Browsing by Subject "Coagulation"

Now showing 1 - 4 of 4
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    Archeogenetics of F11 p.Cys38Arg: a 5400-year-old mutation identified in different southwestern European countries
    (American Society of Hematology, 2019) Morena-Barrio, María Eugenia de la; Salloum-Asfar, Salam; Esteban, Julio; Morena-Barrio, Belén de la; Altisent, Carmen; Martín-Fernández, Laura; Gueguen, Paul; Padilla, José; Miñano, Antonia; Parra, Rafael; Vicente, Vicente; Vidal, Francisco; Bauduer, Frederic; Carbonell, Pablo; Corral, Javier; Medicina
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    Open Access
    Evolutionary trade-offs in kidney injury and repair
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Lei, Yutian; Anders, Hans Joachim
    Evolutionary medicine has proven helpful to understand the origin of human disease, e.g. in identifying causal roles of recent environmental changes impacting on human physiology (environmentphenotype mismatch). In contrast, diseases affecting only a limited number of members of a species often originate from evolutionary trade-offs for usually physiologic adaptations assuring reproductive success in the context of extrinsic threats. For example, the G1 and G2 variants of the APOL1 gene supporting control of Trypanosoma infection come with the trade-off that they promote the progression of kidney disease. In this review we extend the concept of evolutionary nephrology by discussing how the physiologic adaptations (danger responses) to tissue injury create evolutionary trade-offs that drive histopathological changes underlying acute and chronic kidney diseases. The evolution of multicellular organisms positively selected a number of danger response programs for their overwhelming benefits in assuring survival such as clotting, inflammation, epithelial healing and mesenchymal healing, i.e. fibrosis and sclerosis. Upon kidney injury these danger programs often present as pathomechanisms driving persistent nephron loss and renal failure. We explore how classic kidney disease entities involve insufficient or overshooting activation of these danger response programs for which the underlying genetic basis remains largely to be defined. Dissecting the causative and hierarchical relationships between danger programs should help to identify molecular targets to control kidney injury and to improve disease outcomes.
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    Improvement of coagulation-flocculation process using anionic polyacrylamide as coagulant aid.
    (Elsevier, 2005) Aguilar Sanchís, María Isabel; Sáez, José; Llorens Pascual del Riquelme, Mercedes; Soler, Antonio; Ortuño Sandoval, Juan Francisco; Meseguer Zapata, Víctor Francisco; Fuentes, Ana; Ingeniería Química
    A physicochemical treatment (coagulation-flocculation) was applied to a slaughterhouse wastewater, using anionic polyacrylamide as coagulant aid to improve the settling velocity of the flocs formed with the coagulants used: ferric sulphate, aluminium sulphate and polyaluminium chloride. The optimum speed and stirring time for the flocculation stage were ascertained along with the optimum pH and coagulant and coagulant aid doses. The speed and coagulation time were initially set according to recommendations in the literature concerning the treatment of this type of water. Chemical Oxygen Demand (COD), Biochemical Oxygen Demand at five days (BOD5) and Total Suspended Solids (TSS) were recorded at the beginning and end of each experiment in order to monitor the process. Once the optimal conditions had been established, several parameters were measured in order to assess the coagulation-flocculation process: particle number and size, sludge volume, nutrients (ammonia nitrogen, total Kjeldahl nitrogen, albuminoid nitrogen, orthophosphate, total phosphorus) and the residual concentration of iron and aluminium in clarified water. Anionic polyacrylamide, when added with ferric sulphate or polyaluminium chloride led to a significant increase in the settling speed.
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    N-Glycosylation as a Tool to Study Antithrombin Secretion, Conformation, and Function.
    (MDPI, 2021-06-06) Águila Martínez, Sonia; Noto, Rosina; Luengo-Gil, Ginés; Espín, Salvador; Bohdan, Nataliya; Morena Barrio, María Eugenia de la; Peñas, Julia; Rodenas, Maria Carmen; Vicente García, Vicente; Corral de la Calle, Javier; Manno, Mauro; Martínez-Martínez, Irene; Medicina Interna
    N-linked glycosylation is a crucial post-translational modification involved in protein folding, function, and clearance. N-linked glycosylation is also used therapeutically to enhance the half-lives of many proteins. Antithrombin, a serpin with four potential N-glycosylation sites, plays a pivotal role in hemostasis, wherein its deficiency significantly increases thrombotic risk. In this study, we used the introduction of N-glycosylation sites as a tool to explore what effect this glycosylation has on the protein folding, secretion, and function of this key anticoagulant. To accomplish this task, we introduced an additional N-glycosylation sequence in each strand. Interestingly, all regions that likely fold rapidly or were surrounded by lysines were not glycosylated even though an Nglycosylation sequon was present. The new sequon in the strands of the A- and B-sheets reduced secretion, and the B-sheet was more sensitive to these changes. However, the mutations in the strands of the C-sheet allowed correct folding and secretion, which resulted in functional variants. Therefore, our study revealed crucial regions for antithrombin secretion and could potentially apply to all serpins. These results could also help us understand the functional effects of natural variants causing type-I deficiencies.