1,721,227 research outputs found
S. Pasquinelli, G. Rusmini (a cura di), “Badare non basta. Il lavoro i cura: attori, progetti, politiche”
No full textRecensione al volume di S. Pasquinelli, G. Rusmini (a cura di), “Badare non basta. Il lavoro i cura: attori, progetti, politiche” .Book Review: S. Pasquinelli, G. Rusmini (a cura di), “Badare non basta. Il lavoro i cura: attori, progetti, politiche”
Canossi (G. G.), Dardari (M.), Cartesi (N.), Brunelli (B.), Pasquinelli (G.), Anatomie angiographique du Chien
No full textMarcenac Ch. Canossi (G. G.), Dardari (M.), Cartesi (N.), Brunelli (B.), Pasquinelli (G.), Anatomie angiographique du Chien. In: Bulletin de l'Académie Vétérinaire de France tome 122 n°3, 1969. pp. 117-118
RUNX-1 and CD44 as markers of resident stem cell derivation in undifferentiated intimal sarcoma of pulmonary artery.
No full textVasuri F, Resta L, Fittipaldi S, Malvi D & Pasquinelli G (2012) Histopathology RUNX-1 and CD44 as markers of resident stem cell derivation in undifferentiated intimal sarcoma of pulmonary artery Aims: To report a rare case of undifferentiated intimal sarcoma (UIS) of the pulmonary artery in a 44-year-old woman, and to study it by electron microscopy and a novel immunohistochemical (IHC) panel that recognizes markers of endothelial and haematopoietic stemness, in order to extend current knowledge about the histogenesis of this rare neoplasm. Methods and results: Immunohistochemical reactions for CD31, CD34, α-smooth muscle actin (α-SMA), caldesmon, calponin, actin, desmin, epithelial membrane antigen, WT1, CD117, Ki67, nestin, RUNX-1, platelet-derived growth factor, NG2, CD44, CD90 and CD105 were performed manually or automatically. Neoplastic cells were negative for CD31 and CD34, but positive for calponin, nestin, WT1, CD44, and RUNX-1. Electron microscopy was performed after osmium tetroxide fixation and staining with lead citrate and uranyl acetate. Ultrastructurally, tumour cells had slightly irregular nuclei, cisternae of rough endoplasmic reticulum, and punctate intercellular junctions. Conclusions: We report a case of pulmonary artery UIS expressing previously unreported markers, i.e. RUNX-1, nestin, WT1, and CD44, that are commonly seen in different stages of the vascular differentiation hierarchy. These findings, together with the negativity for mature endothelial and smooth muscle markers, raise the question of whether this neoplasm may derive from a vessel wall-resident stem cell, such as the haemangioblast or an embryonic-like stem cell
Tubulopatia renale prossimale con cristalli
No full textLe discrasie plasmacellulari sono patologie eterogenee causate da una espansione clonale di plasmacellule o linfociti B con produzione abnorme di immunoglobuline monoclonali intatte o frammentate in catene leggere e/o catene pesanti che si depositano causando danni in diversi organi e tessuti dell’organismo. Il rene è l’organo maggiormente coinvolto e il danno da accumulo di catene leggere che ne deriva può interessare tutte le componenti renali (glomerulo, tubulo e interstizio). Le principali entità patologiche associate al danno renale si manifestano con quadri clinici e alterazioni istologiche/morfologiche molto diversi e comprendono la nefropatia da cast, la tubulopatia prossimale, la nefrite tubulo-interstiziale acuta, la malattia da deposizione di catene leggere o pesanti e l’amiloidosi di tipo AL.
Per la diagnosi di queste lesioni, la presenza di un prominente picco monoclonale identificato mediante dosaggio delle catene leggere presenti nel siero e/o nelle urine è affiancata all’esame istologico, immunologico e ultrastrutturale della biopsia renale per definire non solo l’isotipo dell’immunoglobulina coinvolta ma anche l’esatta localizzazione delle catene nefrotossiche nel parenchima renale.
Riportiamo due casi di tubulopatia prossimale con cristalli in un paziente affetto da gammopatia monoclonale di significato non determinato (MGUS; caso n. 1) e in un paziente con mieloma multiplo (caso n. 2). Come riportato dalla letteratura, in questa condizione si osserva un accumulo di catene leggere monoclonali nei citoplasmi delle cellule tubulari prossimali che esita nella formazione di strutture cristalline provviste di forme geometriche differenti. In uno dei due casi, i cristalli risultavano presenti anche nel citoplasma dei podociti glomerulari (caso n. 2). L’indagine in immunofluorescenza ha dimostrato come gli inclusi fossero composti da catene leggere kappa.
