Effect of vascular compression and drug injection time on thrombolytic therapy: Numerical simulation and validation.

Venous thromboembolism (VTE) has been occurring frequently in human society. There is an urgent need to study the influence of several factors on thrombolytic therapy, such as the effects of vascular pressure levels (VPL) and the drug injection time (DIT). Considering blood as a non-Newtonian fluid, valve as a hyperelastic material, and thrombus as a porous medium, a new numerical simulation model of biofluid mechanics incorporating fluid-solid coupling phenomena and biochemical substance reactions is established based on the N-S equations and the convection-diffusion reaction equations. Then, a unique in vitro experimental platform is established to verify the correctness of the constructed mathematical model. The results showed that vascular compression resulted in significant differences in blood flow status localized within the vessel. Vascular compression causes the blood boosting index to fluctuate and the valve displacement values are 135% and 158% greater than the lower VPL, respectively. At the same time, vascular compression weakened vortex intensity, accelerated material transport and response, and improved the treatment. Compared with low VPL, the therapeutic efficacy increased by 7% and 15%, respectively. In addition, when the dose of the drug is high, different injection times can increase the therapeutic effect to different degrees, with a maximum difference of 12%. Our in vitro experiments are similar to the results obtained by numerical simulation, which can verify the reliability of numerical simulation. The computational model proposed and the experimental platform designed in this study have the potential to assist in clinical medication prediction in different venous thromboembolism patients.

Light and classical music therapies attenuate chronic unpredictable mild stress-induced depression via BDNF signaling pathway in mice.

Depression, a pervasive mental health issue, often necessitates innovative therapeutic interventions. This study explores the efficacy of music therapy, a non-pharmacological approach, in ameliorating depression symptoms in a murine model. Employing a chronic unpredictable mild stress (CUMS) model to induce depressionlike behaviors in mice, we investigated the therapeutic potential of four distinct music genres: light, classical, atonal composition, and rock music. Behavioral assessments, including sucrose preference and immobility time, were conducted to evaluate the impact of music therapy. Additionally, we measured the levels of brain-derived neurotrophic factor (BDNF), synaptic proteins and neurogenesis to elucidate the underlying biological mechanisms. Our findings indicated that light and classical music significantly alleviated depression-like behaviors in mice, evidenced by increased sucrose preference and reduced immobility time. Conversely, atonal composition and rock music did not yield similar therapeutic benefits. Biochemically, light and classical music were associated with decreased levels of corticosterone and increased levels of glucocorticoid receptor, alongside enhanced BDNF signaling, synaptic proteins and neurogenesis. In conclusion, the study demonstrates that specific genres of music, notably light and classical music, may contribute to alleviating depression-like symptoms, potentially through mechanisms associated with BDNF signaling and neurogenesis. These results highlight the potential of targeted music therapy as a complementary approach in treating depression, with implications for its incorporation into broader therapeutic regimes. Further re-search is warranted to translate these findings into clinical practice.

Mycobacterium tuberculosis suppresses host antimicrobial peptides by dehydrogenating L-alanine.

Antimicrobial peptides (AMPs), ancient scavengers of bacteria, are very poorly induced in macrophages infected by Mycobacterium tuberculosis (M. tuberculosis), but the underlying mechanism remains unknown. Here, we report that L-alanine interacts with PRSS1 and unfreezes the inhibitory effect of PRSS1 on the activation of NF-κB pathway to induce the expression of AMPs, but mycobacterial alanine dehydrogenase (Ald) Rv2780 hydrolyzes L-alanine and reduces the level of L-alanine in macrophages, thereby suppressing the expression of AMPs to facilitate survival of mycobacteria. Mechanistically, PRSS1 associates with TAK1 and disruptes the formation of TAK1/TAB1 complex to inhibit TAK1-mediated activation of NF-κB pathway, but interaction of L-alanine with PRSS1, disables PRSS1-mediated impairment on TAK1/TAB1 complex formation, thereby triggering the activation of NF-κB pathway to induce expression of AMPs. Moreover, deletion of antimicrobial peptide gene ß-defensin 4 (Defb4) impairs the virulence by Rv2780 during infection in mice. Both L-alanine and the Rv2780 inhibitor, GWP-042, exhibits excellent inhibitory activity against M. tuberculosis infection in vivo. Our findings identify a previously unrecognized mechanism that M. tuberculosis uses its own alanine dehydrogenase to suppress host immunity, and provide insights relevant to the development of effective immunomodulators that target M. tuberculosis.

