Objective To investigate the change of the concentration of IL-2?IL-6?IL-10 in peripheral blood and cerebral spinal fluid (CSF) in monkey's experimental allergic encephalomyelitis (EAE),as to explaining it's function in mechanism and prognosis of the disease. Methods First set up animal models of monkey's EAE. Then separate the animals by their onset symptoms according to the level and the different stages of disease. At the same time survey the blood and CSF concentrations of IL-2?IL-6?IL-10, finally process the findings statistically. Results IL-2 in the first or the third week in the acute stage of EAE (5.0?0.8 and 5.3?1.2,respectively) was obviously higher than that (0.7?0.3) before the onset,P=0.045,0.041 respectively,both IL-6 and IL-10 in recuperation or chronic stage were higher significantly than before the onset,P=0.004 3,0.006 5 respectively. The findings were significant statistically. Conclusion IL-2 up-regulates immunologically,which accelerates the disease. IL-6 and IL-10 down-regulate immunologically,which reduce the disease. The findings may play an important role in studying immunological mechanism of EAE or MS in the future.

Objective:To study demyelinating mechanism of the central nervous system in acute experimental allergic encephalomyelitis(EAE).Methods:EAE in cynomolgus monkeys was induced successfully by homologous brain white matter homogenate. Lymphocyte subset in blood and cerebrospinal fluid was monitored by flow cytometer. Pathological changes in brains of acute EAE monkeys were investigated by immunohistochemistry and electron microscopy. Results:In the CSF of acute EAE, CD4 + lymphocytes increased significantly, and CD8 + lymphocytes and B lymphocytes increased slightly whereas the control was normal. A lot of CD4 + lymphocytes and a few CD8 + lymphocytes infiltrated into temporal deep white matter of acute EAE, whereas the control was normal. Inner laminae of myelin sheath were loose and axon was separated, whereas outer laminae were normal. Although axon was preserved well, oligodendrocyte had a severe edema in cytoplasm with mitochondria swollen, crista blurred or broken, and nucleus lysised partly.Conclusion:It is oligodendrocyte rather than myelin sheath itself which is firstly attacked in the demyelination in EAE.

Objective To investigate the clinical manifestations and possible mechanism of the multiple sclerosis (MS) combined with uveitis Methods Two cases of MS combined with uveitis were clinically observed by electro physiological, brain MRI and oligoclonic band (OB) examinations,the cases were analyzed and subjected to assessment Results Case1, a 56-year-old man had symptoms of one month′s numbness and twenty-day sudden decrease of visual acuity Viusal evoked potential (VEP)showed a postponed latent period of bilateral P100 waves Brain MRI showed multifocal T 2 Wight Image high signs in subcortical white matter of frontal and parietal lobes OB was postive Case 2: a 35-year-old woman, had recurrence of decrease of visual acuity of bilateral both eyes for 12 months and bilateral lower-limbs numbness Latent period of VEP P100 waves and BAEP I-V waves were postponed Brain MRI showed multifocal round-like T 2 Wight Image high signs in white matter of frontal and parietal lobes OB was postive Referring to the essay reported ,MS combined with uveitis was moetly moderate in manifestations Their causes were uncertain It is suggested that MS is not due to auto-antigen but due to S100-? protein derived from star-like cells Conclusion MS combined with uveitis ,unlike other one ,was clinically moderate and the pathological mechanism is unclear It is suggested that autoantigen such as S100-? protein derived from star-like cell results in MS and uveitis, not in MBP

Objective To investigate the correlation between diabetes and brainstem infarction. Methods The diagnozed patients with acute cerebral infarction were recruited in the study. Firstly, they were divided into brainstem infarction group and non-brainstem infarction group, and then they were redivided into brainstem infarction with diabetes, brainstem infarction without diabetes, non-brainstem infarction with diabetes and non-brainstem infarction without diabetes groups according to whether they had diabetes or not. Carotid artery intima-media thickness (IMT) and carotid atherosclerosis were detected and identified with Doppler ultrasound; brain stem infarction and its location were identified with diffusion-weighted imaging; basilar artery atherosclerosis was detected with magnetic resonance angiography (MRA). A multivariate logistic regression analysis was used to screen the different risk factors impacting brainstem infarction. Neurological deficit was evaluated with the modified Rankin Scale (mRS)scores. Results A total of 286 patients with acute cerebral infarction were recruited: brain stem infarction in 63, and 34 of them with diabetes; non-brain stem infarction in 223, and 77 of them with diabetes. The proportions of diabetes (54. 0％ vs. 34. 5%, x2 = 7. 816, P = 0. 005),previous cerebral infarction (38. 1％ vs. 24. 2％ ,x2 =4. 771, P =0. 029), basilar artery atherosclerosis (73.0％ vs. 57. 4％,x2 =5. 028, P =0. 025), as wall as the levels of hemoglobin A1C (HbA1c) (7. 30 ± 2. 42％ vs. 6. 46 ± 1.82％, t = - 2. 531, P = 0. 011 ) and apolipoprotein B (ApoB) (0. 97 ± 0. 33 mmol/L vs. 0. 90 ± 0. 34 mmol/L, t =-2. 180, P = 0. 029) in the brainstem infarction group were significantly higher than those in the non-brainstem infarction group. Multivariate logistic regression analysis showed that diabetes (odds ratio [ OR] 2. 150, 95％confidence interval [ CI] 1. 214-3. 808; P =0. 009) and previous cerebral infarction (OR 1. 835, 95％ CI 1.004-3. 352, P = 0. 048) were the independent risk factors for brainstem infarction. There were significant differences in the levels of HbA1c (P ＜ 0. 001 ), fasting blood glucose (FBG) (P ＜0. 001), ApoB (P =0. 007) and high-density lipoprotein cholesterol (P =0. 018) as well as the proportion of basilar artery atherosclerosis (P = 0. 001 ) among the brainstem infarction with diabetes, without diabetes, non-brainstem infarction with diabetes and without diabetes groups. The levels of HbA1c (8. 81 ±2. 36％), FBG (8. 23 ±3. 12 mmol/L andApoB (1.04 ± 0. 41 mmol/L) as well as the proportion of basilar artery atherosclerosis (85. 3％ )were the highest in the brainstem infarction with diabetes group. Conclusions Diabetes is closely associated with brainstem infarction. Diabetes is more likely to result in pontine infarction.

