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| Acceso al texto completo restringido a Biblioteca INIA Las Brujas. Por información adicional contacte bibliolb@inia.org.uy. |
Registro completo
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Biblioteca (s) : |
INIA Las Brujas. |
Fecha : |
20/11/2015 |
Actualizado : |
24/06/2021 |
Tipo de producción científica : |
Artículos en Revistas Indexadas Internacionales |
Autor : |
MACEDO, J.S.; ROCHA, B.P.; COLODEL, E.M.; FREITAS, S.H.; DORIA, R.G.S.; RIET-CORREA, F.; EVENCIO-NETO, J.; MENDONCA, F.S. |
Afiliación : |
JOSENALDO S. MACEDO; BRENA P. ROCHA; EDSON M. COLODEL; SILVIO H. FREITAS; RENATA G.S. DORIA; FRANKLIN RIET-CORREA, INIA (Instituto Nacional de Investigación Agropecuaria), Uruguay; JOAQUIM EVENCIO-NETO; FABIO S. MENDONCA. |
Título : |
Congenital malformations caused by Stryphnodendron fissuratum (Leg. Mimosoideae) in guinea pigs (Cavia porcellus). |
Fecha de publicación : |
2015 |
Fuente / Imprenta : |
Toxicon, 2015, v. 106, p. 68-71. |
ISSN : |
0041-0101 |
DOI : |
10.1016/j.toxicon.2015.09.003 |
Idioma : |
Inglés |
Contenido : |
ABSTRACT.
The aim of this study was to evaluate the toxicity of Stryphnodendron fissuratum pods in guinea pigs (Cavia porcellus) and test the hypothesis that this plant has teratogenic effects. Thus, sixteen guinea pigs were randomly divided into four groups of four animals each. Groups 10, 20 and 40 consisted of guinea pigs that received commercial food that contained crushed pods of S. fissuratum at concentrations of 10, 20 and 40 g/kg, respectively, during the period of organogenesis. Control group consisted of guinea pigs under the same management conditions that did not receive crushed pods of S. fissuratum in their food. In all experimental groups, the main clinical signs of poisoning consisted of anorexia, prostration, absence of vocalizations, alopecia, diarrhea, and abortions within the adult guinea pigs. Those that did not abort gave birth to weak, malnourished pups, some of which had fetal malformations. The main teratogenic changes consisted of eventration, arthrogryposis, amelia of the forelimbs, anophthalmia, microphthalmia, anotia and agnathia. The reductions in the number of offspring and the malformations observed in the experimental groups suggest that S. fissuratum affects fetal development and is teratogenic.
@ 2015 Elsevier Ltd. All rights reserved. |
Palabras claves : |
ABORTIONS; POISONOUS PLANTS; STRYPHNODENDRON FISSURATUM; TERATOGENESIS. |
Asunto categoría : |
-- |
Marc : |
LEADER 02107naa a2200277 a 4500 001 1053971 005 2021-06-24 008 2015 bl uuuu u00u1 u #d 022 $a0041-0101 024 7 $a10.1016/j.toxicon.2015.09.003$2DOI 100 1 $aMACEDO, J.S. 245 $aCongenital malformations caused by Stryphnodendron fissuratum (Leg. Mimosoideae) in guinea pigs (Cavia porcellus).$h[electronic resource] 260 $c2015 520 $aABSTRACT. The aim of this study was to evaluate the toxicity of Stryphnodendron fissuratum pods in guinea pigs (Cavia porcellus) and test the hypothesis that this plant has teratogenic effects. Thus, sixteen guinea pigs were randomly divided into four groups of four animals each. Groups 10, 20 and 40 consisted of guinea pigs that received commercial food that contained crushed pods of S. fissuratum at concentrations of 10, 20 and 40 g/kg, respectively, during the period of organogenesis. Control group consisted of guinea pigs under the same management conditions that did not receive crushed pods of S. fissuratum in their food. In all experimental groups, the main clinical signs of poisoning consisted of anorexia, prostration, absence of vocalizations, alopecia, diarrhea, and abortions within the adult guinea pigs. Those that did not abort gave birth to weak, malnourished pups, some of which had fetal malformations. The main teratogenic changes consisted of eventration, arthrogryposis, amelia of the forelimbs, anophthalmia, microphthalmia, anotia and agnathia. The reductions in the number of offspring and the malformations observed in the experimental groups suggest that S. fissuratum affects fetal development and is teratogenic. @ 2015 Elsevier Ltd. All rights reserved. 653 $aABORTIONS 653 $aPOISONOUS PLANTS 653 $aSTRYPHNODENDRON FISSURATUM 653 $aTERATOGENESIS 700 1 $aROCHA, B.P. 700 1 $aCOLODEL, E.M. 700 1 $aFREITAS, S.H. 700 1 $aDORIA, R.G.S. 700 1 $aRIET-CORREA, F. 700 1 $aEVENCIO-NETO, J. 700 1 $aMENDONCA, F.S. 773 $tToxicon, 2015$gv. 106, p. 68-71.
