Objective:to study memory impairment of patients with stroke in internal capsule-basal ganglia.Method:40 inpatients with stroke in internal capsule-basal ganglia and 25 aged matched normal control received assessment with MMSE (mini mental state examination), WMS-RC (Wechsler memory scale-Chinese revised), AVMT (auditory verbal memory test) and MPS (memory for pictorial scenes test). The patients were assessed in 20 days after stroke while the loci were determined by cranial CT or MRI.Result:among patients, the total scores of these memory tests were associated with cerebral atrophy, educational level, and leukoaraiosis. The volume of lesion and leukoaraiosis played a major role in memory coding strategy in MPS test. There were still significant differences in above memory tests between patients without cerebral atrophy and the matched controls.Conclusion:damage of sub-cortical rgions, such as lesions of internal capsule-basal ganglia, may cause memory impairment.

AIM: To study the effect of food intake on weight, memory, staying balance and power, and some biochemical indexes in mice. METHODS: In accordance with the average food intake everyday, the animals were divided into five groups: group A took the average food intake fully, group B took 75% of the average food intake, group C took 50% of the average food intake, group D took 25% of the average food intake, and group E did not take any food at all. The weights, memory, staying balance and power were recorded every three days, the biochemical index was recorded on the 10th day. RESULTS: On the 3rd day, the weight and staying balance and power of mice in group E decreased. On the 6th and 9th day, the weight of mice in group ABC increased. Compared with group B and C, the memory group A and D decreased. On the 10th day, the blood glucose concentratoin in of group D decreased, total cholesterol and triglyceride also decreased with the reduction of food intake. CONCLUSION: A food intake of 75%-50% in all helpes to keep a good body status and memory, decreases total cholesterol and triglyceride in blood.

Objective To investigate the 4-year follow up of cognitive function outcomes and characteristics in patients after stroke.Methods Sixty three cases according with the diagnostic standard of acute unifocal subcortical stroke were consecutively collected in neurological ward from December 2009 to November 2010.They were followed up for average four years.Forty one out of them completed the neuropsychology tests identical to the baseline,which covered the general cognition function,attention,execution,memory,language,spatial,etc.According to the standard of clinical diagnosis,cognition function is divided into five degrees,including normal,VCI-ND,mild VaD,moderate VaD,and severe VaD.The improved group had 13 cases whose cognition function was improved by one or more ranks.The progressive group had 12 cases whose cognition function progressed by one or more ranks.The stable group had 16 cases whose cognition function remained the same as the baseline.Results According to qualitative analysis on the baseline versus 4-year follow-up outcome,in 13 improved cases,8 were VCI-ND and 5 were mild VaD.In 16 stable cases,11 were normal,4 were VCI-ND and 1 was mild VaD.In 12 progressive cases,3 were normal (change to mild VaD after follow-up),5 were VCI-ND (change to mild and moderate VaD after follow-up) and 4 were mild VaD (change to moderate VaD after 4-year follow-up).In the comparison of baseline cognition function among the improved,progressive and stable group,there was only one significantly different score (the right number of SCWT-A) in the improved and progressive group.The cognition function of improved group had significant differences in CFT-copy,right number of SCWT-C and the time of TMT-B before versus after follow-up.The cognition function of progressive group had significant differences in AVLT-Delay Recall and CFT-Recall.Conclusion Long-term cognitive function outcome after stroke is heterogenetic.The location of cognitive impairment or progression is not the same model for different cognitive outcome group.

Objective To explore the activity and its possible neural mechanism of brain default mode network by using resting state functional magnetic resonance imaging (fMRI) in patients with mild cognitive impairment (MCI). Methods The 20 amnestic MCI patients and 25 healthy controls were included in this study, and all subjects underwent mini-mental state examination (MMSE), auditory verbal learning test (AVLT) and fMRI. The data were analyzed by amplitude of low frequency fluctuation (ALFF), and the enhanced and weakened regions of ALFF were observed and compared in both MCI patients and healthy controls. Results MMSE and AVLT tests showed that the memory function was seriously impaired in MCI patients compared with healthy controls, which is based on the short and long delayed episodic memory impairment (2.4±1.7 vs. 6.6±1.4, t=3.70, P＜0.01; 2.1±1.6 vs. 6.7±1.5, t=4.16, P＜0.01). The resting state fMRI showed that MCI patients had significant decreases of ALFF in hippocampal formation, parahippocampal cortex and lateral temporal cortex as compared with health controls (t=2.58, 2.43 and 1.75, all P＜0.01), which were closely relevant to the episodic memory. And they had significant increases in temporal-parietal joint and inferior parietal lobule (t=3.14 and 2.77, both P＜0.01). Conclusions MCI patients show significant decreased active intensity of some DMN nodes that is related to episodic memory in resting state. Increased active intensity in MCI patients would be some type of compensation.

