Blood Biomarkers in Minor Stroke and Transient Ischemic Attack

Li, Jiejie; Wang, Yongjun

doi:10.1007/s12264-016-0038-5

Cited by 15 publications

(11 citation statements)

References 51 publications

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“…Brain-derived proteins may be expressed abnormally during acute stroke [ 41 ]. Since ACI led to pulmonary edema and lung inflammation, we aimed to determine whether certain factors that were abnormally expressed due to the damage to the brain permeated into the blood and caused injury to PMVECs in lung tissue.…”

Section: Resultsmentioning

confidence: 99%

Brain-Derived Glia Maturation Factor β Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells

Zhang

Wang

et al. 2018

Neurosci. Bull.

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Brain damage can cause lung injury. To explore the mechanism underlying the lung injury induced by acute cerebral ischemia (ACI), we established a middle cerebral artery occlusion (MCAO) model in male Sprague-Dawley rats. We focused on glia maturation factor β (GMFB) based on quantitative analysis of the global rat serum proteome. Polymerase chain reaction, western blotting, and immunofluorescence revealed that GMFB was over-expressed in astrocytes in the brains of rats subjected to MCAO. We cultured rat primary astrocytes and confirmed that GMFB was also up-regulated in primary astrocytes after oxygen-glucose deprivation (OGD). We subjected the primary astrocytes to Gmfb RNA interference before OGD and collected the conditioned medium (CM) after OGD. We then used the CM to culture pulmonary microvascular endothelial cells (PMVECs) acquired in advance and assessed their status. The viability of the PMVECs improved significantly when Gmfb was blocked. Moreover, ELISA assays revealed an elevation in GMFB concentration in the medium after OGD. Cell cultures containing recombinant GMFB showed increased levels of reactive oxygen species and a deterioration in the state of the cells. In conclusion, GMFB is up-regulated in astrocytes after ACI, and brain-derived GMFB damages PMVECs by increasing reactive oxygen species. GMFB might thus be an initiator of the lung injury induced by ACI.Electronic supplementary materialThe online version of this article (10.1007/s12264-018-0283-x) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Brain-Derived Glia Maturation Factor β Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells

Zhang

Wang

et al. 2018

Neurosci. Bull.

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“…In light of disability from stroke bringing huge personal and societal burden, early recognition and management of high-risk patients is of great importance. Blood markers are promising to aid in the risk stratification and individual treatment of ischemic stroke ( 21 , 22 ). A line of evidence have shown that elevated blood glucose levels are associated with unfavorable outcome in the patients with ischemic stroke ( 3 , 23 – 26 ).…”

Section: Discussionmentioning

confidence: 99%

Effect of Stress Hyperglycemia on Neurological Deficit and Mortality in the Acute Ischemic Stroke People With and Without Diabetes

Quan

Wang

et al. 2020

Front. Neurol.

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Objective: To determine the relationship between stress hyperglycemia and prognosis of acute ischemic stroke people with and without diabetes. Methods: A subgroup of 8,622 acute ischemic stroke people with baseline levels of fasting blood glucose and HbA1c from the China National Stroke Registry II were analyzed. Stress hyperglycemia was measured by glucose/glycated hemoglobin (HbA1c) ratio, calculated by fasting blood glucose divided by HbA1c. Diabetes was diagnosed according to medical history or a HbA1c level of ≥6.5%. The outcomes included severe neurological deficit defined as modified Rankin Scale score of 3 to 5 and all-cause death at 1 year. The associations between glucose/HbA1c ratio and neurological deficit and all-cause death were analyzed via logistic regression model and Cox proportional-hazards model, respectively. Subgroup analyses of participants with or without diabetes were performed separately. Results: Totally 1,189 (13.7%) participants had severe neurological deficit, and 678 (7.9%) died within 1 year. Compared with the lowest quartile, the highest quartiles of glucose/HbA1c ratio were associated with elevated risk of worse neurological deficit (20.1% vs. 13.0%; adjusted OR, 1.83; 95%CI, 1.31-2.54, p = 0.001), and mortality (12.1% vs. 6.6%; adjusted HR, 2.04; 95% CI, 1.47-2.83, p < 0.0001) after adjusted for potential covariates. The association of glucose/HbA1c ratio with neurological deficit remained in the participants with and without diabetes, while it was only significant in the participants without diabetes as for the outcome of mortality. Conclusions: Stress hyperglycemia, measured by glucose/HbA1c ratio, was associated with increased risk of severe neurological deficit and mortality within 1 year in the acute ischemic stroke people.

