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This paper introduces an uncertain mean‐reverting currency model that incorporates floating domestic and foreign interest rates along with an exponential Ornstein–Uhlenbeck exchange rate process, all grounded in uncertainty theory. Pricing formulas for both Asian call and put options are derived within this framework. The parameters of the model are estimated using real financial data from Canada and the United States, including the Canadian Overnight Repo Rate Average (CORRA), the American Federal Funds Effective Rate (AFFER), and the monthly average exchange rate of the US Dollar to the Canadian Dollar (USDCAD). The method of moments is applied to estimate the unknown parameters, and goodness‐of‐fit tests are conducted to validate the parameter estimates. Numerical experiments demonstrate that Asian option prices decrease as domestic and foreign initial interest rates increase. The prices of call and put options show divergent behaviors with respect to the initial exchange rate and the fixed strike price. Additionally, the paper investigates the nonlinear relationship between option prices and expiration time. In the appendix, the uncertain currency model is transformed into a stochastic currency model, and statistical tests confirm its inapplicability to the selected data, thereby substantiating the choice of the uncertain currency model.

Oxidative stress-induced mitochondrial dysfunction and neuronal cell death have important roles in the development of neurodegenerative diseases. Dynamin related protein 1 (Drp1) is a critical factor in regulating mitochondrial dynamics. A variety of posttranslational modifications of Drp1 have been reported, including phosphorylation, ubiquitination, sumoylation and S -nitrosylation. In this study, we found that c-Abl phosphorylated Drp1 at tyrosine 266, 368 and 449 in vitro and in vivo , which augmented the GTPase activity of Drp1 and promoted Drp1-mediated mitochondrial fragmentation. Consistently, c-Abl-mediated phosphorylation is important for GTPase activity of Drp1 and mitochondrial fragmentation. Furthermore, we found that Drp1 phosphorylation mediated by c-Abl is required for oxidative stress-induced cell death in primary cortical neurons. Taken together, our findings reveal that c-Abl-Drp1 signaling pathway regulates oxidative stress-induced mitochondrial fragmentation and cell death, which might be a potential target for the treatment of neurodegenerative diseases.

Activation of the NLRP3 inflammasome results in caspase 1 cleavage, which subsequently leads to IL-1 β and IL-18 secretion, as well as pyroptosis, and aberrant activation of the inflammasome is involved in several diseases such as type 2 diabetes, atherosclerosis, multiple sclerosis, Parkinson’s disease, and Alzheimer’s disease. NLRP3 activity is regulated by various kinases. Genetic and pharmacological inhibition of the hematopoietic cell kinase (HCK), a member of the Src family of non-receptor tyrosine kinases (NRTKs) primarily expressed in myeloid cells, has previously been shown to ameliorate inflammation, indicating that it may be involved in the regulation of microglia function. However, the underlying mechanism is not known. Hence, in this study, we aimed to investigate the role of HCK in NLRP3 inflammasome activation. We demonstrated that HCK silencing inhibited NLRP3 inflammasome activation. Furthermore, the HCK-specific inhibitor, A419259, attenuated the release of IL-1 β and caspase 1(P20) from the macrophages and microglia and reduced the formation of the apoptosis-associated speck-like protein with a CARD domain (ASC) oligomer. We also observed that HCK binds to full length NLRP3 and its NBD(NACHT) and LRR domains, but not to the PYD domain. In vivo , the HCK inhibitor attenuated the LPS-induced inflammatory response in the liver of LPS-challenged mice. Collectively, these results suggested that HCK plays a critical role in NLRP3 inflammasome activation. Our results will enhance current understanding regarding the effectiveness of HCK inhibitors for treating acute inflammatory diseases.

Urban pollution caused by road particles is widely criticized. The complex and changeable internal flow field of the dust suction port has the greatest influence of the dust suction operation effect. The aim of this paper is to explore the influence law of various influencing factors on the flow field characteristics of the sweeper’s dust suction port, and reveal its influence mechanism on the dust suction efficiency of the dust suction port. The results of the study show that: increasing the width and outlet diameter will change the flow field characteristics, and the dust suction efficiency will change accordingly, 500 mm and 280 mm are the best width and outlet diameter respectively. The increase of driving speed will increase the relative speed between the inlet surface and dust particles, causing dust particles to spill. The increase of negative pressure at the outlet will increase the flow field characteristics, but the dust suction efficiency will stop when it increases to a certain value. A new dust suction port structure is proposed to further improve the dust suction efficiency. This study can provide a reference for the design of the dust suction port.

