Relevant bibliographies by topics / Weichmacher

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  2. Dissertations / Theses
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  4. Book chapters

Academic literature on the topic 'Weichmacher'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Weichmacher"

1

Janning, Martina. "Gefährlicher Weichmacher." kma - Klinik Management aktuell 10, no. 03 (March 2005): 74–76. http://dx.doi.org/10.1055/s-0036-1573217.

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In Kinderspielzeug ist der Weichmacher DEHP seit langem verboten. In Medizinprodukten kommt die gesundheitsschädliche Substanz aber nach wie vor zum Einsatz. Neue Richtlinien sollen den Schutz des Patienten erhöhen. Doch das geht Umweltschützern nicht weit genug: Sie fordern ein europaweites Verbot von DEHP-haltigen Produkten.
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Vilgis, Thomas. "Weichmacher Wasser." Physik in unserer Zeit 45, no. 5 (September 2014): 258. http://dx.doi.org/10.1002/piuz.201490094.

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Völkel, W. "HBM auf Weichmacher." Das Gesundheitswesen 79, no. 04 (May 2, 2017): 299–374. http://dx.doi.org/10.1055/s-0037-1601948.

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4

Pakusch, Anne. "Kernhydrierung entgiftet Weichmacher." Nachrichten aus der Chemie 55, no. 7-8 (July 2007): 744. http://dx.doi.org/10.1002/nadc.200750982.

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Brennicke, Axel. "Weichmacher für Getreidekörner." Biologie in unserer Zeit 32, no. 3 (May 2002): 144. http://dx.doi.org/10.1002/1521-415x(200205)32:3<144::aid-biuz144>3.0.co;2-h.

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6

vsc. "Weichmacher fördern Diabetes." Der Hausarzt 49, no. 11 (June 2012): 54. http://dx.doi.org/10.1007/s15200-012-0614-3.

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Reckter, Bettina. "Hirnschäden durch Weichmacher." VDI nachrichten 75, no. 15 (2021): 4. http://dx.doi.org/10.51202/0042-1758-2021-15-4-1.

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Allen, K. W. "Acrylate als polymerisierbare Weichmacher." International Journal of Adhesion and Adhesives 9, no. 2 (April 1989): 67. http://dx.doi.org/10.1016/0143-7496(89)90026-2.

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Malberg, K. "Weichmacher stören frühkindliche Entwicklung." MMW - Fortschritte der Medizin 153, no. 38 (September 2011): 20. http://dx.doi.org/10.1007/bf03371822.

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Malberg, K. "Herzinfarkt durch Weichmacher in Plastik?" MMW - Fortschritte der Medizin 154, no. 4 (March 2012): 38. http://dx.doi.org/10.1007/s15006-012-0240-y.

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Dissertations / Theses on the topic "Weichmacher"

1

Gotthardt, geb Nehring Alexandra [Verfasser]. "Human-Biomonitoring für den alternativen Weichmacher Di(2-ethylhexyl)adipat (DEHA) / Alexandra Gotthardt geb. Nehring." Wuppertal : Universitätsbibliothek Wuppertal, 2021. http://d-nb.info/1240165900/34.

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Mörbitz, Philip [Verfasser], Eckhard [Gutachter] Weidner, and Marcus [Gutachter] Petermann. "Nicht migrierende Weichmacher für Polymilchsäure auf Basis linearer und verzweigter Polycaprolacton-Blockcopolymere / Philip Mörbitz ; Gutachter: Eckhard Weidner, Marcus Petermann ; Fakultät für Maschinenbau." Bochum : Ruhr-Universität Bochum, 2019. http://d-nb.info/1175204994/34.

