<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT02997462</url>
  </required_header>
  <id_info>
    <org_study_id>HUM00049322</org_study_id>
    <nct_id>NCT02997462</nct_id>
  </id_info>
  <brief_title>Monocyte Phenotypic Changes in Heart Failure</brief_title>
  <official_title>Monocyte Phenotypic Changes in Heart Failure</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>University of Michigan</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>University of Michigan</source>
  <oversight_info>
    <has_dmc>No</has_dmc>
    <is_fda_regulated_drug>No</is_fda_regulated_drug>
    <is_fda_regulated_device>No</is_fda_regulated_device>
  </oversight_info>
  <brief_summary>
    <textblock>
      There are many treatments that can improve how long and how well people live with heart&#xD;
      failure when they are outside the hospital. However, the investigators know less about how to&#xD;
      effectively treat hospitalized heart failure patients so that they do not have to return to&#xD;
      the hospital after they go home. Part of the problem is that the investigators don't&#xD;
      understand all of the causes of worsening heart failure.&#xD;
&#xD;
      Previous studies by other researchers suggest that white blood cells called monocytes are&#xD;
      over-active in heart failure. Under normal conditions monocytes help fight infections in the&#xD;
      body, but over-active monocytes release chemicals that could cause abnormal function of the&#xD;
      heart and blood vessels. The investigators' research group believes that over-active&#xD;
      monocytes may be an important reason that heart failure worsens before hospitalization.&#xD;
&#xD;
      In this study the investigators will collect blood samples on the day a patient comes into&#xD;
      the hospital, the day they return home, and the day they come back to the clinic for a&#xD;
      follow-up appointment. The investigators will measure the inflammation in the bloodstream and&#xD;
      the activity of monocytes from the patients' blood to see if there are changes in these&#xD;
      measurements as heart failure improves. The investigators will also call each patient several&#xD;
      times after they return home to ask questions about how they are doing.&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      With over 5 million Americans having heart failure (HF) today and an incidence approaching 10&#xD;
      per 1000 population among persons over the age of 65, HF is a major source or morbidity and&#xD;
      mortality and a significant public health concern facing developed nations. In the US,&#xD;
      decompensated heart failure is the most common reason for hospital admission among persons&#xD;
      older than 65. Yet despite significant advances in the treatment of chronic heart failure,&#xD;
      currently there are very few evidence-based strategies to treat acutely decompensated heart&#xD;
      failure. The incidence of heart failure will likely continue to rise with the increasing&#xD;
      prevalence of HF risk factors (advanced age, hypertension, obesity, diabetes, and other&#xD;
      metabolic diseases). Accordingly, substantial efforts are underway to identify and treat&#xD;
      populations at risk and to understand the molecular drivers of this heterogeneous disease.&#xD;
&#xD;
      The investigators understanding of the pathophysiology of heart failure has evolved from a&#xD;
      'cardiocentric' view focused on mechanical dysfunction to a more global view. Heart failure&#xD;
      is now understood as a complex blend of structural, functional, and neurohormonal&#xD;
      abnormalities manifested both locally and systemically. More recently, several groups have&#xD;
      demonstrated abnormalities in the inflammatory cascade associated with both the initiation&#xD;
      and the progression of heart failure. The innate immune system appears to modulate the&#xD;
      inflammatory component of HF through several mechanisms including the production of&#xD;
      inflammatory cytokines (tumor necrosis factor-α,TNFα; interleukin-6, IL6), reactive oxygen&#xD;
      species, activation of the complement system, as well as through functional modification of&#xD;
      endothelial cells and myeloid cell trafficking.&#xD;
&#xD;
      Monocytes and macrophages are two of the key myeloid mediators of acute and chronic&#xD;
      inflammatory responses. Myeloid dysregulation has been implicated in the pathogenesis of&#xD;
