Complementary Helicity Interchange of Optically Switchable Supramolecular-Enantiomeric Helicenes with (−)-Gel-Sol-(+)-Gel Transition Ternary Logic

A gallamide-containing pseudo­enantio­meric helicene pair bearing a (10<i>R</i>,11<i>R</i>)-dimethoxy­methyl­dibenzo­suberane core can self-assemble by intermolecular amide H-bonding and π-π stacking into bundled helical fibers with helical tunnels of complementary helicity in CH₂Cl₂. The helicenes undergo excellent complementary photoswitchings of ternary logic at 280, 318, and 343 nm through (−)-gel-sol-(+)-gel interconversion

Complementary Helicity Interchange of Optically Switchable Supramolecular-Enantiomeric Helicenes with (−)-Gel-Sol-(+)-Gel Transition Ternary Logic

A gallamide-containing pseudo­enantio­meric helicene pair bearing a (10<i>R</i>,11<i>R</i>)-dimethoxy­methyl­dibenzo­suberane core can self-assemble by intermolecular amide H-bonding and π-π stacking into bundled helical fibers with helical tunnels of complementary helicity in CH₂Cl₂. The helicenes undergo excellent complementary photoswitchings of ternary logic at 280, 318, and 343 nm through (−)-gel-sol-(+)-gel interconversion

Spiro-Shaped <i>cis</i>-Stilbene/Fluorene Hybrid Template for the Fabrication of Small-Molecule Bulk Heterojunction Solar Cells

A spiro core appended with trithiophene arms and α-cyanoacrylate end groups was used for the first time in bulk heterojunction solar cell applications. The resulting device performance was evaluated by its blending with PC₆₁BM, leading to a short-circuit current density (<i>J</i>_sc) of 3.55 mA cm^–2 which was 2.4 and 6.6 times better than those of the open form and nonspiro core analogs. The 1,8-diiodooctane solvent additive suppressed its microcrystalline self-aggregation, leading to a well-defined blend film morphology with reduced domain size and thus enhanced <i>J</i>_sc to 6.14 mA cm^–2 and fill factor to 67.2% by 70% and 135% increase, respectively. The film domain size can be further reduced to 50 nm by its blending with PC₇₁BM, leading to a PCE of 4.87% with an improved <i>J</i>_sc of 7.93 mA cm^–2, a <i>V</i>_oc of 0.97 V, and a fill factor of 64.1%

HTPB delays lung metastasis of 4T1-luc breast cancer cell in animal models.

<p>(<b>A</b>) 4T1-luc mouse breast cancer cells were treated with 1.92 µM HTPB for 48 hours. HTPB did not significantly affect cell growth of 4T1-luc cells during the indicated treatments. (<b>B</b>) Fibronectin assembly on the surface of 4T1-luc cells measured by immunofluorescence analyses showed that HTPB treatment reduced pericellular poly-fibronectin assemblies. (<b>C</b>) The treated 4T1-luc cells were injected intravenously via tail vein into Balb/c mice and observed for the luciferase signals and photographed using IVIS50 for 13 days after drug treatment. HTPB significantly delayed lung metastasis.</p

HTPB inhibits cancer cell migration via reduced activities of matrix metalloproteinases, RhoA, and focal adhesion complex.

<p>(<b>A</b>) The image from trans-well migration assay and (<b>B</b>) wound-healing assay indicated that after 48 hours treatment at non-cytotoxic doses, HTPB inhibited migratory activity in a dose-dependent manner. * <i>P</i><0.05; ** <i>P</i><0.01; scale bars: 400 µm. (<b>C</b>) Gelatin-zymography assay and RhoA-GTP GST pull-down assay showed that MMP-2 and MMP-9 enzyme activities were suppressed and RhoA-GTP expression was reduced in A549 and H1299 cells after 2.5 µM HTPB treatment for 48 hours. (<b>D</b>) Expression of integrin-β1 and phosphorylation of FAK at Tyr-397 were down-regulated in H1299 and A549 cells after HTPB treatment for 48 hours at the indicated doses. (<b>E</b>) HTPB led to F-actin dysregulation by immunofluorescence analyses. Cells were treated with 5 µM HTPB for 48 hours, and then fixed and stained with phalloidin (F-actin). Scale bars: 40 µm.</p

HTPB induces cell cycle arrest and apoptosis.

