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ificant effects on the decrease of SMI in patients with esophageal cancer after radiotherapy and chemotherapy.Conclusions Nutrition intervention can reduce the incidence of delayed chemoradiotherapy during esophageal cancer CCRT and reduce skeletal muscle loss.The decline of SMI is mainly related to the T stage,N stage,and nutrition intervention at baseline.Objective To investigate the clinical features and treatments of programmed death-1(PD-1)inhibitors-induced bullous pemphigoid(BP).Methods The clinicopathological and immunohistological data of patients with PD-1 inhibitors-induced BP from Peking Union Medical Collage Hospital and reported in the literature were retrospectively analyzed.Results Totally 21 cases(15 males and 6 females)were enrolled.The average age was(70.9±9.7)years(56-86 years).The most common primary malignancies were melanoma(38.10%)and lung cancer(33.33%).The average duration from onset of PD-1 inhibitors treatment to diagnosis of BP was(49.1±23.7)weeks.Typical dermatopathological features were sub-epidermal blisters(76.19%)with infiltration of eosinophils(88.24%).Direct immunofluorescence features were linear deposition of complement C3(95%)and IgG(75%)in the basement membrane zone.Anti-BP180-NC16A antibodies were positive in most cases(84.21%).Patients were mainly treated with systemic corticosteroids,whereas biologics such as rituximab and omazumab were also effective.Conclusions The risk of PD-1 inhibitors-induced BP should be recognized by dermatologists and oncologists.Early diagnosis and timely treatment of BP induced by PD-1 inhibitors are important to improve the prognosis.Objective To investigate the effect of pirfenidone on cytokine/chemokine production by alveolar macrophages(AMs)in patients with idiopathic nonspecific interstitial pneumonia(iNSIP)or idiopathic pulmonary fibrosis(IPF).Methods We prospectively enrolled 10 iNSIP patients,11 IPF patients,and 8 non-interstitial lung disease(non-ILD)patients(control group)from our center from January 2015 to December 2018.AMs from bronchoalveolar lavage fluid(BALF)were cultured with or without lipopolysaccharide(LPS)stimulation.The production of Th1 cytokines [soluble tumor necrosis factor receptor(sTNFR)-1,sTNFR-2,and interleukin(IL)-1β],Th2 cytokines [IL-10 and granulocyte-macrophage colony-stimulating factor(GM-CSF)],angiogenic chemokines [IL-18 and macrophage inflammatory protein(MIP)-1β],and angiostatic chemokines [interferon-gama inducible monokines(MIG)and interferon-gama inducible protein(IP-10)] in the culture supernatants were measured by a bead-based assay,Luminex.The effect of pirfenidone on the cytokine/chemokine production was tested at various concentrations(0,0.03,0.10,0.30 mg/ml).Results The spontaneous and LPS-stimulated release of TNF-α,sTNFR-1,sTNFR-2,IL-1β,IL-10,MIP-1β,MIG,and IP-10 by AMs were significantly increased in iNSIP and IPF groups compared with control group(all P0.05).Conclusion Pirfenidone can markedly suppress cytokine/chemokine expression in iNSIP and IPF patients,but the difference is not significant between these two groups of patients.Objective To explore the role of evodiamine in promoting the apoptosis of glioma SHG-44 cells and its mechanism.Methods The in vitro cultured glioma SHG-44 cells were divided into control group and evodiamine group(which was further divided into three subgroups according to the glycoside concentrations).Cell viability was determined by CCK-8 method,cells apoptosis rate by flow cytometry,and nucleus apoptosis by Hoechst 33258 nuclear staining.Cell morphological changes were observed by transmission electron microscope.Protein expressions of Cleaved Caspase-3 and Cleaved Caspase-9 were detected by Western blot analysis.Results Evodiamine significantly inhibited the proliferation of glioma SHG-44 cells.The apoptosis rate of Glioma cells increased in a dose-dependent manner as the evodiamine concentration increased.Evodiamine promoted the expressions of cleaved Caspase-3 and cleaved Caspase-9.Conclusion Evodiamine inhibits glioma cell proliferation by changing the expressions of cleaved Caspase-3 and cleaved Caspase-9.Objective To investigate the effect of miRNA210 on primary myocardial cells in lipopolysaccharide(LPS)-induced myocarditis.Methods CCK8 method was used to detect the effect of miRNA210 on the viability of primary myocardial cells in normal or LPS-induced myocarditis rats.ELISA was performed to detect the secretion of tumor necrosis factor(TNF)-α and interleukin(IL)-1β after miRNA210 treatment.Flow cytometry was used to detect the apoptosis of primary myocardial cells before and after the intervention.Western blotting was used to detect the expression of TNF-α and IL-1β.The expression of apoptosis-related proteins bcl-2,bax,caspase-3,and hypoxia inducible factor 1 (HIF1)-vascular endothelial growth factor(VEGF)were detected by Western blotting.Results CCK8 detection results showed that,compared with the control group,the effect of miRNA210 mimic(t=0.000,P=1.000)and siRNA(t=0.686,P=0.500)interference had no significant difference on primary rat cardiomyocytes.The viability of rat primary cardiomyocytes signific3.181,P=0.033)were decreased after miRNA210 was silenced.Compared with LPS group,the expressions of bax(t= 4.899,P=0.008),HIF1(t=2.833,P=0.047),caspase-3(t=2.877,P=0.045),and VEGF(t= 2.994, P=0.040)were significantly decreased,and the expression of bcl-2 was increased(t=3.392,P=0.017).Conclusion Silencing miRNA210 can attenuate LPS-induced cardiomyocyte injury through HIF1-VEGF-mediated apoptotic pathway.Objective To investigate the effects of quercetin on cell viability,apoptosis,autophagy,and phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/mammalian target of rapamycin(mTOR)signaling pathway in human prostate cell carcinoma PC-3 cells.Methods PC-3 cells were cultured in vitro,and cell viability was detected by CCK-8.Apoptosis was detected by TUNEL staining.Autophagy vesicle was observed by acridine orange staining.Autophagosomes was observed by GFP-LC3 plasmid transfection analysis.Expressions of autophagy-related protein microtubule associated protein 1 light chain 3 fusion protein(LC3)and Beclin-1 and PI3K/Akt/mTOR signaling pathway protein were detected by Western blot analysis.Results Quercetin inhibited cell viability in a dose-time dependent manner and induced apoptosis.Quercetin increased the number of autophagy vesicles and autophagosomes in PC-3 cells.Quercetin increased the expressions of LC3-Ⅱ/LC3-Ⅰ and Beclin-1 in PC-3 cells and decreased the expression of phosphorylated-PI3K,phosphorylated-Akt and phosphorylated-mTOR.
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