Changes in cladoceran and diatom community and its relationship with NAO index and temperature during the last 150 years

<p><strong>S08-P-03 Changes in cladoceran and diatom community and its relationship with NAO index and temperature during the last 150 years</strong></p> <p>Pérez-Martínez, C., Jiménez, L.</p> <p>Institute of Water Research. University of Granada. Spain</p> <p>We explore whether changes in cladoceran and diatom community can be linked to changes in mean temperature and in the NAO index. A high NAO index is associated to drier conditions over southern Europe and yields dust transport from Sahara desert over the western Mediterranean basin during summer. <em>Daphnia pulicaria </em>relative abundance shows an important increase in the lake during the last decades, mainly from 1970, whereas <em>Alona quadrangularis </em>increase occurs from late 80s simultaneously with the decrease of <em>Chydorus sphaericus</em>. <em>Daphnia </em>relative abundance through the core is positively correlated to the NAO index but no with temperature values. The opposite is found for <em>A. quadrangularis </em>and <em>C. sphaericus</em>. The most abundant diatom species and the factor 1 of the principal component analysis performed on diatom assemblage are correlated to temperature values and do not show any relationship with NAO index. A positive correlation between <em>Daphnia </em>and the NAO index is also found for 10 years of <em>Daphnia </em>sampling in Río Seco Lake (1996-98 and 2005- 2011).</p> <p>We hypothesized that <em>D. pulicaria </em>is probably benefited by Saharan dust calcium, because this species is likely limited by Ca in Río Seco Lake and Saharan dust is rich in Ca, whereas other cladoceran and the diatom species are more affected by temperature changes in the lake region.</p

Additional file 1: of Activity of the novel BCR kinase inhibitor IQS019 in preclinical models of B-cell non-Hodgkin lymphoma

Figure S1. IQS019 tyrosine kinase inhibitory profiling. Tyrosine kinase (TK) and tyrosine kinase-like (TKL) kinome tree was elaborated on the basis of residual in vitro kinase activity upon exposure to 100 nM or 1 μM IQS019, by means of Kinome Render software ( http://bcb.med.usherbrooke.ca/kinomerender.php ). Figure S2. Sensitivity of CLL primary cases to IQS019 is independent of IGHV mutational status and involves a caspase-dependent cell death process. (a) CLL primary cells, 9 of them with ummutated (UM) and 6 with mutated (M) IGHV gene, were treated with increasing concentrations of IQS019 for 24h. Cell viability was determined by MTT method. Shown are the median values from each CLL group (UM and M), referred to control, untreated cells. (b) IQS019 induces caspase-dependent cell death in MCL (UPN-1) and in FL (DOHH-2) cell lines, as well as in two representative CLL primary cultures. Cells were exposed for 24 hours to 5 μM IQS019, in the presence of absence of the pan-caspase inhibitor Q-VD-OPh (10 μM). Apoptosis was determined by simultaneous cytofluorimetric detection of Annexin-V and caspase-3/7 activity. (c) A set of 6 CLL primary cultures were treated with IQS019 as indicated, followed by Western Blot detection of phospho-histone H3 (p-H3), using β- actin as a loading control. Figure S3. Flow cytometry determination of CXCR4 membrane expression in B-NHL cell lines. Four representative cell lines were stained with a PE-labeled anti-CXCR4 antibody and analyzed on an Attune cytometer. CXCR4-specific signal (black curves) and isotypic control (grey filled curve) are represented. Figure S4. Safety and PK properties of IQS019-2MeSO3H in mice. (a) Twenty SCID mice (10 males and 10 females) received a single intravenous injection of IQS019-2MeSO3H at a 2 mg/kg, 10 mg/kg, or 50 mg/kg dose, or equivalent volume of vehicle, and animal weight was recorded at days 1, 3, 4, 7, 11, 14, 18 and 21 post-treatment. (b) Mean plasma concentration of IQS019-2MeSO3H in ICR mice over the time, after a single p.o. administration of a 25 mg/kg dose of the compound. Figure S5. Comparison of parental and ibrutinib-resistant derived B-NHL cell line. (a) Dose-response of the UPN-1 parental, and UPN-IbruR derived cell line exposed for 72 hours to increasing concentrations of ibrutinib or IQS019. (b) BTK and PLCG2 exon sequencing in UPN-IbruR cells. (c) Western blot detection of the alternative NF-κB pathway component, p52, in UPN-1 and UPN-IbruR cells. β-actin was used as a loading control. (DOC 3279 kb