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Canitz, Carsten Jörg [Verfasser], Leif-Alexander [Akademischer Betreuer] Garbe, Leif-Alexander [Gutachter] Garbe, and Rudolf [Gutachter] Schneider. "Methodenvalidierung zur Bestimmung der Weichmacher DEHT und DINCH durch die Synthese deuterierter Standards / Carsten Jörg Canitz ; Gutachter: Leif-Alexander Garbe, Rudolf Schneider ; Betreuer: Leif-Alexander Garbe." Berlin : Technische Universität Berlin, 2016. http://d-nb.info/1156017769/34.

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Klöting, Nora, Nico Hesselbarth, Martin Gericke, Anne Kunath, Ronald Biemann, Rima Chakaroun, Joanna Kosacka, et al. "Di-(2-Ethylhexyl)-Phthalate (DEHP) Causes Impaired Adipocyte Function and Alters Serum Metabolites." Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-197823.

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Di-(2-ethylhexyl)-phthalate (DEHP), an ubiquitous environmental contaminant, has been shown to cause adverse effects on glucose homeostasis and insulin sensitivity in epidemiological studies, but the underlying mechanisms are still unknown. We therefore tested the hypothesis that chronic DEHP exposure causes impaired insulin sensitivity, affects body weight, adipose tissue (AT) function and circulating metabolic parameters of obesity resistant 129S6 mice in vivo. An obesity-resistant mouse model was chosen to reduce a potential obesity bias of DEHP effects on metabolic parameters and AT function. The metabolic effects of 10-weeks exposure to DEHP were tested by insulin tolerance tests and quantitative assessment of 183 metabolites in mice. Furthermore, 3T3-L1 cells were cultured with DEHP for two days, differentiated into mature adipocytes in which the effects on insulin stimulated glucose and palmitate uptake, lipid content as well as on mRNA/protein expression of key adipocyte genes were investigated.We observed in female mice that DEHP treatment causes enhanced weight gain, fat mass, impaired insulin tolerance, changes in circulating adiponectin and adipose tissue Pparg, adiponectin and estrogen expression. Serum metabolomics indicated a general increase in phospholipid and carnitine concentrations. In vitro, DEHP treatment increases the proliferation rate and alters glucose uptake in adipocytes. Taken together, DEHP has significant effects on adipose tissue (AT) function and alters specific serum metabolites. Although, DEHP treatment led to significantly impaired insulin tolerance, it did not affect glucose tolerance, HOMA-IR, fasting glucose, insulin or triglyceride serum concentrations. This may suggest that DEHP treatment does not cause impaired glucose metabolism at the whole body level.
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Klöting, Nora, Nico Hesselbarth, Martin Gericke, Anne Kunath, Ronald Biemann, Rima Chakaroun, Joanna Kosacka, et al. "Di-(2-Ethylhexyl)-Phthalate (DEHP) Causes Impaired Adipocyte Function and Alters Serum Metabolites." PLoS one, 2015. https://ul.qucosa.de/id/qucosa%3A14511.

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Di-(2-ethylhexyl)-phthalate (DEHP), an ubiquitous environmental contaminant, has been shown to cause adverse effects on glucose homeostasis and insulin sensitivity in epidemiological studies, but the underlying mechanisms are still unknown. We therefore tested the hypothesis that chronic DEHP exposure causes impaired insulin sensitivity, affects body weight, adipose tissue (AT) function and circulating metabolic parameters of obesity resistant 129S6 mice in vivo. An obesity-resistant mouse model was chosen to reduce a potential obesity bias of DEHP effects on metabolic parameters and AT function. The metabolic effects of 10-weeks exposure to DEHP were tested by insulin tolerance tests and quantitative assessment of 183 metabolites in mice. Furthermore, 3T3-L1 cells were cultured with DEHP for two days, differentiated into mature adipocytes in which the effects on insulin stimulated glucose and palmitate uptake, lipid content as well as on mRNA/protein expression of key adipocyte genes were investigated.We observed in female mice that DEHP treatment causes enhanced weight gain, fat mass, impaired insulin tolerance, changes in circulating adiponectin and adipose tissue Pparg, adiponectin and estrogen expression. Serum metabolomics indicated a general increase in phospholipid and carnitine concentrations. In vitro, DEHP treatment increases the proliferation rate and alters glucose uptake in adipocytes. Taken together, DEHP has significant effects on adipose tissue (AT) function and alters specific serum metabolites. Although, DEHP treatment led to significantly impaired insulin tolerance, it did not affect glucose tolerance, HOMA-IR, fasting glucose, insulin or triglyceride serum concentrations. This may suggest that DEHP treatment does not cause impaired glucose metabolism at the whole body level.
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6

