Sog-Cv-dependent BMP signaling is induced along ectopic wing vein morphogenesis by loss of <i>cdc42</i>.

<p>(A) Adult wing of <i>cdc42²</i>. (B, B′) pMad (B) and lacZ staining (B′) in <i>cdc42²</i> ; <i>dpp^shv-lacZ/+</i>. (C—F) pMad staining (C, E) and adult wing (D, F) of <i>sog^P129D, cdc42</i>² (C, D) and <i>cv⁷⁰</i>, <i>cdc42</i>² (E, F). (G) Quantification of the phenotypes in A, D and F. (H—K) Optical cross-sections of the ectopic CV region (white arrows in B and C). pMad and F-actin (H, J) and ß-integrin (I, K) staining in <i>cdc42²</i> (H, I) and <i>sog^P129D</i>, <i>cdc42</i>² (J, K). The relative ß-integrin accumulation at the basal side of the ectopic CV region by comparing to that of intervein regions is 32±2% (n = 7 wings) in <i>cdc42²</i> (I) and 37±3%, (n = 6 wings) in <i>sog, cdc42</i> (K). (L, M) pMad staining and adult PCV (inset) in <i>sog^P11885</i> (L) and in <i>sog^P11885, cdc42²</i> (M). (N) Quantification of the adult wing phenotypes in L and M. All pupal wings were fixed at 24 hr AP.</p

BMP signaling is required for PCV morphogenesis.

<p>(A) Wild-type <i>yw</i> adult wing. (B, B′) lacZ (B) and pMad (B′) staining of <i>dpp^shv-lacZ</i> at 24 hr AP. The PCV position is indicated by arrows. (C) A current model of Sog-Cv-mediated directional BMP transport from the LVs into the PCV. (D—I) Wild-type <i>yw</i> pupal wing. pMad (D, E, F, G, H, I), F-actin (E′, G′, I′), and ß-integrin (E″, G″, I″) staining at 18 hr AP (D, E), 20 hr AP (F, G), and 24 hr AP (H, I). (J—O) <i>cv⁷⁰</i> pupal wing. pMad (J, K, L, M, N, O), F-actin (K′, M′, O′), and ß-integrin (K″, M″, O″) staining at 18 hr AP (J, K), 20 hr AP (L, M), and 24 hr AP (N, O). (D, F, H, J, L, N) Dorsal view of the PCV region. (E, G, I, K, M, O) Optical cross-sections of the PCV region. Prospective PCV positions are indicated by double-headed arrows at 18 hr AP (E–E″, K–K″).</p

Cv-C mediates PCV morphogenesis downstream of BMP signaling by inactivating various Rho-type small GTPases.

<p>(A) Adult wing of <i>cv-c¹</i>. (B, C) Optical cross-sections of the PCV region. F-actin (B) and ß-integrin (C) staining at 24 hr AP in <i>cv-c¹</i>. (D—H) <i>in situ</i> hybridization of <i>cv-c</i> at 20 hr AP (D) and at 24 hr AP (E) in wild-type <i>yw</i>, and at 20 hr AP (F) and at 24 hr AP (G) in <i>cv⁷⁰</i>, and at 24 hr AP in <i>BS1348>caTkv</i> (H). <i>BS1348-Gal4</i> is intervein-specific Gal4 driver. (I) Genetic interactions of <i>cv-c</i> with various small GTPases. Representative adult wings around the PCV region of each genotype are shown above. (J, K) pMad staining at 24 hr AP in wild-type <i>yw</i> (J) and in <i>cv⁷⁰, cdc42²</i> double mutant (K). (L—L″) Optical cross-sections of the PCV region. pMad (L), F-actin (L′), and ß-integrin (L″) staining at 24 hr AP in <i>cv⁷⁰, cdc42²</i> double mutant. (M) A schematic pathway regulating PCV morphogenesis downstream of BMP signaling.</p

Cv-C is required for Sog-Cv-dependent BMP transport into the PCV region.

<p>(A–C) Genetic interaction of <i>cv-c</i> with <i>sog</i> (A), <i>cv</i> (B), or <i>cv-2</i> (C). Representative adult wings around the PCV region of each genotype are shown. (D) Quantification of adult wing phenotypes in A–C. (E, F) GFP-Dpp distribution (E, F) and pMad staining (E′, F′) at 24 hr AP and adult PCV region (inset) in wild-type <i>yw</i> (<i>shv>GFP-Dpp</i>) (E, E′) and in <i>cv-c</i> (<i>cv-c¹</i>, <i>shv>GFP-Dpp</i>) (F, F′). The PCV position is indicated by arrows. (G) GFP distribution at 24 hr AP in <i>shv>GFP</i>. Despite strong GFP signal in LVs, no dots were observed in the PCV region. (H) Quantification of the number of GFP dots in E, F and G. Statistical significance was determined using Mann-Whitney U test.</p

ß-integrin links Sog-Cv-dependent BMP signaling and PCV morphogenesis.

<p>(A—F) Adult wings (A—C) and pMad staining (D—F) of wild-type <i>yw</i> (A, D), <i>mys¹/mys^nj42</i> (B, E), and <i>mys¹, sog^P129D/mys^nj42</i>, + (C, F). (G) Quantification of adult wing phenotypes in B and C. (H—J) Adult wings of <i>mys^nj42</i> (H), <i>mys^nj42, sog^p129D</i> (I), and <i>cv⁷⁰, mys^nj42</i> (J). (K) Quantification of adult wing phenotype in H—J. (L, M) pMad staining at 24 hr AP and adult PCV (insets) in <i>mys^nj42/+; cv-c¹/cv-c^c524</i> (L) and <i>mys^nj42</i>; <i>cv-c¹/cv-c^c524</i> (M). (N) Quantification of adult wing phenotype in L and M.</p

Patient characteristics categorized by age.

<p>AIDS: Acquired immunodeficiency syndrome; IQR: Interquartile range, LOS: Length of stay, TC: Total charge.</p><p>^a Median age (interquartile range): 68 (15)</p><p>^b Kruskal-Wallis test, all others by chi-square test</p><p>Patient characteristics categorized by age.</p

Univariate analyses of opportunistic infections on in-hospital mortality, length of stay, and total charge.

<p>In-hospital mortality analysed by chi-square test, LOS and TC by Mann–Whitney U test. IQR: Interquartile range; LOS: Length of stay (days); TC: Total charges (US dollars).</p><p>Univariate analyses of opportunistic infections on in-hospital mortality, length of stay, and total charge.</p

Patient characteristics categorized by age.

<p>AIDS: Acquired immunodeficiency syndrome; IQR: Interquartile range, LOS: Length of stay, TC: Total charge.</p><p>^a Median age (interquartile range): 68 (15)</p><p>^b Kruskal-Wallis test, all others by chi-square test</p><p>Patient characteristics categorized by age.</p

Prevalence of OI in adult T-cell leukaemia patients.

<p>HSV: Herpes simplex virus, NTM: Nontuberculous mycobacteria; PCP: Pneumocystis pneumonia; VZV: Varicella zoster virus. Total number of patients: 3712.</p><p>Prevalence of OI in adult T-cell leukaemia patients.</p

Multivariate analyses of OI and other factors on in-hospital mortality and health care costs.

<p>In-hospital mortality analysed by multilevel logistic regression model, log LOS and log TC by multilevel linear regression model, data year by random intercept. AOR: Adjusted odds ratio; AIDS: Acquired immunodeficiency syndrome; B: coefficient; LOS: Length of stay; TC: Total charge.</p><p>Multivariate analyses of OI and other factors on in-hospital mortality and health care costs.</p