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Objective:To understand the current status of depression in older people aged 65 and over in Henan Province, and to study its influencing factors, with a focus on depression in older adults in grandparent families.Methods:A multi-stage stratified cluster sampling method was used.Baseline data about older people aged 65 and over were collected by self-designed questionnaires, the 15-item Geriatric Depression Scale(GDS-15)was used to assess depression.Results:A total of 7673 valid questionnaires about older adults aged 65 and over were collected, and the rate of depression was 29.52%(2265). Logistic regression analysis showed that 15 factors, such type of parenting, religious belief, region, degree of self-care, affected depression in older people aged 65 and above.Compared with regular parenting, grandparenting alone was a protective factor for depression[ OR(95% CI)=0.613(0.499-0.755), P<0.01]; compared with religious belief, no religious belief was a risk factor for depression[ OR(95% CI)=1.281(1.102-1.488), P<0.01]; compared with income ≥￥4000, incomes between ￥1000-1999[ OR(95% CI)=0.638(0.464-0.877), P<0.01], between ￥2000-2999[ OR(95% CI)=0.567(0.432-0.744), P<0.01]and between￥3000-3999[ OR(95% CI)=0.584(0.448-0.761), P<0.01]were protective factors for depression, with higher income showing stronger protection; compared with retirement, working had a protective effect, but the protective strength decreased in the order of working as urban labor, [ OR(95% CI)=0.332(0.273-0.405), P<0.01], as farmers[ OR(95% CI)=0.391(0.296-0.516), P<0.01], and as professionals or managers[ OR(95% CI)=0.514(0.402-0.656), P<0.01]; living in rural areas[ OR(95% CI)=0.686(0.586-0.804), P<0.01]and female[ OR(95% CI)=0.820(0.734-0.917), P<0.01]were risk factors for depression. Conclusions:There is currently a high rate of depression in older people aged 65 and over in Henan Province.Its influence factors are complicated and variable.Intervention measures taken by institutions need to adapt to specific circumstances.
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Objective:To analyze any changes in the functional connectivity between the seed points of the dorsolateral prefrontal cortex (DLPFC) and the whole brain, as well as any fluctuations in the low-frequency amplitude among persons with post-stroke depression (PSD). The aim was to develop correlations among functional imaging results, clinical scales, and inflammation indicators including high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), interleukin 2 (IL-2), interleukin 10 (IL-10), interleukin 17a (IL-17a) and interferon-γ (IFN-γ).Methods:Between 2016 and 2020, 55 ischemic stroke survivors were tested. The 28 scoring 7 or more on the Hamilton Depression Scale (HAMD-17) formed the PSD group, while the 27 others formed the control group. Functional magnetic resonance images were collected, and serum inflammation indicators were determined.Results:When seed points in the left DLPFC were used, in the PSD group the frontal cortex (FC) decreased in one cluster, with a voxel of 129mm3 and the MNI coordinates (x=9, y=30, z=33) indicating that the anatomical automatic labeling (AAL) brain regions were the Cingulum_Ant_L, Cingulum_Mid_R and the frontal_Sup_Medial_L. When the right DLPFC was used as the seed point the FC again decreased in one cluster, with voxels of 44mm 3 and the MNI coordinates (x=-27, y=12, z=47) referring to the AAL brain region of the frontal_Mid_L. In the PSD group, the FC value of abnormal brain areas with the R-DLPFC as the seed point was positively correlated with time since stroke. In the control group, the FC value of abnormal brain areas with L-DLPFC as the seed point was negatively correlated with MoCA, while with R-DLPFC as the seed point it was positively correlated with IFN-γ. The FC values of abnormal areas of the brain showed no significant correlation with other clinical scales, inflammation indicators or lesion volume. Conclusion:Abnormal functional connections within the executive control network and between the salience networks may participate in the mechanism of PSD, and may be related to the time since stroke, cognitive functioning, and IFN-γ levels.
