Search

The structure of the toroidal rotation profile with mixed heating by neutral beam injection (NBI) and electron cyclotron resonance heating (ECH) has been investigated in KSTAR L-mode plasmas. ECH with varying resonance layer positions was used for heating a mix control. The experimental results show that ECH causes a counter-current rotation increment both for off-axis and on-axis ECH heating. For L-mode plasmas, off-axis ECH produces larger counter-current rotation than on-axis ECH. Analysis of ion heat and momentum transport for the ECH L-mode plasmas shows that the electron temperature gradient is the main reason for the degradation of ion heat confinement and also the main driving force for the non-diffusive momentum flux. As a possible mechanism for the counter-current intrinsic torque with ECH, the transition of the turbulence mode from ion temperature gradient (ITG) to the trapped electron mode (TEM) with the resulting sign change of turbulence driven residual stress is suggested. A linear gyro-kinetic analysis shows the ITG → TEM transition occurs in a localized region during ECH injection, and the trend of TEM excitation is consistent with the observed macroscopic trend of the toroidal rotation.

We report recent experimental results from HL-2A and KSTAR on ELM mitigation by supersonic molecular beam injection (SMBI). Cold particle deposition within the pedestal by SMBI is verified in both machines. The signatures of ELM mitigation by SMBI are an ELM frequency increase and ELM amplitude decrease. These persist for an SMBI influence time τI. Here, τI is the time for the SMBI influenced pedestal profile to refill. An increase in fELMSMBI/fELM0 and a decrease in the energy loss per ELM ΔWELM were achieved in both machines. Physical insight was gleaned from studies of density and vΦ (toroidal rotation velocity) evolution, particle flux and turbulence spectra, divertor heat load. The characteristic gradients of the pedestal density soften and a change in vΦ was observed during a τI time. The spectra of the edge particle flux Γ ∼ 〈ṽrñe〉 and density fluctuation with and without SMBI were measured in HL-2A and in KSTAR, respectively. A clear phenomenon observed is the decrease in divertor heat load during the τI time in HL-2A. Similar results are the profiles of saturation current density Jsat with and without SMBI in KSTAR. We note that τI/τp (particle confinement time) is close to ∼1, although there is a large difference in individual τI between the two machines. This suggests that τI is strongly related to particle-transport events. Experiments and analysis of a simple phenomenological model support the important conclusion that ELM mitigation by SMBI results from an increase in higher frequency fluctuations and transport events in the pedestal. © 2014 IAEA, Vienna.

Toroidal rotation profiles have been investigated in KSTAR H-mode plasma using combined auxiliary heating by co-neutral beam injection (NBI) and electron cyclotron resonance heating (ECH). The ion temperature and toroidal rotation are measured with x-ray imaging crystal spectroscopy and charge exchange recombination spectroscopy. H-mode plasma is achieved using co-current 1.3 MW NBI, and a 0.35 MW ECH pulse is added to the flat-top of H-mode. The core rotation profiles, which are centrally peaked in the pure NBI heating phase, flatten when ECH is injected, while the edge pedestal is unchanged. Dramatic decreases in the core toroidal rotation values (ΔVtor/V tor ∼ -30%) are observed when on-axis ECH is added to H-mode. The experimental data show that the decrease of core rotation velocity and its gradient are correlated with the increase of core electron temperature and its gradient, and also with the likely steepening of the density gradient. We thus explore the viability of a hypothesized ITG (ITG ion temperature gradient instability) → TEM (trapped electron mode instability) transition as the explanation of the observed counter-current flow induced by ECH. However, the results of linear microstability analyses using inferred profiles suggest that the TEM is excited only in the deep core, so the viability of the hypothesized explanation is not yet clear. © 2013 IAEA, Vienna.

Previous studies have shown that testosterone activates the GPRC6A-Duox1 axis, resulting in the production of H 2 O 2 which leads to the apoptosis of keratinocytes and ultimately hair loss. Here, we elucidated a molecular mechanism by which the non-genomic action of testosterone regulates cellular redox status in androgenetic alopecia (AGA). Building upon this molecular understanding, we conducted a high-throughput screening assay of Nox inhibitors from a natural compounds library. This screening identified diterpenoid compounds, specifically Tanshinone I, Tanshinone IIA, Tanshinone IIB, and Cryptotanshinone, derived from Salviae Miltiorrhizae Radix . The IC 50 values for Nox isozymes were found to be 2.6-12.9 μM for Tanshinone I, 1.9-7.2 μM for Tanshinone IIA, 5.2-11.9 μM for Tanshinone IIB, and 2.1-7.9 μM for Cryptotanshinone. Furthermore, 3D computational docking analysis confirmed the structural basis by which Tanshinone compounds inhibit Nox activity. These compounds were observed to substitute for NADPH at the π-π bond site between NADPH and FAD, leading to the suppression of Nox activity. Notably, Tanshinone I and Tanshinone IIA effectively inhibited Nox activity heightened by testosterone, consequently reducing the production of intracellular H 2 O 2 and preventing cell apoptosis. In an animal study involving the application of testosterone to the back skin of 8-week-old C57BL/6J mice to inhibit hair growth, subsequent treatment with Tanshinone I or Tanshinone IIA alongside testosterone resulted in a substantial increase in hair follicle length compared to testosterone treatment alone. These findings underscore the potential efficacy of Tanshinone I and Tanshinone IIA as therapeutic agents for AGA by inhibiting Nox activity.

