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To design a model to predict the early prognosis of patients with traumatic brain injury (TBI) based on parameters that can be quickly obtained in emergency conditions from medical history, physical examination, and supplementary examinations.The medical records of TBI patients who were hospitalized in two medical institutions between June 2015 and June 2021 were collected and analyzed. Patients were divided into the training set, validation set, and testing set. The possible predictive indicators were screened after analyzing the data of patients in the training set. Then prediction models were found based on the possible predictive indicators in the training set. Data of patients in the validation set and the testing set was provided to validate the predictive values of the models.Age, Glasgow coma scale score, Apolipoprotein E genotype, damage area, serum C-reactive protein, and interleukin-8 (IL-8) levels, and Marshall computed tomography score were found associated with early prognosis of TBI patients. The accuracy of the early prognosis prediction model (EPPM) was 80%, and the sensitivity and specificity of the EPPM were 78.8% and 80.8% in the training set. The accuracy of the EPPM was 79%, and the sensitivity and specificity of the EPPM were 66.7% and 86.2% in the validation set. The accuracy of the early EPPM was 69.1%, and the sensitivity and specificity of the EPPM were 67.9% and 77.8% in the testing set.Prediction models integrating general information, clinical manifestations, and auxiliary examination results may provide a reliable and rapid method to evaluate and predict the early prognosis of TBI patients.

Spontaneous migration of retained intracranial missiles is uncommon but a potentially serious phenomenon. Our objective is to increase awareness of the risk of spontaneous migration of retained intracranial missiles by reporting our case series of 16 patients. We performed a retrospective single-center study on patients treated for intracranial missile injuries between 2000 and 2010 in Palestine with a particular focus on the migration of retained intracranial missiles. Detailed analyses were made of patients' age, sex, type of injurious agents (metallic bullets/rubber bullets/metallic shrapnel from bomb explosion), initial missile position, site to where the missile migrated, radiological and neurological manifestations, complications, treatment modalities (surgery vs. conservative) and functional outcome by Glasgow outcome scale-extended (GOSE) classification at last follow-up. In a cohort of 190 patients with retained intracranial missiles, we identified 16 (8.4%) patients with spontaneous migration. Patients' age ranged from 10 to 30 years (mean: 18.9 ± 6.4 years). There were only 2 female patients. The missiles that migrated intracranially were metallic bullets (n = 10), rubber bullets (n = 3), and metallic shrapnel from a bomb explosion (n = 3). Among the 16 patients, 10 patients experienced symptoms due to missile migration and were treated surgically, while six patients did not develop new symptoms after missile migration and were managed conservatively. In our case series, 16/190 (8.4%) patients with retained intracranial missiles developed spontaneous migration. Neurosurgeons performing delayed surgery on patients with retained intracranial missiles should be aware of the risk of spontaneous migration and verify the location of the missile after positioning the patient for surgery.

BackgroundCurrent studies indicate a contradictory relationship between decreased mortality risks of spontaneous intracerebral hemorrhage (sICH) and elevated low-density lipoprotein cholesterol (LDL-C) levels. Thus, this meta-analysis was designed to examine the involvement of high LDL-C levels in a lower mortality risk of sICH patients.MethodsPubMed, Cochrane, and Embase databases were searched up to the date of August 3rd, 2022. Pooled odds ratio (OR) with a 95% confidence interval (CI) was estimated for the higher vs. lower serum LDL-C level groups. Subgroup and sensitivity analyses were also carried out. Egger's test was applied to detect any potential publication bias.ResultsOf 629 citations reviewed, 8 eligible cohort studies involving 83,013 patients were enrolled in this meta-analysis. Compared with lower serum LDL-C levels containing patients, higher serum LDL-C patients exhibited significantly decreased risks of 3-month mortality (OR: 0.51; 95%CI: 0.33–0.78; I2 = 47.8%); however, the LDL-C level change wasn't significantly associated with in-hospital mortality risks (OR: 0.92; 95%CI: 0.63–1.33; I2 = 91.4%) among sICH subjects. All studies included were classified as high-quality investigations.ConclusionsThis meta-analysis suggests a higher LDL-C level may decrease the mortality risk in sICH patients. LDL-C level increase is inversely associated with the 3-month mortality risks in these patients but not significantly correlated with the in-hospital mortality risks. Further well-designed prospective studies with extended follow-up periods are needed to confirm these findings and explore underlying cross-talks.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022318318, identifier: PROSPERO 2022 CRD42022318318.

Small object detection has been a research hotspot in the field of computer vision. Especially in complex backgrounds (CBs), SOD faces various challenges, including inconspicuous small object features, object distortion due to CBs interference, and inaccurate object localization due to various noises. So far, many methods have been proposed to improve the SOD content in CBs. In this paper, based on an extensive study of related literature, we first outline the current challenges and some cutting-edge solutions for SOD, and then introduce the complex background interference types present in small object images and the imaging characteristics of different types of images, as well as the characteristics of small objects. Next, the image pre-processing methods are summarized. Based on this, machine learning-based SOD methods and traditional SOD methods are focused on. Finally, the future development direction is given.