Objective To analyze the relationship between diabetics and the onset, clinical outcomes and prognosis of brainstem infarction, and to evaluate the impact of diabetes on brainstem infarction. Method Compare 172 cases of acute brainstem infarction in patients with or without diabetes.Analyze the associated risk factors of patients with brain-stem infarction in diabetics by multi-variate logistic regression analysis. Compare the National Institutes of Health Stroke Scale (NIHSS) and Modified Rankin scale (mRS) Score, pathogenetic condition and the outcome of the two groups in different times. Results The systolic blood pressure ( SBP ), TG, LDL-C, apolipoprotein B ( Apo B ), glutamyl transpeptidase (γ-GT), fibrinogen(Fb), fasting blood glucose (FPG) and glycosylated hemoglobin( HbA1c)in diabetic group were higher than those in non-diabetic group , which was statistically significant ( P ＜ 0. 05 ). From multi-variate logistic regression analysis, γ-GT, Apo B and FPG were the risk predictors of diabetes with brainstem infarction( OR = 1. 017, 4. 667 and 3. 173, respectively), while HDL-C was protective( OR =0. 288). HbA1c was a risk predictor of severity for acute brainstem infarction( OR = 1. 299), while Apo A was beneficial( OR =0. 212). Compared with brain-stem infarction in non-diabetic group, NIHSS score and intensive care therapy of diabetic groups on the admission had no statistically significance, while the NIHSS score on discharge and the outcome at 6 months' of follow-up were statistically significant. Conclusions Diabetes is closely associated with brainstem infarction. Brainstem infarction with diabetes cause more rapid progression, poorer prognosis, higher rates of mortality as well as disability and higher recurrence rate of cerebral infarction.

Objective To investigate the changes in brain MRI scan in neuromyelitis optica (NMO).Methods MRI images in 27 cases with NMO were examined in a retrospective study.Results Twenty-two of 27 patients (81.5%) had abnormal brain MRI findings,which were classified as nonspecific (7 cases),atypical (1 case),multiple sclerosis-like (3 cases) and ventricle-aqueduct-syringocoele lesions (11 cases).The lust type is the most common (40.7%).Furthermore,the analysis showed that the number of brain lesions positively correlated with lag time from the onset to the last MRI scan (r=0.475,P=0.025).Conclusions Brain lesions in NMO are diverse,which might result from different pathogenesis.However,ventricle-aqueduct-syringocoele is the most common lesion.Early brain MRI examination of suspected cases is essential.

Objective To investigate brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) concentrations in serum and cerebrospinal fluid (CSF) in patients with multiple sclerosis (MS) and neuromyelitis optica (NMO),and their neuroprotective effects.Methods Sixty-two patients (49 patients were MS and 13 patients were NMO) and 21 controls were investigated in our studies.The disability severity in MS and NMO patients in their relapse period was assessed by the Expanded Disability Status Scale (EDSS).MRI scanning of brain,spinal cord or optic nerve was examined and the oligoclonal band in serum and CSF were detected.BDNF and GDNF concentrations in serum and CSF were assessed by Liquid Assay.Results There were no significant differences of BDNF (μg/L,5.616±0.650 in serum and 0.186±0.012 in CSF of MS patients;6.584±0.929 in serum and 0.176± 0.006 in CSF of NMO patients) and GDNF (μg/L,0.039 in serum and 0.080 in CSF of MS patients;0.029 in serum and 0.050 in CSF of NMO patients) concentrations in serum and CSF in patients with MS and NMO in relapse,compared with those in controls.There was a positive correlation between BDNF and GDNF concentrations in CSF (r=0.756,P=0.000),and a negative correlation between BDNF and GDNF concentrations in serum (r=-0.329,P=0.018).There were no correlations of BDNF and GDNF concentrations in serum and CSF with EDSS,blood brain barrier index,Delpech index and Tourtellotte synthesis rate.There were no significant differences of BDNF and GDNF concentration in serum and CSF between NMO/MS patients with and without atrophy.Conclusions The level of BDNF in patients with MS and NMO is correlated with that of GDNF,which may have a synergistic neurotrophic effect on MS and NMO.BDNF and GDNF are not associated with the blood-brain harrier destruction and lgG synthesis in central nervous system.However,associations of BDNF and GDNF with functional disability and neuron atrophy in NMO and MS patients still need further studies.

