@article {49668, title = {The fruRBA operon is necessary for Group A Streptococcal growth in fructose and for resistance to neutrophil killing during growth in whole human blood.}, journal = {Infect Immun}, year = {2016}, month = {2016 Jan 19}, abstract = {

Bacterial pathogens rely on the availability of nutrients for survival in the host environment. The phosphoenolpyruvate-phosphotransferase system (PTS) is a global regulatory network connecting sugar uptake with signal transduction. Since the fructose PTS has been shown to impact virulence in several Streptococci, including the human pathogen S. pyogenes (the group A Streptococcus, GAS), we characterized its role in carbon metabolism and pathogenesis in the M1T1 strain 5448. Growth in fructose as a sole carbon source resulted in 103 genes affected transcriptionally, where the fru locus (fruRBA) was the most induced. RT-PCR showed that fruRBA formed an operon, which was repressed by FruR in the absence of fructose, in addition to being under carbon catabolic repression. Growth assays and carbon utilization profiles revealed that although the entire fru operon was required for growth in fructose, FruA was the main transporter for fructose and was also involved in the utilization of three additional PTS sugars: cellobiose, mannitol, and N-acetyl-D-galactosamine. Inactivation of sloR, a fruA homolog that was also up regulated in presence of fructose, failed to reveal a role as a secondary fructose transporter. Whereas the ability of both ΔfruR and ΔfruB mutants to survive in the presence of whole human blood or neutrophils was impaired, the phenotype was not reproduced in murine whole blood, nor were those mutants attenuated in a mouse intraperitoneal infection. Since the ΔfruA mutant exhibited no phenotype in the human or mouse assays, we propose that FruR and FruB are important for GAS survival in a human-specific environment.

}, issn = {1098-5522}, doi = {10.1128/IAI.01296-15}, author = {Valdes, Kayla M and Sundar, Ganesh S and Vega, Luis A and Belew, Ashton T and Islam, Emrul and Binet, Rachel and El-Sayed, Najib M and Le Breton, Yoann and McIver, Kevin S} } @article {49657, title = {Genome-scale study reveals reduced metabolic adaptability in patients with non-alcoholic fatty liver disease}, journal = {Nature Communications}, volume = {7}, year = {2016}, month = {Mar-02-2016}, pages = {8994}, doi = {10.1038/ncomms9994}, url = {http://www.nature.com/doifinder/10.1038/ncomms9994}, author = {{\"o}tyl{\"a}inen, Tuulia and Jerby, Livnat and {\"a}j{\"a}, Elina M. and Mattila, Ismo and {\"a}ntti, Sirkku and Auvinen, Petri and Gastaldelli, Amalia and {\"a}rvinen, Hannele and Ruppin, Eytan and {\v s}i{\v c}, Matej} } @article {49795, title = {The fruRBA Operon Is Necessary for Group A Streptococcal Growth in Fructose and for Resistance to Neutrophil Killing during Growth in Whole Human Blood}, journal = {Infection and Immunity}, volume = {84}, year = {2016}, month = {Dec-04-2017}, pages = {1016 - 1031}, issn = {0019-9567}, doi = {10.1128/IAI.01296-15}, url = {http://iai.asm.org/lookup/doi/10.1128/IAI.01296-15}, author = {Valdes, Kayla M. and Sundar, Ganesh S. and Vega, Luis A. and Belew, Ashton T. and Islam, Emrul and Binet, Rachel and El-Sayed, Najib M. and Le Breton, Yoann and McIver, Kevin S.}, editor = {Camilli, A.} } @booklet {49615, title = {Algorithms in Bioinformatics: 15th International Workshop, WABI 2015}, howpublished = {Lecture Notes in Bioinformatics}, number = {9289}, year = {2015}, month = {September 2015}, pages = {328}, publisher = {Springer}, isbn = {978-3-662-48220-9}, author = {Pop, Mihai and Touzet, H{\'e}l{\`e}ne}, editor = {Istrail, Sorin and Pevzner, Pavel and Waterman, Michael S} } @article {49658, title = {Diversion of aspartate in ASS1-deficient tumours fosters de novo pyrimidine synthesis}, journal = {Nature}, volume = {527}, year = {2015}, month = {Nov-11-2015}, pages = {379 - 383}, issn = {0028-0836}, doi = {10.1038/nature15529}, url = {http://www.nature.com/doifinder/10.1038/nature15529}, author = {Rabinovich, Shiran and Adler, Lital and Yizhak, Keren and Sarver, Alona and Silberman, Alon and Agron, Shani and Stettner, Noa and Sun, Qin and Brandis, Alexander and Helbling, Daniel and Korman, Stanley and Itzkovitz, Shalev and Dimmock, David and Ulitsky, Igor and Nagamani, Sandesh C. S. and Ruppin, Eytan and Erez, Ayelet} } @article {49537, title = {Essential Genes in the Core Genome of the Human Pathogen Streptococcus pyogenes.}, journal = {Sci Rep}, volume = {5}, year = {2015}, month = {2015}, pages = {9838}, abstract = {

Streptococcus pyogenes (Group A Streptococcus, GAS) remains a major public health burden worldwide, infecting over 750 million people leading to over 500,000 deaths annually. GAS pathogenesis is complex, involving genetically distinct GAS strains and multiple infection sites. To overcome fastidious genetic manipulations and accelerate pathogenesis investigations in GAS, we developed a mariner-based system (Krmit) for en masse monitoring of complex mutant pools by transposon sequencing (Tn-seq). Highly saturated transposant libraries (Krmit insertions in ca. every 25 nucleotides) were generated in two distinct GAS clinical isolates, a serotype M1T1 invasive strain 5448 and a nephritogenic serotype M49 strain NZ131, and analyzed using a Bayesian statistical model to predict GAS essential genes, identifying sets of 227 and 241 of those genes in 5448 and NZ131, respectively. A large proportion of GAS essential genes corresponded to key cellular processes and metabolic pathways, and 177 were found conserved within the GAS core genome established from 20 available GAS genomes. Selected essential genes were validated using conditional-expression mutants. Finally, comparison to previous essentiality analyses in S. sanguinis and S. pneumoniae revealed significant overlaps, providing valuable insights for the development of new antimicrobials to treat infections by GAS and other pathogenic streptococci.

