<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.journaloftissueviability.com/?rss=yes"><title>Journal of Tissue Viability</title><description>Journal of Tissue Viability RSS feed: Current Issue. The  Journal of Tissue Viability  is the official publication of the  Tissue Viability 
Society  and is a  quarterly journal concerned with all aspects of the occurrence and treatment of wounds, ulcers and pressure 
sores including patient care, pain, nutrition, wound healing, research, prevention, mobility, social problems and management.
The Journal 
particularly encourages papers covering skin and skin wounds but will consider articles that discuss injury in any tissue.  Articles 
that stress the multi-professional nature of tissue viability are especially welcome.  We seek to encourage new authors as well as well-established 
contributors to the field - one aim of the journal is to enable all participants in tissue viability to share information with colleagues.</description><link>http://www.journaloftissueviability.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2009 Tissue Viability Society. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Tissue Viability</prism:publicationName><prism:issn>0965-206X</prism:issn><prism:volume>19</prism:volume><prism:number>2</prism:number><prism:publicationDate>May 2010</prism:publicationDate><prism:copyright> © 2009 Tissue Viability Society. Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.journaloftissueviability.com/article/PIIS0965206X0900059X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journaloftissueviability.com/article/PIIS0965206X09000540/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journaloftissueviability.com/article/PIIS0965206X09000552/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journaloftissueviability.com/article/PIIS0965206X09000539/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journaloftissueviability.com/article/PIIS0965206X09000618/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journaloftissueviability.com/article/PIIS0965206X09000503/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.journaloftissueviability.com/article/PIIS0965206X0900059X/abstract?rss=yes"><title>Bioengineering research in tissue viability</title><link>http://www.journaloftissueviability.com/article/PIIS0965206X0900059X/abstract?rss=yes</link><description>We are pleased to present this Special Issue on Bioengineering in Tissue Viability to the readership of the journal. Challenges in preventing and treating chronic wounds create one of the most important areas of unsolved medical problems, impacting the life of many, decreasing the quality of life of many others, and costing billions in each country. Chronic wounds affect diverse but at the same time large patient populations, such as those with neuromuscular injuries and diseases, diabetes or geriatric patients. Considering that the size of the elderly population is continuously increasing, and that the number of newly diagnosed diabetes cases is climbing up throughout the Western world, the scale of tissue viability related problems is projected to grow even greater in the near future. Unfortunately, until recently, wounds in soft tissues received relatively little attention from the bioengineering research community.</description><dc:title>Bioengineering research in tissue viability</dc:title><dc:creator>Amit Gefen, Laura E. Edsberg</dc:creator><dc:identifier>10.1016/j.jtv.2009.11.007</dc:identifier><dc:source>Journal of Tissue Viability 19, 2 (2010)</dc:source><dc:date>2009-12-11</dc:date><prism:publicationName>Journal of Tissue Viability</prism:publicationName><prism:publicationDate>2009-12-11</prism:publicationDate><prism:volume>19</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0965-206X(10)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>33</prism:startingPage><prism:endingPage>34</prism:endingPage></item><item rdf:about="http://www.journaloftissueviability.com/article/PIIS0965206X09000540/abstract?rss=yes"><title>The importance of internal strain as opposed to interface pressure in the prevention of pressure related deep tissue injury</title><link>http://www.journaloftissueviability.com/article/PIIS0965206X09000540/abstract?rss=yes</link><description>Abstract: For pressure ulcer prevention an ambitious goal would be the establishment of a mechanical threshold for tissue damage. In the past, several researchers have sought to establish such a threshold often involving the loading time. However, they have not resulted in a unique reliable value that could be used in practice. This limitation is probably due to the focus on interface pressure. The objective of this paper is to clarify to an audience with no conventional background in mechanics, why interface pressure is not the appropriate parameter to define a damage threshold, whereas internal local deformations (strains) may prove more suitable. The paper reveals that it may be possible to identify a damage threshold for healthy skeletal muscle tissue based on local internal deformations.