Kidney Organoid Modeling of WT1 Mutations Reveals Key Regulatory Paths Underlying Podocyte Development.

Wilms tumor-1(WT1) is a crucial transcription factor that regulates podocyte development. However, the epigenomic mechanism underlying the function of WT1 during podocyte development has yet to be fully elucidated. Here, single-cell chromatin accessibility and gene expression maps of foetal kidneys and kidney organoids are generated. Functional implications of WT1-targeted genes, which are crucial for the development of podocytes and the maintenance of their structure, including BMPER/PAX2/MAGI2 that regulates WNT signaling pathway, MYH9 that maintains actin filament organization and NPHS1 that modulates cell junction assembly are identified. To further illustrate the functional importance of WT1-mediated transcriptional regulation during podocyte development, cultured and implanted patient-derived kidney organoids derived from the Induced Pluripotent Stem Cell (iPSCs) of a patient with a heterozygous missense mutation in WT1 are generated. Results from single-cell RNA sequencing (scRNA-seq) and functional assays confirm that the WT1 mutation leads to delays in podocyte development and causes damage to cell structures, due to its failure to activate the targeting genes MAGI2, MYH9, and NPHS1. Notably, correcting the mutation in the patient iPSCs using CRISPR-Cas9 gene editing rescues the podocyte phenotype. Collectively, this work elucidates the WT1-related epigenomic landscape with respect to human podocyte development and identifies the disease-causing role of a WT1 mutation.

Primary immunodeficiency as a cause of immune-mediated kidney diseases.

Primary immunodeficiency (PID) is no longer defined by infections alone, and autoimmunity is an accompanying manifestation of PID. Recurrent infections may trigger autoimmunity through molecular mimicry, bystander activation, or superantigens. The diagnosis of PID is still challenging, but genetic analysis reveals the underlying link between PID and autoimmunity. Mutations in relevant genes affecting central and peripheral immune tolerance, regulatory T-cell function, expansion of autoreactive lymphocytes, antigen clearance, hyperactivation of type I interferon, and NF-κB pathways have all been implicated in triggering autoimmunity in PID. Autoimmunity in PID leads to chronic inflammation, tissue damage, and organ failure and increases the mortality of patients with PID. The kidneys are inextricably linked with the immune system, and kidney diseases can be mediated by both infection and autoimmunity/inflammation in PID patients. The manifestations of kidney involvement in PID patients are very heterogeneous and include lupus nephritis, C3 glomerulopathy, kidney thrombotic microangiopathy, vasculitis, and interstitial nephritis.Patients with PID-caused kidney diseases have defined immune function defects and may benefit from pathway-based biologics, stem cell transplantation, or gene therapy. Early diagnosis and appropriate treatment of PID are crucial for reducing the mortality rate and improving organ function and quality of life.

Delayed-onset seizures after subthalamic nucleus deep brain stimulation surgery for Parkinson's disease.

BACKGROUND: Delayed-onset seizures after deep brain stimulation (DBS) surgery were seldom reported. This study summarized the clinical characteristics of delayed-onset seizures after subthalamic nucleus (STN) DBS surgery for Parkinson's disease (PD) and analyzed risk factors. METHODS: A single-center retrospective study containing consecutive STN-DBS PD patients from 2006 to 2021 was performed. Seizures occurred during the DBS surgery or within one month after DBS surgery were identified based on routine clinical records. Patients with postoperative magnetic resonance imaging (MRI) were included to further analyze the risk factors for postoperative seizures with univariate and multivariate statistical methods. RESULTS: 341 consecutive PD patients treated with bilateral STN-DBS surgery wereidentified, and five patients experienced seizures after DBS surgery with an incidence of 1.47 %. All seizures of the five cases were characterized as delayed onset with average 12 days post-operatively. All seizures presented as generalized tonic-clonic seizures and didn't recur after the first onset. In those seizures cases, peri-electrode edema was found in both hemispheres without hemorrhage and infarction. The average diameter of peri-electrode edema of patients with seizures was larger than those without seizures (3.15 ± 1.00 cm vs 1.57 ± 1.02 cm, p = 0.005). Multivariate risk factor analysis indicated that seizures were only associated with the diameter of peri-electrode edema (OR 4.144, 95 % CI 1.269-13.530, p = 0.019). CONCLUSIONS: Delayed-onset seizures after STN-DBS surgery in PD patients were uncommon with an incidence of 1.47 % in this study. The seizures were transient and self-limiting, with no developing into chronic epilepsy. Peri-electrode edema was a risk factor for delayed-onset seizures after DBS surgery. Patients with an average peri-electrode edema diameter > 2.70 cm had a higher risk to develop seizures.

