Histology and histopathology Vol.21, nº 9 (2006)

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  • Publication
    Open Access
    Neurofibroma with psammoma bodies
    (Murcia : F. Hernández, 2006) Kilmurray, L.G.; Ortega, L.; Martínez, A.; Sanz Esponera, J.
    Neurofibromas are benign tumours of the nerve sheath. Histologically they vary depending on their contents of cells, myxoid stroma and collagen. A 41-year old male with radicular pain had a tumour involving the posterior chest wall. Microscopically it resulted to be a neurofibroma with abundant psammoma bodies. Although these bodies are very frequent in some neoplasias, to our knowledge they have not been described in neurofibromas to date.
  • Publication
    Open Access
    Adult stem and transit-amplifying cell location
    (Murcia : F. Hernández, 2006) Díaz-Flores Jr., L.; Madrid, J.F.; Gutiérrez, Ricardo; Varela, H.; Valladares, Francisco; Álvarez-Argüelles, H.; Díaz-Flores, Lucio
    Adult stem cells (ASC) -able to self renew and to intervene in maintaining the structural and functional integrity of their original tissue- can express greater plasticity than traditionally attributed to them, adopting functional phenotypes and expression profiles of cells from other tissues. Therefore, they could be useful to regenerative medicine and tissue engineering. Transit-amplifying cells (TAC) are committed progenitors among the ASC and their terminally differentiated daughter cells. The ASC reside in a specialized physical location named niche, which constitutes a three-dimensional microenviroment where ASC and TAC are protected and controlled in their selfrenewing capacity and differentiation. The niche can be located near or far from the recruitment point, requiring a short or long-distance cellular migration, respectively. This paper briefly reviews the current status of research about ASC plasticity, transdifferentiation, fusion and functional adaptation mechanisms. Subsequently, ASC and TAC occurrence, characteristics and location have been considered in the skin, cornea, respiratory tract, teeth, gastrointestinal tract, liver, pancreas, salivary glands, kidney, breast, prostate, endometrium, mesenchyma, bone marrow, skeletal and cardiac muscle, nervous system and pituitary gland. Moreover, the role of cancer ASC has also been revised.
  • Publication
    Open Access
    Electron microscopic analysis of glucose-induced endothelial damage in primary culture: Possible mechanism and prevention
    (Murcia : F. Hernández, 2006) Mandal, A.K.; Ping, T.; Caldwell, S.; Bagnell, R.; Hiebert, L.M.
    We previously reported that high glucose treated cultured endothelial cells (ECs) showed intercellular gaps by transmission electron microscopy (TEM). These gaps were abrogated with insulin and/or heparin treatment. Our aims were to assess the severity of injury in ECs treated with high glucose for variable duration, and to further study the protective effects of insulin and/or heparin. Cells were also treated with Lbuthionine sulfoximine (BSO), a glutathione inhibitor, to help understand the mechanism of high glucose injury. Primary porcine ECs were treated with high glucose (30 mM) for 2, 6 or 10 days; and glucose plus insulin (1 U/ml), glucose plus heparin (5 µg/ml), glucose plus insulin plus heparin for 6 days. ECs were treated with BSO (0.001-0.05 mM) for 2 days. Pellets from trypsinized cells were processed for TEM. High glucose treatment revealed apoptosis or necrosis showing variable cell size, abnormal nuclei, condensation of nuclear chromatin, few mitochondria, cell membrane disruption and needle-shaped structures. Changes increased with duration of exposure. In high glucose plus heparin or insulin treated cultures at least one-half of the cells appeared normal. Most ECs were intact when treated with high glucose plus insulin plus heparin. BSO treatment showed dose-dependent changes with low doses showing apoptosis whereas higher doses revealed necrosis similar to high glucose treatment for 6 or 10 days. High glucose-induced EC injury increased with duration of exposure. These data demonstrate that high glucose injury resembles that of BSO treatment, suggesting that glutathione depletion may be involved in EC injury. Insulin and/or heparin protect against high glucose-induced injury.
