Scott J. Denstaedt

ORCID: 0000-0002-9173-5146
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About
Contact & Profiles
Research Areas
  • Sepsis Diagnosis and Treatment
  • Immune Response and Inflammation
  • Immune cells in cancer
  • Intensive Care Unit Cognitive Disorders
  • Neonatal Respiratory Health Research
  • S100 Proteins and Annexins
  • Atrial Fibrillation Management and Outcomes
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Venous Thromboembolism Diagnosis and Management
  • Hemodynamic Monitoring and Therapy
  • Autoimmune and Inflammatory Disorders Research
  • Liver Disease Diagnosis and Treatment
  • Central Venous Catheters and Hemodialysis
  • Immune Cell Function and Interaction
  • Antioxidant Activity and Oxidative Stress
  • Adipokines, Inflammation, and Metabolic Diseases
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Hyperglycemia and glycemic control in critically ill and hospitalized patients
  • Nitric Oxide and Endothelin Effects
  • Eicosanoids and Hypertension Pharmacology
  • Respiratory Support and Mechanisms
  • Renal function and acid-base balance
  • Vascular Anomalies and Treatments
  • Pancreatitis Pathology and Treatment
  • Immune responses and vaccinations

University of Michigan–Ann Arbor
2018-2024

Michigan Medicine
2017-2023

Pulmonary and Critical Care Associates
2017-2022

Case Western Reserve University
2020

University School
2020

University Hospitals Cleveland Medical Center
2013

Wayne State University
2010

Sepsis causes brain dysfunction and neuroinflammation. It is unknown whether neuroinflammation in sepsis initiated by dissemination of bacteria to the sustained persistent infection, or a sterile process resulting solely from circulating inflammatory mediators.

10.1164/rccm.201708-1559oc article EN American Journal of Respiratory and Critical Care Medicine 2017-12-12

Abstract Sepsis commonly results in acute and chronic brain dysfunction, which dramatically increases the morbidity associated with this common disease. Chronic dysfunction animal models of sepsis survival is linked to persistent neuroinflammation expression multiple cytokines. However, we have found previously that microglia predominantly upregulate damage molecule S100A8/A9 after sepsis. In article, show increased brains patients who died S100A8 expressed astrocytes myeloid cells. Using a...

10.4049/jimmunol.1700834 article EN The Journal of Immunology 2018-03-21

Predicting long-term outcomes in sepsis survivors remains a difficult task. Persistent inflammation post-sepsis is associated with increased risk for rehospitalization and death. As surrogate markers of inflammation, complete blood count parameters measured at hospital discharge may have prognostic value survivors. To determine the incremental over clinical characteristics predicting 90-day Electronic health record data was used to identify hospitalizations United States Veterans Affairs...

10.3389/fimmu.2023.1133351 article EN cc-by Frontiers in Immunology 2023-02-28

ABSTRACT Pneumonia is the leading cause of sepsis and septic shock. Patients who survive pneumonia are vulnerable to long-term complications including increased risk neurocognitive dysfunction. This study investigated immune response a non-surgical mouse model Klebsiella pneumoniae pneumosepsis with antibiotic treatment. Pneumosepsis resulted in acutely enhanced expression inflammatory cytokines, chemokines, damage-associated molecular patterns brain spleen. Despite resolution infection,...

10.1097/shk.0000000000001435 article EN Shock 2019-08-13

Millions of people who survive sepsis each year are rehospitalized and die due to late pulmonary complications. To prevent treat these complications, biomarkers molecular mediators must be identified. Persistent immune reprogramming in the form immunoparalysis impaired host defense is proposed mediate complications after sepsis, particularly new infections. However, may also involve enhanced/primed responses secondary stimuli, although their contribution long-term remains understudied. We...

10.1152/ajplung.00123.2021 article EN AJP Lung Cellular and Molecular Physiology 2021-06-23

Early-career clinician-scientists often leave academic medicine, but strong mentorship can help facilitate retention. Beyond the traditional dyadic mentor-mentee relationship, formal peer mentoring provides a rich means to augment career development and foster independence.To describe model for early-career retention of participating in medicine.In 2015, multidisciplinary interprofessional group focused on critical care developed at University Michigan called MICReW (Multidisciplinary...

10.34197/ats-scholar.2022-0039in article EN cc-by-nc-nd ATS Scholar 2022-10-04

A 74-year-old woman presented with an acute stroke. The physical examination showed multiple mucocutaneous telangiectasias, and a diagnosis of hereditary hemorrhagic telangiectasia was made.

10.1056/nejmicm1905896 article EN New England Journal of Medicine 2019-12-25

Background: As critical care practice evolves, the sepsis survivor population continues to expand, often with lingering inflammation in many organs, including liver. Given concurrently increasing of patients NAFLD, this study, we aimed understand long-term effect on pre-existing NAFLD and hyperglycemia. Methods: Male mice were randomized a high-fat diet or control (CD). After 24 weeks diet, inoculated Klebsiella pneumoniae ( Kpa ). Serial glucose tolerance tests, insulin pyruvate challenge...

10.1097/hc9.0000000000000210 article EN cc-by-nc-nd Hepatology Communications 2023-08-09

Factors regulating adipose tissue macrophage recruitment are largely unknown. Since tnf-alpha may promote diabetes in obesity, we hypothesized that be an important mediator of both infiltration and CCR2 expression. To determine the role on bred deficient mice onto leptin receptor background compared obese with without tnf-alpha. Immunohistochemical analysis demonstrated significantly greater percentage Mac-3 positive cells epididymal fat wild-type versus (db/db tnf wt: 12.7 + 1.2 %; db/db...

10.1161/circ.114.suppl_18.ii_904-a article EN Circulation 2006-10-31
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