Objective:To investigate the characteristics of implicit memory and its related factors in schizophrenic patients with negative and positive symptoms.Methods:Ninety-three schizophrenic patients (including 52 cases of negative symptoms group and 41 cases of positive symptoms group) and 30 normal controls (normal group) were tested with the method of Chinese character word completion method. The reaction time and correct rate were recorded and compared with analysis of variance and t-test, and the correlation with demographic factors was analyzed with Pearson correlation analysis. Results:Accuracy of implicit memory test in schizophrenia group: there were statistically significant differences in the accuracy of patients with different course of disease (≤5 years: (38±5)%, 5-15 years: (34±8)%, ≥15 years: (34±7)%, P<0.05).The differences were statistically significant in the accuracy of patients with different education levels(primary school: (35±6)%, junior and senior high school: (34±7)%, secondary college education and above: (39±5)%, P<0.05).The accuracy of patients with education years < 10 years ((34±7)%) was significantly lower than those with education years ≥10 years ((37±6)%, P<0.05).Reaction time results of implicit memory test in schizophrenia group : there were significant differences in reaction time of patients with different disease course(≤5 years: (3 248±971)ms, 5-15 years: (3 515±672)ms, ≥15 years: (3 925±842)ms, P<0.05).The differences were statistically significant in the reaction time of workers ((3 495±712)ms), farmers ((3 870±878)ms) and soldiers ((3 024±924)ms, P<0.05).The reaction time of patients with clozapine ((3 869±871)ms) was significantly higher than that of patients with olanzapine ((3 393±626)ms, P<0.05).Intergroup results of accuracy: the accuracy of normal control group ((40±5)%) was significantly higher than that of negative symptom group ((33±7)%, P<0.01).The accuracy of negative symptom group was significantly lower than that of positive symptom group ((37±6)%, P<0.01).Intergroup reaction time results: the reaction time of normal control group ((2 660±667)ms) was significantly lower than that of negative symptom group ((3 678±951)ms, P<0.01) and positive symptom group ((3 072±865)ms, P<0.05).The reaction time of negative symptom group ((3 678±951)ms)was significantly higher than that of positive symptom group( P<0.01).There was significant negative correlation between the accuracy of implicit memory and the course of disease in schizophrenia ( r=-0.22, P<0.05). Conclusion:The implicit memory of schizophrenic patients is related to the course of disease, taking drugs, and occupation.There may have differences in implicit memory between patients with negative and positive symptoms of schizophrenia.

BACKGROUND:In recent years,the treatment method of injecting bone cement into the intervertebral space has been introduced from abroad for the treatment of lumbar recurrent pain caused by lumbar disc degeneration and intervertebral space narrowing;however,some patients had vertebral fractures after treatment;the fracture may occur because the bone cement injected into the intervertebral space has a poor elastic modulus. OBJECTIVE:To analyze the effect of bone cement with different elastic moduli injected into the intervertebral space on the maximum stress of upper and lower vertebrae using a three-dimensional finite element model. METHODS:A volunteer with normal spine was recruited to obtain CT data.The finite element model of L2-L5 lumbar spine was established using Mimics,Geomagic,SolidWorks,and Ansys.Subsequently,a L3-L4 intervertebral space injection model with different doses(1 mL and 4 mL)of bone cement was established.Four different elastic moduli(1 000,2 000,4 000,and 8 000 MPa)were assigned to bone cement at each dose.Pressure and bending moment were applied on the surface of the L2 vertebral body to analyze the stress on the lower surface of the L3 vertebral body and the upper surface of the L4 vertebral body. RESULTS AND CONCLUSION:(1)In the case of the same amount of bone cement injection,as the elastic modulus of bone cement increased,the stress on the lower surface of L3 vertebral body and the upper surface of L4 vertebral body increased.Among them,the bone cement with an elastic modulus of 1 000 MPa had the least effect on the lower surface of L3 vertebral body and the upper surface of L4 vertebral body.Bone cement with elastic modulus of 8 000 MPa had the greatest effect on the lower surface of L3 vertebral body and the upper surface of L4 vertebral body.Bone cement with different elastic moduli had little effect on the motion range of the whole lumbar spine.(2)The results indicate that injecting bone cement with lower elastic modulus while meeting treatment requirements can reduce the risk of postoperative fractures.

