Attention allocation for decision making queues

We consider the optimal servicing of a queue with sigmoid server performance. There are various systems with sigmoid server performance, including systems involving human decision making, visual perception, human–machine communication and advertising response. Tasks arrive at the server according to a Poisson process. Each task has a deadline that is incorporated as a latency penalty. We investigate the trade-off between the reward obtained by processing the current task and the penalty incurred due to the tasks waiting in the queue. We study this optimization problem in a Markov decision process (MDP) framework. We characterize the properties of the optimal policy for the MDP and show that the optimal policy may drop some tasks; that is, may not process a task at all. We determine an approximate solution to the MDP using the certainty-equivalent receding horizon optimization framework and derive performance bounds on the proposed receding horizon policy. We also suggest guidelines for the design of such queues.     

The P2X7R-NLRP3 and AIM2 Inflammasome Platforms Mark the Complexity/Severity of Viral or Metabolic Liver Damage

P2X7R-NLRP3 and AIM2 inflammasomes activate caspase-1 and the release of cytokines involved in viral-related liver disease. Little is known about their role in non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steato-hepatitis (NASH). We characterized the role of inflammasomes in NAFLD, NASH, and HCV. Gene expression and subcellular localization of P2X7R/P2X4R-NLRP3 and AIM2 inflammasome components were examined in histopathological preparations of 46 patients with biopsy-proven viral and metabolic liver disease using real-time PCR and immunofluorescence. P2X7R, P2X4R, and Caspase-1 are two- to five-fold more expressed in patients with NAFLD/NASH associated with chronic HCV infection than those with metabolic damage only (p ≤ 0.01 for all comparisons). The AIM2 inflammasome is 4.4 times more expressed in patients with chronic HCV infection, regardless of coexistent metabolic abnormalities (p = 0.0006). IL-2, a cytokine playing a pivotal role during chronic HCV infection, showed a similar expression in HCV and NASH patients (p = 0.77) but was virtually absent in NAFLD. The P2X7R-NLRP3 complex prevailed in infiltrating macrophages, while AIM2 was localized in Kupffer cells. Caspase-1 expression correlated with elastography-based liver fibrosis (r = 0.35, p = 0.02), whereas P2X7R, P2X4R, NRLP3, Caspase-1, and IL-2 expression correlated with circulating markers of disease severity. P2X7R and P2X4R play a major role in liver inflammation accompanying chronic HCV infection, especially when combined with metabolic damage, while AIM2 is specifically expressed in chronic viral hepatitis. We describe for the first time the hepatic expression of IL-2 in NASH, so far considered a peculiarity of HCV-related liver damage.     

Robust invariant sets for constrained storage systems

Several items are produced and stored into n buffers in order to supply an external demand without interruptions. We consider the classical problem of determining control laws and smallest buffer levels guaranteeing that an unknown bounded demand is always satisfied. A simple model with n decoupled integrators and n additive bounded disturbances is employed. The coupling arises from bounds on the total production capacity and on the total demand. Invariant set theory for linear and switched linear systems is exploited to compute robust positive invariant sets and controlled robust invariant sets for two commonly adopted scheduling policies. This paper provides the explicit expression of the invariant sets for any arbitrary n.     

Stabilization of strict‐feedback nonlinear systems with input delay using closed‐loop predictors

In this paper, we consider the control problem of strict‐feedback nonlinear systems with time‐varying input and output delays. The approach is based on the usual observer/predictor/feedback approach, but the novelty is the use of the closed‐loop dynamics in the predictor. This approach allows to develop two designs, an instantaneous predictor and a delay differential equation‐based predictor, that both attain the same performance in terms of system trajectories and input signal as in the case with no delays. The design based on delay differential equations allows to build a cascade of predictors to deal with arbitrarily large delay bounds. The resulting controller is much simpler to implement than classical infinite‐dimensional predictors, and it is robust with respect to actuation and measurement disturbances. We illustrate the approach with an application to the control of a chaotic system with input delay. Copyright © 2016 John Wiley & Sons, Ltd.     

A distributed simplex algorithm for degenerate linear programs and multi-agent assignments

In this paper we propose a novel distributed algorithm to solve degenerate linear programs on asynchronous peer-to-peer networks with distributed information structures. We propose a distributed version of the well-known simplex algorithm for general degenerate linear programs. A network of agents, running our algorithm, will agree on a common optimal solution, even if the optimal solution is not unique, or will determine infeasibility or unboundedness of the problem. We establish how the multi-agent assignment problem can be efficiently solved by means of our distributed simplex algorithm. We provide simulations supporting the conjecture that the completion time scales linearly with the diameter of the communication graph.     

Joint near-lossless compression and watermarking of still images for authentication and tamper localization

A system is presented to jointly achieve image watermarking and compression. The watermark is a fragile one being intended for authentication purposes. The watermarked and compressed images are fully compliant with the JPEG-LS standard, the only price to pay being a slight reduction of compression efficiency and an additional distortion that can be anyway tuned to grant a maximum preset error. Watermark detection is possible both in the compressed and in the pixel domain, thus increasing the flexibility and usability of the system. The system is expressly designed to be used in remote sensing and telemedicine applications, hence we designed it in such a way that the maximum compression and watermarking error can be strictly controlled (near-lossless compression and watermarking). Experimental results show the ability of the system to detect tampering and to limit the peak error between the original and the processed images.     

