Efficient algorithm for achieving GWPMM fairness in ATM ABR services

A new explicit rate allocation algorithm is proposed for achieving generic weight-proportional max-min (GWPMM) fairness in asynchronous transfer mode (ATM) available bit rate services. This algorithm scales well with a fixed computational complexity of O(1) and can realise GWPMM fair rate allocation in an ATM network accurately.

A study of the generalised max–min fair rate allocation for ABR control in ATM

In the rate-based flow control for ATM Available Bit Rate service, fairness is an important requirement, i.e. each flow should be allocated a fair share of the available bandwidth in the network. Max–min fairness, which is widely adopted in ATM, is appropriate only when the minimum cell rates (MCRs) of the flows are zero or neglected. Generalised max–min (GMM) fairness extends the principle of the max–min fairness to accommodate MCR. In this paper, we will discuss the formulation of the GMM fair rate allocation, propose a centralised algorithm, analyse its bottleneck structure and develop an efficient distributed explicit rate allocation algorithm to achieve the GMM fairness in an ATM network. The study in this paper addresses certain theoretical and practical issues of the GMM fair rate allocation.

Weighted fairness with MCR guarantee and a general-purpose explicit rate allocation algorithm for ATM ABR service

In this paper, weighted fair rate allocation for ATM available bit rate (ABR) service is discussed with the concern of the minimum cell rate (MCR). Weighted fairness with MCR guarantee has been discussed recently in the literature. In those studies, each ABR virtual connection (VC) is first allocated its MCR, then the remaining available bandwidth is further shared among ABR VCs according to their weights. For the weighted fairness defined in this paper, the bandwidth is first allocated according to each VC's weight; if a VC's weighted share is less than its MCR, it should be allocated its MCR instead of the weighted share. This weighted fairness with MCR guarantee is referred to as extended weighted (EXW) fairness. Certain theoretical issues related to EXW, such as its global solution and bottleneck structure, are first discussed in the paper. A distributed explicit rate allocation algorithm is then proposed to achieve EXW fairness in ATM networks. The algorithm is a general-purpose explicit rate algorithm in the sense that it can realise almost all the fairness principles proposed for ABR so far whilst only minor modifications may be needed.

An enhanced explicit rate algorithm for ABR traffic control in ATM networks

A high performance, low computational complexity rate-based flow control algorithm which can avoid congestion and achieve fairness is important to ATM available bit rate service. The explicit rate allocation algorithm proposed by Kalampoukas et al. is designed to achieve max–min fairness in ATM networks. It has several attractive features, such as a fixed computational complexity of O(1) and the guaranteed convergence to max–min fairness. In this paper, certain drawbacks of the algorithm, such as the severe overload of an outgoing link during transient period and the non-conforming use of the current cell rate field in a resource management cell, have been identified and analysed; a new algorithm which overcomes these drawbacks is proposed. The proposed algorithm simplifies the rate computation as well. Compared with Kalampoukas's algorithm, it has better performance in terms of congestion avoidance and smoothness of rate allocation.

ATM mediated phosphorylation of CHD4 contributes to genome maintenance

Background: In order to maintain cellular viability and genetic integrity cells must respond quickly following the induction of cytotoxic double strand DNA breaks (DSB). This response requires a number of processes including stabilisation of the DSB, signalling of the break and repair. It is becoming increasingly apparent that one key step in this process is chromatin remodelling. Results: Here we describe the chromodomain helicase DNA-binding protein (CHD4) as a target of ATM kinase. We show that ionising radiation (IR)-induced phosphorylation of CHD4 affects its intranuclear organization resulting in increased chromatin binding/retention. We also show assembly of phosphorylated CHD4 foci at sites of DNA damage, which might be required to fulfil its function in the regulation of DNA repair. Consistent with this, cells overexpressing a phospho-mutant version of CHD4 that cannot be phosphorylated by ATM fail to show enhanced chromatin retention after DSBs and display high rates of spontaneous damage. Conclusion: These results provide insight into how CHD4 phosphorylation might be required to remodel chromatin around DNA breaks allowing efficient DNA repair to occur.

