Porous carbons from inverse vulcanised polymers

Elemental sulfur is an underutilised industrial by-product. It has been recently shown that it can be simply and scalably co-polymerised, by “inverse vulcanisation” with organic crosslinkers. The properties of porous carbons, which have extensive uses in science and industry, are influenced by the materials from which they are generated. Reported here are the first examples of porous carbons produced from high-sulfur inverse vulcanised polymers. The materials produced show micro-porosity, gas selectivity, and are doped with sulfur. The simplicity of the technique, and wide range of other potential inverse vulcanised feedstocks, gives scope for transferability and control of properties

The impact of a human IGF-II analog ([Leu27]IGF-II) on fetal growth in a mouse model of fetal growth restriction.

Enhancing placental insulin-like growth factor (IGF) availability appears to be an attractive strategy for improving outcomes in fetal growth restriction (FGR). Our approach was the novel use of [Leu(27)]IGF-II, a human IGF-II analog that binds the IGF-II clearance receptor IGF-IIR in fetal growth-restricted (FGR) mice. We hypothesized that the impact of [Leu(27)]IGF-II infusion in C57BL/6J (wild-type) and endothelial nitric oxide synthase knockout (eNOS(-/-); FGR) mice would be to enhance fetal growth and investigated this from mid- to late gestation; 1 mg·kg(-1)·day(-1) [Leu(27)]IGF-II was delivered via a subcutaneous miniosmotic pump from E12.5 to E18.5. Fetal and placental weights recorded at E18.5 were used to generate frequency distribution curves; fetuse

In situ micropillar deformation of hydrides in Zircaloy-4

Deformation of hydrided Zircaloy-4 has been examined using in situ loading of hydrided micropillars in the scanning electron microscope and using synchrotron X-ray Laue microbeam diffraction. Results suggest that both the matrix and hydride can co-deform, with storage of deformation defects observed within the hydrides, which were twinned. Hydrides placed at the plane of maximum shear stress showed deformation within the hydride packet, whilst packets in other pillars arrested the propagation of shear bands. X-ray Laue peak broadening, prior to deformation, was associated with the precipitation of hydrides, and during deformation plastic rotation and broadening of both the matrix and hydride peaks were observed. Post-mortem TEM of the deformed pillars has indicated a greater density of dislocations associated with the precipitated hydride packets, while the observed broadening of the hydride electron diffraction spots further suggests that plastic strain gradients were induced in the hydrides by compression

Nicotinic acetylcholine receptor expression in human airway correlates with lung function

Nicotine and its derivatives, by binding to nicotinic acetylcholine receptors (nAChRs) on bronchial epithelial cells, can regulate cellular signaling and inflammatory processes. Delineation of nAChR subtypes and their responses to nicotine stimulation in bronchial epithelium may provide information for therapeutic targeting in smoking-related inflammation in the airway. Expression of nAChR subunit genes in 60 bronchial epithelial biopsies and immunohistochemical staining for the subcellular locations of nAChR subunit expression were evaluated. Seven human bronchial epithelial cell lines (HBECs) were exposed to nicotine in vitro for their response in nAChR subunit gene expression to nicotine exposure and removal. The relative normalized amount of expression of nAChR α4, α5, and α7 and immunohistochemical staining intensity of nAChR α4, α5, and β3 expression showed significant correlation with lung function parameters. Nicotine stimulation in HBECs resulted in transient increase in the levels of nAChR α5 and α6 but more sustained increase in nAChR α7 expression. nAChR expression in bronchial epithelium was found to correlate with lung function. Nicotine exposure in HBECs resulted in both short and longer term responses in nAChR subunit gene expression. These results gave insight into the potential of targeting nAChRs for therapy in smoking-related inflammation in the airway.postprin

Edible crabs “Go West”: migrations and incubation cycle of Cancer pagurus revealed by electronic tags

Crustaceans are key components of marine ecosystems which, like other exploited marine taxa, show seasonable patterns of distribution and activity, with consequences for their availability to capture by targeted fisheries. Despite concerns over the sustainability of crab fisheries worldwide, difficulties in observing crabs’ behaviour over their annual cycles, and the timings and durations of reproduction, remain poorly understood. From the release of 128 mature female edible crabs tagged with electronic data storage tags (DSTs), we demonstrate predominantly westward migration in the English Channel. Eastern Channel crabs migrated further than western Channel crabs, while crabs released outside the Channel showed little or no migration. Individual migrations were punctuated by a 7-month hiatus, when crabs remained stationary, coincident with the main period of crab spawning and egg incubation. Incubation commenced earlier in the west, from late October onwards, and brooding locations, determined using tidal geolocation, occurred throughout the species range. With an overall return rate of 34%, our results demonstrate that previous reluctance to tag crabs with relatively high-cost DSTs for fear of loss following moulting is unfounded, and that DSTs can generate precise information with regards life-history metrics that would be unachievable using other conventional means

Se-methylselenocysteine inhibits phosphatidylinositol 3-kinase activity of mouse mammary epithelial tumor cells in vitro

