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<modsCollection>

<note type="usage">
These are references to articles on fascia and collagen motivating the
conceptual model of "adhesions". They draw on research on the increase of
cross-linkages with aging, adaptation of tissue to applied stress, and
cumulative affects of microtrauma.
</note>


<mods ID="Langevin2007">
    <titleInfo>
        <title>Pathophysiological model for chronic low back pain
        integrating connective tissue and nervous system mechanisms</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Helene</namePart>
        <namePart type="given">M</namePart>
        <namePart type="family">Langevin</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">Karen</namePart>
        <namePart type="given">J</namePart>
        <namePart type="family">Sherman</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>2007-01-01</dateIssued>
        <publisher>Churchill Livingstone,</publisher>
    </originInfo>
    <relatedItem type="host">
        <titleInfo>
            <title>Medical hypotheses</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
       Although chronic low back pain (cLBP) is increasingly recognized as
       a complex syndrome with multifactorial etiology, the pathogenic
       mechanisms leading to the development of chronic pain in this
       condition remain poorly understood. This article presents a new,
       testable pathophysiological model integrating connective tissue
       plasticity mechanisms with several well-developed areas of research
       on cLBP (pain psychology, postural control, neuroplasticity). We
       hypothesize that pain-related fear leads to a cycle of decreased
       movement, connective tissue remodeling, inflammation, nervous system
       sensitization and further decreased mobility. In addition to
       providing a new, testable framework for future mechanistic studies
       of cLBP, the integration of connective tissue and nervous system
       plasticity into the model will potentially illuminate the mechanisms
       of a variety of treatments that may reverse these abnormalities by
       applying mechanical forces to soft tissues (e.g. physical therapy,
       massage, chiropractic manipulation, acupuncture), by changing
       specific movement patterns (e.g. movement therapies, yoga) or more
       generally by increasing activity levels (e.g. recreational
       exercise). Non-invasive measures of connective tissue remodeling may
       eventually become important tools to evaluate and follow patients
       with cLBP in research and clinical practice. An integrative
       mechanistic model incorporating behavioral and structural aspects of
       cLBP will strengthen the rationale for a multidisciplinary treatment
       approach including direct mechanical tissue stimulation, movement
       reeducation, psychosocial intervention and pharmacological treatment
       to address this common and debilitating condition.
    </abstract>
    <identifier type="issn">0306-9877</identifier>
    <identifier type="citekey">Langevin2007</identifier>
    <identifier type="doi">10.1016/j.mehy.2006.06.033</identifier>
    <location>
        <url>http://linkinghub.elsevier.com/retrieve/pii/S0306987706004919</url>
    </location>
    <part>
        <date>2007-01-01</date>
        <detail type="volume"><number>68</number></detail>
        <detail type="issue"><number>1</number></detail>
        <extent unit="page">
            <start>74</start>
            <end>80</end>
        </extent>
    </part>
</mods>

<mods ID="Buehler2006">
    <titleInfo>
        <title>Nature designs tough collagen</title>
        <subTitle>Explaining the nanostructure of collagen fibrils</subTitle>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Markus</namePart>
        <namePart type="given">J</namePart>
        <namePart type="family">Buehler</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>2006-08-15</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Proceedings of the National Academy of Sciences</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
       Collagen is a protein material with superior mechanical properties.
       It consists of collagen fibrils composed of a staggered array of
       ultra-long tropocollagen (TC) molecules. Theoretical and molecular
       modeling suggests that this natural design of collagen fibrils
       maximizes the strength and provides large energy dissipation during
       deformation, thus creating a tough and robust material. We find that
       the mechanics of collagen fibrils can be understood quantitatively
       in terms of two critical molecular length scales {chi}S and {chi}R
       that characterize when (i) deformation changes from homogeneous
       intermolecular shear to propagation of slip pulses and when (ii)
       covalent bonds within TC molecules begin to fracture, leading to
       brittle-like failure. The ratio {chi}S/{chi}R indicates which
       mechanism dominates deformation. Our modeling rigorously links the
       chemical properties of individual TC molecules to the macroscopic
       mechanical response of fibrils. The results help to explain why
       collagen fibers found in nature consist of TC molecules with lengths
       in the proximity of 300 nm and advance the understanding how
       collagen diseases that change intermolecular adhesion properties
       influence mechanical properties.
    </abstract>
    <note>10.1073/pnas.0603216103</note>
    <identifier type="citekey">Buehler2006</identifier>
    <location>
        <url>http://www.pnas.org/cgi/content/abstract/103/33/12285</url>
    </location>
    <part>
        <date>2006-8-15</date>
        <detail type="volume"><number>103</number></detail>
        <detail type="issue"><number>33</number></detail>
        <extent unit="page">
            <start>12285</start>
            <end>12290</end>
        </extent>
    </part>
</mods>

