Molecular basis of methyl-salicylate-mediated plant airborne defence.

Aphids transmit viruses and are destructive crop pests1. Plants that have been attacked by aphids release volatile compounds to elicit airborne defence (AD) in neighbouring plants2-5. However, the mechanism underlying AD is unclear. Here we reveal that methyl-salicylate (MeSA), salicylic acid-binding protein-2 (SABP2), the transcription factor NAC2 and salicylic acid-carboxylmethyltransferase-1 (SAMT1) form a signalling circuit to mediate AD against aphids and viruses. Airborne MeSA is perceived and converted into salicylic acid by SABP2 in neighbouring plants. Salicylic acid then causes a signal transduction cascade to activate the NAC2-SAMT1 module for MeSA biosynthesis to induce plant anti-aphid immunity and reduce virus transmission. To counteract this, some aphid-transmitted viruses encode helicase-containing proteins to suppress AD by interacting with NAC2 to subcellularly relocalize and destabilize NAC2. As a consequence, plants become less repellent to aphids, and more suitable for aphid survival, infestation and viral transmission. Our findings uncover the mechanistic basis of AD and an aphid-virus co-evolutionary mutualism, demonstrating AD as a potential bioinspired strategy to control aphids and viruses.

Weak-Interaction Environment in a Composite Electrolyte Enabling Ultralong-Cycling High-Voltage Solid-State Lithium Batteries.

Poly(vinylidene fluoride) (PVDF)-based solid electrolytes with a Li salt-polymer-little residual solvent configuration are promising candidates for solid-state batteries. Herein, we clarify the microstructure of PVDF-based composite electrolyte at the atomic level and demonstrate that the Li+-interaction environment determines both interfacial stability and ion-transport capability. The polymer works as a "solid diluent" and the filler realizes a uniform solvent distribution. We propose a universal strategy of constructing a weak-interaction environment by replacing the conventional N,N-dimethylformamide (DMF) solvent with the designed 2,2,2-trifluoroacetamide (TFA). The lower Li+ binding energy of TFA forms abundant aggregates to generate inorganic-rich interphases for interfacial compatibility. The weaker interactions of TFA with PVDF and filler achieve high ionic conductivity (7.0 × 10-4 S cm-1) of the electrolyte. The solid-state Li||LiNi0.8Co0.1Mn0.1O2 cells stably cycle 4900 and 3000 times with cutoff voltages of 4.3 and 4.5 V, respectively, as well as deliver superior stability at -20 to 45 °C and a high energy density of 300 Wh kg-1 in pouch cells.

CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway.

BACKGROUND: White matter injury (WMI) represents a significant etiological factor contributing to neurological impairment subsequent to Traumatic Brain Injury (TBI). CD36 receptors are recognized as pivotal participants in the pathogenesis of neurological disorders, including stroke and spinal cord injury. Furthermore, dynamic fluctuations in the phenotypic polarization of microglial cells have been intimately associated with the regenerative processes within the injured tissue following TBI. Nevertheless, there is a paucity of research addressing the impact of CD36 receptors on WMI and microglial polarization. This investigation aims to elucidate the functional role and mechanistic underpinnings of CD36 in modulating microglial polarization and WMI following TBI. METHODS: TBI models were induced in murine subjects via controlled cortical impact (CCI). The spatiotemporal patterns of CD36 expression were examined through quantitative polymerase chain reaction (qPCR), Western blot analysis, and immunofluorescence staining. The extent of white matter injury was assessed via transmission electron microscopy, Luxol Fast Blue (LFB) staining, and immunofluorescence staining. Transcriptome sequencing was employed to dissect the molecular mechanisms underlying CD36 down-regulation and its influence on white matter damage. Microglial polarization status was ascertained using qPCR, Western blot analysis, and immunofluorescence staining. In vitro, a Transwell co-culture system was employed to investigate the impact of CD36-dependent microglial polarization on oligodendrocytes subjected to oxygen-glucose deprivation (OGD). RESULTS: Western blot and qPCR analyses revealed that CD36 expression reached its zenith at 7 days post-TBI and remained sustained at this level thereafter. Immunofluorescence staining exhibited robust CD36 expression in astrocytes and microglia following TBI. Genetic deletion of CD36 ameliorated TBI-induced white matter injury, as evidenced by a reduced SMI-32/MBP ratio and G-ratio. Transcriptome sequencing unveiled differentially expressed genes enriched in processes linked to microglial activation, regulation of neuroinflammation, and the TNF signaling pathway. Additionally, bioinformatics analysis pinpointed the Traf5-p38 axis as a critical signaling pathway. In vivo and in vitro experiments indicated that inhibition of the CD36-Traf5-MAPK axis curtailed microglial polarization toward the pro-inflammatory phenotype. In a Transwell co-culture system, BV2 cells treated with LPS + IFN-γ exacerbated the damage of post-OGD oligodendrocytes, which could be rectified through CD36 knockdown in BV2 cells. CONCLUSIONS: This study illuminates that the suppression of CD36 mitigates WMI by constraining microglial polarization towards the pro-inflammatory phenotype through the down-regulation of the Traf5-MAPK signaling pathway. Our findings present a potential therapeutic strategy for averting neuroinflammatory responses and ensuing WMI damage resulting from TBI.

