Abductive hypotheses generation in neural-symbolic systems

Wydział Nauk SpołecznychCelem pracy było opracowanie procedury abdukcyjnej, która działa w oparciu o system neuronalno-symboliczny. Procedura abdukcyjna jest rozumiana jako rozszerzona interpretacja algorytmiczna rozumowania abdukcyjnego, tj. posiadając wiedzę Γ oraz zjawisko ᵠ, którego nie można wyprowadzić z Γ tworzymy nową bazę wiedzy Γ’, która jest zmodyfikowaną wersją Γ, a z której ᵠ jest osiągalne. Hipotezę abdukcyjną definiujemy jako różnicę symetryczną pomiędzy Γ i Γ’. Wymagamy aby powstałe w ten sposób hipotezy abdukcyjne posiadały pewne własności, np. niesprzeczność z bazą wiedzy. Procedura abdukcyjna zaimplementowana została w systemie neuronalno-symbolicznym, który umożliwia tłumaczenie programów logicznych (baza wiedzy Γ oraz cel abdukcyjny ᵠ) na sztuczne sieci neuronowe, uczenie sieci neuronowych przy pomocy algorytmu propagacji wstecznej (proces tworzenia hipotezy abdukcyjnej) oraz tłumaczenie sieci neuronowych na programy logiczne (baza wiedzy Γ’), co umożliwia otrzymanie hipotezy abdukcyjnej.The goal of this work was to create abductive procedure that is implemented in neural-symbolic system. The abductive procedure is understood as extended algorithmic perspective, i.e. having Γ as knowledge base and ᵠ that is not obtainable from Γ we create Γ’ (modified Γ) from which ᵠ is obtainable. The abductive hypothesis is a symmetric difference between Γ and Γ’. We also require abductive hypotheses to fulfill certain conditions. The procedure is implemented in a neural-symbolic system where Γ and ᵠ are represented as a logic program that is translated into a neural network, the neural network is then trained by means of the backpropagation algorithm in such a way that ᵠ becomes obtainable, and then the trained neural network is translated back into a logic program that represents Γ’. The symmetric difference between Γ and Γ’ is the abductive hypothesis

Single-shot simulations of dynamics of quantum dark solitons

Eigenstates of Bose particles with repulsive contact interactions in one-dimensional space with periodic boundary conditions can be found with the help of the Bethe ansatz. The type~II excitation spectrum identified by E. H. Lieb, reproduces the dispersion relation of dark solitons in the mean-field approach. The corresponding eigenstates possess translational symmetry which can be broken in measurements of positions of particles. We analyze emergence of single and double solitons in the course of the measurements and investigate dynamics of the system. In the weak interaction limit, the system follows the mean-field prediction for a short period of time. Long time evolution reveals many-body effects that are related to an increasing uncertainty of soliton positions. In the strong interaction regime particles behave like impenetrable bosons. Then, the probability densities in the configuration space become identical to the probabilities of non-interacting fermions but the wave-functions themselves remember the original Bose statistics. Especially, the phase flips that are key signatures of the solitons in the weak interaction limit, can be observed in the time evolution of the strongly interacting bosons.Comment: 11 pages, 9 figure

Neuropathic alterations of the myenteric plexus neurons following subacute intraperitoneal administration of salsolinol

Introduction. Impairment of the enteric nervous system has been suggested to occur within the pathogenesis of neurodegenerative diseases. Thus, in the current study, we consider salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, SAL) as a substance that can potentially induce myenteric neurodegen­eration. Material and methods. Male Wistar rats were subjected to continuous intraperitoneal dosing of salsolinol (200 mg/kg in total) with osmotic mini-pumps for either two or four weeks. An equivalent group of rats served as the control. Jejunal myenteric neurons were subjected to immunofluorescence staining to detect neuron specific protein — protein gene product (pan-neuronal marker, PGP 9.5), nitric oxide synthase (NOS), choline acetyltransferase (ChAT), Bax-protein and alpha-synuclein. In search of any functional impairment within the gastrointestinal tract, gut motility was assessed by determining the residual solid food contents in the stomach and the small and large intestine transit. Results. The myenteric neuron count, the mean size of the neuron body, the area of ganglia and the diameter of nerve strands were decreased in both of the salsolinol-treated groups compared with the controls. The number of NOS-positive cells was lower in the salsolinol-treated groups, while the number of ChAT-positive cells remained unchanged in comparison with the controls. Neurons expressing the pro-apoptotic Bax protein and alpha-synuclein deposits were observed among the myenteric neurons of the salsolinol-treated rats. Conclusions. Salsolinol evokes enteric neuronal cell death via initiation of apoptosis and leads to the formation of pathological aggregates of alpha-synuclein. Impairment of myenteric neurons, mainly the inhibitory motor neurons, might be responsible for the abnormal intestinal transit. Thus, salsolinol might be regarded as a suitable compound for inducing experimental enteric neurodegeneration in rats

