MDs-NP: a property prediction model construction procedure for naphtha based on molecular dynamics simulation.

In the context of carbon neutrality and carbon peaking, molecular management has become a focus of the petrochemical industry. The key to achieving molecular management is molecular reconstruction, which relies on rapid and accurate calculation of oil properties. Focusing on naphtha, we proposed a novel property prediction model construction procedure (MDs-NP) employing molecular dynamics simulations for property collections and gamma distribution from real analytical data for calculating mole fractions of simulation mixtures. We calculated 348 sets of mixture properties data in the range of 273K to 300K by molecular dynamics simulations. Molecular feature extraction was based on molecular descriptors. In addition to descriptors based on open-source toolkits (RDKit and Mordred), we designed 12 naphtha knowledge (NK) descriptors with a focus on naphtha. Three machine learning algorithms (support vector regression, extreme gradient boosting and artificial neural network) were applied and compared to establish models for the prediction of the density and viscosity of naphtha. Mordred and NK descriptors + support vector regression algorithm achieved the best performance for density. The selected RDKFp and NK descriptors + artificial neural network algorithm achieved the best performance for viscosity. Using ablation studies, T, P_w and CC(C)C are three effective descriptors in NK that can improve the performance of the property prediction models. MDs-NP has the potential to be extended to more properties as well as more-complex petroleum systems. The models from MDs-NP can be used for rapid molecular reconstruction to facilitate construction of data-driven models and intelligent transformation of petrochemical processes.

Predicting circRNA-RBP Binding Sites Using a Hybrid Deep Neural Network.

Circular RNAs (circRNAs) are non-coding RNAs generated by reverse splicing. They are involved in biological process and human diseases by interacting with specific RNA-binding proteins (RBPs). Due to traditional biological experiments being costly, computational methods have been proposed to predict the circRNA-RBP interaction. However, these methods have problems of single feature extraction. Therefore, we propose a novel model called circ-FHN, which utilizes only circRNA sequences to predict circRNA-RBP interactions. The circ-FHN approach involves feature coding and a hybrid deep learning model. Feature coding takes into account the physicochemical properties of circRNA sequences and employs four coding methods to extract sequence features. The hybrid deep structure comprises a convolutional neural network (CNN) and a bidirectional gated recurrent unit (BiGRU). The CNN learns high-level abstract features, while the BiGRU captures long-term dependencies in the sequence. To assess the effectiveness of circ-FHN, we compared it to other computational methods on 16 datasets and conducted ablation experiments. Additionally, we conducted motif analysis. The results demonstrate that circ-FHN exhibits exceptional performance and surpasses other methods. circ-FHN is freely available at https://github.com/zhaoqi106/circ-FHN .

TIMELESS promotes reprogramming of glucose metabolism in oral squamous cell carcinoma.

BACKGROUND: Oral squamous cell carcinoma (OSCC), the predominant malignancy of the oral cavity, is characterized by high incidence and low survival rates. Emerging evidence suggests a link between circadian rhythm disruptions and cancer development. The circadian gene TIMELESS, known for its specific expression in various tumors, has not been extensively studied in the context of OSCC. This study aims to explore the influence of TIMELESS on OSCC, focusing on cell growth and metabolic alterations. METHODS: We analyzed TIMELESS expression in OSCC using western blot, immunohistochemistry, qRT-PCR, and data from The Cancer Genome Atlas (TCGA) and the Cancer Cell Line Encyclopedia (CCLE). The role of TIMELESS in OSCC was examined through clone formation, MTS, cell cycle, and EdU assays, alongside subcutaneous tumor growth experiments in nude mice. We also assessed the metabolic impact of TIMELESS by measuring glucose uptake, lactate production, oxygen consumption, and medium pH, and investigated its effect on key metabolic proteins including silent information regulator 1 (SIRT1), hexokinase 2 (HK2), pyruvate kinase isozyme type M2 (PKM2), recombinant lactate dehydrogenase A (LDHA) and glucose transporter-1 (GLUT1). RESULTS: Elevated TIMELESS expression in OSCC tissues and cell lines was observed, correlating with reduced patient survival. TIMELESS overexpression enhanced OSCC cell proliferation, increased glycolytic activity (glucose uptake and lactate production), and suppressed oxidative phosphorylation (evidenced by reduced oxygen consumption and altered pH levels). Conversely, TIMELESS knockdown inhibited these cellular and metabolic processes, an effect mirrored by manipulating SIRT1 levels. Additionally, SIRT1 was positively associated with TIMELESS expression. The expression of SIRT1, HK2, PKM2, LDHA and GLUT1 increased with the overexpression of TIMELESS levels and decreased with the knockdown of TIMELESS. CONCLUSION: TIMELESS exacerbates OSCC progression by modulating cellular proliferation and metabolic pathways, specifically by enhancing glycolysis and reducing oxidative phosphorylation, largely mediated through the SIRT1 pathway. This highlights TIMELESS as a potential target for OSCC therapeutic strategies.

