Compounds, Kováts Indices, EAD responses, detected rate, and absolute amounts of potential pheromone components collected by CAR/DVB SPME fiber (70 µm) from live calling virgin females of <i>Dendrolimus tabulaeformis</i> or extracted from pheromone glands with hexane.

<p>Compounds, Kováts Indices, EAD responses, detected rate, and absolute amounts of potential pheromone components collected by CAR/DVB SPME fiber (70 µm) from live calling virgin females of <i>Dendrolimus tabulaeformis</i> or extracted from pheromone glands with hexane.</p

Additional file 2: of OsRLCK 57, OsRLCK107 and OsRLCK118 Positively Regulate Chitin- and PGN-Induced Immunity in Rice

Materials and Methods. (DOC 59 kb

Catches of male <i>Dendrolimus tabulaeformis</i> in delta-shaped traps baited with various blends of potential pheromone components between 1 and 14 August 2011 in the experimental forest of Ping'quan city, He'bei province, China.

a<p>Means followed by the same letter in column are not significantly different at the 5% confidence level by Tukey's tests (<i>F</i>_(9,30) = 19.31, <i>p</i><0.001).</p>b<p>“—” indicate the components were not included.</p

Electron impact mass spectral data from components of pheromone gland extracts, and their MTAD and DMDS derivatives for the Chinese pine caterpillar, <i>Dendrolimus tabulaeformis</i>.

a<p>From full-scan spectra. MTAD, 4-methyl-1,2,4-triazoline-3,5-dione. DMDS, dimethyl disulfide.</p

Percentages of males exhibiting three key behaviors in the flight tunnel in response to various doses of <i>Z</i>5,<i>E</i>7-12:OPr blended with fixed amounts of <i>Z</i>5,<i>E</i>7-12:OAc and <i>Z</i>5,<i>E</i>7-12:OH (doses in ng).

<p>Taking flight = TF, (light bars); upwind flight over a 1.2-m distance = UP, (hatched bars with different upper-case letters were significantly different by Tukey's test at <i>p</i> = 0.05 following ANOVA, <i>F</i>_5,12 = 4.30, <i>p</i> = 0.018); and source contact = SC, (dark bars with different lower-case letters were significantly different by Tukey's test at <i>p</i> = 0.05 following ANOVA, <i>F</i>_5,12 = 13.47, <i>p</i><0.001).</p

Simultaneously recorded responses from flame ionization detector (FID, top) and electroantennographic detection (EAD, bottom; sensing element: male <i>D. tabulaeformis</i> antenna) to headspace volatiles collected by SPME from a virgin calling female <i>D. tabulaeformis</i> moth.

<p>Peaks indicated by 1–5 represent <i>Z</i>5-12:OAc (EAD1), <i>Z</i>5-12:OH (EAD2), <i>Z</i>5,<i>E</i>7-12:OAc (EAD3), <i>Z</i>5,<i>E</i>7-12:OPr (EAD4), and <i>Z</i>5,<i>E</i>7-12:OH (EAD5).</p

Additional file 1: Figure S1. of OsRLCK 57, OsRLCK107 and OsRLCK118 Positively Regulate Chitin- and PGN-Induced Immunity in Rice

Aligments of full length amino acid sequences of OsRLCK57, OsRLCK107, OsRLCK118 and other RLCKs. Table S1. Primers used in this study. (DOC 6724 kb

<em>MiR-101</em> Is Involved in Human Breast Carcinogenesis by Targeting <em>Stathmin1</em>

<div><h3>Background</h3><p><em>MicroRNA-101 (miR-101</em>) expression is negatively associated with tumor growth and blood vessel formation in several solid epithelial cancers. However, the role of <em>miR-101</em> in human breast cancer remains elusive.</p> <h3>Results</h3><p><em>MiR-101</em> was significantly decreased in different subtypes of human breast cancer tissues compared with that in adjacent normal breast tissues (<em>P<</em>0.01). Up-regulation of <em>miR-101</em> inhibited cell proliferation, migration and invasion, and promoted cell apoptosis in ER alpha-positive and ER alpha-negative breast cancer cells and normal breast cells. Down-regulation of <em>miR-101</em> displayed opposite effects on cell growth and metastasis. Further investigation revealed a significant inverse correlation between the expression of <em>miR-101</em> and <em>Stathmin1</em> (<em>Stmn1</em>), and <em>miR-101</em> could bind to the 3′-untranslated region (UTR) of <em>Stmn1</em> to inhibit <em>Stmn1</em> translation. The inhibition of cell growth and metastasis induced by up-regulation of <em>miR-101</em> was partially restored by overexpresson of <em>Stmn1</em>. Knockdown of <em>Stmn1</em> attenuates the down-regulation of <em>miR-101-</em>mediated enhancement of cell growth and metastasis. More importantly, <em>in vivo</em> analysis found that <em>Stmn1</em> mRNA and protein level in different subtypes of human breast cancer tissues, contrary to the down-regulation of <em>miR-101</em>, were significantly elevated.</p> <h3>Conclusions</h3><p>This study demonstrates that down-regulation of <em>miR-101</em> in different subtypes of human breast cancer tissues is linked to the increase of cellular proliferation and invasiveness via targeting <em>Stmn1</em>, which highlights novel regulatory mechanism in breast cancer and may provide valuable clues for the future clinical diagnosis of breast cancer.</p> </div

Xylazine Activates Adenosine Monophosphate-Activated Protein Kinase Pathway in the Central Nervous System of Rats

<div><p>Xylazine is a potent analgesic extensively used in veterinary and animal experimentation. Evidence exists that the analgesic effect can be inhibited using adenosine 5’-monophosphate activated protein kinase (AMPK) inhibitors. Considering this idea, the aim of this study was to investigate whether the AMPK signaling pathway is involved in the central analgesic mechanism of xylazine in the rat. Xylazine was administrated via the intraperitoneal route. Sprague-Dawley rats were sacrificed and the cerebral cortex, cerebellum, hippocampus, thalamus and brainstem were collected for determination of liver kinase B1 (LKB1) and AMPKα mRNA expression using quantitative real-time polymerase chain reaction (qPCR), and phosphorylated LKB1 and AMPKα levels using western blot. The results of our study showed that compared with the control group, xylazine induced significant increases in AMPK activity in the cerebral cortex, hippocampus, thalamus and cerebellum after rats received xylazine (<i>P</i> < 0.01). Increased AMPK activities were accompanied with increased phosphorylation levels of LKB1 in corresponding regions of rats. The protein levels of phosphorylated LKB1 and AMPKα in these regions returned or tended to return to control group levels. However, in the brainstem, phosphorylated LKB1 and AMPKα protein levels were decreased by xylazine compared with the control (<i>P</i> < 0.05). In conclusion, our data indicates that xylazine alters the activities of LKB1 and AMPK in the central nervous system of rats, which suggests that xylazine affects the regulatory signaling pathway of the analgesic mechanism in the rat brain.</p></div

The effect of <i>miR-101</i> constructs on the expression level of <i>miR-101</i>.

<p>MCF-7, T47D, MDA-MB-231 and Hs518bst were respectively transfected with pre-miR control, <i>miR-101</i> mimics (A), anti-miR control or <i>miR-101</i> inhibitor (B). The <i>miR-101</i> level was detected by TaqMan miRNA RT-Real Time PCR. U6 serves as an internal reference. The expression of <i>miR-101</i> in control group was set to 1. The <i>y</i>-axis displays the relative log2 ratio of <i>miR-101</i> normalized by <i>U6</i>. **<i>P</i><0.01.</p