Objective To study the effect of Nurrl gene on the differentiation of rats' marrow stromal cells(MSCs) into neurous under the co-inducement of total panax notoginserg saponins(tPNS) and all-trans-retineic acid(ATRA) by coloning the Nurrl gene and transfecting it into MSCs. Methods Expressing plasmids pcDNA3.1-hygro-Nurrl were cloned,then transfected into MSCs with lipofectamine 2000.To begin with,MSCs were subcultured into 6-wells cultured plate at about 5?10~5 cells/well density and the wells were divided into four groups randomly which were Nurrl+tPNS/ATRA group,tPNS/ATRA group,Nurrl group and control group.Secondly,the plasmids were introduced to the MSCs in Nurrl+tPNS/ATRA group and Nurrl group,then protein expression of Nurrl was identified with immunocytochemistry.Thirdly,after the MSCs and plasmids had been co-cultured for 48 hours,cells in Nurrl+tPNS/ATRA group and tPNS/ATRA group were induced with BME in advance then with tPNS/ATRA in due form.For cells in Nurrl and control group,the only difference was that tPNS/ATRA was replaced with the culture.Finally we compared the different percentage of positive cells in four groups with TH,AChE and GABA antibodies by immunocytochemistry method. Results The immunocytochemical test showed that the MSCs transfected with Nurrl gene expressed Nurrl protein.The percentage of positive cells of TH antibody in Nurrl+tPNS/ATRA group was(38.4?4.6)% distinctly higher than that of tPNS/ATRA group,which was(5.9?3.4)%.Conclusion With tPNS/ATRA induced and immunocytochemistry of TH,positive cells percentage in Nurrl+tPNS/ATRA group was higher than that in tPNS/ATRA group,which showed a statistic difference.And the inducing function of tPNS and ATRA in MSCs differentiating into neurons was definite.

Frontotemporal lobar degeneration (FTLD) is a non-Alzheimer dementia syndrome characterized by focal atrophy of the frontal and/or temporal lobes. Recently, it has been found that FTLD is related to the degeneration of tau protein, and is closely associated with corticobasal ganglionic degeneration, progressive supranuclear palsy, and motor neuron disease. This article reviews the progress in etiology, genetics, pathology, clinical features, and diagnostic criteria of FTLD.

OBJECTIVE:To discuss the flow-sheet mode of drugs under digitized management.METHODS:Rational medicine flow-sheet was made based on the outfitting and functional authority of each drug storeroom and dispensary as well as the concrete prescription-filling method.RESULTS&CONCLUSION:The key for the success of digitized drug man?agement in hospital is to clarify a suitable relationship between receiving and dispatching of the medicine thus to keep the drugs in a due logistic network and facilitate the receiving and dispatching and accounting.

Objective To study the neuroprotective effects of adeno viral mediated glial cell line derived neurotrophic factor(GDNF) gene transfer in the treatment of Parkinson's disease. Methods Thirty five SD rats were divided into 3 groups which received perinigral injections of recombinant adenovirus encoding GDNF (Ad GDNF)/ LacZ(Ad LacZ) and PBS, respectively. One week later, intrastriatal injection of 6 hydroxydopamine (6 OHDA) was made to induce progressive degeneration of dopaminergic neurons. The neuroprotective effects of Ad GDNF were evaluated by apomorphine induced rotational behavior, immunohistochemical assay of the tyrosine hydroxylase(TH) positive neurons in the midbrain and measurement of monoamine level in the striatum. RT PCR and ELISA were performed to check the expression of the exogenous GDNF gene in the brain. Results Ad GDNF treated rats showed improved motor functions, better survival of TH positive cells in the lesioned substantia nigra (70% vs 30%) and higher DA levels in the lesioned striatum. The exogenous GDNF gene was efficiently expressed in the midbrain. GDNF protein level in the injection site reached 1 ng/10 mg wet tissue 5 weeks after the adenoviral vector delivery, being 16 20 times of that of the Ad LacZ delivery or PBS treated groups. Conclusions Adeno viral mediated GDNF gene intracerebral transfer significantly protected the dopaminergic neurons of nigrostriatal system from 6 OHDA induced injury and is valuable in the treatment of Parkinson's disease.