INT6/EIF3E interacts with ATM and is required for proper execution of the DNA damage response in human cells

Altered expression of the INT6 gene, encoding the e subunit of the translational initiation factor eIF3, occurs in human breast cancers, but how INT6 relates to carcinogenesis remains unestablished. Here, we show that INT6 is involved in the DNA damage response. INT6 was required for cell survival following γ-irradiation and G(2)-M checkpoint control. RNA interference-mediated silencing of INT6 reduced phosphorylation of the checkpoint kinases CHK1 and CHK2 after DNA damage. In addition, INT6 silencing prevented sustained accumulation of ataxia telangiectasia mutated (ATM) at DNA damage sites in cells treated with γ-radiation or the radiomimetic drug neocarzinostatin. Mechanistically, this result could be explained by interaction of INT6 with ATM, which together with INT6 was recruited to the sites of DNA damage. Finally, INT6 silencing also reduced ubiquitylation events that promote retention of repair proteins at DNA lesions. Accordingly, accumulation of the repair factor BRCA1 was defective in the absence of INT6. Our findings reveal unexpected and striking connections of INT6 with ATM and BRCA1 and suggest that the protective action of INT6 in the onset of breast cancers relies on its involvement in the DNA damage response.

ATM is required for the cellular response to thymidine induced replication fork stress

Genetically distinct checkpoints, activated as a consequence of either DNA replication arrest or ionizing radiation-induced DNA damage, integrate DNA repair responses into the cell cycle programme. The ataxia-telangiectasia mutated (ATM) protein kinase blocks cell cycle progression in response to DNA double strand breaks, whereas the related ATR is important in maintaining the integrity of the DNA replication apparatus. Here, we show that thymidine, which slows the progression of replication forks by depleting cellular pools of dCTP, induces a novel DNA damage response that, uniquely, depends on both ATM and ATR. Thymidine induces ATM-mediated phosphorylation of Chk2 and NBS1 and an ATM-independent phosphorylation of Chk1 and SMC1. AT cells exposed to thymidine showed decreased viability and failed to induce homologous recombination repair (HRR). Taken together, our results implicate ATM in the HRR-mediated rescue of replication forks impaired by thymidine treatment.

RPAS integration within an Australian ATM system : what equipment and which airspace

The Australian Civil Aviation Safety Authority (CASA) currently lists more than 100 separate entities or organisations which maintain a UAS Operator Certificate (UOC) [1]. Approved operations are overwhelmingly a permutation of aerial photography, surveillance, survey or spotting and predominantly, are restricted to Visual Line of Sight (VLOS) operations, below 400 feet, and not within 3 NM of an aerodrome. However, demand is increasing for a Remote Piloted Aerial System (RPAS) regulatory regime which facilitates more expansive operations, in particular unsegregated, Beyond Visual Line of Sight (BVLOS) operations. Despite this demand, there is national and international apprehension regarding the necessary levels of airworthiness and operational regulation required to maintain safety and minimise the risk associated with unsegregated operations. Fundamental to addressing these legitimate concerns will be the mechanisms that underpin safe separation and collision avoidance. Whilst a large body of research has been dedicated to investigating on-board, Sense and Avoid (SAA) technology necessary to meet this challenge, this paper focuses on the contribution of the NAS to separation assurance, and how it will support, as well as complicate RPAS integration. The paper collates and presents key, but historically disparate, threads of Australian RPAS and NAS related information, and distils it with a filter focused on minimising RPAS collision risk. Our ongoing effort is motivated by the need to better understand the separation assurance contribution provided by the NAS layers, in the first instance, and subsequently employ this information to identify scenarios where the coincident collision risk is demonstrably low, providing legitimate substantiation for concessions on equipage and airworthiness standards.

Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes

Metformin is the most commonly used pharmacological therapy for type 2 diabetes. We report a genome-wide association study for glycemic response to metformin in 1,024 Scottish individuals with type 2 diabetes with replication in two cohorts including 1,783 Scottish individuals and 1,113 individuals from the UK Prospective Diabetes Study. In a combined meta-analysis, we identified a SNP, rs11212617, associated with treatment success (n = 3,920, P = 2.9 P×-9, odds ratio = 1.35, 95% CI 1.22-1.49) at a locus containing ATM, the ataxia telangiectasia mutated gene. In a rat hepatoma cell line, inhibition of ATM with KU-55933 attenuated the phosphorylation and activation of AMP-activated protein kinase in response to metformin. We conclude that ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to metformin. © 2011 Nature America, Inc. All rights reserved.

Dominant negative ATM mutations in breast cancer families

BACKGROUND: The ATM gene encoding a putative protein kinase is mutated in ataxia-telangiectasia (A-T), an autosomal recessive disorder with a predisposition for cancer. Studies of A-T families suggest that female heterozygotes have an increased risk of breast cancer compared with noncarriers. However, neither linkage analyses nor mutation studies have provided supporting evidence for a role of ATM in breast cancer predisposition. Nevertheless, two recurrent ATM mutations, T7271G and IVS10-6T-->G, reportedly increase the risk of breast cancer. We examined these two ATM mutations in a population-based, case-control series of breast cancer families and multiple-case breast cancer families. METHODS: Five hundred twenty-five or 262 case patients with breast cancer and 381 or 68 control subjects, respectively, were genotyped for the T7271G and IVS10-6T-->G ATM mutations, as were index patients from 76 non-BRCA1/2 multiple-case breast cancer families. Linkage and penetrance were analyzed. ATM protein expression and kinase activity were analyzed in lymphoblastoid cell lines from mutation carriers. All statistical tests were two-sided. RESULTS: In case and control subjects unselected for family history of breast cancer, one case patient had the T7271G mutation, and none had the IVS10-6T-->G mutation. In three multiple-case families, one of these two mutations segregated with breast cancer. The estimated average penetrance of the mutations was 60% (95% confidence interval [CI] = 32% to 90%) to age 70 years, equivalent to a 15.7-fold (95% CI = 6.4-fold to 38.0-fold) increased relative risk compared with that of the general population. Expression and activity analyses of ATM in heterozygous cell lines indicated that both mutations are dominant negative. CONCLUSION: At least two ATM mutations are associated with a sufficiently high risk of breast cancer to be found in multiple-case breast cancer families. Full mutation analysis of the ATM gene in such families could help clarify the role of ATM in breast cancer susceptibility.

Customer satisfaction survey of the facilities provided by office building “X” in Surabaya

Many high-rise office buildings have been built in Surabaya. The investors have provided complimentary facilities to satisfy their tenants. However, not all given facilities has satisfied the tenants. The purpose of this study is to find out the level of tenant satisfaction in office “X” to the existing facilities and to suggest additional required facilities. Although office “X” is offered the highest rental rate and has known as a prestigious place in Surabaya, only location and public transport have satisfied the Indonesian tenants. Meanwhile, the multi National companies have not satisfied for any existing facilities. Additional ATM facilities and presentable cafeteria, improvement of service and the security system are required by tenants.

A ∑GIi/D/1/∞ queue with heterogeneous input/output slot times

In this paper, we present a ∑GIi/D/1/∞ queue with heterogeneous input/output slot times. This queueing model can be regarded as an extension of the ordinary GI/D/1/∞ model. For this ∑GIi/D/1/∞ queue, we assume that several input streams arrive at the system according to different slot times. In other words, there are different slot times for different input/output processes in the queueing model. The queueing model can therefore be used for an ATM multiplexer with heterogeneous input/output link capacities. Several cases of the queueing model are discussed to reflect different relationships among the input/output link capacities of an ATM multiplexer. In the queueing analysis, two approaches: the Markov model and the probability generating function technique, are adopted to develop the queue length distributions observed at different epochs. This model is particularly useful in the performance analysis of ATM multiplexers with heterogeneous input/output link capacities.