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“…Previous studies have demonstrated that CAN is found in patients with newly-diagnosed diabetes, pre-diabetes, and even the first-degree relatives of type 2 diabetic patients with normal glucose tolerance [ 17 , 18 ]. Although CAN progresses with the duration of diabetes [ 19 ], it can be reversed at the very early stage by interventions on risk factors [ 20 ], just like other nervous system diseases [ 21 ]. Hence, it is of great clinical importance to identify CAN and its characteristics in the early stage of the disease.…”

Section: Discussionmentioning

confidence: 99%

Decreased β-Cell Function is Associated with Cardiovascular Autonomic Neuropathy in Chinese Patients Newly Diagnosed with Type 2 Diabetes

Yang

Zhu

et al. 2018

Neurosci. Bull.

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The influence of β-cell function on cardiovascular autonomic neuropathy (CAN), an important diabetes-related complication, is still unclear. In this study, we aimed to investigate the association between residual β-cell function and CAN in patients newly diagnosed with type 2 diabetes. We enrolled 90 newly-diagnosed type 2 diabetic patients and 37 participants with normal glucose tolerance as controls. The patients were divided into a CAN+ group (diabetic patients with CAN, n = 20) and a CAN− group (diabetic patients without CAN, n = 70) according to the standard Ewing battery of tests. Fasting and postprandial plasma glucose, insulin, and C-peptide were measured. Homeostasis model assessment-beta cells (HOMA-B) and HOMA-insulin resistance (IR) were calculated. The prevalence of CAN in this population was 22.2%. Compared with the CAN− group, the CAN+ group had significantly lower fasting plasma insulin (6.60 ± 4.39 vs 10.45 ± 7.82 μ/L, P = 0.029), fasting C-peptide (0.51 ± 0.20 vs 0.82 ± 0.51 nmol/L, P = 0.004), and HOMA-B (21.44 ± 17.06 vs 44.17 ± 38.49, P = 0.002). Fasting C-peptide was correlated with the Valsalva ratio (r = 0.24, P = 0.043) and the 30:15 test (r = 0.26, P = 0.023). Further analysis showed that fasting C-peptide (OR: 0.041, 95% CI 0.003–0.501, P = 0.012) and HOMA-B (OR: 0.965, 95% CI 0.934–0.996, P = 0.028) were independently associated with cardiovascular autonomic nerve function in this population. The patients with fasting C-peptide values < 0.67 nmol/L were more likely to have CAN than those with C-peptide levels ≥0.67 nmol/L (OR: 6.00, 95% CI 1.815–19.830, P = 0.003). A high prevalence of CAN was found in patients with newly-diagnosed type 2 diabetes. Decreased β-cell function was closely associated with CAN in this population.

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Blood Biomarkers in Minor Stroke and Transient Ischemic Attack

Cited by 15 publications

References 51 publications

Brain-Derived Glia Maturation Factor β Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells

Brain-Derived Glia Maturation Factor β Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells

Effect of Stress Hyperglycemia on Neurological Deficit and Mortality in the Acute Ischemic Stroke People With and Without Diabetes

Decreased β-Cell Function is Associated with Cardiovascular Autonomic Neuropathy in Chinese Patients Newly Diagnosed with Type 2 Diabetes

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