Histology and histopathology Vol.24, nº5 (2009)

Ir a Estadísticas

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    The role of vascular adhesion molecules PECAM-1 (CD 31), VCAM-1 (CD 106), E-Selectin (CD62E) and P-Selectin (CD62P) in severe porcine pancreatitis
    (Murcia: F. Hernández, 2009) Kleinhans, Helge; Kaifi, Jussuf T.; Mann, Oliver; Reinknecht, Felix; Freitag, Marc; Hansen, Bente; Schurr, Paulus G.; Izbicki, Jacob R.; Strate, Tim G.
    Inflammatory cytokines have been shown to mediate organ damage by their action on vascular endothelia and leukocytes, in part by upregulating the expression of adhesion molecules, which in turn convey transmigration of leukocytes into tissue. The upregulation and activation of vascular cell adhesion molecules on the endothelial cells avail firm leukocyte adhesion to the vascular endothelium and enhance their transmigration and consecutive tissue injury. The aim of this study was to evaluate the expresion of vascular adhesion molecules CD 31 (PECAM-1), CD 106 (VCAM-1), CD 62E (E-Selectin) and CD 62P (P-Selectin) in the pancreas and distant organs of pigs suffering from acute necrotizing pancreatitis (AP). AP was induced in 13 pigs by a combination of intravenous cerulein and intraductal glycodeoxycholic acid. For immunostaining of vascular adhesion molecules slides of porcine pancreas, lung, kidney and liver tissue were stained with monoclonal antibodies (Ab) against PECAM-1-1, VCAM-1 E- and PSELECTIN. The endothelial cell expression of CD 31 (PECAM- 1), CD 106 (VCAM), CD 62E (E-Selectin) and CD 62P (P-SELECTIN) in severe porcine pancreatitis is detectable and upregulation is partly significantly.
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    Ultrastructure of myotendinous junctions in tendon-skeletal muscle constructs engineered in vitro
    (Murcia: F. Hernández, 2009) Kostrominova, Tatiana Y.; Calve, Sarah; Arruda, Hellen M.; Larkin, Lisa M.
    During development, the interaction between tenocytes and myotubes leads to the formation of highly specialized muscle-tendon structural interfaces: myotendinous junctions (MTJs). Structural integrity of MTJs is critical for force transmission from contracting muscle through tendon to bone. We recently developed an in vitro model of three-dimensional (3-D) skeletal muscle-tendon constructs to address mechanisms of the MTJs development. We hypothesized that engineered in vitro 3-D skeletal muscle-tendon constructs would develop MTJs ultrastructurally resembling those found during fetal development in vivo. To test this hypothesis we compared MTJs structures in vivo to those developed in 3-D skeletal muscle constructs co-cultured with engineered self-organized tendon constructs (SOT), or segments of adult (ART) or fetal rat tail (FRT) by means of electron microscopy. Our study showed that at sites of termination some of the myofibers of the engineered 3-D skeletal muscle-FRT and -SOT constructs displayed emerging finger-like sarcolemmal projections surrounded by collagen fibers. These structures resemble fetal MTJs in vivo. Muscle-ART constructs did not develop MTJs. Muscle-FRT constructs in addition to muscle and tendon also demonstrated well developed cartilage, possessing high potential for development into bone. The muscle-FRT construct model could be used for studies of developmental mechanisms involved in the establishment of interfaces among all four muscularskeletal tissues: muscle, tendon and cartilage/bone.
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    Metallic gold treatment reduces proliferation of inflammatory cells, increases expression of VEGF and FGF, and stimulates cell proliferation in the subventricular zone following experimental traumatic brain injury
    (Murcia : F. Hernández, 2009) Østergaard Pedersen, Mie; Larsen, Agnete; Sonne Pedersen, Dan; Stoltenberg, Meredin; Penkowa, Milena
    Traumatic brain injury represents a leading cause of morbidity in young individuals and there is an imperative need for neuroprotective treatments limiting the neurologic impairment following such injury. It has recently been demonstrated that bio-liberated gold ions liberated from small metallic gold implants reduce inflammation and neuronal apoptosis, while generating an increased neuronal stem cell response following focal brain damage. In this study mice were subjected to a unilateral traumatic cryo-lesion with concomitant injection of 25-45 μm gold particles near the lesion. Placebo-treated mice subjected to cryo-lesion served as controls. The effects of gold-treatment were investigated by examining gold-induced growth factor expression (VEGF and FGF) in the first two weeks after the insult, and the extent of the neurostimulatory effect of gold was explored by comparing cell proliferation in the subventricular zone as judged by immunohistochemical staining for CDC47. Vimentin staining revealed a decrease in activated microglia and a transient astrogliosis in response to the gold liberation. Moreover, gold ions significantly increase the expression of VEGF and FGF following trauma and a significant increase in cell proliferation in both the ipsilateral and the contralateral subventricular zone was found in response to gold-treatment. In conclusion: we confirmed the previously demonstrated anti-inflammatory effect of bioliberated gold ions, and further show that metallic gold increases growth factor expression and adult neurogenesis.
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    Lysyl oxidases in mammalian development and certain pathological conditions
    (Murcia : F. Hernández, 2009) Mäki, Joni M.
    Lysyl oxidase (LOX) catalyzes the oxidation of the side chain of a peptidyl lysine converting specific lysine and hydroxylysine residues of a–aminoadipic-d- semialdehydes, which form covalent crosslinks in collagens and elastin. Five different but closely related lysyl oxidase isoenzymes have been identified to date, and they seem to have overlapping functions in many tissues. Modification of the extracellular matrix by lysyl oxidases has been shown to be a critical contributor to the development of various organs and certain pathological conditions.
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    Cardiac ischemia and reperfusion in spontaneously diabetic rats with and without application of EGb 761: II. Interstitium and microvasculature
    (Murcia : F. Hernández, 2009) Schneider, Rick; Welt, Klaus; Aust, Wolfram; Löster, Heinz; Fitzl, Günther
    Besides alterations in cardiomyocytes themselves, diabetic cardiopathy is characterized by interstitial and microvascular disorders. On the assumption that a specific heart muscle disease develops due to permanently increased oxidative stress on liberation of oxygen-free radicals, adjuvant application of antioxidative therapeutics appears promising in preventing or delaying long-term diabetic complications and protecting the myocardium against acute ischemia. We have investigated the effects of Ginkgo biloba extract (EGb 761), a radical scavenger, against diabetesinduced myocardial interstitium and microvasculature damage, and against additional ischemia/reperfusion injury in spontaneously diabetic BioBreeding/Ottawa Karlsburg (BB/OK) rats modelling diabetic cardiac infarction. Morphological and morphometric parameters in the heart muscle were evaluated by light and electron microscope. We used immunohistochemistry to investigate collagen protein expression as a marker for tissue remodelling together with endothelial nitric oxide synthase (eNOS) protein expression as a marker for endothelial-dependent vasodilation. We also evaluated inflammation response caused by neuropeptide Substance P and interacting mast cells in the diabetic heart. Our results revealed that A) Diabetic myocardium appears more vulnerable to ischemia/reperfusion injury than normal myocardium with regard to myocardial interstitium and microvessel ultrastructure, as well as eNOS protein expression; B) Inflammation response increases in diabetic animals exposed to ischemia/reperfusion injury compared to controls; C) Pre-treatment of diabetic myocardium with EGb results in an improvement of impaired endothelial-dependent vasodilation in diabetes and additional ischemia/ reperfusion, diminished mast cell and substance P accumulation, and better preserved myocardial ultrastructure compared to unprotected myocardium. In conclusion, EGb may act as a potent therapeutic adjuvant in diabetics with respect to ischemic myocardial injury, and may contribute to preventing late complications in diabetic cardiopathy.