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This work investigates the problem of Multi-dimensional Taylor Network (MTN)-based fault-tolerant control (FTC) for single-input and single-output nonlinear systems in non-strict feedback form. A MTN-based FTC method is presented for nonlinear systems with actuator faults and unmodeled dynamics. The actuator faults are contains both the loss of effectiveness factor of the actuator and a time-varying bias signal. MTN is used to approximate the unknown nonlinear functions, while unmodeled dynamics and dynamical disturbances are handled with the help of dynamical signal functions. A systemically backstepping-based fault-tolerant control scheme is proposed based on Lyapunov stability theory and MTN approximation ability. The suggested technique ensures that all closed-loop system signals are semi-globally uniformly ultimately bounded (SGUUB) and the tracking error converges to a small region around the origin. To demonstrate the effectiveness of the proposed controller design, three examples, including a single-link robot manipulator, are presented.

The External Dinarides fold-thrust belt formed during Mid-Eocene–Oligocene times by SW-propagating thrusting from the Internal Dinarides towards the Adriatic foreland. Although previously considered as structurally quite uniform, recent work reported along-strike contrasting deformation styles in two structural domains within this fold-thrust belt. The two areas with very contrasting deformation styles are separated by the N–S-striking dextral Split-Karlovac Fault, a 250 km long, transpressive transfer fault. The southeastern domain is characterized by a thin-skinned SW-vergent nappe stack in contrast to the northwestern domain, where a set of blind, thick-skinned top-SW thrust duplexes prevail underneath the passive NE-vergent backthrusts. To better understand why the External Dinarides underwent such contrasting along-strike deformation, we reconsidered a temporal and spatial along- and across-strike distribution of Paleo-Mesozoic lithofacies to both sides of the Split-Karlovac Fault and estimated the role of mechanical stratigraphy on deformation styles in this part of the fold-thrust belt. Therefore, we constructed a new 2D kinematic forward model in the western backthrust-dominated domain. Our best-fit forward-modelled balanced cross section across the central Velebit Mtn. portrays a 75 km wide triangle zone. This zone took up at least 47 km of shortening during Eo-Oligocene times. It comprises a set of thin-skinned NE-vergent backthrusts detached in the upper Paleozoic atop a SW-vergent thick-skinned antiformal stack detached in the lower Paleozoic Adriatic basement. The NE-vergent backthrusts likely nucleated at lateral facies boundaries related to extensional half grabens that locally formed during Middle Triassic and Late Jurassic passive margin extension. During the Eo-Oligocene folding and thrusting, the selective inversion of inherited Mesozoic half grabens boundary faults into the NE-vergent backthrusts in the northwestern domain led to the observed along-strike changes in the deformation style of the External Dinarides. A seismotectonic analysis of instrumentally recorded earthquakes suggests contrasting seismic behaviour along the central and southern Velebit transects within the northwestern structural domain. The central Velebit Mtn. triangle structure appears to currently accommodate dominantly strike-slip motion, with reverse faulting being confined to east of the Split-Karlovac Fault. In contrast, seismicity along the southern Velebit cross section appears to be confined to the structurally lowermost parts of the triangle zone and the foreland, while it´s structurally higher parts are less seismically active. Also, a predominance of reverse faulting along this transect suggests ongoing accommodation of shortening in this part. Our results indicate that both the variations in the mechanical stratigraphy and the pre-orogenic structural inheritance obtained during rifting and passive margin stages exert control on contractional structures within the External Dinarides, including the distribution of present-day seismicity.

