Objective To investigate the role of CD4+CD25+FoxP3+ in severe Mycoplasma pneumonia among children.Methods One hundred and forty children with M.pneumoniae pneumonia (65 severe and 75 non-severe) who were hospitalized were enrolled along with forty other children as controls.X-ray was assessed.The proportions of peripheral blood CD4+CD25+FoxP3+cells were determined by flow cytometry.Results Both severe and non-severe children had decreased CD4+CD25+FoxP3+cells as compared with control subjects in acute phase (0.87 ± 0.66％ vs.3.88 ± 2.00％,P ＜ 0.01 and 1.17 ± 0.70％ vs.3.88 ±2.00％,P ＜0.01,respectively).The levels of CD4+CD25+FoxP3+cells in severe children were lower than those in non-severe children in acute phase and recovery phase (0.87 ±0.66％ vs.1.17 ±0.70％,P ＜0.05 and 1.66 ±0.85％ vs.3.61 ± 1.45％,P＜0.01,respectively).Both severe children and non-severe children expressed higher CD4+CD25+FoxP3+cells in recovery phase than in acute phase (1.66 ± 0.85 ％ vs.0.87 ± 0.66％,P ＜0.01 and 3.61 ± 1.45％ vs.1.17 ±0.70％,P ＜0.01,respectively).Conclusion The expression of CD4+CD25+FoxP3+Tregs may play a role in the onset of severity of mycoplasma pneumonia and the low express of CD4+CD25+FoxP3+Tregs in children infected with M.pneumonia may increase the susceptibility to severe mycoplasma pneumonia.

OBJECTIVE To investigate the genetic background and antibiotic resistance of continuously isolated P.aeruginosa strains in Shaoxing.METHODS Eighty six strains of P.aeruginosa were isolated from hospitalized patients,and drug-resistant genes,integrons and transposons were detected by PCR.RESULTS The positive rates of blaCARB,blaVIM,blaDHA,blaTEM,ant(2″)-Ⅰ,aac(6')-Ⅱ,aac(6')-Ⅰb and ant(3″)-Ⅰ were 30.2%,14.0%,3.5%,1.1%,27.9%,24.4%,15.1% and 4.7%.There were clone transmitted phenomenon.CONCLUSIONS There are very high positive percentages of blaCARB,blaVIM,ant(2″)-Ⅰ,aac(6')-Ⅱ,and aac(6')-Ⅰb genes in continuously isolated P.aeruginosa strains.P.aeruginosa can induce clone transmitted hospital infection and it has fulminant prevalence.

Objective Published literatures on the relationship between IL-13 gene polymorphism and the susceptibility of children to bronchial asthma in China were comprehensively analyzed with the use of Meta-analysis to evaluate this relationship.Methods The data were collected from the Medline database,Ovid database,the Cochrane library,and Chinese Biomedical database,and the references of eligible studies were manually screened.Published data related to case-control studies reporting the link between IL-13 polymorphisms and asthma in Chinese children were retrieved through those database.Meta-analysis was conducted to determine whether the IL-13 gene polymorphisms were associated with asthma.Results Eighteen studies were finally accepted for analysis.There were three studies focusing on C-1 112T polymorphism,and six studies focusing on C + 1923T polymorphism,and fourteen studies focusing on G + 2044A polymorphism.There was no evidence to confirm that the genotypes in position IL-13-1112 C/T were associated with asthma in Chinese children [odds ratio(OR) =1.00,95％ CI 0.82-1.22,P =0.98].The OR of asthma for TT/CC genotypes was 1.15 (95 ％ CI 0.57-2.33,P =0.69) and for CT/CC was 1.01 (95 ％ CI 0.82-1.25,P =0.89).There was significant evidence to confirm that the genotypes in position + 1923 C/T were associated with asthma in Chinese children(OR =1.86,95％ CI 1.29-2.67,P =0.000 9).The OR of asthma for TT/CC genotypes was 2.12 (95 ％ CI 1.27-3.56,P =0.004) and for TC/CC was 1.67 (95％ CI 1.18-2.35,P =0.003).There was no correlation between IL-13 + 2044G/A polymorphism and the susceptibility (OR =1.33,95％ CI 0.94-1.88,P =0.11).The OR of asthma for AA/GG genotypes was 1.30 (95 ％ CI 0.76-2.20,P =0.34) and for AG/GG was 1.24(95％ CI 0.90-1.70,P =0.19).Conclusions IL-13 gene + 1923 TT and TC genotypes should be associated with susceptibility of asthma in Chinese children,and the T allele could increase the risk of asthma.No clear relationship was found between the genotype TT/TC at the IL-13-1112 site and the incidence of asthma of children in China,and so was the genotype AA/AG at the IL-13 +2044 site and the incidence.