Fast 3D positioning based on a simplified THz photonic stereo ISAR system.

In this work, a THz stereo inverse synthetic aperture radar scheme based on photonics is proposed, and proof-of-concept experimentally demonstrated, achieving high resolution and fast three-dimensional (3D) positioning of multiple targets. An optical frequency comb and a uni-traveling carrier photodiode are employed to photonically generate a linear frequency-modulation signal at 300-320 GHz. By two incoherent measurements at different angles with one pair of antennas, 3D positioning of plane reflectors over a distance of 0.6 m is successfully accomplished, achieving a resolution of 7.5 mm for both range and azimuth dimensions, and a maximum experimental height error of 4 mm.

Postoperative use of steroids for peri-electrode edema after deep brain stimulation surgery: A retrospective cohort study.

BACKGROUND: To review the incidence and extent of peri-electrode edema after DBS and to clarify the effect of postoperative use of steroids on the peri-electrode edema. METHODS: This retrospective cohort study included 250 patients who underwent bilateral subthalamic nucleus (STN) DBS surgery with intact MRI within 1 month after DBS surgery. Patients were divided into steroid and non-steroid groups, based on postoperative steroids use. The occurrence and extent of peri-electrode edema were compared between the two groups, and other associated factors were analyzed using univariate and multivariate methods. RESULTS: Peri-electrode edema >1 cm3 in at least one hemisphere was reported in 215 (86.00%) patients. The mean volume of peri-electrode edema observed in the steroid group was significantly smaller than in the non-steroid group (8.09 ± 8.47 cm3 vs 17.10 ± 16.90 cm3 , p < 0.001). In the steroid group, 104 (32.91%) of the 316 implanted electrodes present with edema less than 1 cm3 , whereas in the non-steroid group, only 27 (14.67%) of the 184 implanted electrodes present with edema less than 1 cm3 (p < 0.001). Multivariate analysis indicated that lesser peri-electrode edema was significantly associated with postoperative steroids use and general anesthesia. CONCLUSIONS: Peri-electrode edema is common after DBS surgery, and postoperative steroids use reduces the occurrence and extent of peri-electrode edema.

The role of KDM4A-mediated histone methylation on temozolomide resistance in glioma cells through the HUWE1/ROCK2 axis.

Temozolomide (TMZ) resistance presents a significant challenge in the treatment of gliomas. Although lysine demethylase 4A (KDM4A) has been implicated in various cancer-related processes, its role in TMZ resistance remains unclear. This study aims to elucidate the contribution of KDM4A to TMZ resistance in glioma cells and its potential implications for glioma prognosis. We assessed the expression of KDM4A in glioma cells (T98G and U251MG) using qRT-PCR and Western blot assays. To explore the role of KDM4A in TMZ resistance, we transfected siRNA targeting KDM4A into drug-resistant glioma cells. Cell viability was assessed using the CCK-8 assay and the TMZ IC50 value was determined. ChIP assays were conducted to investigate KDM4A, H3K9me3, and H3K36me3 enrichment on the promoters of ROCK2 and HUWE1. Co-immunoprecipitation confirmed the interaction between HUWE1 and ROCK2, and we examined the levels of ROCK2 ubiquitination following MG132 treatment. Notably, T98G cells exhibited greater resistance to TMZ than U251MG cells, and KDM4A displayed high expression in T98G cells. Inhibiting KDM4A resulted in decreased cell viability and a reduction in the TMZ IC50 value. Mechanistically, KDM4A promoted ROCK2 transcription by modulating H3K9me3 levels. Moreover, disruption of the interaction between HUWE1 and ROCK2 led to reduced ROCK2 ubiquitination. Inhibition of HUWE1 or overexpression of ROCK2 counteracted the sensitization effect of si-KDM4A on TMZ responsiveness in T98G cells. Our findings highlight KDM4A's role in enhancing TMZ resistance in glioma cells by modulating ROCK2 and HUWE1 transcription and expression through H3K9me3 and H3K36me3 removal.

