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Objective To investigate the effect of maternal psychological status and family structure on the social emotional development of toddlers.Methods The study was conducted in January 2016,50 toddlers aged 12 to 36 months from one kindergarten in Dalian were selected with cluster random sampling.The parents of toddlers were interviewed,and the questionnaire for background condition,the socialemotional assessment scale for children and SCL-90 for maternal psychological status were applied.The effect of maternal psychological status and family structure on the social-emotion development of toddlers was analyzed.Results The positive rates of externalizing,internalizing,deregulation and competence in 50 toddlers were 24％ (12/50),14％ (7/50),20％ (10/50) and 22％ (11/50),respectively.The scores of obsession and anxiety in high school and college graduate mother group were higher than junior high school group(F =6.488,5.834,all P ＜ 0.05).The scores of obsession,interpersonal relationship,depression and anxiety in unhappy mother group were higher than those in happy mother group (t =7.812,3.860,5.871,6.843,all P ＜ 0.05).Compared to happy mother group,the abnormality rates of externalizing behavior [42％ (10/24)vs.8％ (2/26),x2 =10.667,P =0.001],internalization behavior [25％ (6/24) vs.4％ (1/26),x2 =0.000,P =0.008] and behavior disorder [33％ (8/24)vs.8％ (2/26),x2 =7.200,P =0.007] were significantly higher in unhappy mother group.There were significant differences in positive rate of externalized behavior among mothers with different educational levels (junior high school,high school and college graduate) (8/15,3/17 and 1/18,F =9.757,P ＜0.05).There were significant differences in respond ability of children among families with different structure (single-parent family,joint family,direct family and nuclear family) (3/5,1/4,7/28 and 0/13,F =8.134,P =0.026).Conclusion The abnormal rates of children's externalization,internalization and deregulation behavior are higher for mothers with emotional unhappiness,and the abnormal rate of children's competence in single-parent family,joint family and direct family are higher than that in nuclear family.
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Objective To investigate the protective effects and possible mechanisms of polydatin(PD) on hypoxic-ischemia brain damage(HIBD) in neonatal rat by means of the expression of intercellular cell adhesion molecule( ICAM)-1 in cortex. Methods Fifty-four SD rats were divided into 3 groups at random, shame group (no HIBD), HIBD group (no medication) ,and PD treatment group. 7day-old rat's HIBD model was established by Rice's method. ICAM-1 expression in brain after HIBD was measured in different time by Immunohistochemitry technique. Results In sham group, there were less brain microvessel immunostained positively. In HIBD group,the number of ICAM-1 immuno-positive staining blood vessels increased significantly after 6h, 12h reached peak point. ICAM-1 immunoreactive staining of blood vessels levels continued in the peak after 24h. In PD treatment group, ICAM-1 expression on brain microvascular endothelial decreased after HIBD 6h, 12h, 24h, which was significant compared with HIBD group( P < 0. 05 or P < 0. 01 separately). Conclusion The expression of ICAM-1 was involved in the procedure induced by hypoxic-ischemia. After HIBD, polydatin would downregulate ICAM-1 expression in cerebral microvascular endothelial, and inhibite the inflammatory response.
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Objective To explore the effect of exogenesis VEGF 120 gene on the apoptosis of brain cells in the HIBD of newborn rats. Methods VEGF eukaryotic expression plasmid (pCDNA 3.1/r VEGF 120) was constructed by cloning rat VEGF 120 cDNA into eukaryotic expression vector pCDNA 3.1. The HIBD model was established with seven days old SD rats,and all rats were diveded into two groups at random :contral group 18 rats( every rat model was injected pCDNA 3.1 100 μg immediately after hypoxia-is-chemic.then raised seven days) and therapy group 18 rats (every rat model was injected pCDNA 3.1/ rVEGF 120 100 μg immediately after hypoxia-ischemic). Flow cytometer( FCM) was used to detect the ratio of apoptosis of brain cell. Results There was a significant decrease in the ratio of apoptosis brain cells( control group 17.505 ± 0.949; therapy group 8.93 ± 0. 332). Conclusion The VEGF gene product can reduce apoptosis of brain cells.
ABSTRACT
Objective To explore the protective effects and possible mechanisms of Polydatin (PD)on hypoxic-ischemia brain injury(HIBD) in neonatal rat by means of spatial learning memory and the expression of synaptophysin in hippocampal CA1. Methods Thirty-seven neonatal SD rats were divided into 3 groups at random: normal sham-operated group( no hypoxia and ischemia); HIBD group( no medication) ;PD treatment group. 7-old-day rat' s model of HIBD was established by left carotid artery ligation and 2 h hypoxia. Morris water maze test was used to evaluate cognitive function in the rats after 28-day-old( 21-day later after HI). Immunohistochemical method was used to measure the expression of synaptophysin after the end of Morris water maze test. Results Morris water maze results showed that the mean escape latency of the shamgroup (SG) ,HIBD group (HIBD) and PD treatment group (PD) were (39. 55 ±8. 08) s, (52. 37 ±8.03) s and (43.29 ± 7. 63 ) s respectirely. For PD and SG, the mean escape latency was significantly shorter than the HIBD (P ＜0.05). After training,the mean escape latency in the three groups of rats was shortened gradually. The frequency of platform crossings were 5. 29 ±2.62、2. 36 ± 1.80、4. 25 ± 1. 66 in the SG,HIBD and PD respectirely. The frequency of platform crossings in PD was higher than that of HIBD ( P ＜ 0. 05 ). The swimming time in target quadrant were ( 15.74 ± 3.85) s, ( 10. 63 ± 3.66) s and ( 14. 32 ± 2. 52 ) s in SG, HIBD and PD respectirely. For HIBD ,the swimming time in target quadrant was significantly shorter comparing to SG and PD ( P ＜ 0. 05 ). The expression of synaptophys in hippocampal CA1 in PD ( 0. 295 2 ± 0. 044 3 )were evidently higher than that in the HIBD group (0.261 2 ±0.032 3) at 3 week after operation (P ＜0. 05). Conclusion Spatial learning memory deficits and the decrease of synaptophys in hippocampal CA1 could be induced by hypoxic-ischemia. Polydatin could improve the learning and memory ability in neonatal rats following hypoxic-ischemia brain damage. The mechanisms of improvement with Polydatin treatment is associated with the enhancement of expression of synaptophys.