Mycobacterium tuberculosis produces D-serine under hypoxia to limit CD8+ T cell-dependent immunity in mice.

Adaptation to hypoxia is a major challenge for the survival of Mycobacterium tuberculosis (Mtb) in vivo. Interferon (IFN)-γ-producing CD8+ T cells contribute to control of Mtb infection, in part by promoting antimicrobial activities of macrophages. Whether Mtb counters these responses, particularly during hypoxic conditions, remains unknown. Using metabolomic, proteomic and genetic approaches, here we show that Mtb induced Rv0884c (SerC), an Mtb phosphoserine aminotransferase, to produce D-serine. This activity increased Mtb pathogenesis in mice but did not directly affect intramacrophage Mtb survival. Instead, D-serine inhibited IFN-γ production by CD8+ T cells, which indirectly reduced the ability of macrophages to restrict Mtb upon co-culture. Mechanistically, D-serine interacted with WDR24 and inhibited mTORC1 activation in CD8+ T cells. This decreased T-bet expression and reduced IFN-γ production by CD8+ T cells. Our findings suggest an Mtb evasion mechanism where pathogen metabolic adaptation to hypoxia leads to amino acid-dependent suppression of adaptive anti-TB immunity.

Development of a continuum manipulator with variable bending length and piecewise stiffness for transoral laryngeal surgery.

PURPOSE: Continuum manipulators (CMs) show great potential in transoral laryngeal surgery due to their flexibility. However, CMs for transoral surgery face several issues: large size, which reduces practicality; intersegment coupling, which causes undesired deflection; and a lack of versatility that limits their applicability across different patient groups. METHODS: This work combines a rod-driven proximal segment and a cable-driven distal segment to achieve piecewise stiffness, alleviating the issue of intersegment coupling. A rigid constraint tube is integrated into the proximal segment to diversify its bending behavior. Preliminary experiments are conducted to validate the design concept. RESULTS: The proposed CM has an overall diameter of only 6.5 mm. The proximal segment can achieve a 90° bending with various curvatures. At the working configuration, the coupling error between the proximal segment and the distal segment is less than 1 mm. The effectiveness of the proposed CM is successfully validated using a human model. CONCLUSION: The proposed continuum manipulator possesses the desirable characteristics of small size, low coupling, and high versatility, indicating its great potentialities for the diagnosis and treatment of laryngeal lesion.

Integrated bioinformatics analysis identifies autophagy-associated genes as candidate biomarkers and reveals the immune infiltration landscape in psoriasis.

Autophagy is implicated in the pathogenesis of psoriasis. We aimed to identify autophagy-related biomarkers in psoriasis via an integrated bioinformatics approach. We downloaded the gene expression profiles of GSE30999 dataset, and the "limma" package was applied to identify differentially expressed genes (DEGs). Then, differentially expressed autophagy-related genes (DEARGs) were identified via integrating autophagy-related genes with DEGs. CytoHubba plugin was used for the identification of hub genes and verified by the GSE41662 dataset. Subsequently, a series of bioinformatics analyses were employed, including protein-protein interaction network, functional enrichment, spearman correlation, receiver operating characteristic, and immune infiltration analyses. One hundred and one DEARGs were identified, and seven DEARGs were identified as hub genes and verified using the GSE41662 dataset. These validated genes had good diagnostic value in distinguishing psoriasis lesions. Immune infiltration analysis indicated that ATG5, SQSTM1, EGFR, MAPK8, MAPK3, MYC, and PIK3C3 were correlated with infiltration of immune cells. Seven DEARGs, namely ATG5, SQSTM1, EGFR, MAPK8, MAPK3, MYC, and PIK3C3, may be involved in the pathogenesis of psoriasis, which expanded the understanding of the development of psoriasis and provided important clinical significance for treatment of this disease.

Therapeutic Potential of Danyankang Capsule in High-Fat Diet-Induced Cholelithiasis and Its Impact on Liver FXR Signaling and Gut Microbiota.

