The purpose of this study is to analyze the causes of cost variation in natural disaster prevention projects (NDPP) in Gyeongsangbuk-do and to develop effective cost and risk management strategies. The study collected data by conducting an online survey of 244 stakeholders. Binary logistic regression was used to analyze the impact of various variables on cost deviation, in-cluding project management risk (PMR), project costing and execution risk (PCER), project exe-cution strategy risk (PESR), construction project risk (CPR), project cost and schedule risk (PCSR), project management challenges (PMC), and construction project subcontractor and safety man-agement (CPSSM). The results showed that PMR (OR=3.744, 95% C.I. [1.657, 8.457]), PCER (OR=5.068, 95% C.I. [2.236, 11.484]), PESR (OR=3.447, 95% C.I. [1. 853, 6.413]), CPR (OR=2.292, 95% C.I. [1.020, 5.151]), PCSR (OR=4.817, 95% C.I. [2.250, 10.317]), PMC (OR=2.954, 95% C.I. [1.452, 6. 013]), and CPSSM (OR=2.419, 95% C.I. [1.297, 4.515]) had statistically significant effects on cost deviation. In particular, PMR, PCER, and PESR were identified as the main causes, and the effects of additional factors such as CPSSM were also important. The developed predictive model plays an important role in helping stakeholders of NDPP to manage risks in advance and take appro-priate preventive measures to ensure the success of the project. This study empirically supports the theoretical hypotheses of previous studies and provides a clear understanding of the causes of cost deviation in NDPP, which provides important insights for strategic decision-making and provides a new perspective on risk management.

TGF-ꞵ signaling is a vital regulator for maintaining articular cartilage homeostasis. Runx transcription factors, downstream targets of TGF-ꞵ signaling, have been studied in the context of osteoarthritis (OA). Although Runx partner core binding factor β (Cbfβ) is known to play a pivotal role in chondrocyte and osteoblast differentiation, the role of Cbfβ in maintaining articular cartilage remains obscure. This study investigated Cbfβ as a novel anabolic modulator of TGF-ꞵsignaling and determined its role in articular cartilage homeostasis. Cbfβ significantly decreased in aged mouse articular cartilage and human OA cartilage. Articular chondrocyte-specific Cbfb-deficient mice (Cbfb△ac/△ac) exhibited early cartilage degeneration at 20 weeks old and developed OA at 12 months old. Cbfb△ac/△ac mice showed enhanced OA progression under the surgical-induced mice OA model. Mechanistically, forced expression of Cbfβ rescued Col2α1 and Runx1 expression in Cbfβ-deficient chondrocytes. TGF-ꞵ1-mediated Col2α1 expression failed despite the pSmad3 activation under TGF-ꞵ1 treatment in Cbfβ-deficient chondrocytes. Cbfβ protected Runx1 from proteasomal degradation through Cbfβ/Runx1 complex formation. These results indicate that Cbfβ is a novel anabolic regulator for cartilage homeostasis, suggesting that Cbfβ could protect OA development by maintaining the integrity of the TGF-ꞵ1 signaling pathway in articular cartilage.

Liver fibrosis is a critical health issue with limited treatment options. This study investigates the potential of PGC-Sec, a secretome derived from PGC-1α-overexpressing adipose-derived stem cells (ASCs), as a novel therapeutic strategy for liver fibrosis. Upon achieving a cellular confluence of 70-80%, ASCs were transfected with pcDNA-PGC-1α. PGC-Sec, obtained through concentration of conditioned media using ultrafiltration units with a 3-kDa cutoff, was assessed through in vitro assays and in vivo mouse models. In vitro, PGC-Sec significantly reduced LX2 human hepatic stellate cell proliferation and mitigated mitochondrial oxidative stress compared to control-secretome (Ctrl-Sec). In an in vivo mouse model, PGC-Sec treatment led to notable reductions in hepatic enzyme activity, serum pro-inflammatory cytokine concentrations, and fibrosis-related marker expression. Histological analysis demonstrated improved liver histology and reduced fibrosis severity in PGC-Sec-treated mice. Immunohistochemical staining confirmed enhanced expression of PGC-1α, OPA1 (a mitochondrial function marker), and PPARα (an anti-fibrogenic marker) in the PGC-Sec-treated group, along with reduced Collagen 1A expression (a pro-fibrogenic marker). These findings highlight the therapeutic potential of PGC-Sec in combating liver fibrosis by enhancing mitochondrial biogenesis and function, and promoting antifibrotic processes. PGC-Sec holds promise as a novel treatment strategy for liver fibrosis.