</description><dc:title>The importance of internal strain as opposed to interface pressure in the prevention of pressure related deep tissue injury</dc:title><dc:creator>C.W.J. Oomens, Sandra Loerakker, D.L. Bader</dc:creator><dc:identifier>10.1016/j.jtv.2009.11.002</dc:identifier><dc:source>Journal of Tissue Viability 19, 2 (2010)</dc:source><dc:date>2009-12-14</dc:date><prism:publicationName>Journal of Tissue Viability</prism:publicationName><prism:publicationDate>2009-12-14</prism:publicationDate><prism:volume>19</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0965-206X(10)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>35</prism:startingPage><prism:endingPage>42</prism:endingPage></item><item rdf:about="http://www.journaloftissueviability.com/article/PIIS0965206X09000552/abstract?rss=yes"><title>Computer simulations from a finite-element model for wound contraction and closure</title><link>http://www.journaloftissueviability.com/article/PIIS0965206X09000552/abstract?rss=yes</link><description>Abstract: Some implications from a simplified finite-element model are given in this study. The model takes into account the sequential steps of wound contraction, angiogenesis and wound closure. An innovation in the present study is the combination of these partially overlapping processes, yielding novel insights into the process of wound healing, such as geometry related influences, and could be used to investigate the influence of local injection of hormones that stimulate partial processes occurring during wound healing. These insights can be used to improve wound-healing treatments. The model consists of nonlinearly coupled diffusion–reaction and visco-elastic equations, in which transport, production and decay of oxygen, growth factors and various cell types. The present paper provides results of the healing of deep wounds under several regimes of endothelial and epithelial cell migration, and the results are interpreted in a biological sense.</description><dc:title>Computer simulations from a finite-element model for wound contraction and closure</dc:title><dc:creator>F.J. Vermolen, E. Javierre</dc:creator><dc:identifier>10.1016/j.jtv.2009.11.003</dc:identifier><dc:source>Journal of Tissue Viability 19, 2 (2010)</dc:source><dc:date>2009-12-21</dc:date><prism:publicationName>Journal of Tissue Viability</prism:publicationName><prism:publicationDate>2009-12-21</prism:publicationDate><prism:volume>19</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0965-206X(10)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>43</prism:startingPage><prism:endingPage>53</prism:endingPage></item><item rdf:about="http://www.journaloftissueviability.com/article/PIIS0965206X09000539/abstract?rss=yes"><title>Novel antibiotic-eluting wound dressings: An in vitro study and engineering aspects in the dressing's design</title><link>http://www.journaloftissueviability.com/article/PIIS0965206X09000539/abstract?rss=yes</link><description>Abstract: Wound dressings aim to restore the milieu required for skin regeneration by protecting the wound from environmental threats, including penetration of bacteria, and by maintaining a moist healing environment. A wide variety of wound dressing products targeting various types of wounds and different aspects of the wound healing process are currently available on the market. Ideally, a dressing should be easy to apply and remove, and its design should meet both physical and mechanical requirements; namely water absorbance and transmission rate, handleability and strength. In this article, our novel biodegradable antibiotic-eluting wound dressings are described and the engineering aspects in the design are emphasized. These unique new wound dressings are based on a polyglyconate mesh, coated with a porous Poly(dl-lactic-co-glycolic acid) matrix. They demonstrated excellent mechanical and physical properties and desired release profiles of antibiotic drugs which enable bacterial inhibition. Hence, a new generation of wound dressings is now emerging with clear benefits. These include better protection against infection and reducing the need for frequent dressing changing.</description><dc:title>Novel antibiotic-eluting wound dressings: An in vitro study and engineering aspects in the dressing's design</dc:title><dc:creator>Jonathan J. Elsner, Meital Zilberman</dc:creator><dc:identifier>10.1016/j.jtv.2009.11.001</dc:identifier><dc:source>Journal of Tissue Viability 19, 2 (2010)</dc:source><dc:date>2009-12-07</dc:date><prism:publicationName>Journal of Tissue Viability</prism:publicationName><prism:publicationDate>2009-12-07</prism:publicationDate><prism:volume>19</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0965-206X(10)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>54</prism:startingPage><prism:endingPage>66</prism:endingPage></item><item rdf:about="http://www.journaloftissueviability.com/article/PIIS0965206X09000618/abstract?rss=yes"><title>Deep tissue injury rat model for pressure ulcer research on spinal cord