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Objective:To explore the effect of lncRNA SNHG5 on injury of astrocytes induced by hypoxia/reoxygenation (H/R).Methods:(1) Astrocytes were cultured in vitro. The H/R cell model was established by hypoxia culture for 6 hours and then reoxygenaion culture for 18 hours. Lipofectamine? 2000 liposome method was used to transfect lncRNA SNHG5 into astrocytes. RT-qPCR was used to detect the expression of lncRNA SNHG5 in H/R cells and after transfection. (2) Astrocytes were divided into normal control group, model group, transfection control group (pcDNA-NC was transfected first, then H/R cell model was established) and transfection group (pcDNA-lncRNA SNHG5 was transfected first, then H/R cell model was established). Then the effect of overexpression of lncRNA SNHG5 on astrocytes was observed. (3)The astrocytes transfected with lncRNA SNHG5 and H/R intervention were divided into transfection+ vehicle group (0.1% DMSO incubation) and transfection+ inhibitor group (20 μmol/L LY294002 incubation), and then observe the effect of the inhibitor of PI3K/Akt signaling pathway LY294002 on H/R astrocytes was observed. (4) CCK-8 was used to detect cell proliferation. Flow cytometry was used to detect cell apoptosis. Western blot was used to detect the expression of cell proliferation proteins (Cyclin D1 and Cyclin E), apoptotic proteins (Caspase-3 and Bax), p-PI3K and p-AKT protein. ELISA was used to detect the levels of IL-1β and TNF-α. The colorimetric method was used to detect the level of lactate dehydrogenase(LDH) in cell culture supernatants and the level of malondialdehyde(MDA) and superoxide dismutase(SOD) in cells. SPSS 22.0 software was used for independent sample t-test and one-way ANOVA, and LSD- t test was used for further pairwise comparisons. Results:(1) RT-qPCR results showed that the level of lncRNA SNHG5 in astrocytes induced by H/R was lower than that in the normal cultured cells ( t=33.28, P<0.05). (2) lncRNA SNHG5 overexpression experiment: The cell proliferation activity of the model group was lower than that in the normal control group (CCK-8 OD value: (0.64±0.02), (1.23±0.02), t=62.58, P<0.05). The levels of proliferation proteins Cyclin D1 and Cyclin E in the model group were lower than those of the normal control group ( t=33.54, 32.20, both P<0.05). The cell proliferation activity of the transfection group was higher than that of the transfection control group (CCK-8 OD value: (1.49±0.02), (0.65±0.03), t=69.89, P<0.05), the levels of cell proliferation proteins Cyclin D1 and Cyclin E in the transfection group were lower than those in the transfection control group ( t=24.96, 28.46, both P<0.05). The apoptosis rate of the model group was higher than that of the control group (flow cytometry results: (25.33±1.13)%, (9.06±0.21)%, t=42.47, P<0.05), and the levels of apoptotic proteins Caspase-3 and Bax were also higher than those of the control group ( t=57.41, 41.60, both P<0.05). The Caspase-3 rate of the transfection group was lower than that of the transfection control group((16.56±0.60)%, (25.89±1.18)%, t=21.14, P<0.05), and the levels of apoptotic proteins Caspase-3 and Bax were also higher than those of the transfection control group( t=77.79, 58.34, both P<0.05). The levels of p-PI3K and p-AKT proteins in the model group were lower than those in the control group ( t=56.35, 33.94, both P<0.05), and the levels of p-PI3K and p-AKT proteins in the transfection group were higher than those in the transfection control group ( t=130.14, 76.37, both P<0.05). The results of ELISA showed that the levels of IL-1β and TNF-α in the model group were higher than those in the control group ( t=58.04, 30.63, both P<0.05), but the levels of IL-1β and TNF-α in the transfection group were lower than those in the transfection control group ( t=33.63, 39.01, both P<0.05). The colorimetric method showed that the levels of LDH and MDA in the model group were