Objective To investigate the cognitive impairment characteristics in Parkinson's disease (PD) with mild cognitive impairment(PD-MCI)as well as their related risk factors.Methods In all of the participants, a battery of neuropsychological tests were selected to identify the cognitive deficits; the 2 cognitive screening tests utilized in this study were the MMSE and the CAMCOG-C; the severity of disease was measured using the Hoehn-Yahr;the motor portion of the UPDRS and Webster scale were used to evaluate motor function and PD-MCI were classified according to modified Petersen's criteria.Results Of the 89 PD cases, 56 (63%) were cognitively normal (PDCOGNL), 20 (22%) had MCI and 13 (15%) met criteria for PD dementia (PDD). The cognitive domain abnormal in PD-MCI was orientation, language, memory, attention, praxis, thinking and perception. The PDCOGNL group had no significant differences in age and PD onset versus the PD-MCI group, but had significant difference in the years of education (PD-MCI:4.4±4.3,PDCOGNL:7.1±4.9;q=3.270, P<0.05); PD-MCI also had no significant differences for all of them versus the PDD, but the PDD group had significant differences for them (q=-4.913, -4.997, 4.740,all P<0.01) compared with the PDCOGNL group; there were no significant differences among 3 groups in years of PD duration. Hoehn-Yahr and Webster scale, UPDRS-motor score had negative correlation with PD cognitive function. Conclusions A stage of clinical cognitive impairment in PD can be defined between PDCOGNL and PDD that characterized as PD-MCI. There are multiple domains impaired in PD-MCI. The risk factors of PD cognitive impairment include the elder, later onset and lower education level. There are negative correlation between the severity of disease, motor function and PD cognitive function.

Objective To investigate the ability of decision making under risk condition in patients with Parkinson' s disease (PD),and to explore the neural relationship between basal ganglia and the decision-making ability.Method Twenty-five PD patients and 25 healthy controls (HC) were investigated by Game of Dice Test (GDT) with explicit probability.Results PD patients performed poorly in the entire task,selecting more risky options ( PD:10.88 ± 5.58 ; HC:5.72 ± 3.69 ; t =3.86,P ＜ 0.01 ),compared with healthy controls.In general,the final asset of PD group was negative while the result of HC group was always profitable and the difference was significant ( PD:- 3748.00 ± 3923.87 ; HC:684.00 ± 1764.62 ; t =-5.15,P ＜ 0.01 ).The most frequent choice made by PD patients was one number,which is the most risky one.Accordingly,the most frequent choice made by HC group was three numbers (one number:PD:6.48 ±5.81;HC:1.00 ± 1.44;t =4.58,P ＜0.01; three numbers:PD:2.64 ±2.14;HC:7.04 ±2.54;t =-6.62,P ＜ 0.01 ).The frequency of choosing the risky options was correlated with the rate of using negative feedback( r =-0.59,P =0.003 ),and the result of Stroop test( r =0.55,P =0.004).Conclusion Present study has shown that PD patients have significant impairments in decision-making under risk condition,and the impairments are correlated with executive function and negative feedback.

Objective To investigate the episodic memory monitoring ability in patients with Parkinson' s disease (PD) and explore the mechanism of the episodic memory impairment.Method The feeling-of-knowing (FOK) paradigm were established and subsequently administered in 25 PD patients and 25 healthy control (HC) participants who were matched in age and educational level.Results Compared with healthy control group ( FOK-EM recall 39.67％ ±6.11％ ; recognition 58.42％ ±7.50％ ; FOK accuracy 0.61 ±0.22),the episodic memory and its monitoring ability in PD patients were significantly impaired on the accuracy rate of FOK-EM recall ( 19.33％ ±5.10％,t =-4.833,P ＜0.01 ),recognition (45.93％ ±7.82％,t =-2.497,P ＜0.05) and FOK accuracy( -0.18 ±0.46,t =-5.986,P ＜0.01).Furthermore,the correct judgment and correct recognition of FOK-EM ( 20.47％ ± 10.78％ ) and the correct judgment and false recognition of FOK-EM (29.53％ ±5.62％ ) in the PD group were significantly higher than the HC group ( the correct judgment and correct recognition of FOK-EM:39.47％ ± 9.47％ and the correct judgment and false recognition of FOK-EM:13.90％ ±5.50％ ; t =3.564,P ＜0.05 ; t =2.306,P ＜0.05).Most importantly,the stroop effect was positively correlated with the correct judgment and false recognition of FOK-EM in PD group ( r =0.640,P ＜ 0.05 ).Conclusions In the present study,the PD patients demonstrated an overestimation of their recognition ability of episodic memory,moreover,this impairment of memory monitoring was positively correlated with the deficit of executive function,indicating that this mechanism could be an influential factor of memory disorder in PD.