}, issn = {2045-2322}, doi = {10.1038/srep09838}, author = {Le Breton, Yoann and Belew, Ashton T and Valdes, Kayla M and Islam, Emrul and Curry, Patrick and Tettelin, Herv{\'e} and Shirtliff, Mark E and El-Sayed, Najib M and McIver, Kevin S} } @article {49574, title = {Evolutionary Conservation of Bacterial Essential Metabolic Genes across All Bacterial Culture Media}, volume = {10}, year = {2015}, month = {Aug-04-2016}, pages = {e0123785}, doi = {10.1371/journal.pone.0123785}, url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0123785}, author = {Ish-Am, Oren and Kristensen, David M. and Ruppin, Eytan}, editor = {Thangaraj, Kumarasamy} } @article {49512, title = {Independent Emergence of Artemisinin Resistance Mutations Among Plasmodium falciparum in Southeast Asia}, journal = {Journal of Infectious Diseases}, volume = {211}, year = {2015}, month = {03/2015}, pages = {670 - 679}, issn = {1537-6613}, doi = {10.1093/infdis/jiu491}, author = {Takala-Harrison, S. and Jacob, C. G. and Arze, C. and Michael P. Cummings and Silva, J. C. and Dondorp, A. M. and Fukuda, M. M. and Hien, T. T. and Mayxay, M. and Noedl, H. and Nosten, F. and Kyaw, M. P. and Nhien, N. T. T. and Imwong, M. and Bethell, D. and Se, Y. and Lon, C. and Tyner, S. D. and Saunders, D. L. and Ariey, F. and Mercereau-Puijalon, O. and Menard, D. and Newton, P. N. and Khanthavong, M. and Hongvanthong, B. and Starzengruber, P. and Fuehrer, H.-P. and Swoboda, P. and Khan, W. A. and Phyo, A. P. and Nyunt, M. M. and Nyunt, M. H. and Brown, T. S. and Adams, M. and Pepin, C. S. and Bailey, J. and Tan, J. C. and Ferdig, M. T. and Clark, T. G. and Miotto, O. and MacInnis, B. and Kwiatkowski, D. P. and White, N. J. and Ringwald, P. and Plowe, CV} } @article {49612, title = {Microbiota that affect risk for shigellosis in children in low-income countries}, journal = {Emerg Infect DisEmerg Infect Dis}, volume = {21}, number = {2}, year = {2015}, note = {Lindsay, Brianna
Oundo, Joe
Hossain, M Anowar
Antonio, Martin
Tamboura, Boubou
Walker, Alan W
Paulson, Joseph N
Parkhill, Julian
Omore, Richard
Faruque, Abu S G
Das, Suman Kumar
Ikumapayi, Usman N
Adeyemi, Mitchell
Sanogo, Doh
Saha, Debasish
Sow, Samba
Farag, Tamer H
Nasrin, Dilruba
Li, Shan
Panchalingam, Sandra
Levine, Myron M
Kotloff, Karen
Magder, Laurence S
Hungerford, Laura
Sommerfelt, Halvor
Pop, Mihai
Nataro, James P
Stine, O Colin
U19 090873/PHS HHS/United States
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov{\textquoteright}t
Research Support, U.S. Gov{\textquoteright}t, Non-P.H.S.
United States
Emerg Infect Dis. 2015 Feb;21(2):242-50. doi: 10.3201/eid2101.140795.}, month = {Feb}, pages = {242-50}, edition = {2015/01/28}, abstract = {Pathogens in the gastrointestinal tract exist within a vast population of microbes. We examined associations between pathogens and composition of gut microbiota as they relate to Shigella spp./enteroinvasive Escherichia coli infection. We analyzed 3,035 stool specimens (1,735 nondiarrheal and 1,300 moderate-to-severe diarrheal) from the Global Enteric Multicenter Study for 9 enteropathogens. Diarrheal specimens had a higher number of enteropathogens (diarrheal mean 1.4, nondiarrheal mean 0.95; p<0.0001). Rotavirus showed a negative association with Shigella spp. in cases of diarrhea (odds ratio 0.31, 95\% CI 0.17-0.55) and had a large combined effect on moderate-to-severe diarrhea (odds ratio 29, 95\% CI 3.8-220). In 4 Lactobacillus taxa identified by 16S rRNA gene sequencing, the association between pathogen and disease was decreased, which is consistent with the possibility that Lactobacillus spp. are protective against Shigella spp.-induced diarrhea. Bacterial diversity of gut microbiota was associated with diarrhea status, not high levels of the Shigella spp. ipaH gene.}, isbn = {1080-6059 (Electronic)
1080-6040 (Linking)}, author = {Lindsay, B. and Oundo, J. and Hossain, M. A. and Antonio, M. and Tamboura, B. and Walker, A. W. and Paulson, J. N. and Parkhill, J. and Omore, R. and Faruque, A. S. and Das, S. K. and Ikumapayi, U. N. and Adeyemi, M. and Sanogo, D. and Saha, D. and Sow, S. and Farag, T. H. and Nasrin, D. and Li, S. and Panchalingam, S. and Levine, M. M. and Kotloff, K. and Magder, L. S. and Hungerford, L. and Sommerfelt, H. and Pop, M. and Nataro, J. P. and Stine, O. C.} } @article {49606, title = {Orchestrating high-throughput genomic analysis with Bioconductor.}, volume = {12}, year = {2015}, month = {2015 Feb}, pages = {115-21}, abstract = {

Bioconductor is an open-source, open-development software project for the analysis and comprehension of high-throughput data in genomics and molecular biology. The project aims to enable interdisciplinary research, collaboration and rapid development of scientific software. Based on the statistical programming language R, Bioconductor comprises 934 interoperable packages contributed by a large, diverse community of scientists. Packages cover a range of bioinformatic and statistical applications. They undergo formal initial review and continuous automated testing. We present an overview for prospective users and contributors.

}, keywords = {Computational Biology, Gene Expression Profiling, Genomics, High-Throughput Screening Assays, Programming Languages, software, User-Computer Interface}, issn = {1548-7105}, doi = {10.1038/nmeth.3252}, author = {Huber, Wolfgang and Carey, Vincent J and Gentleman, Robert and Anders, Simon and Carlson, Marc and Carvalho, Benilton S and Bravo, H{\'e}ctor Corrada and Davis, Sean and Gatto, Laurent and Girke, Thomas and Gottardo, Raphael and Hahne, Florian and Hansen, Kasper D and Irizarry, Rafael A and Lawrence, Michael and Love, Michael I and MacDonald, James and Obenchain, Valerie and Ole{\'s}, Andrzej K and Pag{\`e}s, Herv{\'e} and Reyes, Alejandro and Shannon, Paul and Smyth, Gordon K and Tenenbaum, Dan and Waldron, Levi and Morgan, Martin} } @article {49611, title = {Construction of a dairy microbial genome catalog opens new perspectives for the metagenomic analysis of dairy fermented products}, journal = {BMC GenomicsBMC Genomics}, volume = {15}, number = {1}, year = {2014}, pages = {1101}, abstract = {BACKGROUND:Microbial communities of traditional cheeses are complex and insufficiently characterized. The origin, safety and functional role in cheese making of these microbial communities are still not well understood. Metagenomic analysis of these communities by high throughput shotgun sequencing is a promising approach to characterize their genomic and functional profiles. Such analyses, however, critically depend on the availability of appropriate reference genome databases against which the sequencing reads can be aligned.RESULTS:We built a reference genome catalog suitable for short read metagenomic analysis using a low-cost sequencing strategy. We selected 142 bacteria isolated from dairy products belonging to 137 different species and 67 genera, and succeeded to reconstruct the draft genome of 117 of them at a standard or high quality level, including isolates from the genera Kluyvera, Luteococcus and Marinilactibacillus, still missing from public database. To demonstrate the potential of this catalog, we analysed the microbial composition of the surface of two smear cheeses and one blue-veined cheese, and showed that a significant part of the microbiota of these traditional cheeses was composed of microorganisms newly sequenced in our study.CONCLUSIONS:Our study provides data, which combined with publicly available genome references, represents the most expansive catalog to date of cheese-associated bacteria. Using this extended dairy catalog, we revealed the presence in traditional cheese of dominant microorganisms not deliberately inoculated, mainly Gram-negative genera such as Pseudoalteromonas haloplanktis or Psychrobacter immobilis, that may contribute to the characteristics of cheese produced through traditional methods.}, isbn = {1471-2164}, author = {Almeida, Mathieu and Hebert, Agnes and Abraham, Anne-Laure and Rasmussen, Simon and Monnet, Christophe and Pons, Nicolas and Delbes, Celine and Loux, Valentin and Batto, Jean-Michel and Leonard, Pierre and Kennedy, Sean and Ehrlich, Stanislas and Pop, Mihai and Montel, Marie-Christine and Irlinger, Francoise and Renault, Pierre} } @article {49600, title = {Diarrhea in young children from low-income countries leads to large-scale alterations in intestinal microbiota composition.}, volume = {15}, year = {2014}, month = {2014}, pages = {R76}, abstract = {

BACKGROUND: Diarrheal diseases continue to contribute significantly to morbidity and mortality in infants and young children in developing countries. There is an urgent need to better understand the contributions of novel, potentially uncultured, diarrheal pathogens to severe diarrheal disease, as well as distortions in normal gut microbiota composition that might facilitate severe disease.