higher than those in the control group ( t=65.51, 41.85, both P<0.05), but the level of SOD was lower than that in the control group ( t=48.82, P<0.05). The levels of LDH and MDA in the transfection group were lower than those in the transfection control group ( t=37.93, 30.72, both P<0.05), but the level of SOD was higher than that in the transfection control group ( t=30.32, P<0.05). (3) PI3K/Akt signaling pathway inhibition experiment: the cell proliferation activity of the transfection+ inhibitor group was lower than that of the transfection+ vehicle group (CCK-8 OD value: (0.97±0.02), (1.46±0.03), t=15.24, P<0.05), and the related proliferation proteins Cyclin D1 and Cyclin E were also lower ( t=11.41, 13.15, both P<0.05). The apoptosis rate of the transfection+ inhibitor group was higher than that of the transfection+ vehicle group (Flow cytometry: (26.11±0.86)%, (16.06±0.44)%, t=10.45, P<0.05). The apoptosis rate of the transfection+ inhibitor group was higher than that of the transfection+ vehicle group (Flow cytometry: (26.11±0.86)%, (16.06±0.44)%, t=10.45, P<0.05), and the related apoptosis protein Caspase-3 and Bax were also higher ( t=19.06, 13.54, both P<0.05). The expression levels of p-PI3K and p-AKT protein in the transfection+ inhibitor group were lower than those in the transfection+ vehicle group ( t=36.67, 27.34, both P<0.05). ELISA results showed that the levels of IL-1β and TNF-α in the transfection+ inhibitor group were higher than those in the transfection+ vehicle group ( t=15.17, 9.44, both P<0.05). The colorimetric method results showed that the levels of LDH and MDA in the transfection+ inhibitor group were the same as those in the transfection+ vehicle group ( t=15.33, 9.05, both P<0.05), but the level of SOD was lower than the transfection+ vehicle group ( t=11.04, P<0.05). Conclusion:Overexpression of lncRNA SNHG5 may promote the proliferation of astrocytes induced by hypoxia/reoxygenation, and inhibit cell apoptosis, inflammation and oxidative stress.
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Objective To investigate the effects of Edaravone on cognitive dysfunction and on protein expression of the mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK)signaling pathway in elderly patients with acute ischemic stroke. Methods A total of 100 elderly patients with acute ischemic cerebral stroke admitted to our hospital from January 2011 to December 2015 were enrolled in this study.During the corresponding period ,100 healthy individuals receiving regular check-ups were selected as the control group. The effects of Edaravone on cognitive function in elderly patients with acute ischemic cerebral stroke were assessed.Serum proteins related to the MAPK/ERK signaling pathway were assayed. Results Elderly patients with acute ischemic stroke showed obvious cognitive dysfunction ,and scores on memory ,orientation ,attention ,calculation language and recall significantly decreased(P＜0.01)but returned to normal after Edaravone treatment (P＜0.01).Compared with the control group ,serum protein expression of rat sarcoma (Ras) ,rapidly accelerated fibrosarcoma(Raf) ,hypoxia inducible factor-1α(HIF-1α) ,connective tissue growth factor (CTGF),extracellular signal-regulated protein kinase(ERK1),ERK2 ,MAPK/ERK kinase(MEK), interleukin-1(IL-1) ,tumor necrosis factor-α(TNF-α) ,vascular endothelial growth factor (VEGF) , tissue inhibitor of metalloproteinase (TIMP) ,nerve growth factor (NGF)and its receptors was significantly downregulated(P＜0.01) ,while expression of leptin and its receptors was upregulated in elderly patients with acute ischemic cerebral stroke ( P ＜ 0.01 ). Expression levels of the above downregulated proteins clearly recovered after Edaravone treatment ( P ＜ 0.01 ). Conclusions Edaravone has favorable effects on cognition dysfunction in elderly patients with acute ischemic cerebral stroke ,which may be related to the regulation of the MAPK/ERK signaling pathway.