OSA is a heterogeneous disease with variable physio-pathological and clinical manifestations, and it is associated with numerous co-morbidities (1). It is a chronic inflammatory disease with a low degree of activity (2), in which the microbiome is now widely considered to play a role. In the last few decades, research into the microbiome has rapidly evolved and has become a hot topic in basic research, both pre-clinical and clinical. Some recent studies have demonstrated that the gut microbiota (GM), situated in the human gastrointestinal tract and consisting of bacteria, viruses, fungi and protozoa, serves important functions regarding the regulation of the immune and metabolic systems and cerebral physiopathology. It is an example of a dynamic complex system, connected to the organism on a cellular, metabolic, immune and nervous level, a sophisticated network regulated by delicate internal and external equilibria (3)(4). The gut microbiota (GM) is composed of microbial symbionts, commensal or mutualistic but also potentially harmful (i.e. pathobionts), whose equilibrium (homeostasis) is crucial to the modulation of various functions and the aetiology of numerous diseases (5). Two bacterial phyla, Bacteroidetes and Firmicutes, account for 90% of the groups present in the human intestine and are essential for the maintenance of intestinal homeostasis (6)(7). A growing scientific literature supports the existence of bidirectional interaction that unfolds via hormonal, neural and immunological pathways between the brain and the intestine, indicating that this relationship plays a fundamental role in modulating cerebral physiopathology via neuronal development and control of synaptic plasticity (8-9-10-11). Dysbiosis of the microbiota entails alteration of either the bacterial composition, with a reduction in bacterial diversity, or a proliferation of pathological bacteria that triggers the release of proinflammatory cytokines. Dysbiosis entails the release of pathological bacterial lipopolysaccharides (LPSs), called PAMPs (Pathogen Associated Molecular Patterns). PAMPs reduce the gene expression of proteins associated with the \"tight junctions\" of the intestinal epithelium (zonulin-1, occludin, claudin) via the activation of the nuclear factor NF-κB, while the pro-inflammatory cytokines IL-1β, IL-6 and TNF-α are responsible for \"minimal persistent inflammation\" (12-13-14). Experimental studies of model rats have shown that intestinal dysbiosis is implicated in the physio-pathological mechanisms of OSA (15-16-17). Dysbiosis alters the synthesis and degradation of neurotransmitters and the regulation of entero-endocrine signalling pathways that communicate with the central nervous system (CNS) via neurotransmission (18)(19).Here we summarise the possible molecular mechanisms underlying OSA-microbiome interactions and discuss how various factors interact with gut dysbiosis to influence OSA. The physiopathological mechanisms underlying OSA are intermittent nocturnal hypoxia (IH) and sleep fragmentation (SF), which can induce dysbiosis of the gut microbiota (GM), compromise the intestinal barrier, alter intestinal metabolites and generate neuroinflammation (20-21-22). These mechanisms, once activated, lead to secondary cellular oxidative stress, sympathetic activation and systemic inflammation (23-24-25-26).The effects of the microbiota on the brain There is abundant scientific evidence that on the intestinal level, thanks to their ability to produce molecules and neurotransmitters, bacteria can act directly on the CNS via the vagus nerve, the neuroendocrine system and bacterial metabolites (27)(28). Dinan et al. demonstrated in animal models that the GM can influence the physiology of the brain by regulating neurotransmission and synaptogenesis. In their study, they characterised the neurobiochemical profile of the forebrains of mice during three key phases of postnatal development, which coincide with the formation of the gut microbiota. They demonstrated that the molecules derived from intestinal microbes are able to cross the blood-brain barrier (BBB) and that the intestinal microbiome can thus influence cerebral neurodevelopmental trajectories (29)(30). A recent review and meta-analysis observed increased levels of biomarkers of intestinal barrier dysfunction in patients with OSA, and found that these markers correlate with polysomnographic parameters indicating the seriousness of OSA (31). Previous experimental studies performed in the laboratory using rodent-based OSA models had already suggested that the absorption and barrier functions that regulate the intestinal epithelium are sensitive to the intensity of intermittent hypoxia (IH) and that the depth and intensity of IH can directly compromise the integrity of the intestinal epithelium, thereby altering \"tight junctions\" and increasing intestinal permeability and the inflammatory process (32)(33).The systemic inflammatory mechanisms generated by intestinal dysbiosis that determine the neuroinflammatory response are described below (34-35-36). In detail, signal-ligands released by intestinal gram-negative bacteria during dysbiosis generate molecular structures such as lipopolysaccharides, called Pathogen-Associated Molecular Patterns (PAMPs). PAMPs bind to Pattern Recognition Receptors (PRRs) including Toll-Like Receptors (TLRs), which are found on Antigen-Presenting Cells (APCs) such as dendritic cells, macrophages and T lymphocytes. This bond between PAMPs and PRRs activates the APCs, which are involved in the epigenetic, immunological and metabolic reprogramming of the entire organism. At the same time, this activation of receptors is responsible for the release of inflammatory cytokines that reduce the gene expression of proteins associated with the tight junctions of the intestinal epithelium (37)(38). This in turn increases intestinal permeability (involving zonulin-1, occluding and claudin) and the release of the pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) responsible for systemic inflammation (39). In addition to the PAMP/TLR4 signalling pathways, PAMPs can activate another inflammatory mechanism by binding to dendritic cells (DCs), which produce the interleukins IL-1 and IL-18. These can generate biologically active molecules such as the inflammasome NLRP3. Inflammasomes modulate a multitude of signals causing chronic pro-inflammatory responses (40-41-42). Experimental studies conducted in the laboratory on animal models have demonstrated the role of nocturnal intermittent hypoxia (IH) and sleep fragmentation (SF) in causing intestinal dysbiosis, which in turn can intensify the development of the physio-pathological mechanisms of OSA and cause cardiorespiratory and metabolic co-morbidity (43-44-45).Intestinal bacteria produce mainly gamma acid aminobutyric acid (GABA), dopamine (DA), norepinephrine (NE), serotonin (5-HT) and histamine in order to communicate with the enteric nervous system (ENS) (46), but also intermediate compounds such as short-chain fatty acids (SCFAs) (47), tryptophan (48) and secondary bile acids (49). The signals generated by these neurotransmitters and molecules are transported to the brain via the fibres of the vagus nerve (VN). In response, the brain sends return signals to the enterochromaffin cells (ECCs) in the intestinal wall and to the immune system of the intestinal mucosae, again via the fibres of the vagus nerve (50). The activation of the VN improves the integrity of the intestinal wall, reduces peripheral inflammation and inhibits the release of pro-inflammatory cytokines such as IL-1β, IL-6 and TNF-α (51). The signals generated by the hypothalamus reach the pituitary and adrenal glands and communicate with the ECCs via the hypothalamic-pituitary-adrenal axis (HPA) (52). The complex control of entero-endocrine signalling and immune responses maintains the gut microbiota in a state of equilibrium. Although the vagus nerve is in contact with all the layers of the intestinal wall, its fibres do not cross the intestinal wall itself and thus are not in direct contact with the gut microbiota (53). The signals reach the microbiota via neurons ranging in number between 100 and 500 million belonging to the enteric nervous system (ENS). Although the ENS is associated with the VN, it functions independently from it. Recent laboratory studies have demonstrated that the ENS is dynamic and continuously changing (54). The neurons of the ENS represent the biggest nervous system in the human body. The neurons connected to the gastrointestinal tract (GIT) possess various chemical and mechanosensitive receptors that interact with regulatory hormones and peptides released by enterochromaffin cells (ECCs), also known as Kulchitsky cells. Although these cells represent just 1% of the epithelial cells of the GIT, they play an important role in maintaining the homeostasis of the GIT (55). To date, 10 different types of ECCs have been characterised. The receptors on these cells are expressed by enteric neurons, but also by the fibres of the vagus nerve, the brainstem and the hypothalamus (56,57). The ENS, also called the \"brain within the gut\" or \"second brain\" (58), is composed of the myenteric plexus and inner submucosal plexus. It is structurally similar to the brain and operates on the basis of a similar \"chemical platform\" (59). The modulation and development of the neurons of the ENS is controlled by the gut microbiota. The embryogenic development of enteric neurons is based on the presence of microbial cells, as shown in studies conducted on mice (60). The role played by the gut microbiota in association with acetylcholine-type neurotransmitters and neuro-regulatory peptides has been highlighted in recent research conducted on animal models. It has been seen that the secretion of Ach can be stimulated by some species of Lactobacillus (61,62). Lactobacillus rhamnosus jB-1 changes the expression of GABA A receptors in the brain