<mods ID="Schleip2005">
    <titleInfo>
        <title>Active fascial contractility</title>
        <subTitle>Fascia may be able to contract in a smooth muscle-like
        manner and thereby influence musculoskeletal dynamics</subTitle>
    </titleInfo>
    <name type="personal">
        <namePart type="given">R</namePart>
        <namePart type="family">Schleip</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">W</namePart>
        <namePart type="family">Klingler</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">F</namePart>
        <namePart type="family">Lehmann-Horn</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <typeOfResource>text</typeOfResource>
    <originInfo>
        <dateIssued>2005-01-01</dateIssued>
        <publisher>Churchill Livingstone</publisher>
    </originInfo>
    <abstract>
      Dense connective tissue sheets, commonly known as fascia, play an
      important role as force transmitters in human posture and movement
      regulation. Fascia is usually seen as having a passive role,
      transmitting mechanical tension which is generated by muscle activity
      or external forces. However, there is some evidence to suggest that
      fascia may be able to actively contract in a smooth muscle-like
      manner and consequently influence musculoskeletal dynamics. General
      support for this hypothesis came with the discovery of contractile
      cells in fascia, from theoretical reflections on the biological
      advantages of such a capacity, and from the existence of pathological
      fascial contractures. Further evidence to support this hypothesis is
      offered by in vitro studies with fascia which have been reported in
      the literature: the biomechanical demonstration of an autonomous
      contraction of the human lumbar fascia, and the pharmacological
      induction of temporary contractions in normal fascia from rats. If
      verified by future research, the existence of an active fascial
      contractility could have interesting implications for the
      understanding of musculoskeletal pathologies with an increased or
      decreased myofascial tonus. It may also offer new insights and a
      deeper understanding of treatments directed at fascia, such as manual
      myofascial release therapies or acupuncture. Further research to test
      this hypothesis is suggested.
    </abstract>
    <relatedItem type="host">
        <titleInfo>
            <title>Medical Hypotheses</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <identifier type="issn">0306-9877</identifier>
    <identifier type="citekey">Schleip2005</identifier>
    <location>
        <url>http://linkinghub.elsevier.com/retrieve/pii/S0306987705001489</url>
    </location>
    <part>
        <date>2005-01-01</date>
        <detail type="volume"><number>65</number></detail>
        <detail type="issue"><number>2</number></detail>
        <extent unit="page">
            <start>273</start>
            <end>277</end>
        </extent>
    </part>
    <identifier type="doi">10.1016/j.mehy.2005.03.005</identifier>
</mods>