La microscopia elettronica riveste un ruolo determinante per documentare con certezza la presenza di inclusioni cristalline nella tubulopatia prossimale di pazienti affetti da discrasia plasmacellulare
Calcification mechanisms in native atherosclerotic arteries
No full textVascular Calcification, i.e., the ectopic accumulation of calcium phosphate salts in the vessel wall, is associated with atherosclerosis, aging, diabetes, and chronic kidney disease, which thusly contributes to increased cardiovascular morbidity and mortality. Previously considered to be a passive process, vascular calcification is now recognized as an active process similar to bone formation. However, the pathogenetic mechanisms involved in vascular calcification are particularly complex and remain inadequately understood, even though they impact significantly on patient prognosis as well as on the stenting placement and outcome of revascularization. Cellular, subcellular, genetic and molecular mechanisms have been proposed. Of particular importance is the role of the progenitor cells either resident in the vessel wall or circulating that are committed to an osteogenic program as well as transdifferentiation of vascular smooth-muscle cells. In addition, numerous evidences show that metastatic calcification is not as directly related to atherosclerosis as dystrophic is, indicating another mechanism of generation, involving additional metabolic pathways. A better understanding of the pathogenetic mechanisms corroborated with ultrastructural clues, as shown in the present review, will be essential for the development of new therapeutic strategies, in order to prevent and treat vascular calcification
Desmoplastic small round-cell tumor: A case report on the large cell variant with immunohistochemical, ultrastructural, and molecular genetic analysis
No full textA case of large cell desmoplastic small round-cell tumor (DSRCT) is described. The tumor arose in a 23-year-old man who was found to have a 14-cm-diameter omental mass during ultrasonographic examination. The patient died 10 months after surgery. Histologically, the tumor was composed of predominantly large epithelioid cells with foci of anaplasia mimicking metastatic carcinoma. Immunohistochemically, the tumor cells stained with anti-cytokeratin, EMA, desmin, and NSE antisera. Electron microscopy showed secretory lumina, desmosomes, cell processes with microtubules and electron-dense granules, and focal whorls of intermediate filaments. Reverse transcriptase-polymerase chain reaction performed on paraffin block-retrieved tissue demonstrated the EWS/WT-1 fusion transcript characteristic of the t(11;22) (p13;q12). This case illustrates a less common histological pattern of DSRCT, i.e., diffuse large cells, thus supporting the view that this tumor presents a wider morphological spectrum than that previously recognized
Mechanisms of Arterial Calcification: The Role of Matrix Vesicles
No full textVascular calcification is related to vascular diseases, for example, atherosclerosis, and its comorbidities, such as diabetes and chronic kidney disease. In each condition, a distinctive histological pattern can be recognised that may influence technical choices, possible intra-operative complications, and procedure outcomes, no matter if the intervention is performed by open or endovascular means. This review considers the classification and initiating mechanisms of vascular calcification. Dystrophic and metastatic calcifications, Monckeberg's calcification, and genetic forms are firstly outlined, followed by their alleged initiation mechanisms; these include (a) ineffective macrophage efferocytosis; (b) ectopic osteogenesis driven by modified resident or circulating osteoprogenitors. As in physiological bio-mineralisation, active calcification starts with the deposition of cell derived matrix vesicles into the extracellular matrix. To substantiate this belief, an in depth ultra-structural documentation of hydroxyapatite crystal deposition on such vesicles is provided in an ex-vivo human vascular cell model. Revealing the vesicle composition and phenotype in normal and pathological vascular conditions will be essential for the development of new therapeutic strategies, in order to prevent and treat vascular calcification
The Dual Nature of Mesenchymal Stem Cells (MSCs): Yin and Yang of the Inflammatory Process
No full textThe well-known reparative properties of mesenchymal stem cells (MSCs) make them an attractive source for cell-based therapy. In vitro and in vivo studies support an anti-inflammatory role of MSCs by directly targeting immune cells or via the secretion of immunomodulatory factors. MSCs have been isolated from several human normal tissues, even from pathological biopsies and blood samples; in these cases, MSCs displayed peculiar characteristics, suggesting a phenotype transition into a pathological state. Indeed, MSCs derived from inflamed tissues acquired a pro-inflammatory behaviour. In this view, MSCs may be crucial players of many pathways involved in human diseases, especially during the inflammatory cascade. The present chapter will minutely describe the basic biology of human MSCs derived from normal and pathological arteries, focusing on their dual nature as cellular switchers of the inflammatory setting. We will also discuss the emerging role of miRNAs in regulating MSC functions and their potential use as alternative strategies to manipulate MSC efficacy
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