH and acute radiation pneumonitis after three-dimensional conformal radiation treatment in patients with non-small-cell lung cancer.MethodsPulmonary function tests were conducted on 68 inoperable patients (male 42,female 26,median age 52,KPS≥80) before and after three months radiotherapy respectively.After 3 months of follow-up,radiation pneumonitis were graded,and V20,V30 and MLD were derived from dose volume histogram (DVH).ResultsAll patients were treated with radiotherapy at the irradiation dose of 60～70Gy.Acute radiation pneumonitis occurred in 24 patients with 11 Grade Ⅰ,7 Grade Ⅱ,3 Grade Ⅲ,3 Grade Ⅳ.There were no significant difference between the pre-irradiation and the three months after irradiation for FVC (P＞0.05).But there were significant different between pre-irradiation and three months after irradiation for FEV1.0 and DLCO (P＜0.05).V20,V30 and MLD were observed in patients treated with high radiation pneumonitis.ConclusionsThere were close relationships among pulmonary function,DVH and radiation pneumonitis in patients with non-small cell lung cancer.

Objective:To investigate the expression, prognostic value and mechanism of MCM10 in hepatocellular carcinoma (LIHC).Methods:The transcriptome and clinical data of hepatocellular carcinoma were obtained from The Cancer Genome Atlas database, and the rank sum test was used to analyze the expression level of MCM10 in tumor tissues and adjacent tissues. Cox regression analysis was used to analyze the relationship between MCM10 expression level and the survival prognosis of patients with hepatocellular carcinoma. Gene set enrichment analysis (GSEA) was utilized for pathway enrichment analysis between MCM10 high and low group gene expression profiles. The effect of MCM10 knockdown on the proliferation of HepG2 cells was determined by cell counting kit-8 (CCK-8) cell viability assay. The effect of MCM10 knockdown on the expression of G1/S-specific cyclin D1 was detected by Western blot.Results:The expression value of MCM10 in hepatocellular carcinoma was 0.709±0.595, and that in adjacent tissues was 0.077±0.094 ( P<0.0 001). Cox regression analysis showed that high expression of MCM10 was a risk factor and prognostic predictor of overall survival ( HR=1.32, 95% CI: 1.19~1.48) and disease-specific survival ( HR=1.40, 95% CI: 1.22~1.61) in LIHC. GSEA analysis showed that the differentially expressed genes were mainly enriched in cell cycle, p53 signaling pathway and positive regulation of G1-S phase transition, et al. CCK-8 assay showed that MCM10 knockdown could inhibit the proliferation of HepG2 cells. Western blot analysis further confirmed that knockdown of MCM10 expression inhibited the expression of cyclin D1 in HepG2 cells. Conclusions:MCM10 is a risk factor for the prognosis of patients with hepatocellular carcinoma, which can promote the proliferation of hepatoma cells through cyclin D1.

BACKGROUND: Conventional hemodialysis mainly for cleaning uremic micro molecule substance, such as urea nitrogen or creatinine; however, few hemodialyses can clean uremic middle molecule substances (MMS). With prolonged dialysis duration, MMS accumulates in vivo and induces a series of complications. OBJECTIVE: To compare the efficiency of adsorptive dialysis (hemoperfusion unites hemodialysis) and conventional hemodialysis in cleaning uremic MMS. METHODS: Totally 60 maintenance hemodialysis patients were averagely divided into the adsorptive dialysis group and conventional hemodialysis group. First of all, hemoperfusion apparatus and dialyser were connected in series to take the adsorptive dialysis in the adsorptive dialysis group (hemoperfusion apparatus were equipped before dialyser). 120 minutes later, the hemoperfusion apparatus was toke off and continues to hemodialysis for 120 minutes. Duration of conventional hemodialysis was 240 minutes. Changes in clinical symptoms and levels of liver function, kidney function, serum electrolytes, hemocytes and uremic MMS were observed prior to and after treatment. RESULTS AND CONCLUSION: Adsorptive dialysis could remove the MMS notably. Compared with the conventional hemodialysis group, a single 120 minutes treatment could decrease MMS significantly (P < 0.05). The platelet levels were obviously decreased in the adsorptive dialysis group after treatment (P < 0.05), which were significantly different from the conventional hemodialysis group (P < 0.05). There was no significant difference in liver function, kidney function or serum electrolytes concentration. But related symptoms, such as the skin itch, sleep disorders and myalgia, were relieved more or less.

