PittsburghV1, PascalFrancis, Corpus, bibRecord, 000924

Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma

Identifieur interne : 000924 ( PascalFrancis/Corpus ); précédent : 000923; suivant : 000925

Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma

Auteurs : Akram M. Zaaqoq ; Rami Namas ; Khalid Almahmoud ; Nabil Azhar ; QI MI ; Ruben Zamora ; David M. Brienza ; Timothy R. Billiar ; Yoram Vodovotz

Source :

Critical care medicine [ 0090-3493 ] ; 2014.

RBID : Pascal:14-0168428

Descripteurs français

Pascal (Inist)
- Hémorragie, Traumatisme de la moelle épinière, Protéine A, Interleukine 10, Morbidité, Epidémiologie, Homme, Chimiokine, Inflammation, Système nerveux, Pathologie du système nerveux, Réanimation, Soin intensif.

English descriptors

KwdEn :
- Chemokine, Epidemiology, Hemorrhage, Human, Inflammation, Intensive care, Interleukin 10, Morbidity, Nervous system, Nervous system diseases, Protein A, Resuscitation, Spinal cord trauma.

Abstract

Objective: Blunt trauma and traumatic spinal cord injury induce systemic inflammation that contributes to morbidity. Dysregulated neural control of systemic inflammation postinjury is likely exaggerated in patients with traumatic spinal cord injury. We used in silico methods to discern dynamic inflammatory networks that could distinguish systemic inflammation in traumatic spinal cord injury from blunt trauma. Design: Retrospective study. Settings: Tertiary care institution. Patients: Twenty-one severely injured thoracocervical traumatic spinal cord injury patients and matched 21 severely injured blunt trauma patients without spinal cord injury. Intervention: None. Measurements and Main Results: Serial blood samples were obtained from days 1 to 14 postinjury. Twenty-four plasma inflammatory mediators were quantified. Statistical significance between the two groups was determined by two-way analysis of variance. Dynamic Bayesian network inference was used to suggest dynamic connectivity and central inflammatory mediators. Circulating interleukin-10 was significantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1β, soluble interleukin-2 receptor-α, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1 a and 1β, granulocyte-macrophage colony-stimulating factor, and interferon-γ were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury group. Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal cord injury dynamic networks. In a separate validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma inducible protein-10 levels more than or equal to 730 pg/mL had significantly prolonged hospital and ICU stay and days on mechanical ventilator versus patients with plasma inducible protein-10 level less than 730 pg/mL. Conclusion: This is the first study to compare the dynamic systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible protein-10 in driving systemic interleukin-10 and morbidity and highlighting the potential utility of in silico tools to identify key inflammatory drivers.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 14-0168428 INIST
ET :	Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma
AU :	ZAAQOQ (Akram M.); NAMAS (Rami); ALMAHMOUD (Khalid); AZHAR (Nabil); QI MI; ZAMORA (Ruben); BRIENZA (David M.); BILLIAR (Timothy R.); VODOVOTZ (Yoram)
AF :	Department of Critical Care Medicine, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (1 aut.); Department of Surgery, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (2 aut., 3 aut., 4 aut., 6 aut., 8 aut., 9 aut.); Center for Inflammation and Regenerative Modeling, McGowan Institute for Regenerative Medicine, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (2 aut., 6 aut., 7 aut., 8 aut., 9 aut.); Department of Sports Medicine and Nutrition, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (5 aut.); Department of Rehabilitation Science and Technology, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (7 aut.); Department of Bioengineering, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (7 aut.)
DT :	Publication en série; Niveau analytique
SO :	Critical care medicine; ISSN 0090-3493; Coden CCMDC7; Etats-Unis; Da. 2014; Vol. 42; No. 6; Pp. 1487-1497; Bibl. 42 ref.
LA :	Anglais
EA :	Objective: Blunt trauma and traumatic spinal cord injury induce systemic inflammation that contributes to morbidity. Dysregulated neural control of systemic inflammation postinjury is likely exaggerated in patients with traumatic spinal cord injury. We used in silico methods to discern dynamic inflammatory networks that could distinguish systemic inflammation in traumatic spinal cord injury from blunt trauma. Design: Retrospective study. Settings: Tertiary care institution. Patients: Twenty-one severely injured thoracocervical traumatic spinal cord injury patients and matched 21 severely injured blunt trauma patients without spinal cord injury. Intervention: None. Measurements and Main Results: Serial blood samples were obtained from days 1 to 14 postinjury. Twenty-four plasma inflammatory mediators were quantified. Statistical significance between the two groups was determined by two-way analysis of variance. Dynamic Bayesian network inference was used to suggest dynamic connectivity and central inflammatory mediators. Circulating interleukin-10 was significantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1β, soluble interleukin-2 receptor-α, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1 a and 1β, granulocyte-macrophage colony-stimulating factor, and interferon-γ were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury group. Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal cord injury dynamic networks. In a separate validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma inducible protein-10 levels more than or equal to 730 pg/mL had significantly prolonged hospital and ICU stay and days on mechanical ventilator versus patients with plasma inducible protein-10 level less than 730 pg/mL. Conclusion: This is the first study to compare the dynamic systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible protein-10 in driving systemic interleukin-10 and morbidity and highlighting the potential utility of in silico tools to identify key inflammatory drivers.
CC :	002B27B; 002B17A07
FD :	Hémorragie; Traumatisme de la moelle épinière; Protéine A; Interleukine 10; Morbidité; Epidémiologie; Homme; Chimiokine; Inflammation; Système nerveux; Pathologie du système nerveux; Réanimation; Soin intensif
FG :	Cytokine; Pathologie de la moelle épinière; Pathologie du système nerveux central
ED :	Hemorrhage; Spinal cord trauma; Protein A; Interleukin 10; Morbidity; Epidemiology; Human; Chemokine; Inflammation; Nervous system; Nervous system diseases; Resuscitation; Intensive care
EG :	Cytokine; Spinal cord disease; Central nervous system disease
SD :	Hemorragia; Traumatismo de médula espinal; Proteína A; Interleuquina 10; Morbilidad; Epidemiología; Hombre; Quimioquina; Inflamación; Sistema nervioso; Sistema nervioso patología; Reanimación; Cuidado intensivo
LO :	INIST-17751.354000501831030210
ID :	14-0168428