There is growing evidence that NADPH oxidase 4 (Nox4) in hepatocytes contributes to liver inflammation and fibrosis during the development of metabolic dysfunction-associated steatohepatitis (MASH). However, how Nox4 is regulated and leads to liver pathogenesis is unclear. Our previous studies showed that the cytosolic protein SH3 domain-containing Ysc84-like 1 (SH3YL1) regulates Nox4 activity. Here, we asked whether SH3YL1 also participates in liver inflammation and fibrosis during MASH development. We generated that whole body SH3YL1 knockout (SH3YL1 -/- ), Nox4 knockout (Nox4 -/- ) mice, and the hepatocyte-specific SH3YL1 conditional knockout (Alb-Cre/SH3YL1 fl/fl ) mice were fed a methionine/choline-deficient (MCD) diet to induce liver inflammation and fibrosis in pathogenesis of MASH. Palmitate-stimulated primary SH3YL1-and Nox4-deficient hepatocytes and hepatic stellate cells (HSCs) did not generate H 2 O 2 . While the liver of MCD diet-fed wild type (WT) mice demonstrated elevated 3-nitrotyrosine as a protein oxidation and 4-hydroxynonenal adducts as a lipid oxidation and increased liver inflammation, hepatocyte apoptosis, and liver fibrosis, these events were markedly reduced in SH3YL1 -/- , Nox4 -/- , and Alb-Cre/SH3YL1 fl/fl mice. The MCD diet-fed WT mice also showed elevated hepatocyte expression of SH3YL1 protein. Similarly, liver biopsies from MASH patients demonstrated strong hepatocyte SH3YL1 protein expression, whereas hepatocytes from patients with steatosis weakly expressed SH3YL1 and histologically normal patient hepatocytes exhibited very little SH3YL1 expression. The Nox4-SH3YL1 complex in murine hepatocytes elevates their H 2 O 2 production, which promotes the liver inflammation, hepatocyte apoptosis, and liver fibrosis that characterize MASH. This axis may also participate in MASH in humans., Competing Interests: Declaration of competing interest The authors state no conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

In this study, 11 species of the genus Diduga Moore, [1887] are recognized from Thailand, including a new species, Diduga siamensis Bayarsaikhan & Heppner sp. nov., and one newly recorded species, D. scalprata Bayarsaikhan, Li & Bae, 2020. Illustrations of adults and genitalia of the additionally examined species are provided, with a checklist of known species of the genus from this country.

The generation of non-exhausted effector T-cells depends on vaccine's spatiotemporal profile, and untimely delivery and low targeting to lymph node (LN) paracortex by standard bolus immunization show limited efficacy. By recapitulating the dynamic processes of acute infection, a bioadhesive immune niche domain (BIND) is developed that facilitates the delivery of timely-activating conjugated nanovaccine (t-CNV) in a metronomic-like manner and increased the accumulation and retention of TANNylated t-CNV (tannic acid coated t-CNV) in LN by specifically binding to collagen in subcapsular sinus where they gradually transformed into TANNylated antigen-adjuvant conjugate by proteolysis, inducing their penetration into paracortex through the collagen-binding in LN conduit and evoking durable antigen-specific CD8 + T-cell responses. The BIND combined with t-CNV, mRNA vaccine, IL-2, and anti-PD-1 antibody also significantly enhanced cancer immunotherapy by the dynamic modulation of immunological landscape of tumor microenvironment. The results provide material design strategy for dynamic immunomodulation that can potentiate non-exhausted T-cell-based immunotherapy., (© 2024 The Author(s). Advanced Materials published by Wiley‐VCH GmbH.)

Background Aims: Liver fibrosis is characterized by the progressive scarring of liver tissue. Oxidative stress is a critical causal factor of hepatic stellate cell (HSC) activation and the subsequent liver fibrogenesis, but the mechanism is not fully understood. Cysteine sulfinic acid (Cys-SO2H), a modification of reactive cysteine residues, is a unique form of oxidative response that alters the structure and function of proteins. Sulfiredoxin 1 (SRXN1) is responsible for ATP-dependent reduction of the Cys-SO2H to sulfenic acid (Cys-SOH)., Approach Results: We found that the expression of SRXN1 was increased in activated HSCs and in human and mouse fibrotic livers. HSC-specific ablation of Srxn1 or pharmacological inhibition of Srxn1 exacerbated HSC activation and sensitized mice to liver fibrosis. Mechanistically, SRXN1 inhibited HSC activation by de-sulfinylating the phosphatase protein tyrosine phosphatase non-receptor type 12 (PTPN12), which enhanced its phosphatase activity and protein stability, leading to decreased tyrosine phosphorylation and reduced activation of the pro-fibrotic inflammasome protein NLRP3. The anti-fibrotic effect of SRXN1 was abolished when NLRP3 was inhibited. In contrast, overexpression of PTPN12 attenuated NLRP3 activation, and this effect was further amplified by the C164A S-sulfinylation resistant mutant of PTPN12., Conclusions: Our findings have uncovered an important role of SRXN1 and protein S-sulfinylation in HSC activation and liver fibrosis. The SRXN1-PTPN12-NLRP3 axis represents potential therapeutic targets for liver fibrosis., (Copyright © 2024 American Association for the Study of Liver Diseases.)

Current immune checkpoint blockade therapy (ICBT) predominantly targets T cells to harness the antitumor effects of adaptive immune system. However, the effectiveness of ICBT is reduced by immunosuppressive innate myeloid cells in tumor microenvironments (TMEs). Toll-like receptor 7/8 agonists (TLR7/8a) are often used to address this problem because they can reprogram myeloid-derived suppressor cells (MDSCs) and tumor-associated M2 macrophages, and boost dendritic cell (DC)-based T-cell generation; however, the systemic toxicity of TLR7/8a limits its clinical translation. Here, to address this limitation and utilize the effectiveness of TLR7/8a, this work suggests a programmed two-step activation strategy via Antibody-Trojan Immune Converter Conjugates (ATICC) that specifically targets myeloid cells by anti-SIRPα followed by reactivation of transiently inactivated Trojan TLR7/8a after antibody-mediated endocytosis. ATICC blocks the CD47-SIRPα ("don't eat me" signal), enhances phagocytosis, reprograms M2 macrophages and MDSCs, and increases cross-presentation by DCs, resulting in antigen-specific CD8 + T-cell generation in tumor-draining lymph nodes and TME while minimizing systemic toxicity. The local or systemic administration of ATICC improves ICBT responsiveness through reprogramming of the immunosuppressive TME, increased infiltration of antigen-specific CD8 + T cells, and antibody-dependent cellular phagocytosis. These results highlight the programmed and target immunomodulation via ATICC could enhance cancer immunotherapy with minimized systemic toxicities., (© 2024 The Author(s). Advanced Healthcare Materials published by Wiley‐VCH GmbH.)

Species of the genus Diduga Moore are reviewed in Vietnam, with nine species including a new species, D. laocai sp. nov., and two newly recorded species, D. hastata Bayarsaikhan & Bae, 2021 and D. robdevosi Bayarsaikhan & Bae, 2023. Illustrations of adults and male and female genitalia of all examined species are provided.

