Dr. Roderick Allen Barke M.D.
Surgeon | Surgical Critical Care
Department Of Surgery (112) Minneapolis Veterans Minneapolis MN, 55417About
Dr. Roderick Barke is a general surgeon practicing in Minneapolis, MN. Dr. Barke specializes in abdominal contents including the esophagus, stomach, liver, gallbladder, pancreas and often thyroid glands. General surgeons are able to deal with almost any surgical or critical care emergency, also involving the skin or soft tissue trauma. Dr. Barke provides quality surgical service for gravely ill or injured patients and is able to respond quickly due to knowledge of various surgical procedures.
Education and Training
Wayne State Univ Sch of Med, Detroit Mi 1977
Board Certification
SurgeryAmerican Board of SurgeryABS- Surgical Critical Care
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Morphine synergizes with lipopolysaccharide in a chronic endotoxemia model.
- Deficiency of the transcription factor c-fos increases lipopolysaccharide-induced macrophage interleukin 12 production.
- Gram-negative bacterial sepsis and the sepsis syndrome.
- Interleukin-4 regulates macrophage interleukin-12 protein synthesis through a c-fos mediated mechanism.
- Morphine directs T cells toward T(H2) differentiation.
- Morphine modulates lymph node-derived T lymphocyte function: role of caspase-3, -8, and nitric oxide.
- Role of mu-opioid receptor in immune function.
- Morphine sulfate inhibits hypoxia-induced vascular endothelial growth factor expression in endothelial cells and cardiac myocytes.
- The immunosuppressive effects of chronic morphine treatment are partially dependent on corticosterone and mediated by the mu-opioid receptor.
- Mu-opioid receptor mediates chronic restraint stress-induced lymphocyte apoptosis.
- Morphine negatively regulates interferon-gamma promoter activity in activated murine T cells through two distinct cyclic AMP-dependent pathways.
- Chronic morphine treatment differentiates T helper cells to Th2 effector cells by modulating transcription factors GATA 3 and T-bet.
- Morphine impairs host innate immune response and increases susceptibility to Streptococcus pneumoniae lung infection.
- Morphine withdrawal contributes to Th cell differentiation by biasing cells toward the Th2 lineage.
- Morphine induces CD4+ T cell IL-4 expression through an adenylyl cyclase mechanism independent of the protein kinase A pathway.
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