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Background/Objectives: Alnustone (Aln) is an effective compound of Alpinia katsumadae Hayata. Aln possesses various pharmacological activities such as antibacterial, anti-inflammatory, and anti-cancer effects. However, the inhibitory effect of Aln on colorectal cancer (CRC) has not yet been identified. Thus, research was conducted to clarify whether Aln can suppress the proliferative and metastatic ability of CRC cells. Methods: A cell viability assay was performed to confirm the decrease in CRC cell viability following Aln treatment. Flow cytometry was carried out to evaluate the effects of Aln on cell cycle arrest, autophagy, and apoptosis in CRC cells. In addition, a lung metastasis animal model was used to check the inhibitory effect of Aln on the metastasis of CRC cells. Results: Aln remarkably diminished the viability and colony-forming ability of several CRC cell lines. In addition, Aln led to a halt at the G0/G1 phase through downregulating cyclin D1-CDK4 in CRC cells. The upregulation of LC3B and p62 expression by Aln triggered autophagy of CRC cells. Moreover, Aln promoted mitochondrial depolarization, resulting in apoptosis of CRC cells. Oral administration of Aln significantly restrained the metastasized lung tumor nodules. Conclusions: This study demonstrated that Aln can suppress the survival and lung metastasis of CRC cells by promoting cell cycle arrest, autophagy, and apoptosis.

Saikosaponin D (SSD), derived from Bupleurum falcatum L., has various pharmacological properties, including immunoregulatory, anti-inflammatory, and anti-allergic effects. Several studies have investigated the anti-tumor effects of SSD on cancer in multiple organs. However, its role in colorectal cancer (CRC) remains unclear. Therefore, this study aimed to elucidate the suppressive effects of SSD on CRC cell survival and metastasis. SSD reduced the survival and colony formation ability of CRC cells. SSD-induced autophagy and apoptosis in CRC cells were measured using flow cytometry. SSD treatment increased LC3B and p62 autophagic factor levels in CRC cells. Moreover, SSD-induced apoptosis occurred through the cleavage of caspase-9, caspase-3, and PARP, along with the downregulation of the Bcl-2 family. In the in vivo experiment, a reduction in the number of metastatic tumor nodules in the lungs was observed after the oral administration of SSD. Based on these results, SSD inhibits the metastasis of CRC cells to the lungs by inducing autophagy and apoptosis. In conclusion, SSD suppressed the proliferation and metastasis of CRC cells, suggesting its potential as a novel substance for the metastatic CRC treatment.

This study provides a comparative analysis of the evolution of skill formation systems in Japan and South Korea, considering the nuances in active labour market policies (ALMPs) and institutional transformations in the post-industrial landscape. Both nations initially adopted segmentalist skill formation systems; however, they now exhibit divergent paths. Korea, in particular, has undergone institutional changes from segmentalist to a liberal skill formation system, with firms reducing their involvement in skill formation, resulting in a pronounced skill formation gap. Firms have curtailed their role in skill formation in alignment with environmental changes, and ALMPs have primarily centred on job creation for the elderly and small- and medium-sized enterprise employment subsidies. Conversely, Japan has maintained consistent policy approaches despite similar environmental changes. This study highlights that these divergent trajectories are rooted in the different stages of institutional maturity established during industrialization.

This paper discusses the restructuring of the social protection system in the changing labor market by comparing and critically reviewing policy ideas of Universal Basic Income (UBI), Universal Basic Voucher (UBV), and Universal Basic Service (UBS) with a focus on how the Social and Ecological Transition (SET) can be achieved. UBS is a concept often paired with UBI, and UBV is considered a middle way between UBI (cash) and UBS (in-kind). This study first analyzes Korea’s basic income, basic service, and basic voucher cases, according to Bohnenberger’s nine types of social benefits through Standing’s policy evaluation principles. Additionally, we evaluated how each of the benefits included in basic income, basic service, and basic voucher can contribute to social and ecological sustainability in the Korean context. Through this evaluation, to pursue SET in the future, what kind of policy efforts should be accompanied with basic income through a Korean case analysis was discussed. The paper focuses on Korea in particular, as all three policies have been initiated here.

