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Objective To investigate the relationship between cholinergic pathway damage and the executive dysfunction of patients with different degrees of cognitive impairment caused by cerebral white matter lesions(WML). Methods From March,2016 to December,2017,115 patients were recruited,whose characteristics,such as age,gender, education,and history of hypertension,diabetes and stroke were recorded.According to the T2-weighted MRI,80 patients were defined as WML.WML patients were divided into cognitively normal(CN)group(n=41),vascular cognitive impairment of none dementia(VCIND)group(n=21)and vascular dementia(VaD)group(n=18)ac-cording to the result of Montreal Cognitive Assessment(MoCA)and Clinical Dementia Rating(CDR).Other 35 cases without WML and cognitive impairment were as control group.WML under MRI were evaluated with Cho-linergic Pathways Hyperintensities Scale(CHIPS).All the WML patients were assessed with Stroop Color-Word Test,Trail Making Test, Symbol Digital Modalities Test, and Verbal Fluence Test.The correlation between the scores of CHIPS and the executive tests were analysed. Results There was no significant difference in age, gender, level of education, and cardiovascular disease risk factors among four groups(P>0.05),but there were significant differences in scores of MoCA and CHIPS(F>25.781,P<0.001),while the score of MoCA was the least(P<0.01)and the scores of CHIPS were the most in VaD group (P<0.001).The CHIPS scores of left and bilateral hemisphere negatively correlated with all the scores of execu-tive tests(P<0.05),while that of the right hemisphere just correlated with the scores of some executive tests(P<0.05). Conclusion For cognitive impairment after WML,cholinergic pathway damage may relate with the executive function impairment,especially the damage in left cerebral hemisphere.
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Objective To observe the inhibitive effect of electro-acupuncture (EA)at Zusanli points (ST36)on inflammatory mediators of postoperative intra-abdominal adhesions and study the relationship between EA and cholinergic anti-inflammatory pathway.Methods Forty-eight male Wistar rats were divided into 6 groups (each =8):Group A (control),Group B(abdominal adhesions model),Group C (abdominal adhesions plus EA),Group D(sham acu-point control),Group E (abdominal adhesions plus α-bungarotoxin )and Group F (abdominal adhesions plus EA after α-bungarotoxin).Animal models of abdominal adhesion were produced by Chiang’s path.Bilateral Zusanli points (ST36) and shame acupoints were electro-acupunctured at a constant voltage for 1 hour while rats were awake.The ɑ-BGT(1 μg/kg)was injected into the abdominal cavity after surgery.All the rats were sacrificed on the 3rd day,and the levels of inflammatory mediators (TNF-ɑ,NO and NOS)in tissues were evaluated.Results Three days after surgery,the damaged cecum of abdominal adhesion groups developed obvious edema that did not adhere with other tissues.Compared with sham control,the abdominal adhesion resulted in significant elevation of inflammatory mediators (TNF-ɑ,NO and NOS).EA at Zusanli points obviously lowered the elevated levels of inflammatory mediators (P <0.01 and P <0.05).EA at Zusanli points following the injection of ɑ-BGT showed less anti-inflammatory effect(P <0.01).Conclusion EA at Zusanli points significantly lowers the elevated levels of inflammatory mediators after abdominal adhesion challenge.The activation of cholinergic anti-inflammatory pathway might be one of the mechanisms by which Zusanli points exert anti-inflammatory effects.