Multi-omics analysis reveals a feedback loop amplifying immune responses in acute graft-versus-host disease due to imbalanced gut microbiota and bile acid metabolism.

Acute graft-versus-host disease (aGVHD) is primarily driven by allogeneic donor T cells associated with an altered composition of the host gut microbiome and its metabolites. The severity of aGVHD after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is not solely determined by the host and donor characteristics; however, the underlying mechanisms remain unclear. Using single-cell RNA sequencing, we decoded the immune cell atlas of 12 patients who underwent allo-HSCT: six with aGVHD and six with non-aGVHD. We performed a fecal microbiota (16SrRNA sequencing) analysis to investigate the fecal bacterial composition of 82 patients: 30 with aGVHD and 52 with non-aGVHD. Fecal samples from these patients were analyzed for bile acid metabolism. Through multi-omic analysis, we identified a feedback loop involving "immune cell-gut microbes-bile acid metabolites" contributing to heightened immune responses in patients with aGVHD. The dysbiosis of the gut microbiota and disruption of bile acid metabolism contributed to an exaggerated interleukin-1 mediated immune response. Our findings suggest that resistin and defensins are crucial in mitigating against aGVHD. Therefore, a comprehensive multi-omic atlas incorporating immune cells, gut microbes, and bile acid metabolites was developed in this study and used to propose novel, non-immunosuppressive approaches to prevent aGVHD.

Neutrophil extracellular traps facilitate sympathetic hyperactivity by polarizing microglia toward M1 phenotype after traumatic brain injury.

Traumatic brain injury (TBI), particularly diffuse axonal injury (DAI), often results in sympathetic hyperactivity, which can exacerbate the prognosis of TBI patients. A key component of this process is the role of neutrophils in causing neuroinflammation after TBI by forming neutrophil extracellular traps (NETs), but the connection between NETs and sympathetic excitation following TBI remains unclear. Utilizing a DAI rat model, the current investigation examined the role of NETs and the HMGB1/JNK/AP1 signaling pathway in this process. The findings revealed that sympathetic excitability intensifies and peaks 3 days post-injury, a pattern mirrored by the activation of microglia, and the escalated NETs and HMGB1 levels. Subsequent in vitro exploration validated that HMGB1 fosters microglial activation via the JNK/AP1 pathway. Moreover, in vivo experimentation revealed that the application of anti-HMGB1 and AP1 inhibitors can mitigate microglial M1 polarization post-DAI, effectively curtailing sympathetic hyperactivity. Therefore, this research elucidates that post-TBI, NETs within the PVN may precipitate sympathetic hyperactivity by stimulating M1 microglial polarization through the HMGB1/JNK/AP1 pathway.

