Objective To improve theu nderstanding of the characteristci s of death in hospitail zed hc ildren and provide clinical cautionary information to professional healthcarep rovdie rs.Methods A retro-spective analysis was undertaken on thed ata of all children aged 1 month to 11 years who died at the Xinhua H ospital between 2007 and 2014.Demographic details,main causes of deaths,and chronic underyl ingd iseases were reviewed.Results Case fatality rate was 0.58%( 451/77 838 ) .Overall, the most common causes fo deathni hospitalized childer n were pneumo nia 38.80%(175/451),tumor 13.75%(62/451),sepsis 11.97%(54/451),central nerve system infection 8.00%(36/451) and accident 7.32%(33/451).Infectious disea-ses were the maoj r causes of deathi n children younger than 5ye ars of age(66.86%,230/344).In oc ntrast, noninfectious diseases accuo tn ed for mo re deathsni children more than 5 years old(52.34%,56/107).There were 343d eath cases comp licated wiht chronic undelr ying diseases.Congentia la bnormality was the most fre-quent chronic underlying disease observed in infants(59.90%,115/192) and tumor was the main chronic nu -derlying dsi easei not ddlers and elder children(34.36%,89/259).Conclusion Infectious diseasse were the major causes of deta hs,and teh mortality in the study popual tion decreased with age.Tumors and accidents accounted for more deaths in elder children.Chronic underlying diseases were found in most deaths of children.Efficient evaluation and effective intervention of these vulnerable children might save more lives.

Objective To construct a model of Fat-1/APPPS1 transgenic mice and a cellular model of microglia and explore the improvement effect and underlying mechanism of n-3 polyunsaturated fatty acids(n-3 PUFAs)on the learning and memory abilities of APPPS1 mice by regulating microglial activation and polarization.Methods After the male mice with heterozygous Fat-1 genotype were mated with the female ones with heterozygous APPPS1 genotype,genetic identification was used to screen the male offspring with Fat-1/APPPS1 genotype.Then after the male wild-type(WT)mice and those with Fat-1,Fat-1/APPPS1,and APPPS1 genotypes were bred until 9 months old,their learning and memory abilities were evaluated with Morris water maze(MWM)test.In addition,gas chromatography-mass spectrometry(GC-MS)was performed to detect the concentration of PUFAs in the brain,and immunohistochemistry(IHC)was applied to detect the deposition of β-amyloid protein(Aβ)in the hippocampal regions.Moreover,immunofluorescence assay,qRT-PCR,and enzyme-linked immunosorbent assays(ELISA)were conducted to measure inflammation,and transcription and expression of Iba-1(indicating the microglial activation)and CD86 and CD206(indicating microglial polarization)in central nervous system(CNS).After pretreated with DHA+EPA(25 pmol/mL∶25 μmol/mL),microglial model of inflammatory injury was established in immortalized mouse BV2 cells induced by LPS(1 μg/mL).Afterwards,immunofluorescence assay,qRT-PCR and Western blotting were used to detect inflammation and microglial activation and polarization.Results Compared with the APPPS1 mice,endogenous n-3 PUFAs effectively improved the learning and memory disorders in Fat-1/APPPS1 ones(P＜0.05),remarkably alleviated Aβ deposition in the hippocampal regions(P＜0.05),evidently reduced CNS inflammation and microglial activation(P＜0.05)and transformed the activated microglia from M1 to M2(P＜0.05).Furthermore,BV2 cells with DHA+EPA pretreatment obviously resisted LPS-induced cellular inflammation and induced activated ones from M1 to M2(P＜0.05).Conclusion n-3 PUFAs inhibit the microglial activation,regulate the microglial polarization from M1 to M2,reduce CNS inflammation,and thus alleviate learning and memory disorders in APPPS1 mice.