Comparison of Thrombelastography (TEG) in Patients with Acute Cerebral Hemorrhage and Cerebral Infarction.

BACKGROUND The aim of this study was to analyze the changing role of thrombelastography (TEG) by detecting the indexes of TEG in patients with acute cerebral hemorrhage and cerebral infarction, combined with pathogenesis, and to find objective laboratory indexes for the diagnosis and treatment of cerebrovascular diseases. MATERIAL AND METHODS Data from 150 patients were collected, including 69 cases identified as the cerebral infarction group and 81 cases identified as the cerebral hemorrhage group. In addition, 50 healthy adults were selected as a control group. The cerebral hemorrhage group was divided into 3 subgroups according to the amount of bleeding: small hemorrhage group, moderate hemorrhage group, and large hemorrhage group. The diagnosis for each participant was mainly based on computed tomography (CT) and magnetic resonance imaging (MRI). TEG indexes [R value (coagulation reaction time), K value (coagulation time), Angle (reflecting the formation rate of blood clot and the function of fibrinogen), MA (maximum thrombus amplitude), CI (coagulation index)] were measured by TEG YZ5000 instrument. RESULTS The cerebral infarction group had lower R and K values and higher Angle and CI (P<0.05). The cerebral hemorrhage group had higher K value; the Angle and MA were lower in the moderate hemorrhage group and in the large hemorrhage groups (P<0.05). In the cerebral hemorrhage group, Angle and MA were negatively correlated with the amount of cerebral hemorrhage (r=-0.475, -0.394 respectively, P<0.05), and the K value was positively correlated with the amount of cerebral hemorrhage (r=0.337, P<0.05), while the R value had no significant correlation with the amount of cerebral hemorrhage (r=0.251, P>0.05). R and K values in the cerebral infarction group were significantly lower, while Angle, MA, and CI were significantly higher in the cerebral hemorrhage group. CONCLUSIONS K value, Angle, and MA may be of value in the assessment of the amount of cerebral hemorrhage.

Postinfectious inflammation in cerebrospinal fluid is associated with nonconvulsive seizures in subarachnoid hemorrhage patients.

PURPOSE: It was unclear how nonconvulsive seizures (NCS) occurred after subarachnoid hemorrhage (SAH). The aim of this prospective observational study was to determine the association between cerebrospinal fluid postinfectious inflammation and NCS in patients with SAH. METHODS: Demographics and parameters were retrieved from pooled data of all SAH patients monitored by continuous electroencephalography (cEEG) in our Stroke-Intensive Care Unit (Stroke-ICU) over six years period. Patients were divided into two groups (NCS group and non-NCS group). According to clinical and cerebrospinal fluid (CSF) parameters, a logistic regression model was used to analyze the association between CSF inflammation and NCS. RESULTS: The data of 143 SAH patients were analyzed (25 patients with NCS and 118 patients with non-NCS). Median age was 53 years (min - max: 19 years - 90 years). 4.8 % SAH patients were accompanied with NCS. Among these 25 NCS patients, only 2 (8%) had complete control of EEG discharges. After confounders correction, logistic regression analysis showed: SAH patients with older age [P = 0.003, OR = 1.193, 95 %CI (1.062-1.341)], intracranial infections [P = 0.000, OR = 171.939, 95 %CI (18.136-1630.064)] and higher increased modified Fisher Scale (mFS) [P = 0.003, OR = 8.884, 95 %CI (2.125-37.148)] were more likely to develop NCS; furthermore, a high level of CSF interleukin-6 (IL-6) was an independent risk factor for NCS [P = 0.000, OR = 1.015, 95 %CI (1.010-1.020)], with a threshold of 164.9 pg/mL (sensitivity = 0.84, specificity = 0.96). Compared with non-NCS patients, NCS patients were more likely to have poor Glasgow outcome scale (GOS) (1-3) at 3 months after discharge (88 %). CONCLUSIONS: SAH patients with NCS were associated with poor neurological prognosis. With the increase of age and mFS, these patients were more likely to develop NCS. As an intracranial infective mark, a high level of CSF IL-6 was an independent risk factor for NCS. For brain protection of severe brain injury after SAH, we should focus on the increasingly important role of inflammatory response.

