Commit e632b745 authored by Turnhout, M.C. van's avatar Turnhout, M.C. van
Browse files

fix bib

parents b724466f 483402e4
......@@ -101,3 +101,4 @@ slprj/
*.tdo
# repo specific ignores
documentation/BasilLab.pdf
......@@ -2,7 +2,6 @@ Contributing
============
Your contributions and thoughts are highly valued.
In order to conribute to the repo, you need to make a BitBucket account (http://bitbucket.org).
Permissions for the repos can then be requested with the BasilLab-admin: m.c.v.turnhout@tue.nl
Note
......
BasilLab
========
http://mategit.wfw.wtb.tue.nl/STEM/basillab
http://gitlab.tue.nl/STEM/basillab
FYI (for your inspiration): a toolbox to get from raw MRI data to a
3D Abaqus FE model with as little user interaction as possible.
Originally written for specific in vivo experiments by Willeke Traa.
See also: Traa et al. MRI based 3D finite element modelling to investigate deep tissue injury, CMBBE, 2018.
See also:
Traa et al. MRI based 3D finite element modelling to investigate deep tissue injury, CMBBE, 2018.
https://dx.doi.org/10.1080/10255842.2018.1517868
Traa et al. There is an individual tolerance to mechanical loading in compression induced deep tissue injury, Clin. Biomech., 2019.
https://doi.org/10.1016/j.clinbiomech.2019.02.015
using & downloading
===================
You do not need (to run or use) Git to able to use basillab. You can
download your favourite version from http://mategit.wfw.wtb.tue.nl/STEM/basillab
download your favourite version from http://gitlab.tue.nl/STEM/basillab
Once downloaded, the code is yours to (ab)use to your liking (as
long as you do not violate the GPL license).
......@@ -30,7 +34,7 @@ compiling documentation from source
The main file to be compiled is BasilLab.tex
In order to compile from source, you may need some custom LaTeX-files
from stexmf: http://mategit.wfw.wtb.tue.nl/STEM/stexmf
from stexmf: http://gitlab.tue.nl/STEM/stexmf
copyright
=========
......
......@@ -9,12 +9,10 @@
Author = {Armstrong, Sarah J. and Read, Richard A. and Price, Roger},
Journal = {Osteoarthritis \& Cartilage},
Year = {1995},
Month = {March},
Number = {1},
Pages = {25--33},
Volume = {3},
Abstract = {Topographical variation in the articular cartilage and subchondral bone of the normal ovine knee was examined using histological techniques. The articular cartilage was examined grossly, then histological sections were cut and the cartilage thickness and chondrocyte density were measured. Bone mineral density, thickness of the subchondral bone plate (SBP) and volume and surface histomorphometrical parameters and mineral apposition rate were calculated for the subchondral bone. It was found that the articular cartilage on the tibial plateaux was thicker, less cellular, and overlay a thicker SBP than that on the femoral condyles. Similarly, the cartilage in the medial joint compartments was thicker, less cellular and overlying a thicker less dense SBP than that in the lateral joint compartments. There was no variation in bone histomorphometric parameters or mineral apposition rate between regions. Biomechanical testing has shown that loading is not uniform throughout the normal human knee joint. The present results suggest that loading within the ovine knee is also nonuniform, with the central regions of the tibial plateaux bearing greater loads than the femoral condyles, and the medial joint compartment being loaded more than the lateral one. The articular cartilage and subchondral bone have adapted in order to best withstand these variations in loading. These histological findings, plus the topographical variations in cartilage biochemistry reported by Read et al. (Topographical variation in composition, PG-biosynthesis and swelling pressure of cartilages of loaded tibio-femoral joints (Abstract). Proceedings of the Combined Meeting of the Orthopaedic Research Societies of USA, Japan and Canada.(ABSTRACT TRUNCATED AT 250 WORDS)},
Doi = {10.1016/S1063-4584(05)80035-4},
Institution = {School of Veterinary Studies, Murdoch University, Australia.},
......@@ -27,12 +25,10 @@
Author = {Bosboom, E.M.H. and Bouten, C.V.C. and Oomens, C.W.J. and Baaijens, F.P.T. and Nicolay, K.},
Journal = {Journal of Applied Physiology},
Year = {2003},
Month = {December},
Number = {6},
Pages = {2235--2240},
Volume = {95},
