The Clinical Implications of Thrombelastography in the Diagnosis of Acute Cerebral Infarction

Liang, Ying; Wu, Jun; Liu, Jianquan; Liu, Hong; Chen, Juan

doi:10.7754/clin.lab.2017.170803

Cited by 8 publications

(9 citation statements)

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“…Mild cases of cerebral infarction can be completely asymptomatic, but they can also manifest as recurrent limb paralysis or dizziness, which is known as a transient ischemic attack. Individuals with severe cases of cerebral infarction may not only experience limb paralysis, but acute coma and death may also occur in some cases ( 28 , 29 ).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA SNHG1 relieves microglia activation by downregulating miR‑329‑3p expression in an in vitro model of cerebral infarction

Xuan

Min-hai

et al. 2021

Exp Ther Med

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Following cerebral infarction, activated microglia cells can release a large amount of inflammatory cytokines, thereby exacerbating neuronal damage. It has been demonstrated that the long non-coding RNA small nucleolar RNA host gene 1 (SNHG1) exerts a protective effect against cerebral infarction. However, its specific role in cerebral infarction and underlying mechanism have yet to be fully elucidated. The present study aimed to investigate the effects of the SNHG1 and microRNA (miR)-329-3p in cerebral infarction and to determine the underlying molecular mechanisms. An in vitro oxygen-glucose deprivation (OGD) model was established using the BV-2 microglial cell line. The mRNA expression levels of SNHG1 and miR-329-3p were analyzed using reverse transcription-quantitative PCR and the protein expression levels of cleaved caspase-3 and caspase-3 were detected using western blotting. The binding relationship between SNHG1 and miR-329-3p was predicted using starBase and verified using a dual luciferase reporter assay. The release of TNF-α and nitric oxide, as well as caspase-3 activity, were detected using appropriate commercial kits. Flow cytometry analysis was performed to measure cell apoptosis. The results of the present study revealed that the expression levels of SNHG1 were upregulated in the OGD-induced BV-2 cell model. miR-329-3p was discovered to directly target SNHG1, and its mRNA expression levels were downregulated in the OGD-induced BV-2 cell model. The SNHG1-plasmid downregulated miR-329-3p expression levels, while this effect was reversed by transfection with the miR-329-3p mimic. The overexpression of SNHG1 or knockdown of miR-329-3p inhibited OGD-induced BV-2 cell activation. In conclusion, the results of the present study suggested that SNHG1 may reduce microglial cell activity by regulating the expression of miR-329-3p, indicating its potential protective role in cerebral infarction.

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Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA SNHG1 relieves microglia activation by downregulating miR‑329‑3p expression in an in vitro model of cerebral infarction

Xuan

Min-hai

et al. 2021

Exp Ther Med

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“… 38 , 39 In human patients with liver disease, stroke, neoplasia, or in those undergoing surgery, TEG parameters can predict the occurrence of thrombosis. 40 , 41 , 42 , 43 , 44 , 45 In dogs, indirect evidence for an association of high TEG G values with thrombosis comes from the observation that conditions associated with thrombosis, such as immune‐mediated hemolytic anemia, protein‐losing enteropathy, protein‐losing nephropathy, hyperadrenocorticism, and pancreatitis, have TEG parameters compatible with hypercoagulabilty. 36 , 46 Studies that link potential coagulation biomarkers of hypercoagulability in dogs with GBM with actual indices of clinical thrombosis are needed, but will be hampered by the difficulty of making an antemortem diagnosis of thrombosis.…”

Section: Discussionmentioning

confidence: 99%

“…Although some studies have suggested a correlation, 36,37 others have failed to show TEG abnormalities in dogs with confirmed thrombosis 38,39 . In human patients with liver disease, stroke, neoplasia, or in those undergoing surgery, TEG parameters can predict the occurrence of thrombosis 40‐45 . In dogs, indirect evidence for an association of high TEG G values with thrombosis comes from the observation that conditions associated with thrombosis, such as immune‐mediated hemolytic anemia, protein‐losing enteropathy, protein‐losing nephropathy, hyperadrenocorticism, and pancreatitis, have TEG parameters compatible with hypercoagulabilty 36,46 .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of coagulation parameters in dogs with gallbladder mucoceles

