A Convolutional Autoencoder Based Fault Diagnosis Method for a Hydraulic Solenoid Valve Considering Unknown Faults.

The hydraulic solenoid valve is an essential electromechanical component used in various industries to control the flow rate, pressure, and direction of hydraulic fluid. However, these valves can fail due to factors like electrical issues, mechanical wear, contamination, seal failure, or improper assembly; these failures can lead to system downtime and safety risks. To address hydraulic solenoid valve failure, and its related impacts, this study aimed to develop a nondestructive diagnostic technology for rapid and accurate diagnosis of valve failures. The proposed approach is based on a data-driven model that uses voltage and current signals measured from normal and faulty valve samples. The algorithm utilizes a convolutional autoencoder and hypersphere-based clustering of the latent variables. This clustering approach helps to identify patterns and categorize the samples into distinct groups, normal and faulty. By clustering the data into groups of hyperspheres, the algorithm identifies the specific fault type, including both known and potentially new fault types. The proposed diagnostic model successfully achieved an accuracy rate of 98% in classifying the measurement data, which were augmented with white noise across seven distinct fault modes. This high accuracy demonstrates the effectiveness of the proposed diagnosis method for accurate and prompt identification of faults present in actual hydraulic solenoid valves.

Facile Green Synthesis of Titanium Dioxide Nanoparticles by Upcycling Mangosteen (Garcinia mangostana) Pericarp Extract.

In the present report, green synthesis of titanium dioxide nanoparticles (TiO2 NPs) was performed by upcycling mangosteen (Garcinia mangostana) pericarp extract (methanol and ethyl acetate extracts). Field emission scanning electron microscopy images revealed an aggregated structure with a highly porous network of TiO2 NPs. TiO2 NPs synthesized with ethyl acetate extract (EtOAc-TiO2 NPs) exhibited more monodispersity and possessed smoother surfaces than the control TiO2 NPs (Con-TiO2 NPs) and TiO2 NPs synthesized with methanol extract (MeOH-TiO2 NPs). High-resolution X-ray diffraction patterns clearly confirmed that TiO2 NPs had a crystalline nature. A mixture of anatase and rutile was observed in Con-TiO2 NPs and MeOH-TiO2 NPs, while EtOAc-TiO2 NPs had only anatase with the smallest size (12.50 ± 1.81 nm). Ethyl acetate extract contained the highest amount of α-mangostin; thus, the surface of TiO2 NPs was functionalized with ethyl acetate extract. The functionalized TiO2 NPs synthesized with ethyl acetate extract (EtOAc-TiO2-αm) showed the highest 2,2-diphenyl-1-(2,4,6-trinitrophenyl)hydrazyl (DPPH) radical scavenging activity. In vitro cell viability on mouse fibroblast cells (NIH3T3) indicated that the newly synthesized TiO2 NPs did not show any significant cytotoxicity. Therefore, the TiO2 NPs in the present report have the potential to be used in cosmetic applications such as sunscreens.

Bioactive PCL microspheres with enhanced biocompatibility and collagen production for functional hyaluronic acid dermal fillers.

Polymeric microspheres containing magnesium hydroxide (MH) and a bioactive agent (BA), such as apocynin (APO) and astaxanthin (ATX), have been prepared as functional dermal fillers with enhanced physicochemical and biological performance. In this study, polycaprolactone (PCL)-based microspheres were produced with a uniform size of about 30-40 µm by utilizing a membrane emulsification device. MH from the PCL/MH microspheres effectively neutralized acidic products from PCL degradation. For in vitro cell experiments, when acidic degradation products (6-hydroxycaproic acid, HCA) were treated with MH, the acidic pH was neutralized to induce wound healing and suppress inflammation. The microspheres comprised of BA had a sustained release of the BA, without an initial burst release. Remarkably, the ATX added into the microspheres was maintained for 16 weeks and displayed positive attributes, such as tissue regeneration and collagen production improvement, as noted by in vivo testing. Overall, these results suggest that the bioactive PCL microspheres containing ATX have excellent potential as a functional dermal filler for skin aesthetics and facial plastic surgery.

