There was a trend toward improved function over time.
Conclusions: Hemidiaphragm paresis results in significant morbidity after repair of congenital heart defects. Early diagnosis and plication result in timely extubation. The plicated diaphragm demonstrates return of function that may improve over time. This is the first study to numerically quantitate the degree of diaphragm recovery.”
“Nitric oxide (NO) generated
from inducible NO synthase (iNOS) during hepatic injury has been reported to Trametinib cost contribute to cytoprotection or cellular damage. Rebamipide, anti-gastric ulcer drug, has protective effects in a variety of tissue and organ injury. However, it remains unknown whether rebamipide is involved in the regulation of iNOS
gene expression under pathological conditions. We examined whether rebamipide influences the induction of iNOS in hepatocytes exposed to pro-inflammatory cytokine. Primary cultured rat hepatocytes were treated with interleukin (IL)-1 beta in the presence or absence of rebamipide. Pretreatment of cells with rebamipide resulted in up-regulation of iNOS induction by IL-1 beta, followed by increased NO production. PSI-7977 cell line Rebamipide enhanced the degradation of I kappa B alpha and the activation of NF-kappa B. Further, rebamipide super-induced the up-regulation of type I IL-1 receptor (IL-1RI), which is essential for iNOS induction in addition to the I kappa B/NF-kappa B pathway. Transfection experiments revealed that rebamipide increased Montelukast Sodium the transactivation of NOS promoter and the stability of iNOS mRNA. In the latter, rebamipide increased the antisense-tran script corresponding to the 3′-UTR of NOS mRNA, which stabilizes iNOS mRNA by interacting with the 3′-UTR and RNA-binding proteins.
These findings demonstrate that rebamipide up-regulates iNOS by iNOS promoter activation through NF-kappa B, and by its mRNA stabilization presumably through the super-induction of IL-1RI and antisense-transcript. Rebamipide may contribute to a novel potentiated treatment in liver injuries. (c) 2007 Elsevier Inc. All rights reserved.”
“Objective: We sought to investigate the mechanism whereby a particular deformity of the aortic arch, an angulated Gothic shape, might lead to hypertension late after anatomically successful repair of aortic coarctation.
Methods: Fifty-five normotensive patients with anatomically successful repair of aortic coarctation and either a Gothic (angulated) or a Romanesque (smooth and rounded) arch were studied with magnetic resonance angiography and flow mapping in both the ascending and descending aortas. Systolic waveforms, central aortic stiffness, and pulse velocity were measured. We hypothesized that arch angulation would result in enhanced systolic wave reflection with loss of energy across the aortic arch, as well as increased central aortic stiffness.
Results: Twenty patients were found to have a Gothic, and 35 a Romanesque, arch.