The Asian and African distribution of T cingulata versus Europe

The Asian and African distribution of T. cingulata versus Europe for T. ljubarskyi; the thickness of the basidiomes: 2–10 mm. for T. cingulata versus 30 mm. for T. ljubarskyi; the pore pattern

and dissepiments: round and regular, 4–6 per mm., fairly thick dissepiments for T. cingulata versus circular to angular, 3–4 per mm., thin dissepiments for T. ljubarskyi and strikingly different upper surface: FHPI frequently concentrically sulcate and whitish to ochraceous becoming sooty black spreading from the base for T. cingulata versus azonate and whitish to ochraceous becoming pale grayish brown in spots for T. ljubarskyi. Furthermore, according to our own observations, basidiomes of T. ljubarskyi are paler than those of the isotype of T. cingulata which

is rather red brown. Nevertheless these 2 species share several common features: somewhat broadly ellipsoid basidiospores (a very unusual character in this group) with similar sizes strictly pored hymenial surface remaining so during development of the basidiomes and glabrous and somewhat glossy upper surface. ‘Lenzites’ warnieri As mentioned above, ‘Lenzites’ warnieri creates a unique branch according to the topology of the Bayesian tree. This unresolved phylogenetic position is reflected in the fact that the species possesses many morphological features from other genera, and this ultimately would place L. warnieri in a separate genus. This Mediterranean Mocetinostat solubility dmso species is always glabrous and dull, with strictly lamellate hymenial surface (character in common with T. betulina), without parietal crystals on the hyphae (Artolenzites, Leiotrametes). L. warnieri shows superficial skeletal hyphae filled with a brown resinous content not selleck chemical accumulating at the apex (Fig. 4e) and its abhymenial surface turns deep brown with 5% KOH. These 2 features also characterize species of the genus Leiotrametes.

This supports one of the striking points emphasized in this study: there is no correlation at all between type of hymenial surface and Sclareol phylogenetic position of a species within the Trametes-group. The lamellate Lenzites warnieri, Artolenzites elegans and T. betulina are not monophyletic and show no close relationship. Lenzites is therefore discarded. Unfortunately, because of the absence or very weak development of the hymenium in most of our specimens, we cannot rule about the taxonomic significance of the hymenial sword-like pseudo-cystidia previously mentioned for T. betulina, T. gibbosa and L. warnieri (Ryvarden and Gilbertson 1993; Tomšovský et al. 2006). For the same reason, the basidiospores could not be properly analyzed in these species. Nevertheless, while Pieri and Rivoire (2007) revealed that pseudocystidia were not found in T.

For the marginal means (collapsed across condition), *PRE > POST,

For the marginal means (collapsed across condition), *PRE > POST, 24 h, 48 h, and 72 h (p < 0.05); †POST < PRE, 24 h, 48 h, and 72 h (p < 0.05); #PRE < POST, 24 h, 48 h, and 72 h (p < 0.05). There were no condition x time (p > 0.05) interactions and no main effects for condition (p > 0.05) or time (p > 0.05) for systolic blood pressure (Figure 4a), diastolic blood pressure (Figure 4b), or resting heart rate (Figure 4c). Figure 4 Heart rate

and blood pressure. Data presented are means ± standard error of the mean for (a) systolic blood pressure (mmHg), (b) diastolic blood pressure (mmHg), and (c) heart rate (bpm) during the supplement (dashed line, open circles; ANA) and placebo (solid line, closed circles; PLA) conditions assessed Epigenetics inhibitor at baseline (visits 1 or 6)and 72 h after the bout of maximal eccentric exercise.

Discussion The results of the present study did not support our original hypotheses that ANA would improve the recovery of PT, hanging joint angle, relaxed arm circumference, or subjective pain ratings compared to PLA in response to eccentric-induced muscle damage. The protocol used in the present study has been used to elicit muscle damage in previous studies [6, 13, 19, 20]. For example, Beck et al. [13] demonstrated 21-43% decreases in PT of the forearm flexors, while Cockburn et al. [20] reported 15-20% decreases in leg flexion PT. The 23-44% decreases in PT observed in the present study were consistent with Beck et al. [13], but greater than Cockburn et al. [20], which may have been related to the muscle group oxyclozanide studied. Nevertheless, Warren et al. [2] suggested that PT is the single best non-invasive indicator of muscle damage resulting from eccentric exercise, therefore,