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Objective To observe the effect of repetitive transcranial magnetic stimulation (rTMS) on behavior in response to chronic but unpredictable mild stress and explore potential neuroendocrine mechanisms.Methods Forty adult SD male rats were randomly divided into a control group (n =8) and a model preparation group (n=32).The control group was given normal care while a model of depression was induced in the model preparation group through giving an unpredictable mild stimulus (CUMS).The depressive rats were randomly divided into a model group,an rTMS group and a sham rTMS group (8 cases in each group).The rTMS group and sham rTMS groups accepted the rTMS or sham stimulation for 3 weeks.The changes in behavior in each group were quantified using body weight,sucrose consumption and an open field test before and after stimulation.Enzyme-linked immunosorbent assays (Elisas) were conducted to detect plasma adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels.Reverse-transcription polymerase chain reactions (RT-PCRs) were carried out to allow the detection of mRNA expression in hypothalamus related to levels of adrenocorticotropic hormone releasing hormone (CRH).Results After the modeling there were significant differences between the model preparation group and the control group in terms of weight increase,sucrose consumption and open field test results.After rTMS the rate of weight increase,sucrose consumption and the scores in the open field test of the rTMS group had increased significantly more than in the control group.Elisas showed significantly higher plasma ACTH and CORT levels in the model group as well.The average expression of CRH mRNA in the model group was significantly higher than in either of the other two groups.Conclusions rTMS can relieve depression-like behavior induced by chronic stress,at least in rats.This may be related to a downgrading of the hyperactive functioning of the hypothalamus-pituitary-adrenal axis.
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Objective To explore the effects of repetitive transcranial magnetic stimulation (rTMS) on the improve?ment of depressive behavior and the hippocampus brain derived neurotrophic factor (BDNF) expression in chronic stress-induced depression rats. To further investigate the possible molecular mechanism of rTMS treatment for depres?sion. Methods Forty male Sprague-Dawley rats of SPF grade were randomly divided into the blank control group (n=8) and the stress-induced group (n=30). Singly housing and chronic unpredictable mild stress (CUMS) were used to induce the depression model in stress-induced group. Twenty-four model rats were divided into three groups:model group (with no further treatment), rTMS group (receiving 10 Hz rTMS intervention for 3 weeks) and shame group (receiving pseudo TMS treatments for 3 weeks). Weight measurement, sucrose consumption test and open-field test were used to assess the behavior changes. The rat hippocampal CA3 area of BDNF positive staining cell number and expression levels of BDNF mRNA in hippocampus were examined after intervention. Results The weight reduction rate, score of sucrose consump?tion test and the score of open field test were significantly higher in rTMS group than in model group (P<0.05). The num? ber of BDNF staining positive cells in the hippocampal CA3 area was lower in model group and shame group than in the blank control group whereas was higher in the rTMS group than in the model group (P<0.01). Compared with the model group, the BDNF mRNA relative expression was significantly increased in the hippocampus of rTMS group (P<0.01). Conclusion rTMS can improve depressive behaviors of CUMS rats probably through the increase in expression of BDNF in the hippocampal neurons and neuronal regeneration.
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[ ABSTRACT] AIM:To prove the purinergic signaling mechanism of the neuroprotective action of hydrogen sulfide by observing the effects of sodium hydrosulfide ( NaHS) , a donor of hydrogen sulfide, on the cell viability, intracellular Ca2+concentration ( [ Ca2+] i ) and the change of membrane permeability in the PC12 cells injured by adenosine triphos-phate ( ATP) .METHODS: PC12 cells in logarithmic growth phase were randomly divided into 4 groups.In control group, the cells were cultured without ATP treatment.In ATP group, the cells were treated with ATP after cultured for 24 h.In NaHS+ATP group, the cells were incubated with NaHS for 30 min before treated with ATP, and NaHS always exis-ted in the reaction system.In KN-62+ATP group, the cells were pretreated with KN-62 for 30 min, and the other treat-ments were as the same as those in NaHS+ATP group.The cell viability was assessed by MTT assay.The [ Ca2+] i was detected by Fura-2/AM staining.The membrane permeability was observed by staining with fluorescent dye YO-PRO-1. RESULTS:ATP at concentration of 0.3 mmol/L showed no injury effect on the cells.However, the cell viability was dropped gradually in a dose-dependent manner as the ATP at doses of 1, 3, 5 and 10 mmol/L.The decline of cell viability by ATP was obviously reversed by 200 μmol/L of NaHS in the PC12 cells (P<0.05), but exasperated by 800μmol/L of NaHS (P<0.05).At the same time, ATP evoked the increase in [Ca2+]i in a dose-dependent manner, which was inhib-ited by NaHS ( P<0.05) .Furthermore, the YO-PRO-1 uptake induced by ATP in a dose-dependent and time-dependent manner was also reduced by NaHS ( P<0.05) .CONCLUSION:Hydrogen sulfide has protective effect on the PC12 cells injured by ATP.The mechanism may be related to the reverse of the increased [ Ca2+] i and YO-PRO-1 uptake.