Over-expression of long noncoding RNA HOTAIRM1 promotes cell proliferation and invasion in human glioblastoma by up-regulating SP1 via sponging miR-137.

Glioblastoma is the most aggressive malignant brain tumor in adults. Long noncoding RNA HOTAIRM1 (HOX antisense intergenic RNA myeloid 1) has been reported to participate in the progression of various cancers. However, the role of HOTAIRM1 in glioblastoma and its underlying mechanisms are largely unknown. The relative expression levels of HOTAIRM1, miR-137 and specificity protein 1 were detected by quantitative real-time PCR or western blot. The effects of HOTAIRM1 on cell proliferation and invasion were evaluated by Cell Counting Kit-8 assay and Transwell assay, respectively. The interactions among HOTAIRM1, miR-137 and specificity protein 1 were predicted by online softwares and confirmed by luciferase reporter assay and RNA immunoprecipitation assay. The levels of HOTAIRM1 and specificity protein 1 were significantly increased while miR-137 was significantly decreased in glioblastoma tissues and cells. Knockdown of HOTAIRM1 suppressed proliferation and invasion in glioblastoma cells. Moreover, miR-137 was bound to HOTAIRM1, and specificity protein 1 was identified as a target of miR-137. The protein level of specificity protein 1 was repressed by silencing the expression of HOTAIRM1, whereas the effect was restored by inhibiting the expression of miR-137. Downregulation of HOTAIRM1 expression suppressed the proliferation and invasion of glioblastoma cells by down-regulating specificity protein 1 expression via sponging miR-137, indicating a promising strategy for glioblastoma treatment.

A Cumulative Score Based on Preoperative Neutrophil-Lymphocyte Ratio and Fibrinogen in Predicting Overall Survival of Patients with Glioblastoma Multiforme.

OBJECTIVE: We conducted a retrospective analysis to explore the prognostic effect of the cumulative score based on neutrophil-lymphocyte ratio (NLR) and fibrinogen in patients with glioblastoma multiforme (GBM). METHODS: The clinical data of patients with GBM from January 2014 to December 2017 in our hospital were retrospectively analyzed. X-tile software was used to identify the optimal cutoff points of NLR and fibrinogen in predicting prognosis of GBM. Fibrinogen-NLR (F-NLR) score was calculated as following: fibrinogen >3.4 g/dL and NLR >4.1 was identified as F-NLR score of 2, only 1 abnormal index was defined as F-NLR score of 1, and no abnormal indices were classified as F-NLR score of 0. RESULTS: A total of 187 patients with primary GBM were enrolled in this study. Of these patients, 116 patients were men and 71 were women, and the mean age was 55 ± 13.55 years. The cutoffs of lymphocyte, NLR, fibrinogen, and platelet-lymphocyte ratio (PLR) identified by X-tile were 1.8 × 109/L, 4.1 × 109/L, 3.4 mg/dL, and 228.6. There were 87 patients with F-NLR score of 0, 50 patients with F-NLR score of 1, and 50 patients with F-NLR score of 2. In the univariate survival analysis, age, lymphocyte count, fibrinogen, NLR, PLR, F-NLR score of 2, chemotherapy, and radiotherapy were significant predictors of overall survival (OS) in patients with GBM (all P < 0.05). After excluding related parameters, F-NLR score of 2 (hazard ratio [HR], 2.103; 95% confidence interval [CI], 1.401-3.155; P < 0.001) and chemotherapy (HR, 0.650; 95% CI, 0.432-0.977; P = 0.038) were predictive factors of OS for patients with GBM. When stratified by extent of resection, age, and adjuvant chemotherapy and radiotherapy, F-NLR score maintained the prognostic value in patients with GBM (all P < 0.05). CONCLUSIONS: F-NLR score of 2 was a risk predictor of prognosis for patients with GBM.