Lyngbya majuscula Blooms in an Enclosed Marine Environment

Cyanobacterial blooms are a cause of concern because of their potential impacts on the marine environment. In Sentosa Cove, Singapore, Lyngbya majuscula blooms appeared regularly in the highly enclosed boat canals traversing the seafront residential development. This study investigated whether sediments resuspended by physical disturbance liberated nutrients that contribute to the blooms. Sediment resuspension events were mimicked in containers of sediment collected from the canals. Lyngbya majuscula that were incubated in containers with resuspended sediment attained greater biomass than those in filtered seawater only. Levels of iron, phosphates and nitrites in seawater with resuspended sediments were significantly higher than in those without. The results indicate that recurrent L. majuscula blooms in Sentosa Cove could be attributed to nutrient loading from sediment resuspension

Green tea polyphenols ameliorate non-alcoholic fatty liver disease through upregulating AMPK activation in high fat fed Zucker fatty rats

© The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved. To investigate protective effects and molecular mechanisms of green tea polyphenols (GTP) on nonalcoholic fatty liver disease (NAFLD) in Zucker fatty (ZF) rats. METHODS Male ZF rats were fed a high-fat diet (HFD) for 2 wk then treated with GTP (200 mg/kg) or saline (5 mL/kg) for 8 wk, with Zucker lean rat as their control. At the end of experiment, serum and liver tissue were collected for measurement of metabolic parameters, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), inflammatory cytokines and hepatic triglyceride and liver histology. Immunoblotting was used to detect phosphorylation of AMP-activated protein kinase (AMPK) acetyl-CoA carboxylase (ACC), and sterol regulatory element-binding protein 1c (SREBP1c). RESULTS Genetically obese ZF rats on a HFD presented with metabolic features of hepatic pathological changes comparable to human with NAFLD. GTP intervention decreased weight gain (10.1%, P = 0.052) and significantly lowered visceral fat (31.0%, P < 0.01). Compared with ZF-controls, GTP treatment significantly reduced fasting serum insulin, glucose and lipids levels. Reduction in serum ALT and AST levels (both P < 0.01) were observed in GTP-treated ZF rats. GTP treatment also attenuated the elevated TNFα and IL-6 in the circulation. The increased hepatic TG accumulation and cytoplasmic lipid droplet were attenuated by GTP treatment, associated with significantly increased expression of AMPK-Thr172 (P < 0.05) and phosphorylated ACC and SREBP1c (both P < 0.05), indicating diminished hepatic lipogenesis and triglycerides out flux from liver in GTP treated rats. CONCLUSION The protective effects of GTP against HFD-induced NAFLD in genetically obese ZF rats are positively correlated to reduction in hepatic lipogenesis through upregulating the AMPK pathway

Tailoring hyper-heuristics to specific instances of a scheduling problem using affinity and competence functions

Hyper-heuristics are high level heuristics which coordinate lower level ones to solve a given problem. Low level heuristics, however, are not all as competent/good as each other at solving the given problem and some do not work together as well as others. Hence the idea of measuring how good they are (competence) at solving the problem and how well they work together (their affinity). Models of the affinity and competence properties are suggested and evaluated using previous information on the performance of the simple low level heuristics. The resulting model values are used to improve the performance of the hyper-heuristic by tailoring it not only to the specific problem but the specific instance being solved. The test case is a hard combinatorial problem, namely the Hybrid Flow Shop scheduling problem. Numerical results on randomly generated as well as real-world instances are included

Association of a genetic variant in the apolipoprotein A5 gene with the metabolic syndrome in Chinese

Poster Session II: Translational & Clinica: no. 11published_or_final_versionThe 16th Medical Research Conference, The University of Hong Kong, Hong Kong, 22 January 2011. In Hong Kong Medical Journal, 2011, v. 17 suppl. 1, p. 18, abstract no. 1

Enrichment analysis of Alu elements with different spatial chromatin proximity in the human genome

