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Differences in the depth of the water surface affect the hydrodynamics of the ship so there is a possibility that the ship will behave differently in deep water and shallow water. The surface flow generated by the hull varies radically due to the speed of the ship and the effects of water depth. At a certain speed, the ship experiences a critical speed condition, which will affect the total resistance of the ship. This study examines the Fridsma ship's resistance to differences in water depth at several speeds. Numerical computation is used in this study to simulate the characteristics of a planing hull form. The Finite Volume Method (FMV) is used to observe fluid flow due to differences in water level with the RANS (Reynolds-Averaged Navier - Stokes) equation in predicting ship resistance. K-ε was modeled as a turbulent and volume of fluid (VOF) model to represent the air and water phases. This study uses a morphing grid mesh to analyze the shape of the hull in numerical simulations. The total resistance of Fridsma in shallow waters increased at each speed when compared to the total resistance in deep waters. On average in deep waters, it can reduce the total resistance by around 22.34% compared to shallow waters. This is caused by the squat phenomenon that occurs in the hull.

This study demonstrated that both copper oxide nanoparticles (CuO‐NPs) and copper nanoparticles (Cu‐NPs) can cause swelling, inflammation, and cause damage to the mitochondria of alveolar type II epithelial cells in mice. Cellular examinations indicated that both CuO‐NPs and Cu‐NPs can reduce cell viability and harm the mitochondria of human bronchial epithelial cells, particularly Beas‐2B cells. However, it is clear that CuO‐NPs exhibit a more pronounced detrimental effect compared with Cu‐NPs. Using bafilomycin A1 (Bafi A1), an inhibitor of lysosomal acidification, was found to enhance cell viability and alleviate mitochondrial damage caused by CuO‐NPs. Additionally, Bafi A1 also reduces the accumulation of dihydrolipoamide S‐acetyltransferase (DLAT), a marker for mitochondrial protein toxicity, induced by CuO‐NPs. This observation suggests that the toxicity of CuO‐NPs depends on the distribution of copper particles within cells, a process facilitated by the acidic environment of lysosomes. The release of copper ions is thought to be triggered by the acidic conditions within lysosomes, which aligns with the lysosomal Trojan horse mechanism. However, this association does not seem to be evident with Cu‐NPs. In mice, CuO‐NPs caused more extensive lung tissue damage than Cu‐NPs. In Beas‐2B cells, inhibition of lysosomal acidification with Bafi A1 markedly decreased CuO‐NPs‐induced mitochondrial damage. The lysosomal Trojan horse mechanism of aggravates CuO‐NPs‐induced cuproptosis in Beas‐2B cells, which can be reversed by Bafi A1. [ABSTRACT FROM AUTHOR]

Osteoporosis is characterized by an imbalance between osteoclast-mediated bone resorption and osteoblast-related bone formation, particularly increased osteoclastogenesis. However, the mechanisms by which epigenetic factors regulate osteoclast precursor differentiation during osteoclastogenesis remain poorly understood. Here, we show that the specific knockout of the chromatin remodeling factor Arid1a in bone marrow–derived macrophages (BMDMs) results in increased bone mass. The loss of Arid1a in BMDM inhibits cell–cell fusion and maturation of osteoclast precursors, thereby suppressing osteoclast differentiation. Mechanistically, Arid1a increases the chromatin access in the gene promoter region of sialic acid–binding Ig-like lectin 15 (Siglec15) by transcription factor Jun/Fos, which results in the upregulation of Siglec15 and promotion of osteoclast differentiation. However, the loss of Arid1a reprograms the chromatin structure to restrict Siglec15 expression in osteoclast precursors, thereby inhibiting BMDM differentiation into mature osteoclasts. Deleting Arid1a after ovariectomy (a model for postmenopausal bone loss) alleviated bone loss and maintained bone mass. In summary, epigenetic reprogramming mediated by Arid1a loss suppresses osteoclast differentiation and may serve as a promising therapeutic strategy for treating bone loss diseases. Lay Summary: Osteoporosis is a common disease, usually diagnosed by decreased bone density and increased fragility. The people with osteoporosis has higher risk of fractures. Nearly one-third of the aged people will suffer from osteoporosis-related fractures and even lose their lives because of this. Therefore, there is an urgent need for early intervention and effective treatment options for osteoporosis in the aging population. Bone tissue is a highly dynamic tissue that undergoes continuous remodeling throughout an individual's entire life. The balance of remodeling depends on the bone formation mediated by osteoblasts and bone resorption by osteoclasts. When this balance is disrupted, osteoporosis occurs. Thus, the aim of our research is to explore the behind mechanism of this imbalance. Here, we demonstrate that the loss of Arid1a, a chromatin remodeler, leads to chromatin reprogramming that restricts access to promoters by transcription factors such as Jun/Fos, thereby suppressing osteoclast activation and bone resorption. Our findings offer insights into the epigenetic mechanisms underlying osteoporosis and suggest potential strategies for its prevention and treatment. Graphical Abstract [ABSTRACT FROM AUTHOR]

Molybdenum disulfide (MoS2), a typical layered material, has important applications in various fields, such as optoelectronics, catalysis, electronic devices, sensors, and supercapacitors. Extensive research has been carried out on few-layered MoS2 in the field of electrochemistry due to its large specific surface area, abundant active sites and short electron transport path. However, the preparation of few-layered MoS2 is a significant challenge. This work presents a simple one-pot hydrothermal method for synthesizing few-layered MoS2. Furthermore, it investigates the exfoliation effect of different amounts of sodium borohydride (NaBH4) as a stripping agent on the layer number of MoS2. Na+ ions, as alkali metal ions, can intercalate between layers to achieve the purpose of exfoliating MoS2. Additionally, NaBH4 exhibits reducibility, which can effectively promote the formation of the metallic phase of MoS2. Few-layered MoS2, as an electrode for supercapacitor, possesses a wide potential window of 0.9 V, and a high specific capacitance of 150 F g−1 at 1 A g−1. This work provides a facile method to prepare few-layered two-dimensional materials for high electrochemical performance. [ABSTRACT FROM AUTHOR]