Cholelithiasis, commonly known as gallstones, represents a prevalent hepatobiliary disorder. This study aimed to elucidate the therapeutic role and mechanism of Danyankang capsulein treating cholelithiasis induced by a high-fat diet in C57BL/6 mice. The therapeutical potential of Danyankang was assessed through biochemical analyses, histopathological examinations, protein detection, and 16S rDNA sequencing. A high-fat diet resulted in cholelithiasis manifestation in mice, with discernable abnormal serum biochemical indices and disrupted biliary cholesterol homeostasis. Danyankang treatment notably ameliorated liver inflammation symptoms and rectified serum and liver biochemical abnormalities. Concurrently, it addressed biliary imbalances. Elevated expressions of toll-like receptor 4 (TLR4), nuclear factor-kappaB (NF-κB)/pNF-κB, HMGCR, CYP7A1, and CYP8B1 observed at the inception of cholelithiasis, were notably reduced upon Danyankang administration. Furthermore, 16S rDNA analysis revealed a decline in species number and diversity of the intestinal flora in cholelithiasis-treated mice, while the decline was reversed with Danyankang treatment. Danyankang capsules reduced the abundance of Verrucomicrobiota and increased the abundance of Actinobacteriota and Proteobacteria. In conclusion, the present study demonstrates that Danyankang exerts potent therapeutic efficacy against high-fat diet-induced cholelithiasis. This beneficial outcome is potentially linked to the inhibition of the TLR4/pNF-κB and SHP/CYP7A1/CYP8B1 signaling pathways, as well as the enhancement of intestinal flora species abundance.

Mycobacterium tuberculosis inhibits METTL14-mediated m6A methylation of Nox2 mRNA and suppresses anti-TB immunity.

Internal N6-methyladenosine (m6A) modifications are among the most abundant modifications of messenger RNA, playing a critical role in diverse biological and pathological processes. However, the functional role and regulatory mechanism of m6A modifications in the immune response to Mycobacterium tuberculosis infection remains unknown. Here, we report that methyltransferase-like 14 (METTL14)-dependent m6A methylation of NAPDH oxidase 2 (Nox2) mRNA was crucial for the host immune defense against M. tuberculosis infection and that M. tuberculosis-secreted antigen EsxB (Rv3874) inhibited METTL14-dependent m6A methylation of Nox2 mRNA. Mechanistically, EsxB interacted with p38 MAP kinase and disrupted the association of TAB1 with p38, thus inhibiting the TAB1-mediated autophosphorylation of p38. Interaction of EsxB with p38 also impeded the binding of p38 with METTL14, thereby inhibiting the p38-mediated phosphorylation of METTL14 at Thr72. Inhibition of p38 by EsxB restrained liquid-liquid phase separation (LLPS) of METTL14 and its subsequent interaction with METTL3, preventing the m6A modification of Nox2 mRNA and its association with the m6A-binding protein IGF2BP1 to destabilize Nox2 mRNA, reduce ROS levels, and increase intracellular survival of M. tuberculosis. Moreover, deletion or mutation of the phosphorylation site on METTL14 impaired the inhibition of ROS level by EsxB and increased bacterial burden or histological damage in the lungs during infection in mice. These findings identify a previously unknown mechanism that M. tuberculosis employs to suppress host immunity, providing insights that may empower the development of effective immunomodulators that target M. tuberculosis.

An effective co-modification strategy to enhance the cycle stability of LiNi0.8Co0.1Mn0.1O2 for lithium-ion batteries.

Ni-rich cathode materials suffer from rapid capacity fading caused by interface side reactions and bulk structure degradation. Previous studies show that Co is conducive to bulk structure stability and sulfate can react with the residual lithium (LiOH and Li2CO3) on the surface of Ni-rich cathode materials and form a uniform coating to suppress the side reactions between the cathode and electrolyte. Here, CoSO4 is utilized as a modifier for LiNi0.8Co0.1Mn0.1O2 (NCM811) cathode materials. It reacts with the residual lithium on the surface of the NCM811 cathode to form Li-ion conductive Li2SO4 protective layers and Co doping simultaneously during the high-temperature sintering process, which can suppress the side reactions between the Ni-rich cathode and electrolyte and effectively prevent the structural transformation. As a result, the co-modified NCM811 cathode with 3 wt% CoSO4 exhibits an improved cycling performance of 81.1% capacity retention after 200 cycles at 1C and delivers an excellent rate performance at 5C of 187.4 mA h g-1, which is 10.2% higher than that of the pristine NCM811 cathode.