Abstract = {To obtain insight into the etiology of deep pressure sores, understanding of the relationship between prolonged transverse loading and local muscle damage is required. To date, the amount and location of muscle damage have been determined by histological examination. In the present study, we determined whether T2-weighted high-resolution magnetic resonance imaging (MRI) can also be applied to evaluate muscle tissue after prolonged transverse loading. The tibialis anterior muscle and overlying skin in the right hindlimbs of five rats were compressed between an indenter and the tibia. The in vivo magnetic resonance images of the loaded and contralateral hindlimbs were obtained 24 h after load application. The tibialis anterior muscles were then processed for histological examination. In the magnetic resonance images of all five loaded hindlimbs, signal intensity appeared higher in the loaded regions of the muscle compared with the unloaded regions. The location of the higher signal intensity coincided with the location of damage assessed from histology. Also the amount of damage determined with MRI was in good agreement with the amount of damage assessed from histological examination. Because MRI is nondestructive, it is a promising alternative for histology in research on pressure sore etiology, especially in follow-up studies to evaluate the development of muscle damage in time and in clinical studies.},
Doi = {10.1152/japplphysiol.01023.2001},
Institution = {Department of Materials Technology, Eindhoven Univ. of Technology, 5600 MB Eindhoven, The Netherlands. e.m.h.bosboom@tue.nl},
......@@ -50,12 +46,10 @@
Author = {Ceelen, K.K. and Stekelenburg, A. and Loerakker, S. and Strijkers, G.J. and Bader, D.L. and Nicolay, K. and Baaijens, F.P.T. and Oomens, C.W.J.},
Journal = {Journal of Biomechanics},
Year = {2008},
Month = {December},
Number = {16},
Pages = {3399--3404},
Volume = {41},
Abstract = {Prolonged mechanical loading of soft tissues adjacent to bony prominences can lead to degeneration of muscle tissue, resulting in a condition termed pressure-related deep tissue injury. This type of deep pressure ulcers can develop into a severe wound, associated with problematic healing and a variable prognosis. Limited knowledge of the underlying damage pathways impedes effective preventive strategies and early detection. Traditionally, pressure-induced ischaemia has been thought to be the main aetiological factor for initiating damage. Recent research, however, proposes tissue deformation per se as another candidate for initiating pressure-induced deep tissue injury. In this study, different strain parameters were evaluated on their suitability as a generic predictive indicator for deep tissue injury. With a combined animal-experimental numerical approach, we show that there is a reproducible monotonic increase in damage with increasing maximum shear strain once a strain threshold has been exceeded. This relationship between maximum shear strain and damage seems to reflect an intrinsic muscle property, as it applied across a considerable number of the experiments. This finding confirms that tissue deformation per se is important in the aetiology of deep tissue injury. Using dedicated finite element modeling, a considerable reduction in the inherent biological variation was obtained, leading to the proposal that muscle deformation can prove a generic predictive indicator of damage.},
Doi = {10.1016/j.jbiomech.2008.09.016},
Institution = {Department of Biomedical Engineering, Eindhoven University of Technology, P.O. Box 513, Building W-hoog 4.11, 5600 MB Eindhoven, The Netherlands. karlienk@gmail.com},
......@@ -73,8 +67,7 @@
Author = {Richard Dawkins},
Publisher = {Bantam publishers},
Year = {2009},
Edition = {p. 230, 1$^\text{st}$},
Edition = {1$^\text{st}$},
Owner = {mark},
Pages = {230},
Timestamp = {2010.01.19}
......@@ -97,10 +90,8 @@
Author = {Galilei, Galileo},
Publisher = {Modern Library},
Year = {1991},
Address = {New York, U.S.A.},
Note = {Translation of \textsl{Dialogo sopra i due massimi sistemi del mondo} (1632) by Stillman Drake.},
Owner = {tue},
Timestamp = {2013.07.09}
}
......@@ -110,7 +101,6 @@
Author = {Harr{\'e}, Rom},
Publisher = {Oxford University Press},
Year = {2009},
Owner = {tue},
Timestamp = {2015.12.30}