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Objective To explore the effects of repetitive transcranial magnetic stimulation (rTMS) and fluoxetine on depression and cognition in the treatment of post-stroke depression (PSD).Methods A total of 82 PSD patients were divided into a treatment group and a control group using a random number table.Besides conventional neurological therapy,the treatment group was treated with rTMS combined with fluoxetine,while the control group was treated only with fluoxetine.Forty healthy persons acted as normal controls.The Hamilton depression rating scale (HAMD) was used to evaluate depressed emotions,and event-related potential (ERP) P300 and exploratory eye movement (EEM) were used to evaluate cognitive function.The three groups were tested before treatment and after 8 weeks of treatment.Results After 8 weeks of treatment the HAMD scores in both the treatment and control groups had decreased significantly compared with before treatment.The HAMD scores decreased significantly more in the treatment group than in the control group.Before treatment,the N2 and P3 iatencies of P300 in the treatment and control groups were significant longer than those in the normal group,and the average amplitude of P3 in the treatment and control groups was significantly lower than among the normal controls.Before treatment,the number of eye fixations (NEF) and the average responsive search score (RSS) in the treatment group and control groups were significantly lower than in the normal group.After 8 weeks after treatment,the N2 and P3 latencies were significantly shorter and the amplitude of P3 was significantly higher in the treatment and control groups than before treatment.The NEF and the average RSS in the treatment and control groups had increased significantly compared with before treatment.All of these indexes improved significantly more in the treatment group than in the control group.Conclusion rTMS combined with fluoxetine can improve depression and cognitive function among PSD patients better than antidepressant treatment alone.
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Objective To study and analyze the relation between cognitive impairment and apolipoprotein E(ApoE) gene polymorphism in post-stroke depression patients(PSD).Methods The patients were divided into PSD group(83 cases) and brain stroke group(96 cases) by using the 24-item Hamilton Depression Rating Scale (HAMD-24),and healthy volunteers were selected as a control group(53 cases).Cognitive function was evaluated by using the event-related potential (ERP) P300 and single nucleotide polymorphisms of ApoE exon 4 of 112 (rs429358) and 158 (rs7412) were determined by using gene sequencing method.Results 1.Compared with the brain stroke group and the control group,latency in ERP including N2 and P3 of PSD group was significantly prolonged (P＜ 0.05 ),while the amplitude of P3 in PSD was significantly lower(P＜ 0.05 ).2.e3/ε4 genotype frequency in PSD group(24 cases) was significantly higher than that in the control group(7 cases) (P＜0.05).The e4/4 genotype fiequency in PSD group (8 cases) was significantly higher than that in brain stroke group (2 cases) (P ＜ 0.05 ).The e4 allele rate in PSD group ( 24.7％ ) was significantly higher than that in both brain stroke group (16.1％) and contro] group(9.4％ ) (all P＜0.05).3.The PSD patients with ε4 allele had significantly higher score of HAMD-24 and prolonged latency of N2 and P3 than those without e4 allele (P ＜ 0.05 ).Conclusion There is cognitive impairment in PSD patients.The ApoE ε4 allele may associate with the cognitive impairment and depression in PSD patients.
