Differential reinforcement of cGAS-STING pathway-involved immunotherapy by biomineralized bacterial outer membrane-sensitized EBRT and RNT.

Radiotherapy (RT), including external beam radiation therapy (EBRT) and radionuclide therapy (RNT), realizes physical killing of local tumors and activates systemic anti-tumor immunity. However, these effects need to be further strengthened and the difference between EBRT and RNT should be discovered. Herein, bacterial outer membrane (OM) was biomineralized with manganese oxide (MnO2) to obtain OM@MnO2-PEG nanoparticles for enhanced radio-immunotherapy via amplifying EBRT/RNT-induced immunogenic cell death (ICD) and cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) activation. OM@MnO2-PEG can react with H2O2 and then gradually produce O2, Mn2+ and OM fragments in the tumor microenvironment. The relieved tumor hypoxia improves the radio-sensitivity of tumor cells, resulting in enhanced ICD and DNA damage. Mn2+ together with the DNA fragments in the cytoplasm activate the cGAS-STING pathway, further exhibiting a positive role in various aspects of innate immunity and adaptive immunity. Besides, OM fragments promote tumor antigen presentation and anti-tumor macrophages polarization. More importantly, our study reveals that OM@MnO2-PEG-mediated RNT triggers much stronger cGAS-STING pathway-involved immunotherapy than that of EBRT, owing to the duration difference of RT. Therefore, this study develops a powerful sensitizer of radio-immunotherapy and uncovers some differences between EBRT and RNT in the activation of cGAS-STING pathway-related anti-tumor immunity.

Hierarchical mixed-model expedites genome-wide longitudinal association analysis.

A hierarchical random regression model (Hi-RRM) was extended into a genome-wide association analysis for longitudinal data, which significantly reduced the dimensionality of repeated measurements. The Hi-RRM first modeled the phenotypic trajectory of each individual using a RRM and then associated phenotypic regressions with genetic markers using a multivariate mixed model (mvLMM). By spectral decomposition of genomic relationship and regression covariance matrices, the mvLMM was transformed into a multiple linear regression, which improved computing efficiency while implementing mvLMM associations in efficient mixed-model association expedited (EMMAX). Compared with the existing RRM-based association analyses, the statistical utility of Hi-RRM was demonstrated by simulation experiments. The method proposed here was also applied to find the quantitative trait nucleotides controlling the growth pattern of egg weights in poultry data.

Study on the correlation between B vitamins and breast cancer.

BACKGROUND: Relevant studies suggest that serum vitamin level is related to the risk of breast cancer, and dietary pattern and drug supplementation can significantly affect the level of vitamin in the body. Therefore, intervention of vitamin level in the body is expected to be a potential strategy to reduce the risk of breast cancer. However, the current epidemiological findings of serum vitamin levels and breast cancer risk are inconsistent, and the relationship between serum vitamin and breast cancer is still controversial. In this study, we compared the serum vitamin expression levels of healthy people, benign breast patients, and breast cancer patients, and evaluated the relationship between B vitamin levels and breast cancer risk. METHODS: The study used liquid chromatography-tandem mass spectrometry to determine the serum vitamin levels of 520 people who attended Yunnan Cancer Hospital from September 2020 to December 2020. After screening by exclusion criteria, 38 patients with benign breast diseases, 87 patients with breast cancer and 91 healthy controls were finally included. The kruskal-wallis H test was used to compare the differences in serum vitamin levels of subjects. Χ2 test was used to evaluate the relationship between B vitamin level and age,BMI,TNM staging,Ki-67,Her-2,surgery and chemotherapy, and other baseline characteristics and through binary logistic regression analysis, calculating odds ratio and 95% confidence interval (CI) to evaluate the relationship between B vitamins and breast cancer risk. CONCLUSION: The levels of VitB1 and VitB5 in the serum of breast cancer patients and patients with benign breast diseases were higher than those in the healthy control group, while the expression levels of VitB3 in breast cancer patients were lower than those in the healthy control group and the breast benign disease groups. The level of VitB1 was positively correlated with breast cancer risk. The VitB3 level was negatively correlated with breast cancer risk. The VitB5 level is not significantly related to the risk of breast cancer.