The ongoing coronavirus disease 2019 (COVID-19) pandemic presents serious public health threats. Omicron, the current most prevalent strain of COVID-19, has a low fatality rate and very high transmissibility, so the number of patients with mild symptoms of COVID-19 is rapidly increasing. This change of pandemic challenges medical systems worldwide in many aspects, including sharp increases in demands for hospital infrastructure, critical shortages in medical equipment, and medical staff. Predicting deterioration in mild patients could alleviate these problems. A novel scoring system was proposed for predicting the deterioration of patients whose condition may worsen rapidly and those who all still mild or asymptomatic. Retrospective cohorts of 954 and 2,035 patients that quarantined in the Residential Treatment Center were assembled for derivation and external validation of mild COVID-19, respectively. Deterioration was defined as transfer to a local hospital due to worsening condition of the patients during the 2-week isolation period. A total of 15 variables: sex, age, seven pre-existing conditions (diabetes, hypertension, cardiovascular disease, respiratory disease, liver disease, kidney disease, and organ transplant), and five vital signs (systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), body temperature, and oxygen saturation (SpO2)) were collected. A scoring system was developed using seven variables (age, pulse rate, SpO2, SBP, DBP, temperature, and hypertension) with significant differences between the transfer and not transfer groups in logistic regression. The proposed system was compared with existing scoring systems that assess the severity of patient conditions. The performance of the proposed scoring system to predict deterioration in patients with mild COVID-19 showed an area under the receiver operating characteristic (AUC) of 0.868. This is a statistically significant improvement compared to the performance of the previous patient condition assessment scoring systems. During external validation, the proposed system showed the best and most robust predictive performance (AUC = 0.768; accuracy = 0.899). In conclusion, we proposed a novel scoring system for predicting patients with mild COVID-19 who will experience deterioration which could predict the deterioration of the patient's condition early with high predictive performance. Furthermore, because the scoring system does not require special calculations, it can be easily measured to predict the deterioration of a patients' condition. This system can be used as effective tool for early detection of deterioration in mild COVID-19 patients., (© 2024. The Author(s).)

The development of an efficient adsorbent for the simultaneous capture of large amounts of benzene, toluene, ethylbenzene, and xylene isomers (BTEX) is an important and challenging issue. Here, through a stepwise screening of 10,142 metal-organic framework (MOF) structures from the computation-ready, experimental (CoRE) MOF database, 65 MOFs are proposed as promising adsorbent candidates for BTEX capture by considering the structures with accessible pore sizes for BTEX adsorption, sufficient hydrophobicity, high benzene selectivity (>0.2), and large total BTEX uptake (>3 mmol/g). Among the top-performing MOFs in terms of the BTEX matrix (total BTEX uptake × benzene selectivity), EGUELUY01 was synthesized, and it exhibited large uptakes (≈5 mmol/g) for all BTEX components at concentrations of 1200-1500 ppm, which are superior to the BTEX uptake of the benchmark adsorbent, activated carbon. Moreover, some structure-property relationships required for BTEX adsorbents are provided through the obtained large-scale simulation data and machine learning analysis. The determined relationships will be useful for the future development of efficient BTEX adsorbents.

In the present study, we report a pantropical family Attevidae of the superfamily Yponomeutoidea in Cambodia for the first time. A new species, Atteva chalco sp. nov., and two newly recorded species, A. fabriciella Swederus, 1787, A. wallengreni Sohn and Wu, 2013 are reported. Illustrations of adults, male and female genitalia, diagnoses, and descriptions are provided.

Angiotensin II (AngII) induces the contraction and proliferation of vascular smooth muscle cells (VSMCs). AngII activates phospholipase C-β (PLC-β), thereby inducing Ca 2+ mobilization as well as the production of reactive oxygen species (ROS). Since contraction is a unique property of contractile VSMCs, signaling cascades related to the proliferation of VSMCs may differ. However, the specific molecular mechanism that controls the contraction or proliferation of VSMCs remains unclear. AngII-induced ROS production, migration, and proliferation were suppressed by inhibiting PLC-β3, inositol trisphosphate (IP 3 ) receptor, and NOX or by silencing PLC-β3 or NOX1 but not by NOX4. However, pharmacological inhibition or silencing of PLC-β3 or NOX did not affect AngII-induced VSMC contraction. Furthermore, the AngII-dependent constriction of mesenteric arteries isolated from PLC-β3 ∆SMC , NOX1 -/- , NOX4 -/- and normal control mice was similar. AngII-induced VSMC contraction and mesenteric artery constriction were blocked by inhibiting the L-type calcium channel Rho-associated kinase 2 (ROCK2) or myosin light chain kinase (MLCK). The activation of ROCK2 and MLCK was significantly induced in PLC-β3 ∆SMC mice, whereas the depletion of Ca 2+ in the extracellular medium suppressed the AngII-induced activation of ROCK2, MLCK, and vasoconstriction. AngII-induced hypertension was significantly induced in NOX1 -/- and PLC-β3 ∆SMC mice, whereas LCCA ligation-induced neointima formation was significantly suppressed in NOX1 -/- and PLC-β3 ∆SMC mice. These results suggest that PLC-β3 is essential for vascular hyperplasia through NOX1-mediated ROS production but is nonessential for vascular constriction or blood pressure regulation., (© 2024. The Author(s).)

