TWO CASES OF YOUNG CHILDREN WITH ACUTE SEVERE ASTHMA TREATED BY NONINVASIVE POSITIVE PRESSURE VENTILATION VIA A HELMET.

We used noninvasive positive pressure ventilation (NPPV) with a helmet-type mask in two young children with acute severe bronchial asthma. The intervention was well-tolerated, because the helmet-type mask caused no pain or discomfort, as compared to the face mask. Tracheal intubation can be avoided by the start of the NPPV. Thus, the respiratory symptoms improved by the use of NPPV in children with acute severe asthma with respiratory muscle fatigue and failure of medical treatment.

Inhibitory effect of açaí (Euterpe oleracea Mart.) pulp on IgE-mediated mast cell activation.

The palm fruit açaí is known to have potential health benefits due to its antioxidant scavenging capacities. Pretreatment of IgE-sensitized mouse primary cultured mast cells with açaí pulp resulted in the dramatic suppression of antigen-induced degranulation in a dose-dependent manner. Similarly, açaí suppressed IgE-mediated degranulation and transcription of the cytokine genes from a cultured mast cell line of rat basophilic leukemia (RBL)-2H3 cells. Açaí could selectively inhibit FcεRI signaling pathways. Furthermore, the FcεRI-mediated complementary signaling pathway was also suppressed by açaí. These results demonstrate that açaí is a potent inhibitor of IgE-mediated mast cell activation.

Selective inhibition of Fcepsilon RI-mediated mast cell activation by a truncated variant of Cbl-b related to the rat model of type 1 diabetes mellitus.

Ubiquitin-protein ligase Cbl-b negatively regulates high affinity IgE receptor (FcepsilonRI)-mediated degranulation and cytokine gene transcription in mast cells. In this study, we have examined the role of a truncated variant of Cbl-b related to the rat model of type 1 diabetes mellitus using the mast cell signaling model. Overexpression of the truncated Cbl-b that lacks the C-terminal region did not suppress the activation of proximal and distal signaling molecules leading to degranulation. FcepsilonRI-mediated tyrosine phosphorylation of Syk, Gab2, and phospholipase C-gamma1, and activation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAP kinase), and inhibitor of nuclear factor kappaB kinase (IKK), and generation of Rac1 are unaffected in cells overexpressing the truncated Cbl-b in the lipid raft. On the other hand, FcepsilonRI-mediated transcriptional activation of nuclear factor of activated T cells (NFAT), and transcription of interleukin-3 (IL-3) and IL-4 mRNA are inhibited by overexpression of the truncated variant of Cbl-b. This suppression parallels the re-compartmentalization of specific effector molecules in the lipid raft. These structural and functional analyses reveal the mechanism underlying the selective inhibition of cellular signaling by the truncated variant of Cbl-b related to insulin-dependent diabetes mellitus.

A novel phenoxazine derivative suppresses surface IgM expression in DT40 B cell line.

1. 2-amino-4, 4alpha-dihydro-4alpha, 7-dimethyl-3H-phenoxazine-3-one (Phx) has been demonstrated to be an actinomycin D-like phenoxazine, and to display anti-tumour activity. 2. In this study, we report on the effect of Phx on B cell antigen receptor (BCR) and receptor-mediated signalling in DT40 B cells. 3. Treatment of B cells with Phx for 12 h inhibited BCR-stimulated tyrosine phosphorylation of cellular proteins. 4. B cells exposed to Phx exhibited down-regulation of surface IgM which is part of BCR. In contracts with actinomycin D, Phx rapidly reduced the expression of IgM without decreasing the expression of other signalling molecules. 5. Analysis with confocal microscopy demonstrated that Phx treatment reduced IgM expression both at the cell surface and inside the cell. 6. Treatment of B cells with Phx resulted in the reduction of IgM secretion. Since MG-132, a proteasomal inhibitor, restored IgM contents to the control levels, Phx has the specific effect of accelerating IgM degradation. 7. These results suggest that Phx down-regulates the expression of IgM and inhibits BCR-mediated signalling and IgM secretion. Phx may be useful as an immunosuppressive agent for therapeutic purposes.