Canonical transformation for multivariate mixed model association analyses.

KEY MESSAGE: In extension of Single-RunKing to analyze multiple correlated traits, mvRunKing not only enlarged number of the analyzed phenotypes with canonical transformation, but also improved statistical power to detect pleiotropic QTNs through joint association analysis. Based on genomic variance-covariance matrices, we simplified multivariate mixed model association analysis to multiple univariate ones by using canonical transformation, and then individually implemented univariate association tests in the Single-RunKing. which enlarged number of the analyzed phenotypes. With canonical transformation back to the original scale, the association results would be biologically interpretable. Especially, we rapidly estimated genomic variance-covariance matrices with multivariate GEMMA and optimized separately the polygenic variances (or heritabilities) for only the markers that had large effects or higher significance levels in univariate mixed models, greatly improving computing efficiency for multiple univariate association tests. Beyond one test at once, joint association analysis for quantitative trait nucleotide (QTN) candidates can significantly increase statistical powers to detect QTNs. A user-friendly mvRunKing software was developed to efficiently implement multivariate mixed model association analyses.

Exclusion of alternative exon 33 of CaV1.2 calcium channels in heart is proarrhythmogenic.

Alternative splicing changes the CaV1.2 calcium channel electrophysiological property, but the in vivo significance of such altered channel function is lacking. Structure-function studies of heterologously expressed CaV1.2 channels could not recapitulate channel function in the native milieu of the cardiomyocyte. To address this gap in knowledge, we investigated the role of alternative exon 33 of the CaV1.2 calcium channel in heart function. Exclusion of exon 33 in CaV1.2 channels has been reported to shift the activation potential -10.4 mV to the hyperpolarized direction, and increased expression of CaV1.2Δ33 channels was observed in rat myocardial infarcted hearts. However, how a change in CaV1.2 channel electrophysiological property, due to alternative splicing, might affect cardiac function in vivo is unknown. To address these questions, we generated mCacna1c exon 33-/--null mice. These mice contained CaV1.2Δ33 channels with a gain-of-function that included conduction of larger currents that reflects a shift in voltage dependence and a modest increase in single-channel open probability. This altered channel property underscored the development of ventricular arrhythmia, which is reflected in significantly more deaths of exon 33-/- mice from ß-adrenergic stimulation. In vivo telemetric recordings also confirmed increased frequencies in premature ventricular contractions, tachycardia, and lengthened QT interval. Taken together, the significant decrease or absence of exon 33-containing CaV1.2 channels is potentially proarrhythmic in the heart. Of clinical relevance, human ischemic and dilated cardiomyopathy hearts showed increased inclusion of exon 33. However, the possible role that inclusion of exon 33 in CaV1.2 channels may play in the pathogenesis of human heart failure remains unclear.

Irisin alleviates pressure overload-induced cardiac hypertrophy by inducing protective autophagy via mTOR-independent activation of the AMPK-ULK1 pathway.

