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Objective To investigate the relationship between serum neutrophil elastase(NE),Sortilin and carotid atherosclerotic(CAS)plaque in patients with acute cerebral infarction(ACI)and its predictive value for poor prognosis.Methods A total of 155 patients with ACI admitted to Daxing Teaching Hospital of Cap-ital Medical University from December 2020 to November 2022 were selected as the study objects.According to carotid intima-media thickness(IMT),they were divided into normal IMT group,thickened group and plaque group,and 40 healthy subjects were selected as control group during the same period.The serum levels of NE and Sortilin in all groups were compared and their correlations with IMT were analyzed.ACI patients were followed up for 3 months and divided into good prognosis group and poor prognosis group.Serum NE and Sortilin levels were compared between the two groups.Multivariate Logistic regression was used to ana-lyze the risk factors of poor prognosis in ACI patients.Receiver operating characteristic(ROC)curve was used to predict prognosis.Results The levels of serum NE and Sortilin in control group,IMT normal group,thick-ened group and plaque group were increased successively(P<0.05).Pearson correlation analysis showed that serum NE and Sortilin levels were positively correlated with IMT(r=0.509,0.483,P<0.05).The incidence of poor prognosis in ACI patients was 39.35%.The proportion of diabetes mellitus,age,admission National Institutes of Health Stroke Scale(NIHSS)score,low density lipoprotein cholesterol,total cholesterol,fasting blood glucose,white blood cell count,serum creatinine,NE,uric acid(UA)and Sortilin levels in poor progno-sis group were higher than those in good prognosis group(P<0.05).Multivariate Logistic regression analysis showed that admission NIHSS score and UA,NE and Sortilin levels were independent risk factors for poor prognosis in ACI patients(P<0.05).ROC curve analysis showed that the area under the curve of serum NE,Sortilin and UA alone and combined to predict poor prognosis were 0.695,0.740,0.752 and 0.869,respective-ly.The combined prediction efficiency of serum NE,Sortilin and UA was higher than that of single detection of each indicator.Conclusion The increase of serum NE and Sortilin levels in ACI patients is positively corre-lated with CAS,and is an independent risk factor for poor prognosis in ACI patients.Detection of serum NE and Sortilin levels could help predict the short-term prognosis of ACI patients.
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Objective To investigate the clinical characteristics of sleep disorders (SD)in patients with Alzheimer's disease(AD),and the relationship between SD and cognitive impairment.Methods According to the inclusion and exclusion criteria of AD,89 consecutive AD patients admitted to Beijing Tiantan Hospital from January 2016 to January 2017 were included.The Pittsburgh sleep quality index(PSQI)scale was used to evaluate the overall sleep status.The patients were randomized into the AD with SD(AD-SD) group (PSQI> 7) and the AD without SD (AD-NSD) group (PSQI < 7).The cognitive function of AD patients was evaluated by the Montreal cognitive assessment (MoCA) scale,and the overall cognitive function and cognitive domains were compared between the AD-SD and AD-NSD groups.Results Of the 89 AD patients,71 cases (79.78%)had SD.There was no significant difference in gender,age,age of onset,education level and disease duration between the AD-SD and AD-NSD groups(P>0.05).The factors in the PSQI scale had significant differences between AD-SD 和 AD-NSD groups,including sleep quality,sleep latency,sleep duration,sleep efficiency,sleep disturbance,administration of sleeping medication and daytime dysfunction(P<0.05).Compared with the AD-NSD group,the AD-SD group showed that the total score of MoCA scale was significantly reduced(P<0.05),and the scores of delayed recall and language were significantly decreased(P < 0.05).There was a negative correlation of the sleep time with the total score of MoCA scale and the score of delayed recall in the AD-SD group(r =-0.245 and 0.249,P =0.041 and 0.039).Night SD was negative correlated with the total score of MoCA scale and the score of delayed recall(r=0.248 and-0.283,P =0.038 and 0.018).Conclusions The incidence of AD-SD is up to 79.78%.AD-SD patients have a worse subjective sleep quality,longer time to fall asleep,shorter sleep time,lower sleep efficiency,higher night SD,more use of sleep drugs and more daytime dysfunction.General cognitive dysfunction,delayed recall and language impairment are more obvious in AD-SD patients.In AD-SD group,longer time to fall asleep and night SD are related to the general cognitive function and delayed recall.