<mods ID="Chaitow2003">
    <titleInfo>
        <title>Neuromuscular Techniques in Orthopedics</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Leon</namePart>
        <namePart type="family">Chaitow</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">Judith</namePart>
        <namePart type="family">DeLany</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>2003-03</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Techniques in Orthopaedics</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
      Alternative medicine offers approaches to health care that are
      complementary to or integrative with conventional medicine. Many
      possibilities have emerged from this background, of methods that can
      enhance medical care, such as acupuncture and lymphatic drainage
      techniques. Another method is neuromuscular therapy, which considers
      both local or global causes of pain and dysfunction, as well as
      perpetuating factors that impact the musculoskeletal system.
      Neuromuscular therapy aims specifically to alter the ground substance
      of connective tissue, to deactivate myofascial trigger points and
      reduce ischemia, and to assess and beneficially modify postural
      alignment, musculoskeletal dysfunction, and neural entrapment.
      Additionally, nutritional awareness and emotional distress are
      considered in an effort to alter chronic pain and myofascial
      dysfunction.
    </abstract>
    <identifier type="citekey">Chaitow2003</identifier>
    <identifier type="url">http://tinyurl.com/2se92k</identifier>
    <part>
        <date>2003-03</date>
        <detail type="volume"><number>18</number></detail>
        <detail type="issue"><number>1</number></detail>
        <extent unit="page">
            <start>74</start>
            <end>86</end>
        </extent>
    </part>
</mods>

<mods ID="OConnell2003">
    <titleInfo>
        <title>Bioelectric Responsiveness of Fascia</title>
        <subTitle>A Model for Understanding the Effects of Manipulation</subTitle>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Judith</namePart>
        <namePart type="given">A</namePart>
        <namePart type="family">O'Connell</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>2003-03</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Techniques in Orthopaedics</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
      Embryologically, the largest mesodermal derivative is connective
      tissue encompassing blood, cartilage, bone, and connective tissue
      proper. Collagen is a major component of connective tissue proper and
      more specifically white fibrous tissue. Fascia, the largest component
      of white fibrous tissue, contains linear sheets of collagen found in
      superficial, deep, and subserous layers. Collagen is piezoelectric,
      functioning as a transducer of mechanical and electrical energy.
      Electrical impulses are generated in the collagen by compressive and
      distraction forces within the musculoskeletal system. These impulses
      trigger a cascade of cellular, biomechanical, neural, and
      extracellular events as the body adapts to external stress. In
      response to internal stress, components of the extracellular fluid
      change in polarity and charge affecting fascial motion. This somatic
      dysfunction, whether caused by internal or external stress, is
      identified as tenderness, asymmetry, altered motion, and tissue
      texture changes. Somatic dysfunction is also caused by visceral
      somatic relationships mediated at the level of the spinal cord.
      Specific patterns of somatic dysfunction in the paraspinal connective
      tissue are related to specific organs and act as diagnostic markers.
      Osteopathic manipulative treatment is a manually applied procedure
      used to treat somatic dysfunction. Through the application of
      compressive and distraction forces, the physician identifies altered
      patterns of motion in the fascia. Physicians trained in osteopathic
      manipulative techniques are able to normalize the somatic dysfunction
      and in so doing encourage healing. Physicians able to integrate
      osteopathic manipulative treatment into standard medical and surgical
      care have an advantage in meeting the needs of their patients.
    </abstract>
    <identifier type="citekey">OConnell2003</identifier>
    <identifier type="url">http://tinyurl.com/3b6xcb</identifier>
    <part>
        <date>2003-03</date>
        <detail type="volume"><number>18</number></detail>
        <detail type="issue"><number>1</number></detail>
        <extent unit="page">
            <start>67</start>
            <end>73</end>
        </extent>
    </part>
</mods>