Mycobacterium tuberculosis suppresses host DNA repair to boost its intracellular survival.

Mycobacterium tuberculosis (Mtb) triggers distinct changes in macrophages, resulting in the formation of lipid droplets that serve as a nutrient source. We discover that Mtb promotes lipid droplets by inhibiting DNA repair responses, resulting in the activation of the type-I IFN pathway and scavenger receptor-A1 (SR-A1)-mediated lipid droplet formation. Bacterial urease C (UreC, Rv1850) inhibits host DNA repair by interacting with RuvB-like protein 2 (RUVBL2) and impeding the formation of the RUVBL1-RUVBL2-RAD51 DNA repair complex. The suppression of this repair pathway increases the abundance of micronuclei that trigger the cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway and subsequent interferon-ß (IFN-ß) production. UreC-mediated activation of the IFN-ß pathway upregulates the expression of SR-A1 to form lipid droplets that facilitate Mtb replication. UreC inhibition via a urease inhibitor impaired Mtb growth within macrophages and in vivo. Thus, our findings identify mechanisms by which Mtb triggers a cascade of cellular events that establish a nutrient-rich replicative niche.

Distinct seasonal variations of dissolved organic matter across two large freshwater lakes in China: Lability profiles and predictive modeling.

Biological lability of dissolved organic matter (DOM) is a crucial indicator of carbon cycle and contaminant attenuation in freshwater lakes. In this study, we employed a multi-stage plug-flow bioreactor and spectrofluorometric indices to characterize the seasonal variations in DOM composition and lability across Poyang Lake (PY) and Lake Taihu (TH), two large freshwater lakes in China with distinct hydrological seasonality. Our findings showed that the export of floodplain-derived organics and river-lake interaction led to a remarkable increase in terrestrial aromatic and humic-like DOM with high molecular weights and long turnover times in PY. Consequently, the labile fraction was extremely low (average LDOC% of 3%) during the rising-to-flood season (spring and summer). Conversely, autochthonous production in TH considerably enriched semi-labile (average SDOC% of 26%) and biodegradable DOM (average BDOC% of 34%) during the phytoplankton bloom to post-bloom season (summer and autumn). This was reflected by the accumulation of low-light-absorbing and protein-like components with high biological and fluorescence indices. In the dry and non-bloom season (winter), the better preservation of humic substances maintained the high molecular weight and humic degree of DOM in PY, while the decay of aquatic plants strengthened autochthonous production, resulting in a similar BDOC% of PY samples (23%-34%) to TH samples (18%-33%). We further applied partial least squares regression using DOM optical indices as predictive proxies, which generated a greater prediction strength for BDOC% (R2 = 0.80) compared to SDOC% (R2 = 0.57) and LDOC% (R2 = 0.28). The regression model identified aromaticity (SUVA254) as the most effective and negative predictor and low molecular weight (A250/A365) as the highly and positively influential factor. Our study provides new evidence that the seasonality of DOM lability profiles is regulated by the trade-off between flow-related variation and phytoplankton production, and presents an approach to describe and predict DOM lability across freshwater lakes.

Systematic Evaluation of the Viable Microbiome in the Human Oral and Gut Samples with Spike-in Gram+/- Bacteria.

