Classification and transfer learning of sleep spindles based on convolutional neural networks.

Background: Sleep plays a critical role in human physiological and psychological health, and electroencephalography (EEG), an effective sleep-monitoring method, is of great importance in revealing sleep characteristics and aiding the diagnosis of sleep disorders. Sleep spindles, which are a typical phenomenon in EEG, hold importance in sleep science. Methods: This paper proposes a novel convolutional neural network (CNN) model to classify sleep spindles. Transfer learning is employed to apply the model trained on the sleep spindles of healthy subjects to those of subjects with insomnia for classification. To analyze the effect of transfer learning, we discuss the classification results of both partially and fully transferred convolutional layers. Results: The classification accuracy for the healthy and insomnia subjects' spindles were 93.68% and 92.77%, respectively. During transfer learning, when transferring all convolutional layers, the classification accuracy for the insomnia subjects' spindles was 91.41% and transferring only the first four convolutional layers achieved a classification result of 92.80%. The experimental results demonstrate that the proposed CNN model can effectively classify sleep spindles. Furthermore, the features learned from the data of the normal subjects can be effectively applied to the data for subjects with insomnia, yielding desirable outcomes. Discussion: These outcomes underscore the efficacy of both the collected dataset and the proposed CNN model. The proposed model exhibits potential as a rapid and effective means to diagnose and treat sleep disorders, thereby improving the speed and quality of patient care.

Bidirectional two-sample Mendelian randomization analyses support causal relationships between structural and diffusion imaging-derived phenotypes and the risk of major neurodegenerative diseases.

Previous observational investigations suggest that structural and diffusion imaging-derived phenotypes (IDPs) are associated with major neurodegenerative diseases; however, whether these associations are causal remains largely uncertain. Herein we conducted bidirectional two-sample Mendelian randomization analyses to infer the causal relationships between structural and diffusion IDPs and major neurodegenerative diseases using common genetic variants-single nucleotide polymorphism (SNPs) as instrumental variables. Summary statistics of genome-wide association study (GWAS) for structural and diffusion IDPs were obtained from 33,224 individuals in the UK Biobank cohort. Summary statistics of GWAS for seven major neurodegenerative diseases were obtained from the largest GWAS for each disease to date. The forward MR analyses identified significant or suggestively statistical causal effects of genetically predicted three structural IDPs on Alzheimer's disease (AD), frontotemporal dementia (FTD), and multiple sclerosis. For example, the reduction in the surface area of the left superior temporal gyrus was associated with a higher risk of AD. The reverse MR analyses identified significantly or suggestively statistical causal effects of genetically predicted AD, Lewy body dementia (LBD), and FTD on nine structural and diffusion IDPs. For example, LBD was associated with increased mean diffusivity in the right superior longitudinal fasciculus and AD was associated with decreased gray matter volume in the right ventral striatum. Our findings might contribute to shedding light on the prediction and therapeutic intervention for the major neurodegenerative diseases at the neuroimaging level.

D-mannose alleviates intervertebral disc degeneration through glutamine metabolism.

