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Benjamin Bairrington

Publications and source records attributed to Benjamin Bairrington.

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Bonded Trajectories of the $3x+γ$ Problem

Fix $γ\in \mathbb{Z}_{>0}^{odd}$ and $n\in\mathbb{Z}_{>0}$. We define the function $C_γ:{\mathbb Z}_{>0}\to {\mathbb Z}_{>0}$ such that if $n$ is odd, $C_γ(n)=3n+γ$; and if $n$ is even, $C_γ(n)=n/2$. We define the characteristic mapping $χ_γ: {\mathbb Z}_{>0}\to \{0,\, 1\}$ to be $χ_γ(n)\equiv C_γ(n)\, {\rm mod}\, 2$. Let $n$ start an integral loop of length $N$ associated with the $3x+γ$ Problem. Let $ρ$ and $ν$ be the count of the number of zeros and ones in a single period of $B = \left(χ_γ^i(n)\right)_{i\geq 0}$. In a single period of $B$, let $m_j$ denote the number of zeros between the $(j-1)$th and $j$th one. Let $\mathcal{M}_n$ be the matrix associated to $n$ whose elements are the sequential products of $2^{m_j}$ (e.g. $(2^{m_0},2^{m_0+m_1},2^{m_0+m_1+m_2},...)$). Let $p$ be a prime factor for all the terms in the integral loop starting with $n$ with multiplicity $a>0$. Suppose also that $p$ is a prime factor of $γ$ and $2^ρ- 3^ν$ with multiplicity $b$ and $c$, respectively. Finally assume that $c>b-a$. Then $\det(\mathcal{M}_n) \equiv 0 \pmod p$. We do find examples of this property. Let $ν$ be prime. Let $z_j = 2^{(m_j+2m_{j+1}+3m_{j+2}+...)/ν}$ be a weighted arithmetic average of the $m_j$. We prove that if $p$ is a prime factor of $2^ρ-3^ν$ distinct from $ν$ so that the residue class $p \pmod ν$ generates the whole group $\mathbb{Z}_ν^{*}$ then $p\nmid \det(\mathcal{M}_n)$ if and only if $p\nmid(z_1+...+z_ν)$ and for any $1\leq i<j\leq ν$ we have $z_i \not\equiv z_j \pmod p$. By this, we give an interesting property for the integral loop.

math.GM

Model for competing pathways in protein-aggregation: role of membrane bound proteins

Motivated by the biologically important and complex phenomena of Aβ peptide aggregation in Alzheimer's disease, we introduce a model and simulation methodology for studying protein aggregation that includes extra-cellular aggregation, aggregation on the cell-surface assisted by a membrane bound protein, and in addition, supply, clearance, production and sequestration of peptides and proteins. The model is used to produce equilibrium and kinetic-aggregation phase diagrams for aggregation onset and of reduced stable Aβ monomer concentrations due to aggregation. The methodology we implemented permits modeling of a phenomenon involving orders of magnitude differences in time scales and concentrations which can be retained in the simulation. We demonstrate how to identify ranges of parameter values that give monomer concentration depletion upon aggregation similar to that observed in Alzheimer's disease. We show how very different behavior can be obtained as reaction parameters and protein concentrations vary, and discuss the difficulty reconciling results of experiments from two vastly different concentration regimes. The latter is an important general issue in relating in-vitro and mice based experiments to humans.

q-bio.QM