Objective To explore the attention bias characteristics and impacts of attention training on negative attention bias of undergraduates with sub-clinical depression.Methods The undergraduates whose BDI scores being at the top of 5％ were recruited as participations and assigned to early attention training group and late attention training group using random number table.The dot probe paradigm was used to compare the difference of depressive symptoms and ingredients of attention bias made by different processing phases of attention training.Results (1)The BDI score after the training(87.91± 12.47) was significantly lower than that the former test (97.23±17.72) (F~,32)=4.78,P＜0.05),and the attention bias score in late attention training group (-5.97±2.92) was lower than that in the early attention training group(2.77±2.75) (P＜0.05).The interaction of the stimulus materials presenting time and the measuring time was significant(F(2,64) =4.76,P＜0.05).Simple effect analysis showed that when the time of stimulus material presenting was 1 000 ms,the score of negative attention bias after the test (-4.89 ± 23.66) was significantly lower than pre-test (7.73±26.14) (F(1,33) =5.11,P＜ 0.05).In the pre-test,the negative attention bias scores of the stimulus materials presenting time for 100 ms and 1 000 ms (8.62 ± 27.60,7.73 ± 26.14) were significantly higher than that for 500 ms (-12.80±29.09)(P＜0.05).(2)When the negative disengaged score as a dependent variable,the repetitive measure analysis of variance showed that the interaction effect of the stimulus materials' presenting time and training group type was significant (F(1,32) =4.41,P＜0.05).Simple effect analysis results indicated the negative disengaged score of the late attention training group at post-test (-5.84±7.79) was significantly lower than that at pre-test (24.16±7.35) (P＜0.05).Conclusion The attention training during the late stage of the attention process can efficiently intervene the negative attention bias of undergraduates with sub-clinical depression.

Objective To study the mechanisms of depression by exploring expressional differences of AQPs in the tissues of chronic stress depression rats.Methods Depression model was replicated by unpredicted chronic stress.20 rats were randomly separated into normal control group and model control group,AQP4 and AQP3,AQP8 expressions on hippocampus and gastrointestinal mucosa of rat model with depression were detected by immunochemical staining method.Results Means of optical density of AQP4 of normal group and model group hippocampus were 0.28 ± 0.02,0.22 ± 0.06 respectively,and the difference between two groups was significant statistically(t value was 2.756,P＜0.05).The expression of AQP3 on gastric mucosa and colonic mucosa between two groups had no significant statistically(t value were 1.814,1.812,P＞0.05).Two groups'means of optical density of AQP3 on small intestinal mucosa were 0.15 ± 0.02,0.17 ± 0.02,and the difference was significant statistically (t value was 2.769,P＜0.05).Two groups'means of AQP8 optical density in gastric mucosa were 0.15± 0.01,0.19 ± 0.04 ;0.16 ± 0.01 and 0.21 ± 0.04 in small intestinal mucosa;0.16 ± 0.01 and 0.22 ± 0.04 in colonic mucosa,and the differences were significant statistically(t values were 3.139,5.113,4.534,P＜0.05,P＜0.01,P＜0.01).Conclusion The expression of AQP4 on depression model rat hippocampus are lower than those of the normal group ; and the expression of AQP3 on gastric mucosa and colonic mucosa are no change obviously,but it(')s up-regulation on small intestinal mucosa.The expressions of AQP8 on gastric mucosa and small intestinal mucosa and colonic mucosa are up-regulating.

AIM:To explore the effect of Delta-like ligand 4 (Dll4)-Notch signaling pathway blockade on the development of Thelper 17(Th17) cells in the asthmatic mice.METHODS:Male BALB/c mice were randomly divided into 5 groups:control group, asthma group, normal saline group, anti-Dll4 antibody group, and immunoglobulin G group.The protein expression of Dll4 was detected by immunohistochemical staining.The proportion of Th17 cells in mouse spleen isolated CD4+ T cells was measured by flow cytometry.The protein expression of Th17 transcription factor retinoid-related orphan receptor γt (RORγt) was determined by Western blot.The serum level of interleukin (IL)-17 was measured by enzyme-linked immunosorbent assay (ELISA).RESULTS:The expression of Dll4 in the lung tissues from asthma group significantly increased as compared with anti-Dll4 antibody group.The proportion of Th17 cells in CD4+ T cells was significantly down-regulated, and the protein expression of RORγt in the lung tissues was significantly reduced in anti-Dll4 antibody group compared with asthma group (P<0.05).Moreover, the serum level of IL-17 in anti-Dll4 antibody group was significantly reduced compared with asthma group (P<0.01).CONCLUSION:The blockade of Dll4-Notch signaling pathway inhibits the differentiation of Th17 cells in asthmatic mice.

