Chungnam National University

Eco-friendly next-generation energy storage devices with high energy density are required to meet the increasing demand for sustainable and green electronics. However, their manufacturing requires a lot of chemical precursors and is usually accompanied by chemical waste; it also involves laborious and time-consuming processes such as mixing, heat treating, casting, and drying. Here, we proposed that mass production of microsupercapacitors (MSCs) for green electronics can be achieved by embedding manganese monoxide (MnO) on wood-derived laser-induced-graphene (LIG) via femtosecond laser direct writing (FsLDW) technique. The direct synthesis of MnO/LIG hetero-nanostructures on wood was realized by drop-casting a small amount of precursor between the first and second FsLDW. The preceding FsLDW thermochemically converted wood into LIG while the following FsLDW converted the precursor into MnO, resulting in MnO/LIG hetero-nanostructures. As-fabricated MnO/LIG MSC exhibited enhanced areal capacitance (35.54 mF cm−2 at 10 mV s−1) and capacitance retention (approximately 82.31% after 10,000 cycles) with only a small inclusion of Mn sources (0.66 mg cm−2) and short production time (10 min cm−2), which attributes to operate light-emitting diodes, digital clocks, and electronic paper as well. This approach enables the green, facile, fast, and cost-effective fabrication of future sustainable energy storage devices from biomass for next-generation green electronics.

Recent advances in high‐performance thermoelectric materials have sparked significant interest, particularly in SnTe, a mid‐temperature group‐IV chalcogenide that is both eco‐friendly and cost‐effective. However, compared to other group‐IV chalcogenides, there remains a substantial scope for enhancing the thermoelectric performance of SnTe. In the past four years (since 2020), numerous compelling reports have proposed novel strategies to narrow this gap and boost the performance of SnTe‐based materials, thereby building upon previous advancements. These recent advancements are comprehensively summarized in this timely review. This review reports three essential facets critical to the advancement of high‐performance SnTe materials: electrical properties, thermal properties, and the overly overlooked mechanical properties. First, a brief theoretical exposition is presented, subsequently detailing empirically verified techniques for achieving superior SnTe‐based materials. The intrinsic prevalence of tin vacancies (VSn) in SnTe classifies it as a p‐type thermoelectric material. Here, it is unveiled for the first time, recent significant breakthroughs in the development of n‐type SnTe. This advancement enables the development of an all‐SnTe‐based thermoelectric device. Additional attention is devoted to emerging trends that further amplify the performance of SnTe. With persistent efforts, achieving a ZT greater than 2 in SnTe‐based materials is inevitable.

Invasive non-indigenous species have been reported to cause harm to ecosystems, including freshwater ecosystems, and reduce species abundance. As the world became more alert to the introduction of non-indigenous species, the demands for developing preliminary management measures have also increased. Thus, this study aimed to develop a habitat suitability assessment approach for non-indigenous freshwater fish with cost-effective data access. This approach utilized the Köppen-Geiger climate classification maps and fish occurrence data to predict the present (1980–2016) and future (2071–2100) habitat suitability of Oreochromis niloticus and Poecilia reticulata in South Korea. A fuzzy inference system was applied to relate climatic variables based on the Köppen-Geiger climate classification and species occurrence records. The results indicate that the habitat of the two species is limited to sites near sources of thermal pollution (for overwintering) in the present, and habitable area will expand in the future as the temperature increases. This approach is expected to aid non-experts in decision-making processes regarding non-indigenous freshwater fish management by evaluating potential habitats through the transfer of quantitative climate variables into linguistic or intuitive variables. Further augmentation in the climate zone classification method is expected to aid developing management strategies. Additionally, this approach is anticipated to facilitate the application of habitat prediction results by shortening the gap between experts and non-experts.