Excessive sodium intake is recognized as a potential risk factor for various diseases, including kidney disease. However, limited research has been conducted on the relationship between sodium intake and kidney disease in the general population. This study aimed to explore the association between sodium intake and the risk of kidney disease, utilizing multivariable logistic regression and spline interpolation models. Twelve-year prospective cohort data were analyzed, and participants were categorized based on their sodium intake. Kidney disease was defined by the presence of proteinuria and a reduction in estimated glomerular filtration rate below 60 ml/min/1.73m². In the overall population, sodium intake exceeding 2g/day was not significantly associated with kidney dysfunction (adjusted OR: 0.84, 95% CI: 0.67–1.04, p = 0.113). However, in subgroup analyses, individuals with diabetes who consumed more than 5g/day of sodium had a significantly increased risk of kidney dysfunction (adjusted OR: 3.76, 95% CI: 1.36–10.30, p = 0.01). Across both the general population and subgroup analyses, sodium intake was not significantly associated with proteinuria. These findings suggest that while sodium intake may not have a substantial impact on kidney function in the general population, it may play a critical role in accelerating kidney dysfunction in individuals with comorbidities such as diabetes.

Inborn errors of TLR3-dependent IFN-α/β- and IFN-λ-mediated immunity in the CNS can underlie herpes simplex virus 1 (HSV-1) encephalitis (HSE). The respective contributions of IFN-α/β and IFN-λ are unknown. We report a child homozygous for a genomic deletion of the entire coding sequence and part of the 3'-UTR of the last exon of IFNAR1, who died of HSE at the age of 2 years. An older cousin died following vaccination against measles, mumps, and rubella at 12 months of age, and another 17-year-old cousin homozygous for the same variant has had other, less severe, viral illnesses. The encoded IFNAR1 protein is expressed on the cell surface but is truncated and cannot interact with the tyrosine kinase TYK2. The patient's fibroblasts and EBV-B cells did not respond to IFN-α2b or IFN-β, in terms of STAT1, STAT2, and STAT3 phosphorylation or the genome-wide induction of IFN-stimulated genes. The patient's fibroblasts were susceptible to viruses, including HSV-1, even in the presence of exogenous IFN-α2b or IFN-β. HSE is therefore a consequence of inherited complete IFNAR1 deficiency. This viral disease occurred in natural conditions, unlike those previously reported in other patients with IFNAR1 or IFNAR2 deficiency. This experiment of nature indicates that IFN-α/β are essential for anti-HSV-1 immunity in the CNS.

Dysbiosis is an environmental factor that affects the induction of axial spondyloarthritis (axSpA) pathogenesis. In the present study, we investigated differences in the gut microbiota of patients with axSpA and revealed an association between specific gut microbiota and their metabolites, and SpA pathogenesis. Using 16S rRNA sequencing data derived from feces samples of 33 axSpA patients and 20 healthy controls (HCs), we examined the compositions of their gut microbiomes. As a result, axSpA patients were found to have decreased α-diversity compared to HCs, indicating that axSpA patients have less diverse microbiomes. In particular, at the species level, and were more abundant in axSpA patients than in HCs, whereas , a butyrate-producing bacteria, was more abundant in HCs. Thus, we decided to investigate whether was associated with health conditions by inoculating (0.1, 1, and 10 μg/mL) or by administrating butyrate (0.5 mM) into CD4 T cells derived from axSpA patients. The levels of IL-17A and IL-10 in the CD4 T cell culture media were then measured. We also assessed osteoclast formation by administrating butyrate to the axSpA-derived peripheral blood mononuclear cells. The CD4 IL-17A T cell differentiation, IL-17A levels were decreased, whereas IL-10 was increased by inoculation. Butyrate reduced CD4 IL-17A T cell differentiation and osteoclastogenesis. We found that CD4 IL-17A T cell polarization was reduced, when or butyrate were introduced into curdlan-induced SpA mice or CD4 T cells of axSpA patient. Consistently, butyrate treatment was associated with the reduction of arthritis scores and inflammation levels in SpA mice. Taken together, we concluded that the reduced abundance of butyrate-producing microbes, particularly , may be associated with axSpA pathogenesis.