[ ABSTRACT] AIM:To investigate the genetic cause of 2 Chinese families with Marfan syndrome .METHODS:The clinical and laboratory investigations were performed in the 2 unrelated Chinese families .Family 1 had 1 patient with cardiac problem.Family 2 had 2 patients:one died, and the other with respiratory and cardiac problems .Next generation sequencing and Sanger sequencing in the Marfan syndrome causal gene FBN1 were performed in the patient , his unaffected sister and the parents of family 1.Sanger sequencing covering all the exons and intron-exon boundaries were performed in the patient and the parents in family 2.Bioinformatic analysis was engaged in the variations unravelled .Fifty healthy indi-viduals were also investigated in the same manner .RESULTS:Both patients were diagnosed with Marfan syndrome .A no-vel mutation c.4685G>A (p.Cys1562Tyr) was detected in the patient of family 1 but was absent in his parents and the unaffected sister .This is a previously unreported novel mutation .In the mutation a conserved Cys was substituted by a Tyr in amino acid 1562 affecting a TGF-βbinding domain and the secondary structure in the encoded protein .We also detected the mutation c.3706T>C (p.Cys1236Arg) in the patient of family 2.It was absent in the unaffected parents , and there-fore was a de novo mutation too.This mutation has been previously reported and known to be associated with neonatal Marfan syndrome .Both mutations were absent in the 50 healthy controls .We also compared the genotype and phenotypes of the 2 families.CONCLUSION:We report 2 de novo mutations in 2 Chinese families with Marfan syndrome .One of the 2 mutations is novel.The phenotype of the mutation c.4685G>A(p.Cys1562Tyr) in family 1 is associated with classical Marfan syndrome, while that of c.3706T>C (p.Cys1236Arg) in family 2 is with neonatal type of Marfan syndrome .De novo mutations may be a cause for a proportion of mutations underlying the disease .The novel mutation also expends the mutational spectrum of the FBN1 gene.

AIM: To observe the effects of the human acidic fibroblast growth factor mutant (mhaFGF), lacking 27 amino acids at N-terminal, on the proliferation and signal transduction of the hepatocarcinoma cells. METHODS: The hepatocarcinoma cells were treated with human acidic fibroblast growth factor (haFGF) and mhaFGF, respectively. The expression levels of the signal proteins, Grb2 and Erk1/2, in the hepatocarcinoma cells were detected by semi-quantitative Western-blotting after treated for 15 min. The mitogenic activity of both haFGF and mhaFGF was detected by MTT method and the cell cycle was analysed by flow cytometer (FCM) after treated for 48 h. RESULTS: The mitogenic activity and the ratio of G 1 and S phase cells in mhaFGF-treated cells were markedly lower than that of the haFGF, and close to that of the control group. The expression level of both Grb2 and Erk1/2 in the mhaFGF-treated cells were lower than those in the haFGF- treated cells. CONCLUSION: The decrease in the mitogenic activity of mhaFGF is probably associated to its down-regulating the expression of the signal molecular, MAPK-ERK1/2 and Grb2.

Objective To analyze the characterization of cognitive function in Parkinson's disease with dementia and Alzheimer's disease. Methods Cognitive function was examined in Parkinson's disease with dementia (PDD) patients ( n = 30) , Alzheimer's disease (AD) patients ( n = 30) and healthy elderly control subjects ( n = 60) . Neuropsychological evaluation contained semantic fluency test, phonemic fluency test, action fluency test, objective and action naming tests. Results In PDD group , the score of semantic fluency test is 9. 33 ±2. 78, 6. 17 ± 1.67 of phonemic fluency test and 7.03 ±2. 34 of action fluency test,it is 6.90 ±2.47, 7.87±2.01,8.30±3. 17 of AD group. The score of objective and action naming tests is 36.33 ±3.39, 17.63 ±2. 17 in PDD group,while AD patients is 33.23 ±3.56 and 22.33 ±2.37. The verbal fluency tests and naming tests were impaired in PDD and AD patients compared with the healthy elderly control group (P ＜ 0. 01 ), phonemic fluency, action fluency and action naming were more impaired in PDD patients compared with the AD group , while semantic fluency and objective naming were more impaired in AD patients (P ＜ 0. 01 ). Conclusions Executive function deficit and naming impairment are found in PDD and AD patients, it shows that PDD is characterized by the addition of cortical dysfunction upon a predominant and progressive fronto-subcortical impairment. There is subcortical dysfunction in AD patients.