Background Breast cancer is one of the most common cancers in women and is closely associated with obesity. Gremlin-2 (GREM2), an antagonist for bone morphogenetic proteins (BMPs), has been considered an inhibitor of adipogenic differentiation in adipose-derived stromal/stem cells. However, the role of GREM2 in breast cancer cells remains largely unknown, and its signaling mechanism has yet to be clarified. Methods Bioinformatics analysis was conducted using public databases. Breast cancer cells overexpressing mock or GREM2 were used for in vitro and in vivo studies. Cell viability, colony formation, migration, and animal studies were performed to investigate the role of GREM2 in breast cancer cells. Screening of target genes affected by GREM2 overexpression in breast cancer cells was performed through RNA sequencing (RNA-seq) analysis. Results The expression level of GREM2 mRNA was significantly reduced in both breast cancer tissues and cell lines. Kaplan-Meier analysis showed that low expression of GREM2 and high methylation of the GREM2 promoter were each associated with poor patient survival. The low mRNA expression of GREM2 in breast cancer cells was increased by the demethylating agent decitabine. Breast cancer cells overexpressing GREM2 decreased cell proliferation when compared to control cells, both in vitro and in vivo. Through comparison of RNA-seq analysis between cell lines and tissue samples, gene ontologies that were consistently upregulated or downregulated by GREM2 in breast cancer were identified. In particular, the expression of inhibitor of DNA-binding-1 (ID1) was repressed by GREM2. BMP2 is one of the upstream regulators that increases the expression of ID1, and the expression of ID1 reduced by GREM2 was restored by overexpression of BMP2. Also, the migration ability of breast cancer cells, which had been suppressed by GREM2, was restored by BMP2 or ID1. Conclusions Low expression of GREM2 in breast cancer cells is associated with hypermethylation of the GREM2 promoter, which may ultimately contribute to poor patient survival. GREM2 participates in regulating the expression of various genes, including ID1, and is involved in suppressing the proliferation of breast cancer cells. This suggests that GREM2 has the potential to act as a novel tumor suppressor in breast cancer.

Therapeutic angiogenesis by intentional formation of blood vessels is essential for treating various ischemic diseases, including limb ischemia. Because Wnt/β-catenin and angiopoietin-1/Tie2 signaling play important roles in endothelial survival and vascular stability, coactivation of these signaling pathways can potentially achieve therapeutic angiogenesis. In this study, we developed a bifunctional antibody fusion, consisting of a Tie2-agonistic antibody and the Furin domains of R-spondin 3 (RSPO3), to simultaneously activate Tie2 and Wnt/β-catenin signaling. We identified a Tie2-agonistic antibody T11 that cross-reacted with the extracellular domain of human and mouse Tie2, and evaluated its ability to increase endothelial cell survival and tube formation. We generated a bifunctional T11–RF12 by fusing T11 with the Furin-1 and −2 domains of RSPO3. T11–RF12 could bind not only to Tie2, but also to LGR5 and ZNRF3, which are counterparts of the Furin-1 and −2 domains. T11–RF12 significantly increased Wnt/β-catenin signaling, as well as the formation of capillary-like endothelial tubes, regardless of the presence of Wnt ligands. Coactivation of Tie2 and Wnt/β-catenin signaling by T11–RF12 increased the blood flow, and thereby reduced foot necrosis in a mouse hindlimb ischemia model. In particular, T11–RF12 induced therapeutic angiogenesis by promoting vessel stabilization through pericyte coverage and retaining endothelial expression of Frizzled 10 and active β-catenin. These results indicate that the agonistic synergism of Tie2 and Wnt/β-catenin signaling achieved using T11–RF12 is a novel therapeutic option with potential for treating limb ischemia and other ischemic diseases.

