Feature extraction based on microstate sequences for EEG-based emotion recognition.

Recognizing emotion from Electroencephalography (EEG) is a promising and valuable research issue in the field of affective brain-computer interfaces (aBCI). To improve the accuracy of emotion recognition, an emotional feature extraction method is proposed based on the temporal information in the EEG signal. This study adopts microstate analysis as a spatio-temporal analysis for EEG signals. Microstates are defined as a series of momentary quasi-stable scalp electric potential topographies. Brain electrical activity could be modeled as being composed of a time sequence of microstates. Microstate sequences provide an ideal macroscopic window for observing the temporal dynamics of spontaneous brain activity. To further analyze the fine structure of the microstate sequence, we propose a feature extraction method based on k-mer. K-mer is a k-length substring of a given sequence. It has been widely used in computational genomics and sequence analysis. We extract features that are based on the D 2 ∗ statistic of k-mer. In addition, we also extract four parameters (duration, occurrence, time coverage, GEV) of each microstate class as features at the coarse level. We conducted experiments on the DEAP dataset to evaluate the performance of the proposed features. The experimental results demonstrate that the fusion of features in fine and coarse levels can effectively improve classification accuracy.

Preclinical Evidence and Possible Mechanisms of Rhodiola rosea L. and Its Components for Ischemic Stroke: A Systematic Review and Meta-Analysis.

Background: Rhodiola rosea L. has long been used as traditional medicines in Europe and Asia to treat a variety of common conditions and diseases including Alzheimer's disease, cardiovascular disease, cognitive dysfunctions, cancer, and stroke. Previous studies reported that Rhodiola rosea L. and its components (RRC) improve ischemia stroke in animal models. Here, we conducted a systematic review and meta-analysis for preclinical studies to evaluate the effects of RRC and the probable neuroprotective mechanisms in ischemic stroke. Methods: Studies of RRC on ischemic stroke animal models were searched in seven databases from inception to Oct 2021. The primary measured outcomes included the neural functional deficit score (NFS), infarct volume (IV), brain water content, cell viability, apoptotic cells, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells, B-cell lymphoma-2 (Bcl-2) level and tumor necrosis factor-α (TNF-α) level. The secondary outcome measures were possible mechanisms of RRC for ischemic stroke. All the data were analyzed via RevMan version 5.3. Results: 15 studies involving 345 animals were identified. Methodological quality for each included studies was accessed according to the CAMARADES 10-item checklist. The quality score of studies range from 1 to 7, and the median was 5.53. Pooled preclinical data showed that compared with the controls, RRC could improve NFS (Zea Longa (p < 0.01), modified neurological severity score (mNSS) (p < 0.01), rotarod tests (p < 0.01), IV (p < 0.01), as well as brain edema (p < 0.01). It also can increase cell viability (p < 0.01), Bcl-2 level (p < 0.01) and reduce TNF-α level (p < 0.01), TUNEL-positive cells (p < 0.01), apoptotic cells (p < 0.01). Conclusion: The findings suggested that RRC can improve ischemia stroke. The possible mechanisms of RRC are largely through antioxidant, anti-apoptosis activities, anti-inflammatory, repressing lipid peroxidation, antigliosis, and alleviating the pathological blood brain barrier damage.

Anti-Yo antibody-positive paraneoplastic cerebellar degeneration in a patient with possible cholangiocarcinoma: A case report and review of the literature.

BACKGROUND: Paraneoplastic cerebellar degeneration (PCD), which is rare in clinical practice, is closely related to autoimmunity. Cases positive for anti-Yo antibodies (anti-Purkinje cytoplasmic antibody 1) are the main subtype of PCD. PCD is subacute cerebellar degeneration, and while it progresses over weeks to months, its resultant deficits last much longer. Cancer patients with anti-Yo antibody-positive PCD are very rare. Most of them are breast cancer or ovarian cancer patients but also occasionally lung cancer patients. CASE SUMMARY: A 61-year-old woman presented with sudden vertigo, nausea, and vomiting for approximately 10 d. The patient's neurological examination showed torsion with downbeat nystagmus and ataxia of the right limb and trunk. Laboratory examination found that the patient's cerebrospinal fluid and serum were anti-Yo antibody-positive, positron emission tomography computed tomography showed an increased metabolic rate in the retroperitoneal lymph nodes, and the pathology of lymph node punctures in the retroperitoneum and neck suggested adenocarcinoma of the pancreaticobiliary duct, which strengthens the hypothesis of paraneoplastic origin. Intravenous immunoglobulin (IVIg) 0.4 g/kg/d for 5 d and methylprednisolone 160 mg for 3 d were initiated, which was reduced to 80 mg for 3 d and then to 40 mg for 7 d. After treatment with IVIg and a steroid, the patient's vertigo and ataxia alleviated. CONCLUSION: The patient's vertigo and ataxia alleviated after treatment, suggesting that early immunotherapeutic intervention may have certain value in stopping neurological loss.