In hypertrophic hearts, autophagic flux insufficiency is recognized as a key pathology leading to maladaptive cardiac remodeling and heart failure. This study aimed to illuminate the cardioprotective role and mechanisms of a new myokine and adipokine, irisin, in cardiac hypertrophy and remodeling. Adult male wild-type, mouse-FNDC5 (irisin-precursor)-knockout and FNDC5 transgenic mice received 4 weeks of transverse aortic constriction (TAC) alone or combined with intraperitoneal injection of chloroquine diphosphate (CQ). Endogenous FNDC5 ablation aggravated and exogenous FNDC5 overexpression attenuated the TAC-induced hypertrophic damage in the heart, which was comparable to the protection of irisin against cardiomyocyte hypertrophy induced by angiotensin II (Ang II) or phenylephrine (PE). Accumulated autophagosome and impaired autophagy flux occurred in the TAC-treated myocardium and Ang II- or PE-insulted cardiomyocytes. Irisin deficiency caused reduced autophagy and aggravated autophagy flux failure, whereas irisin overexpression or supplementation induced protective autophagy and improved autophagy flux, which were reversed by autophagy inhibitors Atg5 siRNA, 3-MA and CQ. Irisin boosted the activity of only AMPK but not Akt and MAPK family members in hypertrophic hearts and cultured cardiomyocytes and further activated ULK1 at Ser555 but not Ser757 and did not affect the mTOR-S6K axis. Blockage of AMPK and ULK1 with compund C and SBI-0206965, respectively, both abrogated irisin's protection against cardiomyocyte hypertrophic injury and reversed its induction of both autophagy and autophagy flux. Our results suggest that irisin protects against pressure overload-induced cardiac hypertrophy by inducing protective autophagy and autophagy flux via activating AMPK-ULK1 signaling.

Structural and functional conservation of half-smooth tongue sole Cynoglossus semilaevis RIP3 in cell death signalling.

Receptor interacting protein kinase 3 (RIP3) has emerged as an essential molecular regulator in human inflammation with accumulating evidence in vertebrates. However, the structure and functions of RIP3 in teleosts remains elusive. Here we identified one RIP3 homologue from half-smooth tongue sole Cynoglossus semilaevis, designated CsRIP3. The open reading frame (ORF) of CsRIP3 contained 1491 nucleotides and encoded a protein with 496 amino acids (Mw = 55.44 kDa). CsRIP3 expression was detected in various tissues in half-smooth tongue soles. CsRIP3 expression was up-regulated after pathogens i.e. Vibrio and poly (i:c) treatment in vivo, indicating its possible role in teleost immune response. Further analysis using human cells demonstrated that CsRIP3 exhibited highly conserved pro-apoptotic and pro-necroptotic functions in comparison with human RIP3. In conclusion, for the first time we reported the homologous structure and functions of CsRIP3 in inflammatory cell death, which provides novel perspectives on fish immunity studies in future.

SIRT6 protects cardiomyocytes against ischemia/reperfusion injury by augmenting FoxO3α-dependent antioxidant defense mechanisms.

SIRT6, a member of the NAD(+)-dependent class III deacetylase sirtuin family, has been revealed to play important roles in promoting cellular resistance against oxidative stress. The formation of reactive oxygen species (ROS) and oxidative stress are the crucial mechanisms underlying cellular damage and dysfunction in cardiac ischemia/reperfusion (I/R) injury, but the role of SIRT6 in I/R-induced ROS and oxidative stress is poorly understood. In this study, by using heterozygous SIRT6 knockout (SIRT6(+/-)) mice and cultured neonatal cardiomyocyte models, we investigated how SIRT6 mediates oxidative stress and myocardial injury during I/R. Partial knockout (KO) of SIRT6 aggravated myocardial damage, ventricular remodeling, and oxidative stress in mice subjected to myocardial I/R, whereas restoration of SIRT6 expression by direct cardiac injection of adenoviral constructs encoding SIRT6 reversed these deleterious effects of SIRT6 KO in the ischemic heart. In addition, partial deletion of the SIRT6 gene decreased myocardial functional recovery following I/R in a Langendorff perfusion model. Similarly, the protective effects of SIRT6 were also observed in cultured cardiomyocytes following hypoxia/reoxygenation. Intriguingly, SIRT6 was noticed to up-regulate AMP/ATP and then activate the adenosine 5'-monophosphate-activated protein kinase (AMPK)-forkhead box O3α (FoxO3α) axis and further initiated the downstream antioxidant-encoding gene expression (manganese superoxide dismutase and catalase), thereby decreasing cellular levels of oxidative stress and mediating cardioprotection in the ischemic heart. These results suggest that SIRT6 protects the heart from I/R injury through FoxO3α activation in the ischemic heart in an AMP/ATP-induced AMPK-dependent way, thus upregulating antioxidants and suppressing oxidative stress.

