Objective To explore the evaluation for apraxia of speech (AOS) with Chinese. Methods 20 Chinese cases with AOS were assessed with Chinese material referred from Motor Speech Evaluation (MSE) using. Results The subtest of multiple repetitions of multisyllabic words was the most difficult and single repetitions of monosyllabic words was the easiest for AOS patients (P<0.05). The score of the short sentences negatively correlated with both the scores of repetition ability (r=-0.865) and the fluency of speech (r=-0.614) (P<0.001).Conclusion Chinese material referred from MSE can be used for evaluation of AOS with Chinese.

This article reviewed the language characteristics of Down's syndrome, cerebral palsy, autism and hearing impairment, including the relevant factors and early manifestations.

Objective To explore the changes of nitric oxide (NO) and nitric oxide synthase (NOS) of the aged rat brain, and the relationship between this change and neuronal apoptosis. Methods Five month old and 30 month old rats were used in the study. NO level and NOS activity were measured by Griess reaction and high presssure liquid chromatography. Neuronal NOS(nNOS) gene and bcl 2 gene were examined by in situ hybradization; nNOS protein level and free calcium level in synaptosome were determined by immunohistochemical method and Fura 2 fluorescence probe respectively. Apoptosis was observed using terminal transferase marking method. Results NO level and nNOS activity in the brain tissue of aged rats was (2 61?0 10) ?mol/L and (398 22?21 62) fmol?mg -1 ?min -1 , respectively,being significantly higher than that of the young rats(1 54?0 15) ?mol/L and (234 38?16 24)fmol?mg -1 ?min -1 respectively. Also both the nNOS gene transcription and protein expression increased in aged rats while bcl 2 gene expression reduced with aging. Free calcium level in synaptosome of aged and young rats was (485 26?28 48) nmol/L and (372 99?19 20) nmol/L respectively. Apoptosis in brain tissue was observed in aged rats, but not in young ones. Conclusions The increase of NO level in the aged rat brain is due to the increase of nNOS activity which is at least partially determined by the increased gene expression. Abnormal enhancement of NO in the aged rats may cause damage, even death of the brain. As an anti oxidant, bcl 2 gene expression reduced with aging and resulted in the brain tissue more vulnerable to oxidative stress and thus produced more lesions. Therefore, it is a promising method to screen and develop drugs that can be anti apoptotic and anti oxidative, and reduce the formation of pathologic NO to prevent and retard brain aging.

Animals ; Antioxidants ; pharmacology ; Ascorbic Acid ; pharmacology ; Cumulative Trauma Disorders ; metabolism ; Lipid Peroxidation ; drug effects ; Male ; Muscle, Skeletal ; injuries ; pathology ; Oxidation-Reduction ; Oxidative Stress ; drug effects ; Rats

[Objective]A new limited contact femoral supracondylar interlocking intramedullary nail(LCFSIIN) was made,which was part of a new custom-made hemi-knee joint,to improve the results of childrens' limb salvage.[Method]A new LCFSIIN was performed and the stress of bolts,intramedullary nails and bone were analyzed by finite dement analysis(FEA) while the bolts were implanted in different angulafions-0?,15?,30?,45?and 60?.[Result]The results of FEA show that the stress of bolts,bone and nails with 15? insertion angles of bolt was the tiniest and well distributed.Stress of bone with 0? insertion angles was more obvious than that with 15?,30?and 45?.The more the angles,the stress of proximal bolt became more obvious and the stress of distal bolt decreasing.[Conclusion]This new LCFSIIN can reduce destruction of biological environment of bone and is easy in use in limb salvage surgery of allograft.

Objective To establish a mathematical model for describing and predicting the effectiveness of physical therapy on lumbar disc hernation(LDH).Methods Daily comprehensive physical therapy interventions including lumbar traction,mobilization and physical agents were administered to 31 LDH patients for 10 sessions.A visual analogue scale was used to measure the pain intensity before each session.The logistic curve model was used in the regression analysis.The first 2 to 9 pain measurements were involved in different predictive models,and the predictive results were compared among different models.Results In regression analysis,the global R2 was 0.719.In predicting analysis,the more measurements involved in the predictive model,the more effective the prediction.The predictive power was low when the model included less than 4 measurements.the prediction power was high when more than 5 measurements were used in the model.Conclusion The logistic model can describe and predict the effectiveness of multiple physical therapy on LDH patients.