Background Neuroinflammation is one of the most important processes in secondary injury after traumatic brain injury (TBI). Triggering receptor expressed on myeloid cells 2 (TREM2) has been proven to exert neuroprotective effects in neurodegenerative diseases and stroke by modulating neuroinflammation, and promoting phagocytosis and cell survival. However, the role of TREM2 in TBI has not yet been elucidated. In this study, we are the first to use COG1410, an agonist of TREM2, to assess the effects of TREM2 activation in a murine TBI model. Methods Adult male wild-type (WT) C57BL/6 mice and adult male TREM2 KO mice were subjected to different treatments. TBI was established by the controlled cortical impact (CCI) method. COG1410 was delivered 1 h after CCI via tail vein injection. Western blot analysis, immunofluorescence, laser speckle contrast imaging (LSCI), neurological behaviour tests, brain electrophysiological monitoring, Evans blue assays, magnetic resonance imaging (MRI), and brain water content measurement were performed in this study. Results The expression of endogenous TREM2 peaked at 3 d after CCI, and it was mainly expressed on microglia and neurons. We found that COG1410 improved neurological functions within 3 d, as well as neurological functions and brain electrophysiological activity at 2 weeks after CCI. COG1410 exerted neuroprotective effects by inhibiting neutrophil infiltration and microglial activation, and suppressing neuroinflammation after CCI. In addition, COG1410 treatment alleviated blood brain barrier (BBB) disruption and brain oedema; furthermore, COG1410 promoted cerebral blood flow (CBF) recovery at traumatic injury sites after CCI. In addition, COG1410 suppressed neural apoptosis at 3 d after CCI. TREM2 activation upregulated p-Akt, p-CREB, BDNF, and Bcl-2 and suppressed TNF-α, IL-1β, Bax, and cleaved caspase-3 at 3 d after CCI. Moreover, TREM2 knockout abolished the effects of COG1410 on vascular phenotypes and microglial states. Finally, the neuroprotective effects of COG1410 were suppressed by TREM2 depletion. Conclusions Altogether, we are the first to demonstrate that TREM2 activation by COG1410 alleviated neural damage through activation of Akt/CREB/BDNF signalling axis in microglia after CCI. Finally, COG1410 treatment improved neurological behaviour and brain electrophysiological activity after CCI. Graphical Abstract

The characteristic X-ray of a target is of considerable significance in industrial applications and medical diagnosis and treatment, and its intensity is closely related to the incident electron en...

Cellular traffic prediction at mobile edges is extremely valuable to ultra high-reliability low-latency (URLLC) communication of 5G. Many network actions depend on this prediction technology, ranging from radio resource scheduling, edge node sharing, and traffic control, to network slicing and dynamic network function virtualization. However, accurate prediction for cellular traffic flow is a tough challenge, since irregular and dramatic fluctuations of network traffic, caused by continuous topology update and multifarious service requests, occur frequently. Motivated by these investigations, we propose a deep multi-reservoir regression learning network for cellular traffic prediction, called mRDLN, supporting multi-access edge computing. This architecture is a uniform and consistent system with functional modules of smoothing, feature extraction, and multi-reservoir regression. This is the first attempt to enhance deep neural computing considering a combined regression scheme in the framework of a deep belief network, where multiple echo state networks are integrated to perform local supervised learning instead of the original single approximator. On highly bursty cellular traffic traces, experimental simulations show that our mRDLN consistently outperforms the state-of-the-art models, and the superior prediction is further verified by means of statistical analysis.

Plant annexins are a kind of conserved Ca2+-dependent phospholipid-binding proteins which are involved in plant growth, development and stress tolerance. Radish is an economically important annual or biennial root vegetable crop worldwide. However, the genome-wide characterization of annexin (RsANN) gene family remain largely unexplored in radish. In this study, a comprehensive identification of annexin gene family was performed at the whole genome level in radish. In total, ten RsANN genes were identified, and these putative RsANN proteins shared typical characteristics of the annexin family proteins. Phylogenetic analysis showed that the RsANNs together with annexin from Arabidopsis and rice were clustered into five groups with shared similar motif patterns. Chromosomal localization showed that these ten RsANN genes were distributed on six chromosomes (R3-R8) of radish. Several cis-elements involved in abiotic stress response were identified in the promoter regions of RsANN genes. Expression profile analysis indicated that the RsANN genes exhibited tissue-specific patterns at different growth stages and tissues. The Real-time quantitative PCR (RT-qPCR) revealed that the expression of most RsANN genes was induced under various abiotic stresses including heat, drought, salinity, oxidization and ABA stress. In addition, stress assays showed that overexpression of RsANN1a improved plant’s growth and heat tolerance, while artificial microRNAs (amiRNA)-mediated knockdown of RsANN1a caused dramatically decreased survival ratio of Arabidopsis plants. These findings not only demonstrate that RsANN1a might play a critical role in the heat stress response of radish, but also facilitate clarifying the molecular mechanism of RsANN genes in regulating the biological process governing plant growth and development.

Background and Purpose: Several pieces of evidence suggest that serum lactate hydrogenase (LDH) level is associated with the pathological process of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). This research aimed to investigate the associations of serum LDH level with the occurrence of DCI in aSAH patients. Methods: A total of 122 patients diagnosed with aSAH within 72h of onset were retrospectively enrolled. The serum levels of LDH between 7:00-8:00 am on day 1, day 3 and day 7, patients’ demographics, and clinical features were collected. Computed tomography perfusion was performed within 7 days after aSAH. The occurrence of DCI was recorded during the hospitalization. Results: Among all the enrolled patients, 43 (35.2%) developed DCI during hospitalization. Patients occurred DCI were always accompanied by more serious clinical features and found with higher serum LDH levels. LDH levels on day 3 and day 7 after onset were independently associated with the occurrence of DCI and showed high predictive value according to the receiver operating characteristic (ROC) curve. Moreover, there was a strong correlation between LDH and mean cerebral blood flow, transit time, and mean time to peak. Conclusions: Serum LDH level on day 3 and day 7 may be a valuable, convenient, and rapid predictive indicator for the occurrence of DCI in aSAH patients.

Meningiomas are the most common primary intracranial neoplasm with diverse pathological types and complicated clinical manifestations. The fifth edition of the WHO Classification of Tumors of the Central Nervous System (WHO CNS5), published in 2021, introduces major changes that advance the role of molecular diagnostics in meningiomas. To follow the revision of WHO CNS5, this expert consensus statement was formed jointly by the Group of Neuro-Oncology, Society of Neurosurgery, Chinese Medical Association together with neuropathologists and evidence-based experts. The consensus provides reference points to integrate key biomarkers into stratification and clinical decision making for meningioma patients.Practice guideline REgistration for transPAREncy (PREPARE), IPGRP-2022CN234.

Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating cerebrovascular disease with high mortality and morbidity. In recent years, a large number of studies have focused on the mechanism of early brain injury (EBI) and delayed cerebral ischemia (DCI), including vasospasm, neurotoxicity of hematoma and neuroinflammatory storm, after aSAH. Despite considerable efforts, no novel drugs have significantly improved the prognosis of patients in phase III clinical trials, indicating the need to further re-examine the multifactorial pathophysiological process that occurs after aSAH. The complex pathogenesis is reflected by the destruction of the dynamic balance of the energy metabolism in the nervous system after aSAH, which prevents the maintenance of normal neural function. This review focuses on the fluid metabolic pathways of the central nervous system (CNS), starting with ruptured aneurysms, and discusses the dysfunction of blood circulation, cerebrospinal fluid (CSF) circulation and the glymphatic system during disease progression. It also proposes a hypothesis on the metabolic disorder mechanism and potential therapeutic targets for aSAH patients. Cover Image for this issue: https://doi.org/10.1111/jnc.15384.

Aim To establish an artery and venous sinus occlusion image score (AVOIS) which is compatible in both cerebral arteries and venous system diseases. Methods A total of 188 consecutive patients with the final diagnosis of anterior circulation infarct (ACI) and 56 consecutive patients with cerebral venous and sinus thrombosis (CVST) were retrospectively studied. The AVOIS was developed based on the severity of occlusive changes of main intracranial arteries and venous sinuses (present = 0, partial occlusion = 1, absent = 2), and divided into four groups (CVST group: 0, 1‐5, 6‐10, >10. ACI group: 0, 1‐5, 6‐10, >10) arbitrarily. A receiver operating characteristic (ROC) curve was applied to discover the sensitivity and specificity of AVOIS. The National Institutes of Health Stroke Scale (NIHSS), Clot Burden Score (CBS) were set as the reference. Logistic regression models were developed to adjust for baseline clinical variables and AVOIS. Length of hospital stay (LOS) was also evaluated using the Kaplan‐Meier estimator. Results For the CVST group, a positive correlation between AVOIS and NIHSS was discovered (Spearman's ρ = 0.54, p, A novel score system called the Artery and Venous Sinus Occlusion Image Score (AVOIS) was developed based on quantification analysis of the intracranial thrombus in both artery and venous sinus (Table 1). According to the CTA or MRA, anterior circulation and venous sinuses were allotted different scores (present = 0, partial occlusion = 1, absent = 2) by researchers. The total score on AVOIS in anterior circulation or venous sinus was accumulated to 14 points.

Deposition defects arising during automated fibre placement (AFP) reduces production rate and creates wastage from rejected parts. This issue can be alleviated by identifying and reacting to those defects in real-time during deposition. To demonstrate the concept, this study augmented an AFP process with profilometry sensors and software control. Description of the machine, its sensors, and the control system is provided. In the experiment, representative bonding defects at the tow level representative of a typical AFP layup were introduced. These defects were picked up by the profilometry sensors, and the machine automatically adjusted the process parameters when the defects reached the nip point. Microscopy revealed that such a procedure can influence the material microstructure and reduce in-plane waviness in the final cured laminate. This demonstrates the feasibility of the observe-think-react concept in AFP and provides another step toward real-time defect monitoring and correction in composites manufacturing.

Early brain injury (EBI) is a major contributor to the high mortality and morbidity after subarachnoid hemorrhage (SAH). Inflammatory responses and neuronal apoptosis are important causes of EBI. Because 5- lipoxygenase (5-LOX) is known to be involved various central nervous system diseases, we investigated the effects of 5-LOX inhibition during EBI after SAH. Zileuton and LY294002 were used to inhibit expression of 5-LOX and Akt, respectively. We found that 5-LOX expression was significantly increased in the cytoplasm of cortical neurons after SAH and was accompanied by upregulated expression of the inflammatory factors LTB4, TNF-α, IL-1β and IL-6; upregulation of the pro-apoptotic factor Bax; downregulation of the anti-apoptotic factor Bcl-2; and an increased apoptosis rate. Gastric Zileuton administration significantly suppressed all of those effects and improved neurological function. Zileuton also upregulated activated (phosphorylated) AKT levels, and these beneficial effects of Zileuton were abolished by intracerebroventricular infusion of the PI3K inhibitor LY294002. Taken together, these findings indicate that 5-LOX mediates pro-inflammatory and pro-apoptotic effects that contribute to EBI after SAH and that those effects are suppressed by activation of PI3K/Akt signaling. This suggests targeting 5-LOX may be an effective approach to treating EBI after SAH.

The single-crystal yielding and hardening behavior of polycrystals is important for understanding their mechanical behavior. Many parameters (> 10) are usually required to achieve this for magnesium alloys based on physics-based models. However, the efficient and precise determination of these parameters is a very challenging task. An efficient and practical method is proposed herein to determine the parameter set by dividing the parameters into those for yielding and hardening, thereby significantly reducing the time cost of automatic parameter calibration. This method is then applied to calibrate the parameter set used in the viscoplastic self-consistent (VPSC) model to describe the mechanical behavior of the rare-earth magnesium alloy ZEK100 from multiple mechanical test data. The obtained best-fit parameters can be considered realistic and nearly unique, and can successfully reproduce the mechanical behavior and textural evolution. This procedure can be generally applied to calibrate near-unique parameters in other materials and constitutive models.

The thermal quenching of light emission is a critical bottleneck that hampers the real-world application of lead halide perovskite nanocrystals in both electroluminescent and down-conversion light-emitting diodes. Here, we report CsPbBr3 perovskite nanocrystals with a temperature-independent emission efficiency of near unity and constant decay kinetics up to a temperature of 373 K. This unprecedented regime is obtained by a fluoride post-synthesis treatment that produces fluorine-rich surfaces with a wider energy gap than the inner nanocrystal core, yielding suppressed carrier trapping, improved thermal stability and efficient charge injection. Light-emitting diodes incorporating these fluoride-treated perovskite nanocrystals show a low turn-on voltage and spectrally pure green electroluminescence with an external quantum efficiency as high as 19.3% at 350 cd m−2. Importantly, nearly 80% of the room-temperature external quantum efficiency is preserved at 343 K, in contrast to the dramatic drop commonly observed for standard CsPbBr3 perovskite nanocrystal light-emitting diodes. These results provide a promising pathway for high-performance, practical light-emitting diodes based on perovskite nanostructures. Fluoride-treated CsPbBr3 nanocrystals emit light with near unity efficiency at temperatures of up to 373 K.