<mods ID="Mueller2002">
    <titleInfo>
        <title>Tissue Adaptation to Physical Stress</title>
        <subTitle>A Proposed "Physical Stress Theory" to Guide Physical
        Therapist Practice, Education, and Research</subTitle>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Michael</namePart>
        <namePart type="given">J</namePart>
        <namePart type="family">Mueller</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">Katrina</namePart>
        <namePart type="given">S</namePart>
        <namePart type="family">Maluf</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>2002-04-01</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Physical Therapy</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
      The purpose of this perspective is to present a general theory--the
      Physical Stress Theory (PST). The basic premise of the PST is that
      changes in the relative level of physical stress cause a predictable
      adaptive response in all biological tissue. Specific thresholds
      define the upper and lower stress levels for each characteristic
      tissue response. Qualitatively, the 5 tissue responses to physical
      stress are decreased stress tolerance (eg, atrophy), maintenance,
      increased stress tolerance (eg, hypertrophy), injury, and death.
      Fundamental principles of tissue adaptation to physical stress are
      described that, in the authors' opinion, can be used to help guide
      physical therapy practice, education, and research. The description
      of fundamental principles is followed by a review of selected
      literature describing adaptation to physical stress for each of the 4
      main organ systems described in the Guide to Physical Therapist
      Practice (ie, cardiovascular/pulmonary, integumentary,
      musculoskeletal, neuromuscular). Limitations and implications of the
      PST for practice, research, and education are presented.
    </abstract>
    <identifier type="citekey">Mueller2002</identifier>
    <location>
        <url>http://www.ptjournal.org/cgi/content/abstract/82/4/383</url>
    </location>
    <part>
        <date>2002-4-1</date>
        <detail type="volume"><number>82</number></detail>
        <detail type="issue"><number>4</number></detail>
        <extent unit="page">
            <start>383</start>
            <end>403</end>
        </extent>
    </part>
</mods>

<mods ID="Bailey2001">
    <titleInfo>
        <title>Molecular mechanisms of ageing in connective tissues</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Allen</namePart>
        <namePart type="given">J</namePart>
        <namePart type="family">Bailey</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>2001-05-31</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Mechanisms of Ageing and Development</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
      The outward manifestations of tissue ageing occurring in the elderly
      primarily involve the two major structural proteins of the body,
      collagen and elastin. The changes in these proteins are associated
      with intermolecular cross-linking and side-chain modifications.
      Cross-linking involves two different mechanisms, a precise enzymic
      process during development and maturation, and a subsequent
      non-enzymic adventitious reaction with glucose during ageing. The
      latter glycation reactions are the major cause of tissue dysfunction
      in the elderly due to cross-linking, which stiffens the tissues, and
      to side-chain modification, which alters normal cell-matrix
      interactions. Photoageing by UV involves two competing reactions,
      chain cleavage and cross-linking, the former predominating on
      long-term exposure. The molecular mechanisms involved are gradually
      being unravelled and will lead to the development of inhibitors of
      these deleterious effects of ageing.
    </abstract>
    <identifier type="citekey">Bailey2001</identifier>
    <identifier type="doi">10.1016/S0047-6374(01)00225-1</identifier>
    <part>
        <date>2001-05-31</date>
        <detail type="volume"><number>122</number></detail>
        <detail type="issue"><number>7</number></detail>
        <extent unit="page">
            <start>735</start>
            <end>755</end>
        </extent>
    </part>
</mods>

<mods ID="Frost2000">
    <titleInfo>
        <title>Why the ISMNI and the Utah paradigm? Their role in skeletal
        and extraskeletal disorders.</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">H</namePart>
        <namePart type="given">M</namePart>
        <namePart type="family">Frost</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>2000-Sep</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>J Musculoskelet Neuronal Interact</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
        <identifier type="issn">1108-7161</identifier>
        <part>
            <date>2000-Sep</date>
            <detail type="volume"><number>1</number></detail>
            <detail type="issue"><number>1</number></detail>
            <extent unit="page">
                <start>5</start>
                <end>5</end>
            </extent>
        </part>
    </relatedItem>
    <abstract>
      Besides bringing problems, aging can let the mind's eye see more
      clearly than before, and it can let us express ourselves better. As
      age, experience and common sense examine today's skeletal medicine
      and surgery two questions keep popping up: A) How did we fail?; B)
      How to make it better? The Utah paradigm of skeletal physiology and
      the seminal ISMNI offer some answers, but exploiting them faces
      problems.
    </abstract>
    <identifier type="citekey">Frost2000</identifier>
    <identifier type="url">http://www.ismni.org/jmni/pdf/1/frost.pdf</identifier>
</mods>