Research Note: Xylooligosaccharide directly attenuates Salmonella Typhimurium colonization and its induction of impairments in intestinal barrier and growth performance of broilers.

Xylooligosaccharide (XOS) is known as a prebiotic, however, it is unknown whether XOS can directly protect against bacterial infection. This study aimed to investigate the direct inhibitory effects of XOS on Salmonella Typhimurium colonization and the inductive impairments in gut health and growth performance in broilers. We first probed the inhibitory effects of XOS on S. Typhimurium adhesion and its induction of intestinal epithelial cell (IPEC-J2) injuries. Afterward, 168 one-day-old yellow-feathered broilers were randomly divided into 3 groups (7 replicates/group): negative control (NC, received a basal diet), positive control (PC, received a basal diet with S. Typhimurium challenge) and XOS group (PC birds + 1,500 mg/kg XOS). All birds except those in NC were orally challenged with S. Typhimurium from 8 to 10 d of age. Parameters were analyzed on d 11. The results showed that XOS inhibited S. Typhimurium adhesion and the inductive injuries of IPEC-J2 cells by lowering (P < 0.05) certain adhesion-related genes expression of this bacterium. It also alleviated S. Typhimurium-induced increase (P < 0.05) in the expression of certain inflammatory cytokines and tight junction (TJ) proteins of IPEC-J2 cells. Supplementing XOS to S. Typhimurium-challenged broilers attenuated the elevations (P < 0.05) in S. Typhimurium colonization of ileal mucosa and its translocation to the liver and spleen, as well as increased (P < 0.05) certain TJ proteins expression of ileum. Besides, XOS addition normalized S. Typhimurium-induced impairments (P < 0.05) in ileal morphology, final body weight and average daily gain in broilers. Collectively, supplemental XOS directly suppressed intestinal colonization of S. Typhimurium by diminishing its adhesiveness and subsequently mitigated destructions in intestinal barriers, thus contributing to weaken growth retardation in challenged broilers. Our findings provide a new insight into the mechanisms of XOS limiting Salmonella infection in chickens.

Evaluation of the significance of complement-related genes mutations in atypical postinfectious glomerulonephritis: a pilot study.

BACKGROUND: Postinfectious glomerulonephritis with C3-dominant glomerular deposition (C3-PIGN) involves C3-dominant glomerular deposition without immunoglobulin. Atypical C3-PIGN involves persistent hypocomplementemia. We investigated the clinical features and explored complement-related gene mutations in atypical PIGN patients. METHODS: We enrolled atypical C3-PIGN patients and collected data regarding the clinical presentation and pathological characteristics and follow-up data. We measured the levels of complement associated antibodies and performed whole-exome sequencing (WES) to detect mutations in complement-related genes. RESULTS: The analysis included six atypical C3-PIGN patients. All patients were antistreptolysin-O (ASO) positive. All patients had varying degrees of hematuria, and four patients had proteinuria. None of the patients were positive for complement-related antibodies. All patients possessed mutations of genes related to the complement pathway, including alternative complement pathway genes-CFI, CFH, CFHR3, CFHR5; the lectin pathway gene-MASP2; and the common complement pathway gene-C8A. The rare variant of CFHR3 has been reported in C3 glomerulonephritis. During 56-73 months of follow-up, the levels of urine markers in three patients recovered within 6 months, and the remaining patients had abnormal urine test results over 12 months. Patients who received glucocorticoid therapy recovered faster. CONCLUSIONS: Our study suggested that complement-related gene mutations may be an important cause of persistent hypocomplementemia in atypical C3-PIGN patients. In addition to variations in alternate pathway-related genes, we also found variations in lectin pathway-related genes, especially MASP2 genes. Although the overall prognosis was good, atypical C3-PIGN patients exhibited a longer period for recovery. Our results suggested that atypical C3-PIGN patients should receive more medical attention and need testing for mutations in complement-related genes.

Central and peripheral analgesic active components of triterpenoid saponins from Stauntonia chinensis and their action mechanism.