Ocean sensor data prediction has become a promising means for smart ocean monitoring. In alternative solutions, deep neural networks (DNNs) are considered as a good choice. The determination of activation functions in DNNs has a significant effect on training speed and nonlinear approximation. In this paper, the effect of activation functions on a deep computing model called deep belief echo-state network (DBEN) is studied in the scenario of ocean time series prediction. Here, different forms, including hyperbolic tangent, rectified linear unit, exponential linear unit, swish, softplus and their variants, are considered. The purpose is to investigate, from the perspectives of accuracy and training efficiency, whether certain activation function in DBEN is completely universal for the different tasks of ocean sensor data processing or not. On a great deal of real-world ocean time series of different characteristics, the results show that the selection of activation functions in DBEN is task-related. Specially, these newly introduced activation functions are more beneficial to the accurate predictions for conventional and chemical data sets compared with sigmoid benchmark. The statistical analysis further verifies this finding.

Background Traumatic brain injury (TBI) is a disease with high mortality and morbidity, which leads to severe neurological dysfunction. Neurogenesis has provided therapeutic options for treating TBI. Brain derived neurotrophic factor (BDNF) plays a key role in neuroblasts migration. We aimed to investigate to the key regulating principle of BDNF in endogenous neuroblasts migration in a mouse TBI model. Methods In this study, controlled cortical impact (CCI) mice (C57BL/6J) model was established to mimic TBI. The sham mice served as control. Immunofluorescence staining and enzyme-linked immunosorbent assay were performed on the CCI groups (day 1, 3, 7, 14 and 21 after CCI) and the sham group. All the data were analyzed with Student’s t-test or one-way or two-way analysis of variance followed by Tukey’s post hoc test. Results Our results revealed that neuroblasts migration initiated as early as day 1, peaking at day 7, and persisted till day 21. The spatiotemporal profile of BDNF expression was similar to that of neuroblasts migration, and BDNF level following CCI was consistently higher in injured cortex than in subventricular zone (SVZ). Reactive astrocytes account for the major resource of BDNF along the migrating path, localized with neuroblasts in proximity. Moreover, injection of exogenous CC chemokine ligand 2 (CCL2), also known as monocyte chemoattractant protein-1, at random sites promoted neuroblasts migration and astrocytic BDNF expression in both normal and CCI mice (day 28). These provoked neuroblasts can also differentiate into mature neurons. CC chemokine ligand receptor 2 antagonist can restrain the neuroblasts migration after TBI. Conclusions Neuroblasts migrated along the activated astrocytic tunnel, directed by BDNF gradient between SVZ and injured cortex after TBI. CCL2 might be a key regulator in the above endogenous neuroblasts migration. Moreover, delayed CCL2 administration may provide a promising therapeutic strategy for late neurogenesis post-trauma.

Delayed cerebral ischemia (DCI) is the most severe complication after subarachnoid hemorrhage (SAH), and cortical spreading depolarization (CSD) is believed to play a vital role in it. However, the dynamic changes in cerebral blood flow (CBF) in response to CSD in typical SAH models have not been well investigated. Here, SAH was established in mice with endovascular perforation. Subsequently, the spontaneous CBF dropped instantly and then returned to baseline rapidly. After KCl application to the cortex, subsequent hypoperfusion waves occurred across the groups, while a lower average perfusion level was found in the SAH groups (days 1-7). Moreover, in the SAH groups, the number of CSD decreased within day 7, and the duration and spreading velocity of the CSD increased within day 3 and day 14, respectively. Next, we continuously monitored the local field potential (LFP) in the prefrontal cortex. The results showed that the decrease in the percentage of gamma oscillations lasted throughout the whole process in the SAH group. In the chronic phase after SAH, we found that the mice still had cognitive deficits but experienced no obvious tissue damage. In summary, SAH negatively affects the CBF responses to CSD and the spontaneous LFP activity and causes long-term cognitive deficits in mice. Based on these findings, in the specific phase after SAH, DCI is induced or exacerbated more easily by potential causers of CSD in clinical practice (edema, erythrocytolysis, inflammation), which may lead to neurological deterioration.

Neutrophil extracellular traps (NETs) play a major role in intrinsic immunity by limiting and killing pathogens. Recently, a series of studies have confirmed that NETs are closely associated with vascular injury and microthrombosis. Furthermore, NETs play an important role in neuroinflammation after ischemic and hemorrhagic stroke. Neuroinflammation and microthrombosis after subarachnoid hemorrhage are key pathophysiological processes associated with poor prognosis, but their crucial formation mechanisms and interventions remain to be elucidated. Could NETs, as an emerging and important pathogenesis, be a new therapeutic target after subarachnoid hemorrhage?

Background Nontuberculous mycobacteria (NTM) usually invades vulnerable hosts. Disseminated NTM (dNTM) infection can affect nearly all organs and be easily misdiagnosed as metastatic carcinoma or other systemic diseases, especially in seemingly immunocompetent hosts. Identification of underlying immunodeficiency is critical for the diagnosis and treatment of dNTM. Adult-onset immunodeficiency (AOID) with anti-IFN-γ autoantibodies has recently been recognized as a crucial but frequently neglected risk factor for dNTM infection. Frequent relapses of infection are common in AOID patients despite appropriate anti-infective treatment and B-cell-depleting therapy has shown some promising results. Herein, we report a case of dNTM infection mimicking malignancy in an AOID patient who was successfully treated with rituximab. Case presentation A middle-aged male presented with fever, productive cough, multifocal skin abscesses and multiple osteolytic lesions with pathological fractures. Chest CT revealed consolidation of the lingula while bronchoscopy showed a mass completely blocking the airway opening of the inferior lingual segment. Metagenomic next-generation sequencing and mycobacterial culture of skin pus and bronchoalveolar lavage fluid reported Mycobacterium Colombiense, confirming the diagnosis of dNTM infection. However, anti-NTM antibiotics alone failed to prevent disease relapse and progression. Further evaluation indicated undetectable serum IFN-γ concentration and high-titer autoantibodies against IFN-γ, suggesting that AOID was the underlying reason for dNTM. Rituximab was added to treatment and successfully controlled the infection without relapse at one-year follow-up. Conclusion We reported a rare case of disseminated Mycobacterium Colombiense infection manifested with pulmonary mass, pathological fracture and dermapostasis in a host with AOID. Our case demonstrated that AOID should be screened when patients get the episode of disseminated NTM infection particularly when other risk factors are excluded. Besides prolonged anti-NTM therapy, AOID-associated NTM infection should be treated with B-cell-depleting therapy to prevent recurrence.

