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The authors discuss the existence and uniqueness of asymptotically stable unpredictable solutions for some quasilinear differential equations. Two principal novelties are in the basis of this research. The first one is that all coordinates of the solution are unpredictable functions. That is, solutions are strongly unpredictable. Secondly, perturbations are strongly unpredictable functions in the time variable. Examples with numerical simulations are presented to illustrate the theoretical results.

The purpose of this paper is to study the dynamics of Hopfield neural networks with impulsive effects, focusing on Poisson stable rates, synaptic connections, and unpredictable external inputs. Through the symmetry of impulsive and differential compartments of the model, we follow and extend the principal dynamical ideas of the founder. Specifically, the research delves into the phenomena of unpredictability and Poisson stability, which have been examined in previous studies relating to models of continuous and discontinuous neural networks with constant components. We extend the analysis to discontinuous models characterized by variable impulsive actions and structural ingredients. The method of included intervals based on the B-topology is employed to investigate the networks. It is a novel approach that addresses the unique challenges posed by the sophisticated recurrence.

Abstract Temporally unpredictable stimuli influence behavior across species, as previously demonstrated for sequences of simple threats and rewards with fixed or variable onset. Neuroimaging studies have identified a specific frontolimbic circuit that may become engaged during the anticipation of temporally unpredictable threat (U-threat). However, the neural mechanisms underlying processing of temporally unpredictable reward (U-reward) are incompletely understood. It is also unclear whether these processes are mediated by overlapping or distinct neural systems. These knowledge gaps are noteworthy given that disruptions within these neural systems may lead to maladaptive response to uncertainty. Here, using functional magnetic resonance imaging data from a sample of 159 young adults, we showed that anticipation of both U-threat and U-reward elicited activation in the right anterior insula, right ventral anterior nucleus of the thalamus and right inferior frontal gyrus. U-threat also activated the right posterior insula and dorsal anterior cingulate cortex, relative to U-reward. In contrast, U-reward elicited activation in the right fusiform and left middle occipital gyrus, relative to U-threat. Although there is some overlap in the neural circuitry underlying anticipation of U-threat and U-reward, these processes appear to be largely mediated by distinct circuits. Future studies are needed to corroborate and extend these preliminary findings.

Vitiligo is a common primary, limited or generalized skin depigmentation disorder. Its pathogenesis is complex, multifactorial and unclear. For this reason, few animal models can simulate the onset of vitiligo, and studies of drug interventions are limited. Studies have found that there may be a pathophysiological connection between mental factors and the development of vitiligo. At present, the construction methods of the vitiligo model mainly include chemical induction and autoimmune induction against melanocytes. Mental factors are not taken into account in existing models. Therefore, in this study, mental inducement was added to the monobenzone (MBEH)-induced vitiligo model. We determined that chronic unpredictable mild stress (CUMS) inhibited the melanogenesis of skin. MBEH inhibited melanin production without affecting the behavioral state of mice, but mice in the MBEH combined with CUMS (MC) group were depressed and demonstrated increased depigmentation of the skin. Further analysis of metabolic differences showed that all three models altered the metabolic profile of the skin. In summary, we successfully constructed a vitiligo mouse model induced by MBEH combined with CUMS, which may be better used in the evaluation and study of vitiligo drugs.

Today, computer vision systems are tested by their accuracy in detecting and localizing instances of objects. As an alternative, and motivated by the ability of humans to provide far richer descriptions and even tell a story about an image, we construct a “visual Turing test”: an operator-assisted device that produces a stochastic sequence of binary questions from a given test image. The query engine proposes a question; the operator either provides the correct answer or rejects the question as ambiguous; the engine proposes the next question (“just-in-time truthing”). The test is then administered to the computer-vision system, one question at a time. After the system’s answer is recorded, the system is provided the correct answer and the next question. Parsing is trivial and deterministic; the system being tested requires no natural language processing. The query engine employs statistical constraints, learned from a training set, to produce questions with essentially unpredictable answers—the answer to a question, given the history of questions and their correct answers, is nearly equally likely to be positive or negative. In this sense, the test is only about vision. The system is designed to produce streams of questions that follow natural story lines, from the instantiation of a unique object, through an exploration of its properties, and on to its relationships with other uniquely instantiated objects. Significance In computer vision, as in other fields of artificial intelligence, the methods of evaluation largely define the scientific effort. Most current evaluations measure detection accuracy, emphasizing the classification of regions according to objects from a predefined library. But detection is not the same as understanding. We present here a different evaluation system, in which a query engine prepares a written test (“visual Turing test”) that uses binary questions to probe a system’s ability to identify attributes and relationships in addition to recognizing objects.

[This corrects the article DOI: 10.3389/fphar.2023.1149185.].

