Hardware software co-design of the Aho-Corasick algorithm: Scalable for protein identification?

Pattern matching is commonly required in many application areas and bioinformatics is a major area of interest that requires both exact and approximate pattern matching. Much work has been done in this area, yet there is still a significant space for improvement in efficiency, flexibility, and throughput. This paper presents a hardware software co-design of Aho-Corasick algorithm in Nios II soft-processor and a study on its scalability for a pattern matching application. A software only approach is used to compare the throughput and the scalability of the hardware software co-design approach. According to the results we obtained, we conclude that the hardware software co-design implementation shows a maximum of 10 times speed up for pattern size of 1200 peptides compared to the software only implementation. The results also show that the hardware software co-design approach scales well for increasing data size compared to the software only approach

Hardware accelerated protein inference framework

Protein inference plays a vital role in the proteomics study. Two major approaches could be used to handle the problem of protein inference; top-down and bottom-up. This paper presents a framework for protein inference, which uses hardware accelerated protein inference framework for handling the most important step in a bottom-up approach, viz. peptide identification during the assembling process. In our framework, identified peptides and their probabilities are used to predict the most suitable reference protein cluster for a given input amino acid sequence with the probability of identified peptides. The framework is developed on an FPGA where hardware software co-design techniques are used to accelerate the computationally intensive parts of the protein inference process. In the paper we have measured, compared and reported the time taken for the protein inference process in our framework against a pure software implementation

Genetic polymorphisms associated with antimalarial antibody levels in a low and unstable malaria transmission area in southern Sri Lanka.

ABSTRACT: BACKGROUND: The incidence of malaria in Sri Lanka has significantly declined in recent years. Similar trends were seen in Kataragama, a known malaria endemic location within the southern province of the country, over the past five years. This is a descriptive study of anti-malarial antibody levels and selected host genetic mutations in residents of Kataragama, under low malaria transmission conditions. METHODS: Sera were collected from 1,011 individuals residing in Kataragama and anti-malarial antibodies and total IgE levels were measured by a standardized ELISA technique. Host DNA was extracted and used for genotyping of selected SNPs in known genes associated with malaria. The antibody levels were analysed in relation to the past history of malaria (during past 10 years), age, sex, the location of residence within Kataragama and selected host genetic markers. RESULTS: A significant increase in antibodies against Plasmodium falciparum antigens AMA1, MSP2, NANP and Plasmodium vivax antigen MSP1 in individuals with past history of malaria were observed when compared to those who did not. A marked increase of anti-MSP1(Pf) and anti-AMA1(Pv) was also evident in individuals between 45-59 years (when compared to other age groups). Allele frequencies for two SNPs in genes that code for IL-13 and TRIM-5 were found to be significantly different between those who have experienced one or more malaria attacks within past 10 years and those who did not. When antibody levels were classified into a low-high binary trait, significant associations were found with four SNPs for anti-AMA1(Pf); two SNPs for anti-MSP1(Pf); eight SNPs for anti-NANP(Pf); three SNPs for anti-AMA1(Pv); seven SNPs for anti-MSP1(Pv); and nine SNPs for total IgE. Eleven of these SNPs with significant associations with anti-malarial antibody levels were found to be non- synonymous. CONCLUSIONS: Evidence is suggestive of an age-acquired immunity in this study population in spite of low malaria transmission levels. Several SNPs were in linkage disequilibrium and had a significant association with elevated antibody levels, suggesting that these host genetic mutations might have an individual or collective effect on inducing or/and maintaining high anti-malarial antibody levels