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Objective To investigate the risk factors for acute ischemic stroke in patients with lower extremity atherosclerosis (LEA).Methods The consecutive patients with acute ischemic stroke admitted to hospital within 7 d after onset were enrolled retrospectively.Color Doppler flow imaging was used to detect LEA.The demographic characteristics,vascular risk factors,and laboratory parameters were identified and analyzed.Results A total of 156 patients with acute ischemic stroke were enrolled,including 138 with LEA.Univariate analysis showed that age (69.5± 11.8 years vs.60.4± 11.5 years;t =3.063,P =0.003) and the proportion of patients with hypertension (81.1％ vs,55.6％;x2 =2.467,P =0.014) in the LEA group were significantly higher than those in the non-LEA group.Multivariate logistic regression analysis showed that after adjustment for confounders such as gender,baseline systolic blood pressure,diabetes mellitus,and ischemic heart disease,age (odds ratio [OR] 1.059,95％ confidence interval [CI] 1.016-1.105;P=0.007),and hypertension (OR 3.128,95％ CI 1.084-9.026,P =0.035) were the independent risk factors for acute ischemic stroke complicated with LEA.Conclusions Age and hypertension are associated with acute ischemic stroke complicated with LEA.
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Objective To explore the effects of astrocytes in cervical spinal cord posterior horn on allodynia in rat models of migraine.Methods Fifty-four male SD rats were randomly divided into 9 groups (each group n =6): blank group,sham surgery group,new inflammatory soup 3 d group (IS 3 d group),new inflammatory soup 7 d group(IS 7 d group),saline group,fluorocitrate (FCA)prevention group,FCA prevention control group,FCA treatment group,FCA treatment control group.Following the IS stimulation in the rat dual matter,Von-Frey hair was used to monitor the pain threshold of periorbital skin.Immunofluorescence technique was used to observe the expression of specific marker of astrocyte,glial fibrilary acidic protein (GFAP),and neuron activation marker,C-fos.Results ①Von-Frey hair study showed the thresholds of IS 3 d group and IS 7 d group were significantly decreased compared with the control group(3 d:5.3 ±0.3 vs 6.4 ±0.3,F =40.15;7 d:3.0 ±0.3 vs 6.3 ±0.2,F =382.5,both P ＜0.01).The pain thresholds of FCA prevention group and FCA treatment group both began to significantly increase at the day 4 (FCA prevention:5.5 ± 5.1 vs 5.1 ± 0.2,F =16.00 ;FCA treatment:4.3 ± 0.2 vs 3.0 ± 0.2,F =138.0,both P ＜ 0.01).②GFAP immunofluorescence showed that the mean optical density (A) values of IS 3 d group and IS 7 d group were significantly increased compared with the control group(3 d:24.5 ±4.4 vs 14.8 ± 2.5,F =32.54;7 d:38.9 ± 7.1 vs 14.6 ± 1.8,F =63.56,both P ＜ 0.01).()C-fosimmunofluorescence showed that mean A value of IS 3 d group was significantly increased compared with the control group (20.4 ± 2.3 vs 8.4 ± 1.1,F =129.0,P ＜ 0.01).The difference was not significant between the IS 7 d group and the control group.Conclusions Activated astrocytes contribute to the facial allodynia induced by chronic dural inflammation.Its inhibitor FCA could both prevent and treat the allodynia behaviour.All of these suggest that astrocytes may not only contribute to the initiation of mechanical allodynia but also the maintenance.
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Objective To observe the changes on the neurogenic inflammation-related factors in the dura mater of the rat model of migraine and investigate the possible mechanism of the pain of migraine.Methods SD rats were randomly divided into stimulation group ( n = 32 ) and sham group ( n = 32 ).Unilateral trigeminal ganglion was stimulated to induce migraine for rats in the stimulation group. Rats in the sham group were subjected to sham surgery. The levels of calcitonin gene-related peptide (CGRP) in the blood of jugular vein in the stimulation side were measured by radioimmunoassay. The levels of histamine in peripheral blood and prostaglandin E2 (PGE2 ) in the dura mater were determined by enzyme-linked immunosorbent assay (ELISA). The number of mast cells and percentage of their degranulation in the dura mater were determined under a microscope after toluidine blue staining. Cyclooxygenase 2 (COX-2)expression in the dura mater was evaluated by immunohistochemical staining and western blot analysis. Results In the stimulation group, the level of CGRP in the ipsilateral jugular vein was (82. 84 ± 16. 24)pg/ml and in the sham group was (59. 20 ±11.66) pg/ml (t = -3.34, P ＜ 0. 05 ). The level of histamine in the ipsilateral jugular vein was ( 11.59 ± 1.20) ng/ml and in the sham group was (9. 87 ±0. 88) ng/ml (t = - 3. 27, P ＜ 0. 05). The number of mast cells in the dura mater decreased from 15.46 ± 2. 40 in the stimulation group to 11.63 ± 1.67 in the sham group ( t = 3.71, P ＜ 0. 05 ). Degranulation of mast cells in the dura mater significantly increased from 14. 09% ±4. 53% in the sham group to 29. 10% ±9. 39% in the stimulation group (t = - 4. 07, P ＜ 0. 05 ). The level of PGE2 in the stimulation group was ( 382. 30 ±20. 90) pg/ml and in the sham group was (80. 70 ± 10. 60) pg/ml (t = - 16. 674, P ＜0. 05). The number of COX-2 positive cells significantly increased from 42. 00 ± 18.40 in the sham group to 139.00 ±20. 50 in the stimulation group (t = -7. 994, P ＜0. 05). Also the COX-2 protein level was elevated from 19. 50 ±9. 20 in the sham group to 359. 20 ±21.90 in the stimulation group (t = -5. 190, P ＜0. 05). Conclusions Electrical stimulation on the unilateral trigeminal ganglion induces neurogenic inflammation in the dura mater. Changes on the neurogenic inflammation-related factors are probably the essential pathophysiological mechanism underlying the pain in migraine.