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[Display omitted] • A Pt RTD was fabricated on turbine blades using DIW technology for the first time. • The sandwich structure enables the Pt RTD to exhibit high-temperature stability performance comparable to armored thermocouples. • The performance and preparation methods of the Pt RTD demonstrate promising potential for real-world applications. High-temperature resistance temperature detectors (RTDs) are gaining significant attention for various promising applications, including aeroengines, steel metallurgy, and construction machinery. However, it remains a critical challenge in developing RTDs on curved metal substrates without involving high-cost and complicated manufacturing processes. Herein, a metal-based sandwich type thick-film platinum (Pt) RTD for in-situ temperature monitoring of hot-end components is developed through a facile and high-efficient tape mask process and direct ink writing (DIW) technology. The liquid-formed glass–ceramic insulating layer and protective layer effectively immobilize the Pt particles within a sandwich structure, resulting in adequate protection from volatilization and aggregation of the Pt sensitive layer. Meanwhile, the insulating/protective layer exhibits outstanding insulation performance. Additionally, the fabricated Pt RTD achieved excellent repeatability, ultra-high stability (with a temperature drift rate of 0.7%/h at 800 °C), and high accuracy (0.92% full-scale) in the range of 50–800 °C. As an application example, the Pt RTD was fabricated on the surface of a turbine blade to verify its functionality at temperatures up to 800 °C. The exceptional performance and flexible fabrication process indicate that the Pt RTD is a promising candidate for in-situ temperature monitoring of critical aeroengine components. [ABSTRACT FROM AUTHOR]

Correlation filter has demonstrated the power in object tracking, benefiting from its superior speed and competitive performance. However, existing correlation filter based trackers (CFTs) are fragile for some inherent defects caused by the boundary effect. To address this issue, we propose a novel correlation filter based tracking framework by integrating three highly collaborative components, including a fast target proposal module, a distractor-aware filter, and a correlation filter based refiner. Specifically, the target proposal aims at determining some target-like regions in contexts efficiently, which provides target-like patches to learn a distractor-aware filter and detect. Multi-region strategy enlarges space fields for learning and prediction. The filter learned from both target and distractors enhances its ability to identify background. Therefore, our method is capable of evaluating multiple candidates in wider context with less risk of drifting to distractors, namely multi-anchor detection. Besides, the proposed Proposal-Detect-Refine hierarchical searching process progressively achieves data alignment between testing and training samples, which benefits for reliable model prediction. A refiner is used to fine-tune positions after multi-anchor detection for lessening error accumulation and preventing model from drifting. Comprehensive experiments on five challenging datasets, i.e. OTB2013, OTB2015, VOT2017, VOT19, and TC128, demonstrate that the proposed method achieves superior performance against the state-of-the-art methods. [ABSTRACT FROM AUTHOR]

Correlation filter (CF) based trackers have shown promising performance in object tracking. However, both the accuracy and efficiency of existing CF based trackers are limited. In this paper, we propose a robust and real-time object tracking framework, based on a canonical CF tracker. Specifically, we first propose an adaptive model update strategy for preventing the tracker from being contaminated when the target is occluded or disappears in sight. Then, we propose a multimodal validation method for reducing tracking failures, which is capable of generating potential candidates adaptively and evaluating them with a siamese network. In addition, we build a template library online to augment the discriminability of the employed siamese network. Experimental results over OTB-13 and OTB-15 benchmark datasets demonstrate that our method outperforms state-of-the-art ones. Especially, on OTB-15, our method not only achieves a relative gain of 12.3% in AUC score but also runs at a high tracking speed, i.e., 58.3 frames per second, in comparison with the baseline CF tracker. [ABSTRACT FROM AUTHOR]

• A decline in the FOXP3medium Tregs has a clinical correlation with early relapse in MCD. • Glucocorticoid treatment attenuates mTORC1 activation and replenishes the FOXP3medium Tregs population. • Baseline levels of FOXP3medium Tregs and mTORC1 activity serve as reliable predictors for MCD relapse. • mTORC1 inhibition restores impaired Treg conversion and IL-10 production in CD4+ T cells of MCD patients. • This study suggests potential therapeutic avenues targeting the mTORC1 pathway for Treg normalization in podocytopathies. Minimal change disease (MCD) usually responds to glucocorticoids (GCs) but relapses in most cases. Relapse pathogenesis after complete remission (CR) remains unclear. We hypothesized that FOXP3+ T regulatory cell (Treg) dysregulation may drive early relapses (ER). In this study, a cohort of 23 MCD patients were treated with a conventional GC regimen for the initial onset of nephrotic syndrome. Upon GC withdrawal, seven patients suffered from ER, while 16 patients sustained remission (SR) during the 12-month follow-up. Patients with ER had reduced FOXP3+ Treg proportions compared with healthy controls. Treg reduction, accompanied by IL-10 impairment, was ascribed to a proportional decline of FOXP3medium rather than FOXP3high cells. GC-induced CR was marked by a rise in the proportions of FOXP3+ and FOXP3medium cells compared to baseline levels. These increases declined in patients with ER. The expression level of phosphorylated ribosomal protein S6 was used to track the dynamic shifts in mTORC1 activity within CD4+ T cells of MCD patients at various stages of treatment. Baseline mTORC1 activity was inversely correlated with FOXP3+ and FOXP3medium Treg proportion. The mTORC1 activity in CD4+ T cells served as a reliable indicator for ER and demonstrated improved performance when paired with FOXP3 expression. Mechanically, targeting mTORC1 intervention by siRNAs sufficiently altered the conversion pattern of CD4+ T cell to FOXP3+ Treg. Taken together, the activity of mTORC1 in CD4+ T cells can act as a credible predictor for ER in MCD, especially when combined with FOXP3 expression, and may offer a potential therapeutic avenue for the treatment of podocytopathies. [ABSTRACT FROM AUTHOR]

Polymer-derived ceramics (PDCs) is considered to be a promising material for extreme environments such as aero-engine and hypersonic vehicles. However, current methods for PDCs thin films focus on 2D forms, hindering the applications for 3D curved structures where the majority of objects hold complex curvilinear surfaces. To overcome these limitations, a new conformal 3D printing system was developed for in situ preparation of the PDCs films on the curved surfaces for the first time by material extrusion. Through conformal algorithm development and process parameters exploration, different patterns on curved surfaces were realized. Subsequently, a conformal thin film temperature sensor (CTFTS) was fabricated on an alumina cylinder and tested at a high temperature of 800 °C. The results showed that the repeatability of multi-cycles was excellent and the resistance change rate was less than 1 % for half an hour of holding at 400 °C, 600 °C, and 800 °C. Given the high performance of the CTFTS on curved surfaces and the surface compatibility, CTFTS was fabricated conformally on a silicon nitride ceramic bearing and an alumina ceramic bolt, respectively. In the flame test and the rotation test, the CTFTS could detect in situ temperature in real-time with a response better than the commercial thermocouple. Therefore, the PDCs thin film conformal fabrication technique in this study is a highly promising approach for bringing PDCs films to practical applications, as well as a reference for multi-material conformal 3D printing. [Display omitted] • Conformal 3D printing of functional polymer-derived ceramics(PDCs) thin films on curved surfaces was achieved. • The conformal thin film temperature sensor(CTFTS) of PDCs was fabricated via conformal direct ink writing. • The CTFTS was applied for the real-time temperature monitoring under the actual rotation test and the flame test. [ABSTRACT FROM AUTHOR]

The restriction measures have not significantly affected the ESRD patients on peritoneal dialysis as compared to the patients undergoing hemodialysis at hospital facility. Novel coronavirus disease in hemodialysis (HD) patients: report from one HD center in Wuhan, China. Dear Editor, The recent outbreak of coronavirus disease 2019 (COVID-19) in Wuhan, China, caused by the newly identified SARS-CoV-2 has claimed more than 80,000 people in China. [Extracted from the article]