Association between homotopic connectivity and clinical symptoms in first-episode schizophrenia.

Background: Abnormal functional connectivity (FC) in the brain has been observed in schizophrenia patients. However, studies on FC between homotopic brain regions are limited, and the results of these studies are inconsistent. The aim of this study was to compare homotopic connectivity between first-episode schizophrenia (FES) patients and healthy subjects and assess its correlation with clinical symptoms. Methods: Thirty-one FES patients and thirty-three healthy controls (HC) were included in the study. The voxel-mirrored homotopic connectivity (VMHC) method of resting-state functional magnetic resonance imaging (rs-fMRI) was used to analyse the changes in homotopic connectivity between the two groups. The 5-factor PANSS model was used to quantitatively evaluate the severity of symptoms in FES patients. Partial correlation analysis was used to assess the correlation between homotopic connectivity changes and clinical symptoms. Results: Compared to those in the HC group, VMHC values were decreased in the paracentral lobule (PL), thalamus, and superior temporal gyrus (STG) in the FES group (P < 0.05, FDR correction). No significant differences in white matter volume (WMV) within the subregion of the corpus callosum or in brain regions associated with reduced VMHC were observed between the two groups. Partial correlation analyses revealed that VMHC in the bilateral STG of FES patients was positively correlated with negative symptoms (rleft = 0.46, p < 0.05; rright = 0.47, p < 0.05), and VMHC in the right thalamus was negatively correlated with disorganized/concrete symptoms (rright = 0.45, p < 0.05). Conclusion: Our study revealed that homotopic connectivity is altered in the resting-state brain of FES patients and correlates with the severity of negative symptoms; this change may be independent of structural changes in white matter. These findings may contribute to the development of the abnormal connectivity hypothesis in schizophrenia patients.

Attention Spiking Neural Networks.

Brain-inspired spiking neural networks (SNNs) are becoming a promising energy-efficient alternative to traditional artificial neural networks (ANNs). However, the performance gap between SNNs and ANNs has been a significant hindrance to deploying SNNs ubiquitously. To leverage the full potential of SNNs, in this paper we study the attention mechanisms, which can help human focus on important information. We present our idea of attention in SNNs with a multi-dimensional attention module, which infers attention weights along the temporal, channel, as well as spatial dimension separately or simultaneously. Based on the existing neuroscience theories, we exploit the attention weights to optimize membrane potentials, which in turn regulate the spiking response. Extensive experimental results on event-based action recognition and image classification datasets demonstrate that attention facilitates vanilla SNNs to achieve sparser spiking firing, better performance, and energy efficiency concurrently. In particular, we achieve top-1 accuracy of 75.92% and 77.08% on ImageNet-1 K with single/4-step Res-SNN-104, which are state-of-the-art results in SNNs. Compared with counterpart Res-ANN-104, the performance gap becomes -0.95/+0.21 percent and the energy efficiency is 31.8×/7.4×. To analyze the effectiveness of attention SNNs, we theoretically prove that the spiking degradation or the gradient vanishing, which usually holds in general SNNs, can be resolved by introducing the block dynamical isometry theory. We also analyze the efficiency of attention SNNs based on our proposed spiking response visualization method. Our work lights up SNN's potential as a general backbone to support various applications in the field of SNN research, with a great balance between effectiveness and energy efficiency.

Sparser spiking activity can be better: Feature Refine-and-Mask spiking neural network for event-based visual recognition.