<mods ID="Kraushaar1999">
    <titleInfo>
        <title>
            Current Concepts Review - Tendinosis of the Elbow (Tennis
            Elbow). Clinical Features and Findings of Histological,
            Immunohistochemical, and Electron Microscopy Studies
       </title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Barry</namePart>
        <namePart type="given">S</namePart>
        <namePart type="family">Kraushaar</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">Robert</namePart>
        <namePart type="given">P</namePart>
        <namePart type="family">Nirschl</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>1999-02-01</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Journal of Bone and Joint Surgery</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <identifier type="citekey">KRAUSHAAR1999</identifier>
    <location>
        <url>http://www.ejbjs.org/cgi/content/full/81/2/259</url>
    </location>
    <part>
        <date>1999-2-1</date>
        <detail type="volume"><number>81</number></detail>
        <detail type="issue"><number>2</number></detail>
        <extent unit="page">
            <start>259</start>
            <end>78</end>
        </extent>
    </part>
</mods>

<mods ID="Bailey1998">
    <titleInfo>
        <title>Mechanisms of maturation and ageing of collagen</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Allen</namePart>
        <namePart type="given">J</namePart>
        <namePart type="family">Bailey</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">Robert</namePart>
        <namePart type="given">Gorden</namePart>
        <namePart type="family">Paul</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">Lynda</namePart>
        <namePart type="family">Knott</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>1998-12-01</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Mechanisms of Ageing and Development</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
      The outward manifestations of tissue ageing occurring in the elderly
      primarily involve the two major structural proteins of the body,
      collagen and elastin. The changes in these proteins are associated
      with intermolecular cross-linking and side-chain modifications.
      Cross-linking involves two different mechanisms, a precise enzymic
      process during development and maturation, and a subsequent
      non-enzymic adventitious reaction with glucose during ageing. The
      latter glycation reactions are the major cause of tissue dysfunction
      in the elderly due to cross-linking, which stiffens the tissues, and
      to side-chain modification, which alters normal cell-matrix
      interactions. Photoageing by UV involves two competing reactions,
      chain cleavage and cross-linking, the former predominating on
      long-term exposure. The molecular mechanisms involved are gradually
      being unravelled and will lead to the development of inhibitors of
      these deleterious effects of ageing.
    </abstract>
    <identifier type="citekey">Bailey1998</identifier>
    <identifier type="doi">10.1016/S0047-6374(98)00119-5</identifier>
    <part>
        <date>1998-12-01</date>
        <detail type="volume"><number>106</number></detail>
        <detail type="issue"><number>1-2</number></detail>
        <extent unit="page">
            <start>1</start>
            <end>56</end>
        </extent>
    </part>
</mods>

<mods ID="Piez1997">
    <titleInfo>
        <title>History of extracellular matrix: a personal view.</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">K</namePart>
        <namePart type="given">A</namePart>
        <namePart type="family">Piez</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>1997-Aug</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Matrix Biol</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
        <identifier type="issn">0945-053X</identifier>
        <location>
            <url></url>
        </location>
        <part>
            <date>1997-Aug</date>
            <detail type="volume"><number>16</number></detail>
            <detail type="issue"><number>3</number></detail>
            <extent unit="page">
                <start>85</start>
                <end>85</end>
            </extent>
        </part>
    </relatedItem>
    <abstract>
      Before the early 1800s, the "fibers" of connective tissue were
      thought to be the basis of life, which arose by spontaneous
      generation. With the discovery of cells in connective tissue, the
      cellular theory became accepted as the basis of life in about 1850.
      Material outside cells, but presumably made by cells, was recognized
      as the extracellular matrix. In the period from 1930 to 1975, the
      components of extracellular matrix were characterized by physical
      chemical, chemical and cell biological methods. For the major
      collagen of skin, tendon and bone, the molecular and fibril
      structures were determined; the aldehydederived crosslinks were
      discovered; its polypeptide chains were sequenced; and its
      biosynthesis and degradation were defined. This collagen, now type I
      collagen, was shown to be one of many types. The events of this
      period are described from the author's perspective. Since 1975,
      molecular and cell biological techniques have shown that the
      extracellular matrix is not the passive residence of cells but is
      highly interactive and plays a major role in health and
      disease.
    </abstract>
    <identifier type="citekey">Piez1997</identifier>
    <identifier type="doi">10.1016/S0945-053X(97)90037-8</identifier>
</mods>