Thin-film sensors have great advantages over bulk sensors in high-temperature applications, such as non-disturbance and fast response. However, oxidation at high temperatures affects their reliability and could even destroy the sensors. Anti-oxidative coatings or environmental barrier coatings (EBCs) can be used to protect the sensors from oxidation at high temperatures. In this study, a thin-film anti-oxidative coating based on polymer-derived ceramics (PDCs) is proposed. By using a direct-writing technique, the coating was applied to a PDC thermistor, and its electrical resistance was measured from room temperature to 800 °C. The resistance of the thermistor coated with the anti-oxidative coating remained virtually constant throughout four consecutive test runs at temperatures of up to 800 °C. The maximum relative standard deviation of the four runs of the resistance-temperature test data was 5.3%, which is one-third that of the thermistor without anti-oxidative coating. The results indicate that the coating can protect the thin-film thermistor from being oxidized at temperatures ranging from room temperature to 800 °C. The mechanism of anti-oxidation of the coating is that a layer of B 2 O 3 forms on the surface of the coating, which prevents the oxygen from diffusing into the coating at high temperature. The coating provides a simple way of producing coatings for high-temperature applications. • An anti-oxidative coating based on particle-filled SiCN precursor was fabricated via direct-writing. • The anti-oxidative mechanism of the coating is revealed. • The electrical insulating property of the coating is investigated from room temperature to 800℃. • The R-T curves of the PDC thin-film thermistors with and without the coating verify the oxidation resistance of the coating [ABSTRACT FROM AUTHOR]

Background: The pathological patterns underlying PNS in adult are poorly studied in Central China. Methods: This is a retrospective analysis of the clinical and pathologic data involving 627 adult patients with PNS who have been finished the renal biopsies from January 2009 to September 2012 in XiangYa 2nd Hospital of Central South University. Patients enrolled in our study were all from Central China. Results: There were 379 males and 248 females, formed the ratio of 1.53:1. There existed three main sorts of pathological patterns underlying PNS: membranous nephropathy (MN) 26.63%, minimal change disease (MCD) 23.60%, IgA nephropathy (IgAN) 23.39%. Among all biopsies, the proportion of FSGS underlying PNS increased from 5.8% during the period from 2009 to 2010 to 14.7% during the period from 2011 to 2012. The most common complication of PNS was infectious diseases, and MCD underlying PNS ran a higher risk of encountering acute renal injury. IgAN had the highest incidence of hematuresis. The common pathological patterns of PNS differed in age-brackets: IgAN and MCD were the main pathological lesions in patients aged from 16 to 30 years; MN mostly occurs in patients over 30. MCD was the dominating pathological lesions underlying IgAN which expressed as PNS. Conclusions: (1) MN was the most frequent pathological pattern underlying PNS, the proportion of FSGS underlying PNS increased during the last 2 years. (2) The common pathological patterns of PNS differed in age-brackets and pathological patterns correlated to the complications or comorbidities of PNS to some extent. [ABSTRACT FROM AUTHOR]

Background Mechanical catheter dysfunction caused by omentum entrapment remains a major complication of peritoneal dialysis (PD) therapy. The purpose of this study was to determine the outcomes of omentum folding at the time of primary open catheter insertion. Methods From March 2008 to December 2012, a total of 67 PD subjects were enrolled in the study and randomly assigned to receive either regular open insertion (ROI group, n = 33) or open insertion with omentum folding (OIOF group, n = 34). The primary outcome was defined as PD catheter tip migration with dysfunction. A systematic review was performed to analyze the outcomes of omentum management in PD catheter implantation, based on published data from 1990 to 2013. Results There was no statistical difference in baseline patient characteristics between the ROI and OIOF groups. Nine (27.3%) patients in the ROI group presented with catheter malposition in the late stage (>60 days) of the study, significantly more than in the OIOF group (two; 5.9%) (P = 0.049). Significant differences in catheter survival rate between the two groups were observed in the late stage (P = 0.030) and over the entire study period (P = 0.028). A higher incidence of irreversible catheter dysfunction was shown in the ROI group (15.2%), whereas none occurred in the OIOF group (P = 0.031). No statistical difference was determined in other catheter-related complications or patient survival rate. There were no statistical differences in peritoneal transport characteristics or dialysis adequacy between the two groups upon evaluation at 3, 6 and 12 months. Systemic review of current publications suggested that PD catheter placement with omentum management could lead to less irreversible catheter dysfunction and improved outcome of catheter survival. Conclusions Our data suggest that omentum folding at the initial time of open catheter placement can significantly reduce the risk of catheter tip migration with dysfunction and improve the outcome of the PD technique. [ABSTRACT FROM PUBLISHER]

Abstract: Patients with nephrotic syndrome (NS) carry a high risk of venous thromboembolism (VTE) due to the abnormalities in coagulation and fibrinolysis. Although massive urine protein loss is considered to trigger the cascade of hypercoagulation, the exact nature of VTE in NS patients still remains obscure, especially in some cases when VTE occurs far before the presence of nephrotic proteinuria. Recent findings illustrate that loss of local glomerular homeostasis, like disturbance of cytokine profiles in endothelial cells or aberrant cellular crosstalks in glomerulus, is sufficient to initiate the development of thrombotic disease in glomerulonephropathy. Emerging data have highlighted the glomerular endothelial cell as a key regulator of local homeostasis, which might mediate the haemostatic derangement in the beginning of glomerular disease by expression of numerous prothrombotic factors and result in the subsequent predilection of VTE in NS. As the glomerulus-derived circulating factors are all collected and flushed into the renal vein directly, it is reasonable to suggest that increased release of glomerulus-derived thrombotic regulators, particularly from endothelial cells, may play a significant role in the highest proclivity for the renal vein as the site of thrombosis in NS. In this review, we thus discuss the current understandings of thromboembolism in NS with focus on how the glomerular endothelial cell involves in the pathogenesis of VTE, which may help to increase our understandings in the anti-thrombotic therapy for patients with NS. [Copyright &y& Elsevier]

The article obtains the uniform local asymptotics of the overshoot of a random walk with heavy-tailed increments. When the overshoot is in (x + y, x + y + T] for some 0

Thin-film sensors have wide applications in the fields of high-temperature measurement, such as in the hot section of aero engines. Polymer-derived ceramics (PDCs) are diversified, ease to shape, and resistant to thermal shock. However, they are seldom used as sensitive parts of thin-film sensors due to the oxidation of PDC thin films. To solve this challenging problem, pyrolysis of PDC thin films in vacuum is proposed in this work, and the anti-oxidation performances are verified in a high-temperature sensor based on such a PDC thin film. The temperature measurement experiment shows that the PDC thin-film temperature sensor with thickness of about 10 µm pyrolyzed in vacuum can measure temperature from room temperature to 800 ℃, which provides a feasible way for fabrication of high-temperature PDC thin-film sensors such as heat flux sensors and strain sensors. [ABSTRACT FROM AUTHOR]

• DNA methyltransferase 3B was aberrantly elevated in IgAN PBMC. • DNA methyltransferase 1 might be protective in IgA nephropathy. • Mainly DNA methyltransferase 3B was associated with pathology of IgA nephropathy. DNA methylation, especially DNA methyltransferases (DNMTs), is involved in the pathogenesis of many autoimmune diseases through regulating immune function. This study aimed to explore the potential role of DNMTs in IgA nephropathy (IgAN). We evaluated mRNA expressions of DNMT1 , DNMT3A , DNMT3B along with β1,3-galactosyltransferase (C1GALT1) in peripheral blood mononuclear cells (PBMCs), and measured galactose-deficient IgA1 (Gd-IgA1) levels in plasma. The expression intensity of DNMT1 and DNMT3B in the renal specimen of IgAN patients were also detected. Results showed DNMT3B , not DNMT1 or DNMT3A , was notably increased in IgAN patients compared to controls and associated with pathologic types. However, DNMT1 and C1GALT1 were found positively correlated with estimated glomerular filtration rate (eGFR) and negatively correlated with 24 h Urine protein in IgAN patients. No association was found between DNMT1 and Gd-IgA1. The expressions of DNMT3B and DNMT1 were barely observed in IgAN renal biopsy specimens. In conclusion, for the first time, we identified the relations of DNMTs and C1GALT1 to the clinical state and pathology of IgAN patients, which provide new clues for IgAN. [ABSTRACT FROM AUTHOR]