Osteoarthritis (OA) reduces the quality of life as a result of the pain caused by continuous joint destruction. Inactivated Lactobacillus (LA-1) ameliorated osteoarthritis and protected cartilage by modulating inflammation. In this study, we evaluated the mechanism by which live LA-1 ameliorated OA. To investigate the effect of live LA-1 on OA progression, we administered LA-1 into monosodium iodoacetate (MIA)-induced OA animals. The pain threshold, cartilage damage, and inflammation of the joint synovial membrane were improved by live LA-1. Furthermore, the analysis of intestinal tissues and feces in the disease model has been shown to affect the systems of the intestinal system and improve the microbiome environment. Interestingly, inflammation of the intestinal tissue was reduced, and the intestinal microbiome was altered by live LA-1. Live LA-1 administration led to an increase in the level of Faecalibacterium which is a short-chain fatty acid (SCFA) butyrate-producing bacteria. The daily supply of butyrate, a bacterial SCFA, showed a tendency to decrease necroptosis, a type of abnormal cell death, by inducing autophagy and reversing impaired autophagy by the inflammatory environment. These results suggest that OA is modulated by changes in the gut microbiome, suggesting that activation of autophagy can reduce aberrant cell death. In summary, live LA-1 or butyrate ameliorates OA progression by modulating the gut environment and autophagic flux. Our findings suggest the regulation of the gut microenvironment as a therapeutic target for OA.

Transparent antennas have been continuously developed for integration with solar cells, vehicular communications, and ultra-high-speed communications such as 5G in recent years. A transparent antenna takes advantage of spatial extensibility more so than all other antennas in terms of wide range of usable area. In addition, the production price of transparent antennas is steadily decreasing due to the development of nano-process technology. This paper reviews published studies of transparent antennas classified by various materials in terms of optical transmittance and electrical, sheet resistance. The transparent electrodes for the transparent antenna are logically classified and the transparent antennas are described according to the characteristics of each electrode. Finally, the contributions transparent antennas can make toward next-generation 5G high-speed communication are discussed.

Osteoarthritis (OA), the most common form of arthritis, is characterized by pain and cartilage damage; it usually exhibits gradual development. However, the pathogenesis of OA remains unclear. This study was undertaken to improve the understanding and treatment of OA. OA was induced in 7-week-old Wistar rats by intra-articular injection of monosodium iodoacetate (MIA); subsequently, the rats underwent oral administration of Bifidobacterium longum BORI ( B . BORI). The effects of B . BORI were examined in chondrocytes and an MIA-induced OA rat model. In the rats, B . BORI-mediated effects on pain severity, cartilage destruction, and inflammation were recorded. Additional effects on mRNA and cytokine secretion were analyzed by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay. Paw withdrawal threshold, paw withdrawal latency, and weight-bearing assessments revealed that pain severity in MIA-induced OA rats was decreased after B . BORI treatment. Histopathology analyses and three-dimensional surface renderings of rat femurs from micro-computed tomography images revealed cartilage protection and cartilage loss inhibition effects in B . BORI-treated OA rats. Immunohistochemical analyses of inflammatory cytokines and catabolic markers (e.g., matrix metalloproteinases) showed that the expression levels of both were reduced in tissue from B . BORI-treated OA rats. Furthermore, B . BORI treatment decreased the expression levels of the inflammatory cytokine monocyte chemoattractant protein-1 and inflammatory gene factors (e.g., inflammatory cell death markers) in chondrocytes. The findings indicate that oral administration of B . BORI has therapeutic potential in terms of reducing pain, progression, and inflammation in OA.