the results of the present study suggested that the magnitude of muscle damage that occurred was consistent with or greater than previous studies using the same protocol. Interestingly, these previous studies [13, 20] and click here others [10] have also demonstrated that this muscle damage protocol has elicited decreases in PT that were sensitive to dietary supplement interventions to improve recovery. However, in the present study there were no differences between ANA and PLA conditions during the recovery of PT, hanging joint angle, relaxed arm circumference, or subjective pain rating within 72 h after eccentric exercise. Thus, our conclusion was that ANA supplementation had no effect on recovery of muscle strength, joint stiffness, arm swelling, or pain using this model of muscle damage. Connelly et al.

Hum Mol Genet 2007, 16:2333–2340 PubMedCrossRef 46 Balding DJ: A

Hum Mol Genet 2007, 16:2333–2340.PubMedCrossRef 46. Balding DJ: A tutorial on statistical methods for population association studies. Nat Rev

Genet 2006,7(10):781–791.PubMedCrossRef 47. Wilcken B, Bamforth F, Li Z, Zhu H, Ritvanen A, Renlund M, Stoll C, Alembik Y, Dott B, Czeizel AE, Gelman-Kohan Z, Scarano G, Bianca S, Ettore G, Tenconi R, Bellato S, Scala I, Mutchinick OM, López MA, De Walle H, Hofstra R, Joutchenko L, Kavteladze L, Bermejo E, Martínez-Frías ML, Gallagher M, Erickson JD, Vollset SE, Mastroiacovo P, Andria G: Geographical and ethnic variation of the 677C > T allele of 5,10 methylenetetrahydrofolate reductase (MTHFR): findings Selleckchem Ganetespib from over 7000 newborns from 16 areas world wide. J Med Genet 2003, 40:619–625.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions All authors participated to the conception, design, interpretation, elaboration of the findings of the study, drafting and revising the final elaborate. In particular, Dr. VB designed the study, wrote the paper and with Dr. FPC and Dr. LM performed patients genotyping experiments. Dr. SP selected and enrolled the patients and performed FDG PET-CT studies. Dr. AS performed quantitative PET measurements and with Dr. GR and Dr. SN analysed data. Prof. CG, Prof. MCG and Prof. CM participated in the elaboration

of the findings of the study, drafting and revising the final elaborate. All authors read and approved the final content of the manuscript.”
“Background Ovarian cancer remains learn more leading cause of death among patients with different gynecological

neoplasms. Although majority of the patients see more respond to the primary treatment with debulking surgery followed by paclitaxel and platinum-based chemotherapy, many of them experience relapse of the disease within few years after first-line therapy. Platinum compounds introduction to the ovarian cancer treatment was a corner stone in the therapy of this malignancy. Paclitaxel addition to platinum improves the results of chemotherapy [1, 2]. Nevertheless about one quarter of the patients does not respond to the therapy and those who initially benefit Phospholipase D1 from the treatment incline to experience disease recurrence. There are no molecular agents known to predict the response to the chemotherapy in ovarian cancer as well as patients’ outcome. Revelation of such markers could result in a more effective patient selection to the certain regimens and development of tailored chemotherapy in ovarian cancer. Recently, microtubule associated protein (MAP) Tau has been identified as a potential marker of response to paclitaxel in breast cancer. Tau protein (50–64 kD), a product of gene located in chromosome 17 (17q21) shows the ability of combining to beta-tubulin.

3, which was also found, associated with tumorigenicity [26] In

3, which was also found, associated with tumorigenicity [26]. In this study, we showed that Mir-29a negatively regulated expression of B-Myb (Figure 5), which is a transcription factor broadly involved in regulating cell cycle and apoptosis and probably is a promoting factor for cancer [27]. Downstream effectors of B-Myb,

