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Search Results: 1 - 10 of 33107 matches for " Antonio Giordano "
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CRT-D Upgrading in a Patient with Persistent Left Superior Vena Cava and Right Superior Vena Cava Atresia Using the Novel Active-Fixation Quadripolar Left Ventricular Lead  [PDF]
Sergio Conti, Antonio Taormina, Vito Bonomo, Umberto Giordano, Giuseppe Sgarito
World Journal of Cardiovascular Diseases (WJCD) , 2018, DOI: 10.4236/wjcd.2018.89045
Abstract: The persistence of left superior vena cava (PLSVC) is the most common congenital anomaly of the venous return system to the heart. Because of the increasing number of patients referred for cardiac resynchronization therapy (CRT) devices implantations, it is expected to encounter this venous anatomic variation. Left ventricular lead placement at an appropriate site is an integral and technically challenging part of successful CRT. In case of cardiac abnormalities could be difficult to achieve an optimal cardiac rhythm management devices implantation. Previous reports in patients with PLSVC highlighted the challenges to achieve an optimal cardiac rhythm device implantation. Recently, a new quadripolar active fixation left ventricular lead is available for CRT device implantation. Hereby we report a case of a device upgrading from dual-chamber pacemaker to CRT with defibrillator backup using the active fixation left ventricular quadripolar lead in a patient with PLSVC and right superior vena cava atresia.
Screening and genetic diagnosis of Hemoglobinopathies in Southern and Northern Europe: Two examples
Antonio Amato,Piero C Giordano
Mediterranean Journal of Hematology and Infectious Diseases , 2009, DOI: 10.4084/mjhid.2011.
Abstract: Prevention of Hemoglobinopathies has developed around the world based upon the experience done in pioneering endemic countries and is now facing a new phase in non-endemic areas with a recent immigration history. We describe two situations, taking Latium (central Italy) and The Netherlands as two models for endemic and non-endemic countries both confronted with a large multi-ethnic immigrant society. We present prevention results and discuss aspects such as local knowledge and organization. We illustrate the importance of issues like information, carrier diagnostics, screening, counseling and prenatal diagnosis in particular situation of contrasting interest an different ethical opinions. We conclude by underlining the importance of implementing primary prevention at the European level, based upon better information, diagnostics and counseling.
Online Leader Selection for Multi-Agent Collective Tracking and Formation Maintenance
Antonio Franchi,Paolo Robuffo Giordano
Mathematics , 2013,
Abstract: In this paper we propose an extension of the popular leader-follower framework for multi-agent collective tracking and formation maintenance. We introduce a new paradigm, the online leader selection, which allows the agent group to persistently select the identity of the current leader in order to maximize the tracking performance of an exogenous velocity command while maintaining a given formation and across a (possibly time-varying) communication-graph topology. By employing two of the most widely used fully-decentralized multi- agent coordination schemes (a first-order and second-order ones), we theoretically analyze the effects of a leader change and propose two corresponding error metrics able to adequately characterize the tracking performance of the multi-agent group. Both the group performance and the choice of the right metrics are found to depend upon the spectral properties of a special directed graph induced by the identity of the chosen leader. By exploiting the proposed analysis and distributed estimation techniques, we then detail two fully-decentralized adaptive controllers able to periodically select the best leader among the neighbors of the current leader. Numerical simulations show that the application of the proposed technique results in an clear improvement of the overall performance of the group behavior.
The retinoblastoma family: twins or distant cousins?