Rothenbacher, Klaus Peter. "Einfluß der Chiralität auf Metabolismus und Toxizität des PVC-Weichmachers DEHP /." [S.l. : s.n.], 1997. http://www.gbv.de/dms/bs/toc/231422105.pdf.

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Dutescu, Ralf Michael [Verfasser], and H. G. [Akademischer Betreuer] Wahl. "Expressionsanalyse der nukleären Rezeptoren PPAR-α/γ-1/γ-2 [PPAR-alpha, gamma-1, gamma-2] und der Transkriptionsfaktoren T-bet und GATA-3 nach Stimulation von dermalen Endothelzellen mit den Weichmacher, Di(2-ethylhexyl)phthalat-Metaboliten-2-Ethylhexanol und 4-Heptanon / Ralf Michael Dutescu. Betreuer: H. G. Wahl." Marburg : Philipps-Universität Marburg, 2011. http://d-nb.info/1013288459/34.

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Hofmann, Peter Josef. "Aufbau eines Reportergenassays zur Untersuchung der Wechselwirkung endokriner Disruptoren mit der T 3-regulierten Transaktivierung." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2008. http://dx.doi.org/10.18452/15813.

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Das Schilddrüsenhormon Triiodthyronin (T3) ist ein essenzieller Regulator physiologischer Prozesse der Entwicklung, des Wachstums und im Intermediärstoffwechsel. Täglich werden zahlreiche natürliche und synthetische Stoffe aufgenommen, die mit dem endokrinen System interferieren und deshalb als Endokrine Disruptoren (ED) bezeichnet werden. Zur Untersuchung einer direkten Interferenz von ED mit den Schilddrüsenhormonrezeptoren (TR) und ihrer transkriptionellen Aktivität wurde im Rahmen dieser Arbeit ein neues Luziferase-basiertes T3 Reportergensystem mit TRalpha1-transfizierten humanen Leberzellen aufgebaut. Durch Validierung mit dem synthetischen TR-Agonisten GC-1 und dem Antagonisten NH-3 konnte nachgewiesen werden, dass dieser Assay ein hoch-sensitives System zur Analyse von agonistischen sowie antagonistischen Effekten von Testsubtanzen darstellt. Zur Bestimmung der endokrinen Aktivitäten einiger humanrelevanter Vertreter aus den Stoffkategorien der Nahrungsmittel, Kosmetika, Pestizide und Industriechemikalien wurden Dosis-Wirkungskurven in Aktivierungs- und T3-Kompetitionsexperimenten ermittelt. In mikromolaren Konzentrationen wirkten von insgesamt 21 Testsubstanzen einige als reine Agonisten oder Antagonisten während andere gemischt agonistische/antagonistische Effekte hatten. Aufgrund ihrer hier beobachteten Effekte und der gegebenen Humanexposition wird eine eingehendere Analyse von 4-Methylbenzyliden Campher, 4-Nonylphenol, Acetochlor, Benzophenon 2, Benzophenon 3, Bisphenol A, Genistein, Octylmethoxycinnamat, Tetrabromobisphenol A und Xanthohumol empfohlen. Außerdem erwiesen sich einige Metaboliten von Schilddrüsenhormonen als potente Agonisten im T3-Reportergenassay und bedürfen weiterer Aufmerksamkeit. Für die molekulare Charakterisierung der Einflüsse solcher Substanzen auf die T3-regulierte Transaktivierung konnte mit dem hier etablierten Bioassay ein zuverlässiges neues Testsystem für reproduzierbare Screeningserien geschaffen werden.
Triiodothyronine (T3) is a crucial regulator of many physiological processes during development, growth and metabolism. A variety of natural and synthetic substances, which are collectively termed endocrine disrupters (ED) due to their interference with the endocrine system, is taken up on a daily base. A novel luciferase-based T3-responsive reporter gene system employing a human liver cell line transfected with thyroid hormone receptor (TR) alpha1 was established in this work to elucidate the potential molecular interference of certain