Event-based visual, a new visual paradigm with bio-inspired dynamic perception and µs level temporal resolution, has prominent advantages in many specific visual scenarios and gained much research interest. Spiking neural network (SNN) is naturally suitable for dealing with event streams due to its temporal information processing capability and event-driven nature. However, existing works SNN neglect the fact that the input event streams are spatially sparse and temporally non-uniform, and just treat these variant inputs equally. This situation interferes with the effectiveness and efficiency of existing SNNs. In this paper, we propose the feature Refine-and-Mask SNN (RM-SNN), which has the ability of self-adaption to regulate the spiking response in a data-dependent way. We use the Refine-and-Mask (RM) module to refine all features and mask the unimportant features to optimize the membrane potential of spiking neurons, which in turn drops the spiking activity. Inspired by the fact that not all events in spatio-temporal streams are task-relevant, we execute the RM module in both temporal and channel dimensions. Extensive experiments on seven event-based benchmarks, DVS128 Gesture, DVS128 Gait, CIFAR10-DVS, N-Caltech101, DailyAction-DVS, UCF101-DVS, and HMDB51-DVS demonstrate that under the multi-scale constraints of input time window, RM-SNN can significantly reduce the network average spiking activity rate while improving the task performance. In addition, by visualizing spiking responses, we analyze why sparser spiking activity can be better. Code.

A Co-driven Functional Electrical Stimulation Control Strategy by Dynamic Surface Electromyography and Joint Angle.

Functional electrical stimulation (FES) is widely used in neurorehabilitation to improve patients' motion ability. It has been verified to promote neural remodeling and relearning, during which FES has to produce an accurate movement to obtain a good efficacy. Therefore, many studies have focused on the relationship between FES parameters and the generated movements. However, most of the relationships have been established in static contractions, which leads to an unsatisfactory result when applied to dynamic conditions. Therefore, this study proposed a FES control strategy based on the surface electromyography (sEMG) and kinematic information during dynamic contractions. The pulse width (PW) of FES was determined by a direct transfer function (DTF) with sEMG features and joint angles as the input. The DTF was established by combing the polynomial transfer functions of sEMG and joint torque and the polynomial transfer functions of joint torque and FES. Moreover, the PW of two FES channels was set based on the muscle synergy ratio obtained through sEMG. A total of six healthy right-handed subjects were recruited in this experiment to verify the validity of the strategy. The PW of FES applied to the left arm was evaluated based on the sEMG of the right extensor carpi radialis (ECR) and the right wrist angle. The coefficient of determination (R 2) and the normalized root mean square error (NRMSE) of FES-included and voluntary wrist angles and torques were used to verify the performance of the strategy. The result showed that this study achieved a high accuracy (R 2 = 0.965 and NRMSE = 0.047) of joint angle and a good accuracy (R 2 = 0.701 and NRMSE = 0.241) of joint torque reproduction during dynamic movements. Moreover, the DTF in real-time FES system also had a nice performance of joint angle fitting (R 2 = 0.940 and NRMSE = 0.071) and joint torque fitting (R 2 = 0.607 and NRMSE = 0.303). It is concluded that the proposed strategy is able to generate proper FES parameters based on sEMG and kinematic information for dynamic movement reproduction and can be used in a real-time FES system combined with bilateral movements for better rehabilitation.

Passive Non-Line-of-Sight Imaging Using Optimal Transport.

Passive non-line-of-sight (NLOS) imaging has drawn great attention in recent years. However, all existing methods are in common limited to simple hidden scenes, low-quality reconstruction, and small-scale datasets. In this paper, we propose NLOS-OT, a novel passive NLOS imaging framework based on manifold embedding and optimal transport, to reconstruct high-quality complicated hidden scenes. NLOS-OT converts the high-dimensional reconstruction task to a low-dimensional manifold mapping through optimal transport, alleviating the ill-posedness in passive NLOS imaging. Besides, we create the first large-scale passive NLOS imaging dataset, NLOS-Passive, which includes 50 groups and more than 3,200,000 images. NLOS-Passive collects target images with different distributions and their corresponding observed projections under various conditions, which can be used to evaluate the performance of passive NLOS imaging algorithms. It is shown that the proposed NLOS-OT framework achieves much better performance than the state-of-the-art methods on NLOS-Passive. We believe that the NLOS-OT framework together with the NLOS-Passive dataset is a big step and can inspire many ideas towards the development of learning-based passive NLOS imaging. Codes and dataset are publicly available (https://github.com/ruixv/NLOS-OT).

