Differential long noncoding RNA expressions in peripheral blood mononuclear cells for detection of acute ischemic stroke.

Long noncoding RNAs (lncRNAs) have been highlighted to be involved in the pathological process of ischemic stroke (IS). The purpose of the present study was to investigate the expression profile of lncRNAs in peripheral blood mononuclear cells (PBMCs) of acute IS patients and to explore their utility as biomarkers of IS. Distinctive expression patterns of PBMC lncRNAs were identified by an lncRNA microarray and individual quantitative real-time PCR (qRT-PCR) in four independent sets for 206 IS, 179 healthy controls (HCs), and 55 patients with transient ischemic attack (TIA). A biomarker panel (lncRNA-based combination index) was established using logistic regression. LncRNA microarray analysis showed 70 up-regulated and 128 down-regulated lncRNAs in IS patients. Individual qRT-PCR validation demonstrated that three lncRNAs (linc-DHFRL1-4, SNHG15, and linc-FAM98A-3) were significantly up-regulated in IS patients compared with HCs and TIA patients. Longitudinal analysis of lncRNA expression up to 90 days after IS showed that linc-FAM98A-3 normalized to control levels by day 7, while SNHG15 remained increased, indicating the ability of lncRNAs to monitor IS dynamics. Receiver-operating characteristic (ROC) curve analysis showed that the lncRNA-based combination index outperformed serum brain-derived neurotrophic factor (BDNF) and neurone-specific enolase (NSE) in distinguishing IS patients from TIA patients and HCs with areas under ROC curve of more than 0.84. Furthermore, the combination index increased significantly after treatment and was correlated with neurological deficit severity of IS. The panel of these altered lncRNAs was associated with acute IS and could serve as a novel diagnostic method.

The Short-term Prognostic Value of the Triglyceride-to-high-density Lipoprotein Cholesterol Ratio in Acute Ischemic Stroke.

The triglyceride (TG)-to-high-density lipoprotein cholesterol (HDL-C) ratio (TG/HDL-C) is a simple approach to predicting unfavorable outcomes in cardiovascular disease. The influence of TG/HDL-C on acute ischemic stroke remains elusive. The purpose of this study was to investigate the precise effect of TG/HDL-C on 3-month mortality after acute ischemic stroke (AIS). Patients with AIS were enrolled in the present study from 2011 to 2017. A total of 1459 participants from a single city in China were divided into retrospective training and prospective test cohorts. Medical records were collected periodically to determine the incidence of fatal events. All participants were followed for 3 months. Optimal cutoff values were determined using X-tile software to separate the training cohort patients into higher and lower survival groups based on their lipid levels. A survival analysis was conducted using Kaplan-Meier curves and a Cox proportional hazards regression model. A total of 1459 patients with AIS (median age 68.5 years, 58.5% male) were analyzed. Univariate Cox regression analysis confirmed that TG/HDL-C was a significant prognostic factor for 3-month survival. X-tile identified 0.9 as an optimal cutoff for TG/HDL-C. In the univariate analysis, the prognosis of the TG/HDL-C >0.9 group was markedly superior to that of TG/HDL-C ≤0.9 group (P<0.001). A multivariate Cox regression analysis showed that TG/HDL-C was independently correlated with a reduced risk of mortality (hazard ratio [HR], 0.39; 95% confidence interval [CI], 0.24-0.62; P<0.001). These results were confirmed in the 453 patients in the test cohort. A nomogram was constructed to predict 3-month case-fatality, and the c-indexes of predictive accuracy were 0.684 and 0.670 in the training and test cohorts, respectively (P<0.01). The serum TG/HDL-C ratio may be useful for predicting short-term mortality after AIS.

ß-arrestin2 functions as a key regulator in the sympathetic-triggered immunodepression after stroke.