}
......@@ -120,7 +110,6 @@
Author = {Loerakker, S. and Stekelenburg, A. and Strijkers, G.J. and Rijpkema, J.J.M. and Baaijens, F.P.T. and Bader, D.L. and Nicolay, K. and Oomens, C.W.J.},
Journal = {Annals of Biomedical Engineering},
Year = {2010},
Month = {August},
Number = {8},
Pages = {2577--2587},
......@@ -142,12 +131,10 @@
Author = {Loerakker, S. and Oomens, C.W.J. and Manders, E. and Schakel, T. and Bader, D.L. and Baaijens, F.P.T. and Nicolay, K. and Strijkers, G.J.},
Journal = {Magnetic Resonance In Medicine},
Year = {2011},
Month = {August},
Number = {2},
Pages = {528--537},
Volume = {66},
Abstract = {Pressure ulcers are localized areas of soft tissue breakdown due to mechanical loading. Susceptible individuals are subjected to pressure relief strategies to prevent long loading periods. Therefore, ischemia-reperfusion injury may play an important role in the etiology of pressure ulcers. To investigate the inter-relation between postischemic perfusion and changes in skeletal muscle integrity, the hindlimbs of Brown Norway rats were subjected to 4-h ischemia followed by 2-h reperfusion. Dynamic contrast-enhanced MRI was used to examine perfusion, and changes in skeletal muscle integrity were monitored with T2-weighted MRI. The dynamic contrast-enhanced MRI data showed a heterogeneous postischemic profile in the hindlimb, consisting of areas with increased contrast enhancement (14-76\% of the hindlimb) and regions with no-reflow (5-77\%). For T2, a gradual increase in the complete leg was observed during the 4-h ischemic period (from 34 to 41 msec). During the reperfusion phase, a heterogeneous distribution of T2 was observed. Areas with increased contrast enhancement were associated with a decrease in T2 (to 38 msec) toward preischemic levels, whereas no-reflow areas exhibited a further increase in T2 (to 42 msec). These results show that reperfusion after prolonged ischemia may not be complete, thereby continuing the ischemic condition and aggravating tissue damage.},
Doi = {10.1002/mrm.22801},
Institution = {Soft Tissue Biomechanics and Engineering, Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands. s.loerakker@tue.nl},
......@@ -164,12 +151,10 @@
Author = {Loerakker, S. and Manders, E. and Strijkers, G.J. and Nicolay, K. and Baaijens, F.P.T. and Bader, D.L. and Oomens, C.W.J.},
Journal = {Journal of Applied Physiology},
Year = {2011},
Month = {October},
Number = {4},
Pages = {1168--1177},
Volume = {111},
Abstract = {Deep tissue injury (DTI) is a severe form of pressure ulcer where tissue damage starts in deep tissues underneath intact skin. In the present study, the contributions of deformation, ischemia, and reperfusion to skeletal muscle damage development were examined in a rat model during a 6-h period. Magnetic resonance imaging (MRI) was used to study perfusion (contrast-enhanced MRI) and tissue integrity (T2-weighted MRI). The levels of tissue deformation were estimated using finite element models. Complete ischemia caused a gradual homogeneous increase in T2 (∼20\% during the 6-h period). The effect of reperfusion on T2 was highly variable, depending on the anatomical location. In experiments involving deformation, inevitably associated with partial ischemia, a variable T2 increase (17-66\% during the 6-h period) was observed reflecting the significant variation in deformation (with two-dimensional strain energies of 0.60-1.51 J/mm) and ischemia (50.8-99.8\% of the leg) between experiments. These results imply that deformation, ischemia, and reperfusion all contribute to the damage process during prolonged loading, although their importance varies with time. The critical deformation threshold and period of ischemia that cause muscle damage will certainly vary between individuals. These variations are related to intrinsic factors, such as pathological state, which partly explain the individual susceptibility to the development of DTI and highlight the need for regular assessments of individual subjects.},
Doi = {10.1152/japplphysiol.00389.2011},
Institution = {Soft Tissue Biomechanics and Engineering, Dept. of Biomedical Engineering, Eindhoven Univ. of Technology, P.O. Box 513, 5600 MB Eindhoven, The Netherlands. s.loerakker@tue.nl},
......@@ -187,10 +172,8 @@
