Jörg Schröder
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Jörg Schröder has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
Frank Stüber
1 shared publicationKarl-Hermann Staubach
1 shared publicationPeter Zabel
1 shared publicationVolker Kahlke
1 shared publication
Latest Publications
- Open Access
- 1 November 1998
- Published by American Medical Association (AMA) in Archives of Surgery
- Vol. 133 (11) , 1200-1205
Gender Differences in Human Sepsis
DESPITE IMPROVEMENT in surgical and critical care management, the prognosis of sepsis and subsequent multiple organ dysfunction remained unchanged during the past decades.1 The common pathway of multiple organ dysfunction is a severe inflammatory reaction resulting from systemic cytokine release.2 In response to the initiating proinflammatory reaction, with tumor necrosis factor (TNF-α), interleukin (IL) 1 and IL-6 playing the predominant role, the body also mounts an immediate anti-inflammatory response. Among the diverse agents, different interleukins, such as IL-10, have profound anti-inflammatory effects that are suggested to control the proinflammatory reaction.3
- 1 November 1998
- Published by American Medical Association (AMA) in Archives of Surgery
- Vol. 133 (11) , 1200-1205
Open AccessGender Differences in Human Sepsis
DESPITE IMPROVEMENT in surgical and critical care management, the prognosis of sepsis and subsequent multiple organ dysfunction remained unchanged during the past decades.1 The common pathway of multiple organ dysfunction is a severe inflammatory reaction resulting from systemic cytokine release.2 In response to the initiating proinflammatory reaction, with tumor necrosis factor (TNF-α), interleukin (IL) 1 and IL-6 playing the predominant role, the body also mounts an immediate anti-inflammatory response. Among the diverse agents, different interleukins, such as IL-10, have profound anti-inflammatory effects that are suggested to control the proinflammatory reaction.3