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        <title>Editor's picks</title>
        <link>http://www.biomedcentral.com/bmcmed/</link>
        <description>The editor's pick of recent articles published by BMC Medicine</description>
        <dc:date>2013-05-17T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7015/11/133" />
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7015/11/131" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7015/11/130" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7015/11/129" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7015/11/128" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7015/11/127" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1741-7015/11/126" />
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/133">
        <title>Patient advocacy and dsm-5</title>
        <description>The revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM) provides a useful opportunity to revisit debates about the nature of psychiatric classification. An important debate concerns the involvement of mental health consumers in revisions of the classification. One perspective argues that psychiatric classification is a scientific process undertaken by scientific experts and that including consumers in the revision process is merely pandering to political correctness. A contrasting perspective is that psychiatric classification is a process driven by a range of different values and that the involvement of patients and patient advocates would enhance this process. Here we draw on our experiences with input from the public during the deliberations of the Obsessive Compulsive-Spectrum Disorders subworkgroup of DSM-5, to help make the argument that psychiatric classification does require reasoned debate on a range of different facts and values, and that it is appropriate for scientist experts to review their nosological recommendations in the light of rigorous consideration of patient experience and feedback.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/133</link>
                <dc:creator>Dan J Stein</dc:creator>
                <dc:creator>Katharine A Phillips</dc:creator>
                <dc:source>BMC Medicine 2013, 11:133</dc:source>
        <dc:date>2013-05-17T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
                            <dc:title>OCD diagnosis revised in DSM-5</dc:title>
                            <dc:description>&lt;p&gt;Dan Stein and Katharine Phillips comment on the patient experience that has helped define the psychiatric classification of obsessive-compulsive spectrum disorders (OCD) in DSM-5, and&amp;nbsp;describe the importance of taking patient opinion into account.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Medicine</prism:publicationName>
        <prism:issn>1741-7015</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>133</prism:startingPage>
        <prism:publicationDate>2013-05-17T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/132">
        <title>Personalized medicine in psychiatry: problems and promises</title>
        <description>The central theme of personalized medicine is the premise that an individual&apos;s unique physiologic characteristics play a significant role in both disease vulnerability and in response to specific therapies. The major goals of personalized medicine are therefore to predict an individual&apos;s susceptibility to developing an illness, achieve accurate diagnosis, and optimize the most efficient and favorable response to treatment. The goal of achieving personalized medicine in psychiatry is a laudable one, because its attainment should be associated with a marked reduction in morbidity and mortality. In this review, we summarize an illustrative selection of studies that are laying the foundation towards personalizing medicine in major depressive disorder, bipolar disorder, and schizophrenia. In addition, we present emerging applications that are likely to advance personalized medicine in psychiatry, with an emphasis on novel biomarkers and neuroimaging.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/132</link>
                <dc:creator>Uzoezi Ozomaro</dc:creator>
                <dc:creator>Claes Wahlestedt</dc:creator>
                <dc:creator>Charles B Nemeroff</dc:creator>
                <dc:source>BMC Medicine 2013, 11:132</dc:source>
        <dc:date>2013-05-16T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
                            <dc:title>Personalized medicine in psychiatry</dc:title>
                            <dc:description>&lt;p&gt;Charles Nemeroff and colleagues review the genetics, epigenetics, biomarkers, treatment response and environmental factors of mood disorders and schizophrenia, and describe the impact of neuroimaging on personalized medicine in psychiatry.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Medicine</prism:publicationName>
        <prism:issn>1741-7015</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>132</prism:startingPage>
        <prism:publicationDate>2013-05-16T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/131">
        <title>Depression as a risk factor for adverse outcomes in coronary heart disease</title>
        <description>Background:
Depression is firmly established as an independent predictor of mortality and cardiac morbidity in patients with coronary heart disease (CHD). However, it has been difficult to determine whether it is a causal risk factor, and whether treatment of depression can improve cardiac outcomes. In addition, research on biobehavioral mechanisms has not yet produced a definitive causal model of the relationship between depression and cardiac outcomes.DiscussionKey challenges in this line of research concern the measurement of depression, the definition and relevance of certain subtypes of depression, the temporal relationship between depression and CHD, underlying biobehavioral mechanisms, and depression treatment efficacy.SummaryThis article examines some of the methodological challenges that will have to be overcome in order to determine whether depression should be regarded as a key target of secondary prevention in CHD.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/131</link>