Public relations' fundamental functions date back to the dawn of human civilisation. The study assessed the relationship between public relation, corporate image and customer affective commitment at MTN in Ghana. The study employed a quantitative study approach, explanatory study design and the positivist study paradigm. Four hundred (400) clients were chosen for the study. A self-administered questionnaire solicited the customers' views on the stated objectives. Data were analysed using SMART PLS 4.0.8.4. The study findings revealed that public relation affects customer affective commitment, public relation impacts corporate image, corporate image predict customer affective commitment, and corporate image fully mediates the relationship between public relation and customer affective commitment. The study informed government officials and policymakers on public relation-related factors that directly and indirectly affect customer affective commitment, which will help guide policy. This study is the first to test the relationship between public relation, corporate image and customers' affective commitment at MTN Limited in a developing country like Ghana. Comprehending the intricate relationship between public relations, company image, and customer involvement is essential for firms, customers, and society. This study investigates how corporate image influences the connection between public relations and customer emotional involvement. Specifically, the study examined how public relation influence customer affective commitment, assess the effect of public relation on corporate image and analyse the impact of corporate image on customer affective commitment and assess the mediating role of corporate image on the relationship between public relation and customer affective commitment. By revealing these mechanisms, organisations will create more impactful PR tactics, improving brand reputation and fostering long-term success. This research advocates for openness, accountability, and ethical behaviour, enabling customers to make well-informed decisions and cultivating trust between businesses and stakeholders. This attempt ultimately benefits the general public by promoting a fairer and more enduring marketplace.