The study of correlation between nomogram prediction of uric acid and different chemotherapy regimens in breast cancer patients.

Background: High levels of serum uric acid (SUA) are associated with a poor survival rate of breast cancer. Meanwhile, a sharp increase in SUA after chemotherapy may lead to tumor lysis syndrome (TLS). We created and validated a nomogram to help doctors better manage the patient's SUA level ahead of time in this study. Methods: From July 2012 to June 2021, 206 patients with breast cancer undergoing chemotherapy participated in the study. They are randomly divided into training set (n=137) and validation set (n=69). Univariate and multivariate logistic regression analysis was used to screen the independent predictors of the risk of elevated uric acid in the whole training set data. The receiver operating characteristic (ROC) curve and decision curve assessed the accuracy and clinical application value of nomogram. Results: We confirmed that body mass index (BMI), age, menopause, EC-T chemotherapy (epirubicin-cyclophosphamide followed by paclitaxel) and THP + C-T (pirarubicin-cyclophosphamide followed by paclitaxel) are independent risk factors for high SUA. We established a nomogram for high SUA risk prediction to help clinicians make individualized choice of chemotherapy regimen. In the training cohort, the area under the ROC curve (AUC) showed statistical accuracy (AUC =0.796). Decision curve analysis proved the clinical value of the nomogram. Conclusions: This nomogram can be used to calculate the specific likelihood of high SUA in patients with breast cancer undergoing chemotherapy with different chemotherapy options.

Prim-O-glucosycimifugin attenuates liver injury in septic mice by inhibiting NLRP3 inflammasome/caspase-1 signaling cascades in macrophages.

BACKGROUND: Liver dysfunction and liver failure are serious complications of sepsis, directly leading to septic progression and death. Now, there is no specific therapeutics available for sepsis-related liver dysfunction. Prim-O-glucosylcimifugin (POG), a chromone richest in the roots of Saposhnikovia divaricata (Turcz.) Schischk, is usually used to treat headache, rheumatoid arthritis and tetanus. While, the underlying mechanisms of POG against sepsis-induced liver damage and dysfunction are still not clear. PURPOSE: To study the anti-sepsis effect of POG, and its pharmacological mechanism to protect liver injury by weakening the function of macrophages in septic livers through inhibiting NOD-like receptor protein 3 (NLRP3) inflammasome pathway. METHOD: In vivo experiments, septic mouse model was induced by cecal ligation and puncture (CLP), and then the mortality was detected, liver inflammatory damages and plasma biomarkers of liver injury were evaluated by histopathological staining and biochemical assays, respectively. In vitro experiments, mouse primary peritoneal macrophages were treated with lipopolysaccharide (LPS) and ATP, and then the activated-inflammasomes, macrophage migration and polarization were detected by ASC immunofluorescence staining, transwell and flow cytometry assays, respectively. NLRP3 inflammasome components NLRP3, caspase-1, IL-1ß and IL-18 protein expressions were detected using western blot assays, and the contents of IL-1ß and IL-18 were measured by ELISA assays. RESULTS: POG treatment significantly decreased the mortality, liver inflammatory damages, hepatocyte apoptosis and plasma biomarkers of liver injury in CLP-challenged male WT mice, which were comparable to those in ibuprofen (a putative anti-inflammatory drug)-supplemented septic male WT mice and septic NLRP3 deficient-male mice. POG supplementation significantly suppressed NLRP3 inflammasome activation in septic liver tissues and cultured macrophages, by significantly reducing NLRP3, cleaved-caspase-1, IL-1ß and IL-18 levels, the activated-inflammasome ASC specks, and macrophage infiltration and migration, as well as M1-like polarization, but significantly increasing M2-like polarization. These findings were similar to the pharmacological effects of ibuprofen, NLRP3 deficiency, and a special NLRP3 inhibitor, MCC950. CONCLUSION: POG protected against sepsis by inhibiting NLRP3 inflammasome-mediated macrophage activation in septic liver and attenuating liver inflammatory injury, indicating that it may be a potential anti-sepsis drug candidate.