                <dc:creator>Kenneth E Freedland</dc:creator>
                <dc:creator>Robert M Carney</dc:creator>
                <dc:source>BMC Medicine 2013, 11:131</dc:source>
        <dc:date>2013-05-15T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
                            <dc:title>Depression: a risk factor for heart disease?</dc:title>
                            <dc:description>&lt;p&gt;Kenneth Freedland and Robert Carney argue that depression predicts coronary heart disease (CHD) but better methods are required to ascertain whether depression is a causal risk factor for CHD, which could help determine treatment strategies for CVD prevention.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Medicine</prism:publicationName>
        <prism:issn>1741-7015</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>131</prism:startingPage>
        <prism:publicationDate>2013-05-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/130">
        <title>Depression as a non-causal variable risk marker in coronary heart disease</title>
        <description>Background:
After decades of investigations, explanations for the prospective association between depression and coronary heart disease (CHD) are still incomplete.DiscussionDepression is often suggested to be causally related to CHD. Based on the available literature, we would rather argue that depression can best be regarded as a variable risk marker, that is, a variable that fluctuates together with mechanisms leading to poor cardiovascular fitness. Despite numerous efforts, no evidence is found that manipulation of depression alters cardiovascular outcomes - a key premise for determining causality. To explain the concept of a variable risk marker, we discuss several studies on the heterogeneity of depression suggesting that depression is particularly harmful for the course of cardiovascular disease when it appears to be a physiological consequence of the cardiovascular disease itself.SummaryWe conclude that instead of depression being a causal risk factor for CHD, the association between depression and CHD is likely confounded, at least by the cardiac disease itself.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/130</link>
                <dc:creator>Anna Meijer</dc:creator>
                <dc:creator>Marij Zuidersma</dc:creator>
                <dc:creator>Peter Jonge</dc:creator>
                <dc:source>BMC Medicine 2013, 11:130</dc:source>
        <dc:date>2013-05-15T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
                            <dc:title>Depression is non-causal in CHD</dc:title>
                            <dc:description>&lt;p&gt;Peter de Jonge and colleagues argue that, although there is a link between coronary heart disease (CHD) and depression, this association is confounded by heterogeneity, such that depression is a non-causal risk factor CHD.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Medicine</prism:publicationName>
        <prism:issn>1741-7015</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>130</prism:startingPage>
        <prism:publicationDate>2013-05-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/129">
        <title>Understanding the somatic consequences of depression: biological mechanisms and the role of depression symptom profile</title>
        <description>Depression is the most common psychiatric disorder worldwide. The burden of disease for depression goes beyond functioning and quality of life and extends to somatic health. Depression has been shown to subsequently increase the risk of, for example, cardiovascular, stroke, diabetes and obesity morbidity. These somatic consequences could partly be due to metabolic, immuno-inflammatory, autonomic and hypothalamic-pituitary-adrenal (HPA)-axis dysregulations which have been suggested to be more often present among depressed patients. Evidence linking depression to metabolic syndrome abnormalities indicates that depression is especially associated with its obesity-related components (for example, abdominal obesity and dyslipidemia). In addition, systemic inflammation and hyperactivity of the HPA-axis have been consistently observed among depressed patients. Slightly less consistent observations are for autonomic dysregulation among depressed patients. The heterogeneity of the depression concept seems to play a differentiating role: metabolic syndrome and inflammation up-regulations appear more specific to the atypical depression subtype, whereas hypercortisolemia appears more specific for melancholic depression. This review finishes with potential treatment implications for the downward spiral in which different depressive symptom profiles and biological dysregulations may impact on each other and interact with somatic health decline.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/129</link>
                <dc:creator>Brenda WJH Penninx</dc:creator>
                <dc:creator>Yuri Milaneschi</dc:creator>
                <dc:creator>Femke Lamers</dc:creator>
                <dc:creator>Nicole Vogelzangs</dc:creator>
                <dc:source>BMC Medicine 2013, 11:129</dc:source>
        <dc:date>2013-05-15T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7015-11-129</dc:identifier>
                            <dc:title>Biological dysregulation in depression</dc:title>
                            <dc:description>&lt;p&gt;Consequences of depression include somatic diseases, such as obesity and cardiovascular disease; Brenda Penninx and colleagues review the biological pathways and their dysregulation between depressive symptoms and somatic health, and describe the therapeutic implications.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Medicine</prism:publicationName>
        <prism:issn>1741-7015</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>129</prism:startingPage>
        <prism:publicationDate>2013-05-15T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/128">
        <title>The DSM-5: Hyperbole, Hope or Hypothesis?</title>