The antagonistic effect of magnesium hydroxide particles on vascular endothelial activation induced by acidic PLGA degradation products.

Although drug-eluting stents (DESs) are mainly coated with biodegradable polymers such as PLGA and PLLA, their acidic degradation products can alter the local microenvironment and affect the homeostasis of adjacent tissue. Previously, we developed anti-inflammatory PLGA-based materials including magnesium hydroxide (MH) to relieve the side effects caused by PLGA degradation. However, the underlying molecular mechanism of its protective effects has not yet been clarified. Here, we demonstrated the pathological mechanism of vascular endothelial activation caused by PLGA by-products. The PLGA by-products accumulated in HCAECs through MCT1, followed by oxidative stress and the activation of the MAPK/NF-κB signaling pathway. Finally, the PLGA by-products increased the expression of VCAM-1 as well as the secretion of proinflammatory cytokines. However, the addition of MH particles significantly diminished the activation of this molecular pathway and the expression of inflammation-related factors induced by acidic PLGA degradation products. Furthermore, Mg2+ released from MH particles restored endothelial function in both intracellular and extracellular spaces. Taken together, MH particles prevent the accumulation of PLGA degradation products in HCAECs, thereby repressing the associated vascular endothelial activation. These findings on the biochemical mechanisms are expected to provide important clues for addressing the safety issues in nearly all biodegradable polymer-based implants.

Rehmannia glutinosa suppresses inflammatory responses elicited by advanced glycation end products.

Fresh rhizome of Rehmannia glutinosa Libosch. (Saeng-jihwang in Korean: SJH) has been prescribed for the treatment of diabetes-associated complications. The purpose of the present study is to investigate the underlying mechanisms of the efficacy of SJH in diabetes-related complications. Decoction was obtained after boiling SJH in water and subsequent lyophilization. The cellular toxicity of SJH was determined by MTT assay. The antioxidant activity of SJH was measured by DPPH and DCFH-DA assays. The effects of SJH on inflammatory responses elicited by AGEs were assessed by western blotting and semi-quantitative RT-PCR analyses. The water extract of SJH had a high free radical scavenging activity in vitro and decreased the level of intracellular ROS in THP-1 cells treated with AGEs. SJH suppressed the expression of pro-inflammatory genes, including TNF-α, MCP-1, IP-10, COX-2, and iNOS; the activation of NF-κB; and the expression of RAGE, a receptor for AGEs, where the expressions of which were induced by AGEs. These results suggest the possibility that SJH can be an alternative therapeutics for diabetes-associated diseases.

Differential inhibitory effects of baicalein and baicalin on LPS-induced cyclooxygenase-2 expression through inhibition of C/EBPbeta DNA-binding activity.

To evaluate the possible mechanisms responsible for the anti-inflammatory effects of baicalein or baicalin, lipopolysaccharide (LPS)-induced inflammatory responses in cultured Raw 264.7 cells were studied. In the present study, baicalein and baicalin, a flavonoid present in the root of Scutellaria baicalensis Georgi, were examined for their effects on LPS-induced cyclooxygenase-2 (COX-2) gene expression in Raw 264.7 macrophages. Baicalein, but not baicalin, inhibited COX-2 gene expression in LPS-induced Raw 264.7 cells. However, both polyphenolic compounds inhibited LPS-induced inducible nitric oxide synthase (iNOS) protein expression, iNOS mRNA expression, and NO production in a dose-dependent manner. To investigate the mechanism by which baicalein inhibits COX-2 gene expression, we examined activation of mitogen-activated protein kinases (MAPKs) in Raw 264.7 cells. We did not observe any significant change in the phosphorylation of MAPKs between baicalein- and baicalin-treated cells. Baicalein and baicalin had no effect on LPS-induced nuclear factor-kappaB (NF-kappaB) and cAMP response element binding protein (CREB) DNA binding activity. Baicalein, but not baicalin, significantly inhibited the DNA binding activity of CCAAT/enhancer binding protein beta (C/EBPbeta) These results indicated that differential effects of baicalein and baicalin on COX-2 gene expression in LPS-induced Raw 264.7 cells were mediated through inhibition of C/EBPbeta DNA binding activity. Taken together, these results suggest that baicalein acts to inhibit inflammation through inhibition of COX-2 gene expression through blockade of C/EBPbeta DNA binding activity.

