Objective The clinical efficacy and safety of L dopa monotherapy and concomitant L dopa therapy with dopamine agonists (bromocriptine or pergolide) of the treatment of Parkinson's disease Methods The clinical trial was performed in the multicentre,open label study L dopa group: 47 cases,L dopa plus bromocriptine group: 43 cases and L dopa plus pergolide group: 48 cases The clinical efficacy was assessed with modified Webster's scale and motor dysfunction rating scale for Parkinson's disease ( MDRSPD ),and safety data included blood hepatic and renal function tests,blood and urine routine tests,arterial blood pressure,heart rate measurements and electrocardiogram were also analyzed at the beginning and end of study The average daily dose of L dopa in levedopa group was (523 3?235 9) mg,The average daily dose of L dopa and bromocriptine were (526 7?241 3) mg and (7 3?1 5) mg in L dopa plus bromocriptine group,respectively The average daily dose of L dopa and pergolide were (558 3?192 9)mg and (0 235?0 045) mg in L dopa plus pergolide group separately Result The clinical improvement was about 74 5%both in assessment of modified Webster's scale and MDRSPD in L dopa group The clinical score was improved in 69 8% (Webster's scale) and 79 1% (MDRSPD) in L dopa plus bromocriptine group,respectively The clinical improved rates were 77 9%( Webster's scale ) and 81 3%( MDRSPD ) in L dopa plus bergolide group The incidence rates of side effects were 27 7%in L dopa group,39 5%in L dopa plus bromocriptine and 18 8%in L dopa plus pergolide groups Conclusion There was an efficacy in treatment of Parkinson's disease in either L dopa monotherapy or combination with bromocriptine or pergolide The treatment of L dopa alone was more effective in the early stage of Parkinson's disease and concomitant L dopa therapy with dopamine agonists were more effective in the advanced stage of Parkinson's disease,pergolide was not only more effective,safe and tolerable,but also fewer adverse events than Bromocriptine was in this short term trial

AIM:To explore the effect of β-asarone on vascular endotheliam and adhesion molecule expression of endothelium induced by β-amyloid peptide from Alzheimer's disease and to estimate the injury repair.METHODS:Cultured ECV304 cells were incubated with freshly solublizeal Aβ1-42 and the mixture of Aβ1-42 and β-asarone,the expression of three central adhesion molecules,CD106,CD62P,CE62E and Ca2+ concentration were examined and apoptosis was recorded by Flow eytometry.Test viability of cells by MTT methods.RESULTS:The results showed that in model group and treated group,ligation of endothelial CD106,CD62P,CE62E,markers for endothelial cell activation and Ca2+ concentration,leads to a lot of release.The livability decreased and the apoptosis increased.Further more,simultaneous treatment of ECV304 cells with β-asarone resulted in the decrease significandy in these three adhesion molecules described above and Ca2+ concentration as well as the livability upper and apoptosis lower.CONCLUSION:CD106,CD62P,CE62E,important inflammational factor of Aβ-induced endothelial injury,may be promotion of the inflammatory scade in vascular endothelial.β-asarone may protect ECV304 cell apoptosis by regulate Ca2+ and expression of cell surface markers.

Objective To study the effect of automobile exhaust pollution saturation of carboxyhemoglobin (COHb) in traffic policemen. Methods 169 traffic policemen working outdoors were selected as a exposure group and 112 traffic policemen working indoors as control group in a traffic policemen detachment in Tangshan. Questionnaires and health examination were conducted in two groups. The carbon monoxide levels in the exhalation were measured in 281 traffic policemen by a micro_smokerlyzer and the corresponding saturation of carboxyhemoglobin (COHb) were read. Results The higher saturation of carboxyhemoglobin were observed in exposure group (2.30%?1.49%) compared with those (1.71%?0.99%) in control group (P

Objective To explore whether the dopamine D1 and D2 receptors were involved in pathogenic mechanism of Parkinsonian mice induced by paraquat. Methods The models of Parkinson's mice were induced by oral paraquat. The levels of dopamine D1 and D2 receptor proteins and the expression of receptor mRNAs in striatum were examined by immunohistochemistry and in situ hybridization, respectively. Results Mice treated by oral paraquat (10mg?day -1 ?kg -1 ) for four months displayed marked hypoactive behavior. The levels of dopamine D1 and D2 receptor proteins in the striatum were significantly decreased by 28% and 29%, respectively (P

AIM:To explore the effect of ?-asarone on vascular endothelium and adhesion molecule expression of endothelium induced by ?-amyloid peptide from Alzheimer's disease and to estimate the injury repair.METHODS:Cultured ECV304 cells were incubated with freshly solublized A?_ 1-42 and the mixture of A?_ 1-42 and ?-asarone,the expression of three central adhesion molecules,CD106,CD62P,CE62E and Ca 2+ concentration were examined and apoptosis was recorded by Flow cytometry.Test viability of cells by MTT methods.RESULTS:The results showed that in model group and treated group,ligation of endothelial CD106,CD62P,CE62E,markers for endothelial cell activation and Ca 2+ concentration,leads to a lot of release.The livability decreased and the apoptosis increased.Further more,simultaneous treatment of ECV304 cells with ?-asarone resulted in the decrease significantly in these three adhesion molecules described above and Ca 2+ concentration as well as the livability upper and apoptosis lower.CONCLUSION:CD106,CD62P,CE62E,important inflammational factor of A?-induced endothelial injury,may be promotion of the inflammatory scade in vascular endothelial.?-asarone may protect ECV304 cell apoptosis by regulate Ca 2+ and expression of cell surface markers.