Triterpenoid saponins from Stauntonia chinensis have been proven to be a potential candidate for inflammatory pain relief. Our pharmacological studies confirmed that the analgesic role of triterpenoid saponins from S. chinensis occurred via a particular increase in the inhibitory synaptic response in the cortex at resting state and the modulation of the capsaicin receptor. However, its analgesic active components and whether its analgesic mechanism are limited to this are not clear. In order to further determine its active components and analgesic mechanism, we used the patch clamp technique to screen the chemical components that can increase inhibitory synaptic response and antagonize transient receptor potential vanilloid 1, and then used in vivo animal experiments to evaluate the analgesic effect of the selected chemical components. Finally, we used the patch clamp technique and molecular biology technology to study the analgesic mechanism of the selected chemical components. The results showed that triterpenoid saponins from S. chinensis could enhance the inhibitory synaptic effect and antagonize the transient receptor potential vanilloid 1 through different chemical components, and produce central and peripheral analgesic effects. The above results fully reflect that "traditional Chinese medicine has multi-component, multi-target, and multi-channel synergistic regulation".

Short- and long-term outcomes of laparoscopic versus open gastrectomy after neoadjuvant chemotherapy: A case-control study using a propensity score matching method.

Background: Neoadjuvant chemotherapy (NACT) is increasingly becoming the recommended treatment for locally advanced gastric cancer (LAGC) with promising results. According to previous reports, few studies have evaluated the benefits of laparoscopic gastrectomy (LG) after NACT. Methods: 135 patients from our center who underwent gastrectomy with NACT were available, including 41 patients of LG and 94 OG between July 2018 and July 2022. To reduce selection bias, we used the nearest neighbor method and set caliper = 0.2 for 3:1 matching between LG and OG groups for propensity score matching method (PSM). After PSM, the matched 41 patients with LG and 80 patients with OG formed the cohort, respectively. Univariate and multivariate Cox analyses were performed on all variables to determine independent risk factors associated with survival. Results: LG had a longer operating time compared to OG [260.00 min (220.00 min, 300.00 min) vs. 200.00 min (160.00 min, 260 min), P < 0.001]. The estimated blood loss, metastatic lymph nodes (LN), total LN examined, postoperative hospital stays, blood transfusion (P>0.05) and the incidence of postoperative complications did not show statistical differences from the OG group (P = 0.084). The type of surgery (LG vs. OG) did not show a significant risk propensity in the univariate and multivariate Cox analysis (HR = 0.69, P = 0.36, 95 % CI: 0.31-1.53). Through the Kaplan-Meier curves, a certain trend showed that the LG group had a better long-term survival outcomes than the OG group, although there was no statistical difference between two groups (P>0.05). Conclusion: LG is a promising treatment option for LAGC patients receiving NACT and had an acceptable safety and efficacy compared to OG.

N-acyl homoserine lactonase attenuates the virulence of Salmonella typhimurium and its induction of intestinal damages in broilers.

This study aimed to investigate the potential mitigating effects of N-acyl homoserine lactonase (AHLase) on the virulence of Salmonella typhimurium and its induction of intestinal damages in broilers. In vitro study was firstly conducted to examine if AHLase treatment could attenuate the virulence of S. typhimurium. Then, an in vivo experiment was performed by allocating 240 broiler chicks at 1 d old into 3 groups (8 replicates per group): negative control (NC), positive control (PC), and PC supplemented with 10,000 U/kg AHLase. All chicks except those in NC were orally challenged by S. typhimurium from 8 to 10 d of age. Parameters were measured on d 11 and 21. The results showed that treatment with 1 U/mL AHLase suppressed the biofilm-forming ability (including biofilm biomass, extracellular DNA secretion and biofilm formation-related gene expression), together with swarming motility and adhesive capacity of S. typhimurium. Supplemental 10,000 U/kg AHLase counteracted S. typhimurium-induced impairments (P < 0.05) in broiler growth performance (including final body weight, average daily gain and average daily feed intake) during either 1-11 d or 12-21 d, and increases (P < 0.05) in the indexes of liver, spleen and bursa of Fabricius on d 11, together with reductions (P < 0.05) in ileal villus height and its ratio to crypt depth on both d 11 and 21. AHLase addition also normalized the increased (P < 0.05) mRNA expression of ileal occludin on both d 11 and 21 in S. typhimurium-challenged broilers. However, neither S. typhimurium challenge nor AHLase addition altered (P > 0.05) serum diamine oxidase activity of broilers. Noticeably, S. typhimurium challenge caused little change in the mRNA expression of ileal inflammatory cytokines except for an increase (P < 0.05) in interleukin-8 expression on d 11, whereas AHLase addition normalized (P < 0.05) this change. In conclusion, AHLase treatment could attenuate the virulence and pathogenicity of S. typhimurium, thus contributing to alleviate S. typhimurium-induced growth retardation and intestinal damages in broilers.