Objective To observe the feasibility of posterior internal fixation with pedicle screw rod system for upper cervical vertebra injury. Methods 16 patients with upper cervical vertebra injury accepted posterior pedicle screw system internal fixation were reviewed. Results Venous plexus behind C2 damaged in operation in a case, who needed a microscope for hemostasis. No complication, such as neurological symptoms worse, cerebrospinal fluid leakage, hematoma and infection of incision happened post operation. The neurological symptoms improved 81.8% in all the 7 cases who complained before operation. No complication was found in the follow-up 3 to 18 months after discharge. Their activities of upper cervical was basically unaffected. Conclusion Posterior internal fixation with pedicle screw rod system can provide stable support for patients with upper cervical injury.

Objective To investigate the effects of dopaminergic medication on decision-making un-der ambiguity in patients with early Parkinson's disease( PD) . Methods Using Iowa Gambling Task ( IGT) for 24 early non-medication idiopathic PD patients( Hoehn and Yahr Scale≤Ⅱlevel) ,24 early idiopathic PD patients with regular dopaminergic medication and also for 24 healthy controls( HC) whose age,gender,and education match to PD patients to test their ability of decision-making under ambiguity. Results The results showed non-medication PD group showed impairments on digtal span and verbal fluency and decision-making task. There was significant difference in IGT task scores among the three groups(F=6.024, P=0.004) . The total net scores of advantageous choices in IGT were significantly lower in non-medication PD group( (-4.50 ±22.19) scores) than medication PD group((8.83±23.24)scores) and healthy group((15.92±15.77) scores) . The difference of net scores in block1 to block5 between non-medication PD group and medication PD group was gradually increased,and the difference of net scores in block5 was significant(P<0.05) . There was no significant difference in total net scores and net scores in block1 to block5 between medication PD group and healthy group(P>0.05) . As the game processing,medication PD group gradually shifted their se-lections toward the advantageous choices. But non-medication group did not exhibit this shift pattern and the performance was much poorer. Meanwhile, the study also indicated the total net scores of advantageous choices for non-medication PD group was positive correlation to the MoCA scores ( r=0.614, P=0.001). Conclusion The present study has shown that non-medication PD group has impairment in decision-making under ambiguity risk condition and prefer to choose risky options. when exogenous complement dopaminergic medication,the risk decision-making ability of medication PD group has been improved.

Objective To explore whether gap junction disturbances are involved in the pathogenesis of levodopa-induced dyskinesia ( LID ). Methods The hemi-parkinsonian ( PD ) rat was treated intraperitoneally with L-dopa methylester (20 mg/kg) and benserazid (10 mg/kg) for 21 days and abnormal involuntary movement was evaluated to establish LID rat model. The experimental animals were divided into three groups: LID group, PD group and normal control group, respectively. The behavior responses of intraperitoneal injection of different doses of carbenoxolon and intracerebroventricular injection of quinine were observed to estimate the effects of gap junctional blockade on the abnormal involuntary movement ( AIM ) in the rat model of LID. Double immunofluorescence labeling was used to analyze the expression of connexin 36 ( Cx36 ) in enkephalin positive medium spiny neurons and parvalbumin ( PV ) positive interneurons in the striatum. Western blottings was used to observe the expression of Cx36 in the striatum and moter cortex. Results Behavioral characteristics indicated that high dose of carbenoxolone ( >60 mg/kg) intraperitoneal injection and intracerebroventricular injection of quinine ( 0.5, 1.0, 2.0 μmol/L, > 2.5 μmol/L ) could decrease the AIM score of LID rats. Western blotting indicated that expression of Cx36 in lesioned striatum and motor cortex of LID rat model was 219.56% ±18.12% and 226.03% ±16.33%, respectively, which induced a significant upregulation in comparison with the normal control group (104.05% ±3.82%, t=15.389, P<0.01;105.27% ±2.82%,t=8.074, P<0.01) and untreated PD group (119.31% ±8.92%, t=13.356, P<0.01; 138.20% ±17.88%, t=5.872, P<0.01). Double immunofluorescence labeling staining revealed that Cx36 expression was increased in Enk-positive striatum neurons in LID model ( 57.59% ±5.36%) compared with that in normal control group (32.67% ±4.22%) and PD group (37.24% ±0.86%, F=78.060, P<0.01). The expression of Cx36 in PV-positive interneurons was also elevated in LID group (68.49% ±11.60%) in comparison with normal control group ( 40.43% ± 2.30%) and PD group ( 31.92% ± 5.68%, F = 39.567, P < 0.01 ).Conclusions The Cx36 expression is generally increased in lesioned striatum and motor cortex of LID rat model. In the striatum, the up-regulation of Cx36 is specifically observed in Enk-positive striatum neurons and in PV-positive interneurons. The dyskinesia behavior of LID rats can be significantly reduced by treatment with gap junction blockade. All these results suggest that gap junction dysfunction may play an important role in the pathogenesis of LID.