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      Diagnosis and management of intralabyrinthine schwannoma: case series and review of the literature

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          Abstract

          Intralabyrinthine schwannoma (ILS) is a rare benign tumor affecting cochlear and vestibular nerves, whose symptoms are generally unspecific and frequently responsible for a late diagnosis. Radiological examinations, with particular reference to magnetic resonance imaging (MRI), represent the only diagnostic technique to identify ILS. On computed tomography ILS can only be indirectly suspected by the presence of surrounding bone remodeling, whereas MRI provides direct visualization of the neoplasm as a filling defect within the labyrinth with vivid contrast enhancement. At the same time, MRI is also helpful in defining ILS anatomical extension into adjacent structures and in planning therapeutic management. Here we report three representative cases of ILS with new pictorial imaging features to improve ILS early detection and optimize subsequent therapeutic management. (www.actabiomedica.it)

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          Most cited references 35

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          Targeting Stim and Orai Proteins as an Alternative Approach in Anticancer Therapy.

          An increase in intracellular Ca2+ concentration plays a key role in the establishment of many cancer hallmarks, including aberrant proliferation, migration, invasion, resistance to apoptosis and angiogenesis. The dysregulation of Ca2+ entry is one of the most subtle mechanisms by which cancer cells overwhelm their normal counterparts and gain the adaptive advantages that result in tumour growth, vascularisation and dissemination throughout the organism. Both constitutive and agonist-induced Ca2+ influx may be mediated by store-dependent as well as store-independent Ca2+ entry routes. A growing body of evidences have shown that different isoforms of Stromal Interaction Molecules (Stim1) and Orai proteins, i.e. Stim1, Stim2, Orai1 and Orai3, underlie both pathways in cancer cells. The alteration in either the expression or the activity of Stim and Orai proteins has been linked to the onset and maintenance of tumour phenotype in many solid malignancies, including prostate, breast, kidney, esophageal, skin, brain, colorectal, lung and liver cancers. Herein, we survey the existing data in support of Stim and Orai involvement in tumourigenesis and provide the rationale to target them in cancer patients. Besides, we summarize the most recent advances in the identification of novel pharmacological tools that could be successfully used in clinical therapy.
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            Acetylcholine induces intracellular Ca2+ oscillations and nitric oxide release in mouse brain endothelial cells.

            Basal forebrain neurons increase cortical blood flow by releasing acetylcholine (Ach), which stimulates endothelial cells (ECs) to produce the vasodilating gasotransmitter, nitric oxide (NO). Surprisingly, the mechanism whereby Ach induces NO synthesis in brain microvascular ECs is unknown. An increase in intracellular Ca2+ concentration recruits a multitude of endothelial Ca2+-dependent pathways, such as Ca2+/calmodulin endothelial NO synthase (eNOS). The present investigation sought to investigate the role of intracellular Ca2+ signaling in Ach-induced NO production in bEND5 cells, an established model of mouse brain microvascular ECs, by conventional imaging of cells loaded with the Ca2+-sensitive dye, Fura-2/AM, and the NO-sensitive fluorophore, DAF-DM diacetate. Ach induced dose-dependent Ca2+ oscillations in bEND5 cells, 300 μM being the most effective dose to generate a prolonged Ca2+ burst. Pharmacological manipulation revealed that Ach-evoked Ca2+ oscillations required metabotropic muscarinic receptor (mAchR) activation and were patterned by a complex interplay between repetitive ER Ca2+ release via inositol-1,4,5-trisphosphate receptors (InsP3Rs) and store-operated Ca2+ entry (SOCE). A comprehensive real time-polymerase chain reaction analysis demonstrated the expression of the transcripts encoding for M3-mAChRs, InsP3R1 and InsP3R3, Stim1-2 and Orai2. Next, we found that Ach-induced NO production was hindered by L-NAME, a selective NOS inhibitor, and BAPTA, a membrane permeable intracellular Ca2+ buffer. Moreover, Ach-elicited NO synthesis was blocked by the pharmacological abrogation of the accompanying Ca2+ spikes. Overall, these data shed novel light on the molecular mechanisms whereby neuronally-released Ach controls neurovascular coupling in blood microvessels.
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              Arachidonic acid-evoked Ca(2+) signals promote nitric oxide release and proliferation in human endothelial colony forming cells.

