86,837 research outputs found
Effect of Total Apple Polyphenols Extract as Inhibitors of Amyloid Protein Aggregation
No full textEffect of Total Apple Polyphenols Extract as Inhibitors of Amyloid Protein Aggregation
By: Guarrasi, Valeria; Rappa, Cinzia Giacoma; Costa, Maria Assunta; et al.
JOURNAL OF CLINICAL GASTROENTEROLOGY Volume: 52 Supplement: 1 Pages: S94-S94 Published: NOV-DEC 201
Tumore adenomatoide
No full textAdenomatoid tumour is a neoplastic process of discussed origin, but the immunohistochemical phenotype leads a mesothelial derivation. The preferential site of origin is the genital apparatus of both sexes, however extragenital cases have been described. The histological pattern varies from tubular formation, to solid growth, to cystic areas. In the present report we described a case of Adenomatoid tumour of the uterus body in a 46 years old patient
Exosomal HSP60 levels and related miRNAs in brain tumors
No full textIn cancer, Extracellular Vesicles (EVs), such as exosomes, contribute to tumor progression by regulating local and systemic parameters [1,2]. Since exosomes are released into body fluids, they may be used in nanomedicine as a valuable source of diagnostic biomarkers [3]. The prognosis of brain tumors is poor even after surgical resection followed by post-operatory chemo- and radio-therapies and it is cogent to find innovative treatments. The discovery that molecular chaperones can be determinant factors in tumorigenesis and the increasing understanding of exosomes, particularly in what refers to their release by tumor cells and contents, including chaperones and miRNA, provide elements to develop novel treatment strategies and means [4]. We measured the chaperone HSP60 and related miRNAs in primary brain tumors and peritumoral cells in vivo to determine levels and distribution. In addition, the presence and levels of HSP60 and miRNAs involved in its regulation were investigated in blood exosomes isolated from tumor patients before and after ablative surgery. Blood and pathological tissue samples were taken on the surgery day, blood was collected at one week, one month, and three months after surgery, and exosomes were isolated. The results revealed distinctive changes in the levels of miRNAs involved in HSP60 regulation in brain tumors, pointing to their potential as biomarkers for diagnosis and patient monitoring during treatment. References [1] Santiago-Dieppa, D. R.; Steinberg, J.; Gonda, D.; et al. Extracellular vesicles as a platform for ‘liquid biopsy’ in glioblastoma patients. Expert Rev. Mol. Diagn. 2014, 14, 819–825. [2] Roma-Rodrigues, C.; Fernandes, A. R.; Baptista, P. V. Exosome in tumour microenvironment: overview of the crosstalk between normal and cancer cells. Biomed Res. Int. 2014, 2014, 179486. [3] Cappello, F.; Logozzi, M.; Campanella, C.; et al. Exosome levels in human body fluids: tumor marker by themselves? Eur. J. Pharm. Sci. 2017, 96. [4] Caruso Bavisotto, C.; Graziano, F.; Rappa, F.; et al. Exosomal Chaperones and miRNAs in Gliomagenesis: State-of-Art and Theranostics Perspectives. Int. J. Mol. Sci. 2018, 19, 2626
Editorial for the special issue “extracellular chaperones and related mirna as diagnostic tools of chronic diseases”
No full textDifferent immunohistochemical levels of Hsp60 and Hsp70 in a subset of brain tumors and putative role of Hsp60 in neuroepithelial tumorigenesis
No full textIn this work we analysed, by immunohistochemistry, a series of brain tumors to detect the levels and cellular distribution of Hsp60 and Hsp70. We found that Hsp60 levels were significantly higher than those of Hsp70 in neuroepithelial tumors, while levels of both molecules were not significantly different from each other in meningeal neoplasms. In particular, Hsp60 immunopositivity was present mainly at the cytoplasmic level, while Hsp70 immunopositivity was found both in the cytoplasm and in the nucleus of tumor cells. The levels of these molecules in healthy control cells were always very low. Finally, Hsp60 and Hsp70 levels did not correlate with the different types (WHO grade) of neoplasm. Our results are partially in agreement with previous studies and suggest that Hsp60 is not increased by a passive phenomenon (e.g., due to the stress caused by the peritumor environment on cancer cells) but may be actively implicated in tumor progression, e.g. inhibiting tumor cell death or antitumor immune system response, as already postulated in vitro. We also briefly discuss the most recent publications on the extramitochondrial localization of Hsp60 in tumor cells and its role in tumor progression.<br /