Pier Claudio, Tiziana Tonini, Antonio Giordano
Genome Biology , 2002, DOI: 10.1186/gb-2002-3-9-reviews3012
Abstract: The three human genes encoding members of the retinoblastoma (Rb) family share some features that are similar to other housekeeping genes, including a lack of the canonical TATA or CAAT boxes found in the promoters of most differentially expressed genes, the presence of a GC-rich zone immediately surrounding the main transcription-initiation site, the presence of multiple consensus sequences for binding the Sp1 transcription factor, and the presence of multiple transcription start sites [1,2,3].The human RB gene (which encodes a protein of 105 kDa and is also called p105) was first identified when both familial and sporadic retinoblastoma, a form of malignant tumor of the retina, were found to be associated with deletions at 13q14 [4,5,6]. The RB transcript is encoded by 27 exons dispersed over about 200 kilobases (kb) of genomic DNA; the exons range from 31 to 1,889 base pairs (bp) in length and the introns range from 80 bp to 60 kb.The human p107 gene (which encodes a protein of 107 kDa and is also known as RBL1) is located at chromosome 20q11.2, a region of special interest because of its association with some myeloid disorders. The arrangement of the p107 gene is similar to that of the other members of the Rb family. It is composed of 22 exons that vary in length from 50 to 840 bp, spanning approximately 100 kb of genomic DNA.The human Rb2 gene (which encodes a protein of 130 kDa and is also called RBL2) maps to chromosome 16q12.2. The Rb2 messenger RNA is 4.6 kb in length; the gene consists of 22 exons and spans over 50 kb of genomic DNA, and the 21 introns vary in size from 82 bp to almost 9 kb.The three Rb-family proteins are also known as 'pocket proteins', after their conserved pocket region, which is composed of two conserved domains (A and B) separated by a spacer (Figure 1). The pocket is important for the binding of other proteins (see below). The exons encoding domain A of the RB gene (exons 11-17), domain B (20-23), and the spacer region between domai
The bad and the good of mesenchymal stem cells in cancer: Boosters of tumor growth and vehicles for targeted delivery of anticancer agents
Umberto Galderisi,Antonio Giordano,Marco G Paggi
World Journal of Stem Cells , 2010,
Abstract: In cancer biology, mesenchymal stem cells (MSCs) display aspects that can appear contradictory. On one hand, these cells possess several features which give them the ability to specifically target and then sustain cancer cells in their ability to survive the multifaceted host response against cancer. On the other hand, due to this excellent aptitude to home-in on tumor tissues, regardless their location in the host’s body, MSCs are considered to be extremely selective vehicles to reach cancer cells specifically. Recently, MSC sustainment of cancer cell growth is a hot research topic. Indeed, these cells are known to sustain tumor angiogenesis and metastasis formation, to create a microenvironment favorable for cancer cell growth and to down-modulate the immune system capabilities in the host organism. On the other hand, since scientists became able to take advantage of their extremely selective capability to target cancer cells, MSCs are now also thought of in a different light. Indeed, MSCs are now considered a promising vehicle for local expression or delivery of even particularly toxic anticancer agents, ranging from Herpes Simplex Virus to locally-acting antineoplastic drugs. On this basis, investigation is now focused on how to impair the pro-neoplastic features of MSCs on one hand whilst taking advantage of their specific tropism toward cancer cells, on the other. As with the two faces of Janus, this review will concisely explore the research activity in these two apparently conflicting fields.
Rigidity Theory in SE(2) for Unscaled Relative Position Estimation using only Bearing Measurements
Daniel Zelazo,Antonio Franchi,Paolo Robuffo Giordano
Mathematics , 2013, DOI: 10.1109/ECC.2014.6862558
Abstract: This work considers the problem of estimating the unscaled relative positions of a multi-robot team in a common reference frame from bearing-only measurements. Each robot has access to a relative bearing measurement taken from the local body frame of the robot, and the robots have no knowledge of a common or inertial reference frame. A corresponding extension of rigidity theory is made for frameworks embedded in the \emph{special Euclidean group} $SE(2) = \mathbb{R}^2 \times \mathcal{S}^1$. We introduce definitions describing rigidity for $SE(2)$ frameworks and provide necessary and sufficient conditions for when such a framework is \emph{infinitesimally rigid} in $SE(2)$. Analogous to the rigidity matrix for point formations, we introduce the \emph{directed bearing rigidity matrix} and show that an $SE(2)$ framework is infinitesimally rigid if and only if the rank of this matrix is equal to $2|\mathcal{V}|-4$, where $|\mathcal{V}|$ is the number of agents in the ensemble. The directed bearing rigidity matrix and its properties are then used in the implementation and convergence proof of a distributed estimator to determine the {unscaled}{} relative positions in a common frame. Some simulation results are also given to support the analysis.