Background Chronic unpredictable mild stress (CUMS) can not only lead to depression-like behavior but also change the composition of the gut microbiome. Regulating the gut microbiome can have an antidepressant effect, but the mechanism by which it improves depressive symptoms is not clear. Short-chain fatty acids (SCFAs) are small molecular compounds produced by the fermentation of non-digestible carbohydrates. SFCAs are ubiquitous in intestinal endocrine and immune cells, making them important mediators of gut microbiome-regulated body functions. The balance between the pro- and anti-inflammatory microglia plays an important role in the occurrence and treatment of depression caused by chronic stress. Non-absorbable antibiotic rifaximin can regulate the structure of the gut microbiome. We hypothesized that rifaximin protects against stress-induced inflammation and depression-like behaviors by regulating the abundance of fecal microbial metabolites and the microglial functions. Methods We administered 150 mg/kg rifaximin intragastrically to rats exposed to CUMS for 4 weeks and investigated the composition of the fecal microbiome, the content of short-chain fatty acids in the serum and brain, the functional profiles of microglia and hippocampal neurogenesis. Results Our results show that rifaximin ameliorated depressive-like behavior induced by CUMS, as reflected by sucrose preference, the open field test and the Morris water maze. Rifaximin increased the relative abundance of Ruminococcaceae and Lachnospiraceae, which were significantly positively correlated with the high level of butyrate in the brain. Rifaximin increased the content of anti-inflammatory factors released by microglia, and prevented the neurogenic abnormalities caused by CUMS. Conclusions These results suggest that rifaximin can regulate the inflammatory function of microglia and play a protective role in pubertal neurodevelopment during CUMS by regulating the gut microbiome and short-chain fatty acids.

A patrolling strategy that defines fare inspection frequencies on a proof-of-payment transportation system is operationally useful to the transit authority when there is a mechanism for its practical implementation. This study addresses the operational implementation of a fare inspection patrolling strategy under an in-station selective inspection policy using an unpredictable patrolling schedule, where the transit authority select a patrolling schedule each day with some probability. The challenge is to determine the set of patrolling schedules and their respective probabilities of being selected whose systematic day-to-day application matches the inspection frequencies that inhibit the action of opportunistic passengers in the medium term. A Stackelberg game approach is used to represent the hierarchical decision making process between the transit authority and opportunistic passengers. The heterogeneity of opportunistic passengers’ decisions to evade fare payment is taken into account. Numerical experiments show that a joint strategy-schedule approach provides good-quality unpredictable patrolling schedules with respect to the optimality gap for large-scale networks.

The purpose of this study was to explore the antidepressant-like effects of vitamin D3 at different doses (1.0, 2.5, and 5.0 mg/kg sc) on a model of depression produced by chronic unpredictable mild stress (CUMS) for 28 days in long-term (3 months) ovariectomized (OVX) adult rats. Sucrose preference (SPT), forced swimming (FST) and open-field (OFT) tests were conducted to examine the depression-like state. Serum corticosterone/adrenocorticotrophic hormone (ACTH) levels and hippocampal brain-derived neurotrophic factor (BDNF) and neurotrophin (NT)-3/NT-4 expressions by ELISA kits and/or western blotting were determined to assess the possible mechanisms of the vitamin D3 effects on the depression-like profile in long-term OVX rats subjected to CUMS. The results showed that vitamin D3 (5.0 mg/kg), as well as fluoxetine treatment, considerably reversed the depression-like state in the SPT and FST, decreased serum corticosterone/ACTH levels, and increased BDNF and NT-3/NT-4 levels in the hippocampus of long-term OVX rats compared to OVX rats with CUMS (p < 0.05). Thus, a high dose of vitamin D3 (5.0 mg/kg sc) could improve the depression-like profile in long-term OVX adult female rats subjected to the CUMS procedure, which might be mediated by the regulation of BDNF and the NT-3/NT-4 signaling pathways in the hippocampus, as well as the corticosterone/ACTH levels of the blood serum.

Accumulating evidence has suggested that the gut microbiome plays an important role in depression. Akkermansia muciniphila (AKK), a next-generation probiotic, shows a beneficial effect on immune and metabolic homeostasis. The relative abundance of AKK was found negatively correlated with depressive symptoms in both clinical and pre-clinical studies. To evaluate the potential antidepressant effect of AKK and explore the possible mechanism, we used chronic alcohol exposure and chronic unpredictable mild stress (CUMS) to induce depressive-like behaviors in mice. We found that oral AKK administration significantly reduced the immobility time in the force swimming test (FST) and tail suspension test (TST) in the mice with chronic alcohol exposure and the CUMS mice. The sucrose preference in the mice receiving AKK was significantly increased in the sucrose preference test (SPT). More importantly, AKK implantation significantly increased the level of 5-HT in the gut and PFC of both the alcohol exposure mice and the CUMS mice. Furthermore, AKK had inhibited the expression of SERT in the gut but not in the brain for both NIAAA and the CUMS model mice. Interestingly, the expression of cFos in enteric nerves in the gut significantly decreased after AKK administration. In conclusion, our study demonstrated the antidepressant effect of AKK in mice exposed to alcohol exposure and CUMS, with the potential mechanism that AKK implantation might lead to an increased level of 5-HT and inhibited SERT expression in the gut, and might alter the gut-to-brain signal through suppression of enteric nerves activation.