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Objective@#To investigate the clinical characteristics of sleep disorders(SD)in patients with Alzheimer's disease(AD), and the relationship between SD and cognitive impairment.@*Methods@#According to the inclusion and exclusion criteria of AD, 89 consecutive AD patients admitted to Beijing Tiantan Hospital from January 2016 to January 2017 were included.The Pittsburgh sleep quality index(PSQI)scale was used to evaluate the overall sleep status.The patients were randomized into the AD with SD(AD-SD)group(PSQI>7)and the AD without SD(AD-NSD)group(PSQI<7). The cognitive function of AD patients was evaluated by the Montreal cognitive assessment(MoCA)scale, and the overall cognitive function and cognitive domains were compared between the AD-SD and AD-NSD groups.@*Results@#Of the 89 AD patients, 71 cases(79.78%)had SD.There was no significant difference in gender, age, age of onset, education level and disease duration between the AD-SD and AD-NSD groups(P>0.05). The factors in the PSQI scale had significant differences between AD-SD和AD-NSD groups, including sleep quality, sleep latency, sleep duration, sleep efficiency, sleep disturbance, administration of sleeping medication and daytime dysfunction(P<0.05). Compared with the AD-NSD group, the AD-SD group showed that the total score of MoCA scale was significantly reduced(P<0.05), and the scores of delayed recall and language were significantly decreased(P<0.05). There was a negative correlation of the sleep time with the total score of MoCA scale and the score of delayed recall in the AD-SD group(r=-0.245 and -0.249, P=0.041 and 0.039). Night SD was negative correlated with the total score of MoCA scale and the score of delayed recall(r=-0.248 and -0.283, P=0.038 and 0.018).@*Conclusions@#The incidence of AD-SD is up to 79.78%.AD-SD patients have a worse subjective sleep quality, longer time to fall asleep, shorter sleep time, lower sleep efficiency, higher night SD, more use of sleep drugs and more daytime dysfunction.General cognitive dysfunction, delayed recall and language impairment are more obvious in AD-SD patients.In AD-SD group, longer time to fall asleep and night SD are related to the general cognitive function and delayed recall.
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Objective To investigate the clinical features of Parkinson disease (PD)with constipation.Methods From October 2013 to August 2015,a total of 204 PD patients were consecutively recruited from the Departments of Geriatrics and Neurology,Beijing Tiantan Hospital,Capital Medical University,and were evaluated by Rome Ⅲ diagnostic criteria for functional constipation and other related scales of motor symptoms(MS)and non-motor symptoms(NMS),the activity of daily living(ADL)and quality of life.Results Overall,131 of 204(64.2%)PD patients with constipation were assigned to the PD-C group and 73 of 204 (35.8%)PD patients without constipation were assigned to the PD-NC group.In the PD-C group,38 of 131(29%)PD patients had constipation before motor symptoms occurred.The mean age and age of onset in the PD-C group were significantly older than those in the PD-NC group (64.13 ± 9.67 vs.58.35 ± 11.37;60.07 ± 10.46 vs.55.10±12.97;F=2.287,4.948;t=3.827,-2.788;P<0.01 for both).Meanwhile,compared with the PD-NC group,the PD-C group was associated with dramatically longer disease duration (2.25,range:1.00-5.00 vs.2.00,range:1.00-3.13;Z =-2.254;P < 0.05),increased scores of the Unified Parkinson Disease Rating Scale (UPDRS) Ⅲ (26.00 scores,range:18.00 37.50 vs.19.00,range:12.50-31.00;Z =-2.349,P < 0.05),more advanced stages on the Hoehn-Yahr (H-Y) scale (2.00 stage,range:1.50-2.50 vs.1.50,range:1.00-2.50;Z=-2.334,P<0.05),higher total numbers of NMS(11.00,range:6.00-15.00 vs.6.00,range:3.00-11.00;Z=-3.715,P<0.05),and higher numbers of NMS occurring before and after MS(before,2.00,range:0.00-4.00 vs.1.00,range:0.00-2.00;after,8.00,range:3.00-14.00 vs.5.00,range:2.00-9.50;Z =-2.612,-2.630,respectively;P<0.05 