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Objective To observe the effects of electrical stimulation of the vagus nerve on sepsis-associated encephalopathy, and to explore its possible mechanism. Methods Forty adult male Sprague-Dawley ( SD ) rats were randomly divided into sham group, model group, vagotomy group ( VGX group ), vagus nerve stimulation group ( VNS group ), with 10 rats in each group. The rat model of sepsis was reproduced by injecting lipopolysaccharide ( LPS ) through femoral vein, and rats of sham group were given the same volume of normal saline. The left cervical vagotomy was performed 30 minutes before LPS administration in VGX group, electrical stimulation of the left vagus nerve was initiated 30 minutes after LPS administration in VNS group. The rats in sham group were sacrificed after receiving electroencephalogram ( EEG ) examinations, and brain specimens were taken. The changes in EEG in the other three groups were monitored at 2, 4 and 6 hours after LPS administration, and the δ wave activity percentage was calculated. The blood was collected from abdominal aorta 6 hours after LPS administration, the rats were sacrificed and brain tissue was harvested. The concentrations of tumor necrosis factor-α ( TNF-α) in plasma and brain were measured with enzyme-linked immunosorbent assay ( ELISA ). The histology and ultrastructure changes in the prefrontal cortex in the rats were observed with both light microscope and transmission electron microscope. Results Compared with sham group, the percentage of δ wave on EEG was significantly increased at 2, 4 and 6 hours after LPS administration in model group [ ( 14.52±0.50 )%, ( 16.70±0.85 )%, ( 17.35±0.36 )%vs. ( 12.60±0.46 )%, all P<0.01 ]. It could be deduced that early brain dysfunction occurred in septic rats. Compared with model group, percentage of δ wave on EEG was significantly reduced at 2, 4, and 6 hours in VNS group [ ( 13.10±0.24 )%vs. ( 14.52±0.50 )%, ( 12.81±0.53 )%vs. ( 16.70±0.85 )%, ( 12.61±0.37 )%vs. ( 17.35±0.36 )%, all P < 0.01 ], while there was no such effect in the VGX group. Compared with sham group, the concentrations of TNF-α in plasma and brain were all increased in model group [ plasma TNF-α( ng/L ): 120.11±5.10 vs. 24.37±1.85, brain TNF-α( ng/L ):165.20±6.31 vs. 14.89±0.83, both P<0.01 ]. Compared with model group, the concentrations of TNF-αin plasma and brain were all significantly decreased in VNS group [ plasma TNF-α( ng/L ):46.72±4.90 vs. 120.11±5.10, brain TNF-α( ng/L ):107.95±1.83 vs. 165.20±6.31, both P<0.01 ], while there was no such effect in the VGX group. Light microscope and transmission electron microscope showed that the damage of brain tissue and neurons in model group and VGX group was more obvious, while that in the VNS group was less severe, though not completely disappeared. Conclusions LPS can lead to sepsis-associated encephalopathy in rats. It was shown that electrical stimulation of the vagus nerve can activate anti-inflammatory effect through cholinergic pathway, and improve the cerebral function, and inhibit the development of sepsis-associated encephalopathy by reducing systemic and cerebral inflammatory reaction.
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@#Objective To investigate the relationship between MRI rating of white matter hyperintensities (WMH) within cholinergic pathway and vascular dementia in Binswanger's disease.Methods 41 patients with Binswanger's disease undergone inspection of MRI. On 4 selected axial images, the severity of WMH in the cholinergic pathways was rated on a 3-point scale for ten regions identified with major anatomical landmarks. The cholinergic pathways hyperintensities scale (CHIPS) were developed by Bocti based immunohistochemical tracings of the cholinergic pathways. Subjects underwent neuropsychological testing with the Mattis Dementia Rating Scale (DRS) to assess cognitive domains of interest (attention, episodic memory, executive functions). Spearman correlation coefficients were used to compute association between CHIPS score and DRS score.Results The total score of DRS, the scores of DRS attention subscale and memory subscale were 105.6±18.2, 29.5±4.2 and 11.3±3.2 respectively. The score of CHIPS was 35.6±13.7. After accounting for age and education in a multiple linear regression model, the CHIP ratings were associated with impaired performance on the DRS ( r=-0.43, P<0.05).Conclusion The MRI rating of WMH within cholinergic pathway has strong correlations with cognitive performance in patients with Binswanger's disease.
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This paper, using acetylcholinesterase (AChE) histochemistry, brain-lesion and di-isopropylfluorophosphate (DFP) pretreatment techniques, studies AChE distribution in the tectum-nucleus isthmi systems in frogs and pigeons. In these two species of animals, the tectal laminae densely stained for AChE are roughly coincided with the retinotectal projections. Staining pattern in the frog nucleus isthmi consists of 3 areas with different staining intensities. The dorsolateral area being most densely stained. In pigeons, the nucleus isthmi pars parvocellularis (Ipc) and pars magnocellularis (Imc) are densely and evenly stained. Following local lesion of tectum, stainings in the frog nucleus isthmi and pigeon Ipc are topographically reduced or disappeared. DFP-treatment shows that tectal cells, with the exception of cells in layer III containing rich AChE, have moderate or low concentrations of AChE. The isthmic cells are rich in AChE. In the tectum-lesioned pigeons, AChE-stained isthmic cells in the topographical area are reduced in number and paler in color. These results suggest that in amphibians and birds both the tectoisthmic projection and the isthmotectal projection could be cholinergic pathways in nature.