ABSTRACT
Objective To compare the characteristics in initial sandplay of college students with high and low gregarious personality,to validate the psychological assessment function of the initial sandplay.Methods Used the 16-PF as the tool to selected the 56 students as the high gregarious group,and 36 students as the low gregarious group.Results On selection of toys,the proportions of high gregarious group were significantly higher than those in low gregarious group in total numbers,plants and daily necessities ((27.77 ± 11.01)vs (20.94 ± 8.76),(7.30 ±6.43)vs(3.25 ±2.85),(3.66 ±2.86)vs(2.25 ±2.57)),and significantly lower in religion toys (0.30 ± 0.47) vs (0.86 ± 1.09).On operation process,the proportion of starting with toys in high gregarious group was significantly higher than that in low gregarious group (94.6％ vs 25％).Their attitudes towards sand were random touch(28.6％ vs 5.6％) and indifference(62.5％ vs 41.7％).They used more grass(55.4％ vs 27.8％),more real characters(83.9％ vs 50％),fewer virtual characters(55.4％ vs 83.3％) and more dynamic changes in creation(14.3％ vs 0％),more applied by the social scene (39.3％ vs 0％).On the theme of sandplay,the high gregarious group was fewer appear by the empty,neglect,injury ((3.6％ vs 19.4％),(0％ vs 8.3％),(0％ vs 8.3％) respectively,P ＜ 0.05).Conclusion The results show that the high and low gregarious personality have significantly characteristics in initial sandplay.Sandplay is valuable to be a personality assessment tool.
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ObjectiveTo summarize the characteristics in initial sandplay of the interpersonal sensitivity (IS) in college students,and validate the psychological assessment function of the initial sandplay.MethodsThe research selected the 32 IS college students and 36 healthy students by the symptom checklist 90(SCL-90).All the 68 students applied the initial sandplay operation.The initial sandplay encoding of information was collected by coding table,and analyzed by t test,Chi-square test.ResultsOn selection of toys,the IS group was significantly lower in total,buildings,plants ( ( 18.63 ± 10.93 ) vs ( 29.81 ± 12.25 ),( 1.47 ± 1.52 ) vs ( 2.39 ± 1.68 ),( 3.41 ±4.39) vs(9.72 ±6.67) ),and significantly more in the others( (0.13 ±0.33) vs(0.00 ± 0.00) ).On space utilization,the IS group was lower than the non-IS group in all fields except the left middle and the middle.On operation process,the IS group on attitude to the sand was untouch(59.4％ vs 22.2％ ),less exposed the blue bottom (71.9％ vs 30.6％ ),less use the bridge(68.8％ vs 38.9％ ),more dissatisfaction with the own sandbox(43.8％vs 2.8％ ),more warfare and abstract scene( ( 18.8％ vs 0％ ),(21.9％ vs 2.8％ ) ),and less family and society scene( ( 12.5％ vs 27.8％ ),(25％ vs 41.7％ ) ).On the theme of sandplay,the is group was more appeared by the confusion,empty,split,limit,neglect,injury,threat theme( (25％ vs 5.6％ ),(37.5％ vs 0％ ),(31.3％ vs 0％ ),(40.6％ vs 5.6％ ),(37.5％ vs 2.8％ ),( 15.6％ vs 0％ ),(50％ vs 5.6％ ) ),and less appeared by the integrate,flow and energy theme ((12.5％ vs 38.9％),(3.1％ vs 50％),(28.1％ vs 58.3％)).ConclusionThe results show that the IS group has significantly characteristics in initial sandplay.Sandplay is valuable to be a clinical psychological assessment.
ABSTRACT
The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension, preeclampsia, and renal-allograft rejection, but the detailed mechanisms remain unclear. In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide, 15 mice were divided into three groups: control group, AT1-EC2-immunized group, and AT1-EC2-immunized and valsartan-treated group. In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times: 0, 5, 10, and 15 days after the experiment. In AT1-EC2-immunized and valsartan-treated group, valsartan was given at a dose of 100 mg/kg every day for 20 days. After the experiment, the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments. The titer of AT1-EC2 was assayed by using ELISA. The level of NOX1 mRNA in the aorta was determined by using RT-PCR. The expression of NOX1 was detected by using Western blotting. Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue. The O(2)∸ production was detected in situ after DHE staining. The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group. There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group. The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group, and the O(2)∸ production increased about 2.7 times as compared with control group. There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group. It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS, and increase vascular inflammation, which can be inhibited by AT1 receptor blocker valsartan. This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.
Subject(s)
Animals , Mice , Aorta , Metabolism , Disease Models, Animal , Mice, Inbred C57BL , NADPH Oxidases , Genetics , Reactive Oxygen Species , Metabolism , Vaccination , MethodsABSTRACT
The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension, preeclampsia, and renal-allograft rejection, but the detailed mechanisms remain unclear. In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide, 15 mice were divided into three groups: control group, AT1-EC2-immunized group, and AT1-EC2-immunized and valsartan-treated group. In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times: 0, 5, 10, and 15 days after the experiment. In AT1-EC2-immunized and valsartan-treated group, valsartan was given at a dose of 100 mg/kg every day for 20 days. After the experiment, the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments. The titer of AT1-EC2 was assayed by using ELISA. The level of NOX1 mRNA in the aorta was determined by using RT-PCR. The expression of NOX1 was detected by using Western blotting. Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue. The O(2)∸ production was detected in situ after DHE staining. The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group, and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group. There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group. The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group, and the O(2)∸ production increased about 2.7 times as compared with control group. There were no significant differences between control group and AT1-EC2-immunized and valsartan-treated group. It is concluded that active immunization with AT1-EC2 can activate NOX1-ROS, and increase vascular inflammation, which can be inhibited by AT1 receptor blocker valsartan. This may partially explain the mechanism of the pathogenesis of inflammatory vascular diseases related to antibody against AT1-EC2.