Atopic dermatitis (AD) is a chronic cutaneous disease with a complex underlying mechanism, and it cannot be completely cured. Thus, most treatment strategies for AD aim at relieving the symptoms. Although corticosteroids are topically applied to alleviate AD, adverse side effects frequently lead to the withdrawal of AD therapy. Tacrolimus (TAC), a calcineurin inhibitor, has been used to treat AD, but its high molecular weight and insolubility in water hinder its skin permeability. Herein, we developed and optimized TAC-loaded chitosan-based nanoparticles (TAC@CNPs) to improve the skin permeability of TAC by breaking the tight junctions in the skin. The prepared nanoparticles were highly loadable and efficient and exhibited appropriate characteristics for percutaneous drug delivery. TAC@CNP was stable for 4 weeks under physiological conditions. CNP released TAC in a controlled manner, with enhanced skin penetration observed. In vitro experiments showed that CNP was non-toxic to keratinocyte (HaCaT) cells, and TAC@CNP dispersed in an aqueous solution was as anti-proliferative as TAC solubilized in a good organic solvent. Importantly, an in vivo AD mouse model revealed that topical TAC@CNP containing ~1/10 of the dose of TAC found in commercially used Protopic® Ointment exhibited similar anti-inflammatory activity to that of the commercial product. TAC@CNP represents a potential therapeutic strategy for the management of AD., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Type 2 innate lymphoid cells (ILC2s) have emerged as key regulators of the immune response in renal inflammatory diseases such as lupus nephritis. However, the mechanisms underlying ILC2 adhesion and migration in the kidney remain poorly understood. Here, we revealed the critical role of integrin α4β7 in mediating renal ILC2 adhesion and function. We found that integrin α4β7 enables the retention of ILC2s in the kidney by binding to VCAM-1, E-cadherin, or fibronectin on structural cells. Moreover, integrin α4β7 knockdown reduced the production of the reparative cytokine amphiregulin (Areg) by ILC2s. In lupus nephritis, TLR7/9 signaling within the kidney microenvironment downregulates integrin α4β7 expression, leading to decreased Areg production and promoting the egress of ILC2s. Notably, IL-33 treatment upregulated integrin α4β7 and Areg expression in ILC2s, thereby enhancing survival and reducing inflammation in lupus nephritis. Together, these findings highlight the potential of targeting ILC2 adhesion as a therapeutic strategy for autoimmune kidney diseases., (© 2024. The Author(s).)

Interleukin-33 (IL-33), a member of the IL-1 family, is a cytokine released in response to tissue damage and is recognized as an alarmin. The multifaceted roles of IL-33 in tumor progression have sparked controversy within the scientific community. However, most findings generally indicate that endogenous IL-33 has a protumor effect, while exogenous IL-33 often has an antitumor effect in most cases. This review covers the general characteristics of IL-33 and its effects on tumor growth, with detailed information on the immunological mechanisms associated with dendritic cells (DCs). Notably, DCs possess the capability to uptake, process, and present antigens to CD8 + T cells, positioning them as professional antigen-presenting cells. Recent findings from our research highlight the direct association between the tumor-suppressive effects of exogenous IL-33 and a novel subset of highly immunogenic cDC1s. Exogenous IL-33 induces the development of these highly immunogenic cDC1s through the activation of other ST2 + immune cells both in vivo and in vitro. Recognizing the pivotal role of the immunogenicity of DC vaccines in DC-based tumor immunotherapy, we propose compelling methods to enhance this immunogenicity through the addition of IL-33 and the promotion of highly immunogenic DC generation., (© 2024. The Author(s).)

The genus Rhagoba from Laos is revised, with three species, R. octomaculalis (Moore, 1867), R. obvellata Du & Li, 2012, and R. flavolineata sp. nov. is reported from Laos for the first time. A key to the Laotian species of Rhagoba is provided, with illustrations of adults and genitalia of examined species.

Background: During the height of the COVID-19 pandemic, the Korean government temporarily allowed full scale telehealth care for safety and usability. However, limited studies have evaluated the impact of telehealth by analyzing the physical and/or mental health data of patients with COVID-19 diagnosis collected through telehealth targeting Korean population., Objective: This study aimed to identify subgroup of depressive symptom trajectories in patients with clinically mild COVID-19 using collected longitudinal data from a telehealth-based contactless clinical trial., Methods: A total of 199 patients with COVID-19 were accrued for contactless clinical trial using telehealth from March 23 to July 20, 2022. Depressive symptoms were measured using the patient health questionnaire-9 on the start day of quarantine, on the final day of quarantine, and 1 month after release from quarantine. Additionally, acute COVID-19 symptoms were assessed every day during quarantine. This study used a latent class mixed model to differentiate subgroups of depressive symptom trajectories and a logistic regression model with Firth's correction to identify associations between acute COVID-19 symptoms and the subgroups., Results: Two latent classes were identified: class 1 with declining linearity at a slow rate and class 2 with increasing linearity. Among COVID-19 symptoms, fever, chest pain, and brain fog 1 month after release from quarantine showed strong associations with class 2 (fever: OR, 19.43, 95% CI, 2.30-165.42; chest pain: OR, 6.55, 95% CI, 1.15-34.61; brain fog: OR, 7.03, 95% CI 2.57-20.95). Sleeping difficulty and gastrointestinal symptoms were also associated with class 2 (gastrointestinal symptoms: OR, 4.76, 95% CI, 1.71-14.21; sleeping difficulty: OR, 3.12, 95% CI, 1.71-14.21)., Conclusion: These findings emphasize the need for the early detection of depressive symptoms in patients in the acute phase of COVID-19 using telemedicine. Active intervention, including digital therapeutics, may help patients with aggravated depressive symptoms., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Sung, Kim, Kim, Bae and Chie.)

Distinct neutrophil populations arise during certain pathological conditions. The generation of dysfunctional neutrophils during sepsis and their contribution to septicemia-related systemic immune suppression remain unclear. In this study, using an experimental sepsis model that features immunosuppression, we identified a novel population of pathogenic CD200R high neutrophils that are generated during the initial stages of sepsis and contribute to systemic immune suppression by enhancing regulatory T (T reg ) cells. Compared to their CD200R low counterparts, sepsis-generated CD200R high neutrophils exhibit impaired autophagy and dysfunction, with reduced chemotactic migration, superoxide anion production, and TNF-α production. Increased soluble CD200 blocks autophagy and neutrophil maturation in the bone marrow during experimental sepsis, and recombinant CD200 treatment in vitro can induce neutrophil dysfunction similar to that observed in CD200R high neutrophils. The administration of an α-CD200R antibody effectively reversed neutrophil dysfunction by enhancing autophagy and protecting against a secondary infection challenge, leading to increased survival. Transcriptome analysis revealed that CD200R high neutrophils expressed high levels of Igf1, which elicits the generation of T reg cells, while the administration of an α-CD200R antibody inhibited T reg cell generation in a secondary infection model. Taken together, our findings revealed a novel CD200R high neutrophil population that mediates the pathogenesis of sepsis-induced systemic immunosuppression by generating T reg cells., (© 2024. The Author(s), under exclusive licence to CSI and USTC.)