Effects of Oxygen Flow during Fabrication by Magnetron Sputtering on Structure and Performance of Zr-Doped HfO2 Thin Films.

Oxygen defects in Hafnium Oxide (HfO2)-based ferroelectric thin films not only are related to the cause of ferroelectricity but also affect the ferroelectric properties of the thin films. This paper, therefore, focuses on the fabrication of Zr:HfO2 thin films by RF (Radio Frequency) magnetron sputtering with Zr-doped HfO2 as the target and examines how oxygen flow impacts the oxygen vacancies and electrical properties thereof. Additionally, TiN thin-film electrodes were prepared by direct current (DC) magnetron reactive sputtering using nitrogen as the reaction gas, the influences of the substrate temperature on the film deposition rate and crystal phase structure were investigated, and the resultant thin-film electrodes with the lowest resistivity were obtained. Furthermore, the ferroelectric hysteresis loop and leakage current density of metal-insulator-metal (MIM) ferroelectric capacitors formed by annealing the 30 nm thick deposited Zr:HfO2 sandwiched between the top and bottom TiN electrodes were measured. The results demonstrate that varying oxygen flow has a considerable effect on oxygen vacancies and the Zr doping concentration of deposited Zr:HfO2 ferroelectric thin films. When the oxygen flow is set to 40 sccm (standard cubic centimeters per minute) and an external electric field strength of 2 mV/cm is applied, the remnant polarization reaches 18 µC/cm2, with a decrease in the leakage current density of 105-6 orders of magnitude.

Design of a Biaxial High-G Piezoresistive Accelerometer with a Tension-Compression Structure.

To meet the measurement needs of multidimensional high-g acceleration in fields such as weapon penetration, aerospace, and explosive shock, a biaxial piezoresistive accelerometer incorporating tension-compression is meticulously designed. This study begins by thoroughly examining the tension-compression measurement mechanism and designing the sensor's sensitive structure. A signal test circuit is developed to effectively mitigate cross-interference, taking into account the stress variation characteristics of the cantilever beam. Subsequently, the signal test circuit of anti-cross-interference is designed according to the stress variation characteristics of the cantilever beam. Next, the finite element method is applied to analyze the structure and obtain the performance indices of the range, vibration modes, and sensitivity of the sensor. Finally, the process flow and packaging scheme of the chip are analyzed. The results show that the sensor has a full range of 200,000 g, a sensitivity of 1.39 µV/g in the X direction and 1.42 µV/g in the Y direction, and natural frequencies of 509.8 kHz and 510.2 kHz in the X and Y directions, respectively.

FOXM1 maintains fatty acid homoeostasis through the SET7-H3K4me1-FASN axis.

Reprogramming of metabolic genes and subsequent alterations in metabolic phenotypes occur widely in malignant tumours, including glioblastoma (GBM). FOXM1 is a potent transcription factor that plays an oncogenic role by regulating the expression of many genes. As a SET domain containing protein, SET7 is a protein lysine methyltransferase which monomethylates histone proteins and other proteins. The epigenetic modification of histones regulates gene expressions by epigenetically modifying promoters of DNAs and inter vening in tumor development. Activation of FASN increased de novo fatty acid (FA) synthesis, a hallmark of cancer cells. Here, we report that FOXM1 may directly promote the transcription of SET7 and activate SET7-H3K4me1-FASN axis, which results in the maintenance of de novo FA synthesis.

CD8 T Cell-Derived Exosomal miR-186-5p Elicits Renal Inflammation via Activating Tubular TLR7/8 Signal Axis.

