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Abstract Background Six-transmembrane epithelial antigen of prostate 3 (STEAP3), an essential constituent of the STEAP family protein, plays a notable role in promoting cancer proliferation and metastasis. Despite the importance of the STEAP gene family in tumor progression, the function of STEAP3 in cervical cancer (CC) remains unclear. Materials and methods The expression of STEAP3 protein in CC tissues and cell lines was identified using immunohistochemistry. The Reduced Representation Bisulfite Sequencing (RRBS) was used to detect global gene DNA methylation in CC tissues and paracancerous tissues. Cell viability, proliferation, migration, and invasion, were evaluated using the Cell Counting Kit-8 (CCK8), 5-ethynyl-2’-deoxyuridine (EdU), wound repair assay, and transwell assay, respectively. RNA sequencing was applied to explore STEAP3-related signaling pathways. Western blotting was performed to detect the expression of related proteins, including epithelial-mesenchymal transition (EMT) and Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling markers. Results Herein, STEAP3 was strongly expressed in CC tissues and associated with poor prognosis. CC samples exhibited lower levels of STEAP3 methylation than normal samples, and the methylation levels of CpG islands in STEAP3 were association with prognosis. In contrast to control group, STEAP3 knockdown suppressed the proliferation and invasion of CC cells and enhanced sensitivity to oxaliplatin. Silencing of STEAP3 led to reduced N-cadherin and vimentin levels and increased E-cadherin expression. RNA sequencing analysis suggested that STEAP3 mediated the activation of the JAK STAT3 signaling pathway. Additionally, inhibition of STEAP3 decreased the phosphorylation of JAK2 and STAT3. Interestingly, colivelin (a STAT3 activator) modified STEAP3-induced cell proliferation, invasion, and expression of related proteins in the EMT and JAK/STAT3 signaling pathway. Conclusion STEAP3 was significantly associated with CC progression mediated via the JAK/STAT3 signaling pathway and may serve as an effective therapeutic target.

Abstract Background Acute monocytic leukemia-M5 (AML-M5) remains a challenging disease due to its high morbidity and poor prognosis. In addition to the evidence mentioned earlier, several studies have shown that programmed cell death (PCD) serves a critical function in treatment of AML-M5. However, the role and relationship between ferroptosis and necroptosis in AML-M5 remains unclear. Methods THP-1 cells were mainly treated with Erastin and IMP-366. The changes of ferroptosis and necroptosis levels were detected by CCK-8, western blot, quantitative real-time PCR, and electron microscopy. Flow cytometry was applied to detect the ROS and lipid ROS levels. MDA, 4-HNE, GSH and GSSG were assessed by ELISA kits. Intracellular distribution of FSP1 was studied by immunofluorescent staining and western blot. Results The addition of the myristoylation inhibitor IMP-366 to erastin-treated acute monocytic leukemia cell line THP-1 cell not only resulted in greater susceptibility to ferroptosis characterized by lipid peroxidation, glutathione (GSH) depletion and mitochondrial shrinkage, as the FSP1 position on membrane was inhibited, but also increased p-RIPK1 and p-MLKL protein expression, as well as a decrease in caspase-8 expression, and triggered the characteristic necroptosis phenomena, including cytoplasmic translucency, mitochondrial swelling, membranous fractures by FSP1 migration into the nucleus via binding importin α2. It is interesting to note that ferroptosis inhibitor fer-1 reversed necroptosis. Conclusion We demonstrated that inhibition of myristoylation by IMP-366 is capable of switching ferroptosis and ferroptosis-dependent necroptosis in THP-1 cells. In these findings, FSP1-mediated ferroptosis and necroptosis are described as alternative mechanisms of PCD of THP-1 cells, providing potential therapeutic strategies and targets for AML-M5.

