Parallel FFT on ATM‐based networks of workstations

We consider parallel computing on a network of workstations using a connection-oriented protocol (e.g., Asynchronous Transfer Mode) for data communication. In a connection-oriented protocol, a virtual circuit of guaranteed bandwidth is established for each pair of communicating workstations. Since all virtual circuits do not have the same guaranteed bandwidth, a parallel application must deal with the unequal bandwidths between workstations. Since most works in the design of parallel algorithms assume equal bandwidths on all the communication links, they often do not perform well when executed on networks of workstations using connection-oriented protocols. In this paper, we first evaluate the performance degradation caused by unequal bandwidths on the execution of conventional parallel algorithms such as the fast Fourier transform and bitonic sort. We then present a strategy based on dynamic redistribution of data points to reduce the bottlenecks caused by unequal bandwidths. We also extend this strategy to deal with processor heterogeneity. Using analysis and simulation we show that there is a considerable reduction in the runtime if the proposed redistribution strategy is adopted. The basic idea presented in this paper can also be used to improve the runtimes of other parallel applications in connection-oriented environments. This revised version was published online in July 2006 with corrections to the Cover Date.     

Multicast scheduling algorithms in mobile networks

We consider the problem of multicasting data to mobile users in a cellular mobile network. In the absence of mobility, a single channel can be used to multicast to all mobile users within a cell. However, mobility combined with the effects of fading necessitates a more complex channel allocation policy. In this paper we develop theoretical bounds on the maximum obtainable efficiency and present algorithms that acheive this bound. Our results hold for the case when mobiles travel on a highway, as well as for the more general case where mobiles roam in a two-dimensional region. This revised version was published online in August 2006 with corrections to the Cover Date.     

A direct antigen-binding assay to screen hybridoma supernatants

A simple and convenient method of directly assaying hybridoma supernatants for the desired monoclonal antibodies is described which obviates the need for labeled second or third antibody conjugates. Culture supernatants (1-5 microliters) were directly spotted onto a nitrocellulose sheet, and additional protein binding sites blocked with bovine serum albumin and incubated with enzyme-labeled, radioactive, or fluorescent antigen. Positive hybridoma supernatants were identified after washing and detection of bound antigen by appropriate means.     

Mitochondrial epigenetics in bone remodeling during hyperhomocysteinemia

The studies into the pathophysiology of viral miRNAs are still in infancy; the interspecies regulation at the miRNA level fuels the spark of the investigation into the repertoire of virus–host interactions. Reports pertaining to the viral miRNAs role in modulating/evading the host immune response are surging up; we initiated this in silico study to speculate the role of human cytomegalovirus (HCMV)-encoded miRNAs on human antiviral mechanisms such as apoptosis and autophagy. The results indicate that both the above mechanisms were targeted by the HCMV miRNAs, located in the unique long region of the HCMV genome. The proapoptotic genes MOAP1, PHAP, and ERN1 are identified to be the potential targets for the miR-UL70-3p and UL148D, respectively. The ERN1 gene plays a role in the initiation of Endoplasmic reticulum stress-induced apoptosis as well as autophagosome formation. This study shows that HCMV employs its miRNA repertoire for countering the cellular apoptosis and autophagy, particularly the mitochondrial-dependent intrinsic pathway of apoptosis. In addition, the homology studies reveal no HCMV miRNA bears sequence homology with human miRNAs.     

Three-dimensional (3D) structure prediction of the American and African oil-palms β-ketoacyl-[ACP] synthase-II protein by comparative modelling

Background: The fatty-acid profile of the vegetable oils determines its properties and nutritional value. Palm-oil obtained from the African oil-palm [Elaeis guineensis Jacq. (Tenera)] contains 44% palmitic acid (C_16:0), but, palm-oil obtained from the American oilpalm [Elaeis oleifera] contains only 25% C16:0. In part, the b-ketoacyl-[ACP] synthase II (KASII) [EC: 2.3.1.179] protein is responsible for the high level of C_16:0 in palm-oil derived from the African oil-palm. To understand more about E. guineensis KASII (EgKASII) and E. oleifera KASII (EoKASII) proteins, it is essential to know its structures. Hence, this study was undertaken. Objective: The objective of this study was to predict three-dimensional (3D) structure of EgKASII and EoKASII proteins using molecular modelling tools. Materials and Methods: The amino-acid sequences for KASII proteins were retrieved from the protein database of National Center for Biotechnology Information (NCBI), USA. The 3D structures were predicted for both proteins using homology modelling and ab-initio technique approach of protein structure prediction. The molecular dynamics (MD) simulation was performed to refine the predicted structures. The predicted structure models were evaluated and root mean square deviation (RMSD) and root mean square fluctuation (RMSF) values were calculated. Results: The homology modelling showed that EgKASII and EoKASII proteins are 78% and 74% similar with Streptococcus pneumonia KASII and Brucella melitensis KASII, respectively. The EgKASII and EoKASII structures predicted by using ab-initio technique approach shows 6% and 9% deviation to its structures predicted by homology modelling, respectively. The structure refinement and validation confirmed that the predicted structures are accurate. Conclusion: The 3D structures for EgKASII and EoKASII proteins were predicted. However, further research is essential to understand the interaction of EgKASII and EoKASII proteins with its substrates.