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 To observe the effect of blood-cooling and blood-stasis-removing Decoction on anti-double-strain DNA ( anti-dsDNA) antibody, anti-nucleosome antibody ( AnuA) and serum levels of interleukin ( IL) -6, 17, 21 in spontaneous systemic lupus erythematosus ( SLE) MRL/lpr experimental rats. Methods The experimental rats were divided into blank control group, model group, and high- and low- dose Chinese medicine groups ( 25.2, 12.6 g/kg respectively) , the treatment lasting 8 weeks. At the end of the experiment, the blood taken from the orbital veins was separated for obtaining serum, and then the serum anti-dsDNA antibody, AnuA, IL-6,17,21 levels were tested by enzyme-linked immunosorbent assay ( ELISA). Results The serum autoantibody and IL-6, 17, 21 levels of rats in the model group were increased significantly as compared with the blank control group ( P<0.01). The serum antibody and cytokine levels of Chinese medicine groups were reduced as compared with the model group, the difference between high-dose Chinese medicine group and model group being significant ( P<0.01). Conclusion Blood-cooling and blood-stasis-removing Decoction has certain effect on reducing the serum levels of anti-dsDNA antibody, AnuA, and IL-6,17,21, which may coniribute to one of its therapeutic mechanisms for SLE.

Objective To discuss the applicated value of systematic nursing intervention in patients with severe pneumonia.Methods 100 patients with severe pneumonia were randomly divided into the study group and the control group,50 cases in each group.The control group was given routine nursing measures.The study group received systematic nursing intervention on the basis of routine nursing measures.The hospitalization time,satisfaction degree, treatment compliance and mentality were observed.Results The SAS scores of the study group before and after nurs-ing were (56.67 ±5.99)points and (38.92 ±5.31 )points,there was statistically significant differences between before and after treatment (t =9.235,P <0.05).The SDS scores of the study group before and after nursing were (62.58 ±6.14)points and (41.15 ±5.26 )points,there was statistically significant difference (t =8.623, P <0.05 ).The hospitalization time ,satisfaction degree and treatment compliance of the study group were (32.9 ± 6.6)days,(8.21 ±1.29)days,6.00%,86.00%,74.00%,which were significantly lower than (45.1 ±10.2)days, (13.56 ±1.77)days,16.00%,52.00%,48.00% of the control group (t =5.254,3.829,χ2 =5.236,8.292, 8.1561,all P <0.05 ).Conclusion Hsystematic nursing intervention can significantly improve the postoperative anxiety and depression,and improve the quality of life of patients with severe pneumonia.

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.

Background and purpose:Pancreatic cancer is one of the most deadly human malignant neoplasms. Resistance to chemotherapeutic drugs is a major reason responsible for poor prognosis in the treatment of pancreatic cancer patients. MicroRNA (miRNA, miR) is a family of small non-coding RNA molecules, dysregulated miRNA is associated with various tumor biological function. miR-33a has been widely reported as a metabolism-related miRNA, while its relationship with drug resistance has little understand. This study was focused on the effect of miR-33a on gemcitabine chemoresistance in pancreatic cancer to bring the novel theoretical basis to chemotherapy for pancreatic cancer.Methods:In situ hybridization and Real-time PCR were used to analyze the miR-33a expressions in pancreatic cancer tissue sample and cell lines, respectively. Cell counting kit 8 (CCK-8) assay was used to calculate the IC50 value of different pancreatic cancer cells.Results:miR-33a was down-regulated in pancreatic cancer tissue and cell lines compared with para-cancerous tissues and normal HEK293T cells. Moreover, miR-33a over expression not only could enhance the chemosensitivity to gemcitabine in pancreatic cancer cells, but also rescue the gemcitabine resistance in pancreatic cancer cells.Conclusion:Down regulation of miR-33a in pancreatic cancer decreases the chemosensitivity to gemcitabine, resulting in development of acquired gemcitabine chemoresistance. It provides the theoretical basis to develop a new molecular targeted drug to combine with chemotherapy for pancreatic cancer.

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.