AIM: To observe skeletal muscle damage of mdx mice after overload exercise, and protection to muscle damage induced by exercise due to myoblast transplantation (MTT). METHODS: Muscle samples of C 57 mice were minced and digested with trypsin, and myoblasts were cultured ex vivo , purified and detected by immunohistochemistry stains. The myoblasts were injected into muscle of left limb of mdx mice, whereas the right limb was injected with DMEM liquid as control. Mice were submitted to exercise for 3 days starting 1 month after MTT, and then Evans blue was injected intravenously through the tail vein. The muscle cryostat sections of mdx mice were made, and then detected the immunofluorescence of dystrophin. Under a fluorescence microscope, the number of fiber stained with Evans blue and dystrophin was counted, analyzed quantitatively with image software. RESULTS: Under a fluorescence microscope, only 10 37%?2 87% muscle fibers in the myoblast grafted muscles were stained with Evans blue. In contrast, 26 82%?14 85% muscle fibers in right control muscles were stained. Significant differences between these two groups were showed ( P

AIM: To investigate the correlation between the expression of neuron-specific protein and apoptosis in the process of differentiation from rat bone marrow stromal cells into neuron with brain-derived neurotrophic factor (BDNF). METHODS: The 5th passage MSCs were induced by BDNF and 2-mercaptoethanol (?-ME), respectively. At 1 h, 6 h, 12 h and 24 h, nestin, neuron specific enolase (NSE), microtubulease associated protein (MAP)-2 and glail fibrillary acidic protein (GFAP) were detected by Western blotting. Cell cycle and apoptosis were examined by flow cytometry. RESULTS: Nestin and NSE of neuron-like cells induced by BDNF and ?-ME were all positive by Western blotting. At 12 h, nestin and NSE turned to negative and apoptosis was detected in ?-ME group, nestin and NSE still positive and apoptosis wasn't detected in BDNF group. Till 24 h, nestin and NSE in BDNF group were negative but apoptosis still not detected. Notably, GFAP (glial astrocyte marker) was detected and MAP-2 wasn't detected in the two induced groups. CONCLUSION: The down-expression of neuron-specific protein correspondingly with apoptosis in the process of differentiation from MSCs into neuron with ?-ME shows that apoptosis may be one of the causes of induced cell death. BDNF induction was not the cause of apoptosis. Other factors may include for the cell death in the presence of neuron-specific protein expression induced by BDNF.

Objeetive To construct the cell DNA damage models for the human CML K562 cell line before or after imarlnib mesylate treatment and observe the repairing process dynamically for investigating the iniluence of imatinib mesylate on the repair function of K562 cells after cell DNA danlage.Methods The MTT assay was used to estimate the optimal pretreatment concentration of imatinib mesylate in K562 cells and Western blot was employed to evaluate the phosphorylation status in K562 cells after imatinib mesylate treatment to estimate BCR/ABL tyrosine kinase inhibition by imatinib mesylate.The comet assay was used to detect the DNA damage induced by hydrogen peroxide at various concentrations in K562 cells with or without the pretreatment of imatinib mesylate.A dynamic observation on the repairing process after cell DNA damage was made by the comet assay.Results The pretreatment by imatinib mesylate for K562 cells was optimized to be at a final concentration of 1 μmol/L for 24 h as revealed by the MTT assay additionly imatinib mesylate treatment at this concentration could effectively inhibit the phosphorylation of the BCR-ABL fusion protein at Tyr177(Deusityrate 0.100±0.018).When compared with the control group(Deusityrate 0.425±0.039),the BCR/ABL phosphorylation at Tyr177 was significantly decreased by (77. 11±5.59) % (t=4. 57,P＜0. 05). The cell DNA damage models for both imatinib mesylate-nontreated and imatinib mesylate-pretreated K562 cell groups were constructed with hydrogen peroxide treatment at a final concentration of 10 μmol/L for 10 min at 4℃ as confirmed by the comet assay. When compared with the control imatinib mesylatenontreatod K562 cell group,the time duration required for the DNA repair in imatinib mesylate-pretreated K562 cell group was significantly prolonged (F= 97.79,P＜0. 05 ). Conclusions The cell DNA damage models for the leukemic K562 cell groups before or after imatinib mesylate treatment were successfully constructed and the tyrosine kinase inhibitor imatinib mesylate for BCR/ABL fusion protein was revealed to attenuate the DNA repair capacity of the K562 cells after DNA damage.