[Display omitted] Thin-film sensors are essential for real-time monitoring of components in high-temperature environments. Traditional fabrication methods often involve complicated fabrication steps or require prolonged high-temperature annealing, limiting their practical applicability. Here, we present an approach using direct ink writing and laser scanning (DIW-LS) to fabricate high-temperature functional thin films. An indium tin oxide (ITO)/preceramic polymer (PP) ink suitable for DIW was developed. Under LS, the ITO/PP thin film shrank in volume. Meanwhile, the rapid pyrolysis of PP into amorphous precursor-derived ceramic (PDC) facilitated the faster sintering of ITO nanoparticles and improved the densification of the thin film. This process realized the formation of a conductive network of interconnected ITO nanoparticles. The results show that the ITO/PDC thin film exhibits excellent stability, with a drift rate of 4.7 % at 1000 °C for 25 h, and withstands temperatures up to 1250 °C in the ambient atmosphere. It is also sensitive to strain, with a maximum gauge factor of −6.0. As a proof of concept, we have used DIW-LS technology to fabricate a thin-film heat flux sensor on the surface of the turbine blade, capable of measuring heat flux densities over 1 MW/m2. This DIW-LS process provides a viable approach for the integrated, rapid, and flexible fabrication of thin film sensors for harsh environments. [ABSTRACT FROM AUTHOR]

Ferroptosis, a defensive strategy commonly employed by the host cells to restrict pathogenic infections, has been implicated in the development and therapeutic responses of various types of cancer. However, the role of ferroptosis in oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV)-induced cancers remains elusive. While a growing number of non-histone proteins have been identified as acetylation targets, the functions of these modifications have yet to be revealed. Here, we show KSHV reprogramming of host acetylation proteomics following cellular transformation of rat primary mesenchymal precursor. Among them, SERPINE1 mRNA binding protein 1 (SERBP1) deacetylation is increased and required for KSHV-induced cellular transformation. Mechanistically, KSHV-encoded viral interleukin-6 (vIL-6) promotes SIRT3 deacetylation of SERBP1, preventing its binding to and protection of lipoyltransferase 2 (Lipt2) mRNA from mRNA degradation resulting in ferroptosis. Consequently, a SIRT3-specific inhibitor, 3-TYP, suppresses KSHV-induced cellular transformation by inducing ferroptosis. Our findings unveil novel roles of vIL-6 and SERBP1 deacetylation in regulating ferroptosis and KSHV-induced cellular transformation, and establish the vIL-6-SIRT3-SERBP1-ferroptosis pathways as a potential new therapeutic target for KSHV-associated cancers. Author summary: Ferroptosis has been implicated in viral infections and the development of cancers, however, its role in oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV)-induced cancers is still unknown. Although abnormal protein lysine acetylation modification has been strongly implicated in tumorigenesis, the exact role of this modification in KSHV-induced cell transformation remains elusive. Our study uncovers the reduction of acetylation of SERPINE1 mRNA binding protein 1 (SERBP1), which is required for KSHV-induced cellular transformation. KSHV-encoded viral interleukin-6 (vIL-6) promotes SIRT3 deacetylation of SERBP1, preventing its binding to and protection of lipoyltransferase 2 (Lipt2) mRNA from mRNA degradation resulting in ferroptosis. A SIRT3-specific inhibitor, 3-TYP, induces ferroptosis and inhibits survival of KSHV-transformed cells. These findings define a novel mechanism contributing to KSHV-induced cellular transformation and provide a rationale for therapeutically targeting lysine acetylation and the associated enzyme for infectious diseases. [ABSTRACT FROM AUTHOR]

Objectives: Conventional glucocorticoid (GC) treatment poses significant risks for opportunistic infections due to its suppressive impact on CD4+ T cells. This study aimed to explore the mechanisms by which GCs modulate the functionality of CD4+ T cells during infection. Methods: We consistently measured FOXP3, inflammatory cytokines and phospho‐S6 ribosomal protein levels in CD4+ T cells from patients undergoing conventional GC treatment. Using Foxp3EGFP animals, we investigated the dynamic activation of the mechanistic target of rapamycin complex 1 (mTORC1) pathway and its correlation with the immunoregulatory function of CD4+ T cells under the influence of GCs. Results: GCs dynamically altered the expression pattern of FOXP3 in CD4+ T cells, promoting their acquisition of an active T regulatory (Treg) cell phenotype upon stimulation. Mechanistically, GCs undermined the kinetics of the mTORC1 pathway, which was closely correlated with phenotype conversion and functional properties of CD4+ T cells. Dynamic activation of the mTORC1 signaling modified the GC‐dampened immunoregulatory capacity of CD4+ T cells by phenotypically and functionally bolstering the FOXP3+ Treg cells. Interventions targeting the mTORC1 pathway effectively modulated the GC‐dampened immunoregulatory capacity of CD4+ T cells. Conclusion: These findings highlight a novel mTORC1‐mediated mechanism underlying CD4+ T cell immunity in the context of conventional GC treatment. [ABSTRACT FROM AUTHOR]

The therapeutic potential of targeting CD4+Foxp3+ regulatory T cells (Tregs) remains controversial under the condition of neuroinflammation. This study aims to explore the neuroprotective role of Tregs in optic nerve ischemia (ONI) and evaluate the therapeutic strategy of Tregs transfer with a focus on targeting the mammalian target of rapamycin (mTOR) pathway. Intraocular pressure was transiently increased in adult C57BL/6 mice to induce ONI. Mucosal tolerance of myelin basic protein (MBP) markedly increased retinal ganglion cell (RGC) survival after ONI through enhanced Tregs suppression. mTOR inhibition significantly promoted the frequency of MBP-immunized Tregs in vitro with increased production of anti-inflammatory cytokines. Transient rapamycin treatment highly promoted the immunosuppressive capacity of Tregs and inhibited retinal inflammation in ONI animals. Intravenous infusion of MBP-immunized Tregs, instead of regular Tregs, beneficially modulated immune activities of host retinal CD11b+ cells and CD4+ effector T cells, leading to significant improvement of RGC survival. Importantly, rapamycin treatment further enhanced the neuroprotective effect of Tregs transfer. Taken together, these findings reveal a fine regulation of mTOR signaling on immunized Tregs after acute retinal injury. Adoptive transfer with targeting-mTOR strategy markedly improves neuronal recovery after ONI, supporting the therapeutic potentials of Tregs in acute and chronic neurological disorder. [ABSTRACT FROM AUTHOR]

The vein–membrane structure inspired by insect wings is applied to the artificial structural design of materials, with the aim of enhancing the intrinsic low strain tolerance and bonding strength of Al2O3 coating. Al2O3 platelets with high aspect ratio are used as veins, forming a bioinspired vein–membrane structure along with the Al2O3 membrane. Further, Al2O3 platelets take "root" in the substrate, forming a bioinspired root–soil interlocking structure. The greatest highlight of this coating is that it can restrict the cracks to the submicron area enclosed by the vein. The multi‐bioinspired structure enabled the Al2O3 coating to sustain strains as high as 8%, which is 2 orders of magnitude higher than the reported failure strain of Al2O3 film. The bonding strength is also increased by at least five times. The vein–membrane structure opens a novel technological space for the artificial structural design of materials. [ABSTRACT FROM AUTHOR]

The thermal degradation of materials strongly influences the weld strength in laser transmission welding (LTW). Weld strength decreases at high temperatures because of material thermal degradation. Hence, it is necessary to investigate this phenomenon. Thermal degradation of polyamide 66 (PA66) was predicted by combining a pyrolysis kinetic model with a 3-D transient thermal model. Thermogravimetric analysis (TGA) was used to study the pyrolysis characteristic of PA66. The TGA data were used to obtain kinetic parameters of PA66 using an n th order model in MATLAB. In addition, material conversion as a function of temperature (time) was analyzed using this kinetic reaction model containing the relevant kinetic parameters. A 3-D transient thermal model based on a volumetric heat source was developed. The temperature-time data of the point located at the maximum temperature was predicted through this thermal analysis model under different weld parameters. This study demonstrates that the predicted power at which the material starts to degrade is generally consistent with the power at which shear strength begins to decrease. The present studies lay a theoretical foundation for the investigation of thermal degradation during LTW. [ABSTRACT FROM AUTHOR]