Transposable elements (TEs) have no longer been totally considered as “junk DNA” for quite a time since the continual discoveries of their multifunctional roles in eukaryote genomes. As one of the most important and abundant TEs that still active in human genome, Alu, a SINE family, has demonstrated its indispensable regulatory functions at sequence level, but its spatial roles are still unclear. Technologies based on 3C(chromosomeconformation capture) have revealed the mysterious three-dimensional structure of chromatin, and make it possible to study the distal chromatin interaction in the genome. To find the role TE playing in distal regulation in human genome, we compiled the new released Hi-C data, TE annotation, histone marker annotations, and the genome-wide methylation data to operate correlation analysis, and found that the density of Alu elements showed a strong positive correlation with the level of chromatin interactions (hESC: r=0.9, P<2.2×1016; IMR90 fibroblasts: r = 0.94, P < 2.2 × 1016) and also have a significant positive correlation withsomeremote functional DNA elements like enhancers and promoters (Enhancer: hESC: r=0.997, P=2.3×10−4; IMR90: r=0.934, P=2×10−2; Promoter: hESC: r = 0.995, P = 3.8 × 10−4; IMR90: r = 0.996, P = 3.2 × 10−4). Further investigation involving GC content and methylation status showed the GC content of Alu covered sequences shared a similar pattern with that of the overall sequence, suggesting that Alu elements also function as the GC nucleotide and CpG site provider. In all, our results suggest that the Alu elements may act as an alternative parameter to evaluate the Hi-C data, which is confirmed by the correlation analysis of Alu elements and histone markers. Moreover, the GC-rich Alu sequence can bring high GC content and methylation flexibility to the regions with more distal chromatin contact, regulating the transcription of tissue-specific genes

Enhancing the antitumor activity of ErbB blockade with histone deacetylase (HDAC) inhibition

Molecular inhibition of the ErbB signaling pathway represents a promising cancer treatment strategy. Preclinical studies suggest that enhancement of antitumor activity can be achieved by maximizing ErbB signaling inhibition. Using cDNA microarrays, we identified histone deacetylase (HDAC) inhibitors as having strong potential to enhance the effects of anti‐ErbB agents. Studies using a 20,000 element (20K) cDNA microarray demonstrate decreased transcript expression of ErbB1 (epidermal growth factor receptor) and ErbB2 in DU145 (prostate) and ErbB2 in SKBr3 (breast) cancer cell lines. Additional changes in the DU145 gene expression profile with potential interaction to ErbB signaling include down‐regulation of caveolin‐1 and hypoxia inducible factor 1‐α (HIF1‐α), and up‐regulation of gelsolin, p19(INK4D) and Nur77. Findings were validated using real time RT‐PCR and Western blot analysis. Enhanced proliferative inhibition, apoptosis induction and signaling inhibition were demonstrated when combining HDAC inhibition with ErbB blockade. These results suggest that used cooperatively, anti‐ErbB agents and HDAC inhibitors may offer a promising strategy of dual targeted therapy. Additionally, microarray data suggest that the beneficial interaction of these agents may not derive solely from modulation of ErbB expression, but may result from effects on other oncogenic processes including angiogenesis, invasion and cell cycle kinetics. © 2005 Wiley‐Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94461/1/21465_ftp.pd

An essential role for the Id1/PI3K/Akt/NFkB/survivin signalling pathway in promoting the proliferation of endothelial progenitor cells in vitro

The enhancement of re-endothelialisation is a critical therapeutic option for repairing injured blood vessels. Endothelial progenitor cells (EPCs) are the major source of cells that participate in endothelium repair and contribute to re-endothelialisation by reducing neointima formation after vascular injury. The over-expression of the inhibitor of differentiation or DNA binding 1 (Id1) significantly improved EPC proliferation. This study aimed to investigate the effects of Id1 on the phosphatidylinositol-3-kinase (PI3K)/Akt/nuclear factor kappa B (NFκB)/survivin signalling pathway and its significance in promoting EPC proliferation in vitro. Spleen-derived EPCs were cultured as previously described. Id1 was presented at low levels in EPCs, and was rapidly up-regulated by stimulation with vascular endothelial growth factor. We demonstrated that transient transfection of Id1 into EPCs activated the PI3K/Akt/NFκB/survivin signalling pathway and promoted EPC proliferation. The proliferation of EPCs was extensively inhibited by silencing of endogenous Id1, and knockdown of Id1 expression led to suppression of PI3K/Akt/NFκB/survivin signalling pathway in EPCs. In addition, blockade by the PI3K-specific inhibitor LY294002, Akt inhibitor, the NFκB inhibitor BAY 11-7082, the survivin inhibitor Curcumin, or the survivin inhibitor YM155 reduced the effects of Id1 transfection. These results suggest that the Id1/PI3K/Akt/NFκB/survivin signalling pathway plays a critical role in EPC proliferation. The Id1/PI3K/Akt/NFκB/survivin signalling pathway may represent a novel therapeutic target in the prevention of restenosis after vascular injury

Charge-changing cross section measurements of 300 MeV/nucleon 28^{28}Si on carbon and data analysis

Charge-changing cross section ($\sigma_{\text{cc}}$) measurements via the transmission method have made important progress recently aiming to determine the charge radii of exotic nuclei. In this work, we report a new $\sigma_{\text{cc}}$ measurement of 304(9) MeV/nucleon $^{28}$Si on carbon at the second Radioactive Ion Beam Line in Lanzhou (RIBLL2) and describe the data analysis procedure in detail. This procedure is essential to evaluate the systematic uncertainty in the transmission method. The determined $\sigma_{\mathrm{cc}}$ of 1125(11) mb is found to be consistent with the existing data at similar energies. The present work will serve as a reference in the $\sigma_{\text{cc}}$ determinations at RIBLL2.Comment: 9 pages, 13 figures, to be published in Chinese Physics

Review on Superconducting Materials

Short review of the topical comprehension of the superconductor materials classes Cuprate High-Temperature Superconductors, other oxide superconductors, Iron-based Superconductors, Heavy-Fermion Superconductors, Nitride Superconductors, Organic and other Carbon-based Superconductors and Boride and Borocarbide Superconductors, featuring their present theoretical understanding and their aspects with respect to technical applications.Comment: A previous version of this article has been published in \" Applied Superconductivity: Handbook on Devices and Applications \", Wiley-VCH ISBN: 978-3-527-41209-9. The new extended and updated version will be published in \" Encyclopedia of Applied Physics \", Wiley-VC

Intrathecal lidocaine pretreatment attenuates immediate neuropathic pain by modulating Nav1.3 expression and decreasing spinal microglial activation

<p>Abstract</p> <p>Background</p> <p>Intrathecal lidocaine reverses tactile allodynia after nerve injury, but whether neuropathic pain is attenuated by intrathecal lidocaine pretreatment is uncertain.</p> <p>Methods</p> <p>Sixty six adult male Sprague-Dawley rats were divided into three treatment groups: (1) sham (Group S), which underwent removal of the L₆transverse process; (2) ligated (Group L), which underwent left L₅spinal nerve ligation (SNL); and (3) pretreated (Group P), which underwent L₅SNL and was pretreated with intrathecal 2% lidocaine (50 μl). Neuropathic pain was assessed based on behavioral responses to thermal and mechanical stimuli. Expression of sodium channels (Nav_1.3and Nav_1.8) in injured dorsal root ganglia and microglial proliferation/activation in the spinal cord were measured on post-operative days 3 (POD₃) and 7 (POD₇).</p> <p>Results</p> <p>Group L presented abnormal behavioral responses indicative of mechanical allodynia and thermal hyperalgesia, exhibited up-regulation of Nav_1.3and down-regulation of Nav_1.8, and showed increased microglial activation. Compared with ligation only, pretreatment with intrathecal lidocaine before nerve injury (Group P), as measured on POD₃, palliated both mechanical allodynia (<it>p </it>< 0.01) and thermal hyperalgesia (<it>p </it>< 0.001), attenuated Nav_1.3up-regulation (<it>p </it>= 0.003), and mitigated spinal microglial activation (<it>p </it>= 0.026) by inhibiting phosphorylation (activation) of p38 MAP kinase (<it>p </it>= 0.034). p38 activation was also suppressed on POD₇(<it>p </it>= 0.002).</p> <p>Conclusions</p> <p>Intrathecal lidocaine prior to SNL blunts the response to noxious stimuli by attenuating Nav_1.3up-regulation and suppressing activation of spinal microglia. Although its effects are limited to 3 days, intrathecal lidocaine pretreatment can alleviate acute SNL-induced neuropathic pain.</p