Sequential activation strategy of triazinyl resorufin for high selectivity fluorescence GSH detection.

The abnormally elevated expression level of glutathione (GSH) has been observed in various human cancer cells and tissue. Thus, effective methods for glutathione detection are of great importance in early diagnosis of cancer. However, many fluorescent probes for GSH detection suffer from the interference of the abundantly existent nucleophilic biomolecules in biological environment. In this work, we propose a sequential activation strategy to overcome this problem by designing and synthesizing a series of 1,3,5-triazinyl resorufin turn-on fluorescent probe (Probes 1-3). As two electrophilic sites are presented in probes, GSH sequentially reacts with the resorufin and the triazine moiety, resulting in significant fluorescence augmentation (up to 165.0-fold). Designed probes possess low limit of detection as low as 1.8 µM). Cellular fluorescent imaging has been successfully applied to selectively detect GSH in several living cells.

Regional cerebral metabolism alterations and functional connectivity in individuals with opioid use disorder: An integrated resting-state PET/fMRI study.

Individuals with opioid use disorder (OUD) have been reported to show abnormal brain metabolism and impaired coupling among brain networks such as the default mode network (DMN), salience network (SN), and executive control network (ECN). However, the characteristics of brain glucose metabolism and its related functions in the brain networks in individuals with OUD remain unknown. Thirty-six individuals with OUD and thirty matched healthy controls (HCs) were recruited in this integrated positron emission tomography/magnetic resonance imaging (PET/MRI) study. Differences in glucose metabolism were analyzed by using 18F-fluorodeoxyglucose (18F-FDG), and the corresponding coupling characteristics of the individuals with OUD were also analyzed. The individuals with OUD showed widespread bilateral hypometabolism in the middle temporal gyrus (MTG), superior temporal gyrus, angular gyrus, supramarginal gyrus, inferior parietal lobe, Rolandic operculum, and left insula, but obvious hypermetabolism in the brainstem and left cerebellum. Meanwhile, in individuals with OUD, the hypometabolism of right MTG which is included in the DMN was accompanied by decreased coupling with the left superior frontal gyrus and right superior parietal gyrus which are included in the ECN. Furthermore, individuals with OUD showed a positive correlation between the duration of heroin use and glucose metabolism of the left MTG. The individuals with OUD were characterized by widespread bilateral hypometabolism in the temporal and parietal regions but obvious hypermetabolism in the brainstem and left cerebellum. The results suggest that the hypometabolism in the temporal and parietal regions might be related to DMN dysfunction and the hypermetabolism in the brainstem and left cerebellum may be compensate for other brain regions showing hypometabolism. In particular, hypometabolism in the self-referential-related DMN regions in OUD might attenuate their relationships with the inhibitory-control-related ECN regions. These findings highlight the importance of evaluating the metabolic and functional profiles of the right MTG in future studies on the treatment of OUD.

Effects of non-invasive brain stimulation over supplementary motor area in people with Parkinson's disease: a protocol for a systematic review and meta-analysis of randomised controlled trials.