injury</title><link>http://www.journaloftissueviability.com/article/PIIS0965206X09000618/abstract?rss=yes</link><description>Abstract: Many rat/mouse pressure ulcer (PU) models have been developed to test different hypotheses to gain deeper understanding of various causative risk factors, the progress of PUs, and assessing effectiveness of potential treatment modalities. The recently emphasized deep tissue injury (DTI) mechanism for PU formation has received increased attention and several studies reported findings on newly developed DTI animal models. However, concerns exist for the clinical relevance and validity of these models, especially when the majority of the reported rat PU/DTI models were not built upon SCI animals and many of the DTI research did not simulate well the clinical observation. In this study, we propose a rat PU and DTI model which is more clinically relevant by including chronic SCI condition into the rat PU model and to simulate the role of bony prominence in DTI formation by using an implant on the bone–tissue interface. Histological data and imaging findings confirmed that the condition of chronic SCI had significant effect on pressure induced tissue injury in a rat PU model and the including a simulated bony prominence in rat DTI model resulted in significantly greater injury in deep muscle tissue. Further integration of the SCI condition and the simulated bony prominence would result a rat PU/DTI model which can simulate even more accurately the clinical phenomenon and yield more clinically relevant findings.</description><dc:title>Deep tissue injury rat model for pressure ulcer research on spinal cord injury</dc:title><dc:creator>Fang Lin, Atek Pandya, Andrew Cichowski, Mauli Modi, Briana Reprogle, Dongkeun Lee, Norio Kadono, Mohsen Makhsous</dc:creator><dc:identifier>10.1016/j.jtv.2009.11.009</dc:identifier><dc:source>Journal of Tissue Viability 19, 2 (2010)</dc:source><dc:date>2009-12-14</dc:date><prism:publicationName>Journal of Tissue Viability</prism:publicationName><prism:publicationDate>2009-12-14</prism:publicationDate><prism:volume>19</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0965-206X(10)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>67</prism:startingPage><prism:endingPage>76</prism:endingPage></item><item rdf:about="http://www.journaloftissueviability.com/article/PIIS0965206X09000503/abstract?rss=yes"><title>Candidate biomarkers for deep tissue damage from molecular biological and biochemical aspects</title><link>http://www.journaloftissueviability.com/article/PIIS0965206X09000503/abstract?rss=yes</link><description>Abstract: Suspected deep tissue injury (DTI) is a new category of pressure ulcer (PU), and defined as an ulcer that developed from a deep tissue (subcutaneous tissue) region and deteriorates towards the superficial skin. DTI is a serious clinical problem because it cannot be detected at an early stage and rapidly deteriorates to a deep PU. Consequently, there is a requirement for the identification of novel biomarkers to detect damage to the deep tissue including deep muscle tissue. For this purpose, it is essential to understand the molecular and cellular mechanisms of DTI formation and deterioration. This article reviews the recent progress in studies on the hypoxia-related mechanisms of DTI, and introduces our attempts to establish novel biomarkers for detecting deep muscle damage. Hypoxia-inducible factor 1 α subunit (HIF1-α) is a widely used marker for hypoxic conditions. We detected increased expression and localization of HIF1-α in the deep muscle tissue of PU model rats, indicating that HIF1α is a key molecule in DTI and a valuable biomarker for hypoxia in DTI in the research field. From the biochemical aspect, we focused on creatine phosphokinase (CPK). CPK is an intracellular enzyme related to energy metabolism, and its level in serum has been extensively used as a diagnostic marker for muscle injury. We attempted to estimate muscle injury from the CPK levels in exudates, which can be collected non-invasively and reflect the microenvironmental conditions. Our results using PU model rats suggested that exudate CPK could be a more sensitive biomarker than serum CPK for deep muscle tissue injury, and could be applicable for clinical diagnosis of DTI.</description><dc:title>Candidate biomarkers for deep tissue damage from molecular biological and biochemical aspects</dc:title><dc:creator>Takeo Minematsu, Gojiro Nakagami, Yunita Sari, Tomoko Akase, Junko Sugama, Takashi Nagase, Hiromi Sanada</dc:creator><dc:identifier>10.1016/j.jtv.2009.10.004</dc:identifier><dc:source>Journal of Tissue Viability 19, 2 (2010)</dc:source><dc:date>2010-03-11</dc:date><prism:publicationName>Journal of Tissue Viability</prism:publicationName><prism:publicationDate>2010-03-11</prism:publicationDate><prism:volume>19</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0965-206X(10)X0003-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>77</prism:startingPage><prism:endingPage>83</prism:endingPage></item></rdf:RDF>