86,807 research outputs found
Filippo Collino. Alessandro, 1756. Olimpia, 1756
No full textIl testo presenta due capolavori dello scultore Filippo Collino, scolpiti a Roma durante il periodo di formazione accademica
Peroxisome Proliferator-Activated Receptors (PPARs) in Glucose Control
No full textThe peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that control lipid and glucose metabolism. PPARs regulate gene expression by binding with retinoid X receptor as a heterodimeric partner to specific DNA sequences, termed PPAR response elements. In addition, PPARs may modulate gene transcription by directly interfering with other transcription factor pathways in a DNA-binding independent manner. To date, three different PPAR isoforms, designated α, β/δ, and γ, have been identified. PPAR-γ was the first isoform demonstrated to affect carbohydrate metabolism and PPAR-γ agonists, the thiazolidinediones, are now in clinical use for the treatment of insulin resistance. Unexpectedly, later studies revealed that also the other two isoforms modulate glucose metabolism. Here we summarize our understanding on how these nuclear receptor isoforms are involved in the control of glucose metabolism, describing some of the novel regulatory mechanisms. In addition, this chapter reviews the evidence and recent developments relating to the role of some foods containing natural compounds as PPAR agonists
I meccanismi del danno cronico renale nelle nefropatie e la loro possibile reversibilità [Mechanisms causing chronic renal injury in kidney disease and their possible reversibility]
No full textMuch study has been dedicated to the understanding of the mechanisms leading to the progression of renal injury and to the development of strategies to limit this progression or possibly induce tissue regeneration. Among several identified mechanisms, the role of angiotensin II is widely recognized. Moreover, the progression of glomerular damage is characterized by capillary loss, reduction of the proliferative response, and production of antiangiogenic factors. Several lines of evidence support the potential effect of therapeutic startegies aimed at interfering with angiotensin II or stimulating angiogenesis in order to reduce the progression of renal injury. Recent work has underlined the potential of strategies involving the use of stem cells. Different populations of stem cells have been identified in the adult kidney. During renal injury, stem cells derived from the bone marrow that migrate through the circulation to the kidney may contribute to tissue repair. The regenerative potential of stem cells could be exploited by administration of ex vivo expanded stem cell populations or by the development of techniques to expand and differentiate local stem cells
Release of MicroRNA-Containing Vesicles Can Stimulate Angiogenesis and Metastasis in Renal Carcinoma
No full textRenal cell carcinoma is a common form of urologic tumor, with low incidence but a high metastatic rate at diagnosis and high frequency of relapse. Renal cell carcinoma comprises a heterogeneous group of subtypes, classified according to their histopathological features and clinical behavior. Diagnostic approaches used to identify malignant tissue are based on immunohistochemical techniques. However, new molecular methods have been recently proposed for profiling and staging renal tumors based on their microRNA (miRNAs) expression. In fact, miRNAs have been shown to have abnormal levels in many cancers compared with their normal tissue counterparts. For this reason, along with the fact that they are present in biological fluids, miRNAs could serve as a useful diagnostic tool. Moreover, miRNAs may modify the translational profile of cells through direct degradation of their target mRNAs or by blocking their translation into functional proteins. The biological function of secretory miRNAs requires protection from extracellular degrading enzymes, which is achieved by envelopment of miRNAs within extracellular vesicles (EVs), which are subsequently secreted. EVs are a heterogeneous population of vesicles that includes shedding vesicles and exosomes, and are variable in size, composition, and releasing mechanisms. Following uptake, EVs are able to induce epigenetic modifications in target cells by the transfer of active proteins, lipids, RNA, and miRNAs. Therefore, through the transfer of selected miRNAs, tumor-released EVs may provide oncogenic signals to stromal cells. In particular, EVs released from renal carcinoma stem cells contain miRNAs that are potentially involved in triggering angiogenesis and metastasis
CD133 + cells as a therapeutic target for kidney diseases
No full textIntroduction: The availability of antibodies recognizing the glycosylation-dependent expression of AC133 epitope of CD133 allowed the identification of stem cells in different human tissues. In the kidney, CD133 has been identified as a marker of progenitor cells within the nephron, both in the cortex and in the inner medulla, showing features of non-differentiated mesenchymal progenitors. In addition, CD133 may be considered a marker of renal repair, as the hypoxic microenvironment occurring after injury may favor the acquirement of CD133 progenitor properties by cells of the nephron. Areas covered: Areas covered in this review include CD133 expression that, in renal pathology, has been related to excessive proliferation and/or reduced differentiation of renal progenitors, which occurs in polycystic kidney disease and glomerular diseases. Also included are data from literature, which by contrast, indicate CD133 cannot be considered a promising marker for renal cancer stem cells. Expert opinion: CD133 could be of interest as a possible therapeutic target for nonmalignant renal pathology. Selective targeting of CD133 may allow pharmacological approaches to control proliferation or induce differentiation of CD133 + cells. In the light of a possible role of CD133 in the regulation of the anaerobic glycolytic metabolism, CD133 modulation could be of therapeutic interest in renal regeneration or diseases. Successful exploitation of CD133 will nevertheless require a better understanding of its molecular function
Extracellular vesicles as regulators of tumor fate: Crosstalk among cancer stem cells, tumor cells and mesenchymal stem cells
No full textThe tumor microenvironment comprises a heterogeneous population of tumorigenic and non-tumorigenic cells. Cancer stem cells (CSCs) and mesenchymal stem cells (MSCs) are components of this microenvironment and have been described as key regulators of different aspects of tumor physiology. They act differently on the tumor: CSCs are described as tumor initiators and are associated with tumor growth, drug resistance and metastasis; MSCs can integrate the tumor microenvironment after recruitment and interact with cancer cells to promote tumor modifications. Extracellular vesicles (EVs) have emerged as an important mechanism of cell communication under the physiological and pathological conditions. In cancer, secretion of EVs seems to be one of the main mechanisms by which stem cells interact with other tumor and non-tumor cells. The transfer of bioactive molecules (lipids, proteins and RNAs) compartmentalized into EVs triggers different responses in the target cells, regulating several processes in the tumor as angiogenesis, tumor invasiveness and immune escape. This review focuses on the role of CSCs and MSCs in modulating the tumor microenvironment through secretion of EVs, addressing different aspects of the multidirectional interactions among stem cells, tumor and tumor-associated cells
Extracellular vesicles derived from renal cancer stem cells induce a pro-tumorigenic phenotype in mesenchymal stromal cells
No full textRenal carcinomas have been shown to contain a population of cancer stem cells (CSCs) that present self-renewing capacity and support tumor growth and metastasis. CSCs were shown to secrete large amount of extracellular vesicles (EVs) that can transfer several molecules (proteins, lipids and nucleic acids) and induce epigenetic changes in target cells. Mesenchymal Stromal Cells (MSCs) are susceptible to tumor signalling and can be recruited to tumor regions. The precise role of MSCs in tumor development is still under debate since both pro- and anti-tumorigenic effects have been reported. In this study we analysed the participation of renal CSC-derived EVs in the interaction between tumor and MSCs. We found that CSC-derived EVs promoted persistent phenotypical changes in MSCs characterized by an increased expression of genes associated with cell migration (CXCR4, CXCR7), matrix remodeling (COL4A3), angiogenesis and tumor growth (IL-8, Osteopontin and Myeloperoxidase). EV-stimulated MSCs exhibited in vitro an enhancement of migration toward the tumor conditioned medium. Moreover, EV-stimulated MSCs enhanced migration of renal tumor cells and induced vessel-like formation. In vivo, EV-stimulated MSCs supported tumor development and vascularization, when co-injected with renal tumor cells. In conclusion, CSC-derived EVs induced phenotypical changes in MSCs that are associated with tumor growth
Analysis and clustering of microRNA array: a new efficient and reliable computational method
No full textMicroRNAs (miRNAs) play determinant roles in gene expression and several cellular processes of mammalian. These processes include differentiation, development, apoptosis, and cancer pathomechanisms. In detail, miRNAs are known to regulate the expression of keys genes relevant to cancer and potentially to other diseases [1-3]. MiRNAs are short noncoding RNAs having a central function in gene expression, since miRNAs are involved in cellular differentiation processes [4, 5], organism developments [6], and apoptosis. Furthermore, recent studies provide growing evidence of the contribution of miRNAs in cancer cellular mechanisms. Therefore, the analysis and the correct identification of miRNAs expression levels play a key role for better understanding and classifying cancer and other diseases. In parallel with the drastic growing of interest into the study of miRNAs, the support of systems and tools that allow an efficient and more robust analysis of miRNA's expression levels become increasing mandatory to have a better disease identification
A Selective IκB Kinase Inhibitor (IKK16) Attenuates The Organ Injury / Dysfunction Associated With Haemorrhagic Shock In The Rat
No full textThe Fano normal function
No full textAbstractThe Fano surface F of lines in the cubic threefold V is naturally embedded in the intermediate Jacobian J(V), we call “Fano cycle” the difference F−F−, this is homologous to 0 in J(V). We study the normal function on the moduli space which computes the Abel–Jacobi image of the Fano cycle. By means of the related infinitesimal invariant we can prove that the primitive part of the normal function is not of torsion. As a consequence we get that, for a general V, F−F− is not algebraically equivalent to zero in J(V) (proved also by van der Geer and Kouvidakis (2010) [15] with different methods) and, moreover, that there is no divisor in JV containing both F and F− and such that these surfaces are homologically equivalent in the divisor.Our study of the infinitesimal variation of Hodge structure for V produces intrinsically a threefold Ξ(V) in the Grassmannian of lines G in P4. We show that the infinitesimal invariant at V attached to the normal function gives a section of a natural bundle on Ξ(V) and more specifically that this section vanishes exactly on Ξ∩F, which turns out to be the curve in F parameterizing the “double lines” in the threefold. We prove that this curve reconstructs V and hence we get a Torelli-like result: the infinitesimal invariant for the Fano cycle determines V
- …
