Belousov-Zhabotinsky type reactions: the non-linear behavior of chemical systems

Chemical oscillators are open systems characterized by periodic variations of some reaction species concentration due to complex physico-chemical phenomena that may cause bistability, rise of limit cycle attractors, birth of spiral waves and Turing patterns and finally deterministic chaos. Specifically, the Belousov-Zhabotinsky reaction is a noteworthy example of non-linear behavior of chemical systems occurring in homogenous media. This reaction can take place in several variants and may offer an overview on chemical oscillators, owing to its simplicity of mathematical handling and several more complex deriving phenomena. This work provides an overview of Belousov-Zhabotinsky-type reactions, focusing on modeling under different operating conditions, from the most simple to the most widely applicable models presented during the years. In particular, the stability of simplified models as a function of bifurcation parameters is studied as causes of several complex behaviors. Rise of waves and fronts is mathematically explained as well as birth and evolution issues of the chaotic ODEs system describing the Györgyi-Field model of the Belousov-Zhabotinsky reaction. This review provides not only the general information about oscillatory reactions, but also provides the mathematical solutions in order to be used in future biochemical reactions and reactor designs

Nonlocal Singular Problems and Applications to MEMS

We consider fourth order nonlinear problems which describe electrostatic actuation in MicroElectroMechanicalSystems (MEMS) both in the stationary case and in the evolution case; we prove existence, uniqueness and regularity theorems by exploiting the Near Operators Theory

Constructing Lifshitz solutions from AdS

Under general assumptions, we show that a gravitational theory in d+1 dimensions admitting an AdS solution can be reduced to a d-dimensional theory containing a Lifshitz solution with dynamical exponent z=2. Working in a d=4, N=2 supergravity setup, we prove that if the AdS background is N=2 supersymmetric, then the Lifshitz geometry preserves 1/4 of the supercharges, and we construct the corresponding Killing spinors. We illustrate these results in examples from supersymmetric consistent truncations of type IIB supergravity, enhancing the class of known 4-dimensional Lifshitz solutions of string theory. As a byproduct, we find a new AdS4 x S1 x T(1,1) solution of type IIB.Comment: 29 pages, no figures; v2 minor corrections, a reference adde

Non-primary progressive language impairment in neurodegenerative conditions: protocol for a scoping review

BACKGROUND: Progressive language difficulties arise in many neurodegenerative conditions, causing significant impact upon patients and families. This occurs most obviously in primary progressive aphasia (PPA) but can also occur within other forms of progressive disease. In these cases, language decline may be significant, but as they are not the presenting or dominant symptom, may be overlooked in favour of more prominent cognitive, behaviour or motor deficits. To date, there has been no systematic investigation into non-primary progressive aphasia. This scoping review aims to describe the currently reported language impairments found in non-language-led dementias and identify their clinical relevance, defined as the impact on everyday living. It also seeks to identify the reported interventions for language impairment in this patient group to-date. METHOD: We will conduct a scoping review of published studies that have assessed and/or treated aphasia in people diagnosed with a neurodegenerative condition other than primary progressive aphasia. The systematic search will include the electronic databases PubMed, MEDLINE, OVID-EMBASE, PsycINFO, and speechBITE, using search terms for specific non-language-led dementia subtypes. Findings will be mapped and described according to the type of language difficulties identified and rehabilitation approaches employed. Intervention studies will be evaluated for their methodological rigour using validated scales. DISCUSSION: This scoping review will provide an overview of the types of aphasia found in neurodegenerative conditions where language dysfunction is not the primary focus. Current treatment approaches (and gaps in the provision of treatment) will be identified

When it is not primary progressive aphasia: A scoping review of spoken language impairment in other neurodegenerative dementias

