Initialize latexmk and research report

.gitignore

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+*.swp

doc/research/.latexmkrc

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+$pdf_mode = 1;
+$pdf_previewer = 'start evince';
+
+@default_files = ('research.tex');
+
+# Make latexmk -c remove .bbl file
+$bibtex_use = 2;
+
+# Make the glossaries package happy
+add_cus_dep('glo', 'gls', 0, 'run_makeglossaries');
+add_cus_dep('acn', 'acr', 0, 'run_makeglossaries');
+
+sub run_makeglossaries {
+    my ($base_name, $path) = fileparse($_[0]);
+    system("makeglossaries '$base_name'");
+}
+
+push @generated_exts, 'glo', 'gls', 'glg';
+push @generated_exts, 'acn', 'acr', 'alg';
+$clean_ext .= ' %R.ist %R.xdy';

doc/research/references.bib

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+@article{levental2009,
+   abstract = {Tumors are characterized by extracellular matrix (ECM) remodeling and stiffening. The importance of ECM remodeling to cancer is appreciated; the relevance of stiffening is less clear. We found that breast tumorigenesis is accompanied by collagen crosslinking, ECM stiffening, and increased focal adhesions. Induction of collagen crosslinking stiffened the ECM, promoted focal adhesions, enhanced PI3 kinase (PI3K) activity, and induced the invasion of an oncogene-initiated epithelium. Inhibition of integrin signaling repressed the invasion of a premalignant epithelium into a stiffened, crosslinked ECM and forced integrin clustering promoted focal adhesions, enhanced PI3K signaling, and induced the invasion of a premalignant epithelium. Consistently, reduction of lysyl oxidase-mediated collagen crosslinking prevented MMTV-Neu-induced fibrosis, decreased focal adhesions and PI3K activity, impeded malignancy, and lowered tumor incidence. These data show how collagen crosslinking can modulate tissue fibrosis and stiffness to force focal adhesions, growth factor signaling and breast malignancy. © 2009 Elsevier Inc. All rights reserved.},
+   author = {Kandice R. Levental and Hongmei Yu and Laura Kass and Johnathon N. Lakins and Mikala Egeblad and Janine T. Erler and Sheri F.T. Fong and Katalin Csiszar and Amato Giaccia and Wolfgang Weninger and Mitsuo Yamauchi and David L. Gasser and Valerie M. Weaver},
+   doi = {10.1016/J.CELL.2009.10.027},
+   issn = {0092-8674},
+   issue = {5},
+   journal = {Cell},
+   keywords = {CELLBIO,HUMDISEASE},
+   month = {11},
+   pages = {891-906},
+   pmid = {19931152},
+   publisher = {Cell Press},
+   title = {Matrix Crosslinking Forces Tumor Progression by Enhancing Integrin Signaling},
+   volume = {139},
+   year = {2009},
+}
+@generic{frantz2010,
+   author = {Christian Frantz and Kathleen M. Stewart and Valerie M. Weaver},
+   doi = {10.1242/jcs.023820},
+   issn = {00219533},
+   issue = {24},
+   journal = {Journal of Cell Science},
+   month = {12},
+   pages = {4195-4200},
+   pmid = {21123617},
+   title = {The extracellular matrix at a glance},
+   volume = {123},
+   year = {2010},
+}

doc/research/research.tex

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+\documentclass[a4paper]{article}
+
+\usepackage{csquotes}
+\usepackage[acronym]{glossaries}
+\usepackage[utf8x]{inputenc}
+\usepackage{siunitx}
+
+\makeglossaries{}
+\newacronym{cis}{CiS}{Cells in Silico}
+\newacronym{cpm}{CPM}{Cellular Potts Model}
+\newacronym{ecm}{ECM}{Extracellular Matrix}
+\newacronym{mcs}{MCS}{Monte-Carlo Step}
+\newacronym{nastja}{NAStJA}{Neoteric Autonomous Stencil code for Jolly Algorithms}
+
+\begin{document}
+
+\title{Research Summary}
+\author{Paul Brinkmeier}
+\date{June 2023}
+\maketitle
+
+\section{\acrfull{ecm}}
+
+For an extensive overview, see \cite{frantz2010}.
+
+\begin{itemize}
+	\item The \acrshort{ecm} constitutes the non-cellular parts of all tissues.
+	\item It consists of:
+	\begin{itemize}
+		\item Fibrous proteins, most importantly collagen, elastin and fibronectin.
+		\item Up to 30\% collagen.
+                      Forms fibrils and fibers of different sizes which can \enquote{stick together} to make up networks.
+		      There are a bunch of different collagen types.
+		\item Proteoglycans, which fill the interstitial space in the form of a hydrated gel.
+	\end{itemize}
+	\item Cells move through and remodel their \acrshort{ecm}, which in turn changes their behavior. \\
+	      $\implies$ \emph{in silico} models need to take this into account.
+	\item Different tissues have different \acrshortpl{ecm}.
+\end{itemize}
+
+\subsection{Properties of the Extracellular Matrix}
+
+Our approach takes a macroscopic view of the \acrshort{ecm}.
+Individual fibrils/fibers should not be modeled.
+Nevertheless we include some microscopic properties.
+
+\begin{itemize}
+	\item \textbf{Density}
+	\item \textbf{Stiffness}: Matrix stiffness has an effect on tumor gowth, e.g. \cite{levental2009}.
+	Measured using Young's modulus/elastic modulus which is given in \si{\Pa}.
+	\item \textbf{Viscoelasticity}
+	\item \textbf{Pore size}
+\end{itemize}
+
+\cite{frantz2010} mentions Matrigel™ and collagen type I gels, so we will focus on these.
+
+\section{\acrfull{cpm}}
+
+\begin{itemize}
+	\item The \acrshort{cpm} is a grid-based Monte-Carlo simulation for cells.
+	\item Each cell consists of many voxels.
+              These voxels contain its cell ID.
+	\item In each \acrfull{mcs}, a random voxel copies the cell ID of its neighbor.
+	\item The hamiltonian $H$ gives the energy of a generation. It depends on the volume and surface of cells and their reciprocal adhesion.
+	\item A \acrshort{mcs} is always accepted if it reduces $H$.
+              If it does not reduce $H$, it is accepted probabilistically.
+\end{itemize}
+
+\section{\acrshort{nastja} \& \acrshort{cis}}
+
+\begin{itemize}
+	\item \acrfull{nastja} is a massively parallel stencil code solver based on OpenMPI.
+	\item \acrfull{cis} is an implementation of the \acrshort{cpm} in \acrshort{nastja}.
+\end{itemize}
+
+\section{The \acrshort{ecm} in the \acrshort{cpm}}
+
+\clearpage
+
+\section{Glossary}
+
+\printglossary[type=\acronymtype]
+
+\bibliographystyle{plain}
+\bibliography{references}
+
+\end{document}