Background: and Purpose This study aimed to determine the changes in cerebral blood flow (CBF) in patients who received different durations of hemodialysis (HD) using arterial spin labeling magnetic resonance imaging. Methods: The study included 46 patients who received HD and 24 demographically similar healthy controls (HCs). Patients who received HD were divided into three subgroups based on its duration: HD-1 (n=15, dialysis duration ≤24 months), HD-2 (n=16, dialysis duration >24 and ≤72 months), and HD-3 (n=15, dialysis duration ≥73 months). All subjects completed the Mini Mental State Examination and Montreal Cognitive Assessment tests, and the patients who received HD underwent laboratory tests. Group-level differences in the global and regional CBFs between patients who received HD and HCs were assessed. Correlation analysis was performed to evaluate the associations among CBF, clinical variables, and cognitive function. Results: Compared with HCs, global and regional CBFs were significantly increased in the HD-1 and HD-2 groups (p<0.05), but there was no significant difference in the HD-3 group (p>0.05). However, compared with the HD-1 group, the HD-3 group had significantly decreased global and regional CBFs (p<0.05). The cognitive function was worse in patients who received long-term HD than in HCs. Increased dialysis duration and hemoglobin level were predictive risk factors for decreased CBF in patients who received long-term HD. Conclusions Patients who received long-term HD with normal CBF had worse cognitive function, which may be related to increased dialysis duration.

Objective:To explore the interventional effect of β-sitosterol on ovalbumin(OVA)-induced allergic asthma rats and its potential mechanism.Methods:SD male rats were randomly divided into normal group(CON),model group(M),positive drug dexamethasone group(DEX,0.075 mg/kg)and β-sitosterol group(Sit,50 mg/kg).A rat model of allergic asthma was estab-lished by intraperitoneal injection of OVA with aluminum hydrogen solution,and nebulized inhalation of OVA to stimulate.Rats were given intragastric administration 30 min before aerosol challenge,and after continuous administration for 7 days,the indicators of cough and asthma and tracheal phenol red excretion were detected.HE staining was used to observe pathological changes of lung tis-sue.Flow cytometry was used to detect reactive oxygen species(ROS)generation,apoptosis level and ratios of Th17 and Treg cells in peripheral blood.Biochemical method was used to detect contents of MDA,and activities of T-SOD and GSH-Px in rat lung tissues.ELISA was used to detect levels of Th17 and Treg-related cytokines(TNF-α,IL-4,IL-6,IL-17A,and IL-35).Results:Compared with model group,β-sitosterol significantly prolonged the incubation period of cough and gasp in rats with allergic asthma,reduced the frequency of cough and gasping,and promoted the excretion of phenol red in trachea;significantly reduced inflammatory infiltration in lung tissue of asthmatic rats;observably reduced MDA content in lung tissue,ROS of primary lung cell and apoptosis levels of asthmatic rats,increased the activities of T-SOD and GSH-Px;markedly reduced proportion of Th17 cells and levels of pro-inflammatory cyto-kines TNF-α,IL-4,IL-6 and IL-17A,increased proportion of Treg cells and levels of anti-inflammatory cytokine IL-35.Conclusion:β-sitosterol can ameliorate airway inflammation and oxidative damage in OVA-induced allergic asthmatic rats,and its mecha-nism may be related to the regulation of β-sitosterol on Th17/Treg immune imbalance and oxidative stress response.

Inhibition of human epidermal growth factor receptor 2 mediated cell signaling pathway is an important therapeutic strategy for HER2-positive cancers. Although monoclonal antibodies are currently used as marketed drugs, their large molecular weight, high cost of production and susceptibility to proteolysis could be a hurdle for long-term application. In this study, we reported a strategy for the development of artificial antibody based on