Sentence examples for systemic deactivation from inspiring English sources

Consistent with previous results concerning alveolar macrophage deactivation, we observed a systemic deactivation of monocytes in septic neutropenic ARDS.

Speculating that our results are in line with previous evidence of a systemic deactivation of monocyte antigen or leukocytes described in septic patients [ 11], however, is tempting.

It has been suggested that the secreted circulating form in humans may play a role in systemic deactivation of chemotactic cytokines, ensuring that the peptides are only active at the local site where they are released.

While local immunosuppression is associated with a good prognosis in non-neutropenic patients with ARDS [ 16], a systemic immunosuppression (monocyte deactivation, neutropenia) could be inappropriate in neutropenic patients with septic ARDS and could participate in increased mortality.

A cylinder deactivation system helps trim fuel consumption.

Monocytes display altered behaviour in response to systemic inflammation; this has been called "deactivation" and is characterised by reduced HLA-DR expression and attenuated tumour necrosis factor-α (TNF) release in response to lipopolysaccharide (LPS) stimulus1.

In summary, our data regarding brain injury suggest that brain-derived cytokines as well as direct brain-stem irritation can trigger strong sympathetic activation leading to a systemic IL-10 release and monocytic deactivation which, as a sign of severe systemic immunodepression, is associated with a high risk of infectious complications.

Remarkably, this was associated with monocytic deactivation – a sign of systemic immunodepression and a high risk of infectious complications.Finally, these data were validated in patients with accidental brain injury, in whom we demonstrated a correlation between the severity of injury, sympathetic activation, IL-10 plasma levels and the incidence of infectious complications.

It happens because serotonin-like substances are directly released into the systemic circulation through the ovarian venous system, bypassing hepatic deactivation.

In this process the catecholamine-mediated systemic IL-10 release that causes monocytic deactivation may be a key mechanism.

Whether the activation or deactivation of metabolically sensitive KATP channels and their regulation of systemic metabolic homeostasis and cellular excitability ultimately contribute to neuronal hyperexcitability and the subsequent degeneration of neural networks that are linked to hyperexcitable cells in ALS remains unknown.