Because of great polar differences and poor compatibility, polyethylene (PE) and polyamide 66 (PA66) cannot be welded by laser transmission welding (LTW), even though they are widely used in our daily life. In this paper, using grafting modification technology to improve the welding performance between PE and PA66 is researched. First of all, two ways of the graft modified polyethylene (TGMPE) that the strong polar and reactive maleic anhydride (MAH) and glycidyl methacrylate (GMA) are grafted to PE respectively are introduced. Also, the mechanical and thermal performances of TGMPE are tested which show that the grafting modification has small influence on them. After TGMPE and PA66 are welded by laser, the high welding strength is found and the mechanism of the weldability between them is researched, which reveals that two reasons account for the high welding strength. For one thing, by observing the welding region micro morphology, it is not difficult to find that the grafting modification makes low interfacial tension, good compatibility, and strong interfacial adhesion between PE and PA66. At the same time, the good compatibility makes them easy to diffuse mutually, which causes some locking structures formed in the welding region. For another, the X-ray photoelectron spectrometer proves that chemical reactions are involved between TGMPE and PA66, which make the welding performance better. Afterward, the tensile failure forms of the welding are researched. At last, the welding strength of the MAH modified polyethylene and PA66 is compared to the GMA modified polyethylene and PA66. [ABSTRACT FROM AUTHOR]

Background Acute kidney injury (AKI) is a public health problem with no specific therapies in the clinic and the underlying pathogenesis of AKI remains obscure. Bombesin receptor-activated protein (BRAP, C6ORF89 protein) was initially discovered as a ligand for a previously orphan G-protein-coupled receptor bombesin-like receptor-3. At present, accepted biological effects of BRAP include cell cycle progression, wound repair and the activation of histone deacetylases. However, its role in kidney disease is unknown. In this study we have investigated the role of BRAP and underlying mechanisms involved in cisplatin (CP)-induced AKI. Methods Here we used Bc004004 (homologous of C6ORF89 in mice) knockout mice and HK2 cells to investigate the effect of BRAP on AKI in vitro and in vivo. We analyzed ChIP-Seq and RNA-Seq data to search for the upstream regulators of BRAP and downstream mediators of BRAP action in AKI. Immunostaining, real-time polymerase chain reaction (PCR), co-immunoprecipitation, a dual-luciferase reporter assay and ChIP-PCR assay were applied to reveal the upstream and downstream regulation mechanism of BRAP during cisplatin-induced AKI. Results BRAP was downregulated in mice and human kidneys with AKI. Global Bc004004 deletion alleviated tubular cell apoptosis and necroptosis in CP-induced AKI mice, whereas local overexpression of BRAP in kidneys aggravated them. Pan-caspase inhibitor Z-VAD pretreatment attenuated CP-induced blood creatinine increase and kidney injury in wild-type mice but not in BRAP -/- mice. The activation of mixed lineage kinase like-domain was magnified by Z-VAD in CP-treated mice, especially in BRAP -/- mice. The cytoprotective effect of Z-VAD was more substantial than necrostatin-1 (Nec-1, an inhibitor of necroptosis) in CP-treated human kidney proximal tubular epithelial (HK2) cells. Furthermore, Nec-1 pretreatment reduced the CP-induced cell death in BRAP overexpression HK2 cells but did not work in cells with normal BRAP levels. We determined that CP treatment activated the nuclear factor-κB subunit P65 and inhibition of P65 increased the messenger RNA (mRNA) levels of BRAP in HK2 cells. The chromatin immunoprecipitation assay and dual-luciferase reporter gene assay verified P65 binding to the C6ORF89 promoter and reduced its mRNA expression upon CP treatment. Next we found that sirtuin 2 (SIRT2) was downregulated in CP-induced AKI and BRAP levels directly impacted the protein levels of SIRT2. Our findings further confirmed that BRAP regulates the SIRT2 protein levels by affecting SIRT2's interactions with E3 ubiquitin ligase HRD1 and subsequent proteasomal degradation. Conclusions Our results demonstrated that BRAP played an important role in tubular cell apoptosis and necroptosis during CP-induced AKI. Safe and efficient BRAP inhibitors might be effective therapeutic options for AKI. [ABSTRACT FROM AUTHOR]

Background: Mesangial cell proliferation is the most basic pathological feature of immunoglobulin A nephropathy (IgAN); however, the specific underlying mechanism and an appropriate therapeutic strategy are yet to be unearthed. This study aimed to investigate the therapeutic effect of triptolide (TP) on IgAN and the mechanism by which TP regulates autophagy and proliferation of mesangial cells through the CARD9/p38 MAPK pathway. Methods: We established a TP‐treated IgAN mouse model and produced IgA1‐induced human mesangial cells (HMC) and divided them into control, TP, IgAN, and IgAN+TP groups. The levels of mesangial cell proliferation (PCNA, cyclin D1, cell viability, and cell cycle) and autophagy (P62, LC3 II, and autophagy flux rate) were measured, with the autophagy inhibitor 3‐Methyladenine used to explore the relationship between autophagy and proliferation. We observed CARD9 expression in renal biopsies from patients and analyzed its clinical significance. CARD9 siRNA and overexpression plasmids were constructed to investigate the changes in mesangial cell proliferation and autophagy as well as the expression of CARD9 and p‐p38 MAPK/p38 MAPK following TP treatment. Results: Administering TP was safe and effectively alleviated mesangial cell proliferation in IgAN mice. Moreover, TP inhibited IgA1‐induced HMC proliferation by promoting autophagy. The high expression of CARD9 in IgAN patients was positively correlated with the severity of HMC proliferation. CARD9/p38 MAPK was involved in the regulation of HMC autophagy and proliferation, and TP promoted autophagy to inhibit HMC proliferation by downregulating the CARD9/p38 MAPK pathway in IgAN. Conclusion: TP promotes autophagy to inhibit mesangial cell proliferation in IgAN via the CARD9/p38 MAPK pathway. [ABSTRACT FROM AUTHOR]

The use of electrical solder joints for die attachment and interconnection in harsh environments remains a significant challenge. The interconnections between traditional metal solder joints and ceramic/semiconductor devices often fail during thermal cycling owing to mismatched coefficients of thermal expansion. In this study, TiB 2 -modified polymer-derived ceramic (PDC) electrical solder joints were developed for electrical interconnections. Owing to the close contact between the PDC paste and the metal/ceramic/semiconductor, as well as the TiB 2 percolation path formed inside the solder joint, the solder joint exhibited extremely low resistance and reliable electrical connection. Thermal cycling tests showed that the PDC solder joints had negative resistance temperature coefficients, excellent repeatability, and oxidation resistance up to 800 °C. After being oxidized at 800 °C for 24 h, the resistance at the solder joint only changed by 1.4 Ω. This solder joint can not only be used for metal devices but also for ceramic/semiconductor device electrical interconnections in harsh environments. • A TiB 2 -modified PDC solder joint was developed for metal/ceramic/semiconductor device interconnections in harsh environments. • The solder joint exhibited excellent thermal stability and high-temperature oxidation resistance. • The feasibility of solder joints for thin-film sensor interconnections was verified. [ABSTRACT FROM AUTHOR]

A reliable protective layer is one of the main challenges in preventing oxidation of thin film sensors to achieve accurate, effective, and stable readings at high temperatures. In this work, an Al2O3-modified polymer-derived ceramic SiCN composite coating fabricated by a direct-writing technique is utilized as a protective layer for thin film sensors. The microstructure evolution of the Al2O3/SiCN films is examined herein. The protective layer exhibits excellent oxidation resistance and thermal stability at high temperatures up to 1000 °C, which contributes to improving the stability and lifetime of thin film sensors in extreme environments. The TiB2/SiCN thin film resistive grid with the Al2O3/SiCN composite film as a protective layer is fabricated and tested. The results indicate that the coating can protect the TiB2/SiCN thin film resistive grid at high temperatures up to 1000 °C, which is about 200 °C higher than that of the TiB2/SiCN thin film resistive grid without a protective layer. The resistance change rates of the TiB2/SiCN thin film resistive grid with a protective layer are 0.5%/h at 900 °C and 10.7%/h at 1000 °C. [ABSTRACT FROM AUTHOR]