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BACKGROUND:Point resolved spectroscopy (PRESS) or single-voxel spectroscopy (SVS) is always used in the previous researches of magnetic resonance spectroscopy (MRS) and its regions of interest are mainly located in focal zones which can be observed with magnetic resonance imaging (MRI); however, both of them cannot manifest the changes of focal marginal zone. Contrarily, hydrogen magnetic resonance spectroscopy (1H-MRS) can det ect the all regions of brain.OBJECTIVE: To observe the 1H-MRS manifestations of patients with heroin spongiform leucoencephalopathy (HSLE) so as to analyze metabolic regularities of N-acetyl aspartate (NAA), creatine (Cr) and bilineurine (Cho) in brain.DESIGN: Case-contrast observation.SETTING: Department of Neurology, Nanfang Hospital.PARTICIPANTS: Three HSLE patients including 2 males and 1 female who were diagnosed with clinical imaging were selected from the Department of Neurology, Nanfang Hospital from August 2005 to August 2006, and all of them were regarded as the case group. In addition, 10 healthy volunteers were regarded as the control group.METHODS: Siemens Megnetom Vision Plus 1.5T superconductive magnetic resonance (MR) system and standard head coil were used in this study, and then, all subjects were checked with 1H-MRS.MAIN OUTCOME MEASURES: Levels of NAA, Cr and Cho in white matter of frontal, parietal and occipital lobes, metabolic maps of them and ratios of NAA/Cr and Cho/Cr.RESULTS: All 13 subjects were involved in the final analysis. ① NAA level: The level of NAA in white matter of frontal,parietal and occipital lobes of case 1 was lower than that of the subjects in the control group (79.50±21.65, 96.75±16.14,77.05±22.47; 146.07±15.49, 117.77±14.56, 120.83±16.02; P ＜ 0.05, 0.01); meanwhile, white matter of parietal lobes of case 2 and case 3 was also lower than that of subjects in the control group (87.50±7.89, 80.65±11.73, P ＜ 0.01). ② Cr level: There were no significant differences of the Cr level of all subjects in both case group and control group (P＞ 0.05).③ Cho level: Except white matter of frontal lobes in case 1, the level of Cho was lower in the case group than that in the control group (P ＜ 0.01). ④ Ratio of NAA/Cr was lower in the case group than that in the control group, and the radio of Cho/Cr was decreased remarkably. ⑤ Metabolic maps of NAA and Cr manifested a low signal in focal site. ⑥ Ratio of Cho/Cr was obviously reversed in focal marginal zone, but wave of lactic acid was not observed at the same time.CONCLUSION:The area with abnormal metabolites in HSLE patients showed by 1H-MRS is obviously larger than the visible lesion area showed by MRI.There are abnormal metabolites in the adjacent area of HSLE lesions.
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BACKGROUND: The depressive emotion and cognition impairment after cerebral stroke are closely connected with the evolution and curative effect and prognosis of the disease, so how to improve depressive emotion and cognition impairment with reasonable drug has important significance to enhance clinical rehabilitation for the patients.OBJECTIVE: To treat patients with post-stroke depression with fluoxetine hydrochloride, andevaluate the changes of their depressive emotion and cognitive function with self-rating depression scale (SDS) and P300 potential.DESIGN: A randomized controlled trial based on patients. SETTING: Henan Provincial Psychiatric Hospital. PARTICIPANTS: Eighty-two inpatients with the first-attack of poststroke depression, who were selected from the Department of Neurology,Henan Provincial Psychiatric Hospital between December 1999 and June 2003, were divided randomly into treatment group (n=41) and control group (n=41).METHODS: All the patients were given neurological routine treatment;besides, those in the treatment group were treated with fluoxetine hyhad taken other psychotropic drugs before entering the group, fluoxetine oxetine was 20 mg, which was taken orally by 1 tablet every morning. All the patients were evaluated with SDS and P300 potentials test at 1 week (the first evaluation) and 6 weeks (reevaluation) after treatment.latencies of N1, P2, N2 and P3 waves and amplitude of P3 wave in P300 potentials.RESULTS: All the patients in the treatment group (n=41) and control group fore treatment, the scores of SDS and the results of P300 potentials were not Reevaluation: After treatment, the score of SDS in the treatment group was significantly lower than that in the control group (40.32±7.2, 48.31±8.02,t=3.89, P ＜ 0.01); the latencies of N2 and P3 waves in P300 potentials test in the treatment group were obviously lower than those in the control group [(235.5±22.9), (248.3±23.4) ms; (339.1±25.3), (348.6±25.5) ms, P ＜ 0.05],and the amplitude of P3 wave was obviously higher than that in the controlgroup [(6.3±1.9), (4.9±2.0) μV, P ＜ 0.05]. CONCLUSION: Fluoxetine hydrochloride can improve the depressive status and cognitive function after cerebral stroke.Song JG, Zhang ZH, Wang XH, Mu JL.Effects of fluoxetine hydrochloride on depressive symptoms and P300 after cerebral stroke.