such as Cyclin A2 and D1, were also correspondingly regulated by Mir-29a. Cyclin D1 is one of highly over-expressed proteins in breast cancer cells and over-expression of Cyclin D1 protein was found in 40-90% of cases of invasive breast cancer [28]. Cyclin CHIR98014 purchase A2 is involved in S phase and G2-M phase transition and is also over-expressed in various cancers [29–31]. Taken together, in current paper, we showed that Mir-29a may act as a tumor suppressor through its inhibitory function on growth of breast cancer cells, and down-regulating expression of B-Myb by Mir-29a may contribute AZD2281 purchase to this process. References 1. Jemal A, et al.: Cancer statistics, 2009. CA Cancer J Clin 2009,59(4):225–249.PubMedCrossRef 2. Lin Y, et al.: Striking life events associated with primary breast cancer susceptibility in women: a meta-analysis study. J Exp Clin Cancer Res 2013,32(1):53.PubMedCentralPubMedCrossRef 3. Iorio MV, et al.: MicroRNA gene expression deregulation in human

breast cancer. Cancer Res 2005,65(16):7065–7070.PubMedCrossRef 4. Wang C, et al.: MicroRNA-203 suppresses cell proliferation and migration by targeting BIRC5 and LASP1 in human triple-negative breast cancer cells. J Exp

Clin Cancer Res 2012, 31:58.PubMedCentralPubMedCrossRef 5. Bartel DP: MicroRNAs: target recognition and regulatory functions. Cell 2009,136(2):215–233.PubMedCentralPubMedCrossRef 6. Chen F, Hu SJ: Effect of microRNA-34a in cell cycle, differentiation, and apoptosis: a review. J Biochem Mol Toxicol 2012,26(2):79–86.PubMedCrossRef 7. He L, Hannon GJ: MicroRNAs: small RNAs with a big role in gene regulation. Nat Rev Genet 2004,5(7):522–531.PubMedCrossRef 8. Plaisier CL, Pan M, Baliga NS: A miRNA-regulatory network explains how dysregulated miRNAs perturb oncogenic processes Rucaparib across diverse cancers. Genome Res 2012,22(11):2302–2314.PubMedCentralPubMedCrossRef 9. Fan MQ, et al.: Decrease expression of microRNA-20a promotes cancer cell proliferation and predicts poor survival of hepatocellular carcinoma. J Exp Clin Cancer Res 2013,32(1):21.PubMedCentralPubMedCrossRef 10. Calin GA, Croce CM: MicroRNA signatures in human cancers. Nat Rev Cancer 2006,6(11):857–866.PubMedCrossRef 11. Creighton CJ, et al.: Integrated analyses of microRNAs demonstrate their widespread influence on gene expression in high-grade serous ovarian carcinoma. PLoS One 2012,7(3):e34546.PubMedCentralPubMedCrossRef 12. Zhao JJ, et al.: MicroRNA expression profile and identification of miR-29 as a AZD3965 prognostic marker and pathogenetic factor by targeting CDK6 in mantle cell lymphoma. Blood 2010,115(13):2630–2639.PubMedCentralPubMedCrossRef 13. Garzon R, et al.

DNA was removed from each RNA preparation using Turbo DNA-free Ki

DNA was removed from each RNA preparation using Turbo DNA-free Kit (Ambion), according to manufacturer’s instructions. RNA quantity (A260) and purity (A260/280 ratio) were measured

in a NanoDrop 1000 Spectrophotometer,EXEL-2880).html (Thermo Fisher Scientific). cDNA was synthesised from 500 ng RNA using the High-Capacity cDNA Reverse Transcription Kit (Applied Biosystems) in a 20 μl reaction according to manufacturer’s protocols. Five μl of a 1:100 dilution of the cDNA reaction was used as template for qPCR amplification in 25 μl final volumes containing 12.5 μl of Power SYBR Green PCR Master Mix (Applied Biosystems) and 200 nM of each primer. Primers used for qPCR are listed in Table  2. The amplification was performed using StepOne PCR software (Applied Biosystems) with thermal cycling conditions set at 10 min at 95°C, followed by 40 Selleckchem Salubrinal cycles of 15 s at 95°C and 1 min at

60°C. Fluorescence was monitored during each extension phase and a melting curve analysis was performed after each run to confirm the amplification of specific transcripts. Each qPCR of the RNA samples was performed Veliparib in triplicate, no template was added in negative controls, and rpoB was used as internal control. The qPCR analysis was performed on three independent biological replicates. Slopes of the standard curves and PCR efficiency (E) for each primer pair were estimated by amplifying serial dilutions of the cDNA template. For quantification of mRNA transcript levels, Ct (threshold cycle) values of the target genes (gerAA) and the internal control gene (rpoB) derived from the same sample in each real-time PCR reaction were first transformed using the term E-Ct. The expression levels of target genes were then normalized by dividing their transformed Ct-values by the corresponding values obtained for internal control gene [64, 65]. Germination assays Storage water was decanted and the spores were resuspended in autoclaved Milli-Q water (20°C) immediately before heat activation at 65°C in a heating block (QBD2, Grant Instruments Ltd) for 20 min. The Morin Hydrate heat-activated

spores were rapidly cooled down by centrifugation for 3 min 4500 × g at 4°C before resuspension in germination buffer (200 mM K-phosphate buffer pH 7.2). The A600 of the buffered spore suspension was adjusted to ~2.1 (Shimadzu UV- 160A, Shimdazu Europe GMBH). L-Alanine (Sigma) was dissolved in Milli-Q water and filter sterilized prior to use through a 0.45 μm pore size filter. 100 μL of 0.05 – 0.2 M L-Alanine germinant solution was added to 100 μL buffered spore suspension in a 96-well microplate (BD) giving an initial A600 of ~1. Germination was by monitored by reading the drop in absorbance (A600) in a 96-well microplate reader (Tecan Infinite M200). Readings were performed at regular intervals (2 min) and the plate was shaken 10 s prior to each reading.

Singapore Med J 2003,44(8):12–19 2 Jaffe HL, Lichtenstein L, Po

Singapore Med J 2003,44(8):12–19. 2. Jaffe HL, Lichtenstein L, Portis RB: Giant cell tumor of the bone. Its pathological apperance, grading, supposed variant and treatment. Arch Pathol 1940, 30:993–1031. 3. Campanacci M, Baldini N, Boriani S, Sudanese A: Giant cell tumor of bone. J Bone and Joint Surg 1987,69(A):106–114. 4. Faisham WI, Zulmi W, Halim AS, Biswal BM, Mutum SS, Ezane AM:

Aggressive giant cell tumor of the bone. Singapore Med J 2006,47(8):631–633. 5. Faisham WI, Zulmi W, Saim AH, Biswal BM: Pulmonary metastases of giant cell tumor of the bone. Med J Malaysia 2004,59(F):78–81.PubMed 6. Scholzen T, Gerdes J: The Ki 67 protein: from the known and the unknown (review). J Cell physiol 2000, 182:311–322.PubMedCrossRef #selleck randurls[1|1|,|CHEM1|]# 7. Rousseau MA, Luca AH, Lazennec JV: Metachronous multicentric giant cell tumor of the bone in the lower limb. Case report and Ki

67 immuno-histochemistry Selleck MK-8931 study. Virchows Arch 2004, 445:79–82.PubMed 8. Matsui F, Ushigome S, Fuji K: Giant cell tumor of bone. Clinicopathologic study of prognostic factors. Pathol Int 1998,48(9):723–729.CrossRef 9. Matsui F, Ushigome S, Fuji K: Giant cell tumor of bone. An immunohistochemical comparative study. Pathol Int 1998,48(5):355–361.CrossRef 10. Gamberi G, Serra M, Ragazzini P: Identification of markers of possible prognostic value in 57 giant cell tumor of the bone. Oncol Rep 2003,10(2):351–356.PubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions FWI is the group leader and the work represents

his idea in correlation the clinical and basic science of GCT. MSA carried out most of the experimental work, literature review and statistical analysis. MDS and SSM, WZ supervised and evaluated the experimental work, clinical evaluation and also contributed in the discussion and preparation of manuscript. All authors have read and approved the final manuscript.”
“Background Peroxisome proliferator-activated receptor γ (PPARγ) belongs to a family of ligand-activated transcription factors. PPARγ is an intracellular sensor for fatty acids and fatty acid derivatives, CYTH4 which in turn act as endogenous ligands for PPARγ. PPARγ and its ligand activators regulate several lipid and glucose metabolism pathways [1]. In humans, PPARγ is expressed in multiple tissues, including the breast, colon, prostate, lung, placenta, and pituitary tissues [2–5]. PPARγ activation is antiproliferative by virtue of its differentiation-promoting effects. For example, ligands activating PPARγ were effective in arresting the growth of dedifferentiated tumor cells in multiple tumor types [2, 4–9], and they promoted differentiation of tumor cells and inhibited spontaneous metastasis in a xenograft model [7]. However, the mechanism by which PPARγ arrests growth has not been completely clarified.