Purpose: The measurement of heat flux is of importance to the development of aerospace engine as basic physical quantities in extreme environment. Heat radiation is one of the basic forms of heat transfer phenomenon. The structure optimizing can improve the performance and infrared absorptivity of the thin film sensor. Design/methodology/approach: This paper designed one kind of thin film heat flux sensor (HFS) with antireflective coating based on transparent conductive oxide thermopile. The introduced membrane structure is so thin that it has little impact on sensor performance. Fabrication of thin film sensors were fabricated by physical vapor deposition (PVD) process. Findings: The steady-state and dynamic response characteristics of the HFS were investigated by calibration platform. The experimental results shown that the absorptivity of the membrane structure (for1070nm) improved compared with that before optimization. The sensitivity of heat flux gauge was 48.56 µV/ (kW/m2) and its frequency response was determined to be about 1980 Hz. Originality/value: The thin film HFS uses thermopile based on Indium Tin Oxid and In2O3. The antireflective coating is introduced to hot endpoint of HFS to improve sensitivity on laser thermal source. The infrared optical properties of membrane layer structure were investigated. The steady-state and the transient response characteristics of the heat flux sensor were also investigated. [ABSTRACT FROM AUTHOR]

The in situ temperature monitoring of hot components in harsh environments remains a challenging task. In this study, SiBCN thin-film resistance grids with thicknesses of 1.8 μm were fabricated on alumina substrates via direct writing. Owing to their dense microscopic morphology and extremely high graphitisation level, the produced SiBCN films exhibited large high-temperature oxidation resistance and electrical conductivity. The resistance–temperature, stability, and repeatability characteristics of these films were examined in an aerobic environment at temperatures up to 800 °C. The obtained results revealed that the thermistor resistance decreased monotonously with increasing temperature from room temperature to 800 °C. The SiBCN film resistance variations observed during repeated temperature cycling in the regions of 505–620 °C and 610–720 °C were 0.09% and 1.7%, respectively. The high cyclability and stability of the SiBCN thin film thermistor suggested its potential applicability for the in situ temperature monitoring of hot components in harsh environments. • A SiBCN thin-film thermistor with a thickness of 1.8 μm based on polymer-derived ceramics is fabricated via direct writing. • The produced SiBCN thin film exhibits large high-temperature oxidation resistance despite the high content of free carbon. • The resistance–temperature relationship of the SiBCN thin film between room temperature and 800 °C is determined. [ABSTRACT FROM AUTHOR]

A natural polysaccharide-based vehicle is facilely prepared for enantioselective loading of S-naproxen (S-NPX) and its programmed release. Cyclodextrin metal-organic frameworks (CD-MOF) are synthesized through the coordination of K+ with γ-cyclodextrin (γ-CD). Compared with R-NPX, the CD-MOF preferably combines with S-NPX, which can be confirmed by the thermodynamic calculations. The S-NPX loaded CD-MOF (CD-MOF-S-NPX) is grafted with disulfide bond (–S–S–) to improve its hydrophobicity, and the loaded S-NPX is further encapsulated in the chiral cavity of γ-CD by carboxymethyl potato starch (CPS) hydrogels. The intermolecular hydrogen bonding of the CPS hydrogels is prone to be destroyed in mildly basic media (∼pH 8.0), resulting in the swelling of the hydrogels; the –S–S– linkage in the vehicle can be cleaved in the presence of glutathione (GSH), leading to the collapse of the CD-MOF. Therefore, the programmed release of S-NPX can be achieved. Also in this work, the release kinetics is investigated, and the results indicate that the release of S-NPX is controlled by the Higuchi model. • A γ-CD-based vehicle is facilely prepared for chiral separation of the NPX isomers. • The CD-MOF-S-NPX is grafted with –S–S– bond to improve the hydrophobicity. • The loaded S-NPX is further encapsulated by the CPS hydrogels. • Programmed release of S-NPX from the SS-CD-MOF-S-NPX-gel is achieved. • Release kinetics reveals that the release of S-NPX is controlled by Higuchi model. [ABSTRACT FROM AUTHOR]

IgA nephropathy (IgAN) is an essential cause of kidney failure and end-stage kidney disease worldwide. Mesangial hypercellularity is an important characteristic of IgAN, but the underlying mechanism remains unclear. Endoplasmic reticulum (ER) stress is a series of stress responses to restore the function of endoplasmic reticulum. We aimed to explore how ER stress functioned in kidneys of IgAN. We first examined ER stress in IgAN kidneys in vivo and in vitro, by testing the levels of ER stress associated proteins (BIP, p-eIF2α and ATF4). Our results showed that ER stress was activated in IgAN patients, mice and cell model. ER stress activation was related to the distribution of IgA deposition and the degree of mesangial proliferation. To determine the role of ER stress in mesangial cell (MC) proliferation of IgAN, we then tested the levels of ER stress and MC proliferation (cyclin D1, cell viability and cell cycle) through inhibiting ER stress associated proteins. After inhibiting ER stress associated proteins, ER stress was inactivated and cell proliferation was inhibited in MCs. We also explored the correlation between ER stress in the glomerulus and the clinical outcomes of IgAN patients in a prospective study. Patients with lower expression of p-eIF2α or ATF4 had higher rates of hematuria remission, proteinuria remission and clinical remission. In summary, our work outlines that in IgAN, ER stress mediated by eIF2α/ATF4 pathway promotes MC proliferation via up-regulating the expression of cyclin D1. Furthermore, p-eIF2α and ATF4 in the glomerulus negatively correlate with the clinical remission of IgAN patients. • Endoplasmic reticulum (ER) stress was activated in IgAN kidneys, especially in mesangial cells, and was positively correlated with mesangial cell proliferation. • When ER stress was inhibited, the proliferation of pIgA1-induced mesangial cells was inhibited. • ER stress associated proteins, p-eIF2α and ATF4 in the glomerulus, were negatively correlated with the clinical remission of IgAN patients. • EIF2α/ATF4/cyclin D1 axis was activated in IgAN leading to mesangial cell proliferation. [ABSTRACT FROM AUTHOR]

Background: Arteriovenous fistula (AVF) is the preferred vascular access for hemodialysis (HD). However, primary AVF dysfunction represents a major barrier to the long-term success of HD therapy. This study aims to analyze the variables that influence the incidence of first AVF failure in HD patients. Methods: From January 2012 to October 2016, a total of 100 HD subjects from 43 medical centers were enrolled for a retrospective survival analysis of AVF dysfunction. To diminish the potential influence of surgeon experiences, the same operation group in Second Xiangya Hospital performed all studied AVF placements. This study focuses on a Chinese population of idiopathic glomerular disease to avoid the secondary influence of other systemic diseases, including diabetes, hypertension, and autoimmune disorder. AVF dysfunction was defined as lower blood flow during dialysis (≤200 mL/min) or insufficiency of HD treatment caused by reduced blood flow. Results: Among all enrolled subjects, the incidence of AVF dysfunction due to impatency was 27% (n = 27) with a cumulative survival of 84.0, 73.1, and 71.6% in 6, 12, and 24 months of post-placement. AVF survival -analysis revealed a higher incidence of AVF failure in females (p= 0.025) and elderly (p = 0.031) patients. Importantly, AVF dysfunction markedly increased in subjects with higher levels of platelets (PLTs; p = 0.024), severe anemia (p = 0.014), and extended temporary catheter retention (p = 0.020). Further multivariate Cox regression analysis confirmed these variables as independent risk factors for first AVF dysfunction. Meanwhile, no significant difference could be observed according to the levels of body mass index, serum albumin, serum calcium, serum phosphorus, prothrombin time, and activated partial thromboplastin time. Lastly, anti-coagulant treatments seemed to barely influence the outcomes of AVF survival in this study. Conclusion: These findings suggest that primary AVF dysfunction in HD patients is associated with gender, ageing, PLT counting number, hemoglobin level, and retention time of temporary catheter. [ABSTRACT FROM AUTHOR]