Curcumin decreases cell proliferation rates through BTG2-mediated cyclin D1 down-regulation in U937 cells.

Curcumin is a promising chemopreventive agent due to its multiple properties including anti-inflammation, induction of apoptosis and inhibition of signal cascades involving cell proliferation. It has been reported that curcumin-treated cells show decreased expression of cyclin D1, ultimately resulting in decreased cell growth rate. Thus, modulation of cell cycle regulatory proteins by curcumin has been suggested as one of the important mechanisms underlying its chemopreventive effects. However, the precise molecular mechanisms involving down-regulation of cyclin D1 by curcumin are not largely understood. In this study we investigated the mechanisms of cyclin D1 down-regulation by curcumin in U937 cells. Expressions of cyclin D1, particularly at protein and mRNA levels, were clearly decreased in curcumin-treated cells. The stability of cyclin D1 mRNA was not affected by curcumin treatment. Treatment of curcumin increased expression of BTG2 mRNA, a member of anti-proliferative gene family and a negative transcriptional regulator of cyclin D1. Furthermore, overexpression of BTG2 led to down-regulation of cyclin D1 mRNA expression in U937 cells. Nuclear translocation of p65 NF-kappaB is involved in the expression of cyclin D1 mRNA. Treatment of curcumin inhibited nuclear translocation of p65 NF-kappaB. Moreover, the expression of cyclin D1 mRNA was dramatically decreased after co-treatment curcumin with NF-kappaB inhibitors. The data presented here indicate that curcumin-induced down-regulation of cyclin D1 mRNA is mediated by induction of BTG2 as well as inhibition of nuclear translocation of NF-kappaB.

Tetradecanoyl phorbol acetate induces expression of Toll-like receptor 2 in U937 cells: involvement of PKC, ERK, and NF-kappaB.

Toll-like receptors (TLRs) have been identified recently as crucial signaling receptors mediating the innate immune recognition. Though induction of TLR2 or TLR4 by 12-O-tetradecanoyl phorbol 13-acetate (TPA) in leukemia cells has been reported, however, the mechanism by which TPA up-regulates TLR2 or TLR4 remains poorly understood. In this study, we investigated the effect of TPA on induction of TLR2 in U937 cells. TPA markedly induced TLR2 mRNA and protein expressions. TLR2 expression in response to TPA was attenuated by pretreatments with GF109203X and Go6976 (inhibitors of protein kinase C (PKC)) and PD98059 (an inhibitor of extracellular signal-regulated kinases (ERKs)), but not SB203580 (an inhibitor of p38s) and SP600125 (an inhibitor of c-Jun N-terminal kinases), suggesting involvement of PKC and ERKs in this response. Moreover, TPA-induced PKC activation was linked to generation of reactive oxygen species, which were dispensable for TLR2 expression in U937 cells. Pretreatments with GF109203X blocked TPA-induced phosphorylation of ERKs, suggesting activation of ERKs by PKC. In addition, TPA induced nuclear factor-kappaB (NF-kappaB) activation, which was shown by increased nuclear translocation of p65 NF-kappaB and degradation of IkappaB-alpha, a NF-kappaB inhibitory protein. Importantly, TPA-induced TLR2 expression was inhibited by blockage of NF-kappaB activation using NF-kappaB inhibitors, including MG132 and BAY11-7085. Specifically, TPA-induced nuclear translocation of NF-kappaB was effectively attenuated by GF109203X and PD98059, suggesting PKC and ERK regulation of NF-kappaB nuclear localization in response to TPA. Together, these results suggest that TPA-induced TLR2 expression in U937 cells may be at least in part mediated through activation of PKC and ERKs as well as NF-kappaB transcription factor, and that cross-talk between PKC or ERKs and NF-kappaB may exist.