INTRODUCTION: Individuals with Parkinson's disease (PD) often experience initial hesitation, slowness of movements, decreased balance and impaired standing ability, which can significantly impact their independence. Transcranial magnetic stimulation and transcranial direct current stimulation are two widely used and promising non-invasive brain stimulation (NIBS) modalities for treating PD. The supplementary motor area (SMA), associated with motor behaviour and processing, has received increasing attention as a potential stimulation target to alleviate PD-related symptoms. However, the data on NIBS over SMA in PD individuals are inconsistent and has not been synthesised. In this article, we will review the evidence for NIBS over SMA in PD individuals and evaluate its efficacy in improving PD function. METHOD AND ANALYSIS: Randomised controlled clinical trials comparing the effects of NIBS and sham stimulation on motor function, activities of daily living and participation for people with PD will be included. A detailed computer-aided search of the literature will be performed from inception to February 2023 in the following databases: PubMed, EMBASE, Physiotherapy Evidence Database (PEDro), Web of Science (WOS) and The Chinese National Knowledge Infrastructure (CNKI). Two independent reviewers will screen articles for relevance and methodological validity. The PEDro scale will be used to evaluate the risk of bias of selected studies. Data from included studies will be extracted by two independent reviewers through a customised, preset data extraction sheet. ETHICS AND DISSEMINATION: Ethical approval is not required for this systematic review. The study's findings will be presented at scientific meetings and published in peer-reviewed journals. PROSPERO REGISTRATION NUMBER: CRD42023399945.

Research hotspots and trends of transcranial magnetic stimulation in Parkinson's disease: a bibliometric analysis.

Background: Transcranial magnetic stimulation (TMS), as a non-invasive neuromodulation technique, has been widely used in the treatment of Parkinson's disease (PD). The increasing application of TMS has promoted an increasing number of clinical studies. In this paper, a bibliometric analysis of existing studies was conducted to reveal current research hotspots and guide future research directions. Method: Relevant articles and reviews were obtained from the Science Citation Index Expanded of Web of Science Core Collection database. Data related to publications, countries, institutions, authors, journals, citations, and keywords in the studies included in the review were systematically analyzed using VOSviewer 1.6.18 and Citespace 6.2.4 software. Result: A total of 1,894 papers on the topic of TMS in PD between 1991 and 2022 were analyzed and visualized to identify research hotspots and trends in the field. The number of annual publications in this field of study has increased gradually over the past 30 years, with the number of annual publications peaking in 2022 (n = 150). In terms of publications and total citations, countries, institutions, and authors from North America and Western Europe were found to make significant contributions to the field. The current hotspot focuses on the effectiveness of TMS for PD in different stimulation modes or different stimulated brain regions. The keyword analysis indicates that the latest research is oriented to the mechanism study of TMS for motor symptoms in PD, and the non-motor symptoms are also receiving more attention. Conclusion: Our study offers insights into the current hotspots and emerging trends of TMS in the rehabilitation of PD. These findings may serve as a guide for future research and the application of TMS for PD.

TET2 is recruited by CREB to promote Cebpb, Cebpa, and Pparg transcription by facilitating hydroxymethylation during adipocyte differentiation.

Ten-eleven translocation proteins (TETs) are dioxygenases that convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), an important epigenetic mark that regulates gene expression during development and differentiation. Here, we found that the TET2 expression was positively associated with adipogenesis. Further, in vitro and in vivo experiments showed that TET2 deficiency blocked adipogenesis by inhibiting the expression of the key transcription factors CCAAT/enhancer-binding protein beta (C/EBPß), C/EBPα and peroxisome proliferator-activated receptor gamma (PPARγ). In addition, TET2 promoted 5hmC on the CpG islands (CGIs) of Cebpb, Cebpa and Pparg at the initial time point of their transcription, which requires the cAMP-responsive element-binding protein (CREB). At last, specific knockout of Tet2 in preadipocytes enabled mice to resist obesity and attenuated the obesity-associated insulin resistance. Together, TET2 is recruited by CREB to promote the expression of Cebpb, Cebpa and Pparg via 5hmC during adipogenesis and may be a potential therapeutic target for obesity and insulin resistance.

Abnormal cerebral metabolism and metabolic connectivity in individuals with heroin dependence: an integrated resting-state PET/fMRI study in large-scale networks.