RESULTS: We use high throughput 16S rRNA gene sequencing to compare fecal microbiota composition in children under five years of age who have been diagnosed with moderate to severe diarrhea (MSD) with the microbiota from diarrhea-free controls. Our study includes 992 children from four low-income countries in West and East Africa, and Southeast Asia. Known pathogens, as well as bacteria currently not considered as important diarrhea-causing pathogens, are positively associated with MSD, and these include Escherichia/Shigella, and Granulicatella species, and Streptococcus mitis/pneumoniae groups. In both cases and controls, there tend to be distinct negative correlations between facultative anaerobic lineages and obligate anaerobic lineages. Overall genus-level microbiota composition exhibit a shift in controls from low to high levels of Prevotella and in MSD cases from high to low levels of Escherichia/Shigella in younger versus older children; however, there was significant variation among many genera by both site and age.

CONCLUSIONS: Our findings expand the current understanding of microbiota-associated diarrhea pathogenicity in young children from developing countries. Our findings are necessarily based on correlative analyses and must be further validated through epidemiological and molecular techniques.

}, keywords = {Bangladesh, Base Sequence, Case-Control Studies, Child, Preschool, Diarrhea, Infantile, Dysentery, Feces, Female, Gambia, HUMANS, Infant, Infant, Newborn, Intestines, Kenya, Male, Mali, Microbiota, Molecular Typing, Poverty, RNA, Bacterial, RNA, Ribosomal, 16S}, issn = {1474-760X}, doi = {10.1186/gb-2014-15-6-r76}, author = {Pop, Mihai and Walker, Alan W and Paulson, Joseph and Lindsay, Brianna and Antonio, Martin and Hossain, M Anowar and Oundo, Joseph and Tamboura, Boubou and Mai, Volker and Astrovskaya, Irina and Corrada Bravo, Hector and Rance, Richard and Stares, Mark and Levine, Myron M and Panchalingam, Sandra and Kotloff, Karen and Ikumapayi, Usman N and Ebruke, Chinelo and Adeyemi, Mitchell and Ahmed, Dilruba and Ahmed, Firoz and Alam, Meer Taifur and Amin, Ruhul and Siddiqui, Sabbir and Ochieng, John B and Ouma, Emmanuel and Juma, Jane and Mailu, Euince and Omore, Richard and Morris, J Glenn and Breiman, Robert F and Saha, Debasish and Parkhill, Julian and Nataro, James P and Stine, O Colin} } @article {49604, title = {Large hypomethylated blocks as a universal defining epigenetic alteration in human solid tumors.}, volume = {6}, year = {2014}, month = {2014}, pages = {61}, abstract = {

BACKGROUND: One of the most provocative recent observations in cancer epigenetics is the discovery of large hypomethylated blocks, including single copy genes, in colorectal cancer, that correspond in location to heterochromatic LOCKs (large organized chromatin lysine-modifications) and LADs (lamin-associated domains).

METHODS: Here we performed a comprehensive genome-scale analysis of 10 breast, 28 colon, nine lung, 38 thyroid, 18 pancreas cancers, and five pancreas neuroendocrine tumors as well as matched normal tissue from most of these cases, as well as 51 premalignant lesions. We used a new statistical approach that allows the identification of large hypomethylated blocks on the Illumina HumanMethylation450 BeadChip platform.

RESULTS: We find that hypomethylated blocks are a universal feature of common solid human cancer, and that they occur at the earliest stage of premalignant tumors and progress through clinical stages of thyroid and colon cancer development. We also find that the disrupted CpG islands widely reported previously, including hypermethylated island bodies and hypomethylated shores, are enriched in hypomethylated blocks, with flattening of the methylation signal within and flanking the islands. Finally, we found that genes showing higher between individual gene expression variability are enriched within these hypomethylated blocks.

CONCLUSION: Thus hypomethylated blocks appear to be a universal defining epigenetic alteration in human cancer, at least for common solid tumors.

}, issn = {1756-994X}, doi = {10.1186/s13073-014-0061-y}, author = {Timp, Winston and Bravo, H{\'e}ctor Corrada and McDonald, Oliver G and Goggins, Michael and Umbricht, Chris and Zeiger, Martha and Feinberg, Andrew P and Irizarry, Rafael A} } @article {49605, title = {Minfi: a flexible and comprehensive Bioconductor package for the analysis of Infinium DNA methylation microarrays.}, volume = {30}, year = {2014}, month = {2014 May 15}, pages = {1363-9}, abstract = {

MOTIVATION: The recently released Infinium HumanMethylation450 array (the {\textquoteright}450k{\textquoteright} array) provides a high-throughput assay to quantify DNA methylation (DNAm) at \~{}450 000 loci across a range of genomic features. Although less comprehensive than high-throughput sequencing-based techniques, this product is more cost-effective and promises to be the most widely used DNAm high-throughput measurement technology over the next several years.

RESULTS: Here we describe a suite of computational tools that incorporate state-of-the-art statistical techniques for the analysis of DNAm data. The software is structured to easily adapt to future versions of the technology. We include methods for preprocessing, quality assessment and detection of differentially methylated regions from the kilobase to the megabase scale. We show how our software provides a powerful and flexible development platform for future methods. We also illustrate how our methods empower the technology to make discoveries previously thought to be possible only with sequencing-based methods.

AVAILABILITY AND IMPLEMENTATION: http://bioconductor.org/packages/release/bioc/html/minfi.html.