Objective To study the deleterious effect of prolonged hyperoxia exposure on preterm rat lungs. Methods On the 2nd postnatal day, preterm SD rats were randomly assigned to the air group (I) and hyperoxia group (II, exposed to 85% O2). After 3, 7 and 14 days of exposure, the contents of total protein (TP), hydroxyproline (HYP) and malondialdehyde (MDA), total cell counts and differentiation in bronchoalveolar lavage fluid (BALF), ratio of lung wet weight/dry weight (W/D), and lung collagen content were examined. After 3, 7, 14 and 21 days of exposure, lung histopathology and radial alveolar counts (RAC) were performed. Results On day 3 of hyperoxia exposure, only the MDA content increased in Group II (P<0.05). On day 7 and 14, TP, HYP, total cell counts, the percentage of neutrophils in BALF and lung W/D also significantly increased (P<0.05 or 0.01). The differences of lung collagen contents between the two groups were not significant (P>0.05). Hyperoxia exposure resulted in subacute alveolitis and inhibition of lung development on day 7, 14 and 21. RAC was similar between the two groups on day 3 (4.9±0.7 vs 5.0±0.8), but different on day 7 (5.9±0.9 vs 7.1±0.9; P<0.05. On day 14 and 21, RAC decreased more obviously in Group II compared with that in Group I (7.0±0.8 vs 9.9±0.6, 7.3±0.9 vs 10.5±0.8; P<0.01). Conclusions Prolonged exposure to 85% O2 may result in subacute inflammatory lung injury and inhibition of lung development in preterm rats.

· AIM:To investigate the prevalence and related factors of dry eye in primary school pupils in Lanzhou,Gansu Province.· METHODS:From October to November 2016,1347 pupils in two primary schools in Lanzhou,Gansu Province,were randomly selected as subjects.Every pupil was carried on the questionnaire of dry eye and eye inspection to confirm the diagnosis of dry eye.Besides,the prevalence and influencing factors of dry eye in pupils were analyzed by chi-square test,Mann-Whitney U test and logistic regression model.· RESULTS:A total of 1 268 pupils took part in this study and the inclusion ratio was 94.14％;271 individuals were diagnosed as dry eye,and the prevalence rate was 21.37％.Statistical analysis showed that the risk factors of dry eye were male,senior pupils,often using eye drops,poor reading habits,wearing contact lenses,video terminals last for a long time,learning pressure.· CONCLUSION:Dry eye has become one of the main diseases that plagued pupil's life and learning.It should cause wide attention.Considering the above factors,rational use of eye and improve lifestyle will help to reduce the damage to eye of pupils.

A permeabilization method of Micrococcus cells has been established. The obtained penneabilized cells could be used for several batches and in the mean time the intracellular enzymes still keep high activity. This method will undoubtedly increase the productivity of the cells and cut down the cost; therefore, it will be a promising way in the treha-lose industrialization. The experiment shows: after being treated with 5% (v/v) methylbenzene for 40min, the cells in suspension were converted into permeabilized cells, then the latter acted on 10% liquefied starch to produce trehaloae, the conversion ratio could reach 70%. The penneabilized cells could be used at least for 6 batchs (12h per batch) and the intracellular enzyme activity kept steady.