BACKGROUND: Intervertebral disc degeneration (IVDD) is a multifaceted condition characterized by heterogeneity, wherein the balance between catabolism and anabolism in the extracellular matrix of nucleus pulposus (NP) cells plays a central role. Presently, the available treatments primarily focus on relieving symptoms associated with IVDD without offering an effective cure targeting its underlying pathophysiological processes. D-mannose (referred to as mannose) has demonstrated anti-catabolic properties in various diseases. Nevertheless, its therapeutic potential in IVDD has yet to be explored. METHODS: The study began with optimizing the mannose concentration for restoring NP cells. Transcriptomic analyses were employed to identify the mediators influenced by mannose, with the thioredoxin-interacting protein (Txnip) gene showing the most significant differences. Subsequently, small interfering RNA (siRNA) technology was used to demonstrate that Txnip is the key gene through which mannose exerts its effects. Techniques such as colocalization analysis, molecular docking, and overexpression assays further confirmed the direct regulatory relationship between mannose and TXNIP. To elucidate the mechanism of action of mannose, metabolomics techniques were employed to pinpoint glutamine as a core metabolite affected by mannose. Next, various methods, including integrated omics data and the Gene Expression Omnibus (GEO) database, were used to validate the one-way pathway through which TXNIP regulates glutamine. Finally, the therapeutic effect of mannose on IVDD was validated, elucidating the mechanistic role of TXNIP in glutamine metabolism in both intradiscal and orally treated rats. RESULTS: In both in vivo and in vitro experiments, it was discovered that mannose has potent efficacy in alleviating IVDD by inhibiting catabolism. From a mechanistic standpoint, it was shown that mannose exerts its anti-catabolic effects by directly targeting the transcription factor max-like protein X-interacting protein (MondoA), resulting in the upregulation of TXNIP. This upregulation, in turn, inhibits glutamine metabolism, ultimately accomplishing its anti-catabolic effects by suppressing the mitogen-activated protein kinase (MAPK) pathway. More importantly, in vivo experiments have further demonstrated that compared with intradiscal injections, oral administration of mannose at safe concentrations can achieve effective therapeutic outcomes. CONCLUSIONS: In summary, through integrated multiomics analysis, including both in vivo and in vitro experiments, this study demonstrated that mannose primarily exerts its anti-catabolic effects on IVDD through the TXNIP-glutamine axis. These findings provide strong evidence supporting the potential of the use of mannose in clinical applications for alleviating IVDD. Compared to existing clinically invasive or pain-relieving therapies for IVDD, the oral administration of mannose has characteristics that are more advantageous for clinical IVDD treatment.

Verapamil Attenuates the Severity of Tendinopathy by Mitigating Mitochondrial Dysfunction through the Activation of the Nrf2/HO-1 Pathway.

Tendinopathy is a prevalent condition in orthopedics patients, exerting a profound impact on tendon functionality. However, its underlying mechanism remains elusive and the efficacy of pharmacological interventions continues to be suboptimal. Verapamil is a clinically used medicine with anti-inflammation and antioxidant functions. This investigation aimed to elucidate the impact of verapamil in tendinopathy and the underlying mechanisms through which verapamil ameliorates the severity of tendinopathy. In in vitro experiments, primary tenocytes were exposed to interleukin-1 beta (IL-1ß) along with verapamil at a concentration of 5 µM. In addition, an in vivo rat tendinopathy model was induced through the localized injection of collagenase into the Achilles tendons of rats, and verapamil was injected into these tendons at a concentration of 5 µM. The in vitro findings highlighted the remarkable ability of verapamil to attenuate extracellular matrix degradation and apoptosis triggered by inflammation in tenocytes stimulated by IL-1ß. Furthermore, verapamil was observed to significantly suppress the inflammation-related MAPK/NFκB pathway. Subsequent investigations revealed that verapamil exerts a remediating effect on mitochondrial dysfunction, which was achieved through activation of the Nrf2/HO-1 pathway. Nevertheless, the protective effect of verapamil was nullified with the utilization of the Nrf2 inhibitor ML385. In summary, the in vivo and in vitro results indicate that the administration of verapamil profoundly mitigates the severity of tendinopathy through suppression of inflammation and activation of the Nrf2/HO-1 pathway. These findings suggest that verapamil is a promising therapeutic agent for the treatment of tendinopathy, deserving further and expanded research.

Effects of selenium-enriched yeast dietary supplementation on egg quality, gut morphology and caecal microflora of laying hens.