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Pascal:14-0168428

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma</title>
<author><name sortKey="Zaaqoq, Akram M" sort="Zaaqoq, Akram M" uniqKey="Zaaqoq A" first="Akram M." last="Zaaqoq">Akram M. Zaaqoq</name>
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<author><name sortKey="Almahmoud, Khalid" sort="Almahmoud, Khalid" uniqKey="Almahmoud K" first="Khalid" last="Almahmoud">Khalid Almahmoud</name>
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<affiliation><inist:fA14 i1="02"><s1>Department of Surgery, University of Pittsburgh</s1>
<s2>Pittsburgh, PA</s2>
<s3>USA</s3>
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<affiliation><inist:fA14 i1="04"><s1>Department of Sports Medicine and Nutrition, University of Pittsburgh</s1>
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<affiliation><inist:fA14 i1="03"><s1>Center for Inflammation and Regenerative Modeling, McGowan Institute for Regenerative Medicine, University of Pittsburgh</s1>
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<affiliation><inist:fA14 i1="05"><s1>Department of Rehabilitation Science and Technology, University of Pittsburgh</s1>
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<s3>USA</s3>
<sZ>7 aut.</sZ>
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</affiliation>
<affiliation><inist:fA14 i1="06"><s1>Department of Bioengineering, University of Pittsburgh</s1>
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</affiliation>
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<author><name sortKey="Billiar, Timothy R" sort="Billiar, Timothy R" uniqKey="Billiar T" first="Timothy R." last="Billiar">Timothy R. Billiar</name>
<affiliation><inist:fA14 i1="02"><s1>Department of Surgery, University of Pittsburgh</s1>
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<author><name sortKey="Vodovotz, Yoram" sort="Vodovotz, Yoram" uniqKey="Vodovotz Y" first="Yoram" last="Vodovotz">Yoram Vodovotz</name>
<affiliation><inist:fA14 i1="02"><s1>Department of Surgery, University of Pittsburgh</s1>
<s2>Pittsburgh, PA</s2>
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<affiliation><inist:fA14 i1="03"><s1>Center for Inflammation and Regenerative Modeling, McGowan Institute for Regenerative Medicine, University of Pittsburgh</s1>
<s2>Pittsburgh, PA</s2>
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<series><title level="j" type="main">Critical care medicine</title>
<title level="j" type="abbreviated">Crit. care med.</title>
<idno type="ISSN">0090-3493</idno>
<imprint><date when="2014">2014</date>
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<seriesStmt><title level="j" type="main">Critical care medicine</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Chemokine</term>
<term>Epidemiology</term>
<term>Hemorrhage</term>
<term>Human</term>
<term>Inflammation</term>
<term>Intensive care</term>
<term>Interleukin 10</term>
<term>Morbidity</term>
<term>Nervous system</term>
<term>Nervous system diseases</term>
<term>Protein A</term>
<term>Resuscitation</term>
<term>Spinal cord trauma</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Hémorragie</term>
<term>Traumatisme de la moelle épinière</term>
<term>Protéine A</term>
<term>Interleukine 10</term>
<term>Morbidité</term>
<term>Epidémiologie</term>
<term>Homme</term>
<term>Chimiokine</term>
<term>Inflammation</term>
<term>Système nerveux</term>
<term>Pathologie du   système nerveux</term>
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<front><div type="abstract" xml:lang="en">Objective: Blunt trauma and traumatic spinal cord injury induce systemic inflammation that contributes to morbidity. Dysregulated neural control of systemic inflammation postinjury is likely exaggerated in patients with traumatic spinal cord injury. We used in silico methods to discern dynamic inflammatory networks that could distinguish systemic inflammation in traumatic spinal cord injury from blunt trauma. Design: Retrospective study. Settings: Tertiary care institution. Patients: Twenty-one severely injured thoracocervical traumatic spinal cord injury patients and matched 21 severely injured blunt trauma patients without spinal cord injury. Intervention: None. Measurements and Main Results: Serial blood samples were obtained from days 1 to 14 postinjury. Twenty-four plasma inflammatory mediators were quantified. Statistical significance between the two groups was determined by two-way analysis of variance. Dynamic Bayesian network inference was used to suggest dynamic connectivity and central inflammatory mediators. Circulating interleukin-10 was significantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1β, soluble interleukin-2 receptor-α, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1 a and 1β, granulocyte-macrophage colony-stimulating factor, and interferon-γ were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury group. Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal cord injury dynamic networks. In a separate validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma inducible protein-10 levels more than or equal to 730 pg/mL had significantly prolonged hospital and ICU stay and days on mechanical ventilator versus patients with plasma inducible protein-10 level less than 730 pg/mL. Conclusion: This is the first study to compare the dynamic systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible protein-10 in driving systemic interleukin-10 and morbidity and highlighting the potential utility of in silico tools to identify key inflammatory drivers.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma</s1>
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<fA11 i1="01" i2="1"><s1>ZAAQOQ (Akram M.)</s1>
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<fA11 i1="02" i2="1"><s1>NAMAS (Rami)</s1>
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<fA11 i1="03" i2="1"><s1>ALMAHMOUD (Khalid)</s1>
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<fA11 i1="04" i2="1"><s1>AZHAR (Nabil)</s1>
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<fA11 i1="05" i2="1"><s1>QI MI</s1>
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<fA11 i1="06" i2="1"><s1>ZAMORA (Ruben)</s1>
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<fA11 i1="07" i2="1"><s1>BRIENZA (David M.)</s1>
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<fA14 i1="06"><s1>Department of Bioengineering, University of Pittsburgh</s1>
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<fC01 i1="01" l="ENG"><s0>Objective: Blunt trauma and traumatic spinal cord injury induce systemic inflammation that contributes to morbidity. Dysregulated neural control of systemic inflammation postinjury is likely exaggerated in patients with traumatic spinal cord injury. We used in silico methods to discern dynamic inflammatory networks that could distinguish systemic inflammation in traumatic spinal cord injury from blunt trauma. Design: Retrospective study. Settings: Tertiary care institution. Patients: Twenty-one severely injured thoracocervical traumatic spinal cord injury patients and matched 21 severely injured blunt trauma patients without spinal cord injury. Intervention: None. Measurements and Main Results: Serial blood samples were obtained from days 1 to 14 postinjury. Twenty-four plasma inflammatory mediators were quantified. Statistical significance between the two groups was determined by two-way analysis of variance. Dynamic Bayesian network inference was used to suggest dynamic connectivity and central inflammatory mediators. Circulating interleukin-10 was significantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1β, soluble interleukin-2 receptor-α, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1 a and 1β, granulocyte-macrophage colony-stimulating factor, and interferon-γ were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury group. Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal cord injury dynamic networks. In a separate validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma inducible protein-10 levels more than or equal to 730 pg/mL had significantly prolonged hospital and ICU stay and days on mechanical ventilator versus patients with plasma inducible protein-10 level less than 730 pg/mL. Conclusion: This is the first study to compare the dynamic systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible protein-10 in driving systemic interleukin-10 and morbidity and highlighting the potential utility of in silico tools to identify key inflammatory drivers.</s0>