SlimConv: Reducing Channel Redundancy in Convolutional Neural Networks by Features Recombining.

The channel redundancy of convolutional neural networks (CNNs) results in the large consumption of memories and computational resources. In this work, we design a novel Slim Convolution (SlimConv) module to boost the performance of CNNs by reducing channel redundancies. Our SlimConv consists of three main steps: Reconstruct, Transform, and Fuse. It aims to reorganize and fuse the learned features more efficiently, such that the method can compress the model effectively. Our SlimConv is a plug-and-play architectural unit that can be used to replace convolutional layers in CNNs directly. We validate the effectiveness of SlimConv by conducting comprehensive experiments on various leading benchmarks, such as ImageNet, MS COCO2014, Pascal VOC2012 segmentation, and Pascal VOC2007 detection datasets. The experiments show that SlimConv-equipped models can achieve better performances consistently, less consumption of memory and computation resources than non-equipped counterparts. For example, the ResNet-101 fitted with SlimConv achieves 77.84% top-1 classification accuracy with 4.87 GFLOPs and 27.96M parameters on ImageNet, which shows almost 0.5% better performance with about 3 GFLOPs and 38% parameters reduced.

Finite-temperature density-functional-theory investigation on the nonequilibrium transient warm-dense-matter state created by laser excitation.

We present a finite-temperature density-functional-theory investigation of the nonequilibrium transient electronic structure of warm dense Li, Al, Cu, and Au created by laser excitation. Photons excite electrons either from the inner shell orbitals or from the valence bands according to the photon energy, and give rise to isochoric heating of the sample. Localized states related to the 3d orbital are observed for Cu when the hole lies in the inner shell 3s orbital. The electrical conductivity for these materials at nonequilibrium states is calculated using the Kubo-Greenwood formula. The change of the electrical conductivity, compared to the equilibrium state, is different for the case of holes in inner shell orbitals or the valence band. This is attributed to the competition of two factors: the shift of the orbital energies due to reduced screening of core electrons, and the increase of chemical potential due to the excitation of electrons. The finite-temperature effect of both the electrons and the ions on the electrical conductivity is discussed in detail. This work is helpful to better understand the physics of laser excitation experiments of warm dense matter.

Intermedin Inhibits the Ox-LDL-Induced Inflammation in RAW264.7 Cells by Affecting Fatty Acid-Binding Protein 4 Through the PKA Pathway.

Objectives: Macrophages stimulated by oxidized low-density lipoprotein (ox-LDL) play an important role in the occurrence and progression of atherosclerosis. Fatty acid-binding protein 4 (FABP4), mainly existing in macrophages and adipocytes, can influence lipid metabolism and inflammation regulated by macrophages. Herein, we first established the connection between intermedin (IMD: a new peptide that has versatile biological activities in the cardiovascular system) and FABP4 and then investigated the influence of IMD on ox-LDL-induced changes in RAW264.7 macrophages line. Methods: The bioinformatics analysis, such as gene ontology enrichment and protein-protein interactions, was performed. For ox-LDL-stimulated assays, RAW264.7 was first pretreated with IMD and then exposed to ox-LDL. To explore the cell signaling pathways of IMD on inflammatory inhibition, main signaling molecules were tested and then cells were co-incubated with relevant inhibitors, and then exposed/not exposed to IMD. Finally, cells were treated with ox-LDL. The protein and gene expression of FABP4, IL-6, and TNF-α were quantified by WB/ELISA and RT-qPCR. Results: In the ox-LDL-stimulated assays, exposure of the RAW264.7 macrophages line to ox-LDL reduced cell viability and increased the expression of FABP4, as well as induced the release of IL-6 and TNF-α (all p < 0.05). On the other hand, IMD prevented ox-LDL-induced cell toxicity, FABP4 expression, and the inflammatory level in RAW264.7 (all p < 0.05) in a dose-dependent manner. The inhibition of FABP4 and the anti-inflammatory effect of IMD were partially suppressed by the protein kinase A (PKA) inhibitor H-89. Conclusion: IMD can prevent ox-LDL-induced macrophage inflammation by inhibiting FABP4, whose signaling might partially occur via the PKA pathway.