Joint effects of sleep disturbance and renal function impairment on incident new-onset severe metabolic dysfunction-associated steatotic liver disease.

AIM: To elucidate the effects of sleep parameters and renal function on the risk of developing new-onset severe metabolic dysfunction-associated steatotic liver disease (MASLD). MATERIALS AND METHODS: The primary analysis involved a cohort of 305 257 participants. Multivariable Cox models were employed to calculate hazard ratios and 95% confidence intervals. Traditional mediation and two-step Mendelian randomization (MR) analyses were conducted to assess the associations and mediating roles of renal function indicators between sleep and new-onset severe MASLD. RESULTS: Poor sleep score and renal function biomarker score (RFS) were associated with an increased risk of new-onset severe MASLD (all ptrend <0.001). Participants with poor sleep patterns and the highest RFS had a 5.45-fold higher risk of new-onset severe MASLD, compared to those with healthy sleep patterns and the lowest RFS (p < 0.001). The RFS could explain 10.08% of the correlations between poor sleep score and risk of new-onset severe MASLD. Additionally, MR analyses supported a causal link between insomnia and new-onset severe MASLD and revealed a mediating role of chronic kidney disease in the connection between insomnia and new-onset severe MASLD risk. CONCLUSIONS: This study highlights the independent and combined associations of sleep parameters and renal function indicators with new-onset severe MASLD, underscoring the bidirectional communication of the liver-kidney axis and providing modifiable strategies for preventing MASLD.

Biomass-assisted fabrication of rGO-AuNPs as surface-enhanced Raman scattering substrates for in-situ monitoring methylene blue degradation.

Reduced graphene oxide-gold nanoparticles nanocomposites (rGO-AuNPs) with high surface-enhanced Raman scattering (SERS) activity was created by biomass-assisted green synthesis with Lilium casa blanca petals biomass for the first time, and its application for methylene blue (MB) degradation was explored through in-situ monitoring. Lilium casa blanca petals biomass was used as a reducing agent to reduce GO and chloroauric acid successively when carrying out rGO-AuNPs in-situ synthesis while it also acted as a capping agent. The produced rGO had oxygen-containing functional groups which had an outstanding performance in enhancing the SERS effect. Characterization results confirmed that the AuNPs were grafted onto the rGO sheet, and the mechanism study showed that total flavonoids in Lilium casa blanca petals biomass were the main biological compounds involved in the reduction. rGO-AuNPs had a high Raman enhancement factor (EF) which could reach 3.88 × 107. The synthesized nanocomposite also had a good catalytic activity that could be employed as catalyst in MB degradation, and it could complete degradation within 15min. The reaction rate increased linearly with the amount of rGO-AuNPs, and the degradation could be in-situ monitored both by UV and SERS.

Endoscopic mucosal resection of gastrointestinal polyps with a novel low-temperature plasma radio frequency generator: a non-inferiority multi-center randomized control study.

BACKGROUND: To evaluate the efficacy and safety of novel plasma radio frequency generator and its single-use polypectomy snares for endoscopic mucosal resection (EMR) of gastrointestinal (GI) polyps. METHODS: A total of 217 patients with 413 GI polyps were recruited from four centers in China. Patients were assigned to experimental or control groups using a central randomization method. The experimental group used the novel plasma radio frequency generator and its matched single-use polypectomy snares (Neowing, Shanghai), while the control group used the high-frequency electrosurgical unit (Erbe, Germany) and disposable electrosurgical snares (Olympus, Japan). The primary endpoint was the en bloc resection rate, and the non-inferiority margin was set at 10%. Secondary endpoint included operation time, coagulation success rate, intraoperative and postoperative bleeding rate, and perforation rate. RESULTS: The en bloc resection rate was 97.20% (104/107) in the experimental group and 95.45% (105/110) in the control group (P = 0.496). The operation time was 29.14 ± 20.21 min in the experimental group and 30.26 ± 18.74 min in the control group (P = 0.671). The average removal time of a single polyp in the experimental group was 7.52 ± 4.45 min, which was slightly shorter than that in the control group 8.90 ± 6.67 min, with no statistical difference (P = 0.076). The intraoperative bleeding rates of the experimental group and control group were 8.41% (9/107) and 10.00% (11/110), respectively (P = 0.686). No intraoperative perforation occurred in either group. The postoperative bleeding rates of the experimental group and the control group were 1.87% (2/107) and 4.55% (5/110), respectively (P = 0.465). No postoperative perforation occurred in the experimental group (0/107), while one case of delayed perforation occurred in the control group (1/110, 0.91%). There was no statistical difference between the two groups. CONCLUSIONS: Endoscopic mucosal resection of GI polyps with the novel plasma radio frequency generator is safe and effective, and non-inferior to the conventional high-frequency electrosurgical system.

