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To simulate the launching process of missile complex flow, movement, and constraint states, a multifield coupling model is put forward based on a computational fluid dynamics (CFD) method. In this coupled model, a CFD method is used to solve the three-dimensional compressible transient flow, and the six-degree motion of the launching platform is considered, and the virtual contact method is used to deal with the constraint states of the guideway and the slider. The active force and moment are applied to the launching platform to simulate its rolling, pitching, and heaving motions under the 5-level waves. Collision detection is carried out through the minimum clearance distance between the slider and the guideway, and the contact force is handled by a modified Herz collision model. In the problem of launching a missile from the water surface, the change characteristics of the flow field, the load response characteristics, and the relative motion laws of the missile and the launching platform during the catapulting process are investigated. The results show that the motion laws of the projectile and the launch tube in the constrained direction are the same, and the established coupling model is able to simulate the launch separation process of the missile in the constrained state. In addition, the effect of wind load on the missile ejection process is analyzed using the coupled model. [ABSTRACT FROM AUTHOR]

The pulsation of bubbles and the impact load from reverse flow, generated by the evolution of semiclosed initial intermittent bubble multiphase flow during underwater launches, are crucial factors affecting launch safety. This paper employs the mixture multiphase flow model and the interphase heat and mass transfer model to simulate the interaction between the gas inside a partially enclosed cylinder and the water medium outside the cylinder, combined with simulation and piggybacking experiments, to analyze the flow process and load state. The numerical model is further utilized to study the evolution of the multiphase flow field of the semienclosed initial intermittent bubble, the pulsating load of the bubble, the impact load of the inverted water flow, and the influence of structural dimensions on the load. The results show that the initial intermittent bubble in the mouth of the cylinder experiences an expansion–contraction–expansion pulsation process, and as the migration of the interface between the phases results in significant pressure pulsation, the peak pulsation can exceed twice the pressure difference between the initial gas pressure inside the cylinder and the hydrostatic pressure at the mouth of the cylinder. At the late stage of bubble pulsation, a large amount of water with pulsating bubbles flows into the semiclosed cylinder, and the pulsation-induced velocity and gravity are used to form a high-speed inverted water flow. The interaction between the inverted water and the gas inside the cylinder generates an oscillating shock load where the maximum shock load is significantly greater than the ambient pressure load. Additionally, the effect of structural dimensions on the load state under the same intermittent conditions is examined. [ABSTRACT FROM AUTHOR]

Aim: Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disease characterized by progressive death of upper and lower motor neurons, leading to generalized muscle atrophy, paralysis, and even death. Mitochondrial damage and neuroinflammation play key roles in the pathogenesis of ALS. In the present study, the efficacy of A‐1, a derivative of arctigenin with AMP‐activated protein kinase (AMPK) and silent information regulator 1 (SIRT1) activation for ALS, was investigated. Methods: A‐1 at 33.3 mg/kg was administrated in SOD1G93A transgenic mice orally from the 13th week for a 6‐week treatment period. Motor ability was assessed before terminal anesthesia. Muscle atrophy and fibrosis, motor neurons, astrocytes, and microglia in the spinal cord were evaluated by H&E, Masson, Sirius Red, Nissl, and immunohistochemistry staining. Protein expression was detected with proteomics analysis, Western blotting, and ELISA. Mitochondrial adenosine triphosphate (ATP) and malondialdehyde (MDA) levels were measured using an assay kit. Results: A‐1 administration in SOD1G93A mice enhanced mobility, decreased skeletal muscle atrophy and fibrosis, mitigated loss of spinal motor neurons, and reduced glial activation. Additionally, A‐1 treatment improved mitochondrial function, evidenced by elevated ATP levels and increased expression of key mitochondrial‐related proteins. The A‐1 treatment group showed decreased levels of IL‐1β, pIκBα/IκBα, and pNF‐κB/NF‐κB. Conclusions: A‐1 treatment reduced motor neuron loss, improved gastrocnemius atrophy, and delayed ALS progression through the AMPK/SIRT1/PGC‐1α pathway, which promotes mitochondrial biogenesis. Furthermore, the AMPK/SIRT1/IL‐1β/NF‐κB pathway exerted neuroprotective effects by reducing neuroinflammation. These findings suggest A‐1 as a promising therapeutic approach for ALS. [ABSTRACT FROM AUTHOR]