The selection of suitable polymers is pivotal in influencing the electrical performance and the thermal/electrical stabilities of organic electronics. Here, the superior properties induced by deuteration in polymer/2,8‐difluoro‐5,11‐bis(triethylsilylethynyl)anthradithiophene (diF‐TES ADT) blends are systematically investigated. By employing a combination of experimental and computational analyses, the critical factors underlying charge transport and device stabilities in deuterated polymers (d‐polymers) compared to protonated polymers are elucidated. Deuterated polymers exhibit increased mass due to the substitution of hydrogen with deuterium, reducing the zero‐point vibration energy by 1/√2. This reduction leads to enhanced energetic stabilization and the formation of stronger D─C bonds than H─C bonds. Consequently, deuterated polymers exhibit enhanced thermal properties, along with improved insulating properties, which are intrinsically linked to improved device performance. Additionally, the correlation between the electrical properties and bias stability using deuterated poly(methyl methacrylate) (d‐PMMA) and polystyrene (d‐PS) blends are analyzed. Utilizing complementary neutron & X‐ray reflectivity, and photoexcited charge‐collection spectroscopy (PECCS), phase separation and trap dynamics are delved, providing a comprehensive understanding of these relationships. These findings reveal that d‐polymers significantly enhance the electrical performance and stability of the blends, offering valuable insights for the design of advanced materials in organic electronics.

Background Bone remodeling is a continuous and balanced process which relies on the dynamic equilibrium between osteoclastic bone resorption and osteoblastic bone formation. During osteoclast differentiation, pro-osteoclastogenic and anti-osteoclastogenic genes are selectively targeted by positive and negative transcription regulators, respectively. VprBP, also known as DCAF1, is a recently identified kinase and plays an important role in driving epigenetic gene silencing and oncogenic transformation. However, nothing is currently known about a possible involvement of VprBP in signaling pathways that regulate other cellular processes. Results We demonstrate that VprBP stimulates RANKL-induced differentiation of osteoclast precursor cells (OCPs) into mature osteoclasts by suppressing the expression of anti-osteoclastogenic genes through phosphorylation of threonine 120 on histone H2A (H2AT120p). H2AT120p is critical for VprBP function, because abrogating VprBP kinase activity toward H2AT120 transcriptionally reactivates anti-osteoclastogenic genes and significantly attenuates osteoclast differentiation. Consistent with this notion, our in vivo studies established the importance of VprBP-mediated H2AT120p in low bone mass phenotypes and osteoporosis caused by overactive osteoclasts. Conclusions Our data reveal a previously unrecognized function of VprBP in supporting RANKL-induced osteoclast differentiation and the molecular mechanism underlying its action as a negative regulator of anti-osteoclastogenic genes.

The genus Streptococcus is a heterogenous group of commensal and pathogenic bacteria that are normal inhabitants of the human body, including the female genital tract (FGT). In the FGT microbiome, streptococci represent two major groups: the pathogenic group B Streptococci (GBS) and the commensal viridans group streptococci (VGS). Though members of the VGS are frequently detected from the FGT, their role in the FGT microbiome remains underexplored. Here, we report the characterization of Streptococcus sp. K0074, isolated from the vaginal swab of an endometrial cancer patient admitted to the hospital, with no evidence of bacterial vaginosis. Phylogenetic analysis revealed that the strain is a member of the commensal VGS and possibly represents a novel species in the mitis subgroup. The strain demonstrated the production of low molecular weight bacteriocin-like substance with narrow-spectrum antagonistic activity, affecting the growth, biofilm formation, and colonization of aerobic vaginitis (AV)–causing bacterium methicillin-resistant Staphylococcus aureus (MRSA). The putative bacteriocin exhibited cell membrane–permeabilizing activity and exerted negative regulatory effect on the accessory gene regulator and SaeRS two-component systems of MRSA. Collectively, our results suggest that the isolate may modulate the FGT microbiome by inhibiting or displacing specific pathogen. Furthermore, the results presented here highlight new perspectives regarding the existence of VGS in the FGT microbiome and in particular pinpoint the potential clinical significance of the isolated VGS strain Streptococcus sp. K0074 for the treatment of AV caused by MRSA.

