101,969 research outputs found
Virus infections: lessons from pancreas histology
No full textType 1 diabetes mellitus is a chronic autoimmune disease resulting from the progressive immune-mediated destruction of pancreatic beta cells in genetically susceptible individuals, with the likely contribution of environmental factors, among which viruses have been extensively studied. The pathologic hallmark of the disease is insulitis-a process characterized by islet infiltration of immunocompetent cells that has been well characterized in animal models of islet autoimmunity, and to a lesser extent, in humans. Insulitis characterization has provided valuable information to gain insights into the disease pathogenesis. We review the recent literature on the viral contribution to beta-cell destruction and dysfunction in type 1 diabetes, with particular reference to the pathology of the pancreatic islet in humans and in animal models of the disease
Women with severe mutations in the gene 21α-hydroxylase do not express the characteristics phenotype after precocius diagnosis and treatment
No full textP l a n r i t n i n g e n – en källa för information och mystik [Elektronisk resurs]
No full textGalleri Silk bjöd in sju konstnärer till utställningen Planlösning (9 april–16 maj 2021) vilka fick i uppdrag att ”tolka och gestalta varsitt rum”. Jag blev tilldelad hallen. Hallen är navet till lägenheten. Genom ytterdörren når vi hallen, som därefter öppnar upp till resten av lägenhetens rum. Texten jag skrev handlar om vad kan en planritning och en planlösning kan berätta. ”Ritningen är ett dokument. Se framför dig en pappersrulle utrullad över bordet. Lite som en karta. En hel värld öppnar sig. Ett hemligt ark där varje streck har mening. Tänk in doften av det nyss kopierade handritade dokumentet och känslan av papperskvaliteten…
Homologous HSV1 and alpha-synuclein peptides stimulate a T cell response in Parkinson's disease
No full textModeled microgravity alters basal and insulin-mediated metabolic activity of normal and neoplastic cells
No full textEffects of High Glucose Concentrations on PC12 Cells: Possible Implications on Neurodegeneration
No full textHyperglycemia, which arises in type 1 or 2 diabetes, leads to different complications, such as macrovascular disease, nephropathy, retinopathy, and neuropathy. In addition, different cognitive variations are associated with type 1 diabetes. Long-term changes in glucose metabolism might induce effects on the central nervous system (CNS) such as reduced mental performance and loss of consciousness, which could be implicated in neurotoxicity. The direct impact of hyperglycemia and elevated glucose concentrations on neuronal cells remains to be fully elucidated, primarily due to the multifaceted mechanisms underlying glucose neurotoxicity, including apoptosis, oxidative stress, and alterations in signaling cascades. The multifaceted mechanisms further complicate the study of the relationship between diabetes and neurodegeneration. Research in this field is continually advancing, with the aim of investigating these eventual connections and developing more effective preventive and therapeutic strategies. The present study aims to assess the damage induced by different glucose concentrations (from 25 to 150 mM) in a neuronal model, such as PC12 cells, rat pheochromocytoma cells. In glucose-exposed PC12 cells, we have tested oxidative stress, apoptosis, and cell migration by (a) viability screening, (b) intracellular levels of anion superoxide (O2-), (c) extracellular levels of MDA and nitrites, (d) apoptosis, and (e) the wound healing assay. By the cell viability assay, it has emerged that glucose (25-150 mM) showed a stronger effect at the highest concentrations (100 and 150 mM). The increase in MDA and O2- levels was determined in PC12 cells treated with high glucose concentrations (6.5-8.8 fold for MDA). High concentrations (100 and 150 mM) significantly reduced the expression of full-length caspase-3 (2.8-fold and 4.2-fold decrease at 24 and 72 h) and caspase-9 (3.4-fold and 2.8-fold decrease at 24 h and 5-fold decrease at 72 h) compared with control conditions. Finally, the wound healing assay showed different scenarios during the several time points. Indeed, the wound closure rate was reduced in a dose-dependent manner (24 h: control 18%, G 50 mM 9%, 100 and 150 mM 8%; 48 h: control 26%, G 50 mM 20%, G 100 mM 13%, 150 mM 11%), following the treatment with three concentrations considered (50, 100, 150 mM). The results obtained in these experimental conditions highlight that glucose, at high concentrations, induced cell damage and corroborate the hypothesis that it could be involved in neurodegenerative diseases
Space flight affects motility and cytoskeletal structures in human monocyte cell line J-111
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Antiproliferative activity of vanadium compounds: Effects on the major malignant melanoma molecular pathways
No full textMalignant melanoma (MM) is the most fatal skin cancer, whose incidence has critically increased in the last decades. Recent molecular therapies are giving excellent results in the remission of melanoma but often they induce drug resistance in patients limiting their therapeutic efficacy. The search for new compounds able to overcome drug resistance is therefore essential. Vanadium has recently been cited for its anticancer properties against several tumors, but only a few data regard its effect against MM. In a previous work we demonstrated the anticancer activity of four different vanadium species towards MM cell lines. The inorganic anion vanadate(v) (VN) and the oxidovanadium(iv) complex [VO(dhp)2] (VS2), where dhp is 1,2-dimethyl-3-hydroxy-4(1H)-pyridinonate, showed IC50 values of 4.7 and 2.6 μM, respectively, against the A375 MM cell line, causing apoptosis and cell cycle arrest. Here we demonstrate the involvement of Reactive Oxygen Species (ROS) production in the pro-apoptotic effect of these two V species and evaluate the activation of different cell cycle regulators, to investigate the molecular mechanisms involved in their antitumor activity. We establish that VN and VS2 treatments reduce the phosphorylation of extracellular-signal regulated kinase (ERK) by about 80%, causing the deactivation of the mitogen activated protein kinase (MAPK) pathway in A375 cells. VN and VS2 also induce dephosphorylation of the retinoblastoma protein (Rb) (VN 100% and VS2 90%), together with a pronounced increase of cyclin-dependent kinase inhibitor 1 p21 (p21Cip1) protein expression up to 1800%. Taken together, our results confirm the antitumor properties of vanadium against melanoma cells, highlighting its ability to induce apoptosis through generation of ROS and cell cycle arrest by counteracting MAPK pathway activation and strongly inducing p21Cip1 expression and Rb hypo-phosphorylation
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