Browsing by Subject "Pigmentation"

Now showing 1 - 3 of 3
  • Thumbnail Image
    Publication
    Open Access
    A reported case of abnormal pigmentation in the Epaulet grouper Epinephelus stoliczkae (Day, 1875) collected from the Sea of Oman
    (Murcia: Servicio de Publicaciones de la Universidad de Murcia, 2013) Jawad, Llaith A.; Al-Kharusi, Lubna H.
    A specimen of the Epaulet grouper Epinephelus stoliczkae with abnormal pigmentation was obtained from the coast of Muscat City on the Sea of Oman. Differences in the degree of colour aberration, pattern and abnormal patches were observed on both sides of the body of the specimen. Possible causes of this anomaly are discussed.
  • Thumbnail Image
    Publication
    Open Access
    Immunohistochemical evaluation of tissues following bone implant extraction from upper and lower limb
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Bielniková Kryštofová, Hana; Motyka, Oldřich; Židlík, Vladimír; Žiak, Dušan; Szotkovská, Iveta; Škarda, Jozef; Pometlová, Jana; Pleva, Leopold; Havlíček, Miroslav; Čabanová, Kristina
    Fractured bones can regenerate and restore their biological and mechanical properties to the state prior to the damage. In some cases, however, the treatment of fractures requires the use of supportive implants. For bone healing, three processes are essential: the inflammatory phase, the repair phase and the remodelling phase. A proper course of the first - inflammatory - stage is important to ensure a successful fracture healing process. In our study, we evaluated tissue samples immunohistochemically from the area surrounding the fractures of upper and lower limbs (bone tissue, soft tissue, and the implant-adhering tissue) for markers: CD11b, CD15, CD34, CD44, CD68, Cathepsin K, and TRAcP that are linked to the aforementioned phases. In soft tissue, higher expressions of CD68, CD34, CD15 and CD11b markers were observed than in other locations. TRAcP and Cathepsin K markers were more expressed in the bone tissue, while pigmentation, necrosis and calcification were more observed in the implant-adhering tissue. Since even the implant materials commonly perceived as inert elicit the observed inflammatory responses, new surface treatments and materials need to be developed.
  • Thumbnail Image
    Publication
    Open Access
    Lineage-specific gene radiations underlie the evolution of novel betalain pigmentation in Caryophyllales
    (Wiley, 2015-05-13) Brockington, Samuel F.; Yang, Ya; Covshoff, Sarah; Hibberd, Julián M.; Sage, Rowan F.; Wong, Gane K. S.; Moore, Michael J.; Smith, Stephen A.; Gandía Herrero, Fernando; Bioquímica y Biología Molecular "A"
    Betalain pigments are unique to the Caryophyllales and structurally and biosynthetically dis-tinct from anthocyanins. Two key enzymes within the betalain synthesis pathway have beenidentified: 4,5-dioxygenase (DODA) that catalyzes the formation of betalamic acid andCYP76AD1, a cytochrome P450 gene that catalyzes the formation of cyclo-DOPA. We performed phylogenetic analyses to reveal the evolutionary history of the DODA andCYP76AD1 lineages and in the context of an ancestral reconstruction of pigment states weexplored the evolution of these genes in relation to the complex evolution of pigments inCaryophylalles. Duplications within the CYP76AD1 and DODA lineages arose just before the origin of beta-lain pigmentation in the core Caryophyllales. The duplications gave rise to DODA-a andCYP76AD1-a isoforms that appear specific to betalain synthesis. Both betalain-specific isoformswere then lost or downregulated in the anthocyanic Molluginaceae and Caryophyllaceae. Our findings suggest a single origin of the betalain synthesis pathway, with neofunctionaliza-tion following gene duplications in the CYP76AD1 and DODA lineages. Loss of DODA-a andCYP76AD1-a in anthocyanic taxa suggests that betalain pigmentation has been lost twice inCaryophyllales, and exclusion of betalain pigments from anthocyanic taxa is mediated throughgene loss or downregulation. [Correction added after online publication 13 May 2015: in thelast two paragraphs of the Summary the gene name CYP761A was changed to CYP76AD1.]