A taxonomic study of Spilonota Stephens, 1834, in Korea is conducted, and S. prognathana (Snellen, 1883) which had previously been merged with S. albicana (Motschulsky, 1866) is separated again. Additionally, as a result of research based on materials from Incheon National University two new species; S. samseong Choi, Bae & Nasu, S. laticucullusa Choi, Bae & Nasu proposed from Korea. The study provides brief descriptions of Spilonota species in Korea, with illustrations of the adult and genital morphology. Identification key for the known species reported from Korea is included.

Three new species of the cochyline genus Cirrothaumatia Razowski & Becker, 1986 are described and illustrated from submontane Andean sites in Peru (Depts. Amazonas, Junn, and San Martn): C. pichita n. sp., C. huemboana n. sp., and C. moyobamba n. sp. Comments and illustrations are provided for the three previously described species from southern Mexico (Veracruz), Central America (Guatemala, Costa Rica, and Panama), and northern South America (Venezuela: Edo. Aragua; Ecuador: Pichincha Prov.).

A new species Siccia triellipsis sp. nov., is described from Vietnam. Illustrations of the adults and genitalia of the new species are provided.

This work deals with 13 species of oribatid mites from different regions of Korea. Two new species, Humerobates aokii sp. nov. and Humerobates ulleungdoensis sp. nov. are proposed, and 11 known species, Punctoribates ezoensis (Fujikawa, 1982), Tectoribates proximus (Berlese, 1910), Protoribates tohokuensis Fujikawa, 2003, Protoribates capucinus Berlese, 1908, Peloribates pilosus Hammer, 1952, Scheloribates fimbriatus Thor, 1930, Neoribates aurantiacus (Oudemans, 1914), Zygoribatula glabra (Michael, 1890), Pergalumna myrmophila (Berlese, 1914), Trichogalumna boninensis Hagino, Bayartogtokh & Shimano, 2017, and Trichogalumna ohkuboi Hagino, Bayartogtokh & Shimano, 2017 are newly reported for the fauna of Korea. Supplementary descriptions and illustrations of each species along with their distributional data are provided.

A data pipeline was developed to send and receive patient blood management (PBM) data from all medical institutions in Korea. By incorporating the collected data with national big data, the system will be able to generate key performance index for each medical institution. The central PBM system also provides feedback to each individual medical institution.

Nox4-derived H 2 O 2 generation plays an important role in the pathogenesis of chronic kidney diseases (CKDs) such as diabetic nephropathy (DN). Here, we showed that SH3 domain-containing Ysc84-like 1 (SH3YL1), a Nox4 cytosolic activator, regulated DN. Streptozotocin (STZ)-induced type Ⅰ diabetic models in SH3YL1 whole-body knockout (KO) mice and podocyte-specific SH3YL1 conditional KO (Nphs2-Cre/SH3YL1 fl/fl ) mice were established to investigate the function of SH3YL1 in DN. The expression of fibrosis markers and inflammatory cytokines, the generation of oxidative stress, and the loss of podocytes were suppressed in diabetic SH3YL1 KO and Nphs2-Cre/SH3YL1 fl/fl mice, compared to diabetic control mice. To extrapolate the observations derived from diabetic mice to clinical implication, we measured the protein level of SH3YL1 in patients DN. In fact, the SH3YL1 level was increased in patients DN. Overall, the SH3YL1-Nox4 complex was identified to play an important role in renal inflammation and fibrosis, resulting in the development of DN., Competing Interests: The authors declare no competing financial interests., (© 2024 The Authors.)

The genus Xyrosaris Meyrick, 1907 from Korea is reviewed. Two new species, Xyrosaris vaginata sp. nov. and X. triacantha sp. nov. are described from Korea, along with notes on allied species of the genus. In addition, X. insuralis Ponomarenko & Beljaev, 2023 is reported for the first time from Korea, including a new host plant. Key to species, illustrations of adult, male and female genitalia, diagnoses, host plants, and descriptions are provided.

Phospholipase D (PLD) is an enzyme that catalyzes the hydrolysis of phosphatidylcholine into phosphatidic acid and free choline. In mammals, PLD exists in two well-characterized isoforms, PLD1 and PLD2, and it plays pivotal roles as signaling mediators in various cellular functions, such as cell survival, differentiation, and migration. These isoforms are predominantly expressed in diverse cell types, including many immune cells, such as monocytes and macrophages, as well as non-immune cells, such as epithelial and endothelial cells. Several previous studies have revealed that the stimulation of these cells leads to an increase in PLD expression and its enzymatic products, potentially influencing the pathological responses in a wide spectrum of diseases. Metabolic diseases, exemplified by conditions, such as diabetes, obesity, hypertension, and atherosclerosis, pose significant global health challenges. Abnormal activation or dysfunction of PLD emerges as a potential contributing factor to the pathogenesis and progression of these metabolic disorders. Therefore, it is crucial to thoroughly investigate and understand the intricate relationship between PLD and metabolic diseases. In this review, we provide an in-depth overview of the functional roles and molecular mechanisms of PLD involved in metabolic diseases. By delving into the intricate interplay between PLD and metabolic disorders, this review aims to offer insights into the potential therapeutic interventions., Competing Interests: Declaration of competing interest The authors declare no conflict of interests., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background: The genus Nycteola Hübner has been mainly distributed in the Old World and usually feeds on Fagaceae and Salicaceae, but Myrtaceae and Juglandaceae have also been reported. In Korea, the number of this genus has been changed from four to three after 2007, but three or four species are listed confusingly up to now., New Information: The Japanese endemic species Nycteoladufayi Sugi, 1982 are firstly reported for the Continents with its brief biology. Additionally, Korean fauna of nycteolid species are reviewed., (Yeong-Bin Cha, Un-Hong Heo, Ulziijargal Bayarsaikhan, Sora Kim, Yang-Seop Bae.)