• Comprehensive Analysis: The review provides a detailed exploration of the structure, signal transduction, and various ligands of T-cell immunoglobulin and mucin-domain containing-3 (TIM-3), an immune checkpoint molecule. • Clinical Implications: We delve into the role of TIM-3 in the pathogenesis of a range of autoimmune diseases and chronic inflammatory conditions, offering insights into potential therapeutic strategies. • Recent Findings: Our perspectives in the review are not only based on existing literature, but are also informed by our most recent research findings on TIM-3, bringing a fresh outlook to the field. • Bridging Basic Science with Clinical Practice: This review creates a comprehensive resource that merges foundational knowledge with cutting-edge research findings, offering valuable insights for a broad range of readers, including researchers, clinicians, and students. • Timely Contribution: Given the current interest in immune checkpoint molecules like TIM-3, this review makes a significant contribution to the literature, addressing a topic of high relevance in both research and clinical settings. Dysfunctional immune cells participate in the pathogenesis of a variety of autoimmune diseases, although the specific mechanisms remain elusive and effective clinical interventions are lacking. Recent research on immune checkpoint molecules has revealed significant expression of T cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) on the surfaces of various immune cells. These include different subsets of T cells, macrophages, dendritic cells, natural killer cells, and mast cells. Further investigation into its protein structure, ligands, and intracellular signaling pathway activation mechanisms has found that TIM-3, by binding with different ligands, is involved in the regulation of crucial biological processes such as proliferation, apoptosis, phenotypic transformation, effector protein synthesis, and cellular interactions of various immune cells. The TIM-3-ligand axis plays a pivotal role in the pathogenesis of numerous conditions, including autoimmune diseases, infections, cancers, transplant rejection, and chronic inflammation. This article primarily focuses on the research findings of TIM-3 in the field of autoimmune diseases, with a special emphasis on the structure and signaling pathways of TIM-3, its types of ligands, and the potential mechanisms implicated in systemic lupus erythematosus, multiple sclerosis, rheumatoid arthritis, as well as other autoimmune diseases and chronic inflammation. The latest research results in the field of immunology suggest that TIM-3 dysfunction affects various immune cells and participates in the pathogenesis of diseases. Monitoring the activity of its receptor-ligand axis can serve as a novel biological marker for disease clinical diagnosis and prognosis evaluation. More importantly, the TIM-3-ligand axis and the downstream signaling pathway molecules may become key targets for targeted intervention treatment of autoimmune-related diseases. [ABSTRACT FROM AUTHOR]

Abstract Background Immunoglobulin A (IgA) nephropathy (IgAN) is a common primary glomerular disease that potentially leads to renal failure, risk prediction of declining kidney function is crucial for early clinical management. Immunoglobulin G (IgG) is an important constituent of the immune system and serves as the preferred therapeutic target in human autoimmune diseases. However, its role in the progression of IgAN is unclear. Methods From May 2009 to April 2014, 455 patients diagnosed with IgAN at the Second Xiangya Hospital were enrolled in this study; the median follow-up was 42.2 months. All subjects were divided into four groups according to IgG level quartiles. The study endpoint was end-stage renal disease (ESRD) or an irreversible 50% estimated glomerular filtration rate (eGFR) reduction. Clinical data and pathological features of renal biopsy specimens were collected. Results Among IgAN patients, serum IgG levels were directly correlated with the levels of serum albumin and serum IgA but reversely correlated with body weight, systolic blood pressure, and serum creatinine and cholesterol levels. According to stratified analysis of serum IgG, the proportions of composite renal endpoints among the enrolled IgAN patients in the serum IgG concentration subgroups 1 (<7.86), 2 (7.86–10.30), 3 (10.31–12.70), and 4 (>12.71 g/l) were 9.6%, 9.2%, 3.7%, and 3.7% respectively. Importantly, cumulative renal survival rates were significantly higher in the patients with increased serum IgG (p = 0.0114). Serum IgG was also predictive of renal survival, with an HR of 0.745 (95% CI, 0.614 to 0.905, p = 0.003) after adjusting for significant factors in the univariate Cox regression and an HR of 0.871 (95% CI, 0.780 to 0.973, p = 0.014) adjusting for traditional risk factors of IgAN. Conclusion These findings demonstrate that a decreased serum IgG level at the time of renal biopsy is independently associated with a poor renal outcome in IgAN patients. Highlights • Changes of serum IgG in IgAN patients accompanied with other clinical data changes • Renal survival rates were higher in patients with higher serum IgG. • Serum IgG served as an independent predictor of renal outcomes. [ABSTRACT FROM AUTHOR]

Background/Aims: There is an increasing risk of end-stage renal disease (ESRD) among Asian people with immunoglobulin A nephropathy (IgAN). A computer-aided system for ESRD prediction in Asian IgAN patients has not been well studied. Methods: We retrospectively reviewed biopsy-proven IgAN patients treated at the Department of Nephrology of the Second Xiangya Hospital from January 2009 to November 2013. Demographic and clinicopathological data were obtained within 1 month of renal biopsy. A random forest (RF) model was employed to predict the ESRD status in IgAN patients. All cases were initially trained and validated, taking advantage of the out-of-bagging(OOB) error. Predictors used in the model were selected according to the Gini impurity index in the RF model and verified by logistic regression analysis. The area under the receiver operating characteristic(ROC) curve (AUC) and F-measure were used to evaluate the RF model. Results: A total of 262 IgAN patients were enrolled in this study with a median follow-up time of 4.66 years. The importance rankings of predictors of ESRD in the RF model were first obtained, indicating some of the most important predictors. Logistic regression also showed that these factors were statistically associated with ESRD status. We first trained an initial RF model using gender, age, hypertension, serum creatinine, 24-hour proteinuria and histological grading suggested by the Clinical Decision Support System for IgAN (CDSS, www.IgAN.net). This 6-predictor model achieved a F-measure of 0.8 and an AUC of 92.57%. By adding Oxford-MEST scores, this model outperformed the initial model with an improved AUC (96.1%) and F-measure (0.823). When C3 staining was incorporated, the AUC was 97.29% and F-measure increased to 0.83. Adding the estimated glomerular filtration rate (eGFR) improved the AUC to 95.45%. We also observed improved performance of the model with additional inputs of blood urea nitrogen (BUN), uric acid, hemoglobin and albumin. Conclusion: In addition to the predictors in the CDSS, Oxford-MEST scores, C3 staining and eGFR conveyed additional information for ESRD prediction in Chinese IgAN patients using a RF model. [ABSTRACT FROM AUTHOR]

[Display omitted] Glucocorticoids (GCs) are widely used to treat autoimmune and inflammatory diseases, but recent research has challenged the notion that GCs are universally anti-inflammatory. In this study, we investigated the effects of long-term GC exposure on circulating T cells in a retrospective cohort of 5,476 patients with primary glomerular diseases. Our results revealed that GCs altered the composition pattern of circulating leukocytes and the correlation between circulating lymphocytes and serum cytokines in response to infections, as well as the subsets of CD4 + T cells. Specifically, GCs promoted the loss of CD4 + T cells and increased the proportions of CD3 + TIM3 + T cells in response to infections, which correlated with the expression of serum inflammatory cytokines, such as IFNG and IL-10. Using animal models of cecal ligation and puncture, we demonstrated that long-term GC exposure exacerbated apoptosis of CD4 + T cells and cytokine storm during sepsis, which was mechanistically linked to the increase of CD3 + TIM3 + T cells. Notably, we found that CD3 + TIM3 + T cells expressed high levels of multiple cytokine genes during infections, suggesting a potent role of TIM3 in the regulation of T cell biology. In vitro studies further showed that engagement of anti-TIM3 treatment enhanced the inflammatory activity of CD3 + T cells. Our findings suggest a causal relationship between chronic exposure to GCs and an excessive inflammatory response mediated by T cells during infections, which is, at least partly, driven by dysregulation of CD3 + TIM3 + T cells. [ABSTRACT FROM AUTHOR]