CONTACT: khansen@jhsph.edu; rafa@jimmy.harvard.edu

SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

}, keywords = {Aged, algorithms, Colonic Neoplasms, DNA Methylation, Genome, High-Throughput Nucleotide Sequencing, HUMANS, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, software}, issn = {1367-4811}, doi = {10.1093/bioinformatics/btu049}, author = {Aryee, Martin J and Jaffe, Andrew E and Corrada-Bravo, Hector and Ladd-Acosta, Christine and Feinberg, Andrew P and Hansen, Kasper D and Irizarry, Rafael A} } @article {38284, title = {Genetic loci associated with delayed clearance of Plasmodium falciparum following artemisinin treatment in Southeast Asia}, journal = {Proceedings of the National Academy of Sciences of the United States of AmericaProceedings of the National Academy of Sciences of the United States of America}, volume = {110}, year = {2013}, type = {10.1073/pnas.1211205110}, abstract = {The recent emergence of artemisinin-resistant Plasmodium falciparum malaria in western Cambodia could threaten prospects for malaria elimination. Identification of the genetic basis of resistance would provide tools for molecular surveillance, aiding efforts to contain resistance. Clinical trials of artesunate efficacy were conducted in Bangladesh, in northwestern Thailand near the Myanmar border, and at two sites in western Cambodia. Parasites collected from trial participants were genotyped at 8,079 single nucleotide polymorphisms (SNPs) using a P. falciparum-specific SNP array. Parasite genotypes were examined for signatures of recent positive selection and association with parasite clearance phenotypes to identify regions of the genome associated with artemisinin resistance. Four SNPs on chromosomes 10 (one), 13 (two), and 14 (one) were significantly associated with delayed parasite clearance. The two SNPs on chromosome 13 are in a region of the genome that appears to be under strong recent positive selection in Cambodia. The SNPs on chromosomes 10 and 13 lie in or near genes involved in postreplication repair, a DNA damage-tolerance pathway. Replication and validation studies are needed to refine the location of loci responsible for artemisinin resistance and to understand the mechanism behind it; however, two SNPs on chromosomes 10 and 13 may be useful markers of delayed parasite clearance in surveillance for artemisinin resistance in Southeast Asia.}, author = {Takala-Harrison, Shannon and Clark, Taane G. and Jacob, Christopher G. and Michael P. Cummings and Miotto, Olivo and Dondorp, Arjen M. and Fukuda, Mark M. and Nosten, Francois and Noedl, Harald and Imwong, Mallika and Bethell, Delia and Se, Youry and Lon, Chanthap and Tyner, Stuart D. and Saunders, David L. and Socheat, Duong and Ariey, Frederic and Phyo, Aung Pyae and Starzengruber, Peter and Fuehrer, Hans-Peter and Swoboda, Paul and Stepniewska, Kasia and Flegg, Jennifer and Arze, Cesar and Cerqueira, Gustavo C. and Silva, Joana C. and Ricklefs, Stacy M. and Porcella, Stephen F. and Stephens, Robert M. and Adams, Matthew and Kenefic, Leo J. and Campino, Susana and Auburn, Sarah and Macinnis, Bronwyn and Kwiatkowski, Dominic P. and Su, Xin-Zhuan and White, Nicholas J. and Ringwald, Pascal and Plowe, Christopher V.} } @article {38455, title = {Quantitative PCR for Detection of Shigella Improves Ascertainment of Shigella Burden in Children with Moderate-to-Severe Diarrhea in Low-Income Countries}, journal = {Journal of Clinical MicrobiologyJournal of Clinical Microbiology}, volume = {51}, year = {2013}, publisher = {American Society for Microbiology}, isbn = {0095-1137}, author = {Lindsay, Brianna and Ochieng, John B. and Ikumapayi, Usman N. and Toure, Aliou and Ahmed, Dilruba and Li, Shan and Panchalingam, Sandra and Levine, Myron M. and Kotloff, Karen and Rasko, David A.} } @article {38509, title = {Somatic alterations contributing to metastasis of a castration-resistant prostate cancer}, journal = {Human mutationHuman mutation}, volume = {34}, year = {2013}, note = {http://www.ncbi.nlm.nih.gov/pubmed/23636849?dopt=Abstract}, type = {10.1002/humu.22346}, abstract = {Metastatic castration-resistant prostate cancer (mCRPC) is a lethal disease, and molecular markers that differentiate indolent from aggressive subtypes are needed. We sequenced the exomes of five metastatic tumors and healthy kidney tissue from an index case with mCRPC to identify lesions associated with disease progression and metastasis. An Ashkenazi Jewish (AJ) germline founder mutation, del185AG in BRCA1, was observed and AJ ancestry was confirmed. Sixty-two somatic variants altered proteins in tumors, including cancer-associated genes, TMPRSS2-ERG, PBRM1, and TET2. The majority (n = 53) of somatic variants were present in all metastases and only a subset (n = 31) was observed in the primary tumor. Integrating tumor next-generation sequencing and DNA copy number showed somatic loss of BRCA1 and TMPRSS2-ERG. We sequenced 19 genes with deleterious mutations in the index case in additional mCRPC samples and detected a frameshift, two somatic missense alterations, tumor loss of heterozygosity, and combinations of germline missense SNPs in TET2. In summary, genetic analysis of metastases from an index case permitted us to infer a chronology for the clonal spread of disease based on sequential accrual of somatic lesions. The role of TET2 in mCRPC deserves additional analysis and may define a subset of metastatic disease.}, author = {Nickerson, Michael L. and Im, Kate M. and Misner, Kevin J. and Tan, Wei and Lou, Hong and Gold, Bert and Wells, David W. and H{\'e}ctor Corrada Bravo and Fredrikson, Karin M. and Harkins, Timothy T. and Milos, Patrice and Zbar, Berton and Linehan, W. Marston and Yeager, Meredith and Andresson, Thorkell and Dean, Michael and Bova, G. Steven} } @article {38276, title = {Gene expression anti-profiles as a basis for accurate universal cancer signatures}, journal = {BMC bioinformaticsBMC Bioinformatics}, volume = {13}, year = {2012}, note = {http://www.ncbi.nlm.nih.gov/pubmed/23088656?dopt=Abstract}, type = {10.1186/1471-2105-13-272}, abstract = {BACKGROUND: Early screening for cancer is arguably one of the greatest public health advances over the last fifty years. However, many cancer screening tests are invasive (digital rectal exams), expensive (mammograms, imaging) or both (colonoscopies). This has spurred growing interest in developing genomic signatures that can be used for cancer diagnosis and prognosis. However, progress has been slowed by heterogeneity in cancer profiles and the lack of effective computational prediction tools for this type of data. RESULTS: We developed anti-profiles as a first step towards translating experimental findings suggesting that stochastic across-sample hyper-variability in the expression of specific genes is a stable and general property of cancer into predictive and diagnostic signatures. Using single-chip microarray normalization and quality assessment methods, we developed an anti-profile for colon cancer in tissue biopsy samples. To demonstrate the translational potential of our findings, we applied the signature developed in the tissue samples, without any further retraining or normalization, to screen patients for colon cancer