Soilborne diseases are important problems in modern agricultural production. Fusarium oxysporum f. sp. cucumerinum (FOC) is one of the predominant soilborne pathogens threatening cucumber cultivation, especially in Hainan, China. This study assessed FOC-resistant rootstocks using incidence rate, disease severity index (DSI), and area under the disease severity index curve (AUDRC), revealing “JinJiaZhen (Mc-4)” as resistant and “JinGangZhuan 1901 (Mc-18)” as susceptible. Comprehensive transcriptome and metabolome analyses were conducted to investigate the defense mechanisms of these rootstocks, revealing key pathways, such as the mitogen-activated protein kinase (MAPK) signaling pathway, starch and sucrose metabolism, and phenylpropanoid biosynthesis, which are crucial for plant disease resistance. Additionally, the study compared the resistance mechanisms of two other rootstocks, Mc-4 and Mc-18, against FOC infection through transcriptomic and metabolomic analyses. Mc-4 exhibited a higher number of differentially expressed genes (DEGs) related to phenylpropanoid biosynthesis compared to Mc-18. Untargeted metabolomics identified 4093 metabolites, with phenylpropanoid biosynthesis, isoquinoline alkaloid biosynthesis, and porphyrin metabolism as primary annotated pathways. On the sixth day post-inoculation, when the number of DEGs and differentially accumulated metabolites (DAMs) was highest, phenylpropanoid biosynthesis emerged as a key pathway in Mc-4, with 37 DEGs and 8 DAMs identified. Notably, Mc-4 showed upregulated expression of genes encoding enzymes involved in phenylpropanoid biosynthesis and increased accumulation of related metabolites, such as coniferyl-aldehyde, coniferyl alcohol, and coniferyl acetate. These findings highlight the differential defense mechanisms between resistant and sensitive rootstocks and provide insights into plant–pathogen interactions. This study’s results will contribute to the development of better and disease-free cucumber varieties, promoting sustainable agriculture.

ObjectiveTo examine the prognostic values of systemic immune-inflammation indices of hemodialysis (HD) vascular access failure and develop a prediction model for vascular access failure based on the most pertinent systemic immune-inflammation index.Study designA prospective cohort study.Setting & participantsPatients undergoing autogenous HD vascular access surgeries or arteriovenous graft as a permanent hemodialysis access in a tertiary center in southwest China from January 2020 to June 2022.PredictorsSystemic immune-inflammation indices, including NLR, dNLR, AAPR, SIRI, SII, PNI, PLR, and LIPI, and clinical variables.OutcomesThe outcome was defined as survival of the hemodialysis access, with both occluded and stenotic access being considered as instances of access failure.Analytical approachCox proportional hazard regression model.Results2690 patients were included in the study population, of whom 658 experienced access failure during the follow-up period. The median duration of survival for HD vascular access was 18 months. The increased systemic immune-inflammation indices, including dNLR, NLR, SII, PNI, SIRI, PLR, and LIPI, are predictive of HD access failure, with SII demonstrating the strongest prognostic value. A simple SII-based prediction model for HD access failure was developed, achieving C-indexes of 0.6314 (95% CI: 0.6249 – 0.6589) and 0.6441 (95% CI: 0.6212 – 0.6670) for predicting 6- and 12-month access survival, respectively.ConclusionsSystemic immune-inflammation indices are significantly and negatively associated with HD vascular access survival. A simple SII-based prediction model was developed and anticipates further improvement through larger study cohort and validation from diverse centers.

Abstract Circularly polarized light (CPL) detection has wide applications in many fields, where the anisotropy factor (gIph) is an important indicator to characterize the CPL detection performance. So far, many materials with high gIph have been reported, however, the exploration of the regulation of gIph is still in its infancy. Herein, two novel alternating chiral‐achiral cations intercalation‐type chiral hybrid perovskites (CHPs), named (R/S‐1‐phenylpropylamine)(propylamine)PbBr4 (1‐R/S), exhibit above room‐temperature (RT) polar‐phase transition, which greatly regulates the gIph value. The gIph of 1‐R is 0.04 in high‐temperature phase chiral non‐polar (P212121) by applying 5 V bias, interestingly, with the temperature decrease, the gIph value in low‐temperature phase chiral polar (P21) gradually increases (0.22@360K, 0.40@340K, 0.47@320K), and finally reaches a maximum of 0.5 at RT. Such value is not only the highest among 2D CHPs to date, but presents a 12.5‐fold amplification compared with 0.04. Further, this rare phenomenon should be attributed to the built‐in electric field induced by the polar photovoltaic effect, which sheds light on further obtaining CHPs with large gIph.