Selenium (Se) is an essential micronutrient for humans and animals and is a powerful antioxidant that can promote reproductive and immune functions. The purpose of this study was to evaluate the effects of supplemental dietary selenium-enriched yeast (SeY) on egg quality, gut morphology and microflora in laying hens. In total, 100 HY-Line Brown laying hens (45-week old) were randomly allocated to two groups with 10 replicates and fed either a basal diet (without Se supplementation) or a basal diet containing 0.2 mg/kg Se in the form of SeY for 8 weeks. The Se supplementation did not have a significant effect on egg quality and intestinal morphology of laying hens. Based on the 16S rRNA sequencing, SeY dietary supplementation effectively modulated the cecal microbiota structure. An alpha diversity analysis demonstrated that birds fed 100 mg/kg SeY had a higher cecal bacterial diversity. SeY dietary addition elevated Erysipelotrichia (class), Lachnospiraceae (family), Erysipelotrichaceae (family) and Ruminococcus_torques_group (genus; p < .05). Analysis of microbial community-level phenotypes revealed that SeY supplementation decreased the microorganism abundance of facultatively anaerobic and potentially pathogenic phenotypes. Overall, SeY supplementation cannot significantly improve intestinal morphology; however, it modulated the composition of cecal microbiota toward a healthier gut.

The Association Between Thymidylate Synthase Gene Polymorphisms and the Risk of Ischemic Stroke in Chinese Han Population.

Family history of hypertension, smoking, diabetes and alcohol consumption and atherosclerotic plaque were identified as common risk factors in IS. We aimed at investigating the relationship between Thymidylate Synthase (TS) gene polymorphisms and ischemic stroke (IS).This case-control research selected and genotyped three single nucleotide polymorphisms (SNPs)of TS( rs699517, rs2790, and rs151264360) with Sanger sequencing in Chinese Han population. We also adopted logistic regression analysis in genetic models for calculating odds ratios and 95% confidence intervals. Genotype-Tissue Expression(GTEx) database analyzed the tissue-specific expression and TS polymorphisms. The ischemic stroke patients showed higher low-density lipoprotein cholesterol and total homocysteine (tHcy). It was found that patients with the TT genotype of rs699517 and GG genotype of rs2790 had larger degrees of tHcy than those with CC + CT genotypes and AA + AG genotypes, respectively. The genotype distribution of the three SNPs did not deviate from Hardy-Weinberg equilibrium (HWE). Haplotype analysis showed that T-G-del was the major haplotype in IS, and C-A-ins was the major haplotype in controls. GTEx database indicated that the rs699517 and rs2790 increased the expression of TS in healthy human and associated with TS expression level in a single tissue. In conclusion: This study has shown that TS rs699517 and rs2790 were significantly related to ischemic stroke patients.

Effects of dietary supplementation with tea polyphenols and probiotics on laying performance, biochemical parameters intestinal morphology and microflora of laying hens.

This study was conducted to investigate the effects of tea polyphenols (TP) and probiotics (PB) on the production performance, biochemical indices, and gut health of laying hens. A total of 400 Hy-line Brown layers (45 weeks old) were randomly assigned to 8 diet groups for 8-week feeding trial. Compared with the control basal diet (CT), dietary high dosage of TP and PB (HTP-PB) increased egg mass (P < 0.05). Supplementation with HTP-PB improved the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased the malonic dialdehyde (MDA) content (P < 0.05) without affecting the contents of immunoglobulins in the serum. The combination of HTP and PB supplementation promoted the secretion of estradiol (E2) and progesterone (PROG) compared with treatment with TP or PB alone (P < 0.05). The combined use of HTP and PB induced higher jejunal villus height (VH) than the CT group (P < 0.05). Dietary TP and PB could optimize the functional network of intestinal microflora and the interactions between the intestinal microflora and the host. Therefore, the combined use of the high dosage of TP and PB affected laying performance, improved antioxidant capacity, and promoted intestinal health, which may be associated with regulation of the intestinal microbiota.

rTMS treatment for abrogating intracerebral hemorrhage-induced brain parenchymal metabolite clearance dysfunction in male mice by regulating intracranial lymphatic drainage.

