Inflammatory effects of hypothermia and inhaled H2S during resuscitated, hyperdynamic murine septic shock.

Inhaling hydrogen sulfide (H2S) reduced energy expenditure resulting in hypothermia. Because the inflammatory effects of either hypothermia alone or H2S per se still are a matter of debate, we tested the hypothesis whether inhaled H2S amplifies the hypothermia-related modulation of the inflammatory response. Fifteen hours after cecal ligation and puncture or sham laparotomy, anesthetized and mechanically ventilated normothermic and hypothermic mice (core temperature kept at 38°C and 27°C, respectively) received either 100 ppm H2S or vehicle.

Xenon blocks AMPA and NMDA receptor channels by different mechanisms.

The noble gas xenon (Xe) inhibits not only NMDA receptors (NMDARs) but also the two other subtypes of glutamate receptor i.e. AMPA (AMPARs) and kainate receptors.

The effects of thoracic epidural anesthesia on hepatic blood flow in patients under general anesthesia.

Background: Hepatic hypoperfusion is regarded as an important factor in the pathophysiology of perioperative liver injury. Although epidural anesthesia (EDA) is a widely used technique, no data are available about the effects on hepatic blood flow of thoracic EDA with blockade restricted to thoracic segments in humans.

Methods: In 20 patients under general anesthesia, we assessed hepatic blood flow index in the right and middle hepatic vein by use of multiplane transesophageal echocardiography before and after induction of EDA.

Prolonged classical NF-kappaB activation prevents autophagy upon E. coli stimulation in vitro: a potential resolving mechanism of inflammation.

Activation of NF-kappaB is known to prevent apoptosis but may also act as proapoptotic factor in order to eliminate inflammatory cells. Here, we show that classical NF-kappaB activation in RAW 264.7 and bone marrow-derived macrophages upon short E.

Anti-inflammatory interventions of NF-kappaB signaling: potential applications and risks.

Signaling via NF-kappaB is a key process during inflammation and thus constitutes an attractive target for anti-inflammatory therapeutic interventions. Especially during initial hyperinflammatory states of an acute illness such as sepsis or in the course of chronic inflammation and autoimmune diseases inhibition of IKK-driven NF-kappaB activation provides a promising treatment strategy. Given its critical role in innate and adaptive immune responses, however, there is a certain amount of risk due to induced immunodeficiency that may follow inhibitory treatment.

Enhancement of NF-kappaB activation in lymphocytes prevents T cell apoptosis and improves survival in murine sepsis.

Sepsis induces extensive lymphocyte apoptosis that contributes to immunosuppression and mortality. Activation of the canonical NF-kappaB pathway, however, prevents TNF-alpha-induced lymphocyte apoptosis. In this study the function of canonical NF-kappaB in T cells was studied in the context of murine sepsis.

Rapid increase of glial glutamate uptake via blockade of the protein kinase A pathway.

Glutamate is the main excitatory neurotransmitter in the vertebrate central nervous system. Removal of this transmitter from the synaptic cleft by glial and neuronal transporter systems plays an important role in terminating glutamatergic neurotransmission. The effects of different activators and blockers of PKA and PKC on glutamate uptake were studied in primary glial cells cultivated from the rat cortex using the patch-clamp recording technique and immunocytochemical methods.

Escherichia coli prevents phagocytosis-induced death of macrophages via classical NF-kappaB signaling, a link to T-cell activation.

NF-kappaB is a crucial mediator of macrophage inflammatory responses, but its role in the context of pathogen-induced adaptive immune responses has yet to be elucidated. Here, we demonstrate that classical NF-kappaB activation delays phagocytosis-induced cell death (PICD) in Raw 264.7 and bone marrow-derived macrophages (BMDMs) upon ingestion of bacteria from the Escherichia coli laboratory strain Top10.