      diverse diseases including diabetes, tumor metastasis, pulmonary fibrosis, myocardial&#xD;
      infarction, and atherosclerosis. Accumulating evidence suggests that myeloid subsets have&#xD;
      distinct functional properties reflecting their polarization patterns and their interaction&#xD;
      with the local microenvironment. As a framework to study their role in models of clinical&#xD;
      diseases, myeloid populations have been broadly categorized as &quot;inflammatory&quot; and&#xD;
      &quot;anti-inflammatory&quot; based on specific surface markers, cytokine potential, and other&#xD;
      functional properties.&#xD;
&#xD;
      Although the role of myeloid populations in inflammatory disease is now appreciated, the&#xD;
      molecular mechanisms linking these cells to clinical heart failure syndromes remain largely&#xD;
      unknown. The investigators hypothesize that distinct myeloid subsets drive different phases&#xD;
      of acute and chronic heart failure syndromes, and that identification of these subsets and&#xD;
      their functional properties will provide further insight into the pathophysiology of clinical&#xD;
      heart failure.&#xD;
&#xD;
      In order to initially characterize the roles that monocytes play across the spectrum of heart&#xD;
      failure, the investigators will obtain whole-blood samples from acutely decompensated&#xD;
      patients on the date of hospitalization, the date of transfer from the intensive care unit&#xD;
      (ICU) to the general-care telemetry floor (if relevant), the date of hospital discharge, and&#xD;
      at their first outpatient follow-up visit. Subjects will be recruited from the University of&#xD;
      Michigan inpatient heart failure service, which admits approximately 75 patients for&#xD;
      decompensated heart failure each month. Once the samples are obtained, the investigators will&#xD;
      perform flow cytometry to characterize monocyte subsets and their flux in response to&#xD;
      treatment. The investigators will also look at the production of reactive oxygen species by&#xD;
      monocytes and will examine how cytokines and chemokines skew monocyte population subsets and&#xD;
      their gene expression profiles. The investigators will also investigate the energetic state&#xD;
      and flux (aerobic vs. anaerobic metabolic status) of the monocytes.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Recruiting</overall_status>
  <start_date>November 2011</start_date>
  <completion_date type="Anticipated">December 2024</completion_date>
  <primary_completion_date type="Anticipated">December 2023</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Cohort</observational_model>
    <time_perspective>Prospective</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>Change in IL-6 between hospital admission and discharge</measure>
    <time_frame>All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)</time_frame>
    <description>Cytokine</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Lys6c Hi and Lo, Mannose Receptor</measure>
    <time_frame>All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)</time_frame>
    <description>Cell Surface Markers</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>IL-10, IL-13</measure>
    <time_frame>All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)</time_frame>
    <description>Cytokine</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Gene Expression (iNOS, CCL2, Ym1, Fizz, VEGF, MMP2/9)</measure>
    <time_frame>All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)</time_frame>
    <description>Monocyte gene expression</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>microRNA</measure>
    <time_frame>All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)</time_frame>
    <description>miR155, let7, mir-33a</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Monocyte/macrophage morphology</measure>
    <time_frame>All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)</time_frame>
    <description>Macrophages/monocytes will be classified based on their morphology</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Serum F-2 Isoprostanes</measure>
    <time_frame>All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)</time_frame>
    <description>Oxidative stress marker</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>TNF-alpha</measure>
    <time_frame>All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)</time_frame>
    <description>Marker of inflammation</description>