based on genomic measurements from peripheral blood in an independent study (AUC of 0.89). This method achieved higher accuracy than the signature underlying commercially available peripheral blood screening tests for colon cancer (AUC of 0.81). We also confirmed the existence of hyper-variable genes across a range of cancer types and found that a significant proportion of tissue-specific genes are hyper-variable in cancer. Based on these observations, we developed a universal cancer anti-profile that accurately distinguishes cancer from normal regardless of tissue type (ten-fold cross-validation AUC > 0.92). CONCLUSIONS: We have introduced anti-profiles as a new approach for developing cancer genomic signatures that specifically takes advantage of gene expression heterogeneity. We have demonstrated that anti-profiles can be successfully applied to develop peripheral-blood based diagnostics for cancer and used anti-profiles to develop a highly accurate universal cancer signature. By using single-chip normalization and quality assessment methods, no further retraining of signatures developed by the anti-profile approach would be required before their application in clinical settings. Our results suggest that anti-profiles may be used to develop inexpensive and non-invasive universal cancer screening tests.}, keywords = {Area Under Curve, Colonic Neoplasms, Gene Expression Profiling, Genetic Variation, Genomics, HUMANS, Oligonucleotide Array Sequence Analysis, Prognosis, Transcriptome, Tumor Markers, Biological}, author = {H{\'e}ctor Corrada Bravo and Pihur, Vasyl and McCall, Matthew and Irizarry, Rafael A. and Leek, Jeffrey T.} } @article {38421, title = {The partitioned LASSO-patternsearch algorithm with application to gene expression data}, journal = {BMC bioinformaticsBMC Bioinformatics}, volume = {13}, year = {2012}, note = {http://www.ncbi.nlm.nih.gov/pubmed/22587526?dopt=Abstract}, type = {10.1186/1471-2105-13-98}, abstract = {BACKGROUND: In systems biology, the task of reverse engineering gene pathways from data has been limited not just by the curse of dimensionality (the interaction space is huge) but also by systematic error in the data. The gene expression barcode reduces spurious association driven by batch effects and probe effects. The binary nature of the resulting expression calls lends itself perfectly to modern regularization approaches that thrive in high-dimensional settings. RESULTS: The Partitioned LASSO-Patternsearch algorithm is proposed to identify patterns of multiple dichotomous risk factors for outcomes of interest in genomic studies. A partitioning scheme is used to identify promising patterns by solving many LASSO-Patternsearch subproblems in parallel. All variables that survive this stage proceed to an aggregation stage where the most significant patterns are identified by solving a reduced LASSO-Patternsearch problem in just these variables. This approach was applied to genetic data sets with expression levels dichotomized by gene expression bar code. Most of the genes and second-order interactions thus selected and are known to be related to the outcomes. CONCLUSIONS: We demonstrate with simulations and data analyses that the proposed method not only selects variables and patterns more accurately, but also provides smaller models with better prediction accuracy, in comparison to several alternative methodologies.}, keywords = {algorithms, Breast Neoplasms, Computer simulation, Female, Gene expression, Gene Expression Profiling, Genomics, HUMANS, Models, Genetic}, author = {Shi, Weiliang and Wahba, Grace and Irizarry, Rafael A. and H{\'e}ctor Corrada Bravo and Wright, Stephen J.} } @article {38566, title = {Vibrio Cholerae Classical Biotype Strains Reveal Distinct Signatures in Mexico}, journal = {Journal of Clinical MicrobiologyJ. Clin. Microbiol.Journal of Clinical MicrobiologyJ. Clin. Microbiol.}, year = {2012}, type = {10.1128/JCM.00189-12}, abstract = {Vibrio cholerae O1 Classical (CL) biotype caused the 5th and 6th, and probably the earlier cholera pandemics, before the El Tor (ET) biotype initiated the 7th pandemic in Asia in the 1970{\textquoteright}s by completely displacing the CL biotype. Although the CL biotype was thought to be extinct in Asia, and it had never been reported from Latin America, V. cholerae CL and ET biotypes, including hybrid ET were found associated with endemic cholera in Mexico between 1991 and 1997. In this study, CL biotype strains isolated from endemic cholera in Mexico, between 1983 and 1997 were characterized in terms of major phenotypic and genetic traits, and compared with CL biotype strains isolated in Bangladesh between 1962 and 1989. According to sero- and bio-typing data, all V. cholerae strains tested had the major phenotypic and genotypic characteristics specific for the CL biotype. Antibiograms revealed the majority of the Bangladeshi strains to be resistant to trimethoprim/sulfamethoxazole, furazolidone, ampicillin, and gentamycin, while the Mexican strains were sensitive to all of these drugs, as well as to ciprofloxacin, erythromycin, and tetracycline. Pulsed-field gel electrophoresis (PFGE) of NotI-digested genomic DNA revealed characteristic banding patterns for all the CL biotype strains, although the Mexican strains differed with the Bangladeshi strains in 1-2 DNA bands. The difference may be subtle, but consistent, as confirmed by the sub-clustering patterns in the PFGE-based dendrogram, and can serve as regional signature, suggesting pre-1991 existence and evolution of the CL biotype strains in the Americas, independent from that of Asia.}, isbn = {0095-1137, 1098-660X}, author = {Alam, Munirul and Islam, M. Tarequl and Rashed, Shah Manzur and Johura, Fatema-Tuz and Bhuiyan, Nurul A. and Delgado, Gabriela and Morales, Rosario and Mendez, Jose Luis and Navarro, Armando and Watanabe, Haruo and Hasan, Nur- A. and Rita R. Colwell and Cravioto, Alejandro} } @article {38151, title = {Clonal transmission, dual peak, and off-season cholera in Bangladesh}, journal = {Infection Ecology \& EpidemiologyInfection Ecology \& Epidemiology}, volume = {1}, year = {2011}, type = {10.3402/iee.v1i0.7273}, author = {Alam, M. and Islam, A. and Bhuiyan, N. A. and Rahim, N. and Hossain, A. and Khan, G. Y. and Ahmed, D. and Watanabe, H. and Izumiya, H. and Faruque, A. S. G. and Rita R. Colwell} } @article {49556, title = {Direct targeting of Sec23a by miR-200s influences cancer cell secretome and promotes metastatic colonization}, volume = {17}, year = {2011}, month = {Jul-08-2011}, pages = {1101 - 1108}, issn = {1078-8956}, doi = {10.1038/nm.2401}, url = {http://www.nature.com/doifinder/10.1038/nm.2401}, author = {Korpal, Manav and Ell, Brian J and Buffa, Francesca M and Ibrahim, Toni and Blanco, Mario A and {\`a}-Terrassa, Toni and Mercatali, Laura and Khan, Zia and Goodarzi, Hani and Hua, Yuling and Wei, Yong and Hu, Guohong and Garcia, Benjamin A and Ragoussis, Jiannis and Amadori, Dino and Harris, Adrian L and Kang, Yibin} } @article {49746, title = {Direct targeting of Sec23a by miR-200s influences cancer cell secretome and promotes metastatic colonization.}, journal = {Nat Med}, volume = {17}, year = {2011}, month = {2011 Sep}, pages = {1101-8}, abstract = {