  • Publication
    Open Access
    Plasma cell quantification in bone marrow by computer-assisted image analysis
    (Murcia : F. Hernández, 2006) Went, P.; Mayer, S.; Oberholzer, M.; Dirnhofer, S.
    Background: Minor and major criteria for the diagnosis of multiple meloma according to the definition of the WHO classification include different categories of the bone marrow plasma cell count: a shift from the 10- 30% group to the >30% group equals a shift from a minor to a major criterium, while the <10% group does not contribute to the diagnosis. Plasma cell fraction in the bone marrow is therefore critical for the classification and optimal clinical management of patients with plasma cell dyscrasias. The aim of this study was (i) to establish a digital image analysis system able to quantify bone marrow plasma cells and (ii) to evaluate two quantification techniques in bone marrow trephines i.e. computer-assisted digital image analysis and conventional light-microscopic evaluation. The results were compared regarding inter-observer variation of the obtained results. Material and methods: Eighty-seven patients, 28 with multiple myeloma, 29 with monoclonal gammopathy of undetermined significance, and 30 with reactive plasmocytosis were included in the study. Plasma cells in H&E- and CD138-stained slides were quantified by two investigators using light-microscopic estimation and computer-assisted digital analysis. The sets of results were correlated with rank correlation coefficients. Patients were categorized according to WHO criteria addressing the plasma cell content of the bone marrow (group 1: 0-10%, group 2: 11-30%, group 3: >30%), and the results compared by kappa statistics. Results: The degree of agreement in CD138-stained slides was higher for results obtained using the computer-assisted image analysis system compared to light microscopic evaluation (corr.coeff.=0.782), as was seen in the intra- (corr.coeff.=0.960) and inter-individual results correlations (corr.coeff.=0.899). Inter-observer agreement for categorized results (SM/PW: kappa 0.833) was in a high range. Conclusions: Computer-assisted image analysis demonstrated a higher reproducibility of bone marrow plasma cell quantification. This might be of critical importance for diagnosis, clinical management and prognostics when plasma cell numbers are low, which makes exact quantifications difficult.
  • Publication
    Open Access
    Fhit protein is preferentially expressed in the nucleus of monocyte-derived cells and its possible biological significance
    (Murcia : F. Hernández, 2006) Zhao, P.; Hou, N.; Lu, Y.
    The FHIT gene encompassing the most active common human fragile region, FRA3B, has been proposed as a tumour suppressor gene for important common human carcinomas. The mechanism in which Fhit protein exerts its tumour suppressor activity is still obscure. To further understand the Fhit function associated with its intracellular localization we have investigated its cellular localization and distribution in human normal and cancerous tissues. Data of 1500 samples from immunohistochemistry showed that Fhit protein was preferentially and stably expressed in the nucleus of monocyte-derived or histiocytic lineage cells including monocytes of the circulating blood cells, macrophages of the connective tissue, Kupffer cells of the liver, alveolar macrophages or dust cells of the lung, osteoclasts of bone, microglia of the brain, epithelioid cells under chronic inflammatory conditions, foreignbody giant cells, Langerhans cells of the epidermis and dendritic cells of various kinds of human tissue, although the protein could also be infrequently observed in the nucleus of some quiescent epithelial cells. In active cells other than histiocytes, Fhit protein was detected either in cytoplasm or was negative. Neurons expressed Fhit strongly and neuroglial cells did so moderately but only in the cytoplasm. There was no Fhit protein detected in the neutrophils, lymphocytes, plasma cells and lipocytes. The present data showes that the stable nuclear localization of Fhit is not only a special marker for histiocytes with various morphologies but also may suggest the other function concerning Fhit as a signaling molecule related to anti-proliferation function. The detailed biological function related to nuclear localization of Fhit protein in the histiocytes remains to be further studied.