Here, we investigated the role of tanshinone IIA (TSO IIA) in astrocytic swelling caused by ischemia and reperfusion-like injury in an in vitro model and the molecular mechanisms underlying this effect. Primary brain astrocytes were cultured in conditions of glucose and oxygen deprivation and reoxygenation (OGD/R). We investigated the effects of TSO IIA treatment on cell swelling and injury, and the expression levels of AQP4 protein in the plasma membrane. We then studied the involvement of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis in TSO IIA-mediated protection. Treatment with TSO IIA alleviated OGD/R-induced astrocytic swelling and the over-clustering of AQP4 protein in the plasma membrane. In addition, TSO-IIA significantly reduced over-expression of HMGB1, the high levels of NF-κB protein in the nucleus, and of IL-6 protein in cytoplasm and extracellular media induced by OGD/R. Combination of TSO IIA and recombinant HMGB1 reversed these effects. Inhibition of RAGE, the receptor of HMGB1, induced similar results to those of TSO IIA. In addition, exogenous IL-6 reversed TSO IIA-mediated effect on AQP4 over-clustering and cell swelling.TSO IIA significantly reduced astrocyte swelling after OGD/R injury in vitro, via blocking activation of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis and thereby decreasing the expression of AQP4 in plasma membrane.

Support vector machine (SVM) is a powerful machine learning (ML) technology and the distinctive generalization ability makes it one of the most popular approximation tools in the field of Internet-of-Things (IoT)-based marine data processing. However, SVM has been criticized for trial and error of parameters, especially, kernel function. How to determine a suitable kernel for SVM in a specific problem has been rather tricky. To give a systematic research of the field, we concentrate on the self-adaptive selection of kernel functions in the framework of SVM for IoT-based marine data prediction. Specifically, we adopt the optimal kernel for obtaining competitive SVM and devises a kernel selection criteria of such high-efficiency models. Experiments are conducted via IoT-based real-world marine data sets of different characteristics. The results demonstrate that our proposed self-adaptive SVM model can autonomously provide a suitable kernel for given marine environmental factor prediction, and outperform the alternative with the linear combination of multiple kernels. Besides, the superior performance is verified from the perspective of statistic analysis.

Although erythropoietin (EPO) has been proven to significantly promote the proliferation of cancer cells, the mechanism for promoting glioma proliferation is poorly understood. Here, we examined the functional role of the AKT/GSK-3β/β-catenin signaling pathway in the EPO-mediated proliferation of glioma. The distribution of EPO and Ki-67 among clinical samples with different WHO grades was plotted by Immunological Histological Chemistry analysis. U87 and U251 glioma cell lines were treated with short hairpin RNA targeting (shEPO), recombinant human erythropoietin (rhEPO) and/or AKT-specific inhibitor (MK-2206). The changes in phosphorylated AKT, nuclear β-catenin, cyclin D1 and p27kip1 expression were detected. Cell cycle distributions and glioma proliferation in vitro and in vivo were analyzed. The expression level of EPO was significantly elevated with the increase of WHO grade and Ki67 in clinical glioma specimens. In vitro, knockdown of endogenous EPO in U87 and U251 cells effectively block the phosphorylation of AKT and GSK-3β and the expression of nuclear β-catenin. shEPO treatment also significantly decreased the expression of cyclin D1 and increased the expression of p27kip1. The cell cycle transition then slowed down and the proliferation of glioma cells or mouse xenograft tumors both decreased. Treatment of cells or tumors with extra rhEPO reversed the above biological effects mediated by shEPO. rhEPO-induced activation of the AKT/GSK-3β/β-catenin pathway and proliferation were abolished by MK-2206. Our study identified the AKT/GSK-3β/β-catenin axis as a critical mediator of EPO-induced glioma proliferation and further provided a clinically significant dimension to the biology of EPO.

Purpose This study aimed to elucidate the biological function and upstream regulatory mechanism of CELSR1 in glioma. Materials and Methods We evaluated the expression of CELSR1 in glioma by TCGA_GEPIA tool, RT-qPCR, and Western blot assays. CCK-8, wound healing, and transwell invasion assays were, respectively, performed to detect the effect of CELSR1 on cell proliferation, migration, and invasion. The upstream regulatory miRNAs of CELSR1 were predicted by TargetScan and validated by luciferase activity reporter assay. Results CELSR1 is overexpressed in glioma (P

Video services have hold a surprising proportion of the whole network traffic in wireless communication networks. Accurate prediction of video traffic can endow networks with intelligence in resource management, especially for the forthcoming beyond the fifth-generation (B5G) networks. However, the existing approaches fail to accurately predict video traffic with all types of frames, due to the natures of strong long-range dependence, self-similarity and burstiness. Obviously, it is unable to meet the QoS and QoE requirements of dynamic bandwidth allocation. In this paper, we propose the feasibility of advanced machine learning methodology applied in nonstationary video traffic prediction, i.e., smoothing-aided support vector machine (SSVM) model. The model utilizes classical smoothing methods to preprocess video traffic by relieving the drastic fluctuation of video stream. It can provide an effective association for the subsequent support vector regression, as the preprocessed data becomes more smooth and continuous than the original unprocessed one. Experimental results show that our proposed model significantly outperforms the state of the art model, i.e., logistic smooth transition autoregressive, in prediction performance. The superior nonlinear approximation capacity is further demonstrated by visualized statistical analysis.