Although the role of miR-200s in regulating E-cadherin expression and epithelial-to-mesenchymal transition is well established, their influence on metastatic colonization remains controversial. Here we have used clinical and experimental models of breast cancer metastasis to discover a pro-metastatic role of miR-200s that goes beyond their regulation of E-cadherin and epithelial phenotype. Overexpression of miR-200s is associated with increased risk of metastasis in breast cancer and promotes metastatic colonization in mouse models, phenotypes that cannot be recapitulated by E-cadherin expression alone. Genomic and proteomic analyses revealed global shifts in gene expression upon miR-200 overexpression toward that of highly metastatic cells. miR-200s promote metastatic colonization partly through direct targeting of Sec23a, which mediates secretion of metastasis-suppressive proteins, including Igfbp4 and Tinagl1, as validated by functional and clinical correlation studies. Overall, these findings suggest a pleiotropic role of miR-200s in promoting metastatic colonization by influencing E-cadherin-dependent epithelial traits and Sec23a-mediated tumor cell secretome.

}, keywords = {Animals, Cadherins, Cell Line, Tumor, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, HUMANS, Mass Spectrometry, Mice, Mice, Inbred BALB C, Microarray Analysis, MicroRNAs, Neoplasm Metastasis, Statistics, Nonparametric, Vesicular Transport Proteins}, issn = {1546-170X}, doi = {10.1038/nm.2401}, author = {Korpal, Manav and Ell, Brian J and Buffa, Francesca M and Ibrahim, Toni and Blanco, Mario A and Celi{\`a}-Terrassa, Toni and Mercatali, Laura and Khan, Zia and Goodarzi, Hani and Hua, Yuling and Wei, Yong and Hu, Guohong and Garcia, Benjamin A and Ragoussis, Jiannis and Amadori, Dino and Harris, Adrian L and Kang, Yibin} } @article {49829, title = {Effective detection of rare variants in pooled DNA samples using Cross-pool tailcurve analysis}, journal = {Genome Biology}, volume = {12}, year = {2011}, month = {Jan-01-2011}, pages = {R93}, issn = {1465-6906}, doi = {10.1186/gb-2011-12-9-r93}, url = {http://genomebiology.biomedcentral.com/articles/10.1186/gb-2011-12-9-r93}, author = {Niranjan, Tejasvi S and Adamczyk, Abby and Bravo, Hector and Taub, Margaret A and Wheelan, Sarah J and Irizarry, Rafael and Wang, Tao} } @article {49831, title = {Increased methylation variation in epigenetic domains across cancer types}, journal = {Nature Genetics}, volume = {43}, year = {2011}, month = {Feb-06-2013}, pages = {768 - 775}, issn = {1061-4036}, doi = {10.1038/ng.865}, url = {http://www.nature.com/doifinder/10.1038/ng.865}, author = {Hansen, Kasper Daniel and Timp, Winston and Bravo, H{\'e}ctor Corrada and Sabunciyan, Sarven and Langmead, Benjamin and McDonald, Oliver G and Wen, Bo and Wu, Hao and Liu, Yun and Diep, Dinh and Briem, Eirikur and Zhang, Kun and Irizarry, Rafael A and Feinberg, Andrew P} } @article {38347, title = {Influence of host gene transcription level and orientation on HIV-1 latency in a primary-cell model}, journal = {Journal of virologyJournal of virology}, volume = {85}, year = {2011}, note = {http://www.ncbi.nlm.nih.gov/pubmed/21430059?dopt=Abstract}, type = {10.1128/JVI.02536-10}, abstract = {Human immunodeficiency virus type 1 (HIV-1) establishes a latent reservoir in resting memory CD4(+) T cells. This latent reservoir is a major barrier to the eradication of HIV-1 in infected individuals and is not affected by highly active antiretroviral therapy (HAART). Reactivation of latent HIV-1 is a possible strategy for elimination of this reservoir. The mechanisms with which latency is maintained are unclear. In the analysis of the regulation of HIV-1 gene expression, it is important to consider the nature of HIV-1 integration sites. In this study, we analyzed the integration and transcription of latent HIV-1 in a primary CD4(+) T cell model of latency. The majority of integration sites in latently infected cells were in introns of transcription units. Serial analysis of gene expression (SAGE) demonstrated that more than 90\% of those host genes harboring a latent integrated provirus were transcriptionally active, mostly at high levels. For latently infected cells, we observed a modest preference for integration in the same transcriptional orientation as the host gene (63.8\% versus 36.2\%). In contrast, this orientation preference was not observed in acutely infected or persistently infected cells. These results suggest that transcriptional interference may be one of the important factors in the establishment and maintenance of HIV-1 latency. Our findings suggest that disrupting the negative control of HIV-1 transcription by upstream host promoters could facilitate the reactivation of latent HIV-1 in some resting CD4(+) T cells.}, keywords = {CD4-Positive T-Lymphocytes, Cells, Cultured, Gene Expression Profiling, Gene Expression Regulation, Viral, HIV-1, HUMANS, Transcription, Genetic, Virus Integration, Virus Latency}, author = {Shan, Liang and Yang, Hung-Chih and Rabi, S. Alireza and H{\'e}ctor Corrada Bravo and Shroff, Neeta S. and Irizarry, Rafael A. and Zhang, Hao and Margolick, Joseph B. and Siliciano, Janet D. and Siliciano, Robert F.} } @article {49832, title = {Influence of Host Gene Transcription Level and Orientation on HIV-1 Latency in a Primary-Cell Model}, journal = {Journal of Virology}, volume = {85}, year = {2011}, month = {Jan-06-2011}, pages = {5384 - 5393}, issn = {0022-538X}, doi = {10.1128/JVI.02536-10}, url = {http://jvi.asm.org/cgi/doi/10.1128/JVI.02536-10https://syndication.highwire.org/content/doi/10.1128/JVI.02536-10}, author = {Shan, L. and Yang, H.-C. and Rabi, S. A. and Bravo, H. C. and Shroff, N. S. and Irizarry, R. A. and Zhang, H. and Margolick, J. B. and Siliciano, J. D. and Siliciano, R. F.} } @proceedings {38367, title = {MDMap: A system for data-driven layout and exploration of molecular dynamics simulations}, year = {2011}, month = {2011}, type = {10.1109/BioVis.2011.6094055}, abstract = {Contemporary molecular dynamics simulations result in a glut of simulation data, making analysis and discovery a difficult and burdensome task. We present MDMap, a system designed to summarize long-running molecular dynamics (MD) simulations. We represent a molecular dynamics simulation as a state transition graph over a set of intermediate (stable and semi-stable) states. The transitions amongst the states together with their frequencies represent the flow of a biomolecule through the trajectory space. MDMap automatically determines potential intermediate conformations and the transitions amongst them by analyzing the conformational space explored by the MD simulation. MDMap is an automated system to visualize MD simulations as state-transition diagrams, and can replace the current tedious manual layouts of biomolecular folding landscapes with an automated tool. The layout of the representative states and the corresponding transitions among them is presented to the user as a visual synopsis of the long-running MD simulation. We compare and contrast multiple presentations of the state transition diagrams, such as conformational embedding, and spectral, hierarchical, and force-directed graph layouts. We believe this system could provide a road-map for the visualization of other stochastic time-varying simulations in a variety of different domains.}, keywords = {Biology, biomolecular, computing, data, digital, driven, DYNAMICS, exploration, folding, graph, landscapes, Layout, MDMap, method, molecular, processes, simulation, Simulations, space, state, Stochastic, THEORY, time-varying, Trajectory, transition}, author = {Patro, R. and Ip, Cheuk Yiu and Bista, S. and Cho, S. S. and Thirumalai, D. and Varshney, Amitabh} } @article {38508, title = {Social Snapshot: A System for Temporally Coupled Social Photography}, journal = {Computer Graphics and Applications, IEEEComputer Graphics and Applications, IEEE}, volume = {31}, year = {2011}, type = {10.1109/MCG.2010.107}, abstract = {Social Snapshot actively acquires and reconstructs temporally dynamic data. The system enables spatiotemporal 3D photography using commodity devices, assisted by their auxiliary sensors and network functionality. It engages users, making them active rather than passive participants in data acquisition.