[Objective]To compare the differences of neuromyelitis optica spectrum disorder(NMOSD)and multiple sclerosis (MS) on pregnancy ,and analyze the mutual impact of pregnancy on the diseases.[Methods]Prospectively collected clinical information of 235 NMOSD patients and 125 MS patients ,including the annualized relapse rate (ARR),the Expanded Disability Status Scale(EDSS)and pregnancy outcomes. 70 NMOSD patients and 30 MS patients were screened out as information patients. The ARR and EDSS score in two groups were compared during the year before pregnancy,during pregnancy and after 1 year postpartum, respectively. 50 cases of normal pregnant women for the same period as the control group ,then to compared the difference of three groups on pregnancy outcomes.[Results]Attacks occurring during pregnancy or one year after childbirth/abortion in NMOSD and MS were 53.25%(41/77)and 20.00%(7/35)(P=0.001);The ARR during the first 3 months postpartum periods of NMOSD and MS group(2.65,2.51)was significantly higher than during the year before pregnancy(0.27,0.49,P < 0.001)and during pregnancy (0.32,0.2,P<0.001);The EDSS score of two groups increased after 1 year postpartum(3.06 ± 2.16,2.19 ± 1.28)than that during the year before pregnancy(1.58 ± 0.48,1.92 ± 1.29,P < 0.001)and during pregnancy(1.92 ± 1.35,1.67 ± 0.70,P < 0.001). There was no difference on ARR and EDSS score between NMOSD and MS group. NMOSD ,MS and normal control group had no dif?ference on pregnancy outcomes and neonatal weight.[Conclusions]Compared with MS,the attack of NMOSD had more closer relation?ship with pregnancy;both NMOSD and MS would increase the risk of disease relapsing and disability after pregnancy;the diseases had no effect on pregnancy outcomes.

Objective To investigate the effect of splenectomy on infarct volume in middle cerebral artery occlusion in focal cerebral ischemia rats and its possible mechanisms.Methods Eighteen male Sprague-Dawley rats were randomly divided into spleneetomy,sham splenectomy,and control groups (n =6 in each group).A model of middle cerebral artery occlusion (MCAO) was induced by the intraluminal suture method 2 weeks after spleneetomy.The rats were decapitated and their brains were removed after 24 hours.The infarct volume was measured with Nissl body staining The number of macrophages in ischemic cortex was detected with immunofluorescence staining Results The infarct volume in the splenectomy group (34.93％ + 3.23％ )was significantly smaller than that in the sham splenectomy group (74.33％ + 2.36％ ; q =39.399,P ＜ 0.001 ) and the control group (77.30％ + 2.62％ ; q =42.369,P ＜ 0.001 ).However,there was no significant difference between the sham splenectomy group and the control group (q =2.970,P =0.082).The number of macrophages of the ischemic cortex in the splenectomy group (3.4 ± 1.07/per high power field) was significantly less than that in the sham splenectomy group (20.7±4.37/per high power field; q =17.300,P＜0.001) and the control group (18.87 ±4.17/per high power field; q =15.467,P ＜0.001).However,there was no significant difference between the sham splenectomy group and the control goup (q =1.833,P =0.384).Conclusions Splenectomy may reduce the infarct volume by reducing the number of macrophages in ischemic corticalregion.

Objective To explore the role of the polymorphism of HLA-DRB1/DPB1 in patients with multiple scle-rosis (MS) and optica neuromyelitis (NMO). Methods Fifty-three patients with MS, 30 patients with NMO and 93 normal controls were enrolled in the present study. The HLA-DRB1/DPB1 gene polymorphism and allele frequencies were deter-mined by sequencing-based typing. All the subjects were Southern Han Chinese and were born in Southern China. Re-sults The frequencies of DPB1*0501 were higher in NMO patients than in controls, P=0.001, P (corrected)=0.022. The frequencies of DRB1*1602 DPB1*0501 haplotype were higher in NMO patients than in MS patients, P<0.001,P (cor-rected)=0.040. Conclusions There is significant difference in HLA-DRB1/DPB1 gene polymorphism between MS and NMO patients in a Southern Han Chinese population. The HLA-DPB1*0501 allele might be the susceptibility gene poly-morphism of NMO.