Blast furnace gas (BFG) produced from steel industries is generally one of the most important energy supplies in enterprises. Due to a great deal of output, fluctuation, and heterogeneity in data, it is very difficult to provide profound insights into its internal dynamic. In this article, a novel analysis framework is developed for the BFG data processing, considering the recurrence plot (RP) and the recurrence quantification analysis (RQA). The specific aim is to investigate the relationship between BFG output and its potential influencing factors. This framework can be deemed as a uniform and consistent system with functional components of qualitative visualization and quantitative analysis. Concretely, the BFG outputs related to five factors are separately projected to high-dimensional spaces, followed by that their internal dynamics can be embodied through a 2-D recurrence representation of states. Finally, five RQA parameters are used to quantify the influence of these factors on the BFG output. This is the first attempt revealing the relations among the BFG data from the qualitative and quantitative perspectives. The experimental results show that RP can discover the BFG output patterns of laminar state, chaos, and instability over given three states of influencing factors, and the ranked influential degree can be given by a two-stage standard deviation of all considered RQA measures. Besides, we also demonstrate that the temperature of the hot-blast stove is most relevant to the BFG output, while the influence of considered other factors directly depends on the selected series length.

The objective of this study is to propose a definition of intraventricular hemorrhage (IVH) growth and to investigate whether IVH growth is associated with ICH expansion and functional outcome. We performed a prospective observational study of ICH patients between July 2011 and March 2017 in a tertiary hospital. Patients were included if they had a baseline CT scan within 6 h after onset of symptoms and a follow-up CT within 36 h. IVH growth was defined as either any newly occurring intraventricular bleeding on follow-up CT scan in patients without baseline IVH or an increase in IVH volume ≥ 1 mL on follow-up CT scan in patients with initial IVH. Poor outcome was defined as modified Rankin Scale score of 3–6 at 90 days. The association between IVH growth and functional outcome was assessed by using multivariable logistic regression analysis. IVH growth was observed in 59 (19.5%) of 303 patients. Patients with IVH growth had larger baseline hematoma volume, higher NIHSS score and lower GCS score than those without. Of 44 patients who had concurrent IVH growth and hematoma growth, 41 (93.2%) had poor functional outcome at 3-month follow-up. IVH growth (adjusted OR 4.15, 95% CI 1.31–13.20; P = 0.016) was an independent predictor of poor functional outcome (mRS 3–6) at 3 months in multivariable analysis. IVH growth is not uncommon and independently predicts poor outcome in ICH patients. It may serve as a promising therapeutic target for intervention.

Introduction Axonal injury results in long‐term neurological deficits in traumatic brain injury (TBI) patients. Apolipoprotein E (ApoE) has been reported to activate intracellular adaptor protein Disabled‐1 (Dab1) phosphorylation via its interaction with ApoE receptors. The Dab1 pathway acts as a regulator of axonal outgrowth and growth cone formation in the brain. Aims We hypothesized that ApoE may alleviate axonal injury and regulate axonal regeneration via the Dab1 pathway after TBI. Results In this study, we established a model of controlled cortical impact (CCI) to mimic TBI in vivo. Using diffusion tensor imaging to detect white matter integrity, we demonstrated that APOE‐deficient mice exhibited lower fractional anisotropy (FA) values than APOE+/+ mice at 28 days after injury. The expression levels of axonal regeneration and synapse plasticity biomarkers, including growth‐associated protein 43 (GAP43), postsynaptic density protein 95 (PSD‐95), and synaptophysin, were also lower in APOE‐deficient mice. In contrast, APOE deficiency exerted no effects on the levels of myelin basic protein (MBP) expression, oligodendrocyte number, or oligodendrocyte precursor cell number. Neurological severity score (NSS) and behavioral measurements in the rotarod, Morris water maze, and Y maze tests revealed that APOE deficiency caused worse neurological deficits in CCI mice. Furthermore, Dab1 activation downregulation by the ApoE receptor inhibitor receptor‐associated protein (RAP) or Dab1 shRNA lentivirus attenuated the beneficial effects of ApoE on FA values, GAP43, PSD‐95, and synaptophysin expression, and neurological function tests. Additionally, the effects of ApoE on axonal regeneration were further validated in vitro. In a mechanical scratch injury model of primary cultured neurons, recombinant ApoE protein treatment enhanced axonal outgrowth and growth cone formation in injured neurons; however, these effects were attenuated by Dab1 shRNA, consistent with the in vivo results. Conclusion Collectively, these data suggest that ApoE promotes axonal regeneration partially through the Dab1 pathway, thereby contributing to functional recovery following TBI.

Network traffic prediction is a great challenge due to complex statistical properties, generally covering the long-range correlations and self-similarity. To address this issue, this article applies an integrated neural computing model to predict network traffic, namely, enhanced echo-state restricted Boltzmann machine (eERBM). In structure, this model possesses the following functional components of feature learning, information compensation, input superposition, and supervised nonlinear approximation. It is motivated by the introduction of information theory in modeling the hybrid architecture of the echo state network and the restricted Boltzmann machine. This is the first attempt that eERBM is applied in network traffic prediction tasks of different origin and characteristics, considering TCP/IP packet and variable-bit-rate video. By performing a theoretical analysis, we show that eERBM achieves superior nonlinear approximation and robustness in comparison to the baseline methods, and effectively preserves the self-similarity of network traffic traces.

Emerging evidence shows immune-related long noncoding RNAs (ir-lncRNAs) perform critical roles in tumor progression and prognosis assessment. However, the identification of ir-lncRNAs and their clinical significance in human glioblastoma multiforme (GBM) remain largely unexplored. Here, a designed computational frame based on immune score was used to identify differentially expressed ir-lncRNAs (DEir-lncRNAs) from The Cancer Genome Atlas (TCGA) GBM program. The immune-related lncRNA signature (IRLncSig) composed of prognosis-related DEir-lncRNAs selected by Cox regression analysis and its clinical predictive values were verified, which was further validated by another dataset from the Gene Expression Omnibus database (GEO). Subsequently, the association between IRLncSig and immune cell infiltration, immune checkpoint inhibitor (ICI) biomarkers, O6-methylguanine-DNA methyltransferase (MGMT) gene expression, and biological function were also analyzed. After calculation, five prognosis-related ir-lncRNAs were included in the establishment of IRLncSig. The risk assessment based on IRLncSig indicated that the high-IRLncSig-score group was significantly associated with poor prognosis (p < 0.001), significant aggregation of macrophages (p < 0.05), higher ICI biomarker expression, and MGMT gene expression (p < 0.05). Signature-related lncRNAs may be involved in immune activities in the tumorigenesis and progression of GBM. In summary, the novel IRLncSig shows a promising clinical value in predicting the prognosis and immune landscape of GBM.