OBJECTIVE: To investigate the effects of blocking the activation of ERK pathway on the expression of matrix metalloproteinase-9 (MMP-9) and the formation of cerebral edema in SD rats after brain injury. METHODS: Ninety SD rats were randomly divided into 3 equal groups, including a sham-operated group, modified Feeney's traumatic brain injury model group, and ERK inhibition group where the ERK inhibitor SCH772984 (500 μg/kg) was injected via the femoral vein 15 min before brain trauma. At 2 h and 2 days after brain trauma, the permeability of blood-brain barrier was assessed by Evans blue method, the water content of the brain tissue was determined, and the phosphorylation level of ERK and the expression level of MMP-9 mRNA and protein were measured by RT-PCR and Western blotting. RESULTS: Compared with the sham-operated group, the rats with brain trauma exhibited significantly increased level of ERK phosphorylation at 2 h and significantly increased expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). Treatment with the ERK inhibitor significantly decreased the phosphorylation level of ERK after the injury ( < 0.01), suppressed over-expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). The permeability of blood-brain barrier increased significantly 2 h after brain trauma ( < 0.05) and increased further at 2 days ( < 0.01); the water content of the brain did not change significantly at 2 h ( > 0.05) but increased significantly 2 d after the injury ( < 0.01). Treatment with the ERK inhibitor significantly lowered the permeability of blood-brain barrier and brain water content after brain trauma ( < 0.01). CONCLUSIONS Blocking the activation of ERK pathway significantly reduced the over-expression of MMP-9 and alleviates the damage of blood-brain barrier and traumatic brain edema, suggesting that ERK signaling pathway plays an important role in traumatic brain edema by regulating the expression of MMP-9.
Animals ; Blood-Brain Barrier ; Brain Edema ; Brain Injuries, Traumatic ; MAP Kinase Signaling System ; Matrix Metalloproteinase 9 ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To investigate the effects of blocking the activation of ERK pathway on the expression of matrix metalloproteinase-9 (MMP-9) and the formation of cerebral edema in SD rats after brain injury. METHODS: Ninety SD rats were randomly divided into 3 equal groups, including a sham-operated group, modified Feeney's traumatic brain injury model group, and ERK inhibition group where the ERK inhibitor SCH772984 (500 μg/kg) was injected via the femoral vein 15 min before brain trauma. At 2 h and 2 days after brain trauma, the permeability of blood-brain barrier was assessed by Evans blue method, the water content of the brain tissue was determined, and the phosphorylation level of ERK and the expression level of MMP-9 mRNA and protein were measured by RT-PCR and Western blotting. RESULTS: Compared with the sham-operated group, the rats with brain trauma exhibited significantly increased level of ERK phosphorylation at 2 h and significantly increased expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). Treatment with the ERK inhibitor significantly decreased the phosphorylation level of ERK after the injury ( < 0.01), suppressed over-expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). The permeability of blood-brain barrier increased significantly 2 h after brain trauma ( < 0.05) and increased further at 2 days ( < 0.01); the water content of the brain did not change significantly at 2 h ( > 0.05) but increased significantly 2 d after the injury ( < 0.01). Treatment with the ERK inhibitor significantly lowered the permeability of blood-brain barrier and brain water content after brain trauma ( < 0.01). CONCLUSIONS Blocking the activation of ERK pathway significantly reduced the over-expression of MMP-9 and alleviates the damage of blood-brain barrier and traumatic brain edema, suggesting that ERK signaling pathway plays an important role in traumatic brain edema by regulating the expression of MMP-9.
Animals ; Brain Edema ; drug therapy ; etiology ; Brain Injuries, Traumatic ; complications ; drug therapy ; Gene Expression Regulation, Enzymologic ; drug effects ; Indazoles ; pharmacology ; therapeutic use ; MAP Kinase Signaling System ; drug effects ; Matrix Metalloproteinase 9 ; genetics ; Piperazines ; pharmacology ; therapeutic use ; Protein Kinase Inhibitors ; pharmacology ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley