Comparison between the TIVA and inhalation groups.

<p>Comparison between the TIVA and inhalation groups.</p

Postoperative outcome between TIVA and inhalation groups.

<p>Postoperative outcome between TIVA and inhalation groups.</p

Flow chart of the retrospective study.

<p>One hundred and eighty patients were enrolled from medical records using key words “free flap reconstruction”. Four patients were excluded because they also had hypopharynx cancer that needed not only free flap reconstruction but also jejunum tissue transfer. Seven patients were excluded because they either had end-organ disease or a psychiatric disorder that may have complicated their recovery course. Finally, fourteen patients were excluded due to incomplete medical records. A total 156 of patients were included in the final analysis.</p

Furanylazaindoles: Potent Anticancer Agents in Vitro and in Vivo

Preliminary biological data on 7-anilino-6-azaindoles (<b>8</b>–<b>11</b>) suggested that hydrophobic substituents at C7 contribute to enhancement of antiproliferative activity. A novel series of 7-aryl-6-azaindole-1-benzenesulfonamides (<b>12</b>–<b>22</b>) were developed and showed improved cytotoxicity compared to ABT751 (<b>5</b>). The conversion of C7 phenyl rings into C7 heterocycles led to a remarkable improvement of antiproliferative activity. Among all the synthetic products, 7-(2-furanyl)-1-(4-methoxybenzenesulfonyl)-6-azaindole (<b>21</b>) exhibited the most potent anticancer activity against KB, HT29, MKN45, and H460 cancer cell lines with IC₅₀ values of 21.1, 32.0, 27.5, and 40.0 nM, respectively. Bioassays indicated that <b>21</b> not only inhibits tubulin polymerization by binding to tubulin at the colchicine binding site but also arrests the cell cycle at the G2/M phase with slight arrest at the sub-G1 phase. Compound <b>21</b> also functions as a vascular disrupting agent and dose-dependently inhibits tumor growth without significant change of body weight in an HT29 xenograft mouse model. Taken together, compound <b>21</b> has potential for further development as a novel class of anticancer agents

Opening the doors of memory: Is declarative memory a natural kind?

Klein's target article argues that autonoetic consciousness is a necessary condition for memory; this unusually narrow view of the scope of memory implies that only episodic memory is, strictly speaking, memory. The narrow view is opposed to the standard broad view, on which causal connection with past experience is sufficient for memory; on the broad view, both declarative (i.e., episodic and semantic) and procedural memory count as genuine forms of memory. Klein mounts a convincing attack on the broad view, arguing that it opens the "doors of memory" too far, but this commentary contends that the narrow view does not open them far enough. It may be preferable to adopt an intermediate view of the scope of memory, on which causal connection is sufficient for memory only when it involves encoding, storage, and retrieval of content. More demanding than the simple causal condition but less demanding than the autonoesis condition, the encoding-storage-retrieval condition implies that both episodic and semantic memory count as genuine forms of memory but that procedural memory does not

IL-6 induces NED in LNCaP cells and this is concomitant with increased autophagy.

<p>(A) LNCaP cells were treated with 2.5% CDT or 2.5% CDT plus 100 ng/ml IL-6 for 48 hours. The induced neurite elongation was assessed using brightfield microscopy images (40× magnification). (B) The neurite elongation was quantified using the average from 3–5 microscopic fields; <i>bars</i>, SD. (C) LNCaP cells were treated as described in (A). Total cell lysates (TCLs) were prepared and then immunoblotted to detect tubulin III, androgen receptor (AR) and LC3. GAPDH was used as the loading control.</p

A comprehensive RT-qPCR analysis of microarray data of IL-6 treated LNCaP cells.

<p>A comprehensive RT-qPCR analysis of microarray data of IL-6 treated LNCaP cells.</p

Knockdown of beclin1 or Atg5 independently enhances the sensitivity of IL-6-induced NE differentiated LNCaP cells to etoposide.

<p>LNCaP-TR-shBeclin1 (A) and LNCaP-TR-shAtg5 (B) cells were treated with Dox for 48 hours to induced either beclin1 or Atg5 knockdown, respectively, or left untreated. LNCaP control and LNCaP knockdown cells were pre-incubated with 2.5% CDT or 2.5% CDT plus 100 ng/ml IL-6 for 48 hours followed by treatment with 20 µg/ml etoposide for 9 days before the MTT assay. Each data point shown is the mean of three independent experiments; <i>bars</i>, SD.</p

The schematic model of IL-6 regulation of autophagy-dependent NED in PCa cells, LNCaP.

<p>Based on our data, autophagy is essential for PCa cells NED and serves a cytoprotective role in NE differentiated PCa cells. IL-6 induces autophagy-dependent NED through activation AMPK/mTOR pathway and down-modulation of REST. Activation of AMPK inhibits mTOR, a key inhibitor of autophagy, which in-turn activates autophagy pathway. Down-modulation of REST level relieves gene silencer REST-mediated transcriptional repression as part of a relay mechanism found in IL-6 induced autophagy.</p

Chemical inhibition of autophagy flux suppresses IL-6-induced NED in LNCaP cells.

<p>(A) LNCaP-eGFP-LC3 cells were treated with 2.5% CDT or 2.5% CDT plus 100 ng/ml IL-6, in the absence and presence of 50 µM chloroquine (CQ) for 48 hours. This was followed by fixation, nuclear counterstaining with DAPI (blue), and analysis by fluorescence microscopy (FITC, 40× magnification). (B) The neurite elongation was quantified using the average from 3–5 microscopic fields; <i>bars</i>, SD.</p