Background The association between metabolic syndrome (MetS) and chronic obstructive pulmonary disease (COPD) has not been studied well, particularly in young individuals. We investigated the risk of COPD development in young individuals based on MetS and its components. Methods We used the Korean National Health Information Database to identify 6,891,400 individuals aged 20–39 years who participated in the national health check-up service between 2009 and 2012. Then, we identified individuals with MetS and investigated COPD development based on health insurance claims. Cox proportional hazard regression models were used to calculate the adjusted hazard ratio (aHR) for the risk of COPD development. Results During a mean follow-up period of 8.35 years, 13,784 individuals were newly diagnosed with COPD. MetS was associated with an increased risk of COPD (aHR, 1.18; 95% confidence interval [CI], 1.11–1.24). Among the MetS components, except for hyperglycemia, abdominal obesity (aHR, 1.27; 95% CI, 1.19–1.34), hypertension (aHR, 1.05; 95% CI, 1.01–1.10), hypertriglyceridemia (aHR, 1.11; 95% CI, 1.07–1.16), and low high-density lipoprotein cholesterol levels (aHR, 1.16; 95% CI, 1.11–1.22) were significantly associated with COPD development. A higher number of MetS components correlated with an increased risk of COPD development, with the highest risk observed when all five MetS components were present (aHR, 1.55; 95% CI, 1.28–1.87). Conclusion MetS was associated with COPD development in young individuals. The risk of COPD development increased along with the increasing number of MetS components. These findings suggest that careful monitoring for COPD development is necessary in young individuals with MetS, especially those with multiple components of MetS.

Plants have evolved photoreceptors to optimize their development during primary growth, including germination, hypocotyl elongation, cotyledon opening, and root growth, allowing them to adapt to challenging light conditions. The light signaling transduction pathway during seedling establishment has been extensively studied, but little molecular evidence is available for light-regulated secondary growth, and how light regulates cambium-derived tissue production remains largely unexplored. Here, we show that CRYPTOCHROME (CRY)-dependent blue light signaling and the subsequent attenuation of ELONGATED HYPOCOTYL 5 (HY5) movement to hypocotyls are key inducers of xylem fiber differentiation in Arabidopsis thaliana. Using grafted chimeric plants and hypocotyl-specific transcriptome sequencing of light signaling mutants under controlled light conditions, we demonstrate that the perception of blue light by CRYs in shoots drives secondary cell wall (SCW) deposition at xylem fiber cells during the secondary growth of hypocotyls. We propose that HY5 is a blue light–responsive mobile protein that inhibits xylem fiber formation via direct transcriptional repression of NAC SECONDARY WALL THICKENING PROMOTING 3 ( NST3 ). CRYs retain HY5 in the nucleus, impede its long-distance transport from leaf to hypocotyl, and they initiate NST3- driven SCW gene expression, thereby triggering xylem fiber production. Our findings shed light on the long-range CRYs-HY5-NST3 signaling cascade that shapes xylem fiber development, highlighting the activity of HY5 as a transcriptional repressor during secondary growth.

New materials were designed and synthesized by introducing electron donor and acceptor groups using coumarin as the basic unit. In addition, two more materials with similar structures were synthesized for the comparison of their optical properties and stability. The solvent effect and the photo physical aggregation properties of aggregation caused quenching (ACQ) in the ratio of water and DMF were also investigated. In addition, we checked the detection ability for anions, and the optical properties of the materials at different pH were also investigated. The photo stability of these synthesized materials was studied, and interesting results were obtained. Based on these synthesized materials, we produced films by introducing color materials into PLA films. PLA film is characterized by the absence of plastic waste due to carbon reduction and biodegradation effects from using biomass instead of fossil fuels as raw materials, but it has the disadvantage of low light stability. By introducing high-photo stability pigment materials, the photo stability of the film can be corrected, and UV protection can be provided. The UV absorbance and fluorescence intensity of the film with the dye materials were checked, and the mechanical properties and thermal stability of the film changed when the coloring material was introduced compared to the conventional PLA film.

