br Acknowledgements We are indebted to K Basler S

Acknowledgements We are indebted to K. Basler, S. Bray, M. Freeman E. Martín-Blanco and F. Schweisguth for fly lines. Some antisera used in this work were obtained from the Developmental Studies Hybridoma Bank (DSHB) developed under the auspices of the NICHD and maintained by the University of Iowa, Dept. of Biology, Iowa City, Iowa 52242. The work was supported by the University of Hohenheim.
Experimental design
Data, experimental design, materials and methods Data sets comprise of list of 34 aromatase inhibitor which were successfully identified by MALDI-TOF/MS after NnV treatment of H9c2 cell and 2-DE. Among these, 10 proteins were down-regulated and 24 proteins were up-regulated [1]. Differentially expressed (relative spot intensity) proteins and their fold-change along with the up- and down-regulated p-values are summarized in Supplementary Table 1 and Supplementary Table 2, respectively.
Acknowledgments This work was supported by the National Research Foundation of Korea (NRF) Grant funded by the Korea government (MSIP) (No. NRF-2014R1A2A2A01007245) and by the “Jellyfish Monitoring and Mitigation (15-OE-14)” Project funded by the National Fisheries Research and Development Institute, Korea.
Data
Experimental design, materials and methods The reference range study was designed to include patients commonly seen in intensive care units of hospitals in the United States [2]. The list of patients with chronic stable comorbid conditions is presented in Table 1. Table 2 gives a description of patient demographics that were targeted for inclusion. Table 3 provides detailed inclusion criteria used to select the healthy reference range population. The protocols for this investigation were approved by investigational review boards/ethics committees as required by each participating institution. All subjects provided written informed consent. Subjects of ≥21 years age, who provided written informed consent for the study participation, and met the morbidity criteria (Table 1) were selected in the stable chronic morbidity cohort. For apparently healthy subjects, individuals of ≥21 years of age, who provided written informed consent for study participation, and met the healthy criteria (Table 2), were selected for this cohort.
Acknowledgments This work was funded by Astute Medical, San Diego, California, 92121.
Data
Experimental design, materials and methods Unless otherwise stated all materials were obtained from Sigma-Aldrich (St. Louis, MO, USA). Plakortin, methyl 4,8-diethyl-6-methyl-3,6-peroxy-9-dodecenoate, was obtained from the organic extract of the Caribbean sponge Plakortis simplex and purified by combination of column chromatography and HPLC as described [8]. The final purity of the compound was >99%.
Acknowledgments The study was supported by the Italian Ministry for Research (MIUR PRIN2008, Leads ad attività antimalarica di origine naturale. Isolamento, ottimizzazione e valutazione biologica), MIUR Grant 2010C2LKKJ-007 (E.S.), the University of Torino Intramural Funds (E.S.; O.A.S. PROG 101289 2012 and 2013, PROG 102326 2014) and EviMalaR (European Virtual Institute dedicated to Malaria Research) Project no. 242095 (P.A.).
1. Data The multiplex assays with TaqMan probes were carried out to amplify two regions of PIK3CA gene (in exons 9 and 20) and analyze the amplicons by DMA for the presence of the “hot spot” mutations (codons 542–546 and 1047–1049, respectively). This short (about 1.5h) procedure is implemented in the “closed tube” format minimizing the sample cross-contaminations [4].
2. Experimental design, materials and methods
Acknowledgments This work was supported by the N.N. Blokhin Russian Cancer Research Center (grant 10-04-00060).
The data presented in this article further characterize the expression pattern of HO-1 in the rat glomerulus and highlight differences of this expression pattern compared to the expression pattern of a key cellular component, glomerular epithelial cells (GEC). Although, HO-1 has an established protective role in the kidney in which it was shown to minimize injury, a marked induction can be detrimental. In this context, we previously demonstrated that HO-1 induction in the renal glomerulus in response to its natural substrate/inducer, heme, reaches a threshold beyond which protein synthesis is halted and HO-1 protein levels are markedly reduced. The present data demonstrate that this threshold also occurs at the HO-1 mRNA level (a) and is not dependent on release of iron (b), one of the heme:HO reaction byproducts known to be cytotoxic when HO-1 activity reaches high levels. The threshold is also independent of the metal (Fe) moiety of heme (FeProtoporhyrin) as it was also observed when glomeruli were exposed to Cobalt (Co) protoporphyrin, as described in the article to which these data relate . The data presented also demonstrate that the heme-mediated HO-1 induction threshold is inversely proportional to availability of heme. Specifically, increasing availability of free heme by incubating glomeruli with serum lacking hemopexin (HPX), a heme scavenger, lowers the HO-1 induction threshold (a and b). Finally, the data demonstrate that, in contrast to isolated glomeruli, heme-mediated HO-1 induction threshold is not reached in a cellular component of glomeruli (GEC) ().