for both).Additionally,there were significant differences between the groups in the scores of the Hamilton depression scale (HAMD),the Hamilton anxiety scale (HAMA),the Pittsburgh sleep quality index (PSQI),the scales for outcomes in Parkinson disease-autonomic (SCOPA-AUT),the Fatigue severity scale (FSS),the Apathy scale,the Montreal Cognitive Assessment(MoCA)scale,the UPDRS Ⅱ and ADL Scale,and the PDQL-39 (all P<0.05).Binary Logistic regression analysis showed that age,SCOPA-AUT,HAMA and HAMD were risk factors for PD-C(OR=1.091,1.107,1.10 and 1.080;P<0.05 for all).Conclusions PD patients have a high incidence of constipation,and more than a quarter of patients have constipation before MS occurs.Meanwhile,PD patients with constipation are usually associated with old age and late age of onset,long disease duration,severe MS,frequent and severe NMS,bad cognition,emotional state and sleep,severe fatigue,and apathy.Moreover,advanced age,autonomic dysfunction,anxiety and depression increase the risk of PD with constipation.Constipation has a serious negative impact on the activity of daily living and quality of life in PD patients.
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Parkinson's disease (PD) is a common neurodegenerative disorder with typical motor symptoms and a variety of non-motor symptoms,including neuropsychiatric symptoms,autonomic dysfunctions,abnormal sense,sleep disorders and fatigue.Studies showed that several non-motor symptoms,such as olfactory dysfunction,constipation,rapid eye movement sleep behavior disorder,depression and fatigue,can occur before the onset of motor symptoms.Fatigue has been considered as one of the most disabling symptoms,and it has a significant impact on activity of daily living and quality of life,and brings heavy burdens to caregivers.However,fatigue in PD has no special biomarkers,so clinicians are lack of the recognition and intervention.Here,we will expound the prevalence,risk factors,rating scales and potential mechanism relating to neuropathology,neuroinflammation and neurobiochemistry in PD patients with fatigue.
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Objective To construct pcDNA 3.1(+)/HPV 18 E 6 fusion gene and a single-codon mutation pcDNA 3.1(+)/E6 F49R or pcDNA 3.1(+)/E6 F127R fusion gene in eukaryotic expression vector and study the effects on proliferation and apoptosis of cervical carcinoma cell line Hela. Method HPV 18 E6 gene sequence and the single-point mutation HPV 18 E6 F49R or HPV 18 E6 F127R were amplified from total RNA of Hela cell line by reverse transcription- polymerase chain reaction ( RT- PCR), then the gene sequences were respectively inserted into pcDNA 3.1(+) vector to reconstruct recombinant plasmids which were transfected transiently into Hela cells. MTT and RT-PCR were used to test the expression levels of HPV 18 E6 and the growth of HeLa cells after transfected about 48 h. The proliferation and apoptosis of Hela cells were detected respectively by cell counting and AO/EB fluorescent vital staining. Results The pcDNA 3.1(+)/HPV 18 E6, pcDNA 3.1(+)/E6 F49R and pcDNA 3.1(+)/E6 F127R eukaryotic expression vectors were successfully constructed. The gene of HPV 18 E6 was discriminably detected in the HeLa cells which were transfected with the recombinant plasmids. After several days, the proliferation of Hela cells transfected with pcDNA 3.1(+)/E6 F49R or pcDNA 3.1(+)/E6 F127R plasmid were obviously inhibited and the apoptotic rates were significantly increased, then the proliferation of cells transfected with pcDNA(+)/HPV 18 E6 was rather increased slightly, and we could observe the phenomena of early apoptosis and the formation of thekaryopyknosis by fluorescent microscope in the cells transfected with pcDNA 3.1(+)/E6 F49R or pcDNA 3.1(+)/E6 F127R. Conclusion The eukaryotic expressing vectors encoding HPV 18 E6 F49R and HPV 18 E6 F127R provide fundamental basis for the further study on HPV 18 E6 mechanism as well as prevention and treatment of uterine cancer.