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Resource Allocation in Multi-Domain Networks Based on Service Level Specifications
Avallone Stefano,D'Antonio Salvatore,Esposito Marcello,Romano Simon Pietro,Ventre Giorgio The Korea Institute of Information and Commucation 2006 Journal of communications and networks Vol.8 No.1
The current trend toward the utilization of the Internet as a common means for the offer of heterogeneous services imposes to address the issues related to end-to-end service assurance in the inter-domain scenario. In this paper, we first present an architecture for service management in networks based on service level specifications (SLS). The architecture is designed to be independent both of the specific network technology adopted and of the high level service semantics. Then, we focus on a specific functionality of the proposed architecture: Resource allocation in the multi-domain scenario. A distributed admission control algorithm is introduced, its complexity is evaluated and a comparison with related solutions is provided.
Francesco Calì,Alda Ragalmuto,Valeria Chiavetta,Giuseppe Calabrese,Marco Fichera,Mirella Vinci,Giuseppa Ruggeri,Pietro Schinocca,Maurizio Sturnio,Salvatore Romano,IRCCS Oasi Maria SS,Valentino Romano 생화학분자생물학회 2010 Experimental and molecular medicine Vol.42 No.12
Angelman syndrome (AS) is a severe neurobehavioural disorder caused by failure of expression of the maternal copy of the imprinted domain located on 15q11-q13. There are different mechanisms leading to AS: maternal microdeletion, uniparental disomy, defects in a putative imprinting centre, mutations of the E3 ubiquitin protein ligase (UBE3A) gene. However,some of suspected cases of AS are still scored negative to all the latter mutations. Recently, it has been shown that a proportion of negative cases bear large deletions overlapping one or more exons of the UBE3A gene. These deletions are difficult to detect by conventional gene-scanning methods due to the masking effect by the non-deleted allele. In this study, we have used for the first time multiplex ligation-dependent probe amplification (MLPA) and comparative multiplex dosage analysis (CMDA) to search for large deletions affecting the UBE3A gene. Using this approach, we identified a novel causative deletion involving exon 8 in an affected sibling. Based on our results, we propose the use of MLPA as a fast, accurate and inexpensive test to detect large deletions in the UBE3A gene in a small but significant percentage of AS patients.
Cali, Francesco,Ragalmuto, Alda,Chiavetta, Valeria,Calabrese, Giuseppe,Fichera, Marco,Vinci, Mirella,Ruggeri, Giuseppa,Schinocca, Pietro,Sturnio, Maurizio,Romano, Salvatore,Romano, Valentino,Elia, Mau Korean Society for Biochemistry and Molecular Bion 2010 Experimental and molecular medicine Vol.42 No.12
Angelman syndrome (AS) is a severe neurobehavioural disorder caused by failure of expression of the maternal copy of the imprinted domain located on 15q11-q13. There are different mechanisms leading to AS: maternal microdeletion, uniparental disomy, defects in a putative imprinting centre, mutations of the E3 ubiquitin protein ligase (UBE3A) gene. However, some of suspected cases of AS are still scored negative to all the latter mutations. Recently, it has been shown that a proportion of negative cases bear large deletions overlapping one or more exons of the UBE3A gene. These deletions are difficult to detect by conventional gene-scanning methods due to the masking effect by the non-deleted allele. In this study, we have used for the first time multiplex ligation-dependent probe amplification (MLPA) and comparative multiplex dosage analysis (CMDA) to search for large deletions affecting the UBE3A gene. Using this approach, we identified a novel causative deletion involving exon 8 in an affected sibling. Based on our results, we propose the use of MLPA as a fast, accurate and inexpensive test to detect large deletions in the UBE3A gene in a small but significant percentage of AS patients.
Exon deletions of the phenylalanine hydroxylase gene in Italian hyperphenylalaninemics
Francesco Calì,Giuseppa Ruggeri,Mirella Vinci,Concetta Meli,Carla Carducci,Vincenzo Leuzzi,Simone Pozzessere,Pietro Schinocca,Alda Ragalmuto,Valeria Chiavetta,Salvatore Miccichè,Valentino Romano 생화학분자생물학회 2010 Experimental and molecular medicine Vol.42 No.2
A consistent finding of many studies describing the spectrum of mutant phenylalanine hydroxylase (PAH)alleles underlying hyperphenylalaninemia is the impossibility of achieving a 100% mutation ascertainment rate using conventional gene-scanning methods. These methods include denaturing gradient gel electrophoresis (DGGE), denaturing high performance liquid chromatography (DHPLC), and direct sequencing. In recent years, it has been shown that a significant proportion of undetermined alleles consist of large deletions overlapping one or more exons. These deletions have been difficult to detect in compound heterozygotes using gene-scanning methods due to a masking effect of the non-deleted allele. To date, no systematic search has been carried out for such exon deletions in Italian patients with phenylketonuria or mild hyperphenylalaninemia. We used multiplex ligation-dependent probe amplification (MLPA), comparative multiplex dosage analysis (CMDA), and real-time PCR to search for both large deletions and duplications of the phenylalanine hydroxylase gene in Italian hyperphenylalaninemia patients. Four deletions removing different phenylalanine hydroxylase (PAH) gene exons were identified in 12 patients. Two of these deletions involving exons 4-5-6-7-8(systematic name c.353-?_912 + ?del) and exon 6(systematic name c.510-?_706 + ?del) have not been reported previously. In this study, we show that exon deletion of the PAH gene accounts for 1.7% of all mutant PAH alleles in Italian hyperphenylalaninemics.