  </secondary_outcome>
  <number_of_groups>2</number_of_groups>
  <enrollment type="Anticipated">60</enrollment>
  <condition>Heart Failure</condition>
  <condition>Decompensated Heart Failure</condition>
  <arm_group>
    <arm_group_label>Heart Failure</arm_group_label>
    <description>Heart Failure patients admitted to the ICU or Heart Failure Service.&#xD;
No changes in service-directed plan of care for patients.</description>
  </arm_group>
  <arm_group>
    <arm_group_label>Healthy Control</arm_group_label>
    <description>Healthy, age-matched controls.</description>
  </arm_group>
  <biospec_retention>Samples With DNA</biospec_retention>
  <biospec_descr>
    <textblock>
      Blood samples for cytokine measures&#xD;
&#xD;
      Blood samples for monocyte cell surface marker and functional phenotyping&#xD;
    </textblock>
  </biospec_descr>
  <eligibility>
    <study_pop>
      <textblock>
        Heart failure inpatients and age-matched controls&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Non-Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria: Heart Failure Patients:&#xD;
&#xD;
          -  18 years of age or older&#xD;
&#xD;
          -  Patients must be diagnosed with heart failure&#xD;
&#xD;
          -  Patients must be hospitalized at the University of Michigan Hospital for treatment of&#xD;
             heart failure symptoms.&#xD;
&#xD;
        Exclusion Criteria: Heart Failure Patients:&#xD;
&#xD;
          -  Heart attack or other active problem with coronary artery disease&#xD;
&#xD;
          -  Severe kidney failure or need for dialysis&#xD;
&#xD;
          -  An active infection or inflammatory condition&#xD;
&#xD;
          -  A need for treatment that affects the immune system (e.g. systemic steroids,&#xD;
             immunomodulatory therapies)&#xD;
&#xD;
          -  A planned surgery during this hospital admission, including heart transplant or other&#xD;
             heart surgery&#xD;
&#xD;
        Inclusion Criteria: Healthy Control Patients:&#xD;
&#xD;
        - Must be greater than or equal to 65 years of age&#xD;
&#xD;
        Exclusion Criteria: Healthy Control Patients:&#xD;
&#xD;
          -  Diabetes&#xD;
&#xD;
          -  High blood pressure&#xD;
&#xD;
          -  Active cancer&#xD;
&#xD;
          -  Heart disease&#xD;
&#xD;
          -  Lung disease&#xD;
&#xD;
          -  Liver disease&#xD;
&#xD;
          -  Kidney disease&#xD;
&#xD;
          -  Active smoker&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>Accepts Healthy Volunteers</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Scott Hummel, MD MS</last_name>
    <role>Principal Investigator</role>
    <affiliation>University of Michigan</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Adam Stein, MD</last_name>
    <role>Principal Investigator</role>
    <affiliation>University of Michigan</affiliation>
  </overall_official>
  <overall_official>
    <last_name>Sascha Goonewardena, MD</last_name>
    <role>Principal Investigator</role>
    <affiliation>University of Michigan</affiliation>
  </overall_official>
  <overall_contact>
    <last_name>Joanna Wells</last_name>
    <phone>734-232-6383</phone>
    <email>joannamw@med.umich.edu</email>
  </overall_contact>
  <overall_contact_backup>
    <last_name>Scott Hummel, MD MS</last_name>
    <phone>734-764-7440</phone>
    <email>scothumm@med.umich.edu</email>
  </overall_contact_backup>
  <location>
    <facility>
      <name>University of Michigan Health System</name>
      <address>
        <city>Ann Arbor</city>
        <state>Michigan</state>
        <zip>48109</zip>
        <country>United States</country>
      </address>
    </facility>
    <status>Recruiting</status>
    <contact>
      <last_name>Joanna Wells</last_name>
      <phone>734-232-6383</phone>
      <email>joannamw@med.umich.edu</email>
    </contact>
    <investigator>
      <last_name>Scott Hummel, MD MS</last_name>
      <role>Principal Investigator</role>
    </investigator>
    <investigator>
      <last_name>Adam Stein, MD</last_name>
      <role>Sub-Investigator</role>
    </investigator>
    <investigator>
      <last_name>Sascha Goonewardena, MD</last_name>
      <role>Sub-Investigator</role>
    </investigator>
  </location>
  <location_countries>
    <country>United States</country>
  </location_countries>
  <reference>
    <citation>Seidler S, Zimmermann HW, Bartneck M, Trautwein C, Tacke F. Age-dependent alterations of monocyte subsets and monocyte-related chemokine pathways in healthy adults. BMC Immunol. 2010 Jun 21;11:30. doi: 10.1186/1471-2172-11-30.</citation>