0.05).The serum PICP of tubercular meningitis children after 4 neeks glucocorticoid therapy (108.85?46.13) ?g/L was significantly lower than that in control group((154.38)?47.98) ?g/L and glucocorticoid- pretreatment (152.99?44.78) ?g/L (P

Hearing Loss, Sensorineural ; genetics ; Humans

LncRNAH19 has been implicated as having both oncogenic and tumor suppression properties in cancer. LncRNAH19 transcripts also serve as a precursor for miR-675. However, it is unknown whether LncRNAH19 and miR-675 are involved in the migration and invasion of hepatocellular carcinoma (HCC) cells. The purpose of this study was to investigate the effect and mechanism of LncRNAH19 and miR-675 on migration and invasion of HCC cells. The migration and invasion of HCC cells were measured by Transwell migration and invasion assays after transfection of HCC cells with miR-675 inhibitors and LncRNAH19siRNA. The levels of LncRNAH19 and miR-675 were detected by quantitative reverse transcriptase real-time polymerase chain reaction (qRT-PCR), and the protein expression of AKT, GSK-3β and Cdc25A by Western blotting analysis. The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells (P<0.01) as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells (P<0.01) as compared with the control group. Western blotting analysis showed that the expression levels of AKT and Cdc25A were significantly increased (P<0.05), and the expression level of GSK-3β was significantly decreased (P<0.05) after treatment with miR-675 inhibitors and LncRNAH19siRNA as compared with the control group. These findings suggested that inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3β/Cdc25A signaling pathway.

Astrocytes maintain homeostasis of neuronal microenvironment, provide metabolic and trophic support to neurons and modulate neuronal responses to injury. Rotenone specifically inhibits mitochondrial complex I, and long exposure to rotenone may increase the risk for Parkinson's disease (PD) and cause Parkinsonism. However, little is known about the role of astrocytes in the process of rotenone-induced dopaminergic neuron injury. In order to investigate this issue, we used MN9D cells as a cell model of dopaminergic neurons and rotenone as a toxin to initiate mitochondrial deficiency. MN9D cells treated with the normal medium or astrocyte-conditioned medium (ACM) were exposed to different concentrations of rotenone for different time followed by cell viability measurement by MTT assay. Besides, various concentrations of ACM and temporally different treatments were devised to evaluate protective efficiency of ACM. Growth curve of cells in the normal medium or ACM was continuously assessed by cell counting for 8 d. The influence of rotenone and ACM on cellular oxidative stress was determined by DCFH-DA staining followed by flow cytometric analysis. Glutathione (GSH) content after treatment of ACM or rotenone was measured by GSH assay kit. Our results showed that rotenone decreased viability of MN9D cells in a dose-dependent manner and ACM treatment significantly attenuated rotenone toxicity at each concentration. No significant difference in growth rate was observed between the normal medium and ACM treatment. Four concentrations of ACM, namely 1/3ACM, 1/2ACM, 2/3ACM and pure ACM, all displayed protection, increasing cell viability to (124.15+/-0.79)%, (126.59+/-0.82) %, (125.84+/-0.61) % and (117.15+/-1.63) % of the cells exposed directly to rotenone, respectively. Treatment with ACM through the whole experiment except the initial 24 h, 24 h before or at the same time of rotenone addition all exerted protective effects, with cell viability being (110.11+/-2.52)%, (113.30+/-2.36) %, (114.42+/-2.00)% of the cells exposed directly to rotenone, respectively. Conversely, ACM treatment 12 h after rotenone addition had no protective effect, with cell viability being (102.54+/-1.36)% of the cells exposed directly to rotenone. Moreover, ACM treatment up-regulated GSH level in MN9D cells nearly twofold. Incubation with 100 nmol/L rotenone for 24 h depleted GSH level by nearly two thirds of the control, but ACM treatment mitigated the drop of GSH level, maintaining its content at (147.83+/-0.63)% of the control. Consistent with GSH change, rotenone administration resulted in a positive rate of 96.24% of DCF staining, implying a great extent of oxidative stress, whereas treatment with ACM reduced the extent of oxidative stress to a positive rate of 78.31%. Taken together, these findings suggest that astrocytes protect MN9D cells from oxidative stress caused by rotenone, and GSH partially accounts for the protection. Therefore, astrocytes may play a protective role in the process of PD.
Animals ; Astrocytes ; physiology ; Cells, Cultured ; Cytoprotection ; Glutathione ; analysis ; physiology ; Neurons ; drug effects ; metabolism ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Rotenone ; toxicity