Engineering quantum computing technologies: from compact modelling to applications

L'abstract è presente nell'allegato / the abstract is in the attachmen

Enteric Nervous System Abnormalities in Ulcerative Colitis

In the recent years, there is increasing evidence highlighting the crucial role played by ENS in intestinal inflammation, as demonstrated by the growing numbers of studies looking at both morphological and functional alterations in the ENS and its cellular elements, neurons and glial cells. These observations are the results of investigations carried out in both experimental animal models and in intestinal tissues of patients with inflammatory bowel disease. Although morpho-functional abnormalities of the ENS of UC patients have been consistently reported, additional studies are necessary to better understand the changes in the enteric cells, including neurons (of both submucosal and myenteric layers) and glial cells, which control gut functions, such as colonic motility and secretion, in the inflamed gut. This approach will help to prevent enteric neuropathies associated with inflammation and pave the way to future therapeutic options. Targeting neuronal and/or glial alterations during the course of inflammation may represent a novel approach to diminish the entity of tissue damage as well as the lack of long-term effectiveness of classical immunosuppressant agents used in the treatment of UC. Moreover, additional studies investigating the relationship between ENS and immune cells are warranted in order to carry out an in-depth assessment of the role of neurons, glial cells and their derived factors in the modulation of immune/inflammatory responses in the human gut, in light of establishment of new therapeutic approaches towards the treatment of gut inflammatory diseases. One of the main questions that still need to be addressed to is whether the alterations of the ENS precede or are secondary to the inflammatory process within the gut. This will hopefully help to predict the disease outcome in UC, that until now remains a challenge, and for better understanding of the pathogenesis of this disease. In conclusion, the complex interactions of the ENS and the other systems during gut inflammation require a broad perspective from neurophysiology, biochemistry and immunology to completely understand the regulation of inflammatory processes involved in UC. Therefore, important progress in this field can only be achieved by interdisciplinary approaches. Further research in this direction needs to be done for the discovery of longlasting, effective treatment for inflammatory diseases of the gut

S100B inhibitor pentamidine attenuates reactive gliosis and reduces neuronal loss in a mouse model of Alzheimer's disease

Among the different signaling molecules released during reactive gliosis occurring in Alzheimer’s disease (AD), the astrocytederived S100B protein plays a key role in neuroinflammation, one of the hallmarks of the disease. The use of pharmacological tools targeting S100B may be crucial to embank its effects and some of the pathological features of AD. The antiprotozoal drug pentamidine is a good candidate since it directly blocks S100B activity by inhibiting its interaction with the tumor suppressor p53. We used a mouse model of amyloid beta- (A-) induced AD, which is characterized by reactive gliosis and neuroinflammation in the brain, and we evaluated the effect of pentamidine on the main S100B-mediated events. Pentamidine caused the reduction of glial fibrillary acidic protein, S100B, and RAGE protein expression, which are signs of reactive gliosis, and induced p53 expression in astrocytes. Pentamidine also reduced the expression of proinflammatory mediators and markers, thus reducing neuroinflammation in AD brain. In parallel, we observed a significant neuroprotection exerted by pentamidine on CA1 pyramidal neurons. We demonstrated that pentamidine inhibits A-induced gliosis and neuroinflammation in an animal model of AD, thus playing a role in slowing down the course of the disease

Integration of Simulated Quantum Annealing in Parallel Tempering and Population Annealing for Heterogeneous-Profile QUBO Exploration

Simulated Quantum Annealing (SQA) is a heuristic algorithm which can solve Quadratic Unconstrained Binary Optimization (QUBO) problems by emulating the exploration of the solution space done by a quantum annealer. It mimics the quantum superposition and tunnelling effects through a set of correlated replicas of the spins system representing the problem to be solved and performing Monte Carlo steps. However, the effectiveness of SQA over a classical algorithm strictly depends on the cost/energy profile of the target problem. In fact, quantum annealing only performs well in exploring functions with high and narrow peaks, while classical annealing is better in overcoming flat and wide energy-profile barriers. Unfortunately, real-world problems have a heterogeneous solution space and the probability of success of each solver depends on the size of the energy profile region compatible with its exploration mechanism. Therefore, significant advantages could be obtained by exploiting hybrid solvers, which combine SQA and classical algorithms. This work proposes four new quantum-classical algorithms: Simulated Quantum Parallel Tempering (SQPT), Simulated Quantum Population Annealing (SQPA), Simulated Quantum Parallel Tempering - Population Annealing v1 (SQPTPA1) and Simulated Quantum Parallel Tempering - Population Annealing v2 (SQPTPA2). They are obtained by combining SQA, Parallel Tempering (PT), and Population Annealing (PA). Their results are compared with those provided by SQA, considering benchmark QUBO problems, characterized by different profiles. Even though this work is preliminary, the obtained results are encouraging and prove hybrid solvers’ potential in solving a generic optimization problem