}, keywords = {3D, ACQUISITION, computing, coupled, data, Photography, reconstruction, sciences, snapshot, social, spatiotemporal, temporally}, isbn = {0272-1716}, author = {Patro, R. and Ip, Cheuk Yiu and Bista, S. and Varshney, Amitabh} } @article {38570, title = {Warming Oceans, Phytoplankton, and River Discharge: Implications for Cholera Outbreaks}, journal = {The American Journal of Tropical Medicine and HygieneAm J Trop Med HygThe American Journal of Tropical Medicine and HygieneAm J Trop Med Hyg}, volume = {85}, year = {2011}, type = {10.4269/ajtmh.2011.11-0181}, abstract = {Phytoplankton abundance is inversely related to sea surface temperature (SST). However, a positive relationship is observed between SST and phytoplankton abundance in coastal waters of Bay of Bengal. This has led to an assertion that in a warming climate, rise in SST may increase phytoplankton blooms and, therefore, cholera outbreaks. Here, we explain why a positive SST-phytoplankton relationship exists in the Bay of Bengal and the implications of such a relationship on cholera dynamics. We found clear evidence of two independent physical drivers for phytoplankton abundance. The first one is the widely accepted phytoplankton blooming produced by the upwelling of cold, nutrient-rich deep ocean waters. The second, which explains the Bay of Bengal findings, is coastal phytoplankton blooming during high river discharges with terrestrial nutrients. Causal mechanisms should be understood when associating SST with phytoplankton and subsequent cholera outbreaks in regions where freshwater discharge are a predominant mechanism for phytoplankton production.}, isbn = {0002-9637}, author = {Jutla, Antarpreet S. and Akanda, Ali S. and Griffiths, Jeffrey K. and Rita R. Colwell and Islam, Shafiqul} } @article {38210, title = {Diversity and distribution of cholix toxin, a novel ADP-ribosylating factor from Vibrio cholerae}, journal = {Environmental Microbiology ReportsEnvironmental Microbiology Reports}, volume = {2}, year = {2010}, type = {10.1111/j.1758-2229.2010.00139.x}, abstract = {Non-toxigenic non-O1, non-O139 Vibrio cholerae strains isolated from both environmental and clinical settings carry a suite of virulence factors aside from cholera toxin. Among V. cholerae strains isolated from coastal waters of southern California, this includes cholix toxin, an ADP-ribosylating factor that is capable of halting protein synthesis in eukaryotic cells. The prevalence of the gene encoding cholix toxin, chxA, was assessed among a collection of 155 diverse V. cholerae strains originating from both clinical and environmental settings in Bangladesh and Mexico and other countries around the globe. The chxA gene was present in 47\% of 83 non-O1, non-O139 strains and 16\% of 72 O1/O139 strains screened as part of this study. A total of 86 chxA gene sequences were obtained, and phylogenetic analysis revealed that they fall into two distinct clades. These two clades were also observed in the phylogenies of several housekeeping genes, suggesting that the divergence observed in chxA extends to other regions of the V. cholerae genome, and most likely has arisen from vertical descent rather than horizontal transfer. Our results clearly indicate that ChxA is a major toxin of V. cholerae with a worldwide distribution that is preferentially associated with non-pandemic strains.}, isbn = {1758-2229}, author = {Purdy, Alexandra E. and Balch, Deborah and Liz{\'a}rraga-Partida, Marcial Leonardo and Islam, Mohammad Sirajul and Martinez-Urtaza, Jaime and Huq, Anwar and Rita R. Colwell and Bartlett, Douglas H.} } @article {38349, title = {Intensity normalization improves color calling in SOLiD sequencing}, journal = {Nat MethNat MethNat MethNat Meth}, volume = {7}, year = {2010}, type = {10.1038/nmeth0510-336}, isbn = {1548-7091}, author = {Wu, Hao and Irizarry, Rafael A. and H{\'e}ctor Corrada Bravo} } @article {49833, title = {Model-Based Quality Assessment and Base-Calling for Second-Generation Sequencing Data}, journal = {Biometrics}, volume = {66}, year = {2010}, month = {Jan-09-2010}, pages = {665 - 674}, doi = {10.1111/j.1541-0420.2009.01353.x}, url = {http://doi.wiley.com/10.1111/j.1541-0420.2009.01353.xhttps://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111\%2Fj.1541-0420.2009.01353.x}, author = {Bravo, H{\'e}ctor Corrada and Irizarry, Rafael A.} } @article {38417, title = {Overcoming bias and systematic errors in next generation sequencing data}, journal = {Genome medicineGenome medicine}, volume = {2}, year = {2010}, note = {http://www.ncbi.nlm.nih.gov/pubmed/21144010?dopt=Abstract}, type = {10.1186/gm208}, abstract = {Considerable time and effort has been spent in developing analysis and quality assessment methods to allow the use of microarrays in a clinical setting. As is the case for microarrays and other high-throughput technologies, data from new high-throughput sequencing technologies are subject to technological and biological biases and systematic errors that can impact downstream analyses. Only when these issues can be readily identified and reliably adjusted for will clinical applications of these new technologies be feasible. Although much work remains to be done in this area, we describe consistently observed biases that should be taken into account when analyzing high-throughput sequencing data. In this article, we review current knowledge about these biases, discuss their impact on analysis results, and propose solutions.}, author = {Taub, Margaret A. and H{\'e}ctor Corrada Bravo and Irizarry, Rafael A.} } @article {38474, title = {Saliency Guided Summarization of Molecular Dynamics Simulations}, journal = {Scientific Visualization: Advanced ConceptsScientific Visualization: Advanced Concepts}, volume = {1}, year = {2010}, abstract = {We present a novel method to measure saliency in molecular dynamics simulation data. This saliency measure is based on a multiscale center-surround mechanism, which is fast and efficient to compute. We explore the use of the saliency function to guide the selection of representative and anomalous timesteps for summarization of simulations. To this end, we also introduce a multiscale keyframe selection procedure which automatically provides keyframes representing the simulation at varying levels of coarseness. We compare our saliency guided keyframe approach against other methods, and show that it consistently selects superior keyframes as measured by their predictive power in reconstructing the simulation.}, author = {Patro, R. and Ip, C. Y. and Varshney, Amitabh and Hagen, H.} } @article {38522, title = {Tackling the widespread and critical impact of batch effects in high-throughput data}, journal = {Nature reviews. GeneticsNature reviews. Genetics}, volume = {11}, year = {2010}, note = {http://www.ncbi.nlm.nih.gov/pubmed/20838408?dopt=Abstract}, type = {10.1038/nrg2825}, abstract = {High-throughput technologies are widely used, for example to assay genetic variants, gene and protein expression, and epigenetic modifications. One often overlooked complication with such studies is batch effects, which occur because measurements are affected by laboratory conditions, reagent lots and personnel differences. This becomes a major problem when batch effects are correlated with an outcome of interest and lead to incorrect conclusions. Using both published studies and our own analyses, we argue that batch effects (as well as other technical and biological artefacts) are widespread and critical to address. We review experimental and computational approaches for doing so.}, keywords = {biotechnology, Computational Biology, Genomics, Oligonucleotide Array Sequence Analysis, Periodicals as Topic, Research Design, Sequence Analysis, DNA}, author = {Leek, Jeffrey T. and Scharpf, Robert B. and H{\'e}ctor Corrada Bravo and Simcha, David and Langmead, Benjamin and Johnson, W. Evan and Geman, Donald and Baggerly, Keith and Irizarry, Rafael A.} } @article {49834, title = {Examining the relative influence of familial, genetic, and environmental covariate information in flexible risk models}, journal = {Proceedings of the National Academy of Sciences}, volume = {106}, year = {2009}, month = {Jul-05-2010}, pages = {8128 - 8133}, issn = {0027-8424}, doi = {10.1073/pnas.0902906106}, url = {http://www.pnas.org/cgi/doi/10.1073/pnas.0902906106https://syndication.highwire.org/content/doi/10.1073/pnas.0902906106}, author = {Bravo, H. C. and Lee, K. E. and Klein, B. E. K. and Klein, R. and Iyengar, S. K. and Wahba, G.} } @article {49646, title = {The genome of the blood fluke Schistosoma mansoni.}, journal = {Nature}, volume = {460}, year = {2009}, month = {2009 Jul 16}, pages = {352-8}, abstract = {