Objective To construct the transformed mouse BaF3-P210 cell line stably expressing BCR/ABL and to initially investigate the influence of BCR/ABL on the cell biological characteristics of BaF3 cell line. Methods The retroviral vector with bcr/abl gene was transfected into the packaging cell line. The BaF3 cells were infected with the collected viral supernatant. The transgenic BaF3-P210 cell line stably expressing BCR/ABL were screened and subcloned. The integration of the bcr/abl gene in the genome of the target cell was determined by PCR and DNA sequencing,trypan blue staining assay,flow cytometry and MTT assay. Results The bcr/abl gene was integrated into the BaF3 cell genome; RT-PCR and Western blot verified the stable expression of the bcr/abl gene and protein in the screened subclone cell line BaF3-P210. Compared with the control group,the cell proliferation rate was promoted (P

Objective: To investigate the effect of hypertensive disorder complicating pregnancy (HDCP) on the mortality and early complications of premature infants. Methods: The general clinical data of preterm infants with gestational age 24-36^{+ 6} weeks were collected from the cooperative units in the task group from January 1, 2013 to December 31, 2014.According to the severity of HDCP, the infants were divided into 4 groups: HDCP group, preeclampsia group, eclampsia group and non HDCP group, the mortality and major complications of preterm infants were compared, and the influencing factors were analyzed. Results: The mortality rate of preterm in the HDCP group was significantly higher than that of non HDCP group, and there was statistical significance (χ²=9.970, P=0.019). Eclampsia had a highest fatality rate (4.8%) in the early stage, compared with non HDCP group (2.2%), and the difference was statistically significant.Comparison of HDCP group (1.8%) and eclampsia group (3.2%) suggested that there was no statistically significant difference.The incidence of respiratory distress syndrome (RDS) in preterm in HDCP group was significantly higher than that of non HDCP group, and there was statistical significance (χ²=13.241, P=0.004). Eclampsia group showed the highest incidence (35.4%), compared with non HDCP group (16.2%), the difference was statistically significant, but compared with HDCP group (19.9%), preeclampsia group (17.1%), there was no significant diffe-rence.The incidence of bronchopulmonary dysplasia (BPD) in preterm in HDCP group was significantly higher than that of non HDCP group (χ²=9.592, P=0.022), the highest incidence showed up in eclampsia group (9.7%), compared with non HDCP group (2.0%) and HDCP group (1.7%), the difference was statistically significant.But there was no statistically significant difference, compared with preeclampsia group.As the degree of HDCP aggravated, the incidence of BPD gradually rose.There was no significant impact on necrotizing enterocolitis (NEC), retinopathy of prematurity (ROP), intraventricular hemorrhage (IVH) and sepsis of HDCP (χ²=7.054, 7.214, 0.358, 3.852; P=0.070, 0.065, 0.949, 0.278). Considering the overall outcome of the child, that was, whether the child died or survived, he had at least one complication, and HDCP had an effect on it (χ²=15.697, P=0.001), so the incidence increased while the degree of HDCP rose gradually.After adjusting gestational age, birth weight, sex, way of delivery, placental abruption and front placenta, prenatal hormonal, gestational diabetes, neonatal asphyxia and other factors, the results displayed that HDCP was the factor leading to the death of premature baby (OR=2.159, 95%CI: 1.093-4.266), and comparison between preeclampsia and eclampsia showed no statistical difference (P=0.714, 0.389); HDCP had no significant influence on RDS, BDP, ICH, NEC, ROP and sepsis. Conclusions HDCP leads to increased risk of premature death, but also leads to the increased incidence of RDS and BPD, but it had no obvious effect on NEC, ROP, IVH, sepsis and other complications.