Molecular regulation of ZmMs7 required for maize male fertility and development of a dominant male-sterility system in multiple species.

Understanding the molecular basis of male sterility and developing practical male-sterility systems are essential for heterosis utilization and commercial hybrid seed production in crops. Here, we report molecular regulation by genic male-sterility gene maize male sterility 7 (ZmMs7) and its application for developing a dominant male-sterility system in multiple species. ZmMs7 is specifically expressed in maize anthers, encodes a plant homeodomain (PHD) finger protein that functions as a transcriptional activator, and plays a key role in tapetal development and pollen exine formation. ZmMs7 can interact with maize nuclear factor Y (NF-Y) subunits to form ZmMs7-NF-YA6-YB2-YC9/12/15 protein complexes that activate target genes by directly binding to CCAAT box in their promoter regions. Premature expression of ZmMs7 in maize by an anther-specific promoter p5126 results in dominant and complete male sterility but normal vegetative growth and female fertility. Early expression of ZmMs7 downstream genes induced by prematurely expressed ZmMs7 leads to abnormal tapetal development and pollen exine formation in p5126-ZmMs7 maize lines. The p5126-ZmMs7 transgenic rice and Arabidopsis plants display similar dominant male sterility. Meanwhile, the mCherry gene coupled with p5126-ZmMs7 facilitates the sorting of dominant sterility seeds based on fluorescent selection. In addition, both the ms7-6007 recessive male-sterility line and p5126-ZmMs7M dominant male-sterility line are highly stable under different genetic germplasms and thus applicable for hybrid maize breeding. Together, our work provides insight into the mechanisms of anther and pollen development and a promising technology for hybrid seed production in crops.

Analysis of Mean Corpuscular Volume and Red Cell Distribution Width in Patients with Aplastic Anemia.

To explore the characteristics of hemogram in patients with aplastic anemia (AA), especially mean corpuscular volume (MCV) and red cell distribution width (RDW). We examined the blood routine of 180 new-onset AA patients and used 166 patients with myelodysplastic syndrome (MDS) as controls. Among the 180 AA patients, 105 (58.3%) were diagnosed with severe AA (SAA), while 75 (41.7%) were diagnosed with non-severe AA (NSAA). Compared to MDS, patients with SAA generally had unfavorable hemogram, including significantly lower white blood cell (WBC), absolute neutrophil count (ANC), hemoglobin (Hb), platelet (PLT) and reticulocyte counts (RET). However, WBC, ANC and lymphocyte counts were higher in the NSAA group than in the MDS group; Hb and Ret were comparable between the two groups. 8.5% of SAA patients and 58.1% of NSAA patients presented with macrocytic anemia, whereas 25.7% of SAA and 64.0% of NSAA had a high RDW. In the MDS group, 54.7% of patients presented with macrocytic anemia, and 84.7% had increased RDW. WBC, ANC, PLT, and Ret in a high-RDW group (25.7% of SAA) were significantly higher than in a normal-RDW group (74.3% of SAA). Overall, most SAA patients exhibited normocytic-normochromic anemia, and their hemograms decreased more significantly; more than half of NSAA patients showed macrocytic-heterogeneous anemia, and their hemograms were similar to those of MDS. Patients with elevated RDW may have better residual bone marrow hematopoietic function than those with normal RDW but with more severe anemia.

