Objective To observe the clinical curative effecand safety of ordinary intensity modulated and simplified intensi-ty modulated radiotherapy technique combined with transcathetearterial chemoembolization (TACE) fotreating primary hepaticancer(PHC) .MethodTotally 85 caseof Phwere randomly divided into the observation group (n=43) and the control group (n=42) .The observation group adopted the sequential therapy of TACE combined with the simplified intensity modulated radio-therapy(sIMRT) and the control group adopted the sequential therapy of TACE combined with the conventional intensity-modula-ted radiation therapy (cIMRT) .The shorterm curative effect,progresfree survival (PFS) ,overall survival (OS) ,and toxicity and adverse reactionwere observed in the two group.Result85 casewere followed up according to the requirement,2 casein the control group did noparticipated in the effecevaluation due to the unfinished radiotherapy projec.There were no statistically significandifferencebetween the two groupin the shorterm effect(55 .81% v.52 .50% ) ,PFS(25 .51 weekv.28 .06 weeks) and OS(78 .82 weekv.83 .22 weeks) (P＞0 .05) .The main toxicity and adverse reactionwere similain the two group,each i-tem had no statistical difference between the two group(P>0 .05) .Conclusion sIMRcan obtain the curative effecand progno-sisimilato cIMRwithouincreasing the toxicity and adverse reaction,and reducethe trend developing radioactive livedam-age ,which can be used athe routine replace mode of intensity modulated radiotherapy projecof PHC.

Objective To investigate the effects of glycogen synthase kinase-3β (GSK-3β) and β-catenin signaling on the human renal proximal tubular epithelial HK-2 cell injury induced by depleted uranium(DU),and provide a new enlightenment for the development of DU antidotes.Methods H K-2 cells were exposed to different concentrations of DU for 3-24 h,then the protein expressions of kidney injury molecule 1 (KIM-1),neutrophil gelatinase-associated lipocalin (NGAL) and nuclear β-catenin were detected by immunofluorescence staining.The protein expressions of p-GSK-3 β(S9),GSK-3β and cmyc were detected by Western blot assay.HK-2 cells were transiently transfected by GSK-3β (KD) plasmid or treated by TDZD-8 to inhibit the activity of GSK-3β specifically.Other HK-2 cells were transiently transfected by β-catenin plasmid to overexpress the β-catenin protein.Results The percentages of KIM-1 and NGAL-positive cells increased with DU exposure time and concentrations from 300 and 600 μmol/L,and they were significantly higher than those of the blank control at 6-24 h of DU exposure (KIM-1-positive cells:t =11.06,18.97,30.49,P ＜0.05;t =6.79,16.02,85.45,P ＜ 0.05;NGAL-positive cells:t =11.78,11.37,34.29,P ＜0.05;t =7.34,21.63,36.84,P ＜0.05).In contrast,the ratio of p-GSK-3β (S9) to GSK-3β and percentage of nuclear β-catenin-positive cells were significantly higher than that of the blank control at 3-24 h of DU exposure (p-GSK-3β(S9)/GSK-3β:t =3.95,4.69,5.40,3.34,P ＜ 0.05;nuclear β-catenin-positive cells:t =4.61,6.52,36.64,14.93,P ＜ 0.05) with a maximum response at 9 h of DU exposure accompanied with corresponding increase of protein level of c-myc,a downstream target gene of β-catenin.Transient transfection of HK-2 cells with GSK-3β (KD) plasmid significantly inhibited the activity of GSK-3β (t =8.07,P ＜ 0.05) and reduced the DU-increased percentage of KIM-1-positive cells (t =24.77,P ＜ 0.05).Treatment cells with TDZD-8 inhibited the activity of GSK-3β and enhanced the percentage of nuclear β-catenin-positive cells,and it also significantly reduced the percentage of KIM-1-positive cells in HK-2 cells exposed to DU (t =6.25,6.73,P ＜ 0.05).Moreover,overexpression of β-catenin significantly reduced DU-induced cell injury (t =7.48,P ＜ 0.05).Conclusions GSK-3β/β-catenin signaling plays a key role in regulating the DU-induced cytotoxicity of HK-2 cells.Inhibition of GSK-3β activity and overexpression of β-catenin can protect the HK-2 cells from DU-induced damage.

