Boron-Catalyzed Double Hydrofunctionalization Reactions of Unactivated Alkynes

Tandem hydroalkoxylation/hydroallylation and hydroalkoxylation/hydrocyanation reactions of alkyl-substituted unactivated alkynes by catalytic systems based on B­(C₆F₅)₃·<i>n</i>H₂O and silyl nucleophiles were developed. The characteristic high alkynophilicity of B­(C₆F₅)₃ enabled the selective activation of the unactivated alkynes in the presence of the reactive alkene of allylsilane. Moreover, the alkynes were electrophilically activated in the presence of cyanide in this catalytic system. Mechanistic studies suggest that the alkynes are activated by the different catalytic species in the two reactions

Clinicopathological characteristics of patients with primary lung adenocarcinoma.

<p>Clinicopathological characteristics of patients with primary lung adenocarcinoma.</p

Representative images of (left panel) HE staining, (middle panel) IL-38 staining, and (right panel) negative controls.

<p>(A) Human tonsil tissue. (B) Human placenta tissue. (C) Human spleen tissue. HE: Hematoxylin-eosin, IL-38: interleukin-38. Scale bar: 100 μm.</p

Univariate and multivariate analyses of the relationship between IL-38 expression and other patient characteristics.

<p>Univariate and multivariate analyses of the relationship between IL-38 expression and other patient characteristics.</p

Univariate and multivariate analyses of DFS and OS in patients with primary lung adenocarcinoma.

<p>Univariate and multivariate analyses of DFS and OS in patients with primary lung adenocarcinoma.</p

Kaplan-Meier curves according to IL-38 expression in the analysis of PD-L1-negative cases and PD-L1-positive cases.

<p>Kaplan-Meier curves showing (A, C) disease-free and (B, D) overall survival of primary lung adenocarcinoma patients according to IL-38 expression in the analysis of (A, B) PD-L1-negative cases and (C, D) PD-L1-positive cases. IL-38: interleukin-38, PD-L1: programmed cell death-ligand 1.</p

Association between IL-38 expression and clinicopathological factors in patients with primary lung adenocarcinoma.

<p>Association between IL-38 expression and clinicopathological factors in patients with primary lung adenocarcinoma.</p

Association between PD-L1 and IL-38 expression.

<p>(A) PD-L1-positive cases showed higher expression of IL-38 than PD-L1-negative cases (Wilcoxon rank-sum test: <i>P</i> < 0.0001). (B) Representative images of (upper panel) PD-L1 staining and (lower panel) IL-38 staining in a (left panel) PD-L1-negative case and (right panel) PD-L1-positive case. IHC: immunohistochemistry, PD-L1: programmed cell death-ligand 1, IL-38: interleukin-38. Scale bar: 100 μm.</p

Severe airway inflammation accompanied with CD4⁺ T cells and eosinophils in IL-18 Tg mice in a mouse asthma model.

<p>(A) Histological evidence of airway inflammation in OVA-sensitized and challenged mice (group 1). Lung tissues were also obtained from OVA-sensitized and saline-challenged mice (group 2). Original magnification 400X, HE staining. (B) Cells in the BALFs were centrifuged onto glass slides, dried in air, and stained with Wright–Giemsa. Cell populations in the BALFs were calculated as described under Materials and methods. (n = 4 to 6 per each group) *: p<0.05 (C) Flow cytometric analysis was performed to examine CD4⁺ T cells and CD8⁺ T cells using a FC500® flow cytometer (Beckman Coulter, Palo Alto, CA). Anti-mouse CD16/CD32 mAb (2.4G2, PharMingen, San Diego, CA) was used to block the non-specific binding. Isolated BALF cells from mice were stained with PC5-anti-mouse CD4 mAb, FITC-anti-mouse CD8 mAb, and/or control isotype matched mAbs (eBioscience, San Diego, CA). Cell populations were calculated as described under Materials and methods. (n = 4 to 6 per each group) *: p<0.05.</p

Overproduction of IL-18 in lungs increases Th1 and Th2 cytokines, and airway hyperresponsiveness.

<p>(A) The concentrations of IFN-γ, IL-13, IL-1β, and eotaxin in the bronchoalveolar lavage fluids (BALFs) were measured by specific ELISA kits. (n = 4 to 6 per each group) *: p<0.05 (B) On day 19, BALF cells were isolated from OVA-sensitized and challenged mice. Three-color analysis was performed for intracellular cytokine staining. Isolated BALF cells were stained with FITC-anti-mouse CD4 mAb, PE-anti-mouse IL-13 mAb, PC7-anti-mouse IFN-γ mAb, and/or control isotype matched mAbs, as reported previously <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0054623#pone.0054623-Hoshino4" target="_blank">[14]</a>. The lymphocyte population was gated for intracellular cytokine analysis. (C) Mice were anesthetized intraperitoneally with sodium pentobarbital, and their tracheas were cannulated via tracheostomy. The mice were ventilated mechanically (tidal volume, 325 µl; frequency, 120 breaths/minute). A paralytic agent (pancuronium bromide) was administered and airway opening pressure was measured with a differential pressure transducer and was recorded continuously. Stepwise increases of acetylcholine chloride (ACh, catalog no. A-6625, Sigma–Aldrich Chemical) in 0.9% saline (0.6 to 160 mg/ml) were given by an ultrasonic nebulizer (30 seconds). The data were expressed as the provocative concentration 200 (PC200); the concentration at which airway pressure was 200% of its baseline. PC200 was calculated by log-linear interpolation for individual mice. The data were also expressed as airway resistance changes from baseline in response to 9 different doses of Ach (0, 0.625, 1.25, 2.5, 5, 10, 20, 40, 80, and 160 mg/ml). (n = 6 to 10 per each group) *: p<0.05. (D) Serum Total IgE and OVA-specific IgE concentrations were measured. (n = 5 to 12 per each group) *: p<0.05.</p