    <PMID>20565954</PMID>
  </reference>
  <reference>
    <citation>Polidori MC, Pratico D, Savino K, Rokach J, Stahl W, Mecocci P. Increased F2 isoprostane plasma levels in patients with congestive heart failure are correlated with antioxidant status and disease severity. J Card Fail. 2004 Aug;10(4):334-8. doi: 10.1016/j.cardfail.2003.11.004.</citation>
    <PMID>15309701</PMID>
  </reference>
  <reference>
    <citation>Colombo PC, Banchs JE, Celaj S, Talreja A, Lachmann J, Malla S, DuBois NB, Ashton AW, Latif F, Jorde UP, Ware JA, LeJemtel TH. Endothelial cell activation in patients with decompensated heart failure. Circulation. 2005 Jan 4;111(1):58-62. doi: 10.1161/01.CIR.0000151611.89232.3B. Epub 2004 Dec 20.</citation>
    <PMID>15611373</PMID>
  </reference>
  <reference>
    <citation>Levine B, Kalman J, Mayer L, Fillit HM, Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med. 1990 Jul 26;323(4):236-41. doi: 10.1056/NEJM199007263230405.</citation>
    <PMID>2195340</PMID>
  </reference>
  <reference>
    <citation>Deswal A, Petersen NJ, Feldman AM, Young JB, White BG, Mann DL. Cytokines and cytokine receptors in advanced heart failure: an analysis of the cytokine database from the Vesnarinone trial (VEST). Circulation. 2001 Apr 24;103(16):2055-9. doi: 10.1161/01.cir.103.16.2055.</citation>
    <PMID>11319194</PMID>
  </reference>
  <reference>
    <citation>Mann DL, McMurray JJ, Packer M, Swedberg K, Borer JS, Colucci WS, Djian J, Drexler H, Feldman A, Kober L, Krum H, Liu P, Nieminen M, Tavazzi L, van Veldhuisen DJ, Waldenstrom A, Warren M, Westheim A, Zannad F, Fleming T. Targeted anticytokine therapy in patients with chronic heart failure: results of the Randomized Etanercept Worldwide Evaluation (RENEWAL). Circulation. 2004 Apr 6;109(13):1594-602. doi: 10.1161/01.CIR.0000124490.27666.B2. Epub 2004 Mar 15.</citation>
    <PMID>15023878</PMID>
  </reference>
  <reference>
    <citation>Aukrust P, Ueland T, Lien E, Bendtzen K, Muller F, Andreassen AK, Nordoy I, Aass H, Espevik T, Simonsen S, Froland SS, Gullestad L. Cytokine network in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 1999 Feb 1;83(3):376-82. doi: 10.1016/s0002-9149(98)00872-8.</citation>
    <PMID>10072227</PMID>
  </reference>
  <verification_date>February 2023</verification_date>
  <study_first_submitted>March 19, 2012</study_first_submitted>
  <study_first_submitted_qc>December 15, 2016</study_first_submitted_qc>
  <study_first_posted type="Estimate">December 20, 2016</study_first_posted>
  <last_update_submitted>February 16, 2023</last_update_submitted>
  <last_update_submitted_qc>February 16, 2023</last_update_submitted_qc>
  <last_update_posted type="Actual">February 17, 2023</last_update_posted>
  <responsible_party>
    <responsible_party_type>Principal Investigator</responsible_party_type>
    <investigator_affiliation>University of Michigan</investigator_affiliation>
    <investigator_full_name>Scott L. Hummel</investigator_full_name>
    <investigator_title>Associate Professor</investigator_title>
  </responsible_party>
  <keyword>Monocyte</keyword>
  <keyword>Oxidative Stress</keyword>
  <keyword>Endothelial Function</keyword>
  <keyword>Congestive Heart Failure</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Heart Failure</mesh_term>
  </condition_browse>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT02997462
org study id: HUM00049322
nct id: NCT02997462
lead sponsor: 
has dmc: No
is fda regulated drug: No
is fda regulated device: No
There are many treatments that can improve how long and how well people live with heart
      failure when they are outside the hospital. However, the investigators know less about how to
      effectively treat hospitalized heart failure patients so that they do not have to return to
      the hospital after they go home. Part of the problem is that the investigators don't
      understand all of the causes of worsening heart failure.

      Previous studies by other researchers suggest that white blood cells called monocytes are
      over-active in heart failure. Under normal conditions monocytes help fight infections in the
      body, but over-active monocytes release chemicals that could cause abnormal function of the
      heart and blood vessels. The investigators' research group believes that over-active
      monocytes may be an important reason that heart failure worsens before hospitalization.