Inhibitors of Mitochondrial Human Carbonic Anhydrases VA and VB as a Therapeutic Strategy against Paclitaxel-Induced Neuropathic Pain in Mice

Neuropathy development is a major dose-limiting side effect of anticancer treatments that significantly reduces patient’s quality of life. The inadequate pharmacological approaches for neuropathic pain management warrant the identification of novel therapeutic targets. Mitochondrial dysfunctions that lead to reactive oxygen species (ROS) increase, cytosolic Ca²⁺ imbalance, and lactate acidosis are implicated in neuropathic pain pathogenesis. It has been observed that in these deregulations, a pivotal role is played by the mitochondrial carbonic anhydrases (CA) VA and VB isoforms. Hence, preclinical studies should be conducted to assess the efficacy of two novel selenides bearing benzenesulfonamide moieties, named 5b and 5d, and able to inhibit CA VA and VB against paclitaxel-induced neurotoxicity in mice. Acute treatment with 5b and 5d (30–100 mg/kg, per os – p.o.) determined a dose-dependent and long-lasting anti-hyperalgesic effect in the Cold plate test. Further, repeated daily treatment for 15 days with 100 mg/kg of both compounds (starting the first day of paclitaxel injection) significantly prevented neuropathic pain development without the onset of tolerance to the anti-hyperalgesic effect. In both experiments, acetazolamide (AAZ, 100 mg/kg, p.o.) used as the reference drug was partially active. Moreover, ex vivo analysis demonstrated the efficacy of 5b and 5d repeated treatments in reducing the maladaptive plasticity that occurs to glia cells in the lumbar portion of the spinal cord and in improving mitochondrial functions in the brain and spinal cord that were strongly impaired by paclitaxel-repeated treatment. In this regard, 5b and 5d ameliorated the metabolic activity, as observed by the increase in citrate synthase activity, and preserved an optimal mitochondrial membrane potential (ΔΨ) value, which appeared depolarized in brains from paclitaxel-treated animals. In conclusion, 5b and 5d have therapeutic and protective effects against paclitaxel-induced neuropathy without tolerance development. Moreover, 5b and 5d reduced glial cell activation and mitochondrial dysfunction in the central nervous system, being a promising candidate for the management of neuropathic pain and neurotoxicity evoked by chemotherapeutic drugs.     

Epigenetic and Genetic Factors Related to Curve Progression in Adolescent Idiopathic Scoliosis: A Systematic Scoping Review of the Current Literature

Adolescent idiopathic scoliosis (AIS) is a progressive deformity of the spine. Scoliotic curves progress until skeletal maturity leading, in rare cases, to a severe deformity. While the Cobb angle is a straightforward tool in initial curve magnitude measurement, assessing the risk of curve progression at the time of diagnosis may be more challenging. Epigenetic and genetic markers are potential prognostic tools to predict curve progression. The aim of this study is to review the available literature regarding the epigenetic and genetic factors associated with the risk of AIS curve progression. This review was carried out in accordance with Preferential Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines. The search was carried out in January 2022. Only peer-reviewed articles were considered for inclusion. Forty studies were included; fifteen genes were reported as having SNPs with significant association with progressive AIS, but none showed sufficient power to sustain clinical applications. In contrast, nine studies reporting epigenetic modifications showed promising results in terms of reliable markers. Prognostic testing for AIS has the potential to significantly modify disease management. Most recent evidence suggests epigenetics as a more promising field for the identification of factors associated with AIS progression, offering a rationale for further investigation in this field.     

Adipose Tissue Dysfunction and Obesity-Related Male Hypogonadism

Obesity is a chronic illness associated with several metabolic derangements and comorbidities (i.e., insulin resistance, leptin resistance, diabetes, etc.) and often leads to impaired testicular function and male subfertility. Several mechanisms may indeed negatively affect the hypothalamic–pituitary–gonadal health, such as higher testosterone conversion to estradiol by aromatase activity in the adipose tissue, increased ROS production, and the release of several endocrine molecules affecting the hypothalamus–pituitary–testis axis by both direct and indirect mechanisms. In addition, androgen deficiency could further accelerate adipose tissue expansion and therefore exacerbate obesity, which in turn enhances hypogonadism, thus inducing a vicious cycle. Based on these considerations, we propose an overview on the relationship of adipose tissue dysfunction and male hypogonadism, highlighting the main biological pathways involved and the current therapeutic options to counteract this condition.     

A Novel Morphological Parameter Predicting Fibrotic Evolution in Myeloproliferative Neoplasms: New Evidence and Molecular Insights

Philadelphia-negative chronic myeloproliferative neoplasms (MPNs) represent a group of hematological disorders that are traditionally considered as indistinct slow progressing conditions; still, a subset of cases shows a rapid evolution towards myelofibrotic bone marrow failure. Specific abnormalities in the megakaryocyte lineage seem to play a central role in this evolution, especially in the bone marrow fibrosis but also in the induction of myeloproliferation. In this review, we analyze the current knowledge of prognostic factors of MPNs related to their evolution to myelofibrotic bone marrow failure. Moreover, we focused the role of the megakaryocytic lineage in the various stages of MPNs, with updated examples of MPNs in vitro and in vivo models and new therapeutic implications.