T cells play an important role in the development of focal segmental glomerulosclerosis (FSGS). The mechanism underlying such T cell-based kidney disease, however, remains elusive. Here the authors report that activated CD8 T cells elicit renal inflammation and tissue injury via releasing miR-186-5p-enriched exosomes. Continuing the cohort study identifying the correlation of plasma level of miR-186-5p with proteinuria in FSGS patients, it is demonstrated that circulating miR-186-5p is mainly derived from activated CD8 T cell exosomes. Renal miR-186-5p, which is markedly increased in FSGS patients and mice with adriamycin-induced renal injury, is mainly delivered by CD8 T cell exosomes. Depleting miR-186-5p strongly attenuates adriamycin-induced mouse renal injury. Supporting the function of exosomal miR-186-5p as a key circulating pathogenic factor, intravenous injection of miR-186-5p or miR-186-5p-containing T cell exosomes results in mouse renal inflammation and tissue injury. Tracing the injected T cell exosomes shows their preferential distribution in mouse renal tubules, not glomerulus. Mechanistically, miR-186-5p directly activates renal tubular TLR7/8 signal and initiates tubular cell apoptosis. Mutating the TLR7-binding sequence on miR-186-5p or deleting mouse TLR7 largely abolishes renal tubular injuries induced by miR-186-5p or adriamycin. These findings reveal a causative role of exosomal miR-186-5p in T cell-mediated renal dysfunction.

Kidney Involvement in Autoinflammatory Diseases.

Background: Autoinflammatory diseases (AIDs) were first proposed 20 years ago and caused by dysregulation of the innate immune system, leading to episodes of systemic inflammation. Advances in next-generation sequencing and biological technology have resulted in the identification of new monogenic diseases and the corresponding signaling pathways that may guide us in targeted therapy. The kidney is a major target organ of various inflammatory processes. Summary: During systemic inflammation, increased pro-inflammatory cytokines, such as IL-6, IL-1ß, and TNF, lead to over-transcription and release of acute phase reactant serum amyloid A (SAA). Sustained high SAA levels promote a cascade of pathophysiological events, including protein misfolding, protein fragmentation, and aggregation into highly ordered amyloid fibrils. Amyloid fibril deposition in the kidney cause progressive glomerular and vascular damage. Renal AA amyloidosis is a common and severe complication of AIDs, including familial Mediterranean fever, cryopyrin-associated periodic syndromes, TNF receptor-associated periodic fever syndrome, mevalonate kinase deficiency/hyper-IgD and periodic fever syndrome, and deficiency of adenosine deaminase 2. Amyloidosis may even be the first clinical manifestation in some patients, presenting with asymptomatic proteinuria, nephritic syndrome, progressive renal insufficiency, or end-stage kidney disease. In addition, major dysregulated pathways in different AIDs lead to endogenous inflammation, which is due to direct endothelial cytotoxicity caused by IL-1ß, type I interferon, or possibly immune complexes. The kidney is frequently affected by various vasculitis, and kidney involvement is a major determinant of treatment options and outcomes. The renal vasculitis involved in AIDs includes renal artery Takayasu vasculitis, polyarteritis nodosa, and IgA vasculitis. Moreover, other kidney diseases, such as glomerulonephritis, lupus nephritis, and renal tubular dysfunction, were also reported in AIDs. Key Messages: Kidney manifestations can be a coexisting disease seen with AIDs. They may also be one of the characteristics of AIDs. Clinicians should be aware of the possibility that amyloidosis, vasculitis, or other kidney diseases may be associated with AIDs in order to make appropriate diagnosis and treatment. Kidney biopsy may be of great significance. Biologics, which switch off the underlying cytokine-mediated inflammatory process, have the potential to restore organ damage and improve the outcome in the very early stage of the disease.

Recent Research Progress into Zinc Ion Battery Solid-Electrolyte Interfaces.

Aqueous zinc ion batteries (ZIBs) are prospective next-generation energy storage device candidates owing to resource abundance, affordability, eco-friendliness, and safety. The solid-electrolyte interface (SEI) produced in a ZIB by electrolyte/electrode interactions significantly impacts battery performance. The SEI is known to promote dendrite growth, determine the electrochemical stability window, passivate zinc-metal-anodic corrosion, and mutate the electrolyte. Accordingly, the SEI is closely related to the overall property of a ZIB device. This review provides an overview of the impact of SEIs on ZIB performance recently and provides an SEI design strategy based on the formation mechanism, type, and characteristics of the SEI. Finally, future investigational directions for SEIs in ZIBs are expected to lead to a deep understanding of the SEI, enhance ZIB performance, and facilitate their extensive implementation.