BACKGROUND: Increasing evidence suggests that heroin addiction may be related to the dysfunction among the triple brain network (default mode network [DMN], salience network [SN] and executive control network [ECN]). However, the characteristics of glucose metabolism and metabolic connectivity among core regions of the triple brain network remain unknown. Therefore, we hypothesized that individuals with heroin dependence would show abnormal glucose metabolism and accompanied abnormal metabolic connectivity within the triple brain network. METHODS: Individuals with heroin dependence and healthy controls matched for age and sex underwent integrated positron emission tomography/magnetic resonance imaging (PET/MRI). Differences in glucose metabolism and metabolic connectivity among the DMN, SN and ECN were analyzed based on 18F-fluorodeoxyglucose PET and resting-state fMRI data. RESULTS: We included 36 individuals with heroin dependence and 30 matched healthy controls in our study. The heroin dependence group showed a significant reduction of glucose metabolism in the bilateral anterior insula (AI) and inferior parietal lobule (IPL), and a significantly decreased metabolic connectivity between the right AI and the left dorsolateral prefrontal cortex (DLPFC). The daily dose of methadone was negatively correlated with glucose metabolism of the right AI and right IPL. LIMITATIONS: The results revealed the glucose metabolism alterations and metabolic connectivity only within the triple brain network in individuals with heroin dependence; additional brain networks should be investigated in future studies. Although methadone is an opioid with a similar neurophysiological mechanism as heroin, the specific chronic effects of methadone on cerebral metabolism and metabolic connectivity should also be investigated in future studies. CONCLUSION: Our findings suggest that long-term opioid use might, to some extent, be associated with reduced synergistic ability between the SN and ECN, which may be associated with the dysfunction of cognitive control. In particular, the right AI, which showed hypometabolism and related reduction in SN-ECN metabolic connectivity, should receive increasing attention in future studies.

Suppression of preadipocyte determination by SOX4 limits white adipocyte hyperplasia in obesity.

Preadipocyte determination expanding the pool of preadipocytes is a vital process in adipocyte hyperplasia, but the molecular mechanisms underlying this process are yet to be elucidated. Herein, SRY-related HMG box transcription factor 4 (SOX4) was identified as a critical target in response to BMP4- and TGFß-regulated preadipocyte determination. SOX4 deficiency is sufficient to promote preadipocyte determination in mesenchymal stem cells (MSCs) and acquisition of preadipocyte properties in nonadipogenic lineages, while its overexpression impairs the adipogenic capacity of preadipocytes and converts them into nonadipogenic lineages. Mechanism studies indicated that SOX4 activates and cooperates with LEF1 to retain the nuclear localization of ß-catenin, thus mediating the crosstalk between TGFß/BMP4 signaling pathway and Wnt signaling pathway to regulate the preadipocyte determination. In vivo studies demonstrated that SOX4 promotes the adipogenic-nonadipogenic conversion and suppresses the adipocyte hyperplasia. Together, our findings highlight the importance of SOX4 in regulating the adipocyte hyperplasia in obesity.

Amyloid-Gold Nanoparticle Hybrids for Biocompatible Memristive Devices.

Biomolecular materials offer tremendous potential for the development of memristive devices due to their low cost of production, environmental friendliness, and, most notably, biocompatibility. Herein, biocompatible memristive devices based on amyloid-gold nanoparticle hybrids have been investigated. These memristors demonstrate excellent electrical performance, featuring an ultrahigh Roff/Ron ratio (>107), a low switching voltage (<0.8 V), and reliable reproducibility. Additionally, the reversible transition from threshold switching to resistive switching mode was achieved in this work. The arrangement of peptides in amyloid fibrils endows the surface polarity and phenylalanine packing, which provides channels for the migration of Ag ions in the memristors. By modulating voltage pulse signals, the study successfully imitates the synaptic behavior of excitatory postsynaptic current (EPSC), paired-pulse facilitation (PPF), and the transition from short-term plasticity (STP) to long-term plasticity (LTP). More interestingly, Boolean logic standard cells were designed and simulated using the memristive devices. The fundamental and experimental results of this study thus offer insights into the utilization of biomolecular materials for advanced memristive devices.

Brain dynamics in triple-network interactions and its relation to multiple cognitive impairments in mild traumatic brain injury.

Traumatic brain injury (TBI) disrupt the coordinated activity of triple-network and produce impairments across several cognitive domains. The triple-network model posits a key role of the salience network (SN) that regulates interactions with the central executive network (CEN) and default mode network (DMN). However, the aberrant dynamic interactions among triple-network and associations with neurobehavioral symptoms in mild TBI was still unclear. In present study, we used brain network interaction index (NII) and dynamic functional connectivity to examine the time-varying cross-network interactions among the triple-network in 109 acute patients, 41 chronic patients, and 65 healthy controls. Dynamic cross-network interactions were significantly increased and more variable in mild TBI compared to controls. Crucially, mild TBI exhibited an increased NII as enhanced integrations between the SN and CEN while reduced coupling of the SN with DMN. The increased NII also implied much severer and multiple domains of cognitive impairments at both acute and chronic mild TBI. Abnormities in time-varying engagement of triple-network is a clinically relevant neurobiological signature of psychopathology in mild TBI. The findings provided align with and advance an emerging perspective on the importance of aberrant brain dynamics associated with highly disparate cognitive and behavioral outcomes in trauma.