Objective To evaluate the efficacy and safety of gefitinib combined with concurrent thoracic radiotherapy in the treatment of local - advanced non - small cell lung cancer with sensitive EGFR mutations. Methods From June 2015 to December 2016,fifty-six eligible patients in Chongqing Three Gorges Central Hospital were randomly assigned into two groups by one to one ratio,with 28 cases in each group.A group received treatment of gefitinib combined with concurrent thoracic radiotherapy, and B group adopted concurrent chemoradiotherapy. The toxic effects were recorded and all patients were followed up as defined by the study protocol.Primary study endpoints included:severe toxic effects,objective response rate and disease control rate,progression free survival and overall survival.Results Twenty-six patients in A group completed the study,and the severe toxic effects were as followed:interstitial pneumonia(3/26),radiation esophagitis(4/26),myelosuppression,skin rashes and gastrointestinal disruption. Twenty- eight patients in B group completed the study, and the severe toxicity included: interstitial pneumonia (4/26),radiation esophagitis(3/26),myelosuppression,skin rashes and gastrointestinal disruption.No toxicity higher than gradeⅢdeveloped in both two groups,and there were no statistically significant differences in incidence rates of interstitial pneumonia and radiation esophagitis between the two groups ( all P >0. 05 ). Moreover, there were no statistically significant differences in ORR and DCR between the two groups( ORR:61.5% vs.39.3% ,P=0.102;DCR:84. 6% vs. 71. 4% , P =0. 505 ). A group showed the benefit over B group in PFS ( 12. 45 months vs. 10.35 months,P=0.036).However,OS didn＇t reach and needed further follow-up.Conclusion The modality of gefitinib combined with concurrent thoracic radiotherapy in the treatment of local -advanced non -small cell lung cancer with sensitive EGFR mutations is safe and effective,and it yet needs further follow-up.

Objective To investigate the effect of Yigong San(YGS)on learning and memory abilities of rats with lipopolysaccharide(LPS)-induced cognitive decline and explore its possible mechanism in light of intestinal microbiota.Methods Forty SD rats were randomly divided into control group,model group,donepezil(1.3 mg/kg)group,and high-dose(5.25 g/kg)and low-dose(2.63 g/kg)YGS treatment groups.After 24 days of treatment with the corresponding drugs or water by gavage,the rats in the latter 4 groups received an intraperitoneal injection of LPS(0.5 mg/kg)to establish models of Alzheimer's disease(AD).Water maze test and HE staining were used to evaluate the changes in learning and memory abilities and pathomorphology of the hippocampus.The changes in gut microbial species of the rats were analyzed with 16S rRNA sequencing,and the levels of IL-6,TNF-α,and IL-1β in the brain tissue and serum were detected using ELISA.Results Compared with the AD model group,the YGS-treated rats showed significantly shortened escape latency on day 5 after modeling,reduced neuronal degeneration and necrosis in the hippocampus,lowered pathological score of cell damage,and decreased levels IL-6,TNF-α and IL-1β in the brain tissue and serum.The YGS-treated rats showed also obvious reduction of Alpha diversity indicators(ACE and Chao1)of intestinal microbiota with significantly increased abundance of Prevotellaceae species at the family level and decreased abundance of Desulfovibrionaceae,which were involved in such metabolic signaling pathways as cell community prokaryotes,membrane transport,and energy metabolism.Conclusion YGS improves learning and memory abilities and hippocampal pathomorphology in AD rat models possibly by regulating the abundance of intestinal microbial species such as Prevotellaceae to affect the metabolic pathways for signal transduction,cofactors,and vitamin metabolism.

Objective To investigate the effect of Yigong San(YGS)on learning and memory abilities of rats with lipopolysaccharide(LPS)-induced cognitive decline and explore its possible mechanism in light of intestinal microbiota.Methods Forty SD rats were randomly divided into control group,model group,donepezil(1.3 mg/kg)group,and high-dose(5.25 g/kg)and low-dose(2.63 g/kg)YGS treatment groups.After 24 days of treatment with the corresponding drugs or water by gavage,the rats in the latter 4 groups received an intraperitoneal injection of LPS(0.5 mg/kg)to establish models of Alzheimer's disease(AD).Water maze test and HE staining were used to evaluate the changes in learning and memory abilities and pathomorphology of the hippocampus.The changes in gut microbial species of the rats were analyzed with 16S rRNA sequencing,and the levels of IL-6,TNF-α,and IL-1β in the brain tissue and serum were detected using ELISA.Results Compared with the AD model group,the YGS-treated rats showed significantly shortened escape latency on day 5 after modeling,reduced neuronal degeneration and necrosis in the hippocampus,lowered pathological score of cell damage,and decreased levels IL-6,TNF-α and IL-1β in the brain tissue and serum.The YGS-treated rats showed also obvious reduction of Alpha diversity indicators(ACE and Chao1)of intestinal microbiota with significantly increased abundance of Prevotellaceae species at the family level and decreased abundance of Desulfovibrionaceae,which were involved in such metabolic signaling pathways as cell community prokaryotes,membrane transport,and energy metabolism.Conclusion YGS improves learning and memory abilities and hippocampal pathomorphology in AD rat models possibly by regulating the abundance of intestinal microbial species such as Prevotellaceae to affect the metabolic pathways for signal transduction,cofactors,and vitamin metabolism.