Up-regulation of human beta-defensin 2 by interleukin-1beta in A549 cells: involvement of PI3K, PKC, p38 MAPK, JNK, and NF-kappaB.

Induction of human beta-defensin 2 (HBD-2) by interleukin-1beta (IL-1beta) in epithelial cells has been reported. However, the mechanism by which IL-1beta up-regulates HBD-2 remains poorly understood. In this study, we investigated the effect of IL-1beta on induction of HBD-2 in A549 cells. IL-1beta markedly increased HBD-2 mRNA expression in concentration- and time-dependent manners. HBD-2 mRNA expression in response to IL-1beta was attenuated by pretreatment of GF109203X, Go6976, and staurosporine [inhibitors of protein kinase C (PKC)], SB203580 [an inhibitor of p38 mitogen-activated protein kinase (MAPK)], SP600125 [an inhibitor of c-Jun N-terminal kinase (JNK)], and LY294002 [an inhibitor of phosphatidylinositol-3-kinase (PI3K)], but not PD98059 [an inhibitor of extracellular signal-regulated kinase (ERK)], suggesting involvement of PKC, p38 MAPK, JNK, and PI3K in this response. Interestingly, IL-1beta induced nuclear factor-kappaB (NF-kappaB) activation in A549 cells, which was shown by increased nuclear translocation of p65 NF-kappaB and degradation of IkappaB-alpha. Importantly, IL-1beta-induced HBD-2 mRNA expression was inhibited by blockage of NF-kappaB activation using NF-kappaB inhibitors, including pyrrolidine dithiocarbamate and MG132. Specifically, IL-1beta-induced nuclear translocation of NF-kappaB was in part attenuated by LY294002, but not by GF109203X, SB203580, and SP600125, suggesting PI3K-dependent nuclear translocation of NF-kappaB in response to IL-1beta. Together, these results suggest that IL-1beta induces HBD-2 mRNA expression in A549 cells, and the induction seems to be at least in part mediated through activation of NF-kappaB transcription factor as well as activation of signaling proteins of PKC, p38 MAPK, JNK, and PI3K, but not ERK.

Immunomodulatory effects of aqueous-extracted Astragali radix in methotrexate-treated mouse spleen cells.

The present study was conducted to evaluate the immunomodulatory effect of aqueous-extracted Astragali radix (ARE) in methotrexate (MTX)-treated mouse spleen cells. In spleen cell proliferation assay, ARE enhanced mitogenic activity in the dose-response manner. We also investigated the effect of ARE on the reducing of immune suppression caused by MTX in mouse spleen cells. MTX decreased the spleen cell proliferation (IC(50):800 microg/ml). However, ARE significantly reduced the suppression of cell proliferation by MTX in mouse spleen cells. Immunomodulatory effect of ARE were further investigated using reverse transcription polymerase chain reaction (RT-PCR). In RT-PCR, we examined the expressions of various cytokines such as IL-6, IL-1alpha, IL-1beta, IL-12p40, GM-CSF and TNF. Enhancement of IL-1alpha and IL-12p40 mRNA expressions were shown in mouse spleen cells by ARE. In spite of MTX treatment, the expressions of IL-1alpha and IL-12p40 mRNA sustained in spleen cells. These data indicate that (1) ARE has a protective effect of immune suppression, and (2) the immunomodulatory effects of ARE may be, in part, associated with the expressions of IL-1alpha and IL-12p40 mRNA as well as the mitogenic effect on spleen cells.