DOI: 10.11606/d.10.2017.tde-04042017-105643
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<b>Comparative pathology of Neotropical deer:</b> morphological and immunohistochemical evaluation

Abstract: buscar herramientas para responder mis preguntas y nunca darme por vencido. Doctor Soler, tenga la seguridad que mi vocación investigativa se la debo enormemente a usted, para mi usted es un ejemplo integral de persona, gracias por ser mi mentor, profesor, evaluador y ahora amigo. A la doctora Victoria Pereira, por permitirme iniciar en este mundo de los animales silvestres, gracias por la confianza depositada en mí. A las instituciones Parque Jaime Duque, Zoológico Santacruz, CRRFSOC y Fundación Bioandina Col… Show more

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Cited by 1 publication
(2 citation statements)
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“…The first reports of Ins(1 ,4,5)P3-induced Ca2+ release from skeletal muscle SR appeared in 1985 [234, 2351. The evidence in favour of Ins(1,4,5)P3 may be summarized as follows: (a) Ins(1,4,5)P3 releases Ca2 + both from isolated SR terminal cisternae [234] and from skinned fibre preparations [234, 235, 241 -2441; (b) the entire machinery for the synthesis of the Ins(1,4,5)P3 precursor PtdIns(4,5)P2, Ins( 1 ,4,5)P3 formation (G-proteindependent phospholipase C) and Ins(1 ,4,5)P3 degradation [Ins(l ,4,5)P3 5-phosphatase] is present in the plasma membrane of striated muscles [245][246][247][248] and in a few cases, a selective enrichment of these synthetic and metabolic pathways has been found in T-tubules [245, 2481; (c) Ins(1,4,5)P3 levels increase dramatically upon electrical stimulation of skeletal muscles [235]; (d) Ins (1 ,4,5)P3, at micromolar concentrations, increases the opening probability of the Ca2 +-release channel of the SR after vesicle fusion with lipid bilayers [249]. A number of objections have been raised against the physiological role of Ins(1,4,5)P3 as a mediator in EC coupling in striated muscle, the most important being: (a) the release of Ca2 + from skinned skeletal muscle fibers activated by photohydrolyzed Ins (1 ,4,5)P3 is orders of magnitude slower than that observed under physiological conditions [250]; (b) the formation of Ins(1,4,5)P3 in electrically stimulated cells is observed only after tetanus [235]; (c) fiber contraction is not blocked by heparin, a known inhibitor preventing Ins(1 ,4,5)P3 binding to its receptor in smooth muscle and in non-muscle cells [251].…”
Section: Calcium-release Channels O J the Srmentioning
confidence: 99%
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“…The first reports of Ins(1 ,4,5)P3-induced Ca2+ release from skeletal muscle SR appeared in 1985 [234, 2351. The evidence in favour of Ins(1,4,5)P3 may be summarized as follows: (a) Ins(1,4,5)P3 releases Ca2 + both from isolated SR terminal cisternae [234] and from skinned fibre preparations [234, 235, 241 -2441; (b) the entire machinery for the synthesis of the Ins(1,4,5)P3 precursor PtdIns(4,5)P2, Ins( 1 ,4,5)P3 formation (G-proteindependent phospholipase C) and Ins(1 ,4,5)P3 degradation [Ins(l ,4,5)P3 5-phosphatase] is present in the plasma membrane of striated muscles [245][246][247][248] and in a few cases, a selective enrichment of these synthetic and metabolic pathways has been found in T-tubules [245, 2481; (c) Ins(1,4,5)P3 levels increase dramatically upon electrical stimulation of skeletal muscles [235]; (d) Ins (1 ,4,5)P3, at micromolar concentrations, increases the opening probability of the Ca2 +-release channel of the SR after vesicle fusion with lipid bilayers [249]. A number of objections have been raised against the physiological role of Ins(1,4,5)P3 as a mediator in EC coupling in striated muscle, the most important being: (a) the release of Ca2 + from skinned skeletal muscle fibers activated by photohydrolyzed Ins (1 ,4,5)P3 is orders of magnitude slower than that observed under physiological conditions [250]; (b) the formation of Ins(1,4,5)P3 in electrically stimulated cells is observed only after tetanus [235]; (c) fiber contraction is not blocked by heparin, a known inhibitor preventing Ins(1 ,4,5)P3 binding to its receptor in smooth muscle and in non-muscle cells [251].…”
Section: Calcium-release Channels O J the Srmentioning
confidence: 99%
“…Single-channel recordings after fusion of SR vesicles with planar lipid bilayers have shown that Ca2 + release is mediated by a high-conductance channel ( x 100 pS with 50 mM Ca2+ in the lumenal side), with low selectivity for divalent over monovalent ions (pCa2+/pK+ x 5) [238,256,2571. Ca2+, ATP [256, 2571 and Ins(1,4,5)P3 [249] on the cytoplasmatic side affect the opening probability of the channel. In agreement with Ca2 +-efflux experiments from SR vesicles, the cardiac Ca2 +-release channel is more sensitive to activation by Ca2+ and less sensitive to activation by ATP than the skeletal channel [238].…”
Section: Calcium-release Channels O J the Srmentioning
confidence: 99%