Regulatory effects of the long non­coding RNA RP11­543N12.1 and microRNA­324­3p axis on the neuronal apoptosis induced by the inflammatory reactions of microglia.

The present study aimed to examine how the long non­coding RNA (lncRNA) RP11­543N12.1 interacted with microRNA (miR)­324­3p to modify microglials (MIs)­induced neuroblastoma cell apoptosis, which may pose benefits to the treatment of Alzhemier's disease (AD). The cell model of AD was established by treating SH­SY5Y cells with amyloid ß (Aß)25­35, and MI were acquired using primary cell culture technology. The lncRNAs that were differentially expressed between SH­SY5Y and control cells were screened through a microarray assay and confirmed via polymerase chain reaction. In addition, overexpression of RP11­543N12.1 and miR­324­3p was established by transfection of SH­SY5Y cells with pcDNA3.1(+)­RP11­543N12.1 and miR­324­3p mimics, respectively, while downregulation of RP11­543N12.1 and miR­324­3p was achieved by transfection with RP11­543N12.1­small interfering RNA (siRNA) and miR­324­3p inhibitor, respectively. The interaction between RP11­543N12.1 and miR­324­3p was confirmed with a dual­luciferase reporter gene assay. The results revealed that the expression levels of total and phosphorylated tau in SH­SY5Y cells were significantly elevated following Aß25­35 treatment (P<0.05), and RP11­543N12.1 was found to be differentially expressed between the control and Aß25­35­treated cells (P<0.05). Furthermore, the targeted association of RP11­543N12.1 and miR­324­3p was predicted based on miRDB4.0 and PITA databases, and then validated via the dual­luciferase reporter gene assay. SH­SY5Y cells transfected with siRNA or inhibitor, and treated with Aß25­35 displayed cellular survival and apoptosis that were similar to the normal levels (P<0.05). Finally, co­culture of MI and SH­SY5Y cells transfected with RP11­543N12.1­siRNA/miR­324­3p inhibitor significantly enhanced cell apoptosis (P<0.05). In conclusion, RP11­543N12.1 targeted miR­324­3p to suppress proliferation and promote apoptosis in the AD cell model, suggesting that RP11­543N12.1 and miR­324­3p may be potential biomarkers and therapeutic targets for AD.

Association between IL-6-174G/C polymorphism and risk of multiple sclerosis: a meta-analysis.

OBJECTIVE: Interleukin-6 (IL-6) is a pleiotropic cytokine and important mediator of many inflammatory processes, which might affect susceptibility to multiple sclerosis (MS). The aim of this study was to assess the effect of IL-6-174G/C polymorphism on the risk of MS using a meta-analysis. MATERIALS AND METHODS: The Pubmed, ISI Web of Science, Wanfang, VIP, and China National Knowledge Infrastructure databases were screened and six studies were included in the meta-analysis. Pooled odds ratios (ORs) with corresponding 95% confidence intervals (CI) were calculated to evaluate the association between the IL-6-174G/C polymorphism and risk of MS. RESULTS: No significant association between the IL-6-174G/C polymorphism and risk of MS was observed in overall analyses. With stratification according to ethnicity, we found that carriers with the IL-6-174CC genotype had a 1.87-fold increased risk for the development of MS in Asians (recessive model: OR=1.87, 95% CI, 1.08-3.24), but not in Caucasians. CONCLUSION: This meta-analysis provides evidence that the IL-6-174G/C polymorphism may be a risk factor for the development of MS in Asians. Further association studies with a larger sample size are required to confirm the result in different populations.

Interleukin-16 polymorphism is associated with an increased risk of ischemic stroke.

Clinical and experimental data have demonstrated that inflammation plays fundamental roles in the pathogenesis of ischemic stroke. Interleukin-16 (IL-16) is identified as a proinflammatory cytokine that is a key element in the ischemic cascade after cerebral ischemia. We aimed to examine the relationship between the IL-16 polymorphisms and the risk of ischemic stroke in a Chinese population. A total of 198 patients with ischemic stroke and 236 controls were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing method. We found that the rs11556218TG genotype and G allele of IL-16 were associated with significantly increased risks of ischemic stroke (TG versus TT, adjusted OR = 1.88; 95% CI, 1.15-3.07; G versus T, adjusted OR = 1.54; 95% CI, 1.05-2.27, resp.). However, there were no significant differences in the genotype and allele frequencies of IL-16 rs4778889 T/C and rs4072111 C/T polymorphisms between the two groups, even after stratification analyses by age, gender, and the presence or absence of hypertension, diabetes mellitus, hypercholesterolemia, and hypertriglyceridemia. These findings indicate that the IL-16 polymorphism may be related to the etiology of ischemic stroke in the Chinese population.