Objective: To evaluate the clinical value of suprapubic Trocar puncture lithotripsy in the treatment of benign prostatic hyperplasia and bladder stones. Methods: From February 2016 to August 2018, 60 patients with benign prostatic hyperplasia and bladder stones in the Second Hospital of Pujiang County were randomly selected.The patients were divided into transurethral prostatic bipolarplasma electrotomy group(control group, 30 cases) and transurethral prostatic bipolar excision procedure combined with suprapubic Trocar puncture cystinolithotomy group(study group, 30 cases) according to the operation methods.The operation time, stone extraction time, removal of bladder fistula time, catheter extraction time, success of one stone extraction, postoperative complications of the two groups were statistically analyzed. Results: The operation time, stone removal time, bladder fistula removal time and catheter removal time of the study group were significantly shorter than those of the control group(t=6.965, 4.541, 3.365, 3.306, all P<0.05). The success rate of the first stone extraction in the study group was 100.0%(30/30), which was significantly higher than 86.7%(26/30) in the control group (χ²=12.83, P<0.05). The incidence rate of postoperative complications in the study group was 10.0%(3/30), which was significantly lower than 23.3%(7/30) in the control group(χ²=13.34, P<0.05). Conclusion Suprapubic Trocar puncture lithotripsy has high value in the treatment of benign prostatic hyperplasia and bladder stones.

AIM:To investigate the regulatory role of retinoid X receptor(RXR)in oxidative stress response of rat type Ⅱ alveolar epithelial cells(AECII)induced by hypoxia/reoxygenation(HR).METHODS:The AECII were di-vided into control(C)group,HR group,HR+solvent dimethyl sulfoxide(DMSO)group(HD group),HR+RXR agonist 9-cis-retinoic acid(9-RA)group(RA group),and HR+RXR antagonist HX531 group(HX group).Cell Counting Kit-8(CCK-8)method was used to measure the cell viability.Immunofluorescence staining was used to detect the expression of surfactant protein A(SP-A)and RXRα in AECII.Kits were detected to the levels of superoxide dismutase(SOD)and malondialdehyde(MDA)in cells.Transmission electron microscopy was used to observe the ultrastructural changes of the cells.Western blot was used to detect the protein level of nuclear factor E2-related factor 2(Nrf2).RT-PCR was used to detect the expression level of Nrf2 mRNA.RESULTS:Compared with C group,the cell viability and SOD activity in HR,HD,RA and HX groups were decreased significantly(P<0.05),the MDA content were increased significantly(P<0.05),the Nrf2 mRNA and protein expression levels were decreased significantly(P<0.05 or P<0.01),and the immuno-fluorescence expression of RXRα was significantly increased(P<0.01).Compared with HR and HX groups,the cells in RA group showed significantly increased cell viability(P<0.05),increased SOD activity(P<0.05),decreased MDA con-tent(P<0.05),increased Nrf2 mRNA and protein expression levels(P<0.01),and significantly increased immunofluo-rescence expression of RXRα(P<0.01).CONCLUSION:Hypoxia/reoxygenation can aggravate the oxidative stress re-sponse of rat AECII,and RXR agonist intervention can alleviate HR-induced rat AECII injury by inhibiting oxidative stress.

Objective:To explore the association of the impaired cognition and the deposition of β-amyloid (Aβ) in normal cognitive (NC) and mild cognitive impairment (MCI).Methods:From December 2018 to January 2021, 305 subjects (113 males, 192 females; age (64.0±7.7) years) who completed neuropsychological tests and MRI in Shanghai Sixth People′s Hospital, Shanghai Jiao Tong University and 18F-florbetapir (AV45) PET imaging in Huashan Hospital, Fudan University were retrospectively analyzed. The subjects were divided into MCI group and NC group based on neuropsychological tests, and each group was further divided into Aβ-positive and Aβ-negative based on PET imaging results. Independent-sample t test, Mann-Whitney U test and χ2 test were used to analyze the data. Results:There were 118 subjects in MCI group and 187 subjects in NC group. The Aβ-positive rate in MCI group (37.3%, 44/118) was higher than that in NC group (26.2%, 49/187; χ2=4.19, P=0.041). The assessment performances of MCI group in general cognitive function, memory function, language function and executive function were inferior to those of NC group ( t values: from -10.63 to -6.31, z values: from -11.01 to -6.03, all P<0.001). The Auditory Verbal Learning Test-Long Delay Recall (AVLT-LDR) score of Aβ-positive subjects was lower than that of Aβ-negative subjects in MCI group (1.00(0.00, 3.00) and 3.00(1.00, 4.00); z=-2.49, P=0.013). The Montreal Cognitive Assessment Basic (MoCA-B) score of Aβ-positive subjects was lower than that of Aβ-negative subjects in NC group (25.29±2.67 and 26.36±2.42; t=-2.61, P=0.010). Conclusion:Compared to Aβ-negative subjects, MCI patients with Aβ-positive perform worse on memory tests, and NC subjects with Aβ-positive perform worse on general cognitive function.