ED with TR and their transcriptional activity. This assay was validated to be a highly sensitive and reliable tool for analyzing agonistic and antagonistic effects of test compounds using the synthetic TR agonist GC-1 and the antagonist NH-3. Dose-response data of test compounds contained in food, cosmetics, pesticides, plasticizers and other industrial chemicals were obtained after applying the substances alone in activation assays or in combination with T3 in competition assays. In total 21 test compounds were screened of which some acted as pure agonists or antagonists while others were mixed agonists/antagonists in the micromolar concentration range and only one was without effect. Follow-up studies are recommended for some of these substances with regard to their effects as determined in this bioassay and in light of information known on human exposure, i.e., 4-methylbenzyliden camphor, 4-nonylphenol, acetochlor, benzophenone 2, benzophenone 3, bisphenol A, genistein, octylmethoxycinnamate, tetrabromobisphenol A and xanthohumol. In addition some endogenous metabolites of thyroid hormones were surprisingly potent agonists in the T3 reporter gene assay and merit further attention. The novel bioassay established here represents a reliable tool for the screening and molecular characterization of substances interfering with T3-mediated transactivation of gene expression.
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Hunger, Luise Verfasser], Bernd [Akademischer Betreuer] [Fischer, Mathias [Akademischer Betreuer] Faßhauer, and Lutz P. [Akademischer Betreuer] Müller. "Einfluss des Weichmachers Di(2-ethylhexyl)phthalat auf die Adipogenese einer humanen Präadipozytenlinie / Luise Hunger ; Bernd Fischer, Mathias Faßhauer, Lutz P. Müller." Halle, 2015. http://d-nb.info/1116950650/34.

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Ewe, Manuel [Verfasser], Manfred [Akademischer Betreuer] Grote, and Wolfgang [Akademischer Betreuer] Bremser. "Entwicklung und Anwendung einer SBSE-TD/GC/MS-Methode zur Bestimmung von Weichmachern und Antioxidantien in Getränken / Manuel Ewe. Betreuer: Manfred Grote ; Wolfgang Bremser." Paderborn : Universitätsbibliothek, 2012. http://d-nb.info/1036552691/34.

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Books on the topic "Weichmacher"

1

Vašek, Thomas. Die Weichmacher: Das süße Gift der Harmoniekultur. München: Hanser, Carl, 2011.

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2

Wandel, Martin, H. Tengler, and H. Ostromow. Die Analyse von Weichmachern. Springer, 2012.

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Book chapters on the topic "Weichmacher"

1

Bährle-Rapp, Marina. "Weichmacher." In Springer Lexikon Kosmetik und Körperpflege, 589–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_11134.

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Scholz, U., S. Loff, F. Kabs, S. Recks, and K. L. Waag. "Besteht ein Zusammenhang zwischen der TPN-induzierten Cholestase bei Neugeborenen und der Herauslösung von Weichmachern aus Infusionslösungen?" In Deutsche Gesellschaft für Chirurgie, 515–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56698-1_132.

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3

"14 Weichmacher." In Allergieprävention, 163–82. De Gruyter, 2019. http://dx.doi.org/10.1515/9783110561012-014.

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You might also be interested in the extended bibliographies on the topic 'Weichmacher' for particular source types:
Journal articles
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