In this paper, we present a novel model that enhances performance by extending the dual-modality TEVAD model—originally leveraging visual and textual information—into a multi-modal framework that integrates visual, audio, and textual data. Additionally, we refine the multi-scale temporal network (MTN) to improve feature extraction across multiple temporal scales between video snippets. Using the XD-Violence dataset, which includes audio data for violence detection, we conduct experiments to evaluate various feature fusion methods. The proposed model achieves an average precision (AP) of 83.9%, surpassing the performance of single-modality approaches (visual: 73.9%, audio: 67.1%, textual: 29.9%) and dual-modality approaches (visual + audio: 78.8%, visual + textual: 78.5%). These findings demonstrate that the proposed model outperforms models based on the original MTN and reaffirm the efficacy of multi-modal approaches in enhancing violence detection compared to single- or dual-modality methods.

The mammalian retina extracts a multitude of diverse features from the visual scene such as color, contrast, and direction of motion. These features are transmitted separately to the brain by more than 40 different retinal ganglion cell (RGC) subtypes. However, so far only a few genetic markers exist to fully characterize the different RGC subtypes. Here, we present a novel genetic Flrt3-CreERT2 knock-in mouse that labels a small subpopulation of RGCs. Using single-cell injection of fluorescent dyes in Flrt3 positive RGCs, we distinguished four morphological RGC subtypes. Anterograde tracings using a fluorescent Cre-dependent Adeno-associated virus (AAV) revealed that a subgroup of Flrt3 positive RGCs specifically project to the medial terminal nucleus (MTN), which is part of the accessory optic system (AOS) and is essential in driving reflex eye movements for retinal image stabilization. Functional characterization using ex vivo patch-clamp recordings showed that the MTN-projecting Flrt3 RGCs preferentially respond to downward motion in an ON-fashion. These neurons distribute in a regular pattern and most of them are bistratified at the level of the ON and OFF bands of cholinergic starburst amacrine cells where they express the known ON-OFF direction-selective RGC marker CART. Together, our results indicate that MTN-projecting Flrt3 RGCs represent a new functionally homogeneous AOS projecting direction-selective RGC subpopulation.