Uncovering the risk factors of pulmonary hypertension and its mechanisms is crucial for the prevention and treatment of the disease. In the current study, we showed that experimental periodontitis, which was established by ligation of molars followed by orally smearing subgingival plaques from patients with periodontitis, exacerbated hypoxia-induced pulmonary hypertension in mice. Mechanistically, periodontitis dysregulated the pulmonary microbiota by promoting ectopic colonization and enrichment of oral bacteria in the lungs, contributing to pulmonary infiltration of interferon gamma positive (IFNγ+) T cells and aggravating the progression of pulmonary hypertension. In addition, we identified Prevotella zoogleoformans as the critical periodontitis-associated bacterium driving the exacerbation of pulmonary hypertension by periodontitis, and the exacerbation was potently ameliorated by both cervical lymph node excision and IFNγ neutralizing antibodies. Our study suggests a proof of concept that the combined prevention and treatment of periodontitis and pulmonary hypertension are necessary.

The symmetry principle of circuit system shows that we can equate a complex structure in the circuit network to a simple circuit. Hence, this paper only considers a simple series RL circuit and first presents an uncertain RL circuit model based on multifactor uncertain differential equation by considering the external noise and internal noise in an actual electrical circuit system. Then, the solution of uncertain RL circuit equation and the inverse uncertainty distribution of solution are derived. Some applications of solution for uncertain RL circuit equation are also investigated. Finally, the method of moments is used to estimate the unknown parameters in uncertain RL circuit equation.

Background High blood glucose is a well‐established risk factor for poor outcomes in ischemic stroke. However, the underlying molecular mechanisms linking high blood glucose to worsened stroke outcomes remain unclear. Objectives Previous studies have implicated the NLRP3 inflammasome, a key mediator of neuroinflammation, in cerebral ischemia/reperfusion (I/R) injury. Under high blood glucose conditions, NLRP3 activation is amplified, potentially driving a vicious cycle of inflammation and neuronal death. Yet, how high blood glucose specifically modulates NLRP3 activation and its downstream pathways remains unclear. This study aimed to investigate the specific mechanisms by which high glucose enhances NLRP3 inflammasome activity and contributes to worsened brain injury following cerebral I/R. Methods We employed a combination of in vitro and in vivo experimental approaches to explore the impact of high glucose on NLRP3 inflammasome activation and its consequences on ischemic stroke outcomes. In vitro experiments were conducted by culturing various immune cells in high‐glucose conditions to evaluate the activation of the NLRP3 inflammasome and the mitochondrial association of HK2. In vivo, mice with genetic knockouts of Nlrp3, Pycard (the gene encoding ASC), or microglial‐specific Hk2 were subjected to transient middle cerebral artery occlusion (tMCAO). Results Our findings revealed that the activation of the NLRP3 inflammasome was enhanced post cerebral I/R under high glucose and a N‐terminal truncation of NLRP3 (miniNLRP3) was induced. Overexpression of PKA could promote the generation of miniNLRP3, while inhibition of PKA decreased the generation of miniNLRP3. In addition, treatment with pan serine protease could block PKA and LPS mediated generation of miniNLRP3. Overexpression of the N‐terminal truncation of NLRP3 could potentiate the activation of the NLRP3 inflammasome under high glucose conditions by promoting the dissociation of Hexokinase 2 (HK2) from mitochondria. In addition, knockout of Nlrp3, Pycard, or microglial Hk2, could all attenuate cerebral I/R‐induced brain injury under high blood glucose in mice. Conclusion Our study elucidates PKA‐mediated generation of a 30 kD N‐terminal truncation of NLRP3 (miniNLRP3) in a serine protease‐dependent manner, which could potentiate the activation of the NLRP3 inflammasome under high glucose conditions via promoting the dissociation of HK2 from mitochondria. These findings add a new dimension to our understanding of NLRP3 regulation in the context of stroke injury, and suggest that the PKA‐miniNLRP3‐HK2‐NLRP3 pathway is a promising therapeutic strategy to improve stroke outcomes in patients with elevated blood glucose levels. Our study elucidates PKA‐mediated generation of a 30 kD N‐terminal truncation of NLRP3 (miniNLRP3) in a serine protease dependent manner, which could potentiate the activation of the NLRP3 inflammasome under high glucose conditions via promoting the dissociation of HK2 from mitochondria. These findings add a new dimension to our understanding of NLRP3 regulation in the context of stroke injury, and suggest that the PKA‐miniNLRP3‐HK2‐NLRP3 pathway is a promising therapeutic strategy to improve stroke outcomes in patients with elevated blood glucose levels.