Ultrarapid Nanomanufacturing of High-Quality Bimetallic Anode Library toward Stable Potassium-Ion Storage.

Bimetallic alloy nanomaterials are promising anode materials for potassium-ion batteries (KIBs) due to their high electrochemical performance. The most well-adopted fabrication method for bimetallic alloy nanomaterials is tube furnace annealing (TFA) synthesis, which can hardly satisfy the trade-off among granularity, dispersity and grain coarsening due to mutual constraints. Herein, we report a facile, scalable and ultrafast high-temperature radiation (HTR) method for the fabrication of a library of ultrafine bimetallic alloys with narrow size distribution (≈10-20 nm), uniform dispersion and high loading. The metal-anchor containing heteroatoms (i.e., O and N), ultrarapid heating/cooling rate (≈103  K s-1 ) and super-short heating duration (several seconds) synergistically contribute to the successful synthesis of small-sized alloy anodes. As a proof-of-concept demonstration, the as-prepared BiSb-HTR anode shows ultrahigh stability indicated by negligible degradation after 800 cycles. The in situ X-ray diffraction reveals the K+ storage mechanism of BiSb-HTR. This study can shed light on the new, rapid and scalable nanomanufacturing of high-quality bimetallic alloys toward extended applications of energy storage, energy conversion and electrocatalysis.

Evidence of pyroptosis and ferroptosis extensively involved in autoimmune diseases at the single-cell transcriptome level.

BACKGROUND: Approximately 8-9% of the world's population is affected by autoimmune diseases, and yet the mechanism of autoimmunity trigger is largely understudied. Two unique cell death modalities, ferroptosis and pyroptosis, provide a new perspective on the mechanisms leading to autoimmune diseases, and development of new treatment strategies. METHODS: Using scRNA-seq datasets, the aberrant trend of ferroptosis and pyroptosis-related genes were analyzed in several representative autoimmune diseases (psoriasis, atopic dermatitis, vitiligo, multiple sclerosis, systemic sclerosis-associated interstitial lung disease, Crohn's disease, and experimental autoimmune orchitis). Cell line models were also assessed using bulk RNA-seq and qPCR. RESULTS: A substantial difference was observed between normal and autoimmune disease samples involving ferroptosis and pyroptosis. In the present study, ferroptosis and pyroptosis showed an imbalance in different keratinocyte lineages of psoriatic skinin addition to a unique pyroptosis-sensitive keratinocyte subset in atopic dermatitis (AD) skin. The results also revealed that pyroptosis and ferroptosis are involved in epidermal melanocyte destruction in vitiligo. Aberrant ferroptosis has been detected in multiple sclerosis, systemic sclerosis-associated interstitial lung disease, Crohn's disease, and autoimmune orchitis. Cell line models adopted in the study also identified pro-inflammatory factors that can drive changes in ferroptosis and pyroptosis. CONCLUSION: These results provide a unique perspective on the involvement of ferroptosis and pyroptosis in the pathological process of autoimmune diseases at the scRNA-seq level. IFN-γ is a critical inducer of pyroptosis sensitivity, and has been identified in two cell line models.

Efficient and high-throughput pseudorecombinant-chimeric Cucumber mosaic virus-based VIGS in maize.