Schistosoma mansoni is responsible for the neglected tropical disease schistosomiasis that affects 210 million people in 76 countries. Here we present analysis of the 363 megabase nuclear genome of the blood fluke. It encodes at least 11,809 genes, with an unusual intron size distribution, and new families of micro-exon genes that undergo frequent alternative splicing. As the first sequenced flatworm, and a representative of the Lophotrochozoa, it offers insights into early events in the evolution of the animals, including the development of a body pattern with bilateral symmetry, and the development of tissues into organs. Our analysis has been informed by the need to find new drug targets. The deficits in lipid metabolism that make schistosomes dependent on the host are revealed, and the identification of membrane receptors, ion channels and more than 300 proteases provide new insights into the biology of the life cycle and new targets. Bioinformatics approaches have identified metabolic chokepoints, and a chemogenomic screen has pinpointed schistosome proteins for which existing drugs may be active. The information generated provides an invaluable resource for the research community to develop much needed new control tools for the treatment and eradication of this important and neglected disease.

}, keywords = {Animals, Biological Evolution, Exons, Genes, Helminth, Genome, Helminth, Host-Parasite Interactions, Introns, Molecular Sequence Data, Physical Chromosome Mapping, Schistosoma mansoni, Schistosomiasis mansoni}, issn = {1476-4687}, doi = {10.1038/nature08160}, author = {Berriman, Matthew and Haas, Brian J and LoVerde, Philip T and Wilson, R Alan and Dillon, Gary P and Cerqueira, Gustavo C and Mashiyama, Susan T and Al-Lazikani, Bissan and Andrade, Luiza F and Ashton, Peter D and Aslett, Martin A and Bartholomeu, Daniella C and Blandin, Ga{\"e}lle and Caffrey, Conor R and Coghlan, Avril and Coulson, Richard and Day, Tim A and Delcher, Art and DeMarco, Ricardo and Djikeng, Appolinaire and Eyre, Tina and Gamble, John A and Ghedin, Elodie and Gu, Yong and Hertz-Fowler, Christiane and Hirai, Hirohisha and Hirai, Yuriko and Houston, Robin and Ivens, Alasdair and Johnston, David A and Lacerda, Daniela and Macedo, Camila D and McVeigh, Paul and Ning, Zemin and Oliveira, Guilherme and Overington, John P and Parkhill, Julian and Pertea, Mihaela and Pierce, Raymond J and Protasio, Anna V and Quail, Michael A and Rajandream, Marie-Ad{\`e}le and Rogers, Jane and Sajid, Mohammed and Salzberg, Steven L and Stanke, Mario and Tivey, Adrian R and White, Owen and Williams, David L and Wortman, Jennifer and Wu, Wenjie and Zamanian, Mostafa and Zerlotini, Adhemar and Fraser-Liggett, Claire M and Barrell, Barclay G and El-Sayed, Najib M} } @article {38385, title = {Model-based quality assessment and base-calling for second-generation sequencing data}, journal = {Johns Hopkins University, Dept. of Biostatistics Working PapersJohns Hopkins University, Dept. of Biostatistics Working Papers}, year = {2009}, author = {Irizarry, R. A. and H{\'e}ctor Corrada Bravo} } @article {38468, title = {RNA Colony Blot Hybridization Method for Enumeration of Culturable Vibrio Cholerae and Vibrio Mimicus Bacteria}, journal = {Applied and Environmental MicrobiologyAppl. Environ. Microbiol.Applied and Environmental MicrobiologyAppl. Environ. Microbiol.}, volume = {75}, year = {2009}, type = {10.1128/AEM.02007-08}, abstract = {A species-specific RNA colony blot hybridization protocol was developed for enumeration of culturable Vibrio cholerae and Vibrio mimicus bacteria in environmental water samples. Bacterial colonies on selective or nonselective plates were lysed by sodium dodecyl sulfate, and the lysates were immobilized on nylon membranes. A fluorescently labeled oligonucleotide probe targeting a phylogenetic signature sequence of 16S rRNA of V. cholerae and V. mimicus was hybridized to rRNA molecules immobilized on the nylon colony lift blots. The protocol produced strong positive signals for all colonies of the 15 diverse V. cholerae-V. mimicus strains tested, indicating 100\% sensitivity of the probe for the targeted species. For visible colonies of 10 nontarget species, the specificity of the probe was calculated to be 90\% because of a weak positive signal produced by Grimontia (Vibrio) hollisae, a marine bacterium. When both the sensitivity and specificity of the assay were evaluated using lake water samples amended with a bioluminescent V. cholerae strain, no false-negative or false-positive results were found, indicating 100\% sensitivity and specificity for culturable bacterial populations in freshwater samples when G. hollisae was not present. When the protocol was applied to laboratory microcosms containing V. cholerae attached to live copepods, copepods were found to carry approximately 10,000 to 50,000 CFU of V. cholerae per copepod. The protocol was also used to analyze pond water samples collected in an area of cholera endemicity in Bangladesh over a 9-month period. Water samples collected from six ponds demonstrated a peak in abundance of total culturable V. cholerae bacteria 1 to 2 months prior to observed increases in pathogenic V. cholerae and in clinical cases recorded by the area health clinic. The method provides a highly specific and sensitive tool for monitoring the dynamics of V. cholerae in the environment. The RNA blot hybridization protocol can also be applied to detection of other gram-negative bacteria for taxon-specific enumeration.}, isbn = {0099-2240, 1098-5336}, author = {Grim, Christopher J. and Zo, Young-Gun and Hasan, Nur A. and Ali, Afsar and Chowdhury, Wasimul B. and Islam, Atiqul and Rashid, Mohammed H. and Alam, Munirul and Morris, J. Glenn and Huq, Anwar and Rita R. Colwell} } @inbook {38475, title = {Salient Frame Detection for Molecular Dynamics Simulations}, booktitle = {Scientific VisualizationScientific Visualization}, year = {2009}, publisher = {Dagstuhl Seminar Proceedings 09251}, organization = {Dagstuhl Seminar Proceedings 09251}, author = {Kim, Youngmin and Patro, Robert and Ip, Cheuk Yiu and O{\textquoteright}Leary, Dianne P. and Anishkin, Andriy and Sukharev, Sergei and Varshney, Amitabh}, editor = {Ebert, D. S. and Gr, and x6f, and x, and ller, E. and Hagen, H. and Kaufman, A.} } @article {38498, title = {Serogroup, Virulence, and Genetic Traits of Vibrio Parahaemolyticus in the Estuarine Ecosystem of Bangladesh}, journal = {Applied and Environmental MicrobiologyAppl. Environ. Microbiol.Applied and Environmental MicrobiologyAppl. Environ. Microbiol.}, volume = {75}, year = {2009}, type = {10.1128/AEM.00266-09}, abstract = {Forty-two strains of Vibrio parahaemolyticus were isolated from Bay of Bengal estuaries and, with two clinical strains, analyzed for virulence, phenotypic, and molecular traits. Serological analysis indicated O8, O3, O1, and K21 to be the major O and K serogroups, respectively, and O8:K21, O1:KUT, and O3:KUT to be predominant. The K antigen(s) was untypeable, and pandemic serogroup O3:K6 was not detected. The presence of genes toxR and tlh were confirmed by PCR in all but two strains, which also lacked toxR. A total of 18 (41\%) strains possessed the virulence gene encoding thermostable direct hemolysin (TDH), and one had the TDH-related hemolysin (trh) gene, but not tdh. Ten (23\%) strains exhibited Kanagawa phenomenon that surrogates virulence, of which six, including the two clinical strains, possessed tdh. Of the 18 tdh-positive strains, 17 (94\%), including the two clinical strains, had the seromarker O8:K21, one was O9:KUT, and the single trh-positive strain was O1:KUT. None had the group-specific or ORF8 pandemic marker gene. DNA fingerprinting employing pulsed-field gel electrophoresis (PFGE) of SfiI-digested DNA and cluster analysis showed divergence among the strains. Dendrograms constructed using PFGE (SfiI) images from a soft database, including those of pandemic and nonpandemic strains of diverse geographic origin, however, showed that local strains formed a cluster, i.e., {\textquotedblleft}clonal cluster,{\textquotedblright} as did pandemic strains of diverse origin. The demonstrated prevalence of tdh-positive and diarrheagenic serogroup O8:K21 strains in coastal villages of Bangladesh indicates a significant human health risk for inhabitants.}, isbn = {0099-2240, 1098-5336}, author = {Alam, Munirul and Chowdhury, Wasimul B. and Bhuiyan, N. A