Effects of Unsaturated Fatty Acid Esters of Testosterone on Neuronal, Behavioral and Hormonal Parameters in Male Rats Subjected to the Formalin Test  [PDF]
Anna Petroni, Paolo Fiorenzani, Valentina Tomei, Antonio Garofalo, Francesca Aiello, Daniele Della Seta, Antonio Giordano, Stella Vodo, Ilaria Ceccarelli, Anna Maria Aloisi
Open Journal of Endocrine and Metabolic Diseases (OJEMD) , 2014, DOI: 10.4236/ojemd.2014.46017

Chronic diseases are often accompanied by inflammatory and degenerative processes. Estrogens have repeatedly been found to be involved in these processes. Testosterone (T) is the main precursor of estrogen in the brain and T replacement in chronic diseases has become important in recent years, prompting research on new T-conjugated molecules. We recently synthesized three new molecules including unsaturated fatty acid esters: T-linoleate (TL), T-oleate (TO) and T-eicosapentanoate (TEPA). These substances were s.c. administered for 7 days to intact male rats subjected to the formalin test (FT). Three other groups were included as comparisons: NAIVE, receiving no substance, OIL, treated with almond oil (vehicle), and TN, treated with T-undecanoate, a saturated fatty acid. Spontaneous behaviors and pain-induced responses were determined during the FT, hormones (T and dihydrotestosterone, DHT) were determined in blood, while estrogen receptors (ERα and β) were detected at the genomic and proteomic levels in the hippocampus, hypothalamus and spinal cord. In the hippocampus, ERα and ERβ mRNA levels were increased respectively by TN and TL treatments with respect to OIL, whereas the hypothalamus TO and TL

Enhancer of zeste homolog 2 (EZH2) in pediatric soft tissue sarcomas: first implications
Roberta Ciarapica, Lucio Miele, Antonio Giordano, Franco Locatelli, Rossella Rota
BMC Medicine , 2011, DOI: 10.1186/1741-7015-9-63
Abstract: Soft tissue sarcomas (STSs) are a group of heterogeneous malignant neoplasms thought to arise from molecular lesions occurring during the differentiation of mesenchymal stem cells (MSCs) [1]. STSs account for less than 1% of all adult tumors and for about 15% of all pediatric ones, with an estimated 10,520 new cases in the US in 2010 [2,3]. A series of chromosomal translocations have been identified as hallmarks of most STSs, such as t(X;18)(p11.2;q11.2) in synovial sarcoma, t(11;22)(q24;q12) in Ewing's sarcoma, t(2;13)(q35;q14) and t(1;13)(p36;q14) in alveolar rhabdomyosarcoma (RMS). These chromosomal rearrangements result in oncogenic fusion proteins that play direct roles in altering gene expression pattern in STS, promoting tumor aggressiveness. Because of their infiltrating behavior, only 50% of STSs are suitable for radical surgical resection. Moreover, a fraction of STSs are resistant to chemotherapeutic agents, especially the metastatic forms [4]. Doxorubicin, the drug used in standard single-agent chemotherapy protocols for the treatment of metastatic STS, results in only 20% to 25% response rates. Even the combination of doxorubicin with other agents, such as ifosfamide, has not dramatically improved the overall 5-year survival rate, which is no higher than 50% to 60% [4]. Nevertheless, chemotherapy represents the only viable strategy for palliation of symptoms in patients with metastatic disease, improving their quality of life [5]. New promising biological drugs, such as monoclonal antibodies to insulin-like growth factor receptor (IGFR), inhibitors of multityrosine kinases, and mammalian target of rapamycin (mTOR), have been introduced in STS clinical trials (Table 1) [4]. However, disease stabilization is still not seen in many patients, especially those affected by peculiar histological variants or showing poor-risk factors; it is reasonable to hypothesize that a combination of cytotoxic chemotherapy with targeted agents may be more appropriate to imp