PMA (propidium monoazide) is one of the few methods that are compatible with metagenomic sequencing to characterize the live/intact microbiota. However, its efficiency in complex communities such as saliva and feces is still controversial. An effective method for depleting host and dead bacterial DNA in human microbiome samples is lacking. Here, we systematically evaluate the efficiency of osmotic lysis and PMAxx treatment (lyPMAxx) in characterizing the viable microbiome with four live/dead Gram+/Gram- microbial strains in simple synthetic and spiked-in complex communities. We show that lyPMAxx-quantitative PCR (qPCR)/sequencing eliminated more than 95% of the host and heat-killed microbial DNA and had a much smaller effect on the live microbes in both simple mock and spiked-in complex communities. The overall microbial load and the alpha diversity of the salivary and fecal microbiome were decreased by lyPMAxx, and the relative abundances of the microbes were changed. The relative abundances of Actinobacteria, Fusobacteria, and Firmicutes in saliva were decreased by lyPMAxx, as was that of Firmicutes in feces. We also found that the frequently used sample storage method, freezing with glycerol, killed or injured 65% and 94% of the living microbial cells in saliva and feces, respectively, with the Proteobacteria phylum affected most in saliva and the Bacteroidetes and Firmicutes phyla affected most in feces. By comparing the absolute abundance variation of the shared species among different sample types and individuals, we found that sample habitat and personal differences affected the response of microbial species to lyPMAxx and freezing. IMPORTANCE The functions and phenotypes of microbial communities are largely defined by viable microbes. Through advanced nucleic acid sequencing technologies and downstream bioinformatic analyses, we gained an insight into the high-resolution microbial community composition of human saliva and feces, yet we know very little about whether such community DNA sequences represent viable microbes. PMA-qPCR was used to characterize the viable microbes in previous studies. However, its efficiency in complex communities such as saliva and feces is still controversial. By spiking-in four live/dead Gram+/Gram- bacterial strains, we demonstrate that lyPMAxx can effectively discriminate between live and dead microbes in the simple synthetic community and complex human microbial communities (saliva and feces). In addition, freezing storage was found to kill or injure the microbes in saliva and feces significantly, as measured with lyPMAxx-qPCR/sequencing. This method has a promising prospect in the viable/intact microbiota detection of complex human microbial communities.

Regulatory mechanism of Scutellaria baicalensis Georgi on bone cancer pain based on network pharmacology and experimental verification.

Context: Scutellaria baicalensis Georgi (SBG) may relieve bone cancer pain (BCP) by regulating cell proliferation, angiogenesis, and apoptosis. Objective: The mechanism of SBG in the treatment of BCP remains to be further explored. Methods: The active compounds and targets of SBG were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and SwissTargetPrediction databases. BCP-related targets were screened from NCBI and GeneCards databases. Additionally, Cytoscape software was applied to construct network diagrams, and OmicShare platform was used to enrich Gene Ontology (GO) and pathways. Finally, the verification of active compounds and core targets was performed based on quantitative real-time PCR (qRT-PCR). Results: Interestingly, we identified baicalein and wogonin as the main active components of SBG. A total of 41 SBG targets, including VEGFA, IL6, MAPK3, JUN and TNF, were obtained in the treatment of BCP. In addition, pathways in cancer may be an essential way of SBG in the treatment of BCP. Experimental verification had shown that baicalein and wogonin were significantly related to BCP core targets. Conclusions: The active components of SBG have been clarified, and the mechanism of the active components in treating BCP has been predicted and verified, which provides an experimental and theoretical basis for the in-depth elucidation of the pharmacodynamics material basis and mechanism of SBG.

Lagotis brachystachya maxim attenuates chronic alcoholic liver injury combined with gouty arthritis in rats via its anti-inflammatory activity.

Lagotis brachystachya Maxim, a common herb in Tibetan medicine, is mainly used to treat pneumonia, hepatitis, yellow water disease (gouty arthritis). Since long-term heavy drinking is also a risk factor for gouty arthritis, the present study aimed to evaluate the underlying protective role and mechanism of extracts of Lagotis brachystachya (ELB) in chronic alcoholic liver injury combined with gouty arthritis. The rat chronic alcoholic liver injury combined with gouty arthritis model was established by long-term alcohol consumption and monosodium urate (MSU) injection. The therapeutical action of ELB was then evaluated by biochemical measurement, histopathological examination, ankle swelling assessment, and protein detection. According to biochemical measurements and histopathological evaluation, ELB could alleviate the symptoms of alcoholic liver injury combined with gouty arthritis. In addition, chronic alcohol consumption and MSU activated inflammatory-related signaling such as TLR4/MyD88/NF-κB, NLRP3, and JAK2/STAT3 pathways in the liver and synovial tissues, while ELB significantly inhibited the activation of the inflammatory signaling pathway. In conclusion, ELB is protective in rats with chronic alcoholic liver injury and gouty arthritis, possibly mediated by the inhibition of TLR4/MyD88/NF-κB, NLRP3, and JAK2-STAT3 signaling pathways in both the hepatic and synovial tissues.

