15 research outputs found
Heteroaggregation between Isomeric Amido-ethynyl-amidohelicene Tridomain Oligomers
Three isomers, i.e., <i><b>P</b></i><b>4</b><i><b>M</b></i><b>5</b><i><b>P</b></i><b>4</b>-<b>1</b>, <i><b>M</b></i><b>4</b><i><b>P</b></i><b>5</b><i><b>M</b></i><b>4</b>-<b>1</b>, and <i><b>M</b></i><b>4</b><i><b>M</b></i><b>5</b><i><b>M</b></i><b>4</b>-<b>1</b>, of amido-ethynyl-amidohelicene tridomain oligomers were
synthesized. <i><b>P</b></i><b>4</b><i><b>M</b></i><b>5</b><i><b>P</b></i><b>4</b>-<b>1</b> formed four homoaggregate states, i.e.,
all-dimer, amido-dimer, ethynyl-dimer, and random-coil states, by
independent aggregation and disaggregation at the ethynyl and amido
domains. Then, possible combinations of heteroaggregation were examined
between the isomeric tridomain oligomers <i><b>P</b></i><b>4</b><i><b>P</b></i><b>5</b><i><b>P</b></i><b>4</b>-<b>1</b>, <i><b>P</b></i><b>4</b><i><b>M</b></i><b>5</b><i><b>P</b></i><b>4</b>-<b>1</b>, <i><b>M</b></i><b>4</b><i><b>P</b></i><b>5</b><i><b>M</b></i><b>4</b>-<b>1</b>, and <i><b>M</b></i><b>4</b><i><b>M</b></i><b>5</b><i><b>M</b></i><b>4</b>-<b>1</b>. When <i><b>P</b></i><b>4</b><i><b>P</b></i><b>5</b><i><b>P</b></i><b>4</b>-<b>1</b> and <i><b>P</b></i><b>4</b><i><b>M</b></i><b>5</b><i><b>P</b></i><b>4</b>-<b>1</b> were mixed in THF, to which trifluoromethylbenzene was added,
heteroaggregates with an all-dimer structure were formed without forming
homoaggregates. The heteroaggregation initially occurred at the central
ethynyl domain, which was followed by the aggregation at the amido
domains. Heteroaggregates were also formed using the combinations <i><b>P</b></i><b>4</b><i><b>P</b></i><b>5</b><i><b>P</b></i><b>4</b>-<b>1</b>/<i><b>M</b></i><b>4</b><i><b>M</b></i><b>5</b><i><b>M</b></i><b>4</b>-<b>1</b> and <i><b>P</b></i><b>4</b><i><b>M</b></i><b>5</b><i><b>P</b></i><b>4</b>-<b>1</b>/<i><b>M</b></i><b>4</b><i><b>P</b></i><b>5</b><i><b>M</b></i><b>4</b>-<b>1</b>, and
the results indicated an important role for the central ethynyl domain
for heteroaggregation
Molecular Design and Synthesis of Novel Salicyl Glycoconjugates as Elicitors against Plant Diseases
<div><p>A new series of salicyl glycoconjugates containing hydrazide and hydrazone moieties were designed and synthesized. The bioassay indicated that the novel compounds had no <i>in vitro</i> fungicidal activity but showed significant <i>in vivo</i> antifungal activity against the tested fungal pathogens. Some compounds even had superior activity than the commercial fungicides in greenhouse trial. The results of RT-PCR analysis showed that the designed salicyl glycoconjugates could induce the expression of <i>LOX1</i> and <i>Cs-AOS2,</i> which are the specific marker genes of jasmonate signaling pathway, to trigger the plant defense resistance.</p></div
General synthetic procedure for salicylic glycoconjugates.
<p>General synthetic procedure for salicylic glycoconjugates.</p
<i>In vivo</i> antifungal activity against <i>Colletotrichum orbiculare</i>.
<p><i>In vivo</i> antifungal activity against <i>Colletotrichum orbiculare</i>.</p
<i>In vivo</i> antifungal activity against <i>Sphaerotheca fuliginea</i>.
<p><i>In vivo</i> antifungal activity against <i>Sphaerotheca fuliginea</i>.</p
<i>In vitro</i> fungicidal activity against <i>Colletotrichum orbiculare</i>.
<p>A: blank control, B: <b>5d</b>, C: DMSO, D: <b>2b</b>, E: thiophanate-methyl, F: <b>2a</b>.</p
<i>In vivo</i> antifungal activity against five fungus species at 500 µg/mL.
a<p>Control fungicides: a, 70% thiophanate-methyl WP; b, 70% benomyl WP; c, 50% chlorothalonil WP; d, 3% validamycin AS; e, 50% dimethomorph WP.</p><p><i>In vivo</i> antifungal activity against five fungus species at 500 µg/mL.</p
<i>In vitro</i> fungicidal activity against <i>Fusarium oxysporum</i>.
<p>A: blank control, B: <b>5d</b>, C: DMSO, D: <b>2b</b>, E: benomyl, F: <b>2a</b>.</p
Effect of designed compounds on inducing the expression of pathogenesis-related genes in <i>Cucumis sativus</i>.
<p>Effect of designed compounds on inducing the expression of pathogenesis-related genes in <i>Cucumis sativus</i>.</p
Characteristics of alveolar macrophages from murine models of OVA-induced allergic airway inflammation and LPS-induced acute airway inflammation
<div><p>ABSTRACT</p><p><i>Background</i>: Macrophages include the classically activated pro-inflammatory M1 macrophages (M1s) and alternatively activated anti-inflammatory M2 macrophages (M2s). The M1s are activated by both interferon-γ and Toll-like receptor ligands, including lipopolysaccharide (LPS), and have potent pro-inflammatory activity. In contrast, Th2 cytokines activate the M2s, which are involved in the immune response to parasites, promotion of tissue remodeling, and immune regulatory functions. Although alveolar macrophages (AMs) play an essential role in the pulmonary immune system, little is known about their phenotypes. <i>Methods</i>: Quantitative reverse transcription polymerase chain reaction and flow cytometry were used to define the characteristics of alveolar macrophages derived from untreated naïve mice and from murine models of both ovalbumin (OVA)-induced allergic airway inflammation and LPS-induced acute airway inflammation. AMs were co-cultured with CD4<sup>+</sup> T cells and were pulsed with tritiated thymidine to assess proliferative responses. <i>Results</i>: We characterized in detail murine AMs and found that these cells were not completely consistent with the current M1 versus M2-polarization model. OVA-induced allergic and LPS-induced acute airway inflammation promoted the polarization of AMs towards the current M2-skewed and M1-skewed phenotypes, respectively. Moreover, our data also show that CD11c<sup>+</sup> CD11b<sup>+</sup> AMs from the LPS-treated mice play a regulatory role in antigen-specific T-cell proliferation in vitro. <i>Conclusions</i>: These characteristics of AMs depend on the incoming pathogens they encounter and on the phase of inflammation and do not correspond to the current M1 versus M2-polarization model. These findings may facilitate an understanding of their contributions to the pulmonary immune system in airway inflammation.</p></div