Gynecol Oncol 2002, 87:1–7.PubMedCrossRef 24. Kajiyama H, Shibata K, Suzuki S, et al.: Is there any possibility of fertility-sparing surgery in patients with clear-cell carcinoma of the ovary? Gynecol Oncol 2008, 111:523–526.PubMedCrossRef 25. Satoh T, Hatae M, Watanabe Y, et al.: KU-57788 price Outcomes of fertility-sparing surgery for stage I epithelial ovarian cancer: a proposal for patient selection. J Clin Oncol 2010, 28:1727–1732.PubMedCrossRef 26. Kajiyama H, Shibata K, Mizuno M, et

al.: Fertility-sparing surgery in patients with clear-cell carcinoma of the ovary: Is it possible? Hum Reprod 2011, 26:3297–3302.PubMedCrossRef 27. O’Brien ME, Schofield JB, Tan S, et al.: Clear cell epithelial ovarian cancer (mesonephroid): bad prognosis only in early stages. Gynecol Oncol 1993, 49:250–254.PubMedCrossRef 28. Omura GA, Brady MF, Homesley HD, et al.: Long-term follow-up and prognostic factor analysis in advanced ovarian carcinoma: the Gynecologic Oncology Group experience. J Clin Oncol 1991, 9:1138–1150.PubMed 29. Goff BA, Sainz De La Cuesta R, Muntz HG, et al.: Clear cell carcinoma of the ovary: find protocol a distinct histologic type with poor prognosis and resistance to platinum-based chemotherapy in stage III disease. Gynecol Oncol 1996, 60:412–417.PubMedCrossRef 30. VS-4718 Sugiyama T, Yakushiji M, Nishida T, et al.:

Irinotecan (CPT-11) combined with cisplatin in patients with refractory or recurrent ovarian cancer. Cancer Lett 1998, 128:211–218.PubMedCrossRef 31. Ho CM,

Huang YJ, Chen TC, et al.: Pure-type clear cell carcinoma of the ovary as a distinct histological type and improved survival in patients treated with paclitaxel-platinum-based chemotherapy in pure-type advanced disease. Gynecol Oncol 2004, 94:197–203.PubMedCrossRef 32. Enomoto T, Kuragaki C, Yamasaki M: Is clear cell carcinoma and mucinous carcinoma of the ovary sensitive to combination chemotherapy with paclitaxel and Liothyronine Sodium carboplatin? Proc Am Soc Clin Oncol 2003,22(#1797):447. 33. Utsunomiya H, Akahira J, Tanno S, et al.: Paclitaxel-platinum combination chemotherapy for advanced or recurrent ovarian clear cell adenocarcinoma: a multicenter trial. Int J Gynecol Cancer 2006, 16:52–56.PubMedCrossRef 34. Minagawa Y, Kigawa J, Ishihara H, et al.: Synergistic enhancement of cisplatin cytotoxicity by SN-38, an active metabolite of CPT-11, for cisplatin-resistant HeLa cells. Jpn J Cancer Res 1994, 85:966–971.PubMedCrossRef 35. Fukuda M, Nishio K, Kanzawa F, et al.: Synergism between cisplatin and topoisomerase I inhibitors, NB-506 and SN-38, in human small cell lung cancer cells. Cancer Res 1996, 56:789–793.PubMed 36. Noda K, Nishiwaki Y, Kawahara M, et al.: Irinotecan plus cisplatin compared with etoposide plus cisplatin for extensive small-cell lung cancer. N Engl J Med 2002, 346:85–91.PubMedCrossRef 37. Adachi S, Ogasawara T, Yamasaki N, et al.: A pilot study of CPT-11 and cisplatin for ovarian clear cell adenocarcinoma.