Abstract Background Ovarian cancer (OC) is one of the most common malignancies in women. It has a poor prognosis owing to its recurrence and metastasis. Unfortunately, reliable markers for early diagnosis and prognosis of OC are lacking. Our research aimed to investigate the value of the six-transmembrane epithelial antigen of prostate family member 3 (STEAP3) as a prognostic predictor and therapeutic target in OC using bioinformatics analysis. Methods STEAP3 expression and clinical data were acquired from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Gene Expression Omnibus (GEO). Unsupervised clustering was used to identify molecular subtypes. Prognosis, tumor immune microenvironment (TIME), stemness indexes, and functional enrichment analysis were compared between two definite clusters. Through the least absolute shrinkage and selection operator (LASSO) regression analysis, a STEAP3-based risk model was developed, and the predictive effectiveness of this signature was confirmed using GEO datasets. A nomogram was used to predict the survival possibility of patients. Additionally, TIME, tumor immune dysfunction and exclusion (TIDE), stemness indexes, somatic mutations, and drug sensitivity were evaluated in different risk groups with OC. STEAP3 protein expression was detected using immunohistochemistry (IHC). Results STEAP3 displayed marked overexpression in OC. STEAP3 is an independent risk factor for OC. Based on the mRNA levels of STEAP3-related genes (SRGs), two distinct clusters were identified. Patients in the cluster 2 (C2) subgroup had a considerably worse prognosis, higher immune cell infiltration, and lower stemness scores. Pathways involved in tumorigenesis and immunity were highly enriched in the C2 subgroup. A prognostic model based on 13 SRGs was further developed. Kaplan-Meier analysis indicated that the overall survival (OS) of high-risk patients was poor. The risk score was significantly associated with TIME, TIDE, stemness indexes, tumor mutation burden (TMB), immunotherapy response, and drug sensitivity. Finally, IHC revealed that STEAP3 protein expression was noticeably elevated in OC, and overexpression of STEAP3 predicted poor OS and relapse-free survival (RFS) of patients. Conclusion In summary, this study revealed that STEAP3 reliably predicts patient prognosis and provides novel ideas for OC immunotherapy.

Abstract Broadband photodetectors (PDs) with low detection limits hold significant importance to next‐generation optoelectronic devices. However, simultaneously detecting broadband (i.e., X‐ray to visible regimes) and weak lights in a single semiconducting material remains highly challenging. Here, by alloying iodine‐substituted short‐chain cations into the 3D FAPbI3 (FA = formamidine), a new 2D bilayered lead iodide hybrid perovskite, (2IPA)2FAPb2I7 (1, 2IPA = 2‐iodopropylammonium), that enables addressing this challenge is reported. Such a 2D multilayered structure and lead iodide composition jointly endow 1 with a minimized dark current (6.04 pA), excellent electrical property, and narrow bandgap (2.03 eV), which further gives it great potential for detecting broadband weak lights. Consequently, its high‐quality single crystal PDs exhibit remarkable photoresponses to weak ultraviolet–visible lights (377–637 nm) at several tens of nW cm−2 with high responsivities (>102 mA W−1) and significant detectivities (>1012 Jones). Moreover, 1 has an excellent X‐ray detection performance with a high sensitivity of 438 µC Gy−1 cm−2 and an ultralow detection limit of 20 nGy s−1. These exceptional attributes make 1 a promising material for broadband weak lights detection, which also sheds light on future explorations of high‐performance PDs based on 2D hybrid perovskites.

Abstract Organic room temperature phosphorescent materials are very limited to date. Halogen bonding interactions not only promote the intersystem crossing process, but also act as cement and dilute solution, preventing the aggregation induced quenching. Herein, four cocrystals using phenazine (PhZ) as halogen‐bonded acceptor and 1,2,4,5‐tetrabromo‐3,6‐diiodobenzene (BrFB) or 1,2,4,5‐tetrafluoro‐3,6‐diiodobenzene (IFB) as halogen‐bonded donor have been successfully synthesized in definite stoichiometric ratio (PhZ : XFB = 1:1 and 2:1) through simple solvent evaporation method. Among the four cocrystals, the halogen bonding interactions play an important role in assembling properties and the large red spots on Hirshfeld surface imply the strong strength. Notably, the IFB‐PhZ cocrystals exhibit a phosphorescence emission at peak of 733 nm with a lifetime up to 159 µs. The results further suggest the importance of the strength and number of halogen bonds to design organic room temperature phosphorescent materials.

