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Objective:To investigate the relationship between the degree of basilar artery stenosis and the short-term prognosis in patients with isolated pontine infarction.Methods:One hundred and thirty-seven patients with isolated pontine infarction within 1 month after symptom onset admitted to our hospital from April 2016 to April 2018 were consecutively included.Based on modified Rankin scale(mRS)socres, patients were divided into the good outcome group(mRS score≤2)and the poor outcome group(mRS score>2). Venous blood samples were taken for biochemical testing on admission or the next day.Baseline National Institutes of Health Stroke Scale(NIHSS)scores and demographic data were recorded and compared between the two groups.The degree of basilar artery stenosis was assessed by magnetic resonance angiography(MRA), and subjects were divided into the non-stenosis, mild stenosis, middle stenosis and severe stenosis subgroups.Results:There were 108 patients in the good outcome group and 29 in the poor outcome group.The baseline NIHSS score(2.71±0.22 vs.7.10±0.59, t=6.99, P<0.01)and total cholesterol[(4.29±0.101)mmol/L vs.(4.76±0.17)mmol/L, t=2.21, P=0.03]were lower in the good outcome group than in the poor outcome group.The proportion of patients without stenosis was higher(76 or 70.4% vs.5 or 17.2%, χ2=26.70, P<0.01)and the proportion of patients with severe stenosis were lower(4 or 3.7% vs.7 or 24.1%, P=0.002)in the good outcome group than in the poor outcome group.Binary logistics regression analysis showed that baseline NIHSS score( OR=1.658, 95% CI: 1.327-2.071, P=0.000)and degree of basilar artery stenosis( OR=2.071, 95% CI: 1.159-3.701, P=0.014)were risk factors for the short-term prognosis. Conclusions:The degree of basilar artery stenosis is a risk factor for the short-term prognosis in patients with isolated pontine infarction, and patients with severer stenosis will have a poorer prognosis.
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Objective To investigate the correlation between serum uric acid level and short-term outcome of acute isolated pontine infarction. Methods From April 2016 to April 2018, consecutive patients with acute isolated pontine infarction admitted to the Department of Neurology, Kaifeng Central Hospital were enrolled. The baseline clinical data were collected. Fasting venous blood was collected on the day of admission or the morning of the next day for blood biochemical tests. The National Institutes of Health Stroke Scale (NIHSS) was used to assess the severity of neurological deficit. According to the modified Rankin Scale score at discharge or 14 dafter onset, the patients were divided into good outcome group (≤2) and poor outcome group ( > 2 ). Multivariate logistic regression analysis was used to determine the independent risk factors for short-term poor outcome. Results A total of 137 patients were enrolled in the study, 108 (78.8% ) had a good outcome, and 29 (21.2% ) had a poor outcome. The baseline NIHSS score (median [ interquartile range]: 2.5 [1.0-4.0] vs. 8.5 [5.5-10.0 ]; Z= 6.092, P< 0.001 ) and total cholesterol levels (4.290 ± 0.101 mmol/L vs. 4.763 ± 0.171 mmol/L; t=2.214, P=0.028] in the good outcome group were significantly lower than those in the poor outcome group, while serum uric acid level (329.769 ± 8.122μmol/L vs. 257.103 ± 14.290μmol/L; t=4.190, P<0.001) was significantly higher than that in the poor outcome group. Multivariate logistic regression analysis showed that high serum uric acid levels were independently associated with short-term good outcomes in patients with isolated pontine infarction (odds ratio [ OR] 0.377, 95% confidence interval [ CI] 0.203-0.702; P=0.002), while high NIHSS score (OR 1.762, 95% CI 1.375-2.258; P<0.001) and hypertension (OR 5. 353, 95% CI 1.333-21.502; P= 0.018 ) were independently associated with short-term poor outcomes. Conclusion High baseline serum uric acid levels are associated with short-term good outcomes in patients with acute isolated pontine infarction.