BACKGROUND: The discovery of the glymphatic system and meningeal lymphatic vessels challenged the traditional view regarding the lack of a lymphatic system in the central nervous system. It is now known that the intracranial lymphatic system plays an important role in fluid transport, macromolecule uptake, and immune cell trafficking. Studies have also shown that the function of the intracranial lymphatic system is significantly associated with neurological diseases; for example, an impaired intracranial lymphatic system can lead to Tau deposition and an increased lymphocyte count in the brain tissue of mice with subarachnoid hemorrhage. METHODS: In this study, we assessed the changes in the intracranial lymphatic system after intracerebral hemorrhage and the regulatory effects of repeated transcranial magnetic stimulation on the glymphatic system and meningeal lymphatic vessels in an intracerebral hemorrhage (ICH) model of male mice. Experimental mice were divided into three groups: Sham, ICH, and ICH + repeated transcranial magnetic stimulation (rTMS). Three days after ICH, mice in the ICH+rTMS group were subjected to rTMS daily for 7 days. Thereafter, the function of the intracranial lymphatic system, clearance of RITC-dextran and FITC-dextran, and neurological functions were evaluated. RESULTS: Compared with the Sham group, the ICH group had an impaired glymphatic system. Importantly, rTMS treatment could improve intracranial lymphatic system function as well as behavioral functions and enhance the clearance of parenchymal RITC-dextran and FITC-dextran after ICH. CONCLUSION: Our results indicate that rTMS can abrogate ICH-induced brain parenchymal metabolite clearance dysfunction by regulating intracranial lymphatic drainage.

Fullerenol inhibits tendinopathy by alleviating inflammation.

Tendinopathy is a common disease in orthopaedics, seriously affecting tendon functions. However, the effects of non-surgical treatment on tendinopathy are not satisfactory and surgical treatments possibly impair the function of tendons. Biomaterial fullerenol has been proved to show good anti-inflammatory effects on various inflammatory diseases. For in vitro experiments, primary rat tendon cells (TCs) were treated by interleukin-1 beta (IL-1ß) combined with aqueous fullerenol (5, 1, 0.3 µg/mL). Then inflammatory factors, tendon-related markers, migration and signaling pathways were detected. For in vivo experiments, rat tendinopathy model was constructed by local injection of collagenase into Achilles tendons of rats and fullerenol (0.5, 1 mg/mL) was locally injected 7 days after collagenase injection. Inflammatory factors and tendon-related markers were also investigated. Fullerenol with good water-solubility showed excellent biocompatibility with TCs. Fullerenol could increase expression of tendon-related factors (Collagen I and tenascin C) and decrease expression of inflammatory factors (matrix metalloproteinases-3, MMP-3, and MMP-13) and reactive oxygen species (ROS) level. Simultaneously, fullerenol slowed the migration of TCs and inhibited activation of Mitogen-activated protein kinase (MAPK) signaling pathway. Fullerenol also attenuated tendinopathy in vivo, including reduction of fiber disorders, decrease of inflammatory factors and increase of tendon markers. In summary, fullerenol is a promising biomaterial that can be used to treat tendinopathy.

Time-Series Expression Profile Analysis of Post-Traumatic Joint Contracture in Rats at the Early Stages of the Healing Process.

Objective: This study aimed to characterize the gene expression profile at the early stages of the healing process of post-traumatic joint contracture (PTJC). Methods: Twelve rats were used for PTJC model establishment and were divided into four groups according to the sampling time: S0d, S3d, S7d and S2w. Transcriptome sequencing was performed on fibrotic joint capsule samples in four groups followed by bioinformatics analyses including differentially expressed genes (DEGs) screening, Short Time-series Expression Miner (STEM) analysis, network construction, and pathway analysis. Five important genes were validated by qRT-PCR. Results: A total of 1171, 1052 and 793 DEGs were screened in S3d vs S0d, S7d vs S0d, and S2w vs S0d comparison groups, respectively. A total of 383 overlapping genes were screened out, which were significantly enriched in some inflammatory functions and pathways. Through STEM analysis, three clusters were identified, including 105, 57 and 57 DEGs, respectively. Then, based on the cluster genes, 10 genes, such as Il6, Timp1, Cxcl1, Cxcr4 and Mmp3, were further selected after PPI and pathway analyses. The expression levels of Il6, Timp1, Cxcl1, Cxcr4 and Mmp3 were validated by qRT-PCR. Conclusion: The present study screened out several genes with significant changes in expression levels at the early stages of the healing process in PTJC, such as Il6, Timp1, Cxcl1, Cxcr4 and Mmp3. Our study offers a valuable contribution to the understanding pathomechanism of PTJC.

