PubMed Health⌕ Search

Biomedical subjects

B Hwangbo

Publications and source records attributed to B Hwangbo.

2 recordsLinked to original sources

Right heart dysfunction in post-tuberculosis emphysema.

SETTING: University-affiliated general hospital. OBJECTIVE: To evaluate the pump performance of right heart before and after exercise in post-tuberculosis emphysema. DESIGN: In patients with post-tuberculosis or primary emphysema (similar lung volumes), body plethysmography, arterial blood gas analysis and echocardiography were performed at rest and after exercise. Right heart pump performance was evaluated with the ejection fraction. RESULTS: At rest, in post-tuberculosis emphysema, diffusing capacity (mean +/- SE 72.7 +/- 3.9 vs. 91.0 +/- 7.1% of reference) and right ventricular ejection fraction (57.5 + 1.4 vs. 61.3 +/- 1.2%) were lower and PaCO2 (42.7 +/- 1.1 vs. 38.6 +/- 0.7 mmHg) was higher, while lung compliance, airway resistance, PaO2, and alveolar-arterial oxygen difference were not different. After exercise, PaO2 (65.6 +/- 2.8 vs. 80.5 +/- 3.5 mmHg) and right ventricular ejection fraction (51.2 +/- 2.4 vs. 59.6 +/- 1.7%) were lower and PaCO2 (47.0 +/- 1.5 vs. 40.9 +/- 1.5 mmHg) was higher in post-tuberculosis emphysema, whereas alveolar-arterial oxygen difference was not different. PaCO2 and alveolar-arterial oxygen difference increased, and PaO2 and right ventricular ejection fraction decreased in post-tuberculosis emphysema, while they did not significantly change in primary emphysema. CONCLUSION: In post-tuberculosis emphysema, the impairment of gas exchange was more serious. Global assessment should be focused on right heart dysfunction which might be more affected than in primary emphysema.

Blood Gas Analysis↗

NF-kappaB activation is related to the resistance of lung cancer cells to TNF-alpha-induced apoptosis.

In diverse cell types, NF-kappaB transcription factors have been shown to have a role in regulating the apoptotic program, either as essential for the induction of apoptosis or, perhaps more commonly, as blockers of apoptosis. We investigated the role of NF-kappaB activation in the TNF-alpha-mediated apoptosis in lung cancer cells. TNF-alpha-resistant NCI-H157 cells became sensitized to TNF-alpha by prior treatment with cycloheximide, suggesting the presence of newly synthesized antiapoptotic protein(s). We next evaluated whether the transcription of antiapoptotic protein(s) depends on the activation of NF-kappaB. NF-kappaB activation was blocked by either adenovirus-mediated overexpression of IkappaBalpha superrepressor or pretreatment with proteasome inhibitor, MG132. Both methods of blocking NF-kappaB activation enhanced TNF-alpha-induced apoptosis in NCI-H157 cells. These results suggest that NF-kappaB activation confers resistance to TNF-alpha-mediated apoptosis in lung cancer cells.

Adenoviridae↗