Decreased lung function with exacerbation, and progressive decline of FEV(1) were observed in patients with TB-destroyed lung.

The present study provides new insight into health care use and the economic burden of COPD in Korea. Changing patterns of COPD-related medication use could help inform COPD management policies.

SLC30A8 encodes the b-cell-specific zinc transporter-8 (ZnT-8) expressed in insulin secretory granules. The single-nucleotide polymorphism rs13266634 of SLC30A8 is associated with susceptibility to post-transplantation diabetes mellitus (PTDM). We tested the hypothesis that the polymorphic residue at position 325 of ZnT-8 determines the susceptibility to cyclosporin A (CsA) suppression of insulin secretion. INS (insulinoma)-1E cells expressing the W325 variant showed enhanced glucose-stimulated insulin secretion (GSIS) and were less sensitive to CsA suppression of GSIS. A reduced number of insulin granule fusion events accompanied the decrease in insulin secretion in CsA-treated cells expressing ZnT-8 R325; however, ZnT-8 W325-expressing cells exhibited resistance to the dampening of insulin granule fusion by CsA, and transported zinc ions into secretory vesicles more efficiently. Both tacrolimus and rapamycin caused similar suppression of GSIS in cells expressing ZnT-8 R325. However, cells expressing ZnT-8 W325 were resistant to tacrolimus, but not to rapamycin. The Down's syndrome candidate region-1 (DSCR1), an endogenous calcineurin inhibitor, overexpression and subsequent calcineurin inhibition significantly reduced GSIS in cells expressing the R325 but not the W325 variant, suggesting that differing susceptibility to CsA may be due to different interactions with calcineurin. These data suggest that the ZnT-8 W325 variant is protective against CsA-induced suppression of insulin secretion. Tolerance of ZnT-8 W325 to calcineurin activity may account for its protective effect in PTDM.

Clinical prediction indicators such as the pneumonia severity index (PSI) and CURB-65 score are useful, but they are complex and often not followed. Therefore, biomarkers that improve hospital outcome predictions are emerging. This study evaluated the prognostic value of a new sepsis biomarker, serum lysophosphatidylcholine (LPC) concentrations, in community-acquired pneumonia (CAP) patients. We prospectively collected blood samples from emergency department CAP patients on days 1 and 7 (post-admission) and analyzed their plasma LPC concentrations. We retrospectively reviewed patient medical records and analyzed correlations between plasma LPC concentrations and clinical parameters and hospital outcomes. A total of 56 CAP patients were included in this study; 24 (42.9 %) required intubation and 15 (26.8 %) died. The mean LPC concentrations on days 1 (p = 0.015) and 7 (p = 0.002) of hospitalization were significantly lower in the non-survivors. Day 1 LPC concentrations were inversely correlated with the PSI (ρ = -269) and CURB-65 scores (ρ = -386). For predicting hospital mortality, the day 1 LPC concentration was comparable with the CURB-65 or PSI scores. Day 1 LPC cut-off levels <29.6 μmol/L were associated with hospital CAP outcomes, including the need for mechanical ventilation, vasopressors, intensive care unit admission, and hospital mortality. Additionally, day 7 LPC concentrations were correlated with in-hospital mortality. Initial serum LPC concentrations predicted hospital outcomes in CAP patients requiring hospitalization. These values were correlated with prognostic markers, such as the PSI and CURB-65 scores. Additionally, follow-up LPC measurements predicted the clinical course of CAP patients.