Prognostic model for predicting overall survival in patients with glioblastoma: an analysis based on the SEER database.

Predicting the prognosis of glioblastoma (GBM) has always been important for improving survival. An understanding of the prognostic factors for patients with GBM can help guide treatment. Herein, we aimed to construct a prognostic model for predicting overall survival (OS) for patients with GBM. We identified 11,375 patients with pathologically confirmed GBM from the Surveillance, Epidemiology, and End Results database between 2004 and 2015. The 1-, 2-, and 3-year survival probabilities were 48.8%, 22.5%, and 13.1%, respectively. The patients were randomly divided into the training cohort (n = 8531) and the validation cohort (n = 2844). A Cox proportional risk regression model was used to analyze the prognostic factors of patients in the training cohort, and a nomogram was constructed. Then concordance indexes (C-indexes), calibration curves, and receiver operating characteristic (ROC) curves were used to assess the performance of the nomograms by internal (training cohort) and external validation (validation cohort). Log-rank test and univariate analysis showed that age, race, marital status, extent of surgical resection, chemotherapy, and radiation were the prognostic factors for patients with GBM (p < 0.05), which were used to construct nomogram. The C-index of the nomogram was 0.717 (95% confidence interval (CI), 0.710-0.724) in the training cohort, and 0.724 (95% CI, 0.713-0.735) in the validation cohort. The nomogram had a higher areas under the ROC curve value. The nomogram was well validated, which can effectively predict the OS of patients with GBM. Thus, this nomogram could be applied in clinical practice.

A Retrospective Comparative Study of Endoscopic Treatment of Gastrocnemius Contracture using the Modified Soft Tissue Release Kit.

Background and Objectives: This study aimed to evaluate the effectiveness and safety of endoscopic gastrocnemius recession using the self-developed Modified Soft Tissue Release Kit. Materials and Methods: This retrospective review followed up 22 patients (34 feet) who underwent endoscopic surgery and 20 patients (30 feet) who received open surgery between January 2020 and January 2022. The American Orthopedic Foot and Ankle Society (AOFAS) ankle-hindfoot score and the maximum ankle dorsiflexion angle were evaluated preoperatively and at the last follow-up. Postoperative complications were recorded. Patient satisfaction was surveyed at the last follow-up. The comparison between quantitative data was analyzed with the Wilcoxon signed-rank test. The comparison between qualitative data was analyzed with the chi-square test. Results: There was no significant difference in the baseline characteristics between the two groups. The AOFAS score in the endoscopic group increased from 50 (18) points preoperatively to 90 (13) points at the last follow-up; the maximum ankle dorsiflexion angle increased from -7.7 (2.8) degrees to 10.6 (3.6) degrees. The AOFAS score in the open group improved from 47 (15) points preoperatively to 90 (18) points at the last follow-up; the maximum ankle dorsiflexion angle increased from -7.6 (4.0) degrees to 10.7 (3.3) degrees. The change values of the AOFAS scores in the endoscopic and open groups were 39 (15) and 40.5 (11) points, respectively, and there was no significant difference between them. The change values of the maximum ankle dorsiflexion angles in the endoscopic and open groups were 19.5 (4.3) and 19.1 (4.9) degrees, respectively, and there was no significant difference between them. There were no complications, such as sural nerve injury, in both groups. There was no significant difference between the two groups in satisfaction with the surgical outcome. Conclusions: Endoscopic gastrocnemius recession using the Modified Soft Tissue Release Kit can significantly improve the foot function with significant mid-term efficacy and high safety.

Polydopamine-coated 3D-printed ß-tricalcium phosphate scaffolds to promote the adhesion and osteogenesis of BMSCs for bone-defect repair: mRNA transcriptomic sequencing analysis.