        <description>The furore preceding the release of the new edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) is in contrast to the incremental changes to several diagnostic categories, which are derived from new research since its predecessor&#8217;s birth in 1990. While many of these changes are indeed controversial, they do reflect the intrinsic ambiguity of the extant literature. Additionally, this may be a mirror of the frustration of the field&#8217;s limited progress, especially given the false hopes at the dawn of the &#8220;decade of the brain&#8221;. In the absence of a coherent pathophysiology, the DSM remains no more than a set of consensus based operationalized adjectives, albeit with some degree of reliability. It does not cleave nature at its joints, nor does it aim to, but neither does alternate systems. The largest problem with the DSM system is how it&#8217;s used; sometimes too loosely by clinicians, and too rigidly by regulators, insurers, lawyers and at times researchers, who afford it reference and deference disproportionate to its overt acknowledged limitations.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/128</link>
                <dc:creator>Michael Berk</dc:creator>
                <dc:source>BMC Medicine 2013, 11:128</dc:source>
        <dc:date>2013-05-14T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7015-11-128</dc:identifier>
                            <dc:title>Debating the DSM-5 criteria</dc:title>
                            <dc:description>&lt;p&gt;In an editorial to launch our article collection on Current Controversies in Psychiatry, Michael Berk discusses the debate on diagnostic categories in mental health based on the new edition of diagnostic criteria; the DSM-5.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Medicine</prism:publicationName>
        <prism:issn>1741-7015</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>128</prism:startingPage>
        <prism:publicationDate>2013-05-14T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/127">
        <title>Informing DSM-5: biological boundaries between bipolar I disorder, schizoaffective disorder, and schizophrenia</title>
        <description>Background:
The fifth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) opted to retain existing diagnostic boundaries between bipolar I disorder, schizoaffective disorder, and schizophrenia. The debate preceding this decision focused on understanding the biologic basis of these major mental illnesses. Evidence from genetics, neuroscience, and pharmacotherapeutics informed the DSM-5 development process. The following discussion will emphasize some of the key factors at the forefront of the debate.DiscussionFamily studies suggest a clear genetic link between bipolar I disorder, schizoaffective disorder, and schizophrenia. However, large-scale genome-wide association studies have not been successful in identifying susceptibility genes that make substantial etiological contributions. Boundaries between psychotic disorders are not further clarified by looking at brain morphology. The fact that symptoms of bipolar I disorder, but not schizophrenia, are often responsive to medications such as lithium and other anticonvulsants must be interpreted within a larger framework of biological research.SummaryFor DSM-5, existing nosological boundaries between bipolar I disorder and schizophrenia were retained and schizoaffective disorder preserved as an independent diagnosis since the biological data are not yet compelling enough to justify a move to a more neurodevelopmentally continuous model of psychosis.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/127</link>
                <dc:creator>Victoria E Cosgrove</dc:creator>
                <dc:creator>Trisha Suppes</dc:creator>
                <dc:source>BMC Medicine 2013, 11:127</dc:source>
        <dc:date>2013-05-14T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7015-11-127</dc:identifier>
                            <dc:title>DSM-5 retains psychosis diagnosis</dc:title>
                            <dc:description>&lt;p&gt;Victoria Cosgrove and Trisha Suppes agree that boundaries between the diagnosis of bipolar disorder I, schizophrenia and schizoaffective disorder are preserved in the DSM-5 criteria, as there is not yet enough data to justify a continuous model of psychosis.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Medicine</prism:publicationName>
        <prism:issn>1741-7015</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>127</prism:startingPage>
        <prism:publicationDate>2013-05-14T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/126">
        <title>Toward the future of psychiatric diagnosis: the seven pillars of RDoC</title>
        <description>Background:
Current diagnostic systems for mental disorders rely upon presenting signs and symptoms, with the result that current definitions do not adequately reflect relevant neurobiological and behavioral systems - impeding not only research on etiology and pathophysiology but also the development of new treatments.DiscussionThe National Institute of Mental Health began the Research Domain Criteria (RDoC) project in 2009 to develop a research classification system for mental disorders based upon dimensions of neurobiology and observable behavior. RDoC supports research to explicate fundamental biobehavioral dimensions that cut across current heterogeneous disorder categories. We summarize the rationale, status and long-term goals of RDoC, outline challenges in developing a research classification system (such as construct validity and a suitable process for updating the framework) and discuss seven distinct differences in conception and emphasis from current psychiatric nosologies.SummaryFuture diagnostic systems cannot reflect ongoing advances in genetics, neuroscience and cognitive science until a literature organized around these disciplines is available to inform the revision efforts. The goal of the RDoC project is to provide a framework for research to transform the approach to the nosology of mental disorders.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/126</link>