Default mode network mechanisms of repeated transcranial magnetic stimulation in heroin addiction.

Repetitive transcranial magnetic stimulation (rTMS) over the left dorsolateral prefrontal cortex (DLPFC) has been shown to reduce cravings in heroin-dependent (HD) individuals, but the mechanisms underlying the anti-craving effects of rTMS are unknown. Abnormalities in the default mode network (DMN) are known to be consistent findings in HD individuals and are involved in cravings. We assessed the effect of rTMS on DMN activity and its relationship to the treatment response. Thirty HD individuals were included in this self-controlled study, and all HD participants received 10-Hz rTMS 7-session during a week. Data for cravings and withdrawal symptoms and resting-state functional magnetic resonance imaging data were collected before and after rTMS treatment. Thirty demographically matched healthy individuals who did not receive rTMS were included as controls. We focused on changes in coupling seeded from the medial prefrontal cortex (MPFC), posterior cingulate cortex (PCC), and bilateral inferior parietal lobe (IPL), which are the core regions of the DMN. The craving and withdrawal symptom score of HD individuals decreased significantly after rTMS treatment. The left IPL-left middle frontal gyrus coupling and the left IPL-right inferior occipital gyrus coupling decreased significantly, and the changes in the left IPL-left middle frontal gyrus coupling were positively correlated with changes in drug-cue induced cravings. rTMS could modulate the coupling between the DMN and executive control network (ECN). Alterations of the left IPL-left middle frontal gyrus coupling may play an important mechanistic role in reducing drug cue-induced cravings.

Exercise therapy for adolescent idiopathic scoliosis rehabilitation: a bibliometric analysis (1999-2023).

Background: Among the conservative treatments for rehabilitation of adolescent idiopathic scoliosis (AIS), exercise therapy has attracted a large number of studies as its advantages of good clinical effect, high operability, high compliance, few side effects and low cost. We conduct a bibliometric analysis of previous research to identify prevalent areas of study and inform research for the future directions in this paper. Methods: Relevant publications and reviews were collected using the Science Citation Index Expanded from the Web of Science Core Collection. Information from the included studies was analyzed systematically using VOSviewer and Citespace software to identify patterns regarding publications, keywords, authors, citations, countries, institutions and journals. Results: A total of 172 articles published from 1999 to 2023 were identified. Over the last decade, the number of publications has gradually increased, reaching a peak of 21 publications in 2021. China, North America and Western European countries and institutions are leading the way as far as the quantity of publications and the total number of citations are concerned. The current areas of focus are the efficacy of exercise therapy in relation to enhancing the quality of life of adolescents during rehabilitation. Conclusions: This is the first bibliometric analysis that provides a comprehensive review of the research trends and advances in exercise therapy for the rehabilitation of AIS. The study identifies latest research frontiers and hot directions, providing a valuable reference for scholars in the field of exercise therapy.

SOX4 promotes beige adipocyte-mediated adaptive thermogenesis by facilitating PRDM16-PPARγ complex.