Cellular bioactivity and tissue regeneration can be affected by coatings on tissue-engineered scaffolds. Using mussel-inspired polydopamine (PDA) is a convenient and effective approach to surface modification. Therefore, 3D-printed ß-tricalcium phosphate (ß-TCP) scaffolds were coated with PDA in this study. The effects of the scaffolds on the adhesion and osteogenic differentiation of seeded bone marrow mesenchymal stem cells (BMSCs) in vitro and on new-bone formation in vivo were investigated. The potential mechanisms and related differential genes were assessed using mRNA sequencing. It was seen that PDA coating increased the surface roughness of the 3D-printed ß-TCP scaffolds. Furthermore, it prompted the adhesion and osteogenic differentiation of seeded BMSCs. mRNA sequencing analysis revealed that PDA coating might affect the osteogenic differentiation of BMSCs through the calcium signaling pathway, Wnt signaling pathway, TGF-beta signaling pathway, etc. Moreover, the expression of osteogenesis-related genes, such as R-spondin 1 and chemokine c-c-motif ligand 2, was increased. Finally, both the 3D-printed ß-TCP scaffolds and PDA-coated scaffolds could significantly accelerate the formation of new bone in critical-size calvarial defects in rats compared with the control group; and the new bone formation was obviously higher in the PDA-coated scaffolds than in ß-TCP scaffolds. In summary, 3D-printed ß-TCP scaffolds with a PDA coating can improve the physicochemical characteristics and cellular bioactivity of the scaffold surface for bone regeneration. Potential differential genes were identified, which can be used as a foundation for further research.

Extracellular Vesicles as Delivery Shippers for Noncoding RNA-Based Modulation of Angiogenesis: Insights from Ischemic Stroke and Cancer.

Ischemic stroke and systemic cancer are two of the leading causes of mortality. Hypoxia is a central pathophysiological component in ischemic stroke and cancer, representing a joint medical function. This function includes angiogenesis regulation. Vascular remodeling coupled with axonal outgrowth following cerebral ischemia is critical in improving poststroke neurological functional recovery. Antiangiogenic strategies can inhibit cancer vascularization and play a vital role in impeding cancer growth, invasion, and metastasis. Although there are significant differences in the cause of angiogenesis across both pathophysiological conditions, emerging evidence states that common signaling structures, such as extracellular vesicles (EVs) and noncoding RNAs (ncRNAs), are involved in this context. EVs, heterogeneous membrane vesicles encapsulating proteomic genetic information from parental cells, act as multifunctional regulators of intercellular communication. Among the multifaceted roles in modulating biological responses, exhaustive evidence shows that ncRNAs are selectively sorted into EVs, modulating common specific aspects of cancer development and stroke prognosis, namely, angiogenesis. This review will discuss recent advancements in the EV-facilitated/inhibited progression of specific elements of angiogenesis with a particular concern about ncRNAs within these vesicles. The review is concluded by underlining the clinical opportunities of EV-derived ncRNAs as diagnostic, prognostic, and therapeutic agents.

A Retrospective Clinical Study of Endoscopic Treatment of Carpal Tunnel Syndrome using the Modified Soft Tissue Release kit.