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<server><NO>PASCAL 14-0168428 INIST</NO>
<ET>Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma</ET>
<AU>ZAAQOQ (Akram M.); NAMAS (Rami); ALMAHMOUD (Khalid); AZHAR (Nabil); QI MI; ZAMORA (Ruben); BRIENZA (David M.); BILLIAR (Timothy R.); VODOVOTZ (Yoram)</AU>
<AF>Department of Critical Care Medicine, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (1 aut.); Department of Surgery, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (2 aut., 3 aut., 4 aut., 6 aut., 8 aut., 9 aut.); Center for Inflammation and Regenerative Modeling, McGowan Institute for Regenerative Medicine, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (2 aut., 6 aut., 7 aut., 8 aut., 9 aut.); Department of Sports Medicine and Nutrition, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (5 aut.); Department of Rehabilitation Science and Technology, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (7 aut.); Department of Bioengineering, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Critical care medicine; ISSN 0090-3493; Coden CCMDC7; Etats-Unis; Da. 2014; Vol. 42; No. 6; Pp. 1487-1497; Bibl. 42 ref.</SO>
<LA>Anglais</LA>
<EA>Objective: Blunt trauma and traumatic spinal cord injury induce systemic inflammation that contributes to morbidity. Dysregulated neural control of systemic inflammation postinjury is likely exaggerated in patients with traumatic spinal cord injury. We used in silico methods to discern dynamic inflammatory networks that could distinguish systemic inflammation in traumatic spinal cord injury from blunt trauma. Design: Retrospective study. Settings: Tertiary care institution. Patients: Twenty-one severely injured thoracocervical traumatic spinal cord injury patients and matched 21 severely injured blunt trauma patients without spinal cord injury. Intervention: None. Measurements and Main Results: Serial blood samples were obtained from days 1 to 14 postinjury. Twenty-four plasma inflammatory mediators were quantified. Statistical significance between the two groups was determined by two-way analysis of variance. Dynamic Bayesian network inference was used to suggest dynamic connectivity and central inflammatory mediators. Circulating interleukin-10 was significantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1β, soluble interleukin-2 receptor-α, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1 a and 1β, granulocyte-macrophage colony-stimulating factor, and interferon-γ were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury group. Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal cord injury dynamic networks. In a separate validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma inducible protein-10 levels more than or equal to 730 pg/mL had significantly prolonged hospital and ICU stay and days on mechanical ventilator versus patients with plasma inducible protein-10 level less than 730 pg/mL. Conclusion: This is the first study to compare the dynamic systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible protein-10 in driving systemic interleukin-10 and morbidity and highlighting the potential utility of in silico tools to identify key inflammatory drivers.</EA>
<CC>002B27B; 002B17A07</CC>
<FD>Hémorragie; Traumatisme de la moelle épinière; Protéine A; Interleukine 10; Morbidité; Epidémiologie; Homme; Chimiokine; Inflammation; Système nerveux; Pathologie du   système nerveux; Réanimation; Soin intensif</FD>
<FG>Cytokine; Pathologie de la moelle épinière; Pathologie du   système nerveux central</FG>
<ED>Hemorrhage; Spinal cord trauma; Protein A; Interleukin 10; Morbidity; Epidemiology; Human; Chemokine; Inflammation; Nervous system; Nervous system diseases; Resuscitation; Intensive care</ED>
<EG>Cytokine; Spinal cord disease; Central nervous system disease</EG>
<SD>Hemorragia; Traumatismo de médula espinal; Proteína A; Interleuquina 10; Morbilidad; Epidemiología; Hombre; Quimioquina; Inflamación; Sistema nervioso; Sistema nervioso patología; Reanimación; Cuidado intensivo</SD>
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<ID>14-0168428</ID>
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Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma

Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma

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