263 research outputs found
Edificio per abitazioni, negozi e uffici, Studio GPA Monti, 1963-67, corso Magenta 19
Negli anni ’60 lo studio GPA Monti (Gianemilio e Piero Monti, e Anna Bertarini Monti, moglie del primo) ha al suo attivo diversi edifici d’abitazione costruiti all’esterno della seconda circonvallazione di Milano: grazie ad essi ha affinato le proprie attitudini progettuali e, in particolare, il disegno delle facciate. Il complesso d’angolo tra corso Magenta e via Nirone (seguito dall’edificio per uffici e abitazioni in via Carducci 34) è in questo senso esemplare poiché introduce un linguaggio di manifesta modernità, ribadendo il "tipo" del condominio milanese
Assessing the impact of chloride deicer application in the Siskiyou Pass, southern Oregon
by Adam J. Stonewall, Matthew C. Yates, and Gregory E. Granato ; prepared in cooperation with Oregon Department of Transportation.This archived document is maintained by the State Library of Oregon. It is for informational purposes and may not be suitable for legal purposes.Includes bibliographical references (pages 90-93).Mode of access: Internet from the State Library of Oregon U.S. Government Publications Collection.Text in English
2,3,7,8-Tetrachlorodibenzo-p-dioxin influences bovine herpesvirus 1 replication through upregulation of SIRT3 and cytoskeletal reorganization.
Infection of kidney cells (MDBK) with Bovine Herpesvirus 1 (BoHV-1) is affected by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which accelerates BoHV-1-induced apoptosis and increases virus replication. Herein, to elucidate the mechanism through TCDD modifies BoHV-1 infection, we analyzed the modulation of a members of Sirtuin proteins family in MDBK cells. We found that mitochondrial SIRT3 was upregulated during infection. This change was accompanied by cytoskeletal rearrangements and cell extensions. All these trends were drastically modified by TCDD. We hypothesize that, taken together, these results might further clarify the processes responsible for the action of TCDD on the BoHV-1 replication, resulting in enhanced virus production
Fine air particles characterized by X-ray photoelectron spectroscopy induce genotoxicity in RAW-264.7 cells. bstract Book
Global Gene Expression Analysis of Canine Cutaneous Mast Cell Tumour
Introduction:
Currently, prognostic and therapeutic determinations for canine cutaneous mast cell tumors (MCTs) are primarily based on the histological grade. However, the prognostic value of this latter is still highly questionable. In the present study, MCT transcriptome was characterized to identify a set of candidate genes potentially useful for MCT classification and prognosis prediction.
Materials and Methods:
Fifty-two canine MCT biopsies were enrolled in the study. Isolated and purified total RNAs were individually hybridized to the Agilent Canine V2 4x44k DNA microarray. Normalized data were analyzed by using SAM (Significant Analysis of Microarray), PAM (Prediction Analysis of Microarray) and TMeV tools. Furthermore, a Functional Annotation bioinformatic tool (DAVID) was used to classify modulated genes.
Results:
PAM identified 14 transcripts providing the greatest accuracy of class prediction into two classes (mostly referable to High and Low grade MCTs) with a misclassification error equal to 0. The functional analysis of genes differentially expressed (597) between the aforementioned two groups provided evidence that they were involved in cell cycle, DNA replication, p53 signaling pathway, nucleotide excision repair and pyrimidine metabolism. The PCA of all samples, made by using this same panel of genes, clearly identified two clusters (the first two components accounted for the 90.9% of total variance).
Conclusions:
The molecular characterization of canine MCT transcriptome allowed the identification of a gene set that clearly separate differentiated and undifferentiated MCTs. This might potentially be helpful for MCT classification and prognosis.
Supporting grants: RC IZS VE 04/1
Cancer: an oxidative crosstalk between solid tumor cells and cancer associated fibroblasts
Redox balance is associated with the regulation of several cell signalling pathways and functions. In fact, under physiological
conditions, cells maintain a balance between oxidant and antioxidant systems, and reactive oxygen species (ROS) can act as second
messengers to regulate cell proliferation, cell death, and other physiological processes. Cancer tissues usually contain higher levels
of ROS than normal tissues, and this ROS overproduction is associated with tumor development. Neoplastic tissues are very
heterogeneous systems, composed of tumor cells and microenvironment that has a critical role in tumor progression. Cancer
associated fibroblasts (CAFs) represent the main cell type of tumor microenvironment, and they contribute to tumor growth by
undergoing an irreversible activation process. It is known that ROS can be transferred from cancer cells to fibroblasts. In particular,
ROS affect the behaviour of CAFs by promoting the conversion of fibroblasts to myofibroblasts that support tumor progression and
dissemination. Furthermore, the wrecking of redox homeostasis in cancer cells and tumor microenvironment induces a metabolic
reprogramming in tumor cells and cancer associated fibroblasts, giving advantage to cancer growth. This review describes the role
of ROS in tumor growth, by focusing on CAFs activation and metabolic interactions between cancer cells and stromal fibroblasts
Fine air particles characterized by X-ray photoelectron spectroscopy induce genotoxicity in RAW-264.7 cells.
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