Towards Compact Modeling of Noisy Quantum Computers: A Molecular-Spin-Qubit Case of Study

Classical simulation of Noisy Intermediate Scale Quantum computers is a crucial task for testing the expected performance of real hardware. The standard approach, based on solving Schrödinger and Lindblad equations, is demanding when scaling the number of qubits in terms of both execution time and memory. In this article, attempts in defining compact models for the simulation of quantum hardware are proposed, ensuring results close to those obtained with standard formalism. Molecular Nuclear Magnetic Resonance quantum hardware is the target technology, where three non-ideality phenomena—common to other quantum technologies—are taken into account: decoherence, off-resonance qubit evolution, and undesired qubit-qubit residual interaction. A model for each non-ideality phenomenon is embedded into a MATLAB simulation infrastructure of noisy quantum computers. The accuracy of the models is tested on a benchmark of quantum circuits, in the expected operating ranges of quantum hardware. The corresponding outcomes are compared with those obtained via numeric integration of the Schrödinger equation and the Qiskit’s QASMSimulator. The achieved results give evidence that this work is a step forward towards the definition of compact models able to provide fast results close to those obtained with the traditional physical simulation strategies, thus paving the way for their integration into a classical simulator of quantum computers

Role of Non-Caloric Carbonated Beverage Preload During a Standardized Solid and Liquid Meal on Colecistokinin and Ghrelin Levels in Healthy Subjects

Background and Aim: The effects of beverages with carbon dioxide on the gastrointestinal system mainly involve the upper digestive tract, with a possible modification of gastric physiology and change in food intake. No data are available on the relationship between non caloric carbonated beverages intake and gastrointestinal hormones levels. We aimed to verify the effect of a sugar-free carbonated beverage (CB) preload compared to a CB without CO2 (DCB) and water (W), during a standardized solid (SM) and liquid (LM) meal, on colecistokinin (CCK) and ghrelin (Gh) release. Subjects & Methods: After 300 ml of CB, DCB and W, a standardized SM or LM was administered at constant rate (100 kcal/5 min) to ten healthy subjects (4 females, aged 22-30 years; BMI 21-24) on six days in a random order (D1: CB+SM; D2: DCB+SM; D3: W+SM; D4: CB+LM; D5: DCB+LM; D6: W+LM). Eating perceptions (desire to eat, hunger, prospective of food consumption) and maximum satiety (MS) as total kcals intake were measured. CCK and Gh were evaluated on blood samples collected at 0, 10 (after beverage), 30, 60 and 120 min. Hormones values are expressed as ratio with body area surface (BSA) and as peak and nadir for CCK and Gh respectively. All data are expressed as mean±SD. Results: Desire to eat, hunger and prospective of food consumption were not different among beverages and meals. Total kcal intakes at MS were significant increased during SM respect to LM for CB (774±209, 585±299, p<0.01), DCB (837±208, 585±280, p<0.01) andW(783±244, 630±353, p<0.01) respectively, without differences among beverages. No differences were found for CCK and Gh among all beverages during SM or LM. Instead, CCK after CB was higher during SM than LM (1.004±0.514, 0.513±0.243, p<0.05) but not after DCB and W (0.790±0.604, 0.849±0.595, n.s.; 0.712±0.473, 0.873±0.431, n.s.) respectively. Moreover, after all beverages, Gh was higher during SM than LM (CB: 0.314±0.100, 0.206±0.099, p<0.05; DCB: 0.288±0.060, 0.145±0.051, p<0.01; W: 0.307±0.083, 0.170±0.085, p<0.01). Conclusions: Liquid meal determined an earlier satiety respect to a solid meal with a parallel decrease of Ghrelin independently of the kind of beverage preload. A CCK decrease was found only during liquid meal after carbonated beverage preload without influence on kcal intake compared with DCB and W. Studies on the influence of carbon dioxide on CCK release nutrients related need to explain this data

Amyotrophic Lateral Sclerosis and Multiple Sclerosis Overlap: A Case Report

The concurrence of amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) is extremely rare. We reported the case of a 33-year-old woman with a past history of paresthesias at the right hand, who developed progressive quadriparesis with muscular atrophy of limbs and, finally, bulbar signs and dyspnea. Clinical and neurophysiologic investigations revealed upper and lower motor neuron signs in the bulbar region and extremities, suggesting the diagnosis of ALS. Moreover, magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) analysis demonstrated 3 periventricular and juxtacortical lesions, hyperintense in T2 and FLAIR sequences, and 3 liquoral immunoglobulin G (IgG) oligoclonal bands, consistent with diagnosis of primary progressive MS (PPMS). This unusual overlap of ALS and MS leads to the discussion of a hypothetical common pathological process of immunological dysfunction in these two disorders, although the role of immune response in ALS remains ambivalent and unclear