[Display omitted] Conventional glucocorticoid (GC) treatment has a long-term influence on T-cell immunity, resulting in an increased risk of opportunistic infection after drug withdrawal. The underlying mechanisms remain ambiguous. This study demonstrated that long-term GC treatment induced persistent lymphopenia in patients with primary glomerular disease. GCs continuously suppressed the proportion of CD4+ T cells even after the daily dose was tapered down to the physiologic equivalences, leading to a significant decline of the CD4/CD8 ratio. Meanwhile, GCs impaired CD4+ T cell biology, leading to enhanced apoptotic cell death, reduced proliferative capacity, downregulated pro-inflammatory genes, and upregulated immunoregulatory genes. Specifically, GCs altered FOXP3 expression pattern in CD4+ T cells and favored their acquisition of an active T regulatory (Treg) cell phenotype with enhanced IL-10 production upon stimulation. Mechanistically, GCs tampered with the transcriptional regulation of mechanistic target of rapamycin complex 1 (mTORC1) pathway, resulting in an inhibitory impact on the signaling activity. Targeting mTORC1 signaling by siRNAs could sufficiently modify the viability of GC-exposed CD4+ T cells. By high-throughput sequencing of genome-wide DNA methylation and mRNA, we further uncovered a causal relationship between the altered DNA methylation level and transcription activity in a subset of mTORC1 pathway genes in long-term GC exposure. Taken together, this study reveals a novel regulation of mTORC1 signaling, which might dominate the long-term influence of GC on CD4+ T cell biology in a dose-independent manner. [ABSTRACT FROM AUTHOR]

• Highly sensitive and conductive TiB 2 /SiCN high-temperature thin-film strain gauge (TFSG) is fabricated using ultrafast high-temperature sintering (UHS). • UHS technique allows rapid sintering toward the desired phase, controls the grain size and microstructure, promotes the precipitation of free carbon in SiCN matrix in minutes, and suppresses high-temperature oxygen pollution. • A TiB 2 /SiCN TFSG with high sensitivity (GF = 8.6) and low thermal noise is fabricated on alloy substrates and its piezoresistibility at 25–800 ℃ is verified. Polymer-derived ceramic nanocomposites (PDC-NCs) are promising materials for high-temperature thin-film sensor (TFS) applications. However, owing to their inherent high-resistance characteristics and the high-temperature furnace sintering process, it is difficult to integrate PDC-NCs with high-conductive and low high-temperature tolerant alloy/metal components. In this study, an ultrafast high-temperature sintering (UHS) method was employed to prepare PDC-NC TFSs in minutes. The TiB 2 /SiCNO film sintered by the UHS technique shows high-sensitive microstructure and properties to sintering parameters. The UHS technique allows rapid sintering toward the desired phase, controls the grain size and microstructure, promotes the precipitation of free carbon in the SiCNO matrix within minutes, and suppresses high-temperature oxygen pollution. For example, TiB 2 /SiCNO films show high conductivity (18.1 S cm−1 at room temperature) and high-temperature stability (up to 800 ℃). In comparison, these properties are orders of magnitude better than those of samples sintered in the furnace. High-quality films sintered using ultrafast heating and cooling rates can also withstand thermal shocks of up to 1000 ℃. With the UHS technique, high-quality and high-conductivity films can be prepared using an ultrafast sintering rate to prevent substrate thermal damage. The TiB 2 /SiCNO thin-film strain gauge with high sensitivity (GF = 8.6) and low thermal noise was fabricated on alloy substrates, and its high-temperature (25–800 ℃) strain sensing performance was verified. This method offers a new route for co-sintering devices with alloy/metal substrates that suffer from low high-temperature tolerance and regulating the microstructure and electrical performance of these devices. [ABSTRACT FROM AUTHOR]

Typical high-temperature thin-film sensors are fabricated by layer-by-layer deposition and layer-by-layer sintering, which are time and energy consuming. In this study, thin-film strain gauges (TFSGs) were fabricated on superalloy substrate by co-sintering process for the first time. The co-sintering behavior of glassy insulating layer and Pt thin-film resistance grid was studied. Compared with layer-by-layer sintering, the weak interface constraint between the top and sub layers of co-sintered TFSG allows the free in-plane shrinkage of the Pt resistance grid. In the co-sintering process, the glassy SiO 2 in the insulating layer fills the pores in the Pt resistance grid, significantly improving the compactness. Further, no Pt element diffuses into the insulating layer. Owing to the remarkable advantages of the co-sintering process, the co-sintered Pt TFSG not only inherits the high-temperature insulation (2.8 MΩ at 800 °C) of the layer-by-layer sintered insulating layer, but also significantly increases the high-temperature stability of the Pt grid resistance; the resistance change rate of layer-by-layer sintered samples at 800 °C is 7.3 % h−1, while that of co-sintered samples at 800 °C is only 0.9 % h−1. Finally, the high-temperature strain response of co-sintered Pt TFSG up to 800 °C was tested. [Display omitted] • One-step co-sintering process was use to fabricated thin film strain gauge (TFSG) on superalloy. • Through co-sintering, the top layer can shrink in-plane while the sub-layer glass phase fills the pores in the top layer. • The co-sintered TFSG exhibits improved performance at high temperatures. [ABSTRACT FROM AUTHOR]

[Display omitted] • The temperature interference of the conductive composite was eliminated by electron scattering and hopping transport. • The smallest feature unit of electron transport in conducting composites was proposed. • A noninterference strain sensor with a gauge factor > 2300 for static strain sensing was designed. Very few thin-film strain gauges (TFSGs) that exhibit temperature self-compensation have been developed. Their temperature insensitivity range is typically < 100 °C, and they cannot be used for static strain sensing in variable-temperature environments. In this study, environmental interference owing to temperature fluctuations was successfully eliminated by controlling electron scattering and thermally assisted hopping transport in conductive composites. A new temperature-insensitive material was developed. The proposed strategy enables noninterference dynamic strain monitoring over an ultrawide temperature range of 30–300 °C, which is approximately 200 °C higher than that of noninterference TFSGs that have been reported. In particular, we propose the smallest feature unit of electron transport in conducting composites, that is, the pathway of an electron through a conductive particle and adjacent junction. This unit retains all the features of the entire conductive network, such as the temperature-resistivity effect, and is the smallest unit that can fully reflect the electron transport behavior. We manipulated the microstructure such that the static strain affects only the arrangement and number of temperature-insensitive feature units without destroying its internal structure, enabling temperature independence under static strain. The first noninterference TFSG was designed with a gauge factor of > 2300 for static strain sensing. The thermal output strain error at 30–200 °C was < 0.0016%. [ABSTRACT FROM AUTHOR]

The diabetic milieu is believed to change the activity, or result in damage of podocytes-a key component of the glomerular filtration barrier and known to secrete matrix for glomerular basement membrane. This in turn contributes to diabetic nephropathy. However, how podocyte dysfunction is triggered in diabetic nephropathy remains ambiguous. Galectin-1 belongs to Galectin family that bind to β-galactoside residues of glycosylated proteins. We explored whether Galectin-1 is dysregulated in diabetic nephropathy using three different techniques, namely real-time polymerase chain reaction, western blotting, and immunofluorescent staining, to follow the expression of Galectin-1 under high glucose levels in podocytes. High glucose consistently induced Galectin-1 expression. Immunohistochemistry using a Galectin-1-specific antibody also showed elevated Galectin-1 in renal tissues of diabetic patients with manifestation of nephropathy, indicating a correlation of Galectin-1 overexpression with diabetic nephropathy. Upregulation of Galectin-1 is associated with loss of podocin, which is important for the physiological function of podocytes and decreases in the renal tissues of diabetic nephropathy. Increased Galectin-1 is a causal event for the high glucose-induced loss of podocin, since silencing Galectin-1 in podocytes increased podocin expression in the presence of 25 mM glucose. Thus expression of Galectin-1 in diabetic nephropathy may serve as a marker and contribute to disease progression by interfering with podocin expression. [ABSTRACT FROM AUTHOR]