Steroids are the standard treatment for allergic airway inflammation in asthma, but steroid-refractory asthma poses a challenge. Group 2 innate lymphoid cells (ILC2s), such as T helper 2 (T H 2) cells, produce key asthma-related type 2 cytokines. Recent insights from mouse and human studies indicate a potential connection between ILC2s and steroid-resistant asthma. Here, we highlight that lung ILC2s, rather than T H 2 cells, can develop steroid resistance, allowing them to persist and maintain their disease-driving activity even during steroid treatment. The emergence of multipotent IL-5 + IL-13 + IL-17A + ILC2s is associated with steroid-resistant ILC2s. The Janus kinase 3 (JAK3)/signal transducer and activator of transcription (STAT) 3, 5, and 6 pathways contribute to the acquisition of steroid-resistant ILC2s. The JAK3 inhibitor reduces ILC2 survival, proliferation, and cytokine production in vitro and ameliorates ILC2-driven Alternaria -induced asthma. Furthermore, combining a JAK3 inhibitor with steroids results in the inhibition of steroid-resistant asthma. These findings suggest a potential therapeutic approach for addressing this challenging condition in chronic asthma.

The genus Diduga Moore, [1887] is reviewed with 11 species from Laos, including one new species, D. bantha sp. nov. Illustrations of adults and genitalia of all examined species from Laos are provided, with the checklist of Laotian species of the genus Diduga.

Coronavirus has caused many casualties and is still spreading. Some people experience rapid deterioration that is mild at first. The aim of this study is to develop a deterioration prediction model for mild COVID-19 patients during the isolation period. We collected vital signs from wearable devices and clinical questionnaires. The derivation cohort consisted of people diagnosed with COVID-19 between September and December 2021, and the external validation cohort collected between March and June 2022. To develop the model, a total of 50 participants wore the device for an average of 77 h. To evaluate the model, a total of 181 infected participants wore the device for an average of 65 h. We designed machine learning-based models that predict deterioration in patients with mild COVID-19. The prediction model, 10 min in advance, showed an area under the receiver characteristic curve (AUC) of 0.99, and the prediction model, 8 h in advance, showed an AUC of 0.84. We found that certain variables that are important to model vary depending on the point in time to predict. Efficient deterioration monitoring in many patients is possible by utilizing data collected from wearable sensors and symptom self-reports.

Biomass-derived value-added materials such as levulinic acid (LA) are favorable natural resources for producing ester-based biolubricants owing to their biodegradability, nontoxicity, and excellent metal-adhering properties. However, highly active catalysts must be developed to carry out efficient esterification of LA with aliphatic alcohols, especially long-chain aliphatic alcohols. In this study, we developed a novel porous covalent organic polymer catalyst (BPOP-SO 3 H) with dual acid sites, phosphate and sulfonic acid sites, for the esterification of LA. The prepared BPOP-SO 3 H catalyst was verified using various surface analysis techniques. BPOP-SO 3 H exhibited 98% LA conversion with n -butanol and 99% selectivity for butyl levulinate ester within 30 min, which is superior to that of most reported catalysts. BPOP-SO 3 H also showed high LA conversion and ester selectivity when other aliphatic alcohols were used. Moreover, BPOP-SO 3 H showed good recyclability for five consecutive cycles. We believe that incorporating a high density of acid sites into a porous polymer with a large surface area and hierarchical pores is a promising approach for developing heterogeneous acid catalysts for the production of alkyl levulinate esters from LA.

Five new spider species of the genus Pholcus Walckenaer, 1805, P.duryun sp. nov. , P.hwaam sp. nov. , P.mohang sp. nov. , P.worak sp. nov. , and P.yangpyeong sp. nov. , belonging to the P.phungiformes group in the family Pholcidae C. L. Koch, 1850, are newly described from South Korea. These new species were collected from mixed forests in mountainous, hilly, and coastal terrains. This study provides the diagnoses, detailed descriptions, distribution maps, and taxonomic photographs of these new species., Competing Interests: The authors have declared that no competing interests exist., (Chang Moon Jang, Yang Seop Bae, Sue Yeon Lee, Jung Sun Yoo, Seung Tae Kim.)

Obesity is a metabolic disorder that results from an imbalance of energy intake and consumption. As low-grade chronic inflammation caused by obesity can lead to various complications, it is important to develop effective treatments against obesity. In this study, we investigate the effects of WKYMVm, a strong anti-inflammatory agent, against obesity. Administration of WKYMVm into high fat diet (HFD)-induced obese mice significantly attenuated body weight gain, food intake and increased insulin sensitivity. HFD-induced hepatic steatosis and adipose tissue hypertrophy were also markedly ameliorated by WKYMVm. During the maturation of adipocytes, WKYMVm improves lipid metabolism by increasing lipolysis, adipogenesis, mitochondrial biogenesis and fat browning. WKYMVm administration also elicited a decrease in leptin levels, but an increase in leptin sensitivity via regulation of hypothalamic endoplasmic reticulum stress and the leptin receptor cascade. Taken together, our results show that WKYMVm ameliorates obesity by improving lipid metabolism and leptin signalling, suggesting that WKYMVm can be a useful molecule for the development of anti-obesity agents., (© 2023 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Recombinant interleukin-33 (IL-33) inhibits tumor growth, but the detailed immunological mechanism is still unknown. IL-33-mediated tumor suppression did not occur in Batf3 -/- mice, indicating that conventional type 1 dendritic cells (cDC1s) play a key role in IL-33-mediated antitumor immunity. A population of CD103 + cDC1s, which were barely detectable in the spleens of normal mice, increased significantly in the spleens of IL-33-treated mice. The newly emerged splenic CD103 + cDC1s were distinct from conventional splenic cDC1s based on their spleen residency, robust effector T-cell priming ability, and surface expression of FCGR3. DCs and DC precursors did not express Suppressor of Tumorigenicity 2 (ST2). However, recombinant IL-33 induced spleen-resident FCGR3 + CD103 + cDC1s, which were found to be differentiated from DC precursors by bystander ST2 + immune cells. Through immune cell fractionation and depletion assays, we found that IL-33-primed ST2 + basophils play a crucial role in the development of FCGR3 + CD103 + cDC1s by secreting IL-33-driven extrinsic factors. Recombinant GM-CSF also induced the population of CD103 + cDC1s, but the population neither expressed FCGR3 nor induced any discernable antitumor immunity. The population of FCGR3 + CD103 + cDC1s was also generated in vitro culture of Flt3L-mediated bone marrow-derived DCs (FL-BMDCs) when IL-33 was added in a pre-DC stage of culture. FL-BMDCs generated in the presence of IL-33 (FL-33-DCs) offered more potent tumor immunotherapy than control Flt3L-BMDCs (FL-DCs). Human monocyte-derived DCs were also more immunogenic when exposed to IL-33-induced factors. Our findings suggest that recombinant IL-33 or an IL-33-mediated DC vaccine could be an attractive protocol for better tumor immunotherapy., (© 2023. The Author(s).)