Brown and beige fat protect against cold environments and obesity by catabolizing stored energy to generate heat. This process is achieved by controlling thermogenesis-related gene expression and the development of brown/beige fat through the induction of transcription factors, most notably PPARγ. However, the cofactors that induce the expression of thermogenic genes with PPARγ are still not well understood. In this study, we explored the role of SOX4 in adaptive thermogenesis and its relationship with PPARγ. Methods: Whole transcriptome deep sequencing (RNA-seq) analysis of inguinal subcutaneous white adipose tissue (iWAT) after cold stimulation was performed to identify genes with differential expression in mice. Indirect calorimetry detected oxygen consumption rate and heat generation. mRNA levels were analyzed by qPCR assays. Proteins were detected by immunoblotting and immunofluorescence. Interaction of proteins was detected by endogenous and exogenous Co-IP. ChIP-qPCR, FAIRE assay and luciferase reporter assays were used to investigate transcriptional regulation. Results: SOX4 was identified as the main transcriptional effector of thermogenesis. Mice with either adipocyte-specific or UCP1+ cells deletion of SOX4 exhibited significant cold intolerance, decreased energy expenditure, and beige adipocyte formation, which was attributed to decreased thermogenic gene expression. In addition, these mice developed obesity on a high-fat diet, with severe hepatic steatosis, insulin resistance, and inflammation. At the cell level, loss of SOX4 from preadipocytes inhibited the development of beige adipocytes, and loss of SOX4 from mature beige adipocytes reduced the expression of thermogenesis-related genes and energy metabolism. Mechanistically, SOX4 stimulated the transcriptional activity of Ucp1 by binding to PPARγ and activating its transcriptional function. These actions of SOX4 were, at least partly, mediated by recruiting PRDM16 to PPARγ, thus forming a transcriptional complex to elevate the expression of thermogenic genes. Conclusion: SOX4, as a coactivator of PPARγ, drives the thermogenic gene expression program and thermogenesis of beige fat, promoting energy expenditure. It has important physiological significance in resisting cold and obesity.

Repetitive transcranial magnetic stimulation modulates coupling among large-scale brain networks in heroin-dependent individuals: A randomized resting-state functional magnetic resonance imaging study.

The abnormal interactions of three key large-scale brain networks (default mode [DMN], salience and executive control [ECN]) were showed underlie dysfunctions in heroin addiction. Repetitive transcranial magnetic stimulation (rTMS) targeting the left dorsolateral prefrontal cortex (DLPFC) is a potential treatment for heroin addiction. It is unclear whether impaired coupling among the large-scale brain networks would be improved by rTMS in treated heroin-dependent individuals. Thirty-five heroin-dependent individuals were included in this sham-controlled, randomized study. The patients received either active or sham rTMS for 1 week. The craving for heroin and resting-state functional magnetic resonance imaging data were collected before and after 1-week rTMS. Twenty-two healthy subjects were included as controls not receiving rTMS. After 1-week rTMS, only the active rTMS group showed a significant decrease in spontaneous and heroin cue-induced craving. The coupling between left DLPFC (a key node of left ECN) and left parahippocampal gyrus (PHG, included in DMN) significantly increased for the active group with a tendency towards that of controls. The coupling between the right precentral gyrus and three key regions included in DMN (posterior cingulate cortex/precuneus and bilateral inferior parietal cortex) significantly decreased for the active group with a tendency towards that of healthy controls. For the active rTMS individuals, the left DLPFC-PHG coupling negatively correlated with the spontaneous craving and the drug cue-induced craving. It suggested that the rTMS could reduce heroin craving, which might be related to the modulation of ECN-DMN coupling. This finding might shed light on the mechanism of rTMS for heroin addiction treatment.

Identifying the characteristics of brain glucose metabolism using normal 18F-FDG PET database in patients with temporal lobe epilepsy.

OBJECTIVES: This study aimed to measure the global brain glucose metabolism of patients with temporal lobe epilepsy (TLE) using MIMneuro software based on the normal brain glucose metabolism database. METHODS: In this cross-sectional study, 23 patients (11 males and 12 females, mean age 25.6 ± 10.1 years) with TLE who underwent 18F-labeled fluoro-2-deoxyglucose positron emission tomography (18F-FDG PET) were enrolled. 18F-FDG PET images were then imported into MIMneuro software, which can automatically analyze the differences in regional brain glucose metabolism between patients and a normal database, and the results of different brain regions were presented by values of Z-score. RESULTS: In patients with TLE, 18F-FDG PET imaging showed that in addition to the presence of temporal lobe hypometabolism, there was hypometabolism in the ipsilateral hippocampus, parahippocampal gyrus, insula, amygdala, temporal operculum, and bilateral cerebellar hemisphere, while hypermetabolism was found in the contralateral temporal lobe, frontal lobe, parietal lobe, parietal lobule, angular gyrus, and precentral gyrus. There was no significant difference in brain areas between the left and the right temporal lobe seizures (P > 0.05). CONCLUSIONS: We found that TLE has a specific characteristic in terms of brain glucose metabolism, and the underlying mechanism needs to be further studied that may be helpful to localize seizure focus.

