Histology and histopathology Vol.29, nº 1 (2014)
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- PublicationOpen AccessIsoflurane post-conditioning stimulates the proliferative phase of myocardial recovery in an ischemia-reperfusion model of heart injury in rats(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Agnić, Ivan; Vukojevic, Katarina; Saraga-Babić, Mirna; Filipović, Natalija; Grković, IvicaSummary. The application of isoflurane in a postconditioning manner, during early reperfusion following a period of coronary occlusion, has numerous beneficial effects on the ischemic myocardium, including reduction of infarct size. It does so by stimulating a sequence of well studied anti-apoptotic pro-survival mechanisms in a similar manner to various ‘ischemic’ pre-/postconditioning approaches which achieve their cardio protective effects in both laboratory and clinical situations. Proliferation of newly formed blood vessels, resulting in formation of highly vascularized granulation tissue, is an essential stage of infarct healing. It can be evaluated by detecting various angiogenic factors, including vascular endothelial growth factor (VEGF) and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) or by quantification of expression of vascular smooth muscle progenitors, such as Nestin. Expression of these three markers was used to evaluate the effect of early isoflurane post-conditioning in ischemia-reperfusion type cardiac injury. A large reduction in infarct size (59.3% of control), and marked increase of expression of VEGF (43.4%), PECAM1/CD31 (136%) and Nestin (77.9%) was found in experimental animals when compared to control animals that did not receive isoflurane treatment. Hence, based on our results, we can emphasize two morphologically detectable benefits of isoflurane post-conditioning: a marked reduction in infarct size and much better organization/vascularization of necrotic tissue.
- PublicationOpen AccessBCL10 expression and localization in Ocular Adnexa MALT lymphomas: a comparative cytogenetic and immunohistochemical study(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Cerrone, Margherita; Collina, Francesca; De Chiara, Anna; Corazzelli, Gaetano; Curcio, Maria Pia; De Renzo, Amalia; Russo, Filippo; Cantile, Monica; Staibano, Stefania; Strianese, Diego; Tranfa, Fausto; Botti, Gerardo; De Rosa, Gaetano; Franco, RenatoSummary. T(1;14) (p22;q32) involving BCL10 and IGH genes is a rare but recurrent chromosomal aberration in MALT-type lymphoma. It is rarely described in ocular adnexa B cell lymphomas, although nuclear BCL10 shuttling seems to be critical for disease progression in this district. We have evaluated the translocations MALT lymphoma-related in a series of 45 ocular adnexa cases, focusing in particular on their relation with BCL10 expression and its cellular topographic distribution. A prognostic tissue microarray (TMA) with ocular adnexa MALT lymphomas was designed. A study of BCL10 expression and its topographic distribution was performed through immunohistochemistry. In addition the assessment of t(14;18) (q32;q21), t(1;14) (p22;q32) and t(11;18) (q21;q21) was determined by Fluorescent In Situ Hybridization (FISH). Our series revealed t(14;18) (q32;q21) in 6/43 cases (14,3%). t(1;14) (p22;q32), never described in ocular adnexa MALT lymphomas, was observed in 3/31 (9,7%), two of which exhibited the gain of 3’ upstream BCL10 gene signal (4%), whereas no case showed t(11;18) (q21;q21). Moreover, BCL10 expression was observed in 18/45 cases. In particular its nuclear expression was revealed in 12/45 cases, cytoplasmic expression in 5/45 and both cytoplasmic and nuclear expression in 1/45. Statistical analysis demonstrated that while BCL10 cytoplasmic expression is significantly related to the presence of the investigated chromosomal aberrations, in particular with t(14;18) (q32;q21), BCL10 nuclear shuttling does not show any correlation with these translocations. Our data support that BCL10 nuclear distribution is neither related to BCL10 rearrangement nor to other known translocations.