MicroRNAs in rhabdomyosarcoma: pathogenetic implications and translational potentiality
Rossella Rota, Roberta Ciarapica, Antonio Giordano, Lucio Miele, Franco Locatelli
Molecular Cancer , 2011, DOI: 10.1186/1476-4598-10-120
Abstract: In this review, we provide an overview of current knowledge on microRNAs de-regulation in rhabdomyosarcoma. Additionally, we examine the potential of microRNAs as prognostic and diagnostic markers in this soft-tissue sarcoma, and discuss possible therapeutic applications and challenges of a "microRNA therapy".Since the discovery of the function of lin-4, the first discovered canonical microRNA (miRNA) in Caenorhabditis elegans [1-3], more than 1400 miRNAs have been identified in mammals (miRBASE, http://www.mirbase.org webcite), most of which with unknown functions.Mature miRNAs are a class of non-coding ~ 19-25 nucleotide (nt) single-strand RNAs highly conserved across species. They act by binding complementary sequences in the 3'-untranslated regions (UTRs) of a messenger RNA (mRNA) through their "seed" sequence (nt 2-8 at the 5' end), with either incomplete or complete base-pairing. This leads to either translational repression or transcriptional degradation of target mRNAs [4]. The end result is post-transcriptional silencing of selected genes that provides an additional layer of gene expression control and enhances the flexibility of gene regulation. A relatively low stringency requirement for base pairing between a particular miRNA and its target 3'UTR sequences results in the capacity of each miRNA to silence several mRNAs [5]. Consequently, small changes in miRNAs expression can have significant effects on cellular phenotype. Conversely, the same mRNA can be targeted by several miRNAs.Genes encoding for miRNAs are evolutionarily conserved and the majority of these are located in intergenic regions or in antisense orientation, suggesting that they behave as independent transcription units. Other miRNAs can be present in intronic regions and transcribed as part of annotated genes. miRNAs can form clusters transcribed as polycistronic transcripts by RNA polymerase II and/or III [6,7], which undergo sequential steps of maturation (Figure 1) [4,8]. The first step
The Prolyl Isomerase Pin1 Acts Synergistically with CDK2 to Regulate the Basal Activity of Estrogen Receptor α in Breast Cancer
Chiara Lucchetti, Isabella Caligiuri, Giuseppe Toffoli, Antonio Giordano, Flavio Rizzolio
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0055355
Abstract: In hormone receptor-positive breast cancers, most tumors in the early stages of development depend on the activity of the estrogen receptor and its ligand, estradiol. Anti-estrogens, such as tamoxifen, have been used as the first line of therapy for over three decades due to the fact that they elicit cell cycle arrest. Unfortunately, after an initial period, most cells become resistant to hormonal therapy. Peptidylprolyl isomerase 1 (Pin1), a protein overexpressed in many tumor types including breast, has been demonstrated to modulate ERalpha activity and is involved in resistance to hormonal therapy. Here we show a new mechanism through which CDK2 drives an ERalpha-Pin1 interaction under hormone- and growth factor-free conditions. The PI3K/AKT pathway is necessary to activate CDK2, which phosphorylates ERalphaSer294, and mediates the binding between Pin1 and ERalpha. Site-directed mutagenesis demonstrated that ERalphaSer294 is essential for Pin1-ERalpha interaction and modulates ERalpha phosphorylation on Ser118 and Ser167, dimerization and activity. These results open up new drug treatment opportunities for breast cancer patients who are resistant to anti-estrogen therapy.
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