No abstract

Sepsis is a well-recognized healthcare issue worldwide, ultimately resulting in significant mortality, morbidity and resource utilization during and after critical illness. In its most severe form, sepsis causes multi-organ dysfunction that produces a state of critical illness characterized by severe immune dysfunction and catabolism. Sepsis induces the activation of complement factor via 3 pathways and the release of inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin-1beta (IL-1β), resulting in a systemic inflammatory response. The inflammatory cytokines and nitric oxide release induced by sepsis decrease systemic vascular resistance, resulting in profound hypotension. The combination of hypotension and microvascular occlusion results in tissue ischemia and ultimately leads to multiple organ failure. Several clinical and experimental studies have reported that treatment using adsorption of cytokines is beneficial during endotoxemia and sepsis. This review article analyzes the efficacy of CytoSorb® adsorber in reducing the inflammatory response during sepsis. The CytoSorb® adsorber is known to have excellent adsorption rates for inflammatory cytokines such as IL-1β, IL-6, IL-8, IL-10, and TNF-α. Studies have demonstrated that treatment with cytokine adsorbing columns has beneficial effects on the survival rate and inflammatory responses in animal septic models. Additionally, several cases have been reported in which treatment with cytokine adsorbing columns is very effective in hemodynamic stabilization and in preventing organ failure in critically ill patients. Although further investigations and clinical trials are needed, treatment with cytokine adsorbing columns may play an important role in the treatment of sepsis in the near future.

The delayed onset of a facial paresis following termination of vasoactive treatment points to a disturbed microcirculation of the nerve as the main pathophysiological feature. Two groups could be identified on the basis of intraoperative EMG activity. In one group with presence of "A-trains" medication apparently masked the onset of an immediate postoperative facial nerve deficit. Four patients without "A-trains" did not develop a typical delayed facial nerve paresis during vasoactive treatment, but thereafter. The time lag between termination of treatment and onset of a delayed palsy points to a protective effect due to improved microcirculation.

Some strains of Saccharomyces cerevisiae (including strains used in fermentation processes) produce short chain (mainly 8 carbon) oxylipins and not potent inflammatory long chain (20 carbon) oxylipins such as prostaglandins. When acetylsalicylic acid (aspirin) was added to cultures of Sacch. cerevisiae UOFS Y-2330, flocculation was significantly inhibited as well as the production of 3-hydroxy 8:0 thereby linking flocculation and this oxylipin. Furthermore, no traces of 3-hydroxy 8:0 could be detected at the start of flocculation in this yeast. This research is based on (i) reports that yeasts in general can produce bioactive prostaglandins, (ii) findings suggesting a link between aspirinsensitive prostaglandins and biofilm formation by Candida albicans, (iii) the discovery that the addition of low concentrations of aspirin abolish yeast biofilm formation and sexual cell aggregation and (iv) the recent discovery of a novel potent aspirinsensitive pro-inflammatory 3-hydroxy prostaglandin E 2 synthesized by Candida albicans in conjunction with mammalian cells probably during candidiasis.

Using immunofluorescence confocal laser scanning microscopy, immunogold transmission electron microscopy and gas chromatography--mass spectrometry, we demonstrated the presence of 3-hydroxy fatty acids in Cryptococcus neoformans. Our results suggest that these oxylipins accumulate in capsules where they are released as hydrophobic droplets through tubular protuberances into the surrounding medium.