Transcriptome Sequencing Explores the Mechanism of Baicalin on Bone Cancer Pain.

INTRODUCTION: Bone cancer pain is characterized by persistent pain, usually requiring drugs to relieve pain. Baicalin, a flavonoid compound extracted from Scutellaria baicalensis, which has antioxidant and analgesic effects. But, the effect of baicalin on bone cancer pain is unclear. Thus, this study aimed to explore the mechanism of baicalin on SD rats with bone cancer pain. MATERIALS AND METHODS: The MADB-106 breast cancer cells-induced bone pain model was constructed and carried out baicalin treatment. The therapeutic effect of baicalin on bone cancer pain model was observed by hematoxylin-eosin staining and immunofluorescence staining. We also performed transcriptome sequencing analysis of baicalin in the treatment of bone metastases. Also, RT-qPCR and ELISA were used to detect the expression levels of inflammation factors. RESULTS: After baicalin treatment, osteoclast activation was inhibited and the number of bone trabeculae was increased. Baicalin inhibited the protein expression level of inflammatory factors (IL-1ß, IL-6, TNF-α and PGE2) in the bone metastases group. Based on the transcriptome sequencing of the bone metastases group and the baicalin treatment group, baicalin inhibited the expression of ALPP, DUSP1, CYR61, ALPPL2, SPP1 and TLR4. RT-qPCR was also used to validate the expression levels of these cytokine genes. CONCLUSION: Baicalin had a certain inhibitory effect on the SD rat model of bone metastasis cancer. These insights can guide future research on the molecular mechanism of bone cancer pain and provide a theoretical basis for baicalin in the treatment of bone pain caused by breast cancer in the future.

Active components from Lagotis brachystachya maintain uric acid homeostasis by inhibiting renal TLR4-NLRP3 signaling in hyperuricemic mice.

Lagotis brachystachya Maxim is a herb widely used in traditional Tibetan medicine. Our previous study indicated that total extracts from Lagotis brachystachya could lower uric acid levels. This study aimed to further elucidate the active components (luteolin, luteoloside and apigenin) isolated from Lagotis brachystachya and the underlying mechanism in vitro and in vivo. The results showed that treatment with luteolin and luteoloside reversed the reduction of organic anion transporter 1 (OAT1) levels, while apigenin attenuated the elevation of urate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) levels in uric acid-treated HK-2 cells, which was consistent with the finding in the kidneys of potassium oxonate (PO)-induced mice. On the other hand, hepatic xanthine oxidase activity was inhibited by the components. In addition, all of these active components improved the morphology of the kidney in hyperuricemic mice. Moreover, molecular docking showed that luteolin, luteoloside and apigenin could bind Toll-like receptor 4 (TLR4) and NLR family pyrin domain containing 3 (NLRP3). Congruently, western blot analysis showed that the components inhibited TLR4/myeloid differentiation primary response 88 (MyD88)/NLRP3 signaling. In conclusion, these results indicated that luteolin, luteoloside and apigenin could attenuate hyperuricemia by decreasing the production and increasing the excretion of uric acid, which were mediated by inhibiting inflammatory signaling pathways.

Research Progress toward Room Temperature Sodium Sulfur Batteries: A Review.

Lithium metal batteries have achieved large-scale application, but still have limitations such as poor safety performance and high cost, and limited lithium resources limit the production of lithium batteries. The construction of these devices is also hampered by limited lithium supplies. Therefore, it is particularly important to find alternative metals for lithium replacement. Sodium has the properties of rich in content, low cost and ability to provide high voltage, which makes it an ideal substitute for lithium. Sulfur-based materials have attributes of high energy density, high theoretical specific capacity and are easily oxidized. They may be used as cathodes matched with sodium anodes to form a sodium-sulfur battery. Traditional sodium-sulfur batteries are used at a temperature of about 300 °C. In order to solve problems associated with flammability, explosiveness and energy loss caused by high-temperature use conditions, most research is now focused on the development of room temperature sodium-sulfur batteries. Regardless of safety performance or energy storage performance, room temperature sodium-sulfur batteries have great potential as next-generation secondary batteries. This article summarizes the working principle and existing problems for room temperature sodium-sulfur battery, and summarizes the methods necessary to solve key scientific problems to improve the comprehensive energy storage performance of sodium-sulfur battery from four aspects: cathode, anode, electrolyte and separator.