We examined COVID-19 vaccination, incidence, and mortality rates among patients with mental health disorders in South Korea from 1 January 2020 to 31 December 2021. The study found that individuals with mental disorders had higher COVID-19 incidence and mortality than those without. Patients with mood disorders had higher vaccination rates and COVID-19 incidence and mortality than those without mental disorders. In contrast, patients with schizophrenia had lower vaccination rates, slightly lower COVID-19 incidence, and higher COVID-19 mortality. Patients with mental health disorders have been vulnerable to COVID-19, and more attention should be paid to their vaccination and health needs., Competing Interests: Declaration of Competing Interest The authors have no conflicts of interest to declare. Declaration of interest The authors have no conflicts of interest to declare., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Introduction: Multiple sclerosis (MS) is a potentially disabling disease that damages the brain and spinal cord, inducing paralysis of the body. While MS has been known as a T-cell mediated disease, recent attention has been drawn to the involvement of B cells in its pathogenesis. Autoantibodies from B cells are closely related with the damage lesion of central nervous system and worse prognosis. Therefore, regulating the activity of antibody secreting cell could be related with the severity of the MS symptoms., Methods: Total mouse B cells were stimulated with LPS to induce their differentiation into plasma cells. The differentiation of plasma cells was subsequently analyzed using flow cytometry and quantitative PCR analysis. To establish an experimental autoimmune encephalomyelitis (EAE) mouse model, mice were immunized with MOG 35-55 /CFA emulsion., Results: In this study, we found that plasma cell differentiation was accompanied by upregulation of autotaxin, which converts sphingosylphosphorylcholine (SPC) to sphingosine 1-phosphate in response to LPS. We observed that SPC strongly blocked plasma cell differentiation from B cells and antibody production in vitro . SPC downregulated LPS-stimulated IRF4 and Blimp 1, which are required for the generation of plasma cells. SPC-induced inhibitory effects on plasma cell differentiation were specifically blocked by VPC23019 (S1PR1/3 antagonist) or TY52159 (S1PR3 antagonist), but not by W146 (S1PR1 antagonist) and JTE013 (S1PR2 antagonist), suggesting a crucial role of S1PR3 but not S1PR1/2 in the process. Administration of SPC against an EAE mouse model significantly attenuated the symptoms of disease, showing decreased demyelinated areas of the spinal cord and decreased numbers of cells infiltrated into the spinal cord. SPC markedly decreased plasma cell generation in the EAE model, and SPC-induced therapeutic effects against EAE were not observed in μMT mice., Conclusion: Collectively, we demonstrate that SPC strongly inhibits plasma cell differentiation, which is mediated by S1PR3. SPC also elicits therapeutic outcomes against EAE, an experimental model of MS, suggesting SPC as a new material to control MS., Competing Interests: Authors BP and Yoe-SB are preparing patent applications. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Park, Jeong, Hu, Lee, Kim, Bae, Bae and Bae.)

Background: Various renal abnormalities, including hydronephrosis, polycystic kidney disease, and hydroureter, have been reported, and these abnormalities are present in DiGeorge syndrome, renal dysplasia, and acute kidney failure. Previous studies have shown that various genes are associated with renal abnormalities. However, the major target genes of nonobstructive hydronephrosis have not yet been elucidated., Results: We examined neuroblast differentiation-associated protein Ahnak localization and analyzed morphogenesis in developing kidney and ureter. To investigated function of Ahnak, RNA-sequencing and calcium imaging were performed in wild type and Ahnak knockout (KO) mice. Ahnak localization was confirmed in the developing mouse kidneys and ureter. An imbalance of calcium homeostasis and hydronephrosis, which involves an expanded renal pelvis and hydroureter, was observed in Ahnak KO mice. Gene Ontology enrichment analysis on RNA-seq results indicated that 'Channel Activity', 'Passive Transmembrane Transporter Activity' and 'Cellular Calcium Ion Homeostasis' were downregulated in Ahnak KO kidney. 'Muscle Tissue Development', 'Muscle Contraction', and 'Cellular Calcium Ion Homeostasis' were downregulated in Ahnak KO ureter. Moreover, peristaltic movement of smooth muscle in the ureter was reduced in Ahnak KO mice., Conclusions: Abnormal calcium homeostasis causes renal disease and is regulated by calcium channels. In this study, we focused on Ahnak, which regulates calcium homeostasis in several organs. Our results indicate that Ahnak plays a pivotal role in kidney and ureter development, and in maintaining the function of the urinary system., (© 2023. The Author(s).)

