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ABSTRACT: Many patients with asthma or chronic obstructive pulmonary disease receive corticosteroids; thus, prevention and treatment of corticosteroid-induced bone loss is important. Patients taking corticosteroids should maintain a daily calcium [...]

ABSTRACT: Patients with asthma or chronic obstructive pulmonary disease (COPD) may be at increased risk for osteoporosis because of the effects of corticosteroids and other comorbid factors. While excessive use [...]

Coronary artery dissection is an infrequent but serious complication of coronary angioplasty that can lead to periprocedural vessel occlusion, emergency bypass surgery, myocardial infarction or death. Recently, a perfusion balloon cathether was developed that permits passive perfusion of blood through the central lumen of the catheter. It enables prolonged balloon inflations to be performed and has been used to provide distal blood flow after coronary occlusion. To evaluate the effectiveness of the perfusion balloon catheter in patients with major coronary dissections, 36 consecutive patients treated with the perfusion balloon catheter were compared with 46 consecutive patients treated before its availability. The 2 groups were similar in terms of clinical, angiographic and initial procedural characteristics. Use of the perfusion balloon catheter permitted a significantly longer inflation than standard balloon inflation (average 18 [+ or -] 5 min). Angiographic success was significantly greater with the perfusion balloon catheter (84 vs 62% for conventional therapy), whereas complications were markedly reduced (48 vs 78%). With the perfusion balloon catheter there were fewer deaths (2 vs 6%), myocardial infarctions (14 vs 40%) and emergency bypass operations (11 vs 25%). The findings of this retrospective comparison demonstrate that the perfusion balloon catheter is effective for the management of major dissections after coronary angioplasty. The use of the perfusion balloon catheter should be considered when a major coronary dissection occurs and when emergency bypass surgery is contemplated. (Am J Cardiol 1991;67:1056-1060), Percutaneous transluminal coronary angioplasty (PTCA, inserting a balloon-tipped catheter into the coronary arteries to dilate narrowed vessels) is a relatively safe method for improving blood flow to the heart in selected patients with symptomatic coronary artery disease. In 2 to 10 percent of PTCA procedures, dissection of the artery occurs, that is, the inner walls of the vessel separate and the space fills with blood. This complication blocks blood flow, and may cause heart attack or death, and may require emergency coronary artery bypass grafting. One study found that among patients who developed arterial tears and dissection, mortality was 5 percent, and the affected artery became blocked in 21 percent of cases. In addition, these patients have a less favorable long-term outcome. Even with improved techniques, equipment and operator skill in PTCA, in-hospital mortality is 1 percent, 4.3 percent of patients suffer a heart attack, and emergency coronary artery bypass is required in 2 percent of cases. The perfusion balloon catheter, which allows blood to pass through, makes prolonged balloon inflations possible and increases the success rate of the procedure. The effectiveness of perfusion balloon catheters was compared with conventional PTCA in 1,026 patients. With the perfusion balloon catheter, the incidence of major complications was lower, although the results were statistically significant only for heart attacks. Other new techniques that may improve outcomes are laser balloon angioplasty, atherectomy devices (which remove the fatty plaques inside arteries) and intracoronary stents (coils that keep an artery expanded). These techniques are available on a limited basis and require better surgical skills than those necessary for the perfusion balloon catheter. (Consumer Summary produced by Reliance Medical Information, Inc.)

Regulation of gp130 expression in cultured mouse mast cells and role for IL‐6 trans‐signaling in increasing survival and cytokine production. It is reported that human and mouse mast cells express the IL‐27R, which consists of WSX‐1 (the IL‐27Rα subunit) and the signal‐transducing subunit gp130. Although it has been proposed that IL‐27 may negatively regulate mast cell‐dependent, immediate hypersensitivity responses directly, this has yet to be examined specifically. We found that mouse BMMC and primary peritoneal mast cells are unresponsive to IL‐27. Consistent with this, gp130 protein in resting BMMC was not on the cell surface to a measurable degree but was found intracellularly, and data are consistent with incompletely processed N‐linked glycosylation. Furthermore, BMMC constitutively expressed SOCS3, a major negative regulator of gp130 signaling. However, BMMC stimulation with IL‐10 and consequential STAT3 activation increased gp130 expression, which resulted in a functional gp130 receptor on the BMMC cell surface. IL‐10 has not been previously shown to regulate gp130 expression, which on the BMMC surface, permitted IL‐6 trans‐signaling, found to increase survival under limiting conditions and enhance IL‐13 and TNF‐α secretion. This study identifies factors that regulate mouse mast cell gp130 expression and signaling and makes conspicuous the limitations of using cultured mouse mast cells to study the effects of the IL‐6/IL‐12 cytokine family on mast cell biology.

ABSTRACTChallenge with the intracellular protozoan parasite Toxoplasma gondiiinduces a potent CD8+T-cell response that is required for resistance to infection, but many questions remain about the factors that regulate the presentation of major histocompatibility complex class I (MHC-I)-restricted parasite antigens and about the role of professional and nonprofessional accessory cells. In order to address these issues, transgenic parasites expressing ovalbumin (OVA), reagents that track OVA/MHC-I presentation, and OVA-specific CD8+T cells were exploited to compare the abilities of different infected cell types to stimulate CD8+T cells and to define the factors that contribute to antigen processing. These studies reveal that a variety of infected cell types, including hematopoietic and nonhematopoietic cells, are capable of activating an OVA-specific CD8+T-cell hybridoma, and that this phenomenon is dependent on the transporter associated with antigen processing and requires live T. gondii. Several experimental approaches indicate that T-cell activation is a consequence of direct presentation by infected host cells rather than cross-presentation. Surprisingly, nonprofessional antigen-presenting cells (APCs) were at least as efficient as dendritic cells at activating this MHC-I-restricted response. Studies to assess whether these cells are involved in initiation of the CD8+T-cell response to T. gondiiin vivo show that chimeric mice expressing MHC-I only in nonhematopoietic compartments are able to activate OVA-specific CD8+T cells upon challenge. These findings associate nonprofessional APCs with the initial activation of CD8+T cells during toxoplasmosis.

Patients with primary hypogammaglobulinemia have been reported to have encephalopathy, but progressive multifocal leukoencephalopathy (PML) due to JC virus reactivation is a rare cause.