[Cardiac implantable electronic devices (CIED) not an absolute contraindication to MRI]. / Pacemaker ingen absolut kontraindikation för MR-undersökning.

Cardiac implantable electronic devices (CIED) not an absolute contraindication to MRI Conventional cardiac implantable electronic devices (CIED) are presently not an absolute contraindication to magnetic resonance imaging (MRI), which thus is accessible for device patients depending on risk/benefit assessments. While current literature suggests that MRI can be performed without risk if precautions are taken, adverse events have been reported. The number of MR conditional CIEDs is rapidly increasing, and depending on device and electrode combinations, patients can now undergo advanced MRI at 3.0 T without risk, possibly with restriction, e.g. anatomy coverage. This article describes published guidelines, recommendations and complications that may appear during MRI and precautions to avoid and manage them. The recommendations made are based on a thorough literature review and our own experiences reported with the aim to increase the awareness of healthcare professionals so that device patients no longer are excluded from the advantages of MRI as a diagnostic tool.

CD44 deficiency leads to enhanced neutrophil migration and lung injury in Escherichia coli pneumonia in mice.

CD44 is a major cell-surface receptor for hyaluronic acid (HA), a glycosaminoglycan component of extracellular matrix. HA-CD44 interactions have been implicated in leukocyte extravasation into an inflammatory site. This study examined the role of CD44 in acute inflammatory responses during pneumonias induced by Escherichia coli and Streptococcus pneumoniae using CD44-deficient mice. In E. coli-induced pneumonia, neutrophil accumulation in the lungs and edema formation was increased by 84% and 88%, respectively, in CD44-deficient mice compared to wild-type mice. In contrast, no difference was observed between these genotypes in S. pneumoniae-induced pneumonia, and the HA content in the lungs decreased after instillation of S. pneumoniae, but not E. coli, in both genotypes. Studies to determine the mechanisms for this enhanced response showed that: 1) neutrophil apoptosis was not different between these two genotypes in either type of pneumonia; 2) CD44 deficiency resulted in enhanced mRNA expression of several inflammatory genes; and 3) CD44-deficient neutrophils migrated through Matrigel in response to chemoattractants faster and in greater numbers than wild-type neutrophils in vitro and this increase was in part dependent on HA content in the Matrigel. These data demonstrate that CD44 deficiency results in enhanced inflammation in E. coli but not S. pneumoniae-induced pneumonia, suggesting a previously unrecognized role for CD44 in limiting the inflammatory response to E. coli.

Resolution of lung inflammation by CD44.

Successful repair after tissue injury and inflammation requires resolution of the inflammatory response and removal of extracellular matrix breakdown products. We have examined whether the cell-surface adhesion molecule and hyaluronan receptor CD44 plays a role in resolving lung inflammation. CD44-deficient mice succumb to unremitting inflammation following noninfectious lung injury, characterized by impaired clearance of apoptotic neutrophils, persistent accumulation of hyaluronan fragments at the site of tissue injury, and impaired activation of transforming growth factor-beta1. This phenotype was partially reversed by reconstitution with CD44+ cells, thus demonstrating a critical role for this receptor in resolving lung inflammation.