OBJECTIVE: Carpal tunnel syndrome (CTS) is the most common peripheral entrapment neuropathy, and endoscopic carpal tunnel release (ECTR) is one of the minimally invasive procedures for the treatment of CTS. Based on the shortcomings of ECTR, we designed the "Modified Soft Tissue Release Kit" to assist the endoscopic operation. This study aimed to evaluate the effectiveness and safety of endoscopic treatment of CTS using this kit. METHODS: This retrospective review included 57 patients (86 wrists) who underwent ECTR using the "Modified Soft Tissue Release Kit" at our department between January 2017 and August 2019. Three scale scores (i.e., Quick-Disabilities of the Arm, Shoulder, and Hand [QDASH]; Boston Carpal Tunnel Syndrome Questionnaire [BCTSQ]: symptom severity [BCTSQ-SS] and functional status [BCTSQ-FS]) were recorded to assess hand function and symptoms preoperatively, 1 month postoperatively, 3 months postoperatively, and at the last follow-up. We also asked patients to answer a satisfaction question during follow-up. Pre- and post-operation scores were compared using paired Wilcoxon signed-rank test. Spearman's rank-order correlation was used to evaluate the relationship between scale scores and patient satisfaction. RESULTS: A total of 55 patients (83 wrists) were followed up, with an average follow-up of 27.2 ± 9.3 months. The median preoperative QDASH score was 45.5; the scores at 1 month postoperatively, 3 months postoperatively, and the last follow-up were 4.5, 0, and 0, respectively, with a significant decrease noted compared with the preoperative scores (P < 0.001). The median preoperative BCTSQ-SS and BCTSQ-FS scores were 3.3 and 2.8, respectively; the scores at 1 month postoperatively, 3 months postoperatively, and the last follow-up were 1.2, 1.0, and 1.0, and 1.1, 1.0, and 1.0, respectively, all of which decreased significantly compared with the preoperative scores (P < 0.001). The incidence of nerve injury was 0. The incidence of pillar pain was 0 at the last follow-up. One patient showed no improvement in hand symptoms and function postoperatively, and two patients showed long-term recurrence despite postoperative symptom remission. Approximately 94.5% (52/55) of the patients were satisfied or very satisfied with the outcome. CONCLUSIONS: ECTR with the "Modified Soft Tissue Release Kit" can significantly relieve symptoms and improve function in patients with CTS, with significant short- and mid-term efficacy and high safety.

Emergent Management of Tandem Occlusions in Anterior Circulation Stroke: A Single-Centre Experience.

OBJECTIVE: For anterior circulation tandem occlusions, the optimal management strategy for extracranial carotid lesions is controversial. We aimed to compare the efficacy and safety of acute stenting (AS) with balloon angioplasty (BA) only. METHODS: Clinical data were collected from 98 patients with anterior circulation tandem occlusion who underwent endovascular treatment at our center. Of these patients, 64 and 34 were assigned to the AS and BA groups, respectively. The clinical characteristics and outcome data of the 2 groups were analyzed and compared. RESULTS: The proportion of patients with good outcomes was 59.2%. The AS group had a higher rate of successful recanalization (98.4% vs. 82.4%, P = 0.007) and a lower rate of occlusion of the responsible vessel at 90 days (14.1% vs. 32.4%, P = 0.039) than the BA group. The AS group was also significantly better than the BA group in terms of good outcomes (67.2% vs. 44.1%, P = 0.027), but there was no significant difference between the 2 groups in terms of 90-day mortality (6.3% vs. 8.8%, P = 0.691) and asymptomatic intracranial hemorrhage (6.3% vs. 5.9%, P = 1.000). Lower baseline National Institutes of Health Stroke Scale scores were associated with good outcomes (P < 0.001), and the presence of symptomatic intracranial hemorrhage was associated with 90-day mortality (P = 0.003). CONCLUSIONS: Acute stent placement in patients with acute ischemic stroke due to anterior circulation tandem occlusion may have a better outcome than BA alone, and the safety of both approaches is comparable.

MRI Study on the Relationship Between Nerve and Blood Vessel in Unilateral Angiogenic Trigeminal Neuralgia.