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| Acceso al texto completo restringido a Biblioteca INIA Las Brujas. Por información adicional contacte bibliolb@inia.org.uy. |
Registro completo
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Biblioteca (s) : |
INIA Las Brujas. |
Fecha actual : |
07/06/2022 |
Actualizado : |
30/11/2022 |
Tipo de producción científica : |
Artículos en Revistas Indexadas Internacionales |
Circulación / Nivel : |
Internacional - -- |
Autor : |
MACHADO, M.; CASTRO, M.B.; WILSON, T. M.; GONÇALVES , A. A. B.; PORTIANSKY, E.; RIET-CORREA, F.; BARROS, S. S. |
Afiliación : |
MIZAEL MACHADO DA COSTA, INIA (Instituto Nacional de Investigación Agropecuaria), Uruguay; MÁRCIO B. CASTRO, University of Brasilia, Brasília, Brazil; TAIS M. WILSON, University of Brasilia, Brasília, Brazil; ALEXANDRA A. B. GONÇALVES, University of Brasilia, Brasília, Brazil; ENRIQUE L. PORTIANSKY, National University of La Plata, La Plata, Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina; FRANKLIN RIET-CORREA AMARAL, INIA (Instituto Nacional de Investigación Agropecuaria), Uruguay; Federal University of Bahia, Salvador, Brazil; SEVERO S. BARROS, Federal University of Santa Maria, Rio Grande do Sul, Brazil. |
Título : |
Poisoning by Nierembergia veitchii: Effects on vascular smooth muscle cells in the pathogenesis of enzootic calcinosis. |
Fecha de publicación : |
2022 |
Fuente / Imprenta : |
Veterinary Pathology, 2022, Volume 59, Issue 5, pages 814-823. doi: https://doi.org/10.1177/03009858221098430 |
ISSN : |
0300-9858 |
DOI : |
10.1177/03009858221098430 |
Idioma : |
Inglés |
Notas : |
Article history: Article first published online May 19, 2022; Published online September 2022. -- Corresponding Author: Franklin Riet-Correa, Postgraduate Program in Animal Science in the Tropics, School of Veterinary Medicine and Animal Science, Federal University of Bahia, Salvador, Bahia 40170-110, Brazil. Email: franklinrietcorrea@gmail.com -- This work was funded by National Institute of Agricultural Research (INIA) of Uruguay (Project CL 44), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, Brazil, (Finance Code 001) and National University of La Plata (Project V270). A postgraduate scholarship was provided to Mizael Machado by INIA, Uruguay. |
Contenido : |
ABSTRACT - Vascular mineralization is a hallmark of enzootic calcinosis. Histopathological, ultrastructural, and immunohistochemical investigations were performed on the external carotid arteries of seven sheep naturally poisoned by Nierembergia veitchii. Histologically, moderate to marked hyperplasia of the tunica intima was observed without mineralization. The tunica media exhibited mild to severe mineralization and osteochondroid metaplasia. Sheep with enzootic calcinosis showed arterial overexpression of osteopontin and tissue-nonspecific alkaline phosphatase and immunolabeling for osteonectin and osteocalcin in both intima and media layers of the tested arteries. The main ultrastructural finding in the tunica media was a marked phenotypic change of vascular smooth muscle cells from a contractile phenotype (VSMC-C) into a synthetic phenotype (VSMC-S). In the tunica media, VSMC-S produced matrix and extracellular vesicles, forming mineralizable granules associated with arterial mineralization. VSMC-S were also present in the tunica intima, but matrix and extracellular vesicles and mineralization were not observed. The absence of matrix and extracellular vesicles in the intimal hyperplasia, even in the presence of noncollagenous bone proteins, tissue-nonspecific alkaline phosphatase, and vitamin D receptors, reinforces the hypothesis that the presence of matrix and extracellular vesicles are crucial for the development of vascular mineralization in enzootic calcinosis. It is proposed that the two different VSMC-S phenotypes in calcinosis are due to the expression of at least two genetically different types of these cells induced by the action of 1,25(OH)2D3. © The Author(s) 2022. MenosABSTRACT - Vascular mineralization is a hallmark of enzootic calcinosis. Histopathological, ultrastructural, and immunohistochemical investigations were performed on the external carotid arteries of seven sheep naturally poisoned by Nierembergia veitchii. Histologically, moderate to marked hyperplasia of the tunica intima was observed without mineralization. The tunica media exhibited mild to severe mineralization and osteochondroid metaplasia. Sheep with enzootic