Vaccine 2013,32(1):165–179 PubMedCrossRef 5 Gupta S, Maiden MCJ:

Vaccine 2013,32(1):165–179.PubMedCrossRef 5. Gupta S, Maiden MCJ: Exploring the evolution of diversity in pathogen populations. Trends Microbiol 2001,9(4):181–185.PubMedCrossRef 6. Pillai D, Shahinas D, Buzina A, Pollock R, Lau R, Khairnar K, Wong A, Farrell D, Green K, McGeer A, Low D: Genome-wide dissection of globally emergent multi-drug resistant serotype 19A Streptococcus pneumoniae . BMC Genomics 2009,10(1):642.PubMedCentralPubMedCrossRef 7. Frosi G, Biolchi A, Sapio ML, Rigat F, Gilchrist S, Lucidarme J, Findlow J, Borrow R, Pizza M, Giuliani MM, Medini

D: Bactericidal antibody against a representative epidemiological meningococcal serogroup B panel confirms that MATS underestimates 4CMenB vaccine strain coverage. Vaccine 2013,31(43):4968–4974.PubMedCrossRef PLX-4720 purchase 8. Selander RK, Caugant DA, Ochman H, Musser JM, Gilmour MN, Whittam TS: Methods of multilocus enzyme electrophoresis for bacterial population genetics FDA-approved Drug Library cell assay and systematics.

Appl Environ Microbiol 1986,51(5):873–884.PubMedCentralPubMed 9. Hunter SB, Vauterin P, Lambert-Fair MA, Van Duyne MS, Kubota K, Graves L, Wrigley D, Barrett T, Ribot E: Establishment of a universal size standard strain for Use with the PulseNet standardized pulsed-field Gel electrophoresis protocols: converting the national databases to the New size standard. J Clin Microbiol 2005,43(3):1045–1050.PubMedCentralPubMedCrossRef 10. Han H, Zhou H, Li H, Gao Y, Lu Z, Hu K, Xu B: Optimization of Pulse-Field Gel Electrophoresis for Subtyping

of Klebsiella pneumoniae . Int J Environ Res Pub Health 2013,10(7):2720–2731.CrossRef 11. Enright MC, Spratt BG: A multilocus sequence typing scheme for Streptococcus pneumoniae : identification of clones associated with serious invasive disease. Microbiology 1998,144(11):3049–3060.PubMedCrossRef 12. Alternative MLST Primers for S. pyogenes and S. pneumoniae. [http://​www.​cdc.​gov/​ncidod/​biotech/​strep/​alt-MLST-primers.​htm] 13. Enright MC, Knox K, Griffiths D, Crook DWM, Spratt BG: pentoxifylline Molecular typing of bacteria directly from cerebrospinal fluid. EJCMID 2000,19(8):627–630.CrossRef 14. Marimon JM, Ercibengoa M, García-Arenzana JM, Alonso M, Pérez-Trallero E: Streptococcus pneumoniae ocular infections, prominent role of unencapsulated isolates in conjunctivitis. Clin Microbiol Infect 2013,19(7):E298-E305.PubMedCrossRef 15. Hanage WP, Bishop CJ, Lee GM, Lipsitch M, Stevenson A, Rifas-Shiman SL, Pelton SI, Huang SS, Finkelstein JA: Clonal replacement among 19A Streptococcus pneumoniae in Massachusetts, prior to 13 valent conjugate vaccination. Vaccine 2011,29(48):8877–8881.PubMedCentralPubMedCrossRef 16. Xu Q, Kaur R, Casey JR, Adlowitz DG, Pichichero ME, Zeng M: Identification of Streptococcus pneumoniae and Haemophilus influenzae in culture-negative middle ear fluids from children with acute otitis media by combination of multiplex PCR and multi-locus sequencing typing. Int J Pediatr Otorhinolaryngol 2011,75(2):239–244.