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Objective To investigate the role and its mechanism of tumor necrosis factor-α (TNF-α) in post-stroke cognitive impairment (PSCI). Methods Sixty male C57BL/6J mice aged 9-11 weeks were randomly divided into sham operation group, PSCI group, and infliximab group. A PSCI model was induced by middle cerebral artery occlusion. The infliximab group was given infliximab intraperitoneally (10 mg/kg, twice a week), and the PSCI group was injected with an equal volume of normal saline. Water maze and light-dark transition tests were used to evaluate cognitive impairment. Western blot analysis was used to detect hippocampal TNF-α and interleukin-18 ( IL-18 ). The levels of kynurenine and tryptophan in hippocampus were measured by high performance liquid chromatography (HPLC), and the changes of indoleamine 2,3-dioxygenase (IDO) activity (the ratio of kynurenine to tryptophan) were evaluated. Results Morris water maze experiment shows that the escape latency of mice was significantly prolonged in the PSCI group, the target quadrant stay time was significantly shortened, and the number of crossing target quadrants was significantly reduced compared with the sham operation group (all P < 0. 05). The escape latency of the infliximab group was significantly shorter than that of the PSCI group, the target quadrant stay time was significantly prolonged, and the number of crossings increased significantly ( all P < 0. 05 ). Light-dark transition test shows that the latency of the mice was significantly shortened and the number of errors was significantly increased in the PSCI group (all P < 0. 05). The latency of the infliximab group was significantly prolonged compared with the PSCI group, and the number of errors was significantly reduced (all P < 0. 05). Compared with the sham operation group, the levels of TNF-α and IL-18 in the mouse hippocampus of the PSCI group were significantly increased (all P < 0. 05), and the kynurenine/tryptophan ratio was significantly increased (P < 0. 05); the level of TNF-α in hippocampus and the ratio of kynurenine/ tryptophan in the infliximab group were significantly lower than those in the PSCI group (all P < 0. 05). Conclusion TNF-α inhibitor infliximab can alleviate PSCI in mice by reducing IDO activity.
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Objective To investigate the effect of human urinary kallidinogenase (HUK) on cerebral ischemia reperfusion injury in mice.Methods One hundred and ten male ICR mice were randomly divided into sham operation,control and HUK groups.A cerebral ischemia-reperfusion model was induced by transient middle cerebral artery occlusion.The infarct volume was detected by triphenyltetrazolium chloride staining.Bcl-2,Bax,and caspase-3 expression levels in the ischemic cortex were detected by Western blot.Bcl-2 and Bax positive cells in the hippocampal CA1 area on the ischemic side were detected using Immunohistochemical staining.Apoptotic cells in the ischemic cortex were detected by TUNEL staining.Results No infarction and neurological deficits were found in the sham operation group.At 24 h after ischemia-reperfusion,the infarction voltne (P ＜0.01) and neurological deficit score (P =0.02) in the HUK group were significantly lower than those in the control group;at 72 h after ischemia-reperfusion,the infarction volume (P ＜ 0.01) and neurologic deficit score (P =0.03) in the HUK group were also significantly lower than those in the control group.Westem blot analysis showed that the expression level of Bcl-2 in the ischemic cortex in the HUK group was significantly higher than that in the control group (P ＜ 0.001),and the expression levels of caspase-3 (P ＜ 0.001) and Bax (P ＜ 0.001) in the cerebral cortex in the HUK group were significantly lower than those in the control group.No apoptotic cells were found in the sham operation group.The number of apoptotic cells in hippocampal CA1 area (P ＜ 0.01) and the number of Bax positive cells (P ＜0.01) in the HUK group were significantly less than those in the control group,while the number of Bcl-2 positive cells was significantly more in the control group (P ＜ 0.01).Conclusions HUK has a certain protective effect on ischemia-reperfusion injury in mice,its mechanism may be associated with the upregulation of Bcl-2 protein expression and downregulation of caspase-3 and Bax protein expression,thus inhibiting cell apoptosis.