calcinosis showed arterial overexpression of osteopontin and tissue-nonspecific alkaline phosphatase and immunolabeling for osteonectin and osteocalcin in both intima and media layers of the tested arteries. The main ultrastructural finding in the tunica media was a marked phenotypic change of vascular smooth muscle cells from a contractile phenotype (VSMC-C) into a synthetic phenotype (VSMC-S). In the tunica media, VSMC-S produced matrix and extracellular vesicles, forming mineralizable granules associated with arterial mineralization. VSMC-S were also present in the tunica intima, but matrix and extracellular vesicles and mineralization were not observed. The absence of matrix and extracellular vesicles in the intimal hyperplasia, even in the presence of noncollagenous bone proteins, tissue-nonspecific alkaline phosphatase, and vitamin D receptors, reinforces the hypothesis that the presence of matrix and extracellular vesicles are crucial for the development of vascular mineralization in enzootic calcinosis. It ... Presentar Todo |
Palabras claves : |
Arterial mineralization; Arteries; Enzootic calcinosis; Exosomes; Pathogenesis; PLATAFORMA DE SALUD ANIMAL; Toxicity; Vascular smooth muscle cells. |
Asunto categoría : |
L50 Fisiología y bioquímica animal |
Marc : |
LEADER 03391nam a2200313 a 4500 001 1063233 005 2022-11-30 008 2022 bl uuuu u01u1 u #d 022 $a0300-9858 024 7 $a10.1177/03009858221098430$2DOI 100 1 $aMACHADO, M. 245 $aPoisoning by Nierembergia veitchii$bEffects on vascular smooth muscle cells in the pathogenesis of enzootic calcinosis.$h[electronic resource] 260 $aVeterinary Pathology, 2022, Volume 59, Issue 5, pages 814-823. doi: https://doi.org/10.1177/03009858221098430$c1177 500 $aArticle history: Article first published online May 19, 2022; Published online September 2022. -- Corresponding Author: Franklin Riet-Correa, Postgraduate Program in Animal Science in the Tropics, School of Veterinary Medicine and Animal Science, Federal University of Bahia, Salvador, Bahia 40170-110, Brazil. Email: franklinrietcorrea@gmail.com -- This work was funded by National Institute of Agricultural Research (INIA) of Uruguay (Project CL 44), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, Brazil, (Finance Code 001) and National University of La Plata (Project V270). A postgraduate scholarship was provided to Mizael Machado by INIA, Uruguay. 520 $aABSTRACT - Vascular mineralization is a hallmark of enzootic calcinosis. Histopathological, ultrastructural, and immunohistochemical investigations were performed on the external carotid arteries of seven sheep naturally poisoned by Nierembergia veitchii. Histologically, moderate to marked hyperplasia of the tunica intima was observed without mineralization. The tunica media exhibited mild to severe mineralization and osteochondroid metaplasia. Sheep with enzootic calcinosis showed arterial overexpression of osteopontin and tissue-nonspecific alkaline phosphatase and immunolabeling for osteonectin and osteocalcin in both intima and media layers of the tested arteries. The main ultrastructural finding in the tunica media was a marked phenotypic change of vascular smooth muscle cells from a contractile phenotype (VSMC-C) into a synthetic phenotype (VSMC-S). In the tunica media, VSMC-S produced matrix and extracellular vesicles, forming mineralizable granules associated with arterial mineralization. VSMC-S were also present in the tunica intima, but matrix and extracellular vesicles and mineralization were not observed. The absence of matrix and extracellular vesicles in the intimal hyperplasia, even in the presence of noncollagenous bone proteins, tissue-nonspecific alkaline phosphatase, and vitamin D receptors, reinforces the hypothesis that the presence of matrix and extracellular vesicles are crucial for the development of vascular mineralization in enzootic calcinosis. It is proposed that the two different VSMC-S phenotypes in calcinosis are due to the expression of at least two genetically different types of these cells induced by the action of 1,25(OH)2D3. © The Author(s) 2022. 653 $aArterial mineralization 653 $aArteries 653 $aEnzootic calcinosis 653 $aExosomes 653 $aPathogenesis 653 $aPLATAFORMA DE SALUD ANIMAL 653 $aToxicity 653 $aVascular smooth muscle cells 700 1 $aCASTRO, M.B. 700 1 $aWILSON, T. M. 700 1 $aGONÇALVES , A. A. B. 700 1 $aPORTIANSKY, E. 700 1 $aRIET-CORREA, F. 700 1 $aBARROS, S. S.
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