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<p><b>OBJECTIVE</b>To explore the changes of soluble interleukin-2 receptor(sIL-2R) in serum and cerebrospinal fluid (CSF) of patients with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP).</p><p><b>METHODS</b>There were 31 patients with DEACMP, 32 patients with other encephalopathy and 31 controls in this study. The levels of sIL-2R in serum and CSF were detected by ELISA.</p><p><b>RESULTS</b>Serum sIL-2R in patients with DEACMP[(329.21 +/- 160.99)U/ml] was significantly higher than that in control[(115.67 +/- 89.58) U/ml, P < 0.05)], but not significantly different from that in the other encephalopathy group[(367.50 +/- 123.14) U/ml, P > 0.05)]. CSF sIL-2R in patients with DEACMP[(54.48 +/- 43.04) U/ml] measured a little before discharge was significantly lower than that in patients with the other encephalopathy[(110.24 +/- 76.56) U/ml, P < 0.05)], but not significantly different from that in the control group[(34.96 +/- 22.70)U/ml, P > 0.05)]. At the pre-discharged period, CSF sIL-2R in patients with DEACMP[(100.26 +/- 93.65) U/ml] was significantly higher than that at the early stage of hospitalization[(52.28 +/- 43.31) U/ml, P < 0.05)]. No significant difference in serum sIL-2R was found between early stage of hospitalization[(338.34 +/- 161.53) U/ml] and pre-discharge [(351.31 +/- 175.93) U/ml, P > 0.05)].</p><p><b>CONCLUSION</b>The occurrence of DEACMP may be related with immunopathological damage. The sIL-2R levels in serum and CSF may give information about the state of immunological function of the patients with DEACMP and may contribute to determining the patient's condition and prognosis.</p>
Subject(s)
Humans , Brain Diseases , Cerebrospinal Fluid , Allergy and Immunology , Carbon Monoxide Poisoning , Cerebrospinal Fluid , Allergy and Immunology , Enzyme-Linked Immunosorbent Assay , Hospitalization , Receptors, Interleukin-2 , BloodABSTRACT
Objective To explore the change of P300 potentials in first cerebral stroke patients,and to find the objective index in judging the cognition in these patients.Methods P300 potentials test was used for sixty patients with their first episode of single loci stroke and sixty-two healthy people.The results were compared in the two groups.Results Latency periods of N 2 and P 3 of P300 potentials in cerebral stroke group were longer than those in the controls,the amplitude of P 3 of P300 potentials in cerebral stroke group was lower than that in the controls.There was significant difference between the two groups(P0.05).Conclusion P300 potentials can reflect the cognition in cerebral stroke patients,which has remarkable clinical value in making reasonable treatment plan.
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Objective To explore the relevance among the cognition function,the autonomic nerve function,and the serum level of monoamine neurotransmitter in the patients with post-stroke depression(PSD).Methods The event-related potentials(ERP),the sympathetic skin response(SSR),and the serum levels of monoamine neurotransmitter were taken in the 33 cases with PSD(PSD group)and 30 normal collators(NC group),the mean of each target was tested by Pearson multiple correlation analysis.Results Comparing with the NC group,the PSD group demonstrated that the latency phase had been prolonged and the wave amplitude reduced significantly(all P
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Objective To observe the cognitive fuction difference between post-stroke depression(PSD) and non-post-stroke depression(NPSD) patients.To evaluate the clinical value of exploratory eye movement(EEM) and event-related potentials(ERP) on PSD.Methods EEM and ERP test were used for 50 PSD,50 NPSD patients and 48 normal controls.The results were compared.Results The abnormal rate of EEM and ERP test in PSD group were 96%(48/50) and 92%(46/50)respectively,and the abnormal rate of EEM and ERP test in NPSD group were 86%(43/50)and 82%(41/50)respectively.The number of eye fixation(NEF)and the responsive search score(RSS)of PSD and NPSD group were significant lower and the scores of discriminant(D) were significant higher than those in the normal control group(all P