BACKGROUND: Trigeminal neuralgia (TN) is a common cranial nerve disease. OBJECTIVE: To investigate the relationship between the trigeminal nerve and the responsible blood vessel in patients with unilateral vascular trigeminal neuralgia (VTN). METHODS: Thirty patients with unilateral VTN were confirmed by microvascular decompression. RESULTS: Among the 30 patients, the responsible blood vessels were present in 30 cases on the affected side and 17 cases on the uninfected side (1). The location of the intersection of the trigeminal nerve and the responsible blood vessel: the affected side is located 2/5 behind the trigeminal nerve cisternal segment; the healthy side is located 3/5 anterior to the cisternal segment (2). Symptomatic vessels were located within the cistern between the origin and 2/5ths of the cistern length, and non-symptomatic vessels were located beyond the 2/5ths location (3). Direction of intersection: on the affected side, the responsible vessel was located inside and above the trigeminal nerve in 27 cases, (27/30, 90%), and outside and below the trigeminal nerve in 3 cases (3/30, 10%). On the unaffected side, the responsible vessel was located inside and above the nerve in 16 cases (16/17, 94%) and outside and below the nerve in 1 case (1/17, 5.8%) (4). Intersection form: 3 cases (3/30, 10%) on the affected side, the responsible blood vessel contacted the trigeminal nerve, in 26 cases (26/30, 86%) the responsible blood vessel compressed the trigeminal nerve, and in 1 case (1/30, 5%) the responsible blood vessel caused the trigeminal nerve to be twisted; 8 cases (8/17, 47%) of the contralateral side contacted the trigeminal nerve with the responsible blood vessel, and in 9 cases (9/17, 53%) the responsible blood vessel compressed the trigeminal nerve. CONCLUSION: Patients with unilateral VTN have differences in the location and form of the intersection of the trigeminal nerve and the responsible vessel on the affected side and the contralateral side.

A clinical application study of a stent placement assessment.

BACKGROUND: Atherosclerotic acute carotid occlusion is a specific type of stroke, and controversy exists regarding the surgical strategy, that is, whether an internal carotid artery stent should be placed immediately after opening the occluded vessel. There is no objective evaluation system for this procedure. In a previous study, we summarized an evaluation decision system Emergent Carotid Artery Stent placement decision Evaluation System (ECASES) for emergency stent placement. STUDY DESIGN: This is a prospective, single-center, randomized controlled trial. Patients with acute ischemic stroke caused by atherosclerotic carotid artery occlusion confirmed by imaging (computed tomography/magnetic resonance angiography/digital subtraction angiography) will be randomly divided into the study and control groups, with 101 patients in each group. The study group will undergo surgery according to the ECASES system and the control group will undergo surgery according to the operator's experience. The postoperative outcomes of the 2 groups will be compared. STUDY OUTCOMES: Primary outcome: Neurological functional status (modified Rankin Scale and National Institutes of Health Stroke Scale scores) of patients 90 days postoperatively. Secondary outcomes: neurological function changes, hemorrhage events, cerebral edema, postoperative modified treatment in cerebral infarction grade, new cerebral infarction, and reocclusion of responsible vessels. DISCUSSION: Currently, no prospective controlled data exist regarding the efficacy and safety of carotid stenting in the acute phase. Previously, we had developed an ECASES stent placement system for acute carotid artery occlusion. The present study will evaluate the efficacy and safety of ECASES in a randomized, double-blind prospective study and clarify its guiding significance in acute atherosclerotic carotid artery occlusion surgery.

The Immunomodulatory Functions of BTK Inhibition in the Central Nervous System.

Bruton's tyrosine kinase (BTK) is a central signaling node in B cells. BTK inhibition has witnessed great success in the treatment of B-cell malignancies. Additionally, in the immune system, BTK is also a prominent component linking a wide variety of immune-related pathways. Therefore, more and more studies attempting to dissect the role of BTK in autoimmune and inflammation progression have emerged in recent years. In particular, BTK expression was also found to be elevated within the central nervous system (CNS) during neuroinflammation. BTK inhibitors are capable of crossing the blood-brain barrier rapidly to modulate B cell functions, attenuate microglial activities and affect NLRP3 inflammasome pathways within the CNS to improve the outcome of diseases. Thus, BTK inhibition appears to be a promising approach to modulate dysregulated inflammation in the CNS and alleviate destruction caused by excessive inflammatory responses. This review will summarize the immunomodulatory mechanisms in which BTK is involved in the development of neurological diseases and discuss the therapeutic potential of BTK inhibition for the treatment of neuroinflammatory pathology.