Individuals diagnosed with advanced cancer often experience stress and depression, factors linked to worse survival. Curability belief—defined as the hope and expectation of cure through treatment, based on affective forecasting—may differ from the patient’s actual life expectancy (i.e., likelihood estimation) and has shown variable associations with cancer survival. In this study, multivariate Cox regression analyses were used to examine the effect of curability belief and depression on 1-year survival after adjustment for physical factors. Additionally, regularized partial correlations among physical and psychological factors were assessed using mixed graphical models to elucidate their roles in mediating the relationship between curability belief and 1-year survival. This multi-center cohort study, conducted across 13 tertiary hospitals (including four ranked among the ‘World’s Best Specialized Hospitals 2025’ in oncology), involved 382 adults with stage IV advanced cancer and an oncologist-estimated survival of more than 6 months. Baseline data included demographics, primary tumor site, number of metastatic sites, symptom burdens (EORTC QLQ-C15-PAL), performance status (ECOG-PS), depression levels (PHQ-9), anti-cancer treatment type, patient’s life expectancy estimation, and curability belief. Follow-up data included 1-year survival and end-of-life care (place of death) for deceased patients. Multivariate Cox proportional hazards models were used to assess adjusted hazard ratios (aHRs) for curability belief, depression, and their interaction on 1-year survival, adjusting for significant demographic and clinical factors from univariate Cox regressions. The Kaplan–Meier method was used to plot survival probability by curability belief and depression interaction. Mixed graphical models estimated regularized partial correlations among 1-year survival, curability belief, patient’s life expectancy, depression, primary tumor site, anti-cancer treatment type, performance status, and symptom burden. In terms of healthcare utilization, patients with curability belief were more likely to receive standard or advanced anti-cancer therapy, while those without curability belief tended to suspend or discontinue therapy (P < 0.001). Among patients who did not survive the 1-year follow-up (N = 161), end-of-life care settings differed significantly between those with curability belief (predominantly nursing homes and home settings) and those without (primarily hospice and tertiary/secondary hospitals; P = 0.036). In multivariate Cox regression, curability belief (P = 0.003), depression (PHQ-9 score ≥ 10; P = 0.003), and their interaction (P = 0.040) were significantly associated with 1-year survival, after adjusting for sex, residential area, primary tumor site, performance status, anti-cancer treatment type, and symptom burdens (fatigue and appetite loss). The relationship between curability belief and 1-year survival was significant only in patients without depression [PHQ-9 score < 10; aHR (95% CI) = 2.20 (1.31–3.70); P = 0.003]. In the mixed graphical model, node predictability values for curability belief, depression, and 1-year survival were 0.68, 0.50, and 0.70, respectively, with curability belief showing partial correlations with depression (r = 0.30) and patients’ life expectancy (r = 0.20); depression correlated with fatigue (r = 0.53), anorexia (r = 0.16), life expectancy (r = 0.24), performance status (r = 0.23), and curability belief; and 1-year survival correlated with suspended/stopped anti-cancer treatment (r = 0.45), primary tumor site (r = 0.24), and performance status (r = 0.15). Partial correlations of performance status with depression and discontinued treatment mediated the association between curability belief and 1-year survival. Curability belief among stage IV advanced cancer patients with an oncologist-estimated survival of over 6 months was associated with depression levels and patients’ perceived life expectancy estimations. Performance status, depression, and anti-cancer treatment status mediate the relationship between curability belief and improved 1-year survival in patients without depression. Further research using longitudinal modeling of depression, performance status, and healthcare utilization, with curability belief and primary tumor site as covariates, is warranted. Trial registration: Clinical Trial Number (ClinicalTrials.gov): NCT03222258; Study Registration Dates (First submitted: 2017-06-05; First submitted following the QC criteria: 2017-07-16; First posted: 2017-07-19).