<p>(<b>A</b>) The effects of HTPB on cell cycle distribution in A549 and H1299 cells. Cells were treated with 5 µM HTPB for indicated times and assessed by flow cytometry. The percentage of G2/M and sub-G1 fraction population is plotted in the histogram. G2/M arrest and sub-G1 induction are indicated by arrows. (<b>B</b>) HTPB caused apoptotic DNA ladders in A549 and H1299 cells treated with 5 µM HTPB for 48 hours. HTPB induced intrinsic apoptosis. Cells were treated with 5 µM HTPB for indicated times and cell lysates were subjected to Western blot analyses (<b>C</b>) and caspase activity assay (<b>D</b>). Pro-apoptotic proteins Bad and Bak were up-regulated and anti-apoptotic proteins Bcl-2 and Bcl-_XL were down-regulated. Caspases-3 and -9 were up-regulated in both A549 and H1299 cells. Data represent mean ± SEM from three independent experiments. * <i>P</i><0.05; ** <i>P</i><0.01.</p

HTPB effectively induced protein acetylation, apoptosis and pFAK/pAKT inactivation <i>in vivo</i>.

<p>(<b>A</b>) Mice bearing established (about 100∼200 mm³) A549 tumors were injected intraperitoneally with a single dose of HTPB at 50 mg/kg. After treatment for the indicated time, tumors from two representative mice of each time point (a–f) were harvested and subjected to Western blot using anti-actyl-histone H3, H4 and p53 and Bcl-_XL antibodies. (<b>B</b>) Immunohistochemistry analyses were performed using antibody against cleaved-form of caspase-3, p-FAK and p-AKT (brownish color). Original magnification×200.</p

Effect of HTPB on cell viability and on the biomarkers associated with broad inhibition on numerous HDACs.

<p>(<b>A</b>) Chemical structure of HTPB (upper left). Dose-dependent effects of HTPB on cell viability in IMR90, H1299, and A549 cells (lower left). Cells were treated with 0.5–10 µM of HTPB for 48 hours, and cell viability was assessed by MTT assay. A known HDAC inhibitor, SAHA, was used for comparison. (<b>B</b>) HTPB suppressed activities of class I (HDAC1 and HDAC8), class II (HDAC4 and HDAC6), and class IV (HDAC11) HDACs in A549 cells. Data represent mean ± SEM from three independent experiments. *** <i>P</i><0.001. Dose-dependent effects (<b>C</b>) and time-dependent effects (<b>D</b>) of HTPB on the histone and non-histone proteins. SAHA was included for comparison. (<b>E</b>) HTPB induced acetylation of histone H3 and H4 without affecting the total protein levels of HDAC1 and HDAC 6. In addition, HTPB induced p21 protein expression in both A549 (p53 wild-type) and H1299 (p53 null) cells. The immunoblots shown are representatives of three independent experiments.</p

Spirally Configured (<i>cis</i>-Stilbene) Trimers: Steady-State and Time-Resolved Photophysical Studies and Organic Light-Emitting Diode Applications

This article reports for the time-resolved photophysical studies of spirally configured (<i>cis</i>-stilbene) trimers and their spin-coated organic light-emitting diode (OLED) device performances. Transient absorption profiles of spirally configured, ter-(<i>cis</i>-stilbene) were studied by pulse radiolysis. The emission profiles after charge recombination of their incipient radical ions in benzene provides insights into the emission mechanism and efficiency in OLED devices. Blue-, sky blue-, and green-emitting OLED devices for a maximum external quantum efficiency are 4.32%, 4.70%, and 2.77%, respectively, by solution process