Objective To evaluate the role of calcium/calmodulin-dependent kinase Ⅱ alpha (CaMK Ⅱα) in the central nucleus of the amygdale (CeA) in fentanyl-induced hyperalgesia in rats and the relationship with miniature excitatory postsynaptic currents (mEPSCs).Methods Thirty-two male Sprague-Dawley rats,weighing 50-80 g,in which the CeA was successfully cannulated,were randomly divided into 4 groups (n=8 each) using a random number table:control 1 group (group C1),fentanylinduced hyperalgesia 1 group (group FIH1),KN92 group,and KN93 group.Normal saline was injected subcutaneously,and dimethyl sulfoxide (DMSO) was given into the amygdale in group C1.In group FIH1,fentanyl was injected subcutaneously (60 μg/kg per time,4 times in total,15-min interval,cumulative dose of 240 μg/kg) to establish the model of hyperalgesia.In KN92 and KN93 groups,KN92 and KN93 10 nmol were given into the CeA after establishing the model.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal threshold (TWT) were measured at 6 and 7 h after fentanyl or normal saline injection.Another 12 Sprague-Dawley rats were selected and randomly divided into either control 2 group (group C2) or fentanyl-induced hyperalgesia 2 group (group FIH2) using a random number table with 6 rats in each group.The brains were removed and sliced 12 h later,and the frequency and amplitude of mEPSCs were recorded.KN93 10 nmol was then added to the artificial cerebral spinal fluid,and the frequency and amplitude of mEPSCs were recorded by whole cell patch-clamp technique.Results Compared with group C 1,the MWT and TWT were significantly decreased at 6 h after fentanyl or normal saline injection in FIH1,KN92 and KN93 groups,and at 7 h after fentanyl or normal saline injection in FIH and KN92 groups (P＜0.05).Compared with group FIH1,the MWT and TWT were significantly increased at 7 h after fentanyl or normal saline injection in group KN93 (P＜0.05),and no significant change was found in group KN92 (P＞0.05).Compared with group C2,the frequency and amplitude of mEPSCs were significantly increased before administration of KN93 (P ＜ 0.05),and no significant change was found in the frequency and amplitude of mEPSCs after administration of KN93 in group FIH2 (P＞0.05).Compared with the value before KN93 administration,no significant change was found in the frequency and amplitude of mEPSCs after administration of KN93 in group C2 (P＞0.05),and the frequency and amplitude of mEPSCs were significantly decreased after administration of KN93 in group FIH2 (P＜ 0.05).Conclusion Activation of CaMK Ⅱ α in the CeA enhances synaptic excitation in neurons,which is involved in fentanyl-induced hyperalgesia in rats.

AIM　To study the effect of lidamycin on the expression of genes involved in invasion regulation in HCT-8 human colon cancer cells. METHODS　HCT-8 human colon cancer cells were treated with lidamycin (10 nmol*L-1) for 8 h. The effect of lidamycin on the expression of genes were detected by cDNA arrays, Northern blot and RT-PCR. RESULTS　Hybridization of the entire cDNA populations to Atlas Arrays showed that lidamycin down-regulated the expression level of MMP-9 and up-regulated the expression level of TIMP-1. These changes were confirmed by Northern blot and RT-PCR. CONCLUSION　The results indicate that lidamycin may exhibit its anti-invasive activity by inhibitting the production of type IV collagenase whilst enhancing the production of tissue inhibitor metalloproteinase.

AIM: To study the effects of neuregulin-1β (NRG-1β) on the nervous behavioral function, cerebral infarction volume, brain water content (BWC), neuroal apoptosis and aquaporin-4 (AQP-4) expression in astrocytes after cerebral ischemic reperfusion in mice. METHODS: Intraluminal thread methods were applied to establish the middle cerebral artery occlusion reperfusion (MCAO/R) model in mice. Neuregulin-1β (2 μg/kg) was injected into the internal carotid artery for treatment. The nervous behavioral function was evaluated by Bedersons test. The cerebral infarction volume was observed with tetrazolium chloride (TTC) staining. The BWC was measured by calculating the dry-wet weight ratio. The apoptotic positive cells were counted by immunofluorescence assay. The expression of AQP-4 was determined by immunohistochemical method. RESULTS: Nervous behavioral malfunction appeared in all the mice with left middle cerebral artery occlusion (MCAO) and/or reperfusion. The infarction focus showed in the ischemic hemisphere following the injury. The BWC, the numbers of neuroal apoptotic cells and AQP-4 expression in astrocytes were higher than those in sham control group. In MCAO/R+NRG-1β treatment group, the nervous behavioral function at ischemia 24 h significantly improved, the numbers of apoptotic positive cells reduced and the infarction volume decreased significantly than those in MCAO/R group (P<0.05). The BWC and AQP-4 expression in astrocytes showed no significant difference compared with MCAO/R group (P>0.05). In the reperfusion 22 h, 46 h and 70 h groups, the five indexes mentioned above were significantly different from those in the corresponding MCAO/R groups (P<0.05). CONCLUSION: NRG-1β might reduce cerebral edema and infarction volume, and improve the nervous behavioral function via down-regulating the expression of AQP-4 in astrocytes and inhibiting the neuronal apoptosis induced by ischemia reperfusion injury.