• A thin-film temperature sensor was fabricated based on polymer-derived ceramics (PDCs) via direct-writing. • A layer of protective coating made from PDC was applied on the sensor head and improved the repeatability. • The sensitivity and resistance-temperature relationship of SiCN sensor head were investigated. [Display omitted] In-situ monitoring of machines in harsh environment remains challenging due to lack of high-performance sensors. Most of sensors cannot survive over 600 ℃ even with packaging. In this work, an ultra-thin-film temperature sensor was fabricated based on polymer-derived ceramics (PDCs) via direct-writing for aerospace applications. The sensitive film with thickness of 10 µm consists of polymer-derived SiCN filled with TiB 2 , ZrB 2 and SiC nano-particles. The resistance-temperature dependence tests of the sensor indicates that the resistance of the PDC thin film decreases monotonically with rising temperature and exhibits good repeatability at temperatures from room temperature to 800 ℃ in the air environment. The fabricated thin-film sensor shows great potential for high temperature applications and the technological routine provides a feasible pathway for structure/function integration in aerospace manufacture. [ABSTRACT FROM AUTHOR]

Immunoglobulin A nephropathy (IgAN nephropathy, IgAN) is named for the renal pathological features of IgA-dominant immunoglobulin deposition. IgA deposits, however, may also occur in other diseases, from liver disease and inflammation to chronic infections and tumors. Now increasing studies have suggested that galactose-deficient IgA1 (Gd-IgA1) plays a critical role in the pathogenesis of IgAN. This study aims to investigate whether the Gd-IgA1-specific antibody KM55 contributes to differentiating primary IgAN from other diseases with IgA deposits. In this retrospective study, we enrolled 100 Chinese patients with IgA deposits in renal biopsies, including IgAN(n = 40), IgAN with hepatitis B virus antigen deposits(n = 14), IgA vasculitis(n = 16), lupus nephritis(n = 11), incidental IgA deposits(n = 13) and negative controls(n = 6). Double immunostaining of Gd-IgA1 and IgA was performed in all biopsies. There were similar patterns of Gd-IgA1 deposition in primary IgAN, IgA vasculitis, and IgAN with hepatitis B virus antigen deposits. Gd-IgA1 staining could also be seen in patients with lupus nephritis and incidental IgA deposits, but the intensity was significantly lower than IgAN, and the optimal cutoff was 2+ staining for differential diagnosis. Every increase in KM55 staining intensity of 1+ was associated with an increase in the odds of primary IgAN (OR: 4.399; 95% CI: 1.725–11.216). Immunostaining for Gd-IgA1 by KM55 is not specific for IgA nephropathy, but weak or negative staining may favor incidental IgA deposits. [ABSTRACT FROM AUTHOR]

• miR-98-5p was highly expressed in PBMCs of IgAN patients. • miR-98-5p targeted chemokine ligand 3 (CCL3) • CCL3 affected the expression of interleukin-6 (IL-6) and C1GALT1. • miR-98-5p overexpression in PBMCs reduced CCL3 and C1GALT1 and increased IL-6. Increases in galactose-deficient IgA1 (Gd-IgA1) play a crucial role in the pathogenesis of IgA nephropathy (IgAN), and several recent experiments have shown that microRNAs (miRNAs) are involved in regulating the development and physiological function of the kidney. The aims of this study were to identify miRNAs that can affect the pathogenesis of IgAN and reveal the underlying regulatory mechanism of IgA1 glycosylation in peripheral blood. The differentially expressed miRNAs in peripheral blood mononuclear cells (PBMCs) between IgAN patients and healthy controls were screened by high-throughput sequencing, and the targets of these miRNAs were predicted and verified by dual-luciferase reporter assays. We also explored the miRNA regulation of Gd-IgA1 through the transfection of miRNA mimics and related plasmids. The high-throughput sequencing results showed that miR-98-5p was more highly expressed in the PBMCs of IgAN patients compared with healthy controls, and the luciferase reporter gene system confirmed that miR-98-5p might target chemokine ligand 3 (CCL3). The transfection of si-CCL3 confirmed that a decrease in CCL3 can affect the expression of interleukin-6 (IL-6) and C1GALT1. The overexpression of miR-98-5p in PBMCs through the transfection of miR-98-5p mimic reduced the CCL3 and C1GALT1 levels and increased the IL-6 levels, and these changes in PBMCs were attenuated by cotransfection with the CCL3 plasmid. The results showed that in PBMCs, miR-98-5p can target CCL3 to decrease its expression and thereby increase the IL-6 levels, and the resulting increase in IL-6 can decrease C1GALT1 expression. Therefore, miR-98-5p might be involved in the development of IgAN. [ABSTRACT FROM AUTHOR]

• Mesangial cell model of IgA nephropathy was well established by stimulating mesangial cells with aggregated IgA1 in vitro. • Dihydroartemisinin attenuated the proliferation of aggregated IgA1-induced human mesangial cells. • Dihydroartemisinin inhibited the mammalian target of rapamycin/ribosomal protein S6 kinase beta-1 signaling pathway. IgA nephropathy (IgAN) is an autoimmune kidney disease and is the most prevalent form of glomerular kidney disease in China and worldwide. IgA immune complex deposition accompanied by mesangial cell proliferation and mesangial matrix expansion is the most basic pathological feature of IgAN. Dihydroartemisinin (DHA), an antimalarial drug, was recently reported to be effective in treating autoimmune diseases. However, its potential therapeutic role in IgAN is relatively unstudied. The aim of this study was to investigate the pharmacological effects and the underlying mechanisms of DHA in the treatment of IgAN. In this study, renal biopsy specimens were collected for immunohistochemistry. In vitro, 25 μg/ml concentrations of aggregated IgA1 (aIgA1) was used to construct the IgAN mesangial cell model. Stimulated human mesangial cells (HMCs) were treated for 24 h with DHA (0–15 μM) and were collected for western blot analyses. Cell proliferation was assessed by Cell Counting Kit 8 (CCK8) and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. In vitro, our results showed that DHA could downregulate the mammalian target of rapamycin/ribosomal protein S6 kinase beta-1 (mTOR/S6K1) signaling pathway, promote cell autophagy, and ameliorate cell proliferation in aIgA1-induced HMCs. The results suggested that DHA may represent a novel class of mTOR inhibitor and promote an anti-proliferation effect in IgAN HMCs, which provides an alternative approach for IgAN treatment. [ABSTRACT FROM AUTHOR]

Objective: To construct a connective tissue growth factor (CTGF) and red fluorescent protein (RFP)–coexpressed renal tubular epithelial cell that can be used to quantitatively evaluate the CTGF-induced epithelial-mesenchymal transition (EMT). Methods: The CTGF and RFP coding sequences were linked with a “2A” peptide, cloned into an expressing vector, and the HK-C2AR cell clone, which could express CTGF and RFP, were selected from the HK-2 cells after the recombinant plasmid transfection. Then, the CTGF-induced EMT in this cell line was determined, to further determine the association of RFP fluorescence intensity with the CTGF expression or CTGF-induced EMT. CTGF-specific ribonucleic acid (RNA) interference was also used to reconfirm the association. Results: The constructed HK-C2AR cells could stably express RFP and CTGF proportionally, and the CTGF expressed in the cell line could induce EMT of cells, whereas the RFP expressed in the cell could exhibit bright red fluorescence after excitation. After the silence in CTGF, the RFP expression was also decreased, and the CTGF-induced EMT was also inhibited. Conclusion: The CTGF and RFP–coexpressing renal tubular epithelial cell, HK-C2AR, could be used to quantitatively evaluate CTGF-specific small interfering RNAs on EMT by quantitatively detecting the RFP expression. Also, this cell line could be used to quantitatively determine the mechanism of CTGF-induced EMT in renal tubular epithelial cells. [ABSTRACT FROM AUTHOR]