Objective To investigate the relationship between the variation of cerebrospinal fluid pulse pressure and that of intracranial perfusion pressure during the process of increasing intracranial pressure.Methods Fourteen dogs were installed epidurally with latex sacculus to establish models of increased intracranial pressure. The degree of intracranial pressure and volume could be altered by changing the volume of fluid in the sacculus. During the process, pressure transducers were arranged to monitor and record the systematic blood pressure and the variation of the pressure of cerebral ventricle and lumbar subarachnoid space.Results With the continual increasement of intracranial pressure, the cerebral perfusion pressure decreased, and the cerebrospinal fluid pulse pressure correspondingly increased. A positive linear relationship between the variation of intracranial pressure and that of cerebrospinal fluid pulse pressure and a negative linear relationship between the variation of cerebral perfusion pressure and that of cerebrospinal fluid pulse pressure were found.Conclusion During the experimental process of increased intracranial pressure, with the decrease of cerebral perfusion pressure , the cerebrospinal fluid pulse pressure increases. The relationship of variations between them shows a negative linear one. It seems that in the circumstances when the autoregulation of cerebral vessel is injured, the variations of cerebrospinal fluid pulse pressure may produce some useful information as to the changes of intracranial blood flow.

Objective To study the changes of low-frequency-component of intracranial pressure (ICP) fluctuation during intracranial hypertension. Methods 15 healthy mongrel dogs were used to make models of intracranial hypertension by arranging latex sacculus epidurally.The different amount of normal that was injected into latex sacculus led to fluctuation of ICP and alteration of intracranial volume. The pressures in ventricle and lumbar spinal canal were recorded continuously by baroceptor, and the changes of low-frequency-component of ICP fluctuation were studied by frequency-spectrum analysis. Results After increase of intracranial pressure and volume,pulse wave (M wave) with its frequency at 0.1～0.2 Hz showed continually. Conclusion Emerge of M wave may reflect some decrease of intracranial compliance and the beginning of volume compensation failure.

Objective To observe the effects of MPP+ on the expression of inhibin, activin and its receptor ⅡA and cell ability in PC12 cells of rats.Methods The changes of expression of activin?A, activin?B, inhibin? and receptorⅡA mRNAs were assayed by RT-PCR, the change of cell viability was detect by tyrpan blue exclusion method in cultured PC12 cells at 3 h,6 h,12 h,24 h after MPP+ was added and compared with control groups.Results The expression of activin?A, activin?B and activin receptorⅡA mRNAs in PC12 cells were down-regulated significantly after MPP+ administrated at every time point while the expression of inhibin? mRNA remained unchanged. The cell viability decreased at the points of 12 h and 24 h after MPP+ administrated.Conclusion MPP+ may cause the injury of PC12 cells by downregulating the expression of activin and its receptor.

Objective To evaluate the protective role of bone marrow stromal cells (BMSCs) to lactacystin-Parkinson's disease (PD) rats.Methods BMSCs were obtained from adult male SD rats and were expanded, isolated and purified. BMSCs were harvested from 4 to 6 passage and used for transplantation. PD rats that expressed Lewy body and presented lateral rotation were made by injecting 8?g lactacystin into one side of substantia nigra compact part of rat with stereotaxic technique. The rats were transplanted with BMSCs labelled by Brdu by stereotaxic unilateral injection into striatum and transplanted with normal saline as control. The behavior changes of rats and the expression of BDNF, migration, differentiation of BMSCs were examined.Results 71.43% of the rats displayed significant improvement of contralateral behavior after BMSCs transplantation, however there was no change in control group. BMSCs were found in several areas of the brain including striatum, corpus callosum and contralateral cortex. The implanted BMSCs expressed BDNF but no tyrosine hydroxylase.Conclusion BMSCs may play a neuroprotective role in lactacystin-PD rats by secreting BDNF.

Objective To set up the Parkinson's disease(PD)rat model with pathologic characteristic of Lewy body in nigral cells.Methods SD rats were injected respectively with 8 mg Lactacystin(Lactacystin group),sodium saline(NS group)and 12 mg 6-OHDA(6-OHDA group)by stereotaxic unilateral injection into the pars compacta of substantia nigral.The spontaneous and apomorphine-induced contralateral behaviors of rats were observed.The changes of midbrain histology were viewed by microscope;expression of ?-synuclein and tyrosine hydroxylase(TH)positive cells were investigated by immunohistochemistry.The contents of dopamine and homovanillic acid in striatum were determined.Results Rats of NS group did not display abnormal behavior.The animals treated with Lactacystin developed progressively bradykinesia,hypokinesia,tremor,contralateral head tilting,and displayed apomorphine-induced contralateral rotation behavior;3 weeks later the number of TH positive cells were decreased by 83.29% compared with NS group(P