Objectives: Arctigenin (ATG) is a natural product with a variety of biological activity, which can improve the pathological changes of Alzheimer's disease (AD) model mice through multiple mechanisms. This study aims to further elucidate the potential mechanism by which ATG improves memory impairment in AD mice. Methods: Here, we used pR5 mice as an experimental model, and ATG was administered continuously for 90 days. Novel object recognition, Y-maze, and Morris water maze were used to evaluate the therapeutic effect of ATG on memory impairment in AD mice. Immunohistochemical and immunofluorescence analyses were used to evaluate the effects of ATG on tau hyperphosphorylation and neuroinflammation, respectively. Finally, proteomics techniques were used to explore the possible mechanism of ATG. Key findings: ATG significantly improved memory impairment in pR5 mice and inhibited tau phosphorylation in the hippocampus and neuroinflammation in the cortex. According to the proteomic analysis, the altered cognitive function of ATG was associated with the proteins of the tricarboxylic acid cycle and the electron transport chain. Conclusion: These results suggest that ATG is a potential therapeutic agent for diseases related to aberrant energy metabolism that can treat AD by improving mitochondrial function. [ABSTRACT FROM AUTHOR]

A 7-year-old boy was misdiagnosed as having contact dermatitis due to itching and redness of the eyelids. Later, with the assistance of a slit lamp, active pubic lice on the eyelid margin were discovered. Microorganisms and insect eggs were mechanically removed, and itching and redness symptoms complete disappeared after 1 week. [J Pediatr Ophthalmol Strabismus. 2024;61(2)e13–e15.] [ABSTRACT FROM AUTHOR]

Aim: Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disease characterized by progressive death of upper and lower motor neurons, leading to generalized muscle atrophy, paralysis, and even death. Mitochondrial damage and neuroinflammation play key roles in the pathogenesis of ALS. In the present study, the efficacy of A-1, a derivative of arctigenin with AMP-activated protein kinase (AMPK) and silent information regulator 1 (SIRT1) activation for ALS, was investigated., Methods: A-1 at 33.3 mg/kg was administrated in SOD1 G93A transgenic mice orally from the 13th week for a 6-week treatment period. Motor ability was assessed before terminal anesthesia. Muscle atrophy and fibrosis, motor neurons, astrocytes, and microglia in the spinal cord were evaluated by H&E, Masson, Sirius Red, Nissl, and immunohistochemistry staining. Protein expression was detected with proteomics analysis, Western blotting, and ELISA. Mitochondrial adenosine triphosphate (ATP) and malondialdehyde (MDA) levels were measured using an assay kit., Results: A-1 administration in SOD1 G93A mice enhanced mobility, decreased skeletal muscle atrophy and fibrosis, mitigated loss of spinal motor neurons, and reduced glial activation. Additionally, A-1 treatment improved mitochondrial function, evidenced by elevated ATP levels and increased expression of key mitochondrial-related proteins. The A-1 treatment group showed decreased levels of IL-1β, pIκBα/IκBα, and pNF-κB/NF-κB., Conclusions: A-1 treatment reduced motor neuron loss, improved gastrocnemius atrophy, and delayed ALS progression through the AMPK/SIRT1/PGC-1α pathway, which promotes mitochondrial biogenesis. Furthermore, the AMPK/SIRT1/IL-1β/NF-κB pathway exerted neuroprotective effects by reducing neuroinflammation. These findings suggest A-1 as a promising therapeutic approach for ALS., (© 2024 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.)