Dr. Forest Raymond Sheppard MD
Surgeon
887 CONGRESS ST STE 210 PORTLAND ME, 04102About
Dr. Forest Sheppard is a general surgeon practicing in PORTLAND, ME. Dr. Sheppard 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. Sheppard provides quality surgical service for gravely ill or injured patients and is able to respond quickly due to knowledge of various surgical procedures.
Provider Details
Expert Publications
Data provided by the National Library of Medicine- The abdominal compartment syndrome as a second insult during systemic neutrophil priming provokes multiple organ injury.
- Clinically relevant osmolar stress inhibits priming-induced PMN NADPH oxidase subunit translocation.
- Structural organization of the neutrophil NADPH oxidase: phosphorylation and translocation during priming and activation.
- Platelet-activating factor-induced clathrin-mediated endocytosis requires beta-arrestin-1 recruitment and activation of the p38 MAPK signalosome at the plasma membrane for actin bundle formation.
- Platelet-activating factor-mediated endosome formation causes membrane translocation of p67phox and p40phox that requires recruitment and activation of p38 MAPK, Rab5a, and phosphatidylinositol 3-kinase in human neutrophils.
- Inflammatory response is associated with critical colonization in combat wounds.
- Direct Evidence Versus Lack of Direct Evidence and the Impact on HTA Acceptance.
- Rapid Detection of Neutrophil Oxidative Burst Capacity is Predictive of Whole Blood Cytokine Responses.
- Control of severe intra-abdominal hemorrhage with an infusible platelet-derived hemostatic agent in a nonhuman primate (rhesus macaque) model.
- Rapid assessment of shock in a nonhuman primate model of uncontrolled hemorrhage: Association of traditional and nontraditional vital signs to mortality risk.
- Inflammatory Profile in Response to Uncontrolled Hemorrhage in a Non-Human Primate (Rhesus Macaque) Model.
- Severe Hemorrhagic Shock Induces Acute Activation and Expansion of IL-8+/IL-10+ Neutrophils with Enhanced Oxidative Reactivity in Non-Human Primates.
- Non-human primate model of poly-traumatic hemorrhagic shock recapitulates early platelet dysfunction observed following severe injury in humans.
- Tissue injury suppresses fibrinolysis after hemorrhagic shock in nonhuman primates (rhesus macaque).
- Nonhuman primate model of polytraumatic hemorrhagic shock recapitulates early platelet dysfunction observed following severe injury in humans.
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