      In this study the investigators will collect blood samples on the day a patient comes into
      the hospital, the day they return home, and the day they come back to the clinic for a
      follow-up appointment. The investigators will measure the inflammation in the bloodstream and
      the activity of monocytes from the patients' blood to see if there are changes in these
      measurements as heart failure improves. The investigators will also call each patient several
      times after they return home to ask questions about how they are doing.
With over 5 million Americans having heart failure (HF) today and an incidence approaching 10
      per 1000 population among persons over the age of 65, HF is a major source or morbidity and
      mortality and a significant public health concern facing developed nations. In the US,
      decompensated heart failure is the most common reason for hospital admission among persons
      older than 65. Yet despite significant advances in the treatment of chronic heart failure,
      currently there are very few evidence-based strategies to treat acutely decompensated heart
      failure. The incidence of heart failure will likely continue to rise with the increasing
      prevalence of HF risk factors (advanced age, hypertension, obesity, diabetes, and other
      metabolic diseases). Accordingly, substantial efforts are underway to identify and treat
      populations at risk and to understand the molecular drivers of this heterogeneous disease.

      The investigators understanding of the pathophysiology of heart failure has evolved from a
      'cardiocentric' view focused on mechanical dysfunction to a more global view. Heart failure
      is now understood as a complex blend of structural, functional, and neurohormonal
      abnormalities manifested both locally and systemically. More recently, several groups have
      demonstrated abnormalities in the inflammatory cascade associated with both the initiation
      and the progression of heart failure. The innate immune system appears to modulate the
      inflammatory component of HF through several mechanisms including the production of
      inflammatory cytokines (tumor necrosis factor-α,TNFα; interleukin-6, IL6), reactive oxygen
      species, activation of the complement system, as well as through functional modification of
      endothelial cells and myeloid cell trafficking.

      Monocytes and macrophages are two of the key myeloid mediators of acute and chronic
      inflammatory responses. Myeloid dysregulation has been implicated in the pathogenesis of
      diverse diseases including diabetes, tumor metastasis, pulmonary fibrosis, myocardial
      infarction, and atherosclerosis. Accumulating evidence suggests that myeloid subsets have
      distinct functional properties reflecting their polarization patterns and their interaction
      with the local microenvironment. As a framework to study their role in models of clinical
      diseases, myeloid populations have been broadly categorized as "inflammatory" and
      "anti-inflammatory" based on specific surface markers, cytokine potential, and other
      functional properties.

      Although the role of myeloid populations in inflammatory disease is now appreciated, the
      molecular mechanisms linking these cells to clinical heart failure syndromes remain largely
      unknown. The investigators hypothesize that distinct myeloid subsets drive different phases
      of acute and chronic heart failure syndromes, and that identification of these subsets and
      their functional properties will provide further insight into the pathophysiology of clinical
      heart failure.

      In order to initially characterize the roles that monocytes play across the spectrum of heart
      failure, the investigators will obtain whole-blood samples from acutely decompensated
      patients on the date of hospitalization, the date of transfer from the intensive care unit
      (ICU) to the general-care telemetry floor (if relevant), the date of hospital discharge, and
      at their first outpatient follow-up visit. Subjects will be recruited from the University of
      Michigan inpatient heart failure service, which admits approximately 75 patients for
      decompensated heart failure each month. Once the samples are obtained, the investigators will
      perform flow cytometry to characterize monocyte subsets and their flux in response to
      treatment. The investigators will also look at the production of reactive oxygen species by
      monocytes and will examine how cytokines and chemokines skew monocyte population subsets and
      their gene expression profiles. The investigators will also investigate the energetic state
      and flux (aerobic vs. anaerobic metabolic status) of the monocytes.
observational model: Cohort
time perspective: Prospective
measure: Change in IL-6 between hospital admission and discharge
time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
description: Cytokine
measure: Lys6c Hi and Lo, Mannose Receptor
time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
description: Cell Surface Markers
measure: IL-10, IL-13
time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
description: Cytokine
measure: Gene Expression (iNOS, CCL2, Ym1, Fizz, VEGF, MMP2/9)
time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
description: Monocyte gene expression
measure: microRNA
time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
description: miR155, let7, mir-33a
measure: Monocyte/macrophage morphology
time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
description: Macrophages/monocytes will be classified based on their morphology
measure: Serum F-2 Isoprostanes
time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
description: Oxidative stress marker
measure: TNF-alpha
time frame: All scheduled blood draws - hospital admission, discharge (3-14 days after admission), and first post-discharge appointment (5-10 days following discharge)
description: Marker of inflammation
arm group label: Heart Failure
description: Heart Failure patients admitted to the ICU or Heart Failure Service.