IntroductionIdiopathic mesenteric phlebosclerosis colitis (IMP) is a rare condition that impairs colonic venous blood return owing to mesenteric venous sclerosis and fibrosis. At present, many studies have suggested that long-term intake of Chinese herbal medicines is associated with its pathogenesis. IMP has no characteristic clinical manifestations, and most patients with IMP present with acute intestinal obstruction. As a rare disease, the etiology, pathogenesis, pathophysiology, and treatment of IMP are being explored and studied.Case DescriptionA 60-year-old Chinese male patient with IMP was admitted to our hospital for acute intestinal obstruction, received subtotal colectomy and ileostomy after 10 days of ineffective conservative treatment, and was discharged after postoperative supportive treatment for 1 month.ConclusionThere are many causes of intestinal obstruction, and we report a relatively rare one. After failure of conservative treatment, it is necessary to surgically resect part of the diseased bowel.

Inhibitor of DNA binding 2 (Id2) can promote axonal regeneration after injury of the central nervous system. However, whether Id2 can promote axonal regeneration and functional recovery after peripheral nerve injury is currently unknown. In this study, we established a mouse model of bilateral sciatic nerve crush injury. Two weeks before injury, AAV9-Id2-3×Flag-GFP was injected stereotaxically into the bilateral ventral horn of lumbar spinal cord. Our results showed that Id2 was successfully delivered into spinal cord motor neurons projecting to the sciatic nerve, and the number of regenerated motor axons in the sciatic nerve distal to the crush site was increased at 2 weeks after injury, arriving at the tibial nerve and reinnervating a few endplates in the gastrocnemius muscle. By 1 month after injury, extensive neuromuscular reinnervation occurred. In addition, the amplitude of compound muscle action potentials of the gastrocnemius muscle was markedly recovered, and their latency was shortened. These findings suggest that Id2 can accelerate axonal regeneration, promote neuromuscular reinnervation, and enhance functional improvement following sciatic nerve injury. Therefore, elevating the level of Id2 in adult neurons may present a promising strategy for peripheral nerve repair following injury. The study was approved by the Experimental Animal Ethics Committee of Jinan University (approval No. 20160302003) on March 2, 2016.

On-chip microscale vacuum chambers with high sealing performance and electrical feedthroughs are highly desired for microscale vacuum electronic devices and other MEMS devices. In this paper, we report an on-chip microscale vacuum chamber which achieves a high sealing performance by using monolayer graphene as lateral electrical feedthrough. A vacuum chamber with the dimensions of π × 2 mm × 2 mm × 0.5 mm is fabricated by anodically bonding a glass chip with a through-hole between two Si chips in a vacuum, after monolayer graphene electrodes have been transferred to the surface of one of the Si chips. Benefiting from the atomic thickness of monolayer graphene, the leak rate of Si–glass bonding interface with a monolayer graphene feedthrough is measured at less than 2 × 10−11 Pa·m3/s. The monolayer graphene feedthrough exhibits a minor resistance increase from 22.5 Ω to 31 Ω after anodic bonding, showing good electrical conductance. The pressure of the vacuum chamber is estimated to be 185 Pa by measuring the breakdown voltage. Such a vacuum is found to maintain for more than 50 days without obvious degradation, implying a high sealing performance with a leak rate of less than 1.02 × 10−16 Pa·m3/s.

Molecular fluorophores emitting in the second near-infrared (NIR-II) window with good renal excretion ability are favorable for in vivo bio-imaging and clinical applications. So far, renally excretable fluorophores are still less studied. Understanding the influences of molecular structure on optical properties and renal excretion abilities are vital for fluorophore optimization. Herein, a series of shielding unit-donor-acceptor-donor-shielding unit (S-D-A-D-S) NIR-II molecular fluorophores are designed and synthesized with dialkoxy chains substituted benzene as the S unit. The anchoring positions of dialkoxy chains on benzene are tuned as meso-2,6, para-2,5, or ortho-3,4 to afford three fluorophores: BGM6P, BGP6P and BGO6P, respectively. Experimental and calculation results reveal that alkoxy side chains anchored closer to the conjugated backbone can provide better protection from water molecules and PEG chains, affording higher fluorescence quantum yield (QY) in aqueous solutions. Further, these side chains can enable good encapsulation of backbone, resulting in decreased binding with albumin and improved renal excretion. Thus, fluorophore BGM6P with meso-2,6-dialkoxy chains exhibits the highest quantum yield and fastest renal excretion. This work emphasizes the important roles of side chain patterns on optimizing NIR-II fluorophores with high brightness and renal excretion ability.