Virus-induced gene silencing (VIGS) is a versatile and attractive approach for functional gene characterization in plants. Although several VIGS vectors for maize (Zea mays) have been previously developed, their utilities are limited due to low viral infection efficiency, insert instability, short maintenance of silencing, inadequate inoculation method, or abnormal requirement of growth temperature. Here, we established a Cucumber mosaic virus (CMV)-based VIGS system for efficient maize gene silencing that overcomes many limitations of VIGS currently available for maize. Using two distinct strains, CMV-ZMBJ and CMV-Fny, we generated a pseudorecombinant-chimeric (Pr) CMV. Pr CMV showed high infection efficacy but mild viral symptoms in maize. We then constructed Pr CMV-based vectors for VIGS, dubbed Pr CMV VIGS. Pr CMV VIGS is simply performed by mechanical inoculation of young maize leaves with saps of Pr CMV-infected Nicotiana benthamiana under normal growth conditions. Indeed, suppression of isopentenyl/dimethylallyl diphosphate synthase (ZmIspH) expression by Pr CMV VIGS resulted in non-inoculated leaf bleaching as early as 5 d post-inoculation (dpi) and exhibited constant and efficient systemic silencing over the whole maize growth period up to 105 dpi. Furthermore, utilizing a ligation-independent cloning (LIC) strategy, we developed a modified Pr CMV-LIC VIGS vector, allowing easy gene cloning for high-throughput silencing in maize. Thus, our Pr CMV VIGS system provides a much-improved toolbox to facilitate efficient and long-duration gene silencing for large-scale functional genomics in maize, and our pseudorecombination-chimera combination strategy provides an approach to construct efficient VIGS systems in plants.

Submucosal tunneling endoscopic septum division for esophageal diverticulum with a median follow-up of 39 months: a multicenter cohort study.

BACKGROUND AND AIMS: Submucosal tunneling endoscopic septum division (STESD) is an endoscopic minimally invasive technique for treating esophageal diverticulum. The objectives of this study were to evaluate the safety and efficacy of STESD and its impact on patients' quality of life. METHODS: This study included consecutive patients who underwent STESD for esophageal diverticulum from April 2016 to August 2020 in 2 centers (Zhongshan Hospital, Fudan University and Tianjin First Central Hospital). Esophagogram and endoscopic examination were performed before STESD and 30 days after STESD. Patients completed the 36-item Short Form survey (SF-36) before STESD and 1 year after surgery. Clinical symptoms were assessed via telehealth every 6 months until August 2021. Costamagna and Eckardt scores were used to evaluate changes in symptoms. RESULTS: Twenty-one patients were included. Mucosal injury 1 to 2 cm below the septum occurred in 2 patients. No severe surgical adverse events were observed. Median duration of follow-up was 39 months (range, 12-63). Total SF-36 scores increased from 118.7 ± 18.6 before STESD to 132.4 ± 9.1 at 1 year after the procedure (P = .007). SF-36 subscales of general health (P = .002), vitality (P = .004), social functioning (P = .030), and mental health (P = .020) improved significantly after STESD. The mean Costamagna score decreased from 3.83 ± 1.33 to 1.67 ± 1.51 (P = .010), whereas the mean Eckardt score decreased from 3.50 ± .90 to 1.25 ± 1.76 (P = .002). One patient developed symptom recurrence at 10 months after STESD. CONCLUSIONS: STESD is a safe and valid endoscopic minimally invasive surgery for esophageal diverticulum, which can reduce symptoms and improve quality of life.

Long Noncoding RNA LINC00941 Promotes Cell Proliferation and Invasion by Interacting with hnRNPK in Oral Squamous Cell Carcinoma.

Oral squamous cell carcinoma (OSCC) is a prevalent carcinoma of the head, neck and mouth. Recently studies involving the role of long noncoding RNAs (lncRNAs) that play key regulatory roles in altering gene expression has been reported in the context of promoting tumorigenesis. However, the functions of lncRNAs in the context of oral squamous cell carcinoma have not been extensively described. In this study, we report a never identified before lncRNA, LINC00941, which was highly expressed in OSCC tissues and cells. Expression of LINC00941 promoted cell proliferation, migration, invasion, and metastasis of OSCC cells In Vitro by inducing epithelial-mesenchymal transition (EMT) and activating the Wnt/ß-catenin signaling cascade. In silico analyses revealed heterogeneous nuclear ribonucleoprotein K (hnRNPK) to be a strong positive regulator of LINC00941 activity. Experimental verification of this association revealed a direct interaction of LINC00941 and hnRNPK to induce cell growth and invasion by activating EMT in OSCC cells. Therefore, our study reports that LINC00941 promotes progression of OSCC by its interaction with hnRNPK, and it may present a promising strategy for diagnosis and treatment of OSCC.