The thermal expansion properties of the MWCNT/epoxy nanocomposite

The thermal expansion properties of the MWCNT/epoxy nanocomposites were measured using a TMA equipment (TMA-50, Shimadzu Co., Kyoto, Japan). The TMA measurement methodology is described as follows: a rectangular sample (3 cm wide, 3 cm long) was cut from the nanocomposites at a point 3 cm from the parallel portion of the tensile test specimen (according to JIS K 7197 [22]). Specimens were heated from 30°C to 120°C at a scanning rate of 5°C/min in air for continuous measurements. The thermal expansion properties of pure epoxy were similarly

measured for the same specimen size and test conditions. Note that the highest test temperature, i.e., 120°C, is close to the glass transition point of bisphenol-F epoxy resin, which usually ranges from 120°C to 130°C, depending on fabrication conditions. In our tests, it was found that even at 120°C, the obtained thermal expansion rates were still normal and a molten or rubber-like state in epoxy was not identified. Comparison Figure 9 shows the comparison between the thermal expansion properties of the MWCNT/epoxy nanocomposites as determined by multi-scale numerical simulations, theoretical analysis, and ITF2357 chemical structure experimental measurement. In Figure 9a, for GDC-0449 chemical structure uni-directional models, the comparison between the thermal expansion properties by multi-scale

numerical simulation and theoretical prediction was given, in which the relative difference is lower than 15% for the results. In Figure 9b,c, for multi-directional models, the comparisons of experimental, simulated, and theoretical results were shown for different CNT contents (i.e., 1

and 3 wt%). It can be found that the multi-scale numerical simulation results possess a similar trend to the theoretical prediction and experimental measurement as temperature increases. It should be noted that the relative difference is also lower than 15% for all three results. This implies that the present multi-scale numerical simulation is effective in predicting the thermal expansion properties of CNT-based nanocomposites under the condition that the CNT is of a comparatively large size and a good dispersion state in Celecoxib matrix. Figure 10 shows the influence of CNT loading on the thermal expansion rates of the MWCNT/epoxy nanocomposites at high temperature (120°C), which was evaluated by experimental, simulated, and theoretical approaches. From this figure, it can be found that the thermal expansion rate obtained by experiments decreases about 25% at 1 wt% and 35% at 3 wt%. Moreover, a similar trend is observed at a broad temperature range from 30°C to 120°C, in which the thermal expansion rate decreases with CNT loading for each case, and the present numerical simulation and theoretical analysis can effectively predict the experimental measurements.

The conference, organised by Land-Ocean Interactions in the Coast

The conference, organised by Land-Ocean Interactions in the Coastal Zone (LOICZ) and the Yantai Institute of Coastal Zone Research (YICZR), was hosted by YICZR and the Chinese Academy of Sciences, with support from the Centre for Materials and Coastal Research, Helmholtz-Zentrum, Geesthacht, Germany. The aim of the conference was to Selleckchem R788 bring together the

international research community working on land-ocean issues, to showcase the breadth and scope of ongoing research, to help build a community-of-interest in this highly interdisciplinary field, and to inspire new research, theory, and ABT-888 datasheet applied science. The organisers gave priority to an integrated approach by drawing on a diversity of experiences and disciplinary perspectives worldwide in order to generate new levels of understanding and improve policy, decision-making, and planning practice. The conference included a special session on Islands at Risk: Small Island Developing States. Many of the papers in this Special Issue were presented initially in the small islands session, which focussed on the constraints, challenges, and potential strategies for coping with existing and projected coastal hazards in the context of climate change and

extreme events. Many consequences of changes in climate will first be felt in extreme events, which therefore require careful attention along with the potential for climate ‘surprises’. Of the 11 papers in this Special Issue, 6 had their origins in the 2011 Yantai conference. The others are included because of their relevance to the theme of the conference and Selleck AR-13324 their contribution to a broader discussion of small islands issues. While the majority of the papers arise from research undertaken in the Pacific Islands region,

in particular Kiribati and Tuvalu, other papers report research findings for the Bahamas and Trinidad and Tobago. Another paper draws examples from small islands in three major oceans with robust local sea-level projections for 18 small island sites around the world. One paper discusses environmental management in coastal and small-island communities in both Canada and the Caribbean. Still others present findings of research with Cell press global relevance to all SIDS and other small islands. A similar diversity is seen in the authorship of the papers, with representation both from SIDS and from the broader global research community. Figure 1 shows that the papers cover three key aspects of understanding and managing global change in small islands: Fig. 1 Titles, authors and thematic focus of papers in this Special Issue. The papers are organised under three themes related to understanding and managing global change in small islands learning from the past and anticipating the future; understanding and assessing hazards, exposure, risk, vulnerability, resilience, and sustainability; and managing current and future change.