Objective To explore the effect of CD8+T cell subsets on the formation of atheroscle-rosis(AS)in mice.Methods Lasso regression and random forest were employed to identify key infiltrating immune cells in AS blood vessels.Apolipoprotein E gene(ApoE)/recombination acti-vation gene 1(Rag1)double knockout(ApoE/Rag1-DKO)mice were constructed,and then fed with high-fat chow to establish an AS model.The ApoE knockout mice were divided into control group(Con group)and high-fat diet group(HFD group),with 3 mice in each group.And the ApoE/Rag1-DKO mice were divided into DKO+S group[(high-fat diet+phosphate buffer saline(PBS)],DKO+Tem group(high-fat diet with CD8+Tem cell infusion),and DKO+Temra group(high-fat diet with CD8+Temra cell infusion),with 3 mice in each group.Oil red O staining and HE staining were conducted to observe the formation of AS plaques in the vascular walls in the Con,HFD,DKO+S,DKO+Tem,and DKO+Temra groups respectively.Results The results of Lasso regression and random forest showed that CD8+Tem was the most important CD8+T cell subset in the formation of AS.Oil red O staining and HE staining displayed that compared with the Con group,the AS plaque area were significantly larger in the HFD group(P＜0.05);com-pared with the HFD group,there was no significant increase in the AS plaque area in the DKO+S group(P＞0.05);compared with the DKO+S group,the AS plaque area were notably increased in the DKO+Tem group and the DKO+Temra group(P＜0.05).Conclusion CD8+T cell sub-sets are closely associated with the formation of AS in mice,and CD84 Tem and CD84 Temra cells significantly induce the formation.

Objective To investigate the virus-carrying rate of non-polio enteroviruses ( NPEV) in patients with acute flaccid paralysis ( AFP) in Yunnan province of China in 2015 and to analyze the genetic characteristics of enterovirus 71 (EV71) strains. Methods A total of 213 cases under 15 years old with AFP were reported by Center for Disease Control and Prevention ( CDC) of Yunnan Province of China. Virus isolation was conducted for all samples and the serotypes of isolated NPEV strains were identified by VP1 se-quencing. The isolation rates of NPEV in the past consecutive 5 years were analyzed by SPSS22. 0 software. Phylogenetic trees of NPEV and EV71 strains were constructed by MEGA6. 06 software based on neighbor-joining algorithm and Kimura 2-parameter substitution model and the reliability of the phylogenetic trees was determined by bootstrap analysis with 100 pseudo replicate datasets. Results Altogether, 23 NPEV strains were isolated from 213 AFP cases. Among the 23 strains, 7 strains belonged to EV-A group (2 serotypes, 6 strains of which were EV71 ) , 14 strains belonged to EV-B group ( 8 serotypes ) and the other 2 strains belonged to EV-C group. No NPEV strains of EV-D group were identified. Statistical analysis showed that no significant differences in the isolation rates were observed in the past 5 years ( P=0. 101 ) . Conclusion The isolation rate of NPEV in patients with AFP in Yunnan province in 2015 was similar to that of the previ-ous years. The EV71 strains of C4 subgenotype were the predominant strains circulating in Yunnan province.

Objective To investigate the distribution characteristics and risk factors of intracranial atherosclerotic stenosis ischemic stroke. Methods We retrospectively collected 342 consecutive patients with first-ever ischemic stroke. Clinical data was collected including demographics, the presence of risk factors,MRI with MRA and other routine admis?sion laboratory tests. Results Intracranial atherosclerotic stenosis (ICAS) was located most frequently in MCA (47.0%), Extracranial internal carotid artery was the most common affected artery (65.0%) among extracranial atherosclerotic steno? sis (ECAS). MetS (OR=1.586,95%CI:1.232~2.268), ApoB/ApoA1 ratio (OR=1.926,95%CI:1.051~4.288), were as?sociated with ICAS (vs ECAS), whereas hypertension (OR=3.603,95%CI:1.675~12.485), MetS (OR=2.268,95%CI:1.274~6.103), HbA1c (OR=2.015,95%CI:1.182~5.613) and ApoB/ ApoA I ratio (OR=1.948,95%CI:1.157~4.285) were related to ICAS (vs NCAS). Hypertension (OR=2.437,95%CI:1.492~3.505,P=0.005), Hcy (OR=2.437,95%CI:1.492~3.505,P=0.005) and HbA1c (OR=1.769,95%CI:1.034~3.121, P=0.005) were the independent risk factors re?lated to posterior circulation strokes (vs anterior circulation strokes ) in ICAS strokes. Conclusions The occurrence of ICAS may be more frequent than that of ECAS in ischemic stroke. Posterior circulation ICAS strokes seems to be close?ly associated with metabolic derangement.

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 improve differential diagnosis between acute disseminated encephalomyelitis ( ADEM) and classical multiple sclerosis ( CMS).Methods All 20 cases of ADEM and 24 cases of CMS were examined.Their epidemiological and clinical findings,laboratory features and magnetic resonance imaging ( MRI) data were analyzed using x2 test for categorical variables,Wilcoxon Rank-Sum tests for continuous variables.Results ADEM and CMS showed no sex predominance.Patients with ADEM ((27 ±15) years) were younger than CMS ((37 ±13) years,Z= -2.218,P =0.027).The following findings were more commonly seen in ADEM compared with CMS:predemyelinating infectious disease (75% vs 4%,x2 =23.652,P = 0.000),fever (65% vs 4%,x2 =18.609,P = 0.000),meningeal irritation sign (40% vs 0,x2 = 9.189,P =0.002),seizure (25% vs 0,x2 =4.514,P = 0.034),and encephalopathy.ADEM patients were more likely to present with blood leucocytosis ( (11.9 ± 5.8) ×109/L vs (8.0±3.2) ×109/L,Z= -2.030,P=0.042),high C-reactive protein (2.74 mg/L vs 0.49 mg/L,Z = - 3.028,P = 0.002),increased erythrocyte sedimentation rate (11.00 mm/h vs 7.00 mm/h,Z= -2.406,P =0.016),and cerebrospinal fluid leucocytosis (9 × 106/L vs 2×106/L,Z =- 2.781,P = 0.005).There were no differences in cerebrospinal fluid protein and oligoclonal band between the two groups.The following MRI lesions were more commonly seen in ADEM patients:cortical gray matter lesions (14/20,x2=15.213,P=0.000),basal ganglia gray matter lesions (14/20,x2 =8.910,P = 0.003),and brainstem lesions ( 14/20,x2 = 5.867,P = 0.015).In contrast,lesions in subcortical white matter (21/24,x2 = 17.628,P =0.000),periventricular area (21/24,x2 =15.213,P=0.000) and corpus callosum ( 14/24,x2 = 8.640,P = 0.003 ) were more common in the MRI image of CMS patients.The lesions in spinal cord were usually centrally distributed in ADEM (83% ),while peripherally in CMS (85%,x2 = 11.542,P = 0.001).The lesions had poorly defined margins in ADEM (95%),but well defined margins in CMS (75%,x2 =21.787,P = 0.000).Conclusion There are differences in epidemiological and clinical findings,laboratory features and MRI appearances between ADEM and CMS.

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 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.