- PublicationOpen AccessHigh level of CDK4 amplification is a poor prognostic factor in well-differentiated and dedifferentiated liposarcoma(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) Lee, Seung Eun; Kim, Yu Jin; Kwon, Mi Jeong; Choi, Dong Ill; Lee, Jeeyun; Cho, Junhun; Seo, Sung Wook; Kim, Sung Joo; Shin, Young Kee; Choi, Yoon-LaThe amplification of MDM2 and CDK4 is the main molecular feature of well-differentiated liposarcomas (WDLS) and dedifferentiated liposarcomas (DDLS). Although the diagnostic usefulness of this molecular characteristic in liposarcomas has been investigated, its prognostic utility of quantitative gene level has not been explored. The aim of this study was to assess the prognostic significance of level of CDK4 amplification in MDM2-amplified WDLS/DDLS. MDM2 amplification in liposarcomas was confirmed by fluorescence in situ hybridization. The copy number of MDM2 and CDK4 was further determined by quantitative PCR (qPCR) and multiplex ligation-dependent probe amplification. Among 56 MDM2-amplified liposarcomas, 30 cases were assigned as WDLS, and 26 as DDLS. When liposarcomas were classified by qPCR-determined CDK4 amplification levels, the high-CDK4 group showed significantly poorer progression free survival (P=0.001) and disease specific survival (P=0.033) than the low-CDK4 group. However, MDM2 amplification level did not show prognostic significance. In WDLS/DDLS, the level of CDK4 amplification was useful for prognosis prediction and precise stratification of patients for targeted therapy.
- PublicationOpen AccessImpaired hepatocyte maturation, abnormal expression of biliary transcription factors and liver fibrosis in C/EBPα (Cebpa)-knockout mice(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) Akai, Yusuke; Oitate, Takeshi; Koike, Toru; Shiojiri, NobuyoshiInactivation of the C/EBPα gene (Cebpa) in the mouse not only causes impaired hepatocyte maturation, but also induces pseudoglandular structures in the liver parenchyma. The present study was undertaken to determine how the expression of other transcription factors controlling differentiation into hepatocytes and biliary epithelial cells is affected, and how the hepatic architecture, including the bile and vascular systems, is disordered in the fetal knockout liver. Histochemical analyses demonstrated that the expression of HNF1α and HNF4α was heterogeneous in the knockout liver, and that not all parenchymal cells (pseudoglandular) expressed these transcription factors, whereas parenchymal cells in the wild-type liver homogeneously expressed these transcription factors. SOX9, which was expressed only in biliary cells in the wild-type liver, was detectable in many pseudoglandular cells of the knockout liver. Although the pseudoglandular cells often coexpressed SOX9 and HNF1α/HNF4α, cells expressing SOX9 but not expressing HNF1α/HNF4α (biliary cells) were sometimes detectable in the parenchyma. Periportal biliary structures were abnormal in their segregation from the parenchyma and in their expression of the transcription factors and Ep-CAM, a biliary adhesion molecule. These results suggest that the inactivation of the Cebpa gene causes unstable expression of liver-enriched transcription factors or biliary transcription factors and elevated expression of Ep-CAM, which may lead to abnormal biliary morphogenesis in the knockout liver. The impaired maturation of the parenchyma caused elevated expression of PECAM-1, desmin and Foxf1, suggesting that the maturation of the parenchyma plays an important role in the normal histogenesis of nonparenchymal cells (stellate cells and sinusoidal endothelial cells).
- PublicationOpen AccessLong term behavior of biological prostheses used as abdominal wall substitutes(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) Pascual, G.; Sotomayor, S.; Pérez-López, P.; Buján, J.; Bellón, J.M.Background. Despite their degradation in the host organism, the benefits of collagen bioprostheses remain unclear. This study addresses the absorption and long-term host tissue incorporation of several collagen biomeshes. Material and methods. Partial ventral hernial defects created in the abdominal wall of rabbits were repaired using the crosslinked meshes Permacol® or CollaMend®, or the non-crosslinked Surgisis®, Tutomesh® or Strattice®. After 90 and 180 days of implant, morphological studies and morpho-metric analysis of the thickness of the meshes were performed. Immunofluorescence confocal microscopy combined with differential interference contrast (DIC) imaging was used to distinguish newly formed collagen from that comprising the mesh. The macrophage response was examined by immunohisto-chemistry. Results. At 90 days, the thinner non-crosslinked biomeshes Tutomesh and Surgisis were more fully degraded with much of their collagen replaced with loose connective tissue. By 180 days, both implants had been practically fully absorbed. In contrast, in Strattice only the outermost third was infiltrated by neoformed tissue. On both surfaces of the crosslinked meshes, a fibrous capsule with host cells lining its perimeter was observed at both time points, though at 180 days these cells had penetrated the mesh interior. At both implant times, Strattice showed the higher expression of collagen type I while collagen III expression was similar for all the meshes. The non-crosslinked materials elicited lower macrophage counts at both time points, significantly so for Strattice. The macrophage response decreased over time for all the meshes but Surgisis. Conclusions. Strattice, the thicker, more compacted non-crosslinked mesh showed the best balance between tissue incorporation and absorption while eliciting a minimal foreign-body reaction in the long-term.
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