Predictors of the difficulty for endoscopic resection of gastric gastrointestinal stromal tumor and follow-up data.

BACKGROUND AND AIM: Gastrointestinal stromal tumors (GISTs) are among the most common submucosal tumors in the stomach that require therapeutic intervention. We aim to identify the predictors of technical difficulty during endoscopic resection of gastric GIST and to investigate follow-up outcomes. METHODS: Patients with gastric GISTs were reviewed from June 2009 to June 2020 at Zhongshan Hospital. Clinical and pathological features, endoscopic procedure information, and follow-up data were collected and analyzed. A nomogram was developed and validated internally and externally. RESULTS: A total of 628 GISTs were finally analyzed. The difficulty was experienced in 66 cases. GISTs size (2-3 cm: OR 2.431 P = 0.018 and > 3 cm: OR 9.765 P < 0.001), invasion depth beyond submucosal (MP: OR 2.280, P = 0.038 and MP-ex: OR 4.295, P = 0.002), and lack of experience (OR 2.075, P = 0.016) were independent risk factors of difficulty. The nomogram prediction model showed a bias-corrected C-index value of 0.778 and acquired an area under curve (AUC) of 0.756 on the external validation cohort. At the cut-off of 0.15, the nomogram's negative predictive value (NPV) and accuracy (ACC) were 94.9% and 79.8% in identifying non-difficult GISTs. Follow-up results showed that only five GIST patients had local recurrence after endoscopic resection. CONCLUSIONS: Tumor size, invasion depth, and endoscopists' experience were risk factors for the difficulty of endoscopic GIST resection. Our nomogram provided a valuable tool for screening non-difficult GIST resection.

Rapid and simple quantitative identification of Listeria monocytogenes in cheese by isothermal sequence exchange amplification based on surface-enhanced Raman spectroscopy.

Foodborne pathogens detection is important to ensure food safety and human health. In this study, we designed a comet structure to rapidly and sensitively detect foodborne Listeria monocytogenes. This method combined isothermal sequence exchange amplification (SEA) and surface-enhanced Raman spectroscopy. Listeria monocytogenes DNA could be rapidly amplified at a constant temperature via SEA with a pair of modified primers, which rendered the precise thermal control instrumentation unnecessary. Efficient SEA amplification generated a large number of DNA duplexes that could be easily captured by streptavidin-modified magnetic bead and AuMB@Ag-isothiocyanate fluorescein antibody (anti-FITC). AuMB@Ag-anti-FITC was used as a signal probe, which generated a significant excitation signal at 1,616 cm-1 for quantitative detection and analysis. The results displayed sensitive detection of L. monocytogenes in cheese from 2.0 × 101 cfu/mL to 2.0 × 106 cfu/mL within 1.0 h with a detection limit of 7.8 cfu/mL. Furthermore, this comet structure displayed the desirable specificity as its specific primers and amplified DNA ends were attached to streptavidin-modified magnetic beads and AuMB@Ag-anti-FITC, respectively. We expected that the method devised would provide a promising new approach to screening for L. monocytogenes and guarantee the microbiological safety of dairy products.

Constructing a Reinforced and Gradient Solid Electrolyte Interphase on Si Nanoparticles by In-Situ Thiol-Ene Click Reaction for Long Cycling Lithium-Ion Batteries.