<mods ID="Viidik1996">
    <titleInfo>
        <title>Molecular mechanisms of ageing in connective tissues</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Andrus</namePart>
        <namePart type="family">Viidik</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">Hanne</namePart>
        <namePart type="given">Melgaard</namePart>
        <namePart type="family">Nielsen</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">Monika</namePart>
        <namePart type="family">Skalicky</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>1996-07-17</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Mechanisms of Ageing and Development</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
       Regular physical exercise has been shown to have a number of
       benefits compared with sedentary behaviour, such as delaying a
       number of aging changes and increasing the life expectancy but not
       the maximum lifespan. The purpose of this paper is to analyze the
       effects of physical exercise on the connective tissues of the body,
       especially systemic efects. We trained male Sprague-Dawley rats in a
       treadmill from the age of 5 months to 23 months. We analyzed the
       effects of training on tail tendons with respect to thermal
       stability of collagen and biomechanical properties of tendon
       bundles. Although tail tendons are attached to muscles, the are not
       weight-bearing as limb muscle tendons and can. therefore, be
       considered to be subjected mainly to systemic effects. The thermal
       stability of tail tendon collagen was significantly lower or
       'younger' for the trained group compared with the sedentary one. The
       biomechanical parameters were likewise 'younger' with respect to
       maximum stress, although considerably stiffer compared with a
       S-month-old base-line group. This suggests that there are several
       mechanisms, elicited by physical exercise, that act on the
       connective tissues. It can be concluded that life-long physical
       exercise has a beneficial influence on the connective tissues of the
       maturing and aging organism.
    </abstract>
    <identifier type="citekey">Viidik1996</identifier>
    <identifier type="doi">10.1016/0047-6374(96)01729-0</identifier>
    <part>
        <date>1996-07-17</date>
        <detail type="volume"><number>88</number></detail>
        <detail type="issue"><number>3</number></detail>
        <extent unit="page">
            <start>139</start>
            <end>148</end>
        </extent>
    </part>
</mods>

<mods ID="Davis1992">
    <titleInfo>
        <title>Management of Adhesions of the Scapulothoracic Interface</title>
        <subTitle>Scapulocostal Syndrome</subTitle>
    </titleInfo>
    <name type="personal">
        <namePart type="given">R</namePart>
        <namePart type="given">Vincent</namePart>
        <namePart type="family">Davis</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>1992-07-03</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Dynamic Chiropractic</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
       Following trauma to the soft tissue components of the scapulocostal
       interface, traumatic edema is formed. Irrespective of where it
       occurs in the body tissues, the presence of inflammatory edema is
       the antecedent to adhesion formation. This is a well-recognized
       clinicopathological process. If allowed to progress, such adhesions
       formation will inevitably result in loss of motion of the scapula on
       the respective thoracic cage. Such loss of motion then complements
       pathological progression of this lesion to one of complete adhesive
       myofascitis of the scapulothoracic interface. References paper by
       Michele and Eisenberg (1968, Arch. Phys. Med. Rehabil. 49:383) also
       referenced by Travell and Simons.
    </abstract>
    <identifier type="citekey">Davis1992</identifier>
    <location>
        <url>http://www.chiroweb.com/archives/10/14/23.html</url>
    </location>
    <part>
        <date>1992-07-03</date>
        <detail type="volume"><number>10</number></detail>
        <detail type="issue"><number>14</number></detail>
    </part>
</mods>