Background: Tanshione IIA (TSO IIA) has emerged as a powerful anti-inflammatory compound with multiple therapeutic properties. Here, we investigated the role of TSO IIA in astrocytic swelling caused by ischemia and reperfusion-like injury in an in vitro model and the molecular mechanisms underlying this effect. Methods: Primary brain astrocytes were cultured in vitro in conditions of glucose and oxygen deprivation and reoxygenation (OGD/R). We investigated the effects of TSO IIA treatment on cell swelling and injury, and the expression levels of AQP4 protein in the plasma membrane. We then studied the involvement of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis in TSO IIA-mediated protection. Results: Treatment with TSO IIA alleviated OGD/R-induced astrocytic swelling, changes in cell morphology and ultrastructure, the release of LDH, and the over-clustering of AQP4 protein in the plasma membrane. In addition, TSO-IIA significantly reduced over-expression of HMGB1 protein in the cytoplasm and surrounding medium, the high levels of NF-κB protein in the nucleus, and of IL-6 protein in cytoplasm and extracellular media induced by OGD/R. Combination of TSO IIA and recombinant HMGB1 (rHMGB1) reversed these effects. Inhibition of RAGE, the receptor of HMGB1, via administration of FPS-ZM1 (a RAGE antagonist) induced similar results to those of TSO IIA. In addition, exogenous IL-6 reversed TSO IIA-mediated effect on AQP4 protein clustering in the plasma membrane, cell swelling and LDH activity.Conclusions: TSO IIA significantly reduced astrocyte swelling after OGD/R injury in vitro, via blocking activation of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis and thereby decreasing the expression of AQP4 in plasma membrane.

This study aimed to investigate the role of tanshinone IIA (TSO IIA) in astrocytic swelling caused by ischemia–reperfusion-like injury in an in vitro model and the molecular mechanisms underlying this effect. Primary brain astrocytes were cultured under conditions of glucose and oxygen deprivation and reoxygenation (OGD/R). The study explored the effects of TSO IIA treatment on cell swelling and injury and the protein levels of aquaporin 4 (AQP4) in the plasma membrane. It then examined the involvement of the high-mobility group box protein 1 (HMGB1)/receptors for advanced-glycation end products (RAGE)/nuclear factor-kappa B (NF-κB)/interleukin-6 (IL-6) pro-inflammatory axis in TSO IIA-mediated protection. The treatment with TSO IIA alleviated OGD/R-induced astrocytic swelling and the overclustering of AQP4 protein in the plasma membrane. In addition, TSO IIA significantly reduced the overexpression of HMGB1 and the high levels of the NF-κB protein in the nucleus and of the IL-6 protein in the cytoplasm and extracellular media induced by OGD/R. The combination of TSO IIA and recombinant HMGB1 reversed these effects. The inhibition of the RAGE, the receptor of HMGB1, induced results similar to those of TSO IIA. In addition, exogenous IL-6 reversed TSO IIA-mediated effect on AQP4 overclustering and cell swelling. TSO IIA significantly reduced astrocyte swelling after OGD/R injury in vitro, via blocking the activation of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis and thereby decreasing the expression of AQP4 in the plasma membrane.

Background: Tanshione IIA (TSO IIA) has emerged as a powerful anti-inflammatory compound with multiple therapeutic properties. Here, we investigated the role of TSO IIA in astrocytic swelling caused by ischemia and reperfusion-like injury in an in vitro model and the molecular mechanisms underlying this effect. Methods: Primary brain astrocytes were cultured in vitro in conditions of glucose and oxygen deprivation and reoxygenation (OGD/R). We investigated the effects of TSO IIA treatment on cell swelling and injury, and the expression levels of AQP4 protein in the plasma membrane. We then studied the involvement of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis in TSO IIA-mediated protection. Results: Treatment with TSO IIA alleviated OGD/R-induced astrocytic swelling, changes in cell morphology and ultrastructure, the release of LDH, and the over-clustering of AQP4 protein in the plasma membrane. In addition, TSO-IIA significantly reduced over-expression of HMGB1 protein in the cytoplasm and surrounding medium, the high levels of NF-κB protein in the nucleus, and of IL-6 protein in cytoplasm and extracellular media induced by OGD/R. Combination of TSO IIA and recombinant HMGB1 (rHMGB1) reversed these effects. Inhibition of RAGE, the receptor of HMGB1, via administration of FPS-ZM1 (a RAGE antagonist) induced similar results to those of TSO IIA. The combination of HMGB1 and FPS-ZM1 did not alter the effects mediated by FPS-ZM1 alone. In addition, exogenous IL-6 reversed TSO IIA-mediated effect on AQP4 protein clustering in the plasma membrane, cell swelling and LDH activity.Conclusions: TSO IIA significantly reduced astrocyte swelling after OGD/R injury in vitro, via blocking activation of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis and thereby decreasing the expression of AQP4 in plasma membrane.

The main purpose of the study was to explore a reliable way to automatically handle emergency cases, such as intracerebral hemorrhage (ICH). Therefore, an artificial intelligence (AI) system, named, H-system, was designed to automatically recognize medical text data of ICH patients and output the treatment plan. Furthermore, the efficiency and reliability of the H-system were tested and analyzed. The H-system, which is mainly based on a pretrained language model Bidirectional Encoder Representations from Transformers (BERT) and an expert module for logical judgment of extracted entities, was designed and founded by the neurosurgeon and AI experts together. All emergency medical text data were from the neurosurgery emergency electronic medical record database (N-eEMRD) of the First Affiliated Hospital of Chongqing Medical University, Chongqing Emergency Medical Center, and Chongqing First People’s Hospital, and the treatment plans of these ICH cases were divided into two types. A total of 1,000 simulated ICH cases were randomly selected as training and validation sets. After training and validating on simulated cases, real cases from three medical centers were provided to test the efficiency of the H-system. Doctors with 1 and 5 years of working experience in neurosurgery (Doctor-1Y and Doctor-5Y) were included to compare with H-system. Furthermore, the data of the H-system, for instance, sensitivity, specificity, accuracy, positive predictive value (PPV), negative predictive value (NPV), and the area under the receiver operating characteristics curve (AUC), were calculated and compared with Doctor-1Y and Doctor-5Y. In the testing set, the time H-system spent on ICH cases was significantly shorter than that of doctors with Doctor-1Y and Doctor-5Y. In the testing set, the accuracy of the H-system’s treatment plan was 88.55 (88.16–88.94)%, the specificity was 85.71 (84.99–86.43)%, and the sensitivity was 91.83 (91.01–92.65)%. The AUC value of the H-system in the testing set was 0.887 (0.884–0.891). Furthermore, the time H-system spent on ICH cases was significantly shorter than that of doctors with Doctor-1Y and Doctor-5Y. The accuracy and AUC of the H-system were significantly higher than that of Doctor-1Y. In addition, the accuracy of the H-system was more closed to that of Doctor-5Y. The H-system designed in the study can automatically recognize and analyze medical text data of patients with ICH and rapidly output accurate treatment plans with high efficiency. It may provide a reliable and novel way to automatically and rapidly handle emergency cases, such as ICH.