As one major component of extracellular matrix (ECM) in the central nervous system, chondroitin sulfate proteoglycans (CSPGs) have long been known as inhibitors enriched in the glial scar that prevent axon regeneration after injury. Although many studies have shown that CSPGs inhibited neurite outgrowth in vitro using different types of neurons, the mechanism by which CSPGs inhibit axonal growth remains poorly understood. Using cerebellar granule neuron (CGN) culture, in this study, we evaluated the effects of different concentrations of both immobilized and soluble CSPGs on neuronal growth, including cell adhesion, spreading and neurite growth. Neurite length decreased while CSPGs concentration arised, meanwhile, a decrease in cell density accompanied by an increase in cell aggregates formation was observed. Soluble CSPGs also showed an inhibition on neurite outgrowth, but it required a higher concentration to induce cell aggregates formation than coated CSPGs. We also found that growth cone size was significantly reduced on CSPGs and neuronal cell spreading was restrained by CSPGs, attributing to an inhibition on lamellipodial extension. The effect of CSPGs on neuron adhesion was further evidenced by interference reflection microscopy (IRM) which directly demonstrated that both CGNs and cerebral cortical neurons were more loosely adherent to a CSPG substrate. These data demonstrate that CSPGs have an effect on cell adhesion and spreading in addition to neurite outgrowth.

Our previous studies showed that mutant mice with congenital absence of the corticospinal tract (CST) undergo spontaneous remodeling of motor networks to partially compensate for absent CST function. Here, we asked whether voluntary wheel running could further improve locomotor plasticity in CST-deficient mice. Adult mutant mice were randomly allocated to a “runners” group with free access to a wheel, or a “non-runners” group with no access to a wheel. In comparison with non-runners, there was a significant motor improvement including fine movement, grip strength, decreased footslip errors in runners after 8-week training, which was supported by the elevated amplitude of electromyography recording and increased neuromuscular junctions in the biceps. In runners, terminal ramifications of monoaminergic and rubrospinal descending axons were significantly increased in spinal segments after 12 weeks of exercise compared to non-runners. 5-ethynyl-2′-deoxyuridine (EDU) labeling showed that proliferating cells, 90% of which were Olig2-positive oligodendrocyte progenitors, were 4.8-fold more abundant in runners than in non-runners. In 8-week runners, RNAseq analysis of spinal samples identified 404 genes up-regulated and 398 genes down-regulated, and 69 differently expressed genes involved in signal transduction, among which the NF-κB, PI3K-Akt and cyclic AMP (cAMP) signaling were three top pathways. Twelve-week training induced a significant elevation of postsynaptic density protein 95 (PSD95), synaptophysin 38 and myelin basic protein (MBP), but not of brain derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF) and insulin like growth factor-1 (IGF-1). Thus, locomotor training activates multiple signaling pathways, contributes to neural plasticity and functional improvement, and might palliate locomotor deficits in patients.

Nogo-66 receptor (NgR), a common receptor for the three known myelin-associated inhibitors, i.e., Nogo-A, myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein (OMgp), plays a key role in the failure of axonal regeneration in the adult mammalian central nervous system (CNS). Here we report a novel vaccine approach that stimulates the production of anti-NgR antibody to overcome NgR-mediated growth inhibition after spinal cord injury (SCI). We showed that adult rats immunized with recombinant NgR produced high titers of the anti-NgR antibody and that antisera obtained from the immunized rats promoted neurite outgrowth of rat cerebellar neurons on the inhibitory MAG substrate in vitro. In a spinal cord dorsal hemisection model, NgR immunization promoted regeneration of lesioned corticospinal tract (CST) axons, anterogradely labeled with biotin dextran amine (BDA), beyond the lesion site. In a contusive SCI model, NgR immunization markedly reduced the total lesion volume and improved Basso, Beattie, and Bresnahan (BBB) locomotor rating scale and grid walking performance. Thus, the NgR vaccine approach may represent a promising repair strategy to promote structural and functional recovery following SCI.