                <dc:creator>Bruce N Cuthbert</dc:creator>
                <dc:creator>Thomas R Insel</dc:creator>
                <dc:source>BMC Medicine 2013, 11:126</dc:source>
        <dc:date>2013-05-14T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7015-11-126</dc:identifier>
                            <dc:title>Mental disorder diagnosis based on RDoC?</dc:title>
                            <dc:description>&lt;p&gt;Bruce Cuthbert and Thomas Insel argue that future psychiatric nosologies will be informed by the Research Domain Criteria (RDoC) that is based on genetics, neuroscience and behavioural science, which will help achieve precision medicine for mental disorders.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Medicine</prism:publicationName>
        <prism:issn>1741-7015</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>126</prism:startingPage>
        <prism:publicationDate>2013-05-14T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/125">
        <title>Clinical classification in mental health at the cross-roads: which direction next?</title>
        <description>Background:
After 30 years of consensus-derived diagnostic categories in mental health, it is time to head in new directions. Those categories placed great emphasis on enhanced reliability and the capacity to identify them via standardized checklists. Although this enhanced epidemiology and health services planning, it failed to link broad diagnostic groupings to underlying pathophysiology or specific treatment response.DiscussionIt is time to adopt new goals that prioritize the validation of clinical entities and foster alternative strategies to support those goals. The value of new dimensions (notably clinical staging), that are both clinically relevant and directly related to emerging developmental and neurobiological research, is proposed. A strong emphasis on &#8216;reverse translation&#8217; (that is, working back from the clinic to the laboratory) underpins these novel approaches. However, it relies on using diagnostic groupings that already have strong evidence of links to specific risk factors or patterns of treatment response.SummaryThe strategies described abandon the historical divides between clinical neurology, psychiatry and psychology and adopt the promotion of pathways to illness models.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/125</link>
                <dc:creator>Ian B Hickie</dc:creator>
                <dc:creator>Jan Scott</dc:creator>
                <dc:creator>Daniel F Hermens</dc:creator>
                <dc:creator>Elizabeth M Scott</dc:creator>
                <dc:creator>Sharon L Naismith</dc:creator>
                <dc:creator>Adam J Guastella</dc:creator>
                <dc:creator>Nick Glozier</dc:creator>
                <dc:creator>Patrick D McGorry</dc:creator>
                <dc:source>BMC Medicine 2013, 11:125</dc:source>
        <dc:date>2013-05-14T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7015-11-125</dc:identifier>
                            <dc:title>Psychiatric diagnosis: time for change?</dc:title>
                            <dc:description>&lt;p&gt;There is much debate on DSM-5 diagnosis in mental health, and Ian Hickie and colleagues argue for the development of new approaches that identify pathways underlying the illnesses rather than using broad categories to describe psychiatric disorders.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Medicine</prism:publicationName>
        <prism:issn>1741-7015</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>125</prism:startingPage>
        <prism:publicationDate>2013-05-14T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7015/11/124">
        <title>The genomic landscape of chronic lymphocytic leukemia: clinical implications</title>
        <description>A precise understanding of the genomic and epigenomic features of chronic lymphocytic leukemia (CLL) may benefit the study of the disease&#8217;s staging and treatment. While recent reports have shed some light on these aspects, several challenges need to be addressed before translating this research into clinical practice. Thus, even the best candidate driver genes display low mutational rates compared to other tumors. This means that a large percentage of cases do not display clear tumor-driving point mutations, or show candidate driving point mutations with no obvious biochemical relationship to the more frequently mutated genes. This genomic landscape probably reflects either an unknown underlying biochemical mechanism playing a key role in CLL or multiple biochemical pathways independently driving the development of this tumor. The elucidation of either scenario will have important consequences on the clinical management of CLL. Herein, we review the recent advances in the definition of the genomic landscape of CLL and the ongoing research to characterize the underlying biochemical events that drive this disease.</description>
        <link>http://www.biomedcentral.com/1741-7015/11/124</link>
                <dc:creator>Víctor Quesada</dc:creator>
                <dc:creator>Andrew J Ramsay</dc:creator>
                <dc:creator>David Rodríguez</dc:creator>
                <dc:creator>Xose S Puente</dc:creator>
                <dc:creator>Elías Campo</dc:creator>
                <dc:creator>Carlos López-Otín</dc:creator>
                <dc:source>BMC Medicine 2013, 11:124</dc:source>
        <dc:date>2013-05-09T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1741-7015-11-124</dc:identifier>
                            <dc:title>Characterizing leukemia genomics</dc:title>
                            <dc:description>&lt;p&gt;Carlos Lopez-Otin and colleagues review new developments in understanding the genomics of chronic lymphocytic leukemia, and discuss how genomic advances could benefit disease staging and treatment.&lt;/p&gt;</dc:description>
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        <prism:volume>11</prism:volume>
        <prism:startingPage>124</prism:startingPage>
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