Constructing a stable solid electrolyte interphase (SEI) on high-specific-capacity silicon (Si) anode is one of the most effective methods to reduce the crack of SEI and improve the cycling performance of Si anode. Herein, the authors construct a reinforced and gradient SEI on Si nanoparticles by an in-situ thiol-ene click reaction. Mercaptopropyl trimethoxysilane (MPTMS) with thiol functional groups (SH) is first grafted on the Si nanoparticles through condensation reaction, which then in-situ covalently bonds with vinylene carbonate (VC) to form a reinforced and uniform SEI on Si nanoparticles. The modified SEI with sufficient elastic Lix SiOy can homogenize the stress and strain during the lithiation of Si nanoparticles to reduce their expansion and prevent the SEI from cracking. The Si nanoparticles-graphite blending anode with the reinforced SEI exhibits excellent performance with an initial coulombic efficiency of ≈90%, a capacity of 1053.3 mA h g-1 after 500 cycles and a high capacity of 852.8 mA h g-1 even at a high current density of 3 A g-1 . Moreover, the obtained anode shows superior cycling stability under both high loadings and lean electrolyte. The in-situ thiol-ene click reaction is a practical method to construct reinforced SEI on Si nanoparticles for next-generation high-energy-density lithium-ion batteries.

Hemodynamics is associated with vessel wall remodeling in patients with middle cerebral artery stenosis.

OBJECTIVES: To evaluate the relationship between hemodynamics and vessel wall remodeling patterns in middle cerebral artery (MCA) stenosis based on high-resolution magnetic resonance imaging and computational fluid dynamics (CFD). METHODS: Forty consecutive patients with recent ischemic stroke or transient ischemic attack attributed to unilateral atherosclerotic MCA stenosis (50-99%) were prospectively recruited. All patients underwent a cross-sectional scan of the stenotic MCA vessel wall. The parameters of the vessel wall, the number of patients with acute infarction, translesional wall shear stress ratio (WSSR), wall shear stress in stenosis (WSSs), and translesional pressure ratio were obtained. The patients were divided into positive remodeling (PR) and negative remodeling (NR) groups. The differences in vessel wall parameters and hemodynamics were compared. Correlations between the parameters of the vessel wall and hemodynamics were calculated. RESULTS: Of the 40 patients, 16 had PR, 19 had NR, and the other 5 displayed non-remodeling. The PR group had a smaller lumen area (p = 0.004), larger plaque area (p < 0.001), normal wall index (p = 0.004), and higher WSSR (p = 0.004) and WSSs (p = 0.023) at the most narrowed site. The PR group had more enhanced plaques (12 vs 6, p = 0.03). The number of patients with acute stroke in the PR group was more than that in the NR group (11 vs 4, p = 0.01). The remodeling index (r = 0.376, p = 0.026) and plaque area (r = 0.407, p = 0.015) showed a positive correlation with WSSR, respectively. CONCLUSIONS: Hemodynamics plays a role in atherosclerotic plaques and vessel wall remodeling. Individuals with greater hemodynamic values might be more prone to stroke. KEY POINTS: • Stenotic plaques in middle cerebral artery with positive remodeling have smaller lumen area and larger resp. higher plaque area, normal wall index, translesional wall shear stress ratio, and wall shear stress than negative remodeling. • The remodeling index and plaque area are positively correlated with translesional wall shear stress ratio. • Hemodynamic may help to understand the role of positive remodeling in the development of acute stroke.

Effects of tolC on tolerance to bile salts and biofilm formation in Cronobacter malonaticus.

Bile salts is one of essential components of bile secreted into the intestine to confer antibacterial protection. Cronobacter species are associated with necrotizing enterocolitis in newborns and show a strong tolerance to bile salts. However, little attempt has been made to focus on the molecular basis of the tolerance to bile salts. In this study, we investigated the roles of tolC on growth, cell morphology, motility, and biofilm formation ability in Cronobacter malonaticus under bile salt stress. The results indicated that the absence of tolC significantly affected the colony morphology and outer membrane structure in a normal situation, compared with those of the wild type strain. The deletion of tolC caused the decline in resistance to bile salt stress, inhibition of growth, and observable reduction in relative growth rate and motility. Moreover, the bacterial stress response promoted the biofilm formation ability of the mutant strain. The expression of the AcrAB-TolC system (acrA, acrB, and tolC) was effectively upregulated compared with the control sample when exposed to different bile salt concentrations. The findings provide valuable information for deeply understanding molecular mechanisms about the roles of tolC under bile salt stress and the prevention and control of C. malonaticus.