Clinical Value of 3D-Printed Navigation Technology Combined with Neuroendoscopy for Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is the most common form of hemorrhagic stroke with high morbidity and mortality. Rapid and massive bleeding may compress the brain tissue, causing space-occupying and pathological effects, such as reduced local cerebral blood flow, acidosis, and inflammatory and immune responses. Although the development of minimally invasive technique provides a new option for the treatment of ICH, their application is limited due to the difficulty in achieving accurate puncture localization under the guidance of the marks on CT. We selected 30 patients treated with neuroendoscopic surgery guided by 3D-printed navigation technology (experimental group) and 30 patients treated with neuroendoscopic surgery guided by hand-painted on the patient's body surface according to the marks on CT (control group). Our results showed that patients in the experimental group had a lower number of intraoperative punctures, shorter operation time, less intraoperative blood loss, higher hematoma clearance rate, and smaller volume of perihematomal edema than the patients in the control group. Moreover, patients in the experimental group had higher Glasgow Coma Scale score at discharge, shorter postoperative hospitalization time and ICU stay, and a lower rate of postoperative complications, despite the lack of statistically significant differences. In addition, no statistically significant differences were observed in mortality and Glasgow Outcome Scale score between the two groups. In conclusion, 3D-printed navigation technology used for the neuroendoscopic hematoma removal is a more reliable and less invasive approach in the treatment of ICH. This technique has great application prospects and deserves promotion in the future clinical practice.

Variation of rhizosphere microbial community in continuous mono-maize seed production.

Soil microbe is crucial to a healthy soil, therefore its diversities and abundances under different conditions are still need fully understand.The aims of the study were to characterize the community structure and diversity of microbe in the rhizosphere soil after continuous maize seed production, and the relationship between the disease incidence of four diseases and the variation of the rhizosphere microbe. The results showed that different fungal and bacterial species were predominant in different cropping year, and long-term maize seed production had a huge impact on structure and diversity of soil microbial. Ascomycota and Mortierellomycota were the dominant fungal phyla and Mortierella and Ascomycetes represented for a large proportion of genus. A relative increase of Fusarium and Gibberella and a relative decrease of Mortierella, Chrysosporium, Podospora, and Chaetomium were observed with the increase of cropping year. Pathogenic Fusarium, Curvularia, Curvularia-lunata, Cladosporium, Gibberella-baccata, and Plectosphaerellaceae were over-presented and varied at different continuous cropping year, led to different maize disease incidence. Proteobacteria and Actinobacteria ranked in the top two of all bacterial phyla, and genus Pseudarthrobacter, Roseiflexus and RB41 dominated top 3. Haliangium and Streptomyces decreased with the continuous cropping year and mono-cropping of maize seed production increased disease incidence with the increase of cropping year, while the major disease was different. Continuous cropping of maize seed production induced the decrease of protective microbe and biocontrol genera, while pathogenic pathogen increased, and maize are in danger of pathogen invasion. Field management show great effects on soil microbial community.

Long Non-coding RNA MALAT1 Upregulates ZEB2 Expression to Promote Malignant Progression of Glioma by Attenuating miR-124.

Long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been shown to play a critical role in the development of several malignancies. However, the potential molecular mechanism of MALAT1 in glioma remains unclear. In the present study, we found that the expression of MALAT1 was aberrantly increased in both human glioma tissues and cells and associated with poor prognosis in glioma patients. We further found that MALAT1 silencing significantly inhibited glioma cell proliferation while induced cell cycle arrest and apoptosis. In parallel, knockdown of MALAT1 decreased tumor volume in vivo. These results suggested that MALAT1 acts as a functional oncogene, resulting in the oncogenicity in glioma. Nevertheless, the tumor-suppressive effect of MALAT1 silencing was reversed by miR-124. Besides, the relevance of ZEB2 in tumor progression has been studied in several forms of human cancer, and ZEB2 was identified as a target of miR-124 and negatively regulated by miR-124. MALAT1 overexpression or miR-124 inhibitor led to increased expression of ZEB2. In summary, our study depicts a novel pathway of MALAT1/miR-124/ZEB2 that regulates the progression of glioma and might provide a promising strategy for glioma therapy.