              Arachidonic acid (AA) stimulates endothelial cell (EC) proliferation through an increase in intracellular Ca(2+) concentration ([Ca(2+)]i), that, in turn, promotes nitric oxide (NO) release. AA-evoked Ca(2+) signals are mainly mediated by Transient Receptor Potential Vanilloid 4 (TRPV4) channels. Circulating endothelial colony forming cells (ECFCs) represent the only established precursors of ECs. In the present study, we, therefore, sought to elucidate whether AA promotes human ECFC (hECFC) proliferation through an increase in [Ca(2+)]i and the following activation of the endothelial NO synthase (eNOS). AA induced a dose-dependent [Ca(2+)]i raise that was mimicked by its non-metabolizable analogue eicosatetraynoic acid. AA-evoked Ca(2+) signals required both intracellular Ca(2+) release and external Ca(2+) inflow. AA-induced Ca(2+) release was mediated by inositol-1,4,5-trisphosphate receptors from the endoplasmic reticulum and by two pore channel 1 from the acidic stores of the endolysosomal system. AA-evoked Ca(2+) entry was, in turn, mediated by TRPV4, while it did not involve store-operated Ca(2+) entry. Moreover, AA caused an increase in NO levels which was blocked by preventing the concomitant increase in [Ca(2+)]i and by inhibiting eNOS activity with NG-nitro-l-arginine methyl ester (l-NAME). Finally, AA per se did not stimulate hECFC growth, but potentiated growth factors-induced hECFC proliferation in a Ca(2+)- and NO-dependent manner. Therefore, AA-evoked Ca(2+) signals emerge as an additional target to prevent cancer vascularisation, which may be sustained by ECFC recruitment.
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                Author and article information

                Journal
                Acta Biomed
                Acta Biomed
                Acta Bio Medica : Atenei Parmensis
                Mattioli 1885 (Italy )
                0392-4203
                2531-6745
                2020
                13 July 2020
                : 91
                : Suppl 8
                : 136-144
                Affiliations
                [1 ] Department of Neuroscience, Reproductive and Odontostomatologic Sciences, University of Naples “Federico II”, Naples, Italy
                [2 ] CEINGE- Advanced Biotechnology, Naples, Italy
                [3 ] Ospedale Maggiore Policlinico Milano, Milan, Italy
                [4 ] Department of Medicine and Health Sciences “V. Tiberio”, University of Molise, Campobasso, Italy
                [5 ] Department of Neurosciences, “Santobono-Pausilipon” Pediatric Hospital, Naples, Italy
                [6 ] Department of Precision Medicine, University of Campania Luigi Vanvitelli, Naples, Italy
                [7 ] Department of Biotechnological and Applied Clinical Sciences, University of L’Aquila, L’Aquila,Italy
                [8 ] Department of Advanced Biomedical Sciences, University of Naples “Federico II”, Naples, Italy
                Author notes
                Correspondence: Fabio Tortora, MD, Associate Professor Department of Advanced Biomedical Sciences University of Naples “Federico II”, Naples, Italy Via Pansini, 5 - 80131 Naples - Italy Tel: 0039 333 7050711 E-mail: fabio.tortora@ 123456unina.it
                Article
                ACTA-91-136
                10.23750/abm.v91i8-S.9976
                7944674
                32945288
                Copyright: © 2020 ACTA BIO MEDICA SOCIETY OF MEDICINE AND NATURAL SCIENCES OF PARMA

                This work is licensed under a Creative Commons Attribution 4.0 International License

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