Balloon-expandable stent angioplasty in the treatment of vertebral artery stenosis in the V2 segment.

INTRODUCTION: Vertebral artery stenosis is a major cause of posterior circulation ischemia in the elderly. There is not a clear consensus on the optimal therapeutic approach for symptomatic extracranial vertebral artery stenosis. AIM: To evaluate the feasibility and efficacy of balloon-expandable stent angioplasty in the treatment of vertebral artery stenosis in the V2 segment. MATERIAL AND METHODS: Five patients with vertebral artery stenosis (V2 segment) and treatment of percutaneous transluminal stenting from July 2009 to June 2014 were retrospectively evaluated. All patients underwent color Doppler, transcranial color Doppler (TCD), CT angiography (CTA) and cerebral digital subtraction angiography (DSA) preoperatively. Whether there was osseous oppression was determined according to neck computed tomography (CT) and CTA. After the surgery, angiography was performed to determine if there was infarction or bleeding in the intracranial vertebral artery, basilar artery and posterior cerebral artery. The surgical parameters, residual stenosis, complications, etc. were recorded and evaluated. The patients were followed up accordingly. RESULTS: Five patients (3 males, 2 females; average age of 66 ±4.2, range of 54-75) were enrolled in the study. Balloon-expandable stents were successfully implanted in the 5 patients. The mean residual stenosis after the balloon-expandable stenting (preoperative: average, 87.0 ±6.6%, range: 75-93%) was 12.6 ±7.8% (range: 5-25%). The clinical symptoms disappeared or receded. No serious complications occurred. CONCLUSIONS: The balloon-expandable stent angioplasty seemed to be feasible and efficacious in treating vertebral artery stenosis in the V2 segment. Further study with a large sample size is needed.

Treatment of internal carotid artery dissection with Willis covered stent: A case report of recurrent limb weakness and no response to medical therapy.

Internal carotid artery dissection (ICAD) is a major cause of ischemic stroke in young and middle-aged patients. Patients may be asymptomatic or present with symptoms ranging from headache and neck pain to severe cerebral ischemic events. Conventional treatment is medical anticlotting therapy or involves the use of interventional tools, such as endovascular treatment. Anticoagulation or antiplatelet therapy are the primary treatment modalities used to prevent thromboembolic complications from arterial dissections, however, they are unsuitable in certain cases of dissecting aneurysms. In the current study reports the case of a 52-year-old male patient presenting with the primary complaint of left limb weakness. Computed tomography angiography revealed a right ICAD located in the oropharyngeal segment. Subsequently, digital subtraction angiography was performed to assess the oropharyngeal segment. Antithrombotic therapy resulted in no improvement; therefore, endovascular treatment with the insertion of a Willis covered stent was performed, resulting in an improved outcome.

Four FCRL3 Gene Polymorphisms (FCRL3_3, _5, _6, _8) Confer Susceptibility to Multiple Sclerosis: Results from a Case-Control Study.

Multiple sclerosis (MS) is an autoimmune/inflammatory neurodegenerative disease which mainly affects the central nervous system in young adults. Fc-receptor-like-3 (FCRL3) gene, which involved in immune cell regulation, has drawn lots of attentions. This study aims to investigate the association between common polymorphisms of FCRL3 gene and MS risk in a Chinese Han population. Nine single nucleotide polymorphisms (SNPs) were genotyped in 120 patients and 240 healthy controls through PCR assay. t test and chi-square test was conducted to find a possible association between FCRL3 genetic mutations and risk of MS. This analysis results performed that four SNPs, rs7528684 (FCRL3_3), rs945635 (FCRL3_5), rs3761959 (FCRL3_6), and rs2282284 (FCRL3_8), were significantly associated with the risk of MS. Further haplotype analysis showed two haplotypes of FCRL3_3, 5, 6, 8, CCAG and CGAG, presented the significant associations with the susceptibility to MS. Four SNPs in FCRL3 gene could possibly associate with the susceptibility of MS in a Chinese Han population. Moreover, the haplotype analysis confirmed that the linkage disequilibrium exists in polymorphisms in FCRL3. Based on the supporting evidence, we deduced that FCRL3_3C, FCRL3_5C, FCRL3_6A, and FCRL3_8G caused increased risk of MS. Nevertheless, large cohort studies are required in the future to validate the autoimmune function.