Chondroitin sulfate proteoglycans (CSPGs) are major components of the extracellular matrix which mediate inhibition of axonal regeneration after injury to the central nervous system (CNS). Several neuronal receptors for CSPGs have recently been identified; however, the signaling pathways by which CSPGs restrict axonal growth are still largely unknown. In this study, we applied quantitative phosphoproteomics to investigate the global changes in protein phosphorylation induced by CSPGs in primary neurons. In combination with isobaric Tags for Relative and Absolute Quantitation (iTRAQ) labeling, strong cation exchange chromatography (SCX) fractionation, immobilized metal affinity chromatography (IMAC) and LC-MS/MS, we identified and quantified 2214 unique phosphopeptides corresponding to 1118 phosphoproteins, with 118 changing significantly in abundance with CSPG treatment. The proteins that were regulated by CSPGs included key components of synaptic vesicle trafficking, axon guidance mediated by semaphorins, integrin signaling, cadherin signaling and EGF receptor signaling pathways. A significant number of the regulated proteins are cytoskeletal and related proteins that have been implicated in regulating neurite growth. Another highly represented protein category regulated by CSPGs is nucleic acid binding proteins involved in RNA post-transcriptional regulation. Together, by screening the overall phosphoproteome changes induced by CSPGs, this data expand our understanding of CSPG signaling, which provides new insights into development of strategies for overcoming CSPG inhibition and promoting axonal regeneration after CNS injury.

Malignant glioma exhibits immune evasion characterized by highly expressing the immune checkpoint CD47. RNA 5-methylcytosine(m5C) modification plays a pivotal role in tumor pathogenesis. However, the mechanism underlying m5C-modified RNA metabolism remains unclear, as does the contribution of m5C-modified RNA to the glioma immune microenvironment. In this study, we demonstrate that the canonical 28SrRNA methyltransferase NSUN5 down-regulates β-catenin by promoting the degradation of its mRNA, leading to enhanced phagocytosis of tumor-associated macrophages (TAMs). Specifically, the NSUN5-induced suppression of β-catenin relies on its methyltransferase activity mediated by cysteine 359 (C359) and is not influenced by its localization in the nucleolus. Intriguingly, NSUN5 directly interacts with and deposits m5C on CTNNB1 caRNA (chromatin-associated RNA). NSUN5-induced recruitment of TET2 to chromatin is independent of its methyltransferase activity. The m5C modification on caRNA is subsequently oxidized into 5-hydroxymethylcytosine (5hmC) by TET2, which is dependent on its binding affinity for Fe2+ and α-KG. Furthermore, NSUN5 enhances the chromatin recruitment of RBFOX2 which acts as a 5hmC-specific reader to recognize and facilitate the degradation of 5hmC caRNA. Notably, hmeRIP-seq analysis reveals numerous mRNA substrates of NSUN5 that potentially undergo this mode of metabolism. In addition, NSUN5 is epigenetically suppressed by DNA methylation and is negatively correlated with IDH1-R132H mutation in glioma patients. Importantly, pharmacological blockage of DNA methylation or IDH1-R132H mutant and CD47/SIRPα signaling synergistically enhances TAM-based phagocytosis and glioma elimination in vivo. Our findings unveil a general mechanism by which NSUN5/TET2/RBFOX2 signaling regulates RNA metabolism and highlight NSUN5 targeting as a potential strategy for glioma immune therapy. [ABSTRACT FROM AUTHOR]

The heterogeneous micro-interface plays a crucial role in facilitating mass transfer and catalytic conversion. This study aimed to investigate the influence of the surfactant cetyltrimethyl ammonium bromide (CTAB) on micro-interface properties during sonocatalytic degradation of Orange II using bagasse biochar. Our findings indicate that increasing the concentration of CTAB or the dosage of bagasse biochar significantly enhances sonocatalytic degradation efficiency. However, an increase in solution pH was observed to have a detrimental effect on degradation efficiency, while higher ultrasonic power proved beneficial for Orange II degradation when CTAB was present. Moreover, the pseudo-first-order rate constant (Kapp) for the sonocatalytic process was 1.3 times that of the sum of combined Kapp values obtained with ultrasonication and biochar adsorption individually, indicating a substantial synergistic effect when bagasse biochar and ultrasonication are combined in the presence of CTAB. The influence of inorganic anions on sonocatalytic degradation of Orange II, in the presence of CTAB, was relatively weak. Quenching tests using iso-propanol and KBr indicated that free radical chain reactions predominantly occurred at the micro-interface, with limited involvement in bulk solutions during the sonocatalytic degradation process. Overall, our results indicate that OH radicals remained the dominant contributors to the overall reaction. [ABSTRACT FROM AUTHOR]