INTRODUCTION: Se-methylselenocysteine (MSC), a naturally occurring selenium compound, is a promising chemopreventive agent against in vivo and in vitro models of carcinogen-induced mouse and rat mammary tumorigenesis. We have demonstrated previously that MSC induces apoptosis after a cell growth arrest in S phase in a mouse mammary epithelial tumor cell model (TM6 cells) in vitro. The present study was designed to examine the involvement of the phosphatidylinositol 3-kinase (PI3-K) pathway in TM6 tumor model in vitro after treatment with MSC. METHODS: Synchronized TM6 cells treated with MSC and collected at different time points were examined for PI3-K activity and Akt phosphorylation along with phosphorylations of Raf, MAP kinase/ERK kinase (MEK), extracellular signal-related kinase (ERK) and p38 mitogen-activated protein kinase (MAPK). The growth inhibition was determined with a [(3)H]thymidine incorporation assay. Immunoblotting and a kinase assay were used to examine the molecules of the survival pathway. RESULTS: PI3-K activity was inhibited by MSC followed by dephosphorylation of Akt. The phosphorylation of p38 MAPK was also downregulated after these cells were treated with MSC. In parallel experiments MSC inhibited the Raf–MEK–ERK signaling pathway. CONCLUSION: These studies suggest that MSC blocks multiple signaling pathways in mouse mammary tumor cells. MSC inhibits cell growth by inhibiting the activity of PI3-K and its downstream effector molecules in mouse mammary tumor cells in vitro

Causality constraints in AdS/CFT from conformal collider physics and Gauss-Bonnet gravity

We explore the relation between positivity of the energy constraints in conformal field theories and causality in their dual gravity description. Our discussion involves CFTs with different central charges whose description, in the gravity side, requires the inclusion of quadratic curvature corrections. It is enough, indeed, to consider the Gauss-Bonnet term. We find that both sides of the AdS/CFT correspondence impose a restriction on the Gauss-Bonnet coupling. In the case of 6d supersymmetric CFTs, we show the full matching of these restrictions. We perform this computation in two ways. First by considering a thermal setup in a black hole background. Second by scrutinizing the scattering of gravitons with a shock wave in AdS. The different helicities provide the corresponding lower and upper bounds. We generalize these results to arbitrary higher dimensions and comment on some hints and puzzles they prompt regarding the possible existence of higher dimensional CFTs and the extent to which the AdS/CFT correspondence would be valid for them.Comment: 31 pages, 5 figures; v2: typos fixed, cosmetic amendments and references adde

Survivin gene silencing sensitizes prostate cancer cells to selenium growth inhibition

<p>Abstract</p> <p>Background</p> <p>Prostate cancer is a leading cause of cancer-related death in men worldwide. Survivin is a member of the inhibitor of apoptosis (IAP) protein family that is expressed in the majority of human tumors including prostate cancer, but is barely detectable in terminally differentiated normal cells. Downregulation of survivin could sensitize prostate cancer cells to chemotherapeutic agents <it>in vitro </it>and <it>in vivo</it>. Selenium is an essential trace element. Several studies have shown that selenium compounds inhibit the growth of prostate cancer cells. The objective of this study is to investigate whether survivin gene silencing in conjunction with selenium treatment could enhance the therapeutic efficacy for prostate cancer and to elucidate the underlying mechanisms.</p> <p>Methods</p> <p>Expression of survivin was analyzed in a collection of normal and malignant prostatic tissues by immunohistochemical staining. <it>In vitro </it>studies were conducted in PC-3M, C4-2B, and 22Rv1 prostate cancer cells. The effect of selenium on survivin expression was analyzed by Western blotting and semi-quantitative RT-PCR. Survivin gene knockdown was carried out by transfecting cells with a short hairpin RNA (shRNA) designed against survivin. Cell proliferation was quantitated by the 3-(4,5-Dimethylthiazol-2-yl)- 2,5-Diphenyltetrazolium Bromide (MTT) assay and apoptosis by propidium iodide staining followed by flow cytometry analysis. Finally, <it>in vivo </it>tumor growth assay was performed by establishing PC-3M xenograft in nude mice and monitoring tumor growth following transfection and treatment.</p> <p>Results</p> <p>We found that survivin was undetectable in normal prostatic tissues but was highly expressed in prostate cancers. Survivin knockdown or selenium treatment inhibited the growth of prostate cancer cells, but the selenium effect was modest. In contrast to what have been observed in other cell lines, selenium treatment had little or no effect on survivin expression in several androgen-independent prostate cancer cell lines. Survivin knockdown sensitized these cells to selenium growth inhibition and apoptosis induction. In nude mice bearing PC-3M xenografts, survivin knockdown synergizes with selenium in inhibiting tumor growth.</p> <p>Conclusions</p> <p>Selenium could inhibit the growth of hormone-refractory prostate cancer cells both <it>in vitro </it>and <it>in vivo</it>, but the effects were modest. The growth inhibition was not mediated by downregulating survivin expression. Survivin silencing greatly enhanced the growth inhibitory effects of selenium.</p