Osteoarthritis (OA) is a degenerative joint disorder associated with inflammation, functional disability, and high socioeconomic costs. The development of effective therapies against inflammatory OA has been limited owing to its complex and multifactorial nature. The efficacy of Prussian blue nanozymes coated with Pluronic (PPBzymes), US Food and Drug Administration-approved components, and their mechanisms of action have been described in this study, and PPBzymes have been characterized as a new OA therapeutic. Spherical PPBzymes were developed via nucleation and stabilization of Prussian blue inside Pluronic micelles. A uniformly distributed diameter of approximately 204 nm was obtained, which was maintained after storage in an aqueous solution and biological buffer. This indicates that PPBzymes are stable and could have biomedical applications. In vitro data revealed that PPBzymes promote cartilage generation and reduce cartilage degradation. Moreover, intra-articular injections with PPBzymes into mouse joints revealed their long-term stability and effective uptake into the cartilage matrix. Furthermore, intra-articular PPBzymes injections attenuated cartilage degradation without exhibiting cytotoxicity toward the synovial membrane, lungs, and liver. Notably, based on proteome microarray data, PPBzymes specifically block the JNK phosphorylation, which modulates inflammatory OA pathogenesis. These findings indicate that PPBzymes might represent a biocompatible and effective nanotherapeutic for obstructing JNK phosphorylation., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Siyoung Yang, Won reports financial support was provided by Korea Research Institute of Bioscience and Biotechnology. Eun-Jeong Kim, Ho Chul Kang, Won Il Choi, Siyoung Yang reports financial support was provided by National Research Foundation of Korea. Siyoung Yang reports financial support was provided by National Research Council. Ho Chul Kang, Siyoung Yang reports financial support was provided by Korea Health Industry Development Institute. Won Il Choi reports financial support was provided by Korea Institute of Ceramic Engineering and Technology., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The signaling pathways governing acetaminophen (APAP)-induced liver injury have been extensively studied. However, little is known about the ubiquitin-modifying enzymes needed for the regulation of APAP-induced liver injury. Here, we examined whether the Pellino3 protein, which has E3 ligase activity, is needed for APAP-induced liver injury and subsequently explored its molecular mechanism. Whole-body Peli3 -/- knockout (KO) and adenovirus-mediated Peli3 knockdown (KD) mice showed reduced levels of centrilobular cell death, infiltration of immune cells, and biomarkers of liver injury, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), upon APAP treatment compared to wild-type (WT) mice. Peli3 deficiency in primary hepatocytes decreased mitochondrial and lysosomal damage and reduced the mitochondrial reactive oxygen species (ROS) levels. In addition, the levels of phosphorylation at serine 9 in the cytoplasm and mitochondrial translocation of GSK3β were decreased in primary hepatocytes obtained from Peli3 -/- KO mice, and these reductions were accompanied by decreases in JNK phosphorylation and mitochondrial translocation. Pellino3 bound more strongly to GSK3β compared with JNK1 and JNK2 and induced the lysine 63 (K63)-mediated polyubiquitination of GSK3β. In rescue experiments, the ectopic expression of wild-type Pellino3 in Peli3 -/- KO hepatocytes restored the mitochondrial translocation of GSK3β, but this restoration was not obtained with expression of a catalytically inactive mutant of Pellino3. These findings are the first to suggest a mechanistic link between Pellino3 and APAP-induced liver injury through the modulation of GSK3β polyubiquitination., (© 2023. The Author(s).)

Sphingolipids, which are components of cellular membranes and organ tissues, can be synthesized or degraded to modulate cellular responses according to environmental cues, and the balance among the different sphingolipids is important for directing immune responses, regardless of whether they originate, as intra- or extracellular immune events. Recent progress in multiomics-based analyses and methodological approaches has revealed that human health and diseases are closely related to the homeostasis of sphingolipid metabolism, and disease-specific alterations in sphingolipids and related enzymes can be prognostic markers of human disease progression. Accumulating human clinical data from genome-wide association studies and preclinical data from disease models provide support for the notion that sphingolipids are the missing pieces that supplement our understanding of immune responses and diseases in which the functions of the involved proteins and nucleotides have been established. In this review, we analyze sphingolipid-related enzymes and reported human diseases to understand the important roles of sphingolipid metabolism. We discuss the defects and alterations in sphingolipid metabolism in human disease, along with functional roles in immune cells. We also introduce several methodological approaches and provide summaries of research on sphingolipid modulators in this review that should be helpful in studying the roles of sphingolipids in preclinical studies for the investigation of experimental and molecular medicines., (© 2023. The Author(s).)

We designed and developed Remote Patient Monitoring (RPM) system specific for coronavirus (COVID-19) patients, and collected multimodal data. Using the collected data, we explored the trajectories of anxiety symptoms for 199 COVID-19 patients quarantined at home. Two classes were identified using latent class linear mixed model. Thirty-six patients showed an exacerbation of anxiety. Presence of initial psychological symptoms, pain on the start day of quarantine, and abdominal discomfort at one month after finishing the quarantine were associated with exacerbation of anxiety.

Building an integrated data model that includes not only clinical data but also personal health records has become increasingly important. We aimed to build a big data healthcare platform by developing a common data model that can be utilized in the healthcare field. To this end, we acquired health data from various communities to establish community care digital healthcare service models. Further, to improve personal health data interoperability, we ensured conformance to international standards, namely, the Systemized Nomenclature of Medicine Clinical Terms (SNOMED-CT) and transmission standards, namely, Health Level 7 Fast Healthcare Interoperability Resource (HL7 FHIR). Furthermore, FHIR resource profiling was designed to transmit and receive data, following the HL7 FHIR R4 guidelines.

Two new species, Stericta jaeshini Kim & Bae, sp. nov. and S. atroaurantiaca Kim & Bae, sp. nov. are described from Southeast Asia. About 50 species of the genus Stericta have been recorded from Southeast Asia, but it has not been recorded to occur in Laos and Cambodia previously. We record the presence of this genus in these two countries for the first time in this study. Illustrations of adults and genitalia of examined species are provided. v.

Although activin receptor IIB (ACVR2B) is emerging as a novel pathogenic receptor, its ligand and assembled components (or assembly) are totally unknown in the context of osteoarthritis (OA) pathogenesis. The present results suggest that upregulation of ACVR2B and its assembly could affect osteoarthritic cartilage destruction. It is shown that the ACVR2B ligand, activin A, regulates catabolic factor expression through ACVR2B in OA development. Activin A Tg mice (Col2a1-Inhba) exhibit enhanced cartilage destruction, whereas heterozygous activin A KO mice (Inhba +/- ) show protection from cartilage destruction. In silico analysis suggests that the Activin A-ACVR2B axis is involved in Nox4-dependent ROS production. Activin A Tg:Nox4 KO (Col2a1-Inhba:Nox4 -/- ) mice show inhibition of experimental OA pathogenesis. NOX4 directly binds to the C-terminal binding site on ACVR2B-ACVR1B and amplifies the pathogenic signal for cartilage destruction through SMAD2/3 signaling. Together, the findings reveal that the ACVR2B assembly, which comprises Activin A, ACVR2B, ACVR1B, Nox4, and AP-1-induced HIF-2α, accelerates OA development. Furthermore, it is shown that shRNA-mediated ACVR2B knockdown or trapping ligands of ACVR2B abrogate OA development by competitively disrupting the ACVR2B-Activin A interaction. These results suggest that the ACVR2B assembly is required to amplify osteoarthritic cartilage destruction and could be a potential therapeutic target in efforts to treat OA., (© 2023 The Authors. Advanced Science published by Wiley-VCH GmbH.)