Many artificially intelligent systems solve complex health- and agriculture-related problems that require great computational power. Such systems are used for tracking medical records, genome sequence analysis, image-based plant disease detection, food supply chain traceability, and photosynthesis simulation. Massively parallel computers (MPCs) are among those used to solve these computation-intensive problems. MPCs comprise a million nodes; connecting such a large number of nodes is a daunting task. Therefore, hierarchical interconnection networks (HINs) have been introduced to solve this problem. A midimew-connected torus network (MTN) is a HIN that has basic modules (BM) as torus networks that are connected hierarchically by midimew links. This paper presents the performance of MTNs in terms of static topological parameters and cost-effectiveness, as measured through simulations. An MTN was compared with other networks, including mesh, torus, TESH, TTN, MMN, and TFBN. The results showed that our MTN had a low diameter with a high bisection width and arc connectivity. In addition, our MTN had a high cost–performance trade-off factor (CPTF), a high cost-effective factor (CEF), low packing density, and moderate message-traffic density with marginally higher costs, as compared to other networks, due to wire complexity. However, our MTN provided better bandwidth with higher static fault tolerance. Therefore, MTNs are suggested for further evaluation of the effective implementation of MPCs.

As supply chains in today's world become more complex and fragile, enhancing the resilience of maritime transport is increasingly imperative. The COVID-19 epidemic in 2020 exposed the vulnerability of existing supply chains, causing substantial impacts such as supply shortages, procurement constraints, logistics delays and port congestion, highlighting the need to build resilient maritime transportation networks (MTNs) and reigniting research on the resilience of maritime transport. Based on science mapping, we quantitatively analysed the domain of resilience of MTNs. We mainly study the resilience of MTNs from the following aspects: the construction of MTNs and their topological characterization, vulnerability-orientated resilience analysis of MTNs, recovery-orientated resilience analysis of MTNs, investment decision-orientated resilience analysis of MTNs, climate change-orientated resilience analysis of MTNs and pandemic-orientated resilience analysis of MTNs. This study reviews recent advances in MTN resilience research, highlighting research topics, shortcomings and future research agenda.

Multivalued optical logic shows immense promise in modern computing systems with several advantages like ultrahigh computational speed, large amount of data handling capability and high data density. The logic gates are building blocks of computational systems, and all the logic circuits can be realized by cascading different logic gates. This paper proposes a new set of designs for existing logic gates in the Modified Trinary Number system with more efficiency and less complexity. The newly designed gates enable direct cascading of multiple gates and require lesser number of SLMs and Savart plates for realization, hence greatly reducing the circuit complexity of larger circuits. The Optical Tree Architecture of these new logic gates is realized using Spatial Light Modulators (SLM) and Savart plates. Moreover, a comparative study between the newly designed gates and existing gates is also incorporated to demonstrate the reduction in SLMs and Savart plates in the newly developed designs.

This work reports the synthesis and structure of a large porous zeotype network observed within compound (1) using Cu2(piv)4 as the linking unit (piv = pivalate). The slow in situ formation of the hmt ligand (hexamethylenetetramine) appears to be key in generating a µ4-bridging mode of the hmt-node. Attempts to improve the low yield of compound (1) using different solvent layer diffusion methods resulted in the µ3-hmt complexes (2) and (3). Both compounds exhibit a 3D network of two intertwined chiral networks. Strong hydrogen bonding present in (3) leads to the formation of intertwined, DNA-like double-helix structures. The use of bulky solvents in the synthesis of compound (4) leads to the structure crystallizing solvent-free. The packing of (4) is dominated by energy minimization, which is achieved when the 1D-“cylinders” pack into the closest possible arrangement. This work highlights the potential for solvent controlled synthesis of extended copper-hmt systems.