Unraveling Partial Coalescence Between Droplet and Oil-Water Interface in Water-in-Oil Emulsions under a Direct-Current Electric Field via Molecular Dynamics Simulation.

When the electric field strength (E) surpasses a certain threshold, secondary droplets are generated during the coalescence between water droplets in oil and the oil-water interface (so-called the droplet-interface partial coalescence phenomenon), resulting in a lower efficiency of droplet electrocoalescence. This study employs molecular dynamics (MD) simulations to investigate the droplet-interface partial coalescence phenomenon under direct current (DC) electric fields. The results demonstrate that intermolecular interactions, particularly the formation of hydrogen bonds, play a crucial role in dipole-dipole coalescence. Droplet-interface partial coalescence is categorized into five regimes based on droplet morphology. During the contact and fusion of the droplet with the water layer, the dipole moment of the droplet exhibits alternating increases and decreases along the electric field direction. Electric field forces acting on sodium ions and the internal interactions within droplets promote the process of droplet-interface partial coalescence. High field strengths cause significant elongation of the droplet, leading to its fragmentation into multiple segments. The migration of hydrated ions has a dual impact on the droplet-interface partial coalescence, with both facilitative and suppressive effects. The time required for droplet-interface partial coalescence initially decreases and subsequently increases as the field strength increases, depending on the competitive relationship between the extent of droplet stretching and the electric field force. This work provides molecular insights into the droplet-interface coalescence mechanisms in water-in-oil emulsions under DC electric fields.

Nicotine induces apoptosis through exacerbation of blocked alveolar macrophage autophagic degradation in silicosis.

Silica dust mainly attacks alveolar macrophages (AMs). The apoptosis of AMs is correlated with the progress of silicosis. Our previous study showed that autophagic degradation was blocked in AMs from silicosis patients. However, the effects of nicotine on AM autophagy and apoptosis in silicosis are unknown. In this study, we collected AMs from twenty male workers exposed to silica and divided them into observer and silicosis patient groups, according to the tuberous pathological changes observed by X-ray. The AMs from both groups were exposed to nicotine. We found increased levels of LC3, p62, and cleaved caspase-3, decreased levels of LAMP2, and damaged lysosomes after nicotine stimulation of the AMs from both groups. We also found that the autophagy inhibitor 3-methyladenine (3MA) inhibited nicotine-induced apoptosis in the AMs. Furthermore, 3MA reversed both the nicotine-induced decrease in Bcl-2 and the increase in Bax in both groups. These results suggest that nicotine may induce apoptosis by blocking AM autophagic degradation in human silicosis.

Lipopolysaccharides promote pulmonary fibrosis in silicosis through the aggravation of apoptosis and inflammation in alveolar macrophages.

Alveolar macrophages (AMs) play an important defensive role by removing dust and bacteria from alveoli. Apoptosis of AMs is associated with lung fibrosis; however, the relationship between this apoptotic event and environmental factors, such as the presence of lipopolysaccharides (LPSs) in the workplace, has not yet been addressed. To investigate whether exposure to LPS can exacerbate fibrosis, we collected AMs from 12 male workers exposed to silica and incubated them in the presence and absence of LPS for 24 h. We show that the levels of cleaved caspase-3 and pro-inflammatory cytokines interleukin (IL)-1ß, IL-6, and tumor necrosis factor-alpha were increased in these AMs following LPS treatment. Moreover, we demonstrate that LPS exposure aggravated apoptosis and the release of inflammatory factors in AMs in a mouse model of silicosis, which eventually promoted pulmonary fibrosis. These results suggest that exposure to LPS may accelerate the progression of pulmonary fibrosis in silicosis by increasing apoptosis and inflammation in AMs.

TNF-α-TNFR signal pathway inhibits autophagy and promotes apoptosis of alveolar macrophages in coal worker's pneumoconiosis.

OBJECTIVE: Exposure to coal dust causes the development of coal worker's pneumoconiosis (CWP), which is associated with accumulating macrophages in the lower respiratory tract. This study was performed to investigate the effect of tumor necrosis factor-α (TNF-α)-tumor necrosis factor receptor (TNFR) signal pathway on autophagy and apoptosis of alveolar macrophages (AMs) in CWP. METHODS: AMs from controls exposed to coal dust and CWP patients were collected, in which expressions of TNF-α and TNFR1 were determined. Autophagy was observed by transmission electron microscopy, and apoptosis by light microscope and using terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. AMs in CWP patients were treated with TNF-α or anti-TNF-α antibody. Besides, expressions of autophagy marker proteins, apoptosis-related factors, FAS, caspase-8, and receptor-interacting serine-threonine-protein kinase 3 (RIPK3) were determined by western Blot. Activities of caspase-3 and caspase-8 were determined by a fluorescence kit. Flow cytometry was applied to measure the expression of TNFR1 on the surface of the AM. RESULTS: TNF-α expression and TNFR1 expression on the surface of AM, as well as autophagy and apoptotic index were significantly increased in AMs of CWP patients. In response to the treatment of TNF-α, TNF-α expression and TNFR1 expression on the surface of AM as well as LC3I expression were increased, autophagy was decreased, and LC3, LC3II, Beclin1 and B-cell lymphoma 2 expressions decreased, whereas FAS expression and activity and expression of caspase-3 and caspase-8 increased, and apoptotic index increased. Moreover, the situations were reversed with the treatment of anti-TNF-α antibody. CONCLUSION: TNF-α-TNFR signal pathway was involved in the occurrence and development of CWP by activating FAS-caspase-8 and thus inhibiting autophagy while promoting apoptosis of AM.

Load partitioning between the bcc-iron matrix and NiAl-type precipitates in a ferritic alloy on multiple length scales.

An understanding of load sharing among constituent phases aids in designing mechanical properties of multiphase materials. Here we investigate load partitioning between the body-centered-cubic iron matrix and NiAl-type precipitates in a ferritic alloy during uniaxial tensile tests at 364 and 506 °C on multiple length scales by in situ neutron diffraction and crystal plasticity finite element modeling. Our findings show that the macroscopic load-transfer efficiency is not as high as that predicted by the Eshelby model; moreover, it depends on the matrix strain-hardening behavior. We explain the grain-level anisotropic load-partitioning behavior by considering the plastic anisotropy of the matrix and elastic anisotropy of precipitates. We further demonstrate that the partitioned load on NiAl-type precipitates relaxes at 506 °C, most likely through thermally-activated dislocation rearrangement on the microscopic scale. The study contributes to further understanding of load-partitioning characteristics in multiphase materials.