Pavlick

deLaforcade

Penninck

et al. 2021

Veterinary Internal Medicne

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Background: Gallbladder mucocele (GBM) is a common biliary disorder in dogs.Limited information is available on the coagulation status of dogs with GBM.Hypothesis/Objectives: To determine patterns of coagulation alterations in dogs with GBM and correlate them with clinicopathologic abnormalities and ultrasonographic findings of disease severity.Animals: Twenty-three dogs with GBM identified on ultrasound examination were prospectively enrolled.Methods: At the time of GBM identification, blood and urine were collected for CBC, serum biochemical panel, urinalysis, prothrombin time, activated partial thromboplastin time (aPTT), factor VIII, protein C (PC), von Willebrand's factor (vWF), antithrombin activity, fibrinogen, D-dimers, and thromboelastrography (TEG). Gallbladder mucoceles were classified into ultrasound types 1 to 5. Medical records were reviewed for clinical presentation, underlying conditions and to determine if systemic inflammatory response syndrome (SIRS) was present.Results: Based on TEG parameters, maximal amplitude, and G, 19/23 (83%) of dogs with GBM had evaluations consistent with hypercoagulability. On plasma-based coagulation testing, dogs with GBM had increased total PC activity (20/23, 87%), fibrinogen (9/23, 39%), platelet count (9/23, 39%), and D-dimers (6/15, 40%) as well as prolongations in aPTT (9/22, 41%) and low vWF activity (5/21, 24%). No correlation was found between TEG G value and any coagulation or clinical pathology variables, ultrasound stage of GBM or disease severity as assessed by the presence of SIRS.Conclusions and Clinical Importance: Dogs with ultrasonographically identified GBM have changes in whole blood kaolin-activated TEG supporting a hypercoagulable state although traditional plasma-based coagulation testing suggests that a complex state of hemostasis exists.

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“…Research shows that the death/disability rate of ACI within 1 year is high, which is seriously harmful to people's health 2 . The diagnosis and treatment mainly focus on early detection, treatment and prevention 3,4 . There have been studies on the diagnostic value of C‐reactive protein and interleukin‐6 in ACI, but their specificity is not high 3–5 .…”

Section: Introductionmentioning

confidence: 99%

“…The diagnosis and treatment mainly focus on early detection, treatment and prevention 3,4 . There have been studies on the diagnostic value of C‐reactive protein and interleukin‐6 in ACI, but their specificity is not high 3–5 . At present, the diagnosis of ACI depends on the Stroke Scale score, computed tomography (CT), magnetic resonance imaging (MRI) and other imaging methods 6 .…”

Section: Introductionmentioning

confidence: 99%

Plasma miR‐409‐3p promotes acute cerebral infarction via suppressing CTRP3

Song

Zhu

2020

The Kaohsiung J of Med Scie

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Abnormal expression of miR-409-3p has been found in several neurodevelopmental disorders, but whether it is dysregulated in the patients with acute cerebral infarction (ACI) has not been evaluated. The current study mainly focused on the clinical significance and the underlying mechanism of plasma miR-409-3p in the progression of ACI. The level of plasma miR-409-3p was determined in ACI patients (n = 80) and healthy controls (n = 30). Pearson correlation assay was performed to evaluate the association and cardiovascular risk factors. A receiver operating characteristic curve (ROC) was used to evaluate the diagnostic value of plasma miR-409-3p levels in patients with ACI. Dual luciferase reporter assay and western blot were performed to determine the possible target gene of miR-409-3p. Our data showed that the expression of plasma miR-409-3p in the ACI group was higher than that in the healthy controls. Furthermore, Pearson correlation analysis indicated a positive correlation between plasma miR-409-3p and the NIHSS score. ROC analysis indicated that plasma miR-409-3p could differentiate plasma miR-409-3p in ACI patients from healthy controls. Then, we explored the possible target genes of miR-409-3p. Interestingly, C1q and TNF-related 3 (CTRP3), a novel adipose tissue-derived secreted factor, was found to be a target gene of miR-409-3p. We found that knockdown of CTRP3 significantly induced PC12 cell apoptosis, even in PC12 cells transfected with miR-409-3p inhibitor. These data suggested that miR-409-3p induced PC12 cell apoptosis by targeting CTRP3. Altogether, elevated plasma miR-409-3p is correlated with disease severity and may be efficient for the early diagnosis of ACI.

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The Clinical Implications of Thrombelastography in the Diagnosis of Acute Cerebral Infarction

Abstract: TEG results have important clinical implications in the early diagnosis of acute cerebral infarction.

Cited by 8 publications

References 0 publications

Long non‑coding RNA SNHG1 relieves microglia activation by downregulating miR‑329‑3p expression in an in vitro model of cerebral infarction

Long non‑coding RNA SNHG1 relieves microglia activation by downregulating miR‑329‑3p expression in an in vitro model of cerebral infarction

Evaluation of coagulation parameters in dogs with gallbladder mucoceles

Plasma miR‐409‐3p promotes acute cerebral infarction via suppressing CTRP3

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