BACKGROUND: Progressive difficulties with spoken language occur across the spectrum of degenerative dementia. When not a primary presenting and dominant symptom, language difficulties may be overlooked in favor of more prominent cognitive, behavior, or motor deficits. The aim of this scoping review is to examine the extent and nature of the research evidence describing (1) the spoken language impairments found in non-language led dementias, (2) their impact on everyday living, and (3) the reported language interventions. METHODS: We searched PubMed, MEDLINE, OVID-EMBASE, PsycINFO, and SpeechBITE using terms related to spoken language for the following dementia types: Parkinson's disease dementia (PDD), dementia with Lewy bodies (DLB), progressive supranuclear palsy (PSP), cortico-basal syndrome (CBS), behavior variant frontotemporal dementia (bvFTD), early-onset Alzheimer's disease (EOAD), posterior cortical atrophy (PCA), and motor neuron disease associated with FTD (MND+FTD). Risk of bias was assessed with the QualSyst tool. RESULTS: Seventy-three eligible studies were included. A wide range of spoken language impairments were reported, involving both linguistic (e.g., syntactic processing) and other cognitive (e.g., sustained attention) underlying mechanisms. Although the severity of these deficits was scarcely reported, in some cases they manifested as non-fluent, dynamic, and global aphasias. No papers in the review described either the impact of these language impairments on everyday living or language therapies to treat them. DISCUSSION: There is a need to understand better the level of disability produced by language impairment in people living with non–language-led dementias. Our findings suggest three calls for action: (1) research studies should assess the clinical relevance of any spoken language deficits examined, (2) both linguistic and cognitive underlying mechanisms should be fully described (to inform the design of effective language and behavioral interventions), and (3) trials of language therapy should be conducted in those groups of individuals where significant language impairment is proved

A defective ABC transporter of the MRP family, responsible for the bean lpa1 mutation, affects the regulation of the phytic acid pathway, reduces seed myo-inositol and alters ABA sensitivity

We previously identified the lpa1 (low phytic acid) 280-10 line that carries a mutation conferring a 90% reduction in phytic acid (InsP6) content. In contrast to other lpa mutants, lpa1(280-10) does not display negative pleiotropic effects. In the present paper, we have identified the mutated gene and analysed its impact on the phytic acid pathway. Here, we mapped the lpa1(280-10) mutation by bulk analysis on a segregating F2 population, an then, by comparison with the soybean genome, we identified and sequenced a candidate gene. The InsP6 pathway was analysed by gene expression and quantification of metabolites. The mutated Pvmrp1(280-10) cosegregates with the lpa1(280-10) mutation, and the expression level of several genes of the InsP6 pathway are reduced in the lpa1(280-10) mutant as well as the inositol and raffinosaccharide content. PvMrp2, a very similar paralogue of PvMrp1 was also mapped and sequenced. The lpa1 mutation in beans is likely the result of a defective Mrp1 gene (orthologous to the lpa genes AtMRP5 and ZmMRP4), while its Mrp2 paralog is not able to complement the mutant phenotype in the seed. This mutation appears to down-regulate the InsP6 pathway at the transcriptional level, as well as altering inositol-related metabolism and affecting ABA sensitivity

The Controversy of Myopia as a Risk Factor for Glaucoma: a Mathematical Approach

poster abstractPurpose: to quantify how individual variations in anatomical parameters often associated with myopia (e.g. longer ocular axial length (OAL), reduced scleral thickness (ST), lamina cribrosa diameter (LCD) and thickness (LCT)) affect retinal blood flow (RBF) and its sensitivity to ocular perfusion pressure (OPP). Methods: A mathematical model is used to calculate RBF through central retinal artery (CRA), arterioles, capillaries, venules, and central retinal vein (CRV). The flow is time-dependent, driven by systemic pressure and regulated by variable resistances to account for nonlinear effects due to (1) autoregulation (AR), and (2) lamina cribrosa effect on CRA and CRV. The latter is a nonlinear function of intraocular pressure (IOP), cerebrospinal fluid pressure (CSF) and OAL, ST, LCD, and LCT. RBF is computed as the solution of a system of five non-linear ordinary differential equations. The system is solved for different OPP values, obtained by varying independently IOP and mean arterial pressure (MAP), with and without AR. Results: Four representative eyes are compared: Eye 1 (OAL=24mm, ST=1mm, LCD=3mm, LCT=0.4mm), Eye 2 (OAL=28mm, ST=1mm, LCD=3mm, LCT=0.4mm), Eye 3 (OAL=24mm, ST=0.7mm, LCD=2mm, LCT=0.2mm), Eye 4 (OAL=28mm, ST=0.7mm, LCD=2mm, LCT=0.2mm). The model predicts that the cardiac cycle RBF average (RBFav) for eyes with smaller LCD and LCT is notably less than in normal eyes when IOP is elevated and without AR (c). Without AR and reduced MAP, the four eyes show similar RBFav reductions (d). With AR, anatomical changes do not induce notable changes in RBFav, (a) and (b). Conclusions: Reduced LCD and LCT, often associated with myopia, seem to affect RBFav more than elevated OAL. RBFav reductions magnify when AR is impaired, and this might reduce IOP safe levels for eyes with reduced LCD and LCT. These findings suggest that a combination of anatomical and vascular factors might cause certain myopic eyes to be at higher risk for glaucomatous damage than others