La normativa sulla destinazione del corpo allo studio e alla ricerca: una riflessione multidisciplinare sulle questioni ancora aperte
No full textLaw No. 10/2020, supplemented by the regulation established by Presidential Decree No. 47/2023, regulates whole-body donation for education, training and scientific research. This paper aims to analyze, with an interdisciplinary approach, the critical issues and gaps in the legislation that hinder its full implementation. Particular attention will be paid to aspects related to self-determination, information, protection of anonymity and the restitution of the body
GLP-2 as Beneficial Factor in the Glucose Homeostasis in Mice Fed a High Fat Diet
No full textGlucagon like peptide-2 (GLP-2) is a gastrointestinal hormone released in response to dietary nutrients, which acts through a specific receptor, the GLP-2 receptor (GLP-2R). The physiological effects of GLP-2 are multiple, involving also the intestinal adaptation to high fat diet (HFD). In consideration of the well-known relationship between chronic HFD and impaired glucose metabolism, in the present study we examined if the blocking of the GLP-2 signaling by chronic treatment with the GLP-2R antagonist, GLP-2 (3-33), leads to functional consequences in the regulation of glucose metabolism in HFD-fed mice. Compared with animals fed standard diet (STD), mice at the 10th week of HFD showed hyperglycaemia, glucose intolerance, high plasma insulin level after glucose load, increased pancreas weight and β cell expansion, but not insulin resistance. In HFD fed mice, GLP-2 (3-33) treatment for 4 weeks (from the 6th to the 10th week of diet) did not affect fasting glycaemia, but it significantly increased the glucose intolerance, both fasting and glucose-induced insulin levels, and reduced the sensitivity to insulin leading to insulin-resistance. In GLP-2 (3-33)-treated HFD mice pancreas was significantly heavier and displayed a significant increase in β-cell mass in comparison with vehicle-treated HFD mice. In STD mice, the GLP-2 (3-33) treatment did not affect fasted or glucose-stimulated glycemia, insulin, insulin sensitivity, pancreas weight and beta cell mass. The present study suggests that endogenous GLP-2 may act as a protective factor against the dysregulation of the glucose metabolism that occurs in HFD mice, because GLP-2 (3-33) worsens glucose metabolism disorders. J. Cell. Physiol. 230: 3029-3036, 2015. © 2015 Wiley Periodicals, Inc
CMV infection in non functioningadrenal adenoma: Innocent bystander or pathogenetic agent?
No full textGlucagon-like peptide-2 and mouse intestinal adaptation to a high fat diet.
No full textEndogenous glucagon-like peptide-2 (GLP2) is a key mediator of refeeding-induced and
resection-induced intestinal adaptive growth. This study investigated the potential role
of GLP2 in mediating the mucosal responses to a chronic high-fat diet (HFD). In this
view, the murine small intestine adaptive response to a HFD was analyzed and a possible
involvement of endogenous GLP2 was verified using GLP2 (3–33) as GLP2 receptor (GLP2R)
antagonist. In comparison with animals fed a standard diet, mice fed a HFD for 14 weeks
exhibited an increase in crypt–villus mean height (duodenum, 27.5G3.0%; jejunum,
36.5G2.9%; P!0.01), in the cell number per villus (duodenum, 28.4G2.2%; jejunum,
32.0G2.9%; P!0.01), and in Ki67-positive cell number per crypt. No change in the percent
of caspase-3-positive cell in the villus–crypt was observed. The chronic exposure to a HFD
also caused a significant increase in GLP2 plasma levels and in GLP2R intestinal expression.
Daily administration of GLP2 (3–33) (30–60 ng) for 4 weeks did not modify the crypt–villus
height in control mice. In HFD-fed mice, chronic treatment with GLP2 (3–33) reduced the
increase in crypt–villus height and in the cell number per villus through reduction of cell
proliferation and increase in apoptosis. This study provides the first experimental evidence
for a role of endogenous GLP2 in the intestinal adaptation to HFD in obese mice and for
a dysregulation of the GLP2/GLP2R system after a prolonged HFD
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