Effect of Heat Treatments under High Isostatic Pressure on the Transport Critical Current Density at 4.2 K and 20 K in Doped and Undoped MgB2 Wires

Annealing undoped MgB2 wires under high isostatic pressure (HIP) increases transport critical current density (Jtc) by 10% at 4.2 K in range magnetic fields from 4 T to 12 T and significantly increases Jtc by 25% in range magnetic fields from 2 T to 4 T and does not increase Jtc above 4 T at 20 K. Further research shows that a large amount of 10% SiC admixture and thermal treatment under a high isostatic pressure of 1 GPa significantly increases the Jtc by 40% at 4.2 K in magnetic fields above 6 T and reduces Jtc by one order at 20 K in MgB2 wires. Additionally, our research showed that heat treatment under high isostatic pressure is more evident in wires with smaller diameters, as it greatly increases the density of MgB2 material and the number of connections between grains compared to MgB2 wires with larger diameters, but only during the Mg solid-state reaction. In addition, our study indicates that smaller wire diameters and high isostatic pressure do not lead to a higher density of MgB2 material and more connections between grains during the liquid-state Mg reaction

Effect of feeding on the pharmacokinetics of vilazodone in dogs

Vilazodone (VLZ) is a drug approved for the treatment of major depressive disorder in humans but no data are available for dogs. The present study aimed to evaluate the pharmacokinetics of a single oral 40 mg dose of VLZ in healthy Labrador dogs (n = 6) in fasted and fed conditions. Dogs were randomly divided in two (n = 3) groups in a cross-over study design (2 x 2). Group I was administered with VLZ at 40 mg/dog after fasting over-night. Group II was fed prior to and after administration of the same dose. A two-week wash-out period was observed. Plasma samples collected underwent LC-MS/MS analysis. VLZ concentrations were quantified in dogs' plasma in two different windows of time: 30 min to 10 h for the fasted group and 4 h to 35 h for the fed group. The values for t(1/2 lambda z) were statistically different between the groups (fed, 4.6 +/- 1.1 h vs fasted, 1.7 +/- 0.2 h). Tmax drastically changed between the groups (fed, 10 h vs fasted, 1.5 h), while C-max did not significantly vary (fed, 39.4 +/- 5.6 ng/mL vs fasted, 38.7 +/- 4.8 ng/mL). The AUC value was always statistically higher in the fed group. As a result, the average relative oral fasted bioavailability of VLZ was low, 28.8 +/- 6.1%. In conclusion, feeding can affect the pharmacokinetics of VLZ in the dog

Triple immunofluorescence labeling of atherosclerotic plaque components in apoE/LDLR ^{-/-} mice

This paper presents a simple and reliable method of triple immunofluorescence staining that allows simultaneous detection of various cell types present in atherosclerotic plaque of apolipoprotein E and LDL receptor-double knockout (apoE/LDLR -/-) mice. We used combined direct and indirect procedures applying commercially available primary antibodies raised in different species to detect smooth muscle cells (Cy3-conjugated mouse anti-smooth muscle actin, SMA), macrophages (rat anti-CD68) and T lymphocytes (rabbit anti-CD3). Fixation of the material in acetone and modified incubation protocol employing nonfat dry milk in preincubation and incubation media significantly increased the intensity of labeling and effectively quenched the background. Our method offers an efficient way to detect qualitative as well as quantitative changes of macrophages, T lymphocytes and smooth muscle cells in atherosclerotic plaque of apoE/LDLR -/- mice during atherosclerosis development or in response to pharmacological treatment

Sprint Fidelis implantable cardioverter-defibrillators lead patient management and survival: Single center study

Background: Over the last several years significant rises in the use of implanted cardioverter-defibrillators (ICD) have also resulted in a number of associated complications. This number includes lead failure. Sprint Fidelis (SF) ICD lead is regarded as a lead with elevated failure risk. Every center acting in accordance with the guidelines should observe patients more thoroughly especially with recalled leads and run a registry of their follow-up. The aim of this research was to present follow-up of the patients with SF leads (types 6948, 6949) from a single implantation center. Methods: There were 36 SF leads implanted in 36 patients. Mean follow-up period was 76 months (IQR 40.3–86.8). Patients were subjected to regular check-ups in 3 to 6 month intervals. Results: Patients were implanted at a median age of 66.5 years and majority of them had ischemic cardiomyopathy (72%). A majority of the studied population were men (72.2%). Predominantly dual-chamber ICD (ICD-DR) were implanted (50% ICD-DR vs. 47.2% ICD-VR). The guidelines for management of patients implanted with SF were fully implemented. During the follow-up 14 (38.9%) patients died. No deaths were noted that could be attributed to lead failure. In 5 cases lead failure was identified and of these 4 leads were replaced. Median time from implantation to the detection of lead dysfunction was 52 months (IQR 49; 83). The symptoms of failure consisted of: inappropriate shocks, alternating ventricular lead signal, or loss of ventricular stimulation. Conclusions: The follow-up of patients with recalled SF leads in a single center supports that implementation SF management guidelines could be effective in clinical practice