Phase Synchronization of EEG in Bilateral, Cyclical Ankle Alternating Movements of Stroke.

Electroencephalogram (EEG) is a basic physiological signal of human body, which can effectively record the nervous system activities of the brain and contains rich information. The synchronization of EEG signals is not only the key to the exchange of information between different brain regions, but also reflects the neural activity of the brain, which in turn can infer people's cognitive activities. Therefore, studying the phase synchronization of EEG signals after stroke is of great significance for understanding the communication and neuroplasticity of neurons after brain injury. In this paper, the changes of EEG phase synchronization in bilateral, cyclical ankle movements alternately after stroke were studied by Hilbert transform. Ten stroke patients and six healthy adults participated in the test. The results showed that the inter-hemisphere phase synchronization index (inter-PSI) and the global PSI of patients were significantly lower than that of the healthy subjects during the task. The PSI between Cz and the affected sensory cortex associated with lower limb movements was also significantly lower than that in the control group. There was a significant negative correlation between National Institutes of Health Stroke Scale (NIHSS) and cortical synchronization. The above results indicated that PSI under ankle alternating movements may be used as a new biomarker to evaluate the recovery of patients' brain neurons.

Correlation Between Poststroke Balance Function and Brain Symmetry Index in Sitting and Standing Postures.

Balance problems are the main sequelae of stroke, which increases the risk of falling. The assessment of balance ability can guide doctors to formulate rehabilitation plans, thereby reducing the risk of falls. Studies have reported the role of resting-state EEG during sitting in the motor assessment of the upper extremity and prognosis of stroke patients. However, the above research in the sitting posture lacks specificity in evaluating the balance ability of the lower limbs. Herein, this article investigated whether EEG was different in sitting and standing positions with different difficulty levels and validated the feasibility of EEG in assessing body balance ability. The resting-state EEG signals were collected from 11 stroke patients. The pairwise-derived brain symmetry index (pdBSI) was used to identify the differences in EEG-quantified interhemispheric cortical power asymmetry observable in healthy versus cortical and subcortical stroke patients by calculating the absolute value of the difference in power at each pair of electrodes. Subsequently, we computed the pdBSI over different frequency bands. Balance function was assessed using the BBS (Berg Balance Scale). Stroke survivors showed higher pdBSI (1-25 Hz) values in standing posture compared to sitting (p <0.05) and the pdBSI was significantly negatively correlated with BBS (r = -0.671, p =0.034). Additionally, the pdBSI within beta band was also significantly negatively correlated with BBS (r = -0.711, p=0.017). In conclusion, stroke brain asymmetry in standing posture was significantly more severe and the pdBSIs in 1-25Hz and beta hand were related to balance function. BBS and NIHSS was significantly negatively correlated (r = -0.701, p = 0.024), and NIHSS was significantly correlated with age (r = 0.822, p = 0.004). The present study suggests that stroke can seriously affect the body's balance ability. Compared with the sitting posture, the asymmetry of cortical energy in the standing posture can better assess the patient's balance ability.