Model Seleksi Premi Asuransi Jiwa Dwiguna untuk Kasus Multiple Decrement

This article discusses a select survival model for the case of multiple decrements in evaluating endowment life insurance premium for person currently aged ( + ) years, who is selected at age with ℎ years selection period. The case of multiple decrements in this case is limited to two cases. The calculation of the annual premium is done by prior evaluating of the single premium, and the present value of annuity depends on theconstant force assumption

SOD3, AQP5, and pro-SPC proteins in control, moderate, and severe COPD lungs.

<p><b>A</b>. Two bands (32 and 30 kDa) are recognized by a specific polyclonal antibody against human SOD3 (Santa Cruz, sc-32219) via Western blot. The blots were stripped and reprobed with a monoclonal anti-β actin antibody. <b>B</b>. Quantitative densitometry of SOD3 relative to corresponding β actin. One-way ANOVA. *P<0.05 and ***P<0.001 vs control or moderate group. N = 17. <b>C</b>. Representative images of control, moderate, and severe groups. H & E stain. 10×. <b>D</b>. AQP5 proteins are detected by a specific antibody against human AQP5 (Santa Cruz, sc-28628) via Western blot. Pro-SPC is detected (21 kDa) using a specific antibody (Millipore, AB3786). <b>E</b>. Densitometric measurements of AQP5 over β actin. N = 17. *P<0.05 versus controls. <b>F</b>. Relative pro-SPC protein expression. One-way ANOVA. *P<0.05 versus controls and **P<0.01 versus moderate group.</p

Patient demographics.

<p>Values are medians (25^th, 75^th percentile). Perdlco, severity classification of DLCO abnormality (continuous). Severity was grouped using Gold standard according to REV1pd1a (see Methods): Controls ≥80%; Moderate ≥50 and <80%; Severe <50%. Statistical analysis was performed using Mann-Whitney U test and Kruskal-Wallis ANOVA. P value <0.05 was considered significant. ^aP<0.05 compared with Control group; ^bP<0.05 versus moderate stage.</p><p>Patient demographics.</p

Expression of protein levels and COPD severity.

<p><b>A</b>. SOD3, total CFTR (tCFTR), and CFTR in ATI cells (CFTR1) are associated with GOLD classification of COPD (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0109725#s2" target="_blank">Methods</a> for details). <b>B</b>. CFTR expressed in ATII cells correlates with GOLD1. <b>C</b>. β ENaC in ATI cells is positively associated with GOLD1.</p

Association of spirometry and expression of SOD3 and ENaC in COPD lungs.

<p><b>A</b>. Total SOD3 and perdlco. <b>B</b>. α ENaC in ATII cells and spirometry. <b>C</b>. α ENaC expressed in ATI cells and fev1pd1a. <b>D</b>. β ENaC in ATI cells and lung function test. <b>E</b>. Total γ ENaC level and fev1prd1.</p

Positive correlation of CFTR with spirometry test in COPD lungs.

<p><b>A</b>. Total CFTR expression and fev1prd2. <b>B</b>. Expression of CFTR in ATI cells and three spirometric parameters. <b>C</b>. CFTR proteins in ATII cells and spirometry test.</p

Correlation of aquaporin 5 with spirometry test.

<p>Dotted lines were created by linear regression analysis of the paired experimental data.</p

Expression of ENaC proteins.

<p><b>A</b>. Representative Western blots. α (90 kDa), β (95 kDa) and γ ENaC protein signals are found in blots probed with specific antibodies against α (Santa Cruz, sc-22239), β (Santa Cruz, sc-21013), and γ (Abcam, ab3468) subunits. <b>B</b>. Total expression levels of ENaC subunits. β actin is used as a loading control. <b>C & D</b>. Expression of ENaC proteins in ATI and ATII cells. The expression levels of ENaC proteins related to AQP5 (<b>C</b>) and pro-SPC (<b>D</b>) were adjusted to compensate for the alterations in AQP5 and pro-SPC (dotted bars). One-way ANOVA. *P<0.05 and ***P<0.001 versus control groups.</p

p53-mediated induction of PAI-1 expression contributes to increased pulmonary MPO levels in mice with PCSE.

<p>(<b>A</b>) WT mice were exposed to ambient air (control) or PCS (n = 5/group) for 20 weeks. LL collected from these mice was subjected to total cell counting. (<b>B</b>) Total protein in the lavage was quantified from the above exposed mice. (<b>C</b>) Paraffin embedded lung sections from WT, p53- and PAI-1-deficient mice (n = 5mice/group) exposed to ambient air (control) or PCS for 20 weeks were subjected to H&E staining. Representative fields from 1 of 3 sections per subject are shown at X 400 magnification. Lung sections were subjected to IHC analysis for neutrophils using anti-MPO antibody and for macrophages using anti-F4/80 antibody. Neutrophils (<b>D</b>) and macrophages (<b>E</b>) were counted in 10 high-power fields (hpf) are shown as bar graph. (<b>F</b>) Lung homogenate from WT, p53- and PAI-1-deficient mice exposed to ambient air or PCS for 20 weeks were immunoblotted for changes in the levels of MPO using anti-MPO antibody. These membranes were later stripped and analyzed for β-actin to assess loading. Data shown in bar graphs are mean ± SD of two independent experiments (n = 5 mice/group). Differences between treatments are statistically significant *(P<0.05).</p

p53 and PAI-1 are prominently linked to PCSE-induced type II AEC apoptosis.

<p>(<b>A</b>) WT, p53- and PAI-1-deficient mice were exposed to ambient air (control) or PCS for 20 weeks. Lung section obtained from these mice were subjected to TUNEL staining and the bar graph represents percent apoptosis in these groups with error bars and significance *(p<0.005) (n = 5 mice/group). (<b>B</b>) Type II AECs isolated from WT, p53- and PAI-1-deficient mice as described in methods were subjected to TUNEL staining and the bar graph represents percent apoptosis in these groups with error bars and significance *(p<0.005) (n = 5 mice/group). (<b>C</b>) Type II AECs isolated from WT, p53- and PAI-1-deficient mice were subjected to flow cytometric analysis after staining with anti-annexin-v antibody and PI to assess apoptosis. NS = the differences are not statistically significant (n = 5 mice/group). (<b>D</b>) Type II AECs isolated from WT and p53- and PAI-1-deficient mice as described above were immunoblotted for SP-C and β-actin as a loading control.</p