The Effect of W Content on the Microstructure, Mechanics and Electrical Performance of an FeCrCo Alloy.

In this paper, FeCrCoW alloys with different W contents (0.4, 2.1 and 3.4 at%) are designed and studied in order to overcome the existing shortcomings of resistance materials. These resistance materials have high resistivity and a low temperature coefficient of resistivity. It is observed that the addition of W has a remarkable effect on the phase structure of the alloy. In particular, when the W content is 3.4 at%, the single BCC phase of the alloy can be transformed into the BCC and FCC phase. Meanwhile, when analyzed by transmission electron microscopy, there are stacking faults and martensite in FeCrCoW alloy with W content of 3.4 at%. These features are related to excessive W content. In addition, the strength of the alloy can be improved, and the ultimate tensile strength and yield strength are both very high, which are considered as grain-boundary strengthening and solid solution strengthening, caused by the addition of W. The electrical resistivity of the FeCrCoW alloys decreases when the content of W is more than 2.1 at%. The maximum resistivity of the alloy is 170 ± 1.5 µΩ·cm. Moreover, the unique properties of the transition metal allow the alloy to have a low temperature coefficient of resistivity in the temperature range of 298~393 K. The temperature coefficient of resistivity values of the W0.4, W2.1 and W3.4 alloys are -0.0073, -0.0052 and -0.0051 ppm/K. Therefore, this work provides a vision for resistance alloys, which can achieve highly stable resistivity and high strengths in a certain temperature range.

Original self-assembled S-scheme BiOBr-(001)/Bi2SiO5/Bi heterojunction photocatalyst with rich oxygen vacancy for boosting CO2 reduction performance.

Photocatalysis CO2 reduction into high-value-added chemical feedstocks is desirable for simultaneously addressing the solar energy storage, CO2 excess and energy shortage issues. In this work, a kind of original S-scheme BiOBr-(001)/Bi2SiO5/Bi (OSB) heterostructure photocatalyst with rich oxygen vacancies is in-situ synthesized, which significantly promotes the photocatalytic CO2 reduction performance. Interestingly, the lower formation energy of oxygen vacancy exhibits the easy feasibility on the BiOBr-(001) surface via the assistant of ultrasound. There exists the highest photocatalytic CO2 reduction activity to CO of 234.05 µmol g-1h-1 for OSB-20 sample (ultrasound time: 20 min), higher 3.3 times than OSB-0 sample (without ultrasound). Combined with experimental and calculated results, the significative formation mechanism, widened light-response range, highly-efficient separation/transfer paths and improved redox-reduction abilities of photogenerated electron-hole pairs for S-scheme OSB-20 heterostructure are investigated and proposed. Our findings provide new insights for the construction and synthesis of the S-scheme Bi-based heterojunction photocatalyst system.

A Potential Adhesin/Invasin STM0306 Participates in Host Cell Inflammation Induced by Salmonella enterica Serovar Typhimurium.

Salmonella enterica serovar typhimurium (S. Typhimurium) is a common Gram-negative foodborne pathogenic bacterium that causes gastrointestinal disease in humans and animals. It is well known that adhesins and invasins play crucial roles in the infection mechanism of S. Typhimurium. S. Typhimurium STM0306 has been denoted as a putative protein and its functions have rarely been reported. In this study, we constructed the STM0306 gene mutant strain of S. Typhimurium and purified the recombinant STM0306 from Escherichia coli. Deletion of the STM0306 gene resulted in reduced adhesion and invasion of S. Typhimurium to IPEC-J2, Caco-2, and RAW264.7 cells. In addition, STM0306 could bind to intestinal epithelial cells and induced F-actin modulation in IPEC-J2 cells. Furthermore, we found that STM0306 activated the nuclear factor kappa B (NF-κB) signaling pathway and increased the mRNA expression of pro-inflammatory cytokines such as IL-1ß, TNF-α, as well as chemokine CXCL2, thus resulting in cellular inflammation in host cells. In vivo, the deletion of the STM0306 gene led to reduced pathogenicity of S. Typhimurium, as evidenced by lower fecal bacterial counts and reduced body weight loss in S. Typhimurium infected mice. In conclusion, the STM0306 of S. Typhimurium is an important adhesin/invasin involved in the pathogenic process and cellular inflammation of the host.