<mods ID="Threlkeld1992">
    <titleInfo>
        <title>The effects of manual therapy on connective tissue</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">A</namePart>
        <namePart type="given">J</namePart>
        <namePart type="family">Threlkeld</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>1992-12-01</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Physical Therapy</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
       The purpose of this manuscript is to examine the known and
       theoretical mechanical effects of therapeutic manual techniques on
       the connective tissue (CT) of joints and fasciae. Typical CT
       structures that could be influenced by manual techniques will be
       discussed. The behavior of CT under loading and the influence of
       immobilization on CT will be examined. The forces developed during
       manual techniques will be described, and their potential effects on
       the physical properties of CT will be discussed. Research priorities
       regarding the effects of manual therapy on CT will be
       outlined.</abstract>
    <identifier type="citekey">Threlkeld1992</identifier>
    <location>
        <url>http://www.ptjournal.org/cgi/content/abstract/72/12/893</url>
    </location>
    <part>
        <date>1992-12-1</date>
        <detail type="volume"><number>72</number></detail>
        <detail type="issue"><number>12</number></detail>
        <extent unit="page">
            <start>893</start>
            <end>902</end>
        </extent>
    </part>
</mods>


<mods ID="Frost1991a">
    <titleInfo>
        <title>Some ABC's of skeletal pathophysiology. 5. Microdamage physiology</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">H</namePart>
        <namePart type="family">Frost</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>1991-07-08</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Calcified Tissue International</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
      We are finding that structural microdamage plays important roles in
      many clinical problems, so this Editorial discusses it. Repeatedly
      loading and deloading wheels, bolts, beams, and crankshafts can cause
      microscopic cracks that increase in size and number as the loads and
      number of load-deload cycles increases. Eventually so little material
      remains undamaged that the structure suddenly breaks under an
      ordinary load. Engineers call that fatigue damage. All structural
      materials can develop it, including biologic structural materials of
      animals and plants. Named "microdamage" (MDx) in bone in 1963,
      several forms occur in woven and lamellar bone, hyaline cartilage,
      fibrocartilage, tendon, ligament, fascia, and teeth.
    </abstract>
    <note>10.1007/BF02556207</note>
    <identifier type="citekey">Frost1991a</identifier>
    <location>
        <url>http://dx.doi.org/10.1007/BF02556207</url>
    </location>
    <part>
        <date>1991-07-08</date>
        <detail type="volume"><number>49</number></detail>
        <detail type="issue"><number>4</number></detail>
        <extent unit="page">
            <start>229</start>
            <end>231</end>
        </extent>
    </part>
</mods>

<mods ID="Frost1991b">
    <titleInfo>
        <title>Some ABC's of skeletal pathophysiology. 6. The
        growth/modeling/remodeling distinction</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">H</namePart>
        <namePart type="family">Frost</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>1991-09-08</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Calcified Tissue International</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
    </relatedItem>
    <abstract>
      When malfunction of one biologic activity can cause clinical diseases
      while other activities function normally, we may consider that
      activity differs from others and try to find how to control it for
      medical needs. The new skeletal paradigm names five fundamental
      tissue-level activities: growth, modeling, remodeling, repair, and
      inflammation. Each has its own functions, mediator mechanisms, and
      responses to drugs, hormones, mechanics, and other agents. We discuss
      the first three activities.
    </abstract>
    <note>10.1007/BF02556248</note>
    <identifier type="citekey">Frost1991b</identifier>
    <location>
        <url>http://dx.doi.org/10.1007/BF02556248</url>
    </location>
    <part>
        <date>1991-09-08</date>
        <detail type="volume"><number>49</number></detail>
        <detail type="issue"><number>5</number></detail>
        <extent unit="page">
            <start>301</start>
            <end>302</end>
        </extent>
    </part>
</mods>

