Design of reinforced concrete frame structure of exhibition hall

Import 23/08/2017Předmětem bakalářské práce je železobetonová dvoupatrová rámová konstrukce, která má sloužit pro občanskou vybavenost jako výstavní síň. Cílem je navrhnout a posoudit nosné prvky rámové konstrukce, konstrukce schodiště a stropů a založení na základových patkách podle metody mezních stavů, platných norem a konstrukčních zásad. Pro posouzené prvky byly vypracovány výkresy výztuže a stavební výkresy.The subject of Bachelor thesis is two storey reinforced concrete frame structure, which has to serve for civil amenitied as exhibition hall. The aim is to design and assess the support elements of frame structure, the structure of staircase and the ceilings and the foundation on foundation plinths according to the method of limit states, applicable standards and design principles. For assess elements have been created reinforcement drawings and constuction drawings.221 - Katedra konstrukcívýborn

Disruption of Retinol (Vitamin A) Signaling by Phthalate Esters: SAR and Mechanism Studies - Fig 1

<p><b>(A) Major steps in the retinol signaling pathway of vertebrates. (B) Timeline for PE and ROH additions and duration of exposures for the 7 h and 30 h screens.</b> The initial PE concentration was 50 μM. After the addition of ROH, the PE and ROH concentrations were 45 μM and 0.3 μM respectively. The initial and final DMSO concentration was 0.5%. P19 cells were cultured in 96-well plates as described previously [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0161167#pone.0161167.ref011" target="_blank">11</a>].</p

Corexit-EC9527A Disrupts Retinol Signaling and Neuronal Differentiation in P19 Embryonal Pluripotent Cells

<div><p>Corexit-EC9500A and Corexit-EC9527A are two chemical dispersants that have been used to remediate the impact of the 2010 Deepwater Horizon oil spill. Both dispersants are composed primarily of organic solvents and surfactants and act by emulsifying the crude oil to facilitate biodegradation. The potential adverse effect of the Corexit chemicals on mammalian embryonic development remains largely unknown. Retinol (vitamin A) signaling, mediated by <i>all-trans</i> retinoic acid (RA), is essential for neural tube formation and the development of many organs in the embryo. The physiological levels of RA in cells and tissues are maintained by the retinol signaling pathway (RSP), which controls the biosynthesis of RA from dietary retinol and the catabolism of RA to polar metabolites for removal. RA is a potent activating ligand for the RAR/RXR nuclear receptors. Through RA and the receptors, the RSP modulates the expression of many developmental genes; interference with the RSP is potentially teratogenic. In this study the mouse P19 embryonal pluripotent cell, which contains a functional RSP, was used to evaluate the effects of the Corexit dispersants on retinol signaling and associated neuronal differentiation. The results showed that Corexit-EC9500A was more cytotoxic than Corexit-EC9527A to P19 cells. At non-cytotoxic doses, Corexit-EC9527A inhibited retinol-induced expression of the <i>Hoxa1</i> gene, which encodes a transcription factor for the regulation of body patterning in the embryo. Such inhibition was seen in the retinol- and retinal- induced, but not RA-induced, <i>Hoxa1</i> up-regulation, indicating that the Corexit chemicals primarily inhibit RA biosynthesis from retinal. In addition, Corexit-EC9527A suppressed retinol-induced P19 cell differentiation into neuronal cells, indicating potential neurotoxic effect of the chemicals under the tested conditions. The surfactant ingredient, dioctyl sodium sulfosuccinate (DOSS), may be a major contributor to the observed effect of Corexit-EC9527A in the cell.</p></div

Synopsis of connections between fetal malformations induced by PEs and RA deficiency.

<p>Gestational exposure to some phthalates or to a VAD (vitamin A deficient/RA deficient) diet cause a characteristic spectrum of malformations (dysgenesis of seminiferous tubules, seminal vesicles, epididymis, prostate, genital tubercle/hypospadias, and cryptorchidism) in the reproductive system of the male rat fetus; phthalates or VAD also cause malformations in the axial skeleton of both sexes. PE-mediated fetal testosterone (T) deficiency is generally considered to be the cause of male reproductive system malformations. Given that PEs also caused cellular RA deficiency in this in vitro study, PE-mediated RA deficiency is hypothesized (indicated in red) to be an additional cause of malformations in the male rat reproductive system and axial skeleton in utero.</p

The effect of Corexit-9527 on retinoid-induced <i>Hoxa1</i> gene expression in P19 cells.

<p>(A) Corexit-9527 inhibited ROH-induced <i>Hoxa1</i> expression. P19 cells were exposed to the indicated concentrations of Corexit-9527 for 1 or 24 hr followed by 0.3 μM ROH for additional 6 hr. The columns represent the relative <i>Hoxa1</i> expression levels (left axis) that are normalized to the control (no ROH induction). The bars show cell viability (right axis) at the tested doses of Corexit. Values are mean ± s.e.m.; n = 3. (B) The effect of Corexit-9527 on ROH-, RAL- or RA-induced <i>Hoxa1</i> expression. P19 cells were exposed to Corexit-9527 for 1 hr and then were induced by indicated retinoids for additional 6 hr. For each retinoid, the <i>Hoxa1</i> expression levels in the cells that were induced by the cognate retinoid in the absence of Corexit-9527 were set to be 1. Values are mean ± s.e.m.; ***, <i>p</i> < 0.001, n.s., not significant, determined by Student’s <i>t</i>-test using two-tailed distribution and unequal variance; n = 4.</p

The major regulatory steps in the retinol signaling pathway.

<p>The enzymes that are predominantly expressed in P19 cells are listed in parentheses.</p

Effect of Corexit-9527 on ROH-induced P19 cell neuronal differentiation.

<p>(A) A simplified workflow for the P19 cell embryoid body formation and neuronal differentiation assays. (B) Phenotypical characteristics of the 3-day EBs and the 4-day EBs-derived cells. Yellow arrows indicate examples of neurons. (C) Expression of several neuronal marker genes in the P19-derived cells post EBs formation and differentiation procedures. The control cells were mock-treated with DMSO vehicles only throughout the experimental procedures. Values are mean ± s.e.m.; n = 4. **, <i>p</i> < 0.01, ***, <i>p</i> < 0.001.</p

Comparison of short-term and long-term effects of PEs on the induction of <i>Hoxa1</i> expression by ROH.

<p>The same compound numbering used in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0161167#pone.0161167.g002" target="_blank">Fig 2</a> is used in Fig 3. Compounds are arranged in Fig 3A according to their relative inhibitory activity and that format is maintained for the 30 h assay (Fig 3B). The screens were carried out on PE #s 1, 12–20 (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0161167#pone.0161167.g002" target="_blank">Fig 2A</a>) plus DHxP and DBnP which were not screened in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0161167#pone.0161167.g002" target="_blank">Fig 2</a> and, therefore, are not numbered. (A) 7 h screen; (B) 30 h screen; n = 4.</p

Effects of DBuP and DBnP on <i>Hoxa1</i> induction by ROH, RAL, and RA.

<p>The final ROH and RAL concentration were 0.3 μM and the RA concentration was 2.0 nM. n = 4.</p

Comparison of the effects of phthalate diesters and cognate monoesters on the induction of <i>Hoxa1</i> expression by ROH.

<p>P values for phthalate effects on <i>Hoxa1</i> expression compared to +ROH controls are indicated at the top of each bar. n = 4.</p