Objective To study the physical stress reactions of soldiers undergone 100 kilometer march in battle gear,and explore the mechanism of biochemical changes in special military physical training.Methods Thirty four soldiers of armed-police force,averagely aged 18.6?1.6 years,169.3?4.2cm in height,weighted 65.4?4.5kg and with one-year of military physical training experience,were involved in present study.The soldiers were loaded about 25 kilogram of battle gear in a supervised 100 kilometer march in three days.The changes on biochemical index after the march were analyzed.Results After 100 kilometer march in battle gear,significant decline were found in the following biochemistry indexes in the soldiers involved: HB(P

LOVO.PGZ significantly up-regulates the expression of PPAR? in MGC803 and LOVO cells,the expression of PPAR? was higher in combination group than PGZ alone(P

OBJECTIVE:To study the apoptosis of human leukemic cells induced by Dihydroartemisinin and its molecular mechanism.METHODS:Human leukemia K562 cells were treated by Dihydroartemisinin.The inhibitory effect on cell proliferation was assayed by MTT.Fluorescence microscopy was applied to observe the presence of apoptosis.The expression of caspase-3 was assayed with reverse transcription-polymerase chain reaction(RT-PCR).Levels of mitochondrial and cytoplasmic cytochrome C were determined using Western blot.RESULTS:After treatment with Dihydroartemisinin for 48 hours,the IC50 values of human leukemia K562 cells were 8? 10-5mol? L-1 detected at a wavelength of 570nm by MTT.Distinct morphology changes of cell apoptosis such as karyopyknosis and conglomeration were observed by Hoechst33342/PI staining.RT-PCR assay showed the expression of Caspase-3.Western-blot detection showed the decrease of mitochondrial cytochrome C concentration but the positive expression of cytoplasmic cytochrome C concentration.CONCLUSION:Dihydroartemisinin could inhibit proliferation and induce apoptosis of human leakemic K562 cells,this may partially attributed to the promotion of the delivery of cyt-c and the activation of caspase-3.

OBJECTIVE:To detect the expression of genes of leukemia cell line K562 treated by artemisinin using the gene chip technology and to study the mechanism of artemisinin in the inhibition of leukemia cell line K562 on the molecular level. METHODS:K562 cells were treated with artemisinin for 24h,and then the morphological change of K562 cells were observed under invert microscope and fluorescence microscope. The cell cycle state was examined by flow cytometry analysis (FCM). Total RNA samples were extracted and reverse transcribed to cDNA. Cy3-labelled cDNA samples were hybridized with gene chips.The hybridization results were detected by Gene Pix 4100A. RESULTS: Under invert microscope,different degree of shrinkage of K562 cells was noted,karyoschisis was reduced,cell density was decreased and the numbers of drift cells were increased.Under fluorescence microscope,caryotin was highly concentrated,marginalized and agglomerated to relucent clump,i.e.apoptotic body. Flow cytometric analysis showed that ratio of cells in G2 phase increased markedly. Hybridization analysis showed down-regulation of cyclin D1,cdk4,cdk2,cdc2,DNA-PK,DNA-TopoI,mcl-1,erk,jnk and VEGF in the artemisinin-treated K562 cells.CONCLUSION: The mechanism for artemisinin to inhibit the proliferation of leukemia cell line K562 is related to its action to alter the gene expression of certain regulatory substances involved in cell cycle and induce apoptosis of leukemia cell line K562.

Five grams of urea and two milliliters of corn syrup were added into 1 liter ethanoldistilled wastewater with 8% solid dregs The activity of acid resistant ? amylase and glucoamylase produced by inoculated Aspergillus kawachii genetic engineering strain TR12 in the transformed liquid reached a level of 13 42U/mL and 246U/mL respectively after fermentation at 32℃ by the shaking flask for 70 hours The transformed liquid was circularly applied to the ethanol ingredient process without cooking room, not only it didn't influence the ethanol output and quality, but also it could efficiently reduce the pollution of ethanol distilled wastewater and the cost of ethanol production

Objective To find out the expression relation between TP53 and NOTCH1,and to explore their effects in head and neck squamous cell carcinoma.Methods Obtained the differentially expressed genes data of head and neck squamous cell carcinoma from 279 samples in TCGA database.Analyzed the co-expression relation between TP53 and NOTCH1 through Pearson and Spearman method.Cbioportal was used to analyze their co-expressed genes.Establish the co-expression network of TP53 and NOTCH1 with String database.The pathway and function of co-expression network was identified through KEGG and DAVID database respectively.Results Among the 279 samples,TP53 and NOTCH1 was co-expressed in head and neck squamous cell carcinoma.(Pearson score =0.45;Spearman score =0.41) There were 182 interaction pairs of TP53 and NOTCH1 related co-expressed gene according to the String database.(Pearson and Spearman score ＞ 0.3)These genes were enriched in some pathways such as T cell receptor signaling pathway,cell cycle,cell adhesion molecules and so on.These genes were enriched in some tumor related function including immune response,regulation of transposition,regulation of apoptotic process,cell cycle,regulation of GTPase activity and so on.Conclusion TP53 and NOTCH1 was co-expressed.Through establishing co-expressed network of TP53 and NOTCH1 and bioinformatics analysis,their function and signaling pathway were explored.The data generated from this study could provide a new reference in mechanism research of head and neck squamous cell carcinoma.

Heart Diseases ; Humans ; Ryanodine Receptor Calcium Release Channel

Objective To explore the FOXP3-related mechanism underlying head and neck squamous cell carcinoma.Methods We used cbioportal to identify the co-expressed genes of FOXP3 in 279 samples from head and neck squamous cell carcinoma in TCGA database.We used String database to establish the co-expression network of FOXP3.The function of co-expression network was identified through DAVID database.We used miRTarBase and StarBase database to screen the microRNA,lncRNA and circRNA that regulate FOXP3.Finally,Cytoscape software was used to establish FOXP3-related ceRNA network.Results We found 950 FOXP3 related co-expressed gene.(Spearman score over 0.5) These genes were enriched in immune response including T cell,leukocyte and lymphocyte activation.CeRNA network revealed that 2 microRNAs (i.e.,miR-31-5p and miR-210-3p),42 lncRNAs (e.g.,XIST,TUG1,JRK and LINC00473) and 31 circRNAs (e.g.,ZNF223 _hsa_ circ_ 000898 and ISY1 _hsa _circ _001090) could regulate FOXP3.Conclusion We established FOXP3-related ceRNA network and identified 42 lncRNAs and 31 circRNAs that regulate FOXP3.The data generated from this study could provide a new cut point in research and treatment of head and neck squamous cell carcinoma.

Objective To evaluate the effect of fluid load on the prognosis of severe hand , foot and mouth disease in children. Methods The patients with severe hand foot and mouth disease in the emergency department of PICU in our hospital were enrolled as the research object. We would collect demographic characteristics , labora-tory tests and clinical data: age, gender, focus, basic disease, and simplified acute severity score (SAPS)Ⅱ and record the cumulative amount of fluid balance at 24, 48, 72 hours after admission. Results There was a signifi-cant difference on fluid balance at 48 and 72 hours between the survival group and the death group , the death group appeared the positive liquid balance , and there were significant differences in PICU retention time , mechani-cal ventilation rate, MODF involved organs, mortality and other prognostic indicators between the negative fluid balance group and the positive fluid balance group. Conclusion Fluid balance is an important treatment for severe hand foot and mouth disease, and positive liquid balance is related to mortality and other adverse prognosis.