Background: Tanshione IIA (TSO IIA) has emerged as a powerful anti-inflammatory compound with multiple therapeutic properties. Here, we investigated the role of TSO IIA in astrocytic swelling caused by ischemia and reperfusion-like injury in an in vitro model and the molecular mechanisms underlying this effect. Methods: Primary brain astrocytes were cultured in vitro in conditions of glucose and oxygen deprivation and reoxygenation (OGD/R). We investigated the effects of TSO IIA treatment on cell swelling and injury, and the expression levels of AQP4 protein in the plasma membrane. We then studied the involvement of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis in TSO IIA-mediated protection. Results: Treatment with TSO IIA alleviated OGD/R-induced astrocytic swelling, changes in cell morphology and ultrastructure, the release of LDH, and the over-clustering of AQP4 protein in the plasma membrane. In addition, TSO-IIA significantly reduced over-expression of HMGB1 protein in the cytoplasm and surrounding medium, the high levels of NF-κB protein in the nucleus, and of IL-6 protein in cytoplasm and extracellular media induced by OGD/R. Combination of TSO IIA and recombinant HMGB1 (rHMGB1) reversed these effects. Inhibition of RAGE, the receptor of HMGB1, via administration of FPS-ZM1 (a RAGE antagonist) induced similar results to those of TSO IIA. The combination of HMGB1 and FPS-ZM1 did not alter the effects mediated by FPS-ZM1 alone. In addition, exogenous IL-6 reversed TSO IIA-mediated effect on AQP4 protein clustering in the plasma membrane, cell swelling and LDH activity.Conclusions: TSO IIA significantly reduced astrocyte swelling after OGD/R injury in vitro, via blocking activation of the HMGB1/RAGE/NF-κB/IL-6 pro-inflammatory axis and thereby decreasing the expression of AQP4 in plasma membrane.

Subarachnoid hemorrhage (SAH) is a devastating cerebral vascular disease which causes neurological deficits including long-term cognitive deficit. Demyelination of white matter is correlated with cognitive deficit in SAH. Electroacupuncture (EA) is a traditional Chinese medical treatment which protects against cognitive deficit in varies of neurological diseases. However, whether EA exerts protective effect on cognitive function in SAH has not been investigated. The underlying mechanism of remyelination regulated by EA remains unclear. This study aimed to investigate the protective effects of EA on cognitive deficit in a rat model of SAH. SAH was induced in SD rats (n = 72) by endovascular perforation. Rats in EA group received EA treatment (10 min per day) under isoflurane anesthesia after SAH. Rats in SAH and sham groups received the same isoflurane anesthesia with no treatment. The mortality rate, neurological score, cognitive function, cerebral blood flow (CBF), and remyelination in sham, SAH and EA groups were assessed at 21 d after SAH.EA treatment alleviated cognitive deficits and myelin injury of rats compared with that in SAH group. Moreover, EA treatment enhanced remyelination in white matter and promoted the differentiation of OPCs after SAH. EA treatment inhibited the expression of Id2 and promoted the expression of SOX10 in oligodendrocyte cells. Additionally, the cerebral blood flow (CBF) of rats was increased by EA compared with that in SAH group. EA treatment exerts protective effect against cognitive deficit in the late phase of SAH. The underlying mechanisms involve promoting oligodendrocyte progenitor cell (OPC) differentiation and remyelination in white matter via regulating the expression of Id2 and SOX10. The improvement of CBF may also account for the protective effect of EA on cognitive function. EA treatment is a potential therapy for the treatment of cognitive deficit after SAH.

Most patients with subarachnoid hemorrhage (SAH) do not exhibit brain parenchymal injury upon imaging but present significant blood-brain barrier (BBB) disruption and secondary neurological deficits. The aim of this study was to investigate whether stressed astrocytes act as a secondary barrier to exert a protective effect after SAH and to investigate the mechanism of glial limitan formation.A total of 204 adult male C57BL/6 mice and an endovascular perforation SAH model were employed. The spatiotemporal characteristics of glial limitan formation after SAH were determined by immunofluorescence staining and transmission electron microscopy. The molecular mechanisms by which pericytes regulate glia limitans formation were analyzed using polymerase chain reaction, Western blotting, immunofluorescence staining and ELISA in a pericyte-astrocyte contact coculture system. The findings were validated ex vivo and in vivo using lentiviruses and inhibitors. Finally, pericytes were targeted to regulate glial limitan formation, and the effect of the glia limitans on secondary brain injury after SAH was evaluated by flow cytometry and analysis of neurological function.Stress-induced glial limitan formation occurred 1 day after SAH and markedly subsided 3 days after ictus. Pericytes regulated astrocyte glia limitan formation via EphA4/EphrinB2 signaling, inhibited inflammatory cell infiltration and altered neurological function.Astrocyte-derived glia limitans serve as a secondary protective barrier following BBB disruption after SAH in mice, and pericytes can regulate glial limitan formation and alter neurological function via EphA4/EphrinB2 signaling. Strategies for maintaining this secondary protective barrier may be novel treatment approaches for alleviating early brain injury after SAH.

Aquaporins (AQPs) constitute a highly diverse family of channel proteins that transport water and neutral solutes.