Author = {Moerman, Kevin M. and Nederveen, Aart J. and Simms, Ciaran K.},
Booktitle = {Proceedings of the 11th International Symposium on Computer Methods in Biomechanics and Biomedical Engineering},
Year = {2013},
Address = {Salt Lake City, Utah, USA},
Month = {April},
Owner = {tue},
Timestamp = {2015.12.10}
}
......@@ -200,7 +183,6 @@
Author = {\noopsort{Nierop}van Nierop, Bastiaan J. and Stekelenburg, Anke and Loerakker, Sandra and Oomens, Cees W. and Bader, Dan and Strijkers, Gustav J. and Nicolay, Klaas},
Journal = {Journal of Biomechanics},
Year = {2010},
Month = {February},
Number = {3},
Pages = {570--575},
......@@ -223,7 +205,6 @@
Author = {Oomens, C.W.J. and Loerakker, Sandra and Bader, D.L.},
Journal = {Journal of tissue viability},
Year = {2010},
Month = {May},
Number = {2},
Pages = {35--42},
......@@ -246,7 +227,6 @@
Author = {Stekelenburg, A. and Oomens, C.W.J. and Strijkers, G.J. and \noopsort{Graaf}de Graaf, L. and Bader, D.L. and Nicolay, K.},
Journal = {Medical Engineering and Physics},
Year = {2006},
Month = {May},
Number = {4},
Pages = {331--338},
......@@ -269,7 +249,6 @@
Author = {Stekelenburg, A. and Oomens, C.W.J. and Strijkers, G.J. and Nicolay, K. and Bader, D.L.},
Journal = {Journal of Applied Physiology},
Year = {2006},
Month = {June},
Number = {6},
Pages = {1946--1954},
......@@ -292,7 +271,6 @@
Author = {Stekelenburg, Anke and Strijkers, Gustav J. and Parusel, Henry and Bader, Dan L. and Nicolay, Klaas and Oomens, Cees W.},
Journal = {Journal of Applied Physiology},
Year = {2007},
Month = {May},
Number = {5},
Pages = {2002--2011},
......@@ -317,7 +295,6 @@
HowPublished = {Annual MaTe Poster Award of the Materials Technology (MaTe) group (Eindhoven University of Technology, Eindhoven, The Netherlands)},
Month = {December},
Year = {2014},
Owner = {tue},
Timestamp = {2015.12.10},
Url = {http://repository.tue.nl/posters/783267.pdf}
......@@ -330,7 +307,6 @@
HowPublished = {Annual MaTe Poster Award of the Materials Technology (MaTe) group (Eindhoven University of Technology, Eindhoven, The Netherlands)},
Month = {December},
Year = {2015},
Owner = {tue},
Timestamp = {2015.12.10},
Url = {http://repository.tue.nl/posters/801419.pdf}
......@@ -355,11 +331,9 @@
Author = {Traa, Willeke A. and \noopsort{Turnhout}van Turnhout, Mark C. and Nelissen, Jules L. and Strijkers, Gustav J. and Bader, Dan L. and Oomens, Cees W.J.},
Journal = {Clinical Biomechanics},
Year = {2019},
Month = {March},
Pages = {153--160},
Volume = {63},
Abstract = {Background
Deep tissue injury is a type of pressure ulcer which originates subcutaneously due to sustained mechanical loading. The relationship between mechanical compression and damage development has been extensively studied in 2D. However, recent studies have suggested that damage develops beyond the site of indentation. The objective of this study was to compare mechanical loading conditions to the associated damage in 3D.
Methods
......@@ -374,6 +348,5 @@ Individual tolerance is an important factor when considering the mechanical load
Pmid = {30897463},
Timestamp = {2019.03.02}
}
@comment{jabref-meta: databaseType:bibtex;}
@Comment{jabref-meta: databaseType:bibtex;}
......@@ -46,7 +46,7 @@ BasilLab is released under a \href{https://www.gnu.org/licenses/gpl-3.0.en.html}
Note that there is ABSOLUTELY NO WARRANTY; not even for FITNESS FOR A PARTICULAR PURPOSE, and certainly not for MERCHANTABILITY.\warning\\
\noindent BasilLab is available from the \href{mailto:m.c.v.turnhout@tue.nl}{author}. It is maintained in a Git repository that is hosted at \href{https://gitlab.tue.nl/STEM/basillab}{http://\-mategit.wfw.wtb.tue.nl/STEM/basillab}, where you can find the \href{https://gitlab.tue.nl/STEM/basillab/tree/master}{latest version}. The \href{mailto:m.c.v.turnhout@tue.nl}{author} welcomes your contributions.
\noindent BasilLab is available from the \href{mailto:m.c.v.turnhout@tue.nl}{author}. It is maintained in a Git repository that is hosted at \href{https://gitlab.tue.nl/STEM/basillab}{https://gitlab.tue.nl/STEM/basillab}, where you can find the \href{https://gitlab.tue.nl/STEM/basillab/tree/master}{latest version}. The \href{mailto:m.c.v.turnhout@tue.nl}{author} welcomes your contributions.
\section{Honour due and `backward compatibility'}
......
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