<mods ID="McGaw1983">
    <titleInfo>
        <title>A Role for Collagen Phagocytosis by Fibroblasts in Scar Remodeling</title>
        <subTitle>An Ultrastrutural Stereologic Study</subTitle>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Wm</namePart>
        <namePart type="given">Timothy</namePart>
        <namePart type="family">McGaw</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <name type="personal">
        <namePart type="given">A</namePart>
        <namePart type="given">Richard</namePart>
        <namePart type="given">Ten</namePart>
        <namePart type="family">Cate</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <abstract>
      A role for collagen phagocytosis and intracellular degradation by
      fibroblasts during remodeling activity has been suggested by studies
      on several connective tissues characterized by high rates of collagen
      turnover and remodeling. The possible importance of such activity in
      the normal remodeling of scar tissue has been studied by a
      quantitative ultrastructural stereologic measure of collagen
      phagocytosis by fibroblasts at various post-wounding intervals in
      mouse skin scars. The results demonstrate a correlation between the
      peak periods of such phagocytic activity and the interval during
      which collagen fiber reorientation across the scar appears to take
      place.
    </abstract>
    <originInfo>
        <dateIssued>1983-10</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>J Investig Dermatol</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
        <identifier type="issn">0022-202X</identifier>
    </relatedItem>
    <identifier type="citekey">McGaw1983</identifier>
    <location>
        <url>http://dx.doi.org/10.1111/1523-1747.ep12519983</url>
    </location>
    <part>
        <date>1983-10</date>
        <detail type="volume"><number>81</number></detail>
        <detail type="issue"><number>4</number></detail>
        <extent unit="page">
            <start>375</start>
            <end>378</end>
        </extent>
    </part>
</mods>

<mods ID="Nimni1983">
    <titleInfo>
        <title>Collagen: structure, function, and metabolism in normal and
        fibrotic tissues.</title>
    </titleInfo>
    <name type="personal">
        <namePart type="given">Marcel</namePart>
        <namePart type="given">E</namePart>
        <namePart type="family">Nimni</namePart>
        <role>
            <roleTerm authority="marcrelator" type="text">author</roleTerm>
        </role>
    </name>
    <originInfo>
        <dateIssued>1983-Aug</dateIssued>
    </originInfo>
    <typeOfResource>text</typeOfResource>
    <relatedItem type="host">
        <titleInfo>
            <title>Semin Arthritis Rheum</title>
        </titleInfo>
        <originInfo>
            <issuance>continuing</issuance>
        </originInfo>
        <genre authority="marc">periodical</genre>
        <genre>academic journal</genre>
        <identifier type="issn">0049-0172</identifier>
        <part>
            <date>1983-Aug</date>
            <detail type="volume"><number>13</number></detail>
            <detail type="issue"><number>1</number></detail>
            <extent unit="page">
                <start>1</start>
                <end>86</end>
            </extent>
        </part>
    </relatedItem>
    <abstract>
       Collagen is the single most abundant animal protein in mammals
       accounting for about 30% of all proteins. The collagen
       molecules, after being secreted by the cells, assemble into
       characteristic fibers responsible for the functional integrity
       of tissues such as bone, cartilage, skin, and tendon (Fig. 1).
       They contribute a structural framework to other tissues such as
       blood vessels and most organs. Crosslinks between adjacent
       molecules are a prerequisite for the collagen fibers to
       withstand the physical stresses to which they are exposed.
       Significant progress has been made towards understanding the
       functional groups on the molecules that are involved in the
       formation of such crosslinks, their nature, and location. A
       variety of human conditions, normal and pathologic, involve the
       ability of tissues to repair and regenerate their collagenous
       framework.
    </abstract>
    <identifier type="citekey">Nimni1983</identifier>
    <identifier type="doi">10.1016/0049-0172(83)90024-0</identifier>
</mods>

</modsCollection>

