Objective To investigate the influence of aging on motor function,binding activity and protein expression level of striatum dopamine transporter(DAT)of rats. Methods Rolling-bar test was performed to assess motor function.Western blot and 131I-FP-β-CIT up-take ratio were used to evaluate DAT protein 1evel and striatum DAT binding activity respectively. Results There were an age-related decline of rolling-bar latency and striatum 131I-FP-β-CIT up-take ratio in rats older than6 months.There was a significant difference between 6-month-old rats and older rats(12-month-old rats,16-month-old rats,20-month-old rats),and rolling-bar latency was correlated with striatum 131I-FP-β-CIT up-take ratio(r=0.656,P＜0.01).There was no change in DAT protein 1evel during aging process. Conclusions The age-related decline of motor function of rats was correlated with the decreasing of striatum DAT binding activity.The synaptic membrane expression of striatum DAT may decrease in aged rats.

Objective To investigate the role of astrocyte in the lipopolysaccharide-induced damage of dopaminergic neurons. Methods After lipop01ysaccharide was applied to the third generation of rat astrocytes for 24 hours,supernatants of astrocytes culture were collected.The primary middle-brain dopaminergic neuron-enriched culture systems were obtained by neurobasal and ara-c,eoeulture system of both astrocytes and neurons was established by transwell inserts.The lipopolysaccharide was administered into neuron-enriched systems and coculture systems and the change of dopaminergic neurons was detected.At the same time,the supernatants of astrocytes were administered into the neuron-enriched systems,and the survival of dopaminergic neurons and the expression of tyrosine hydroxylase mRNA were observed. Results Lipopolysaccharide had a negative effect on the survival of dopaminergic neurons in a concentration-dependent manner.Both astrocytes and supernatants promoted the survival of dopaminergie neurons,and the former was better than the latter. In the preoccupation of existence of astrocytes,low-concentration lipopolysaccharide promoted the survival of dopaminergic neurons,while high-concentration,decreased.The change of the expression of tyrosine hydroxylase mRNA was similar to the survival of dopaminergic neurons.Conclusions Astrocytes play a protective role in the damage of dopaminergic neurons induced by lipopolysaccharide,and suitable activation of astrocytes would increase the protective effect while excessive activation of astroeytes would attenuate the effect.

Objective To observe the effect of mutant α-synuclein(A30P)in autophagic programmed cell death by transfected PC12 cells and explore its probable role and pathway in PD.Methods The definite PC12 cells which were transfected mutant α-synuclein(A30P)were constructed at first and MPP+,Rapamycin and Wortmanin were administrated to transfected PC12 cells with mutant α-synuclein. Not only the proliferative activity of cells was detected with MTT method but also the ultrastructttre changes of cells and expression of α-synuclein in different circumstance were observed by transmission electron microscopy(TEM),Western Blot and the level of SOD.Results (1)The expression of α-synuclein in groups A30P+Wortmannin and A30P+MPP+was higher than that in group A30P(P＜0.01), particularly.there was more significant expression of α-synuclein in group A30P+Wortmannin.The expression of α-synuclein in group A30P+Rapamycin was weaker than that in group A30P(P＜0.01); (2)The results showed that the SOD level(group A30P+MPP+:3 h:97.49±13.8;12 h:102.7±12.7; 24 h:101.5±11.8;48 h:104.3±12.4)was significantly decreased at various time points after MPP+ treatment compared that of group A30P(t=3.7721,P=0.0017).SOD level gradually increased in A30P +Rapamycin 12 h and showed significant difference at 24 h(121.2±13.0),48 h(124.3±14.1)and 72 h(127.7±13.7)after drug treatment compared with that in group A30P+Wortmannin(t:2.9746, P=0.0083);(3)Mutant α-synuclein(A30P)leading to PC12 cells death by means of autophagy involved α-synuclein accumulation,membrane lipid oxidation,and loss of plasma membrane integrity.Mutant α- synuclein(A30P)mediated the toxicity of MPP+.Rapamycin,an inducer of autophagy,reduced the aggregation of α-synuclein in transfected cells.Meanwhile,Wortmanin,an inhibitor of autophagy,promoted the aggregation of α-synuclein in transfected cells and induced cells to die.Conclusions The abnormal aggregation of α-synuclein induces autophagic programmed cell death in PC12 cells and mutant α-synuclein (A30P)mediates the toxicity of MPP+.Meanwhile,Rapamycin may reduce the aggregation of α-synuclein in transfeeted cells by activation of autophagic pathway.

Objective:To analyze the clinical characteristics and differences of inpatients who have been diagnosed with both cardiovascular and cerebrovascular diseases.The findings from this study will help medical professionals make informed decisions regarding diagnosis and treatment strategies for patients with coexisting cardiovascular and cerebrovascular diseases.Methods:This study included a total of 275 patients who were hospitalized in both the Neurology and Cardiology Departments of our hospital between January 2012 and December 2019.The study compared the treatment, hospitalization, and prognosis of the two departments using retrospective stratified analysis.Results:The majority of patients hospitalized in the Cardiology Department were diagnosed with circulatory system diseases(I00-I99), accounting for 92.0%(253 cases). In the Neurology Department, the main diagnoses were circulatory system diseases(I00-I99), nervous system diseases(G00-G99), symptoms and signs involving circulatory and respiratory systems, cognition, perception, emotional state and behavior(R00-R09, R40-R46), accounting for 69.8%(192 cases), 16.7%(46 cases)and 13.1%(36 cases), respectively.There was a significant difference in the distribution of diagnoses between the Cardiology and Neurology Departments( χ2=67.8, P<0.001). The Cardiology Department had a higher proportion of patients with 5 or more other diagnoses[153(55.6%) vs.59(21.5%)], while Neurology Department had a higher proportion of patients with 2-4 other diagnoses(64.0% vs.36.4%). When comparing the distribution of other diagnoses during hospitalization in the Cardiology Department, the proportion of patients with only one other diagnosis was higher in the first visit group of Neurology Department compared to those with two or more diagnoses, which was statistically significant( χ2=9.3, P=0.03). There was no statistical difference in hospitalization days between the two departments( χ2=2.2, P=0.14). Although there was a significant difference in patient outcomes, with a lower proportion of patients not recovering or dying in the Neurology Department( χ2=4.6, P=0.03), there was no significant difference in the interval between hospitalizations for the two groups(180 d, χ2=0.1, P=0.72; 90 d, χ2=1.8, P=0.18). Conclusions:The need for early prevention, diagnosis, and treatment of patients with both cardiovascular and cerebrovascular diseases is still a pressing concern.Exploring a combined diagnosis and treatment model for multiple diseases may prove useful in overcoming the limitations of the current single disease diagnosis and treatment approach.