Secreted Wnts play diverse roles in a non-cell-autonomous fashion. However, the cell-autonomous effect of unsecreted Wnts remains unknown. Endoplasmic reticulum (ER) stress is observed in specialized secretory cells and participates in pathophysiological processes. The correlation between Wnt secretion and ER stress remains poorly understood. Here, we demonstrated that Drosophila miR-307a initiates ER stress specifically in wingless (wg) -expressing cells through targeting wntless (wls/evi) . This phenotype could be mimicked by retromer loss-of-function or porcupine (porc) depletion and rescued by wg knockdown, arguing that unsecreted Wg triggers ER stress. Consistently, we found that disrupting the secretion of human Wnt5a also induced ER stress in mammalian cells. Furthermore, we showed that a C-terminal KKVY-motif of Wg is required for its retrograde Golgi-to-ER transport, thus inducing ER stress. Next, we investigated if COPI, the regulator of retrograde transport, is responsible for unsecreted Wg to induce ER stress. To our surprise, we found that COPI acts as a novel regulator of Wg secretion. Taken together, this study reveals a previously unknown Golgi-to-ER retrograde route of Wg and elucidates a correlation between Wnt secretion and ER stress during development.

Type I interferon (IFN-I) is critical for a host against viral and bacterial infections via induction of hundreds of interferon-stimulated genes (ISGs), but the mechanism underlying the regulation of IFN-I remains largely unknown. In this study, we first demonstrate that ISG expression is required for optimal IFN-β levels, an effect that is further enhanced by endoplasmic reticulum (ER) stress. Furthermore, we identify mitochondrial calcium uniporter protein (MCU) as a mitochondrial antiviral signaling protein (MAVS)-interacting protein that is important for ER stress induction and amplified MAVS signaling activation. In addition, by performing an ectopic expression assay to screen a library of 117 human ISGs for effects on IFN-β levels, we found that tumor necrosis factor receptor 1 (TNFR1) significantly increases IFN-β levels independent of ER stress. Altogether, our findings suggest that MCU and TNFR1 are involved in the regulation of RIG-I-like receptors (RLR) signaling.

Microbiologically influenced corrosion (MIC) is the process of material degradation in the presence of microorganisms and their biofilms. This is an environmentally assisted type of corrosion, which is highly complex and challenging to fully understand. Different metallic materials, such as steel alloys, magnesium alloys, aluminium alloys, and titanium alloys, have been reported to have adverse effects of MIC on their applications. Though many researchers have reported bacteria as the primary culprit of microbial corrosion, several other microorganisms, including fungi, algae, archaea, and lichen, have been found to cause MIC on metal and non-metal surfaces. However, less attention is given to the MIC caused by fungi, algae, archaea, and lichens. In this review paper, the effects of different microorganisms, including bacteria, fungi, algae, archaea, and lichens, on the corrosion properties of engineering materials have been discussed in detail. This review aims to summarize all of the corrosive microorganisms that directly or indirectly cause the degradation of structural materials. Accusing bacteria of every MIC case without a proper investigation of the corrosion site and an in-depth study of the biofilm and secreted metabolites can create problems in understanding the real cause of the materials’ failure. To identify the real corrosion agent in any environment, it is highly important to study all kinds of microorganisms that exist in that specific environment.