No changes in service-directed plan of care for patients.
arm group label: Healthy Control
description: Healthy, age-matched controls.
Blood samples for cytokine measures

      Blood samples for monocyte cell surface marker and functional phenotyping
study pop: 
sampling method: Non-Probability Sample
criteria: 
gender: All
minimum age: 18 Years
maximum age: N/A
healthy volunteers: Accepts Healthy Volunteers
last name: Scott Hummel, MD MS
role: Principal Investigator
affiliation: University of Michigan
last name: Adam Stein, MD
role: Principal Investigator
affiliation: University of Michigan
last name: Sascha Goonewardena, MD
role: Principal Investigator
affiliation: University of Michigan
last name: Joanna Wells
phone: 734-232-6383
email: joannamw@med.umich.edu
last name: Scott Hummel, MD MS
phone: 734-764-7440
email: scothumm@med.umich.edu
facility: 
status: Recruiting
contact: 
investigator: 
investigator: 
investigator: 
country: United States
citation: Seidler S, Zimmermann HW, Bartneck M, Trautwein C, Tacke F. Age-dependent alterations of monocyte subsets and monocyte-related chemokine pathways in healthy adults. BMC Immunol. 2010 Jun 21;11:30. doi: 10.1186/1471-2172-11-30.
PMID: 20565954
citation: Polidori MC, Pratico D, Savino K, Rokach J, Stahl W, Mecocci P. Increased F2 isoprostane plasma levels in patients with congestive heart failure are correlated with antioxidant status and disease severity. J Card Fail. 2004 Aug;10(4):334-8. doi: 10.1016/j.cardfail.2003.11.004.
PMID: 15309701
citation: Colombo PC, Banchs JE, Celaj S, Talreja A, Lachmann J, Malla S, DuBois NB, Ashton AW, Latif F, Jorde UP, Ware JA, LeJemtel TH. Endothelial cell activation in patients with decompensated heart failure. Circulation. 2005 Jan 4;111(1):58-62. doi: 10.1161/01.CIR.0000151611.89232.3B. Epub 2004 Dec 20.
PMID: 15611373
citation: Levine B, Kalman J, Mayer L, Fillit HM, Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med. 1990 Jul 26;323(4):236-41. doi: 10.1056/NEJM199007263230405.
PMID: 2195340
citation: Deswal A, Petersen NJ, Feldman AM, Young JB, White BG, Mann DL. Cytokines and cytokine receptors in advanced heart failure: an analysis of the cytokine database from the Vesnarinone trial (VEST). Circulation. 2001 Apr 24;103(16):2055-9. doi: 10.1161/01.cir.103.16.2055.
PMID: 11319194
citation: Mann DL, McMurray JJ, Packer M, Swedberg K, Borer JS, Colucci WS, Djian J, Drexler H, Feldman A, Kober L, Krum H, Liu P, Nieminen M, Tavazzi L, van Veldhuisen DJ, Waldenstrom A, Warren M, Westheim A, Zannad F, Fleming T. Targeted anticytokine therapy in patients with chronic heart failure: results of the Randomized Etanercept Worldwide Evaluation (RENEWAL). Circulation. 2004 Apr 6;109(13):1594-602. doi: 10.1161/01.CIR.0000124490.27666.B2. Epub 2004 Mar 15.
PMID: 15023878
citation: Aukrust P, Ueland T, Lien E, Bendtzen K, Muller F, Andreassen AK, Nordoy I, Aass H, Espevik T, Simonsen S, Froland SS, Gullestad L. Cytokine network in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 1999 Feb 1;83(3):376-82. doi: 10.1016/s0002-9149(98)00872-8.
PMID: 10072227
responsible party type: Principal Investigator
investigator affiliation: University of Michigan
investigator full name: Scott L. Hummel
investigator title: Associate Professor
mesh term: Heart Failure