BACKGROUND: Stroke-induced immunodeficiency syndrome (SIDS) is regarded as a protective mechanism for secondary inflammatory injury as well as a contributor to infection complications. Although stroke-induced hyperactivation of the sympathetic system is proved to facilitate SIDS, the involved endogenous factors and pathways are largely elusive. In this study, we aim to investigate the function of beta-arrestin-2 (ARRB2) in the sympathetic-mediated SIDS. METHODS: Splenic ARRB2 expression and the sympathetic system activity were detected after establishing transient models of middle cerebral artery occlusion (MCAO). In addition, a correlation between ARRB2 expression and the sympathetic system activity was analyzed using a linear correlation analysis. Any SIDS reflected in monocyte dysfunction was investigated by measuring inflammatory cytokine secretion and neurological deficit scores and infarct volume were tested to assess neurological outcome. Further, ARRB2 expression in the monocytes was knocked down in vitro by siRNAs. Following the stimulation of noradrenaline and lipopolysaccharide, cytokine secretion and the nuclear factor-κB (NF-κB) pathway were evaluated to gain insight into the mechanisms related to the contribution of ARRB2 to adrenergic-induced monocyte dysfunction. RESULTS: Splenic ARRB2 expression was significantly increased after stroke and also showed a significant positive correlation with the sympathetic system activity. Stroke-induced monocyte dysfunction resulted in an increase of the interleukin-10 (IL-10) level as well as a decrease of the interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) levels. Also, blockade of adrenergic-activity significantly reversed these cytokine levels, and blockade of adrenergic-activity improved stroke-induced neurological results. However, the improved neurological results had no significant correlation with ARRB2 expression. Furthermore, the in vitro results showed that the deficiency of ARRB2 dramatically repealed adrenergic-induced monocyte dysfunction and the inhibition of NF-κB signaling phosphorylation activity. CONCLUSIONS: ARRB2 is implicated in the sympathetic-triggered SIDS, in particular, monocyte dysfunction after stroke. Accordingly, ARRB2 may be a promising therapeutic target for the immunological management of stroke in a clinic.

[The Study of Characteristics of Cladding-Reduced Coated Long-Period Fiber Grating Based on Mode Transition and Dual Peak Resonance].

Based on coupled-mode theory, the mode transition of the high-order cladding modes in a coated long-period tiber grating (LPFG) has been studied firstly; the mode transition region and non-mode transition region of high-order cladding modes are divided. The response characteristic of cladding mode effective index with increasing the overlay thickness is analyzed; the shift of resonant wavelength in the mode transition region will be larger than that in the non-mode transition region. Further, the changes of the resonant wavelength of some high-order cladding modes with grating period are investigated when the cladding radius are different, the shift between two resonant wavelengths of dual peak in the mode transition region is bigger than that in non-mode transition region when the cladding radius are uniform. And the shift between two resonant wavelengths of dual peak will be increased by the decrease of the cladding radius in both mode transition and non-mode transition regions. Finally, the response characteristics of film refractive index of coated LPFG are investigated for a high-order cladding mode while the cladding radius are different and the overlay thickness is located in mode transition region and non-transition mode region, then the optimized design scheme is come up with. The higher sensitivity dual-peak sensor of coated LPFG than the traditional dual-peak sensor will be obtained when the overlay thickness and refractive index is located in the mode transition region and the grating period close to the phase matching turning points. Further, the resolution power of coated LPFG sensor will further be improved by the appropriate reducing of the cladding radius.

Treatment of depression using sleep electroencephalogram modulated repetitive transcranial magnetic stimulation.

BACKGROUND: As a treatment of depression, the efficacy of conventional repetitive transcranial magnetic stimulation (rTMS) is limited, and symptoms recurrence is easy to occur after the treatment. This study aimed to examine the efficacy and safety of sleep electroencephalogram modulated repetitive rTMS (SEM-rTMS) in the treatment of depression. METHODS: After 7 days without psychoactive medication, 164 patients with clinically defined depression were randomly divided into 3 groups: SEM-rTMS group (n = 57), conventional rTMS (C-rTMS, n = 55) group and sham-rTMS group (n = 52). Every patient was treated with the corresponding method for 30 minutes everyday for 10 days. Before and after scores on the 24-item Hamilton rating scale for depression (HAMD-24) and the clinical outcome on the 10th day of therapy for all subjects were analyzed. RESULTS: Twenty-two cases in the SEM-rTMS group obtained improved mood as compared to 6 in the C-rTMS group and 2 in the sham-rTMS group (χ(2) = 15.89, P = 0.0004). After completion of the rTMS phase of the protocol, a (51 ± 5)% reduction of HAMD-24 scores from the baseline in the SEM-rTMS group was found compared with a (34 ± 4)% in the C-rTMS group (q = 26.09, P = 0.001) and a (14 ± 3)% in sham-rTMS group (q = 57.53, P = 0.000). The 88% total effective rate in the SEM-rTMS group was significantly higher than 68% in the C-rTMS group and 20% in the sham-rTMS group (χ(2) = 12.01, P = 0.0025). No significant side effects were noted. CONCLUSION: SEM-rTMS is an effective and safe way for treating depression with repetitive transcranial magnetic stimulation (ChiCTR-TRC-00000438).