Three-dimensional single-pixel imaging (3D SPI) has become an attractive imaging modality for both biomedical research and optical sensing. 3D-SPI techniques generally depend on time-of-flight or stereovision principle to extract depth information from backscattered light. However, existing implementations for these two optical schemes are limited to surface mapping of 3D objects at depth resolutions, at best, at the millimeter level. Here, we report 3D light-field illumination single-pixel microscopy (3D-LFI-SPM) that enables volumetric imaging of microscopic objects with a near-diffraction-limit 3D optical resolution. Aimed at 3D space reconstruction, 3D-LFI-SPM optically samples the 3D Fourier spectrum by combining 3D structured light-field illumination with single-element intensity detection. We build a 3D-LFI-SPM prototype that provides an imaging volume of ~390 × 390 × 3,800 µm³ and achieves 2.7-µm lateral resolution and better than 37-µm axial resolution. Its capability of 3D visualization of label-free optical absorption contrast is demonstrated by imaging single algal cells in vivo. Our approach opens broad perspectives for 3D SPI with potential applications in various fields, such as biomedical functional imaging. [ABSTRACT FROM AUTHOR]

The optimum mechanical properties of Fe-0.17C-2.10Mn-0.51Si steel are achieved by adjusting annealing and quenching temperatures. Annealing at 790 °C for 300 s, followed by quenching at 310 °C for 15 s and partitioning at 460 °C for 50 s, results in a tensile strength of 831.8 MPa and an elongation of 27.6 %. This is attributed to a higher volume fraction (13.1 %) and mechanical stability of retained austenite (RA), along with smaller grain size (3.99 µm) and a high proportion of high-angle grain boundaries (83.3 %), enhancing the transformation-induced plasticity (TRIP) effect. With increasing annealing and quenching temperatures, grain size increases. However, annealing temperature raises dislocation density, while quenching temperature reduces it. The fraction of RA initially increases and then decreases with higher annealing and quenching temperatures. XRD analysis shows carbide precipitation at 730 °C shifts peaks to lower angles, while dissolution at 850 °C and 910 °C leads to lattice expansion. Minimal peak shifts at 790 °C correlate with optimal properties. Micro-texture analysis reveals γ-fiber {111}//ND texture in BCC and Rotated-Goss texture in austenite, contributing to the balanced strength and ductility. This study offers insights into optimizing Q&P treatment for excellent mechanical performance.

Abstract Employees in enterprises face numerous challenges due to the severe employment situation and job pressure. Sales personnel and research and development (R&D) personnel in companies are particularly susceptible to mental health issues due to the unique nature and complexity of their work. This study aims to explore the psychological health issues among sales personnel and R&D personnel in high-tech enterprises. Twenty-four R&D personnel (23 males and 1 female) and twenty-six sales personnel (25 males and 1 female) were recruited. The participants’ psychological health conditions were assessed using the Symptom Checklist-90 (SCL-90) and verbal fluency tasks combined with functional near-infrared spectroscopy (VFT-fNIRS), while their work stress level was evaluated using the Personal Stress Questionnaire (PSQ) and Personal Resources Questionnaire (PRQ). The results indicated significantly higher brain activities in the right dorsolateral prefrontal cortex and bilateral Broca’s areas of the R&D group compared to the sales group. The R&D group had significantly lower scores in the total score and multiple dimensions of SCL-90, such as somatization, obsession-compulsion, depression, anxiety, hostility, and paranoia. In addition, the R&D group exhibited significantly lower psychological and physical tension reactions compared to the sales group in PSQ. Based on the PRQ, the R&D group obtained significantly higher scores in self-care compared to the sales group. In conclusion, the mental health status of the R&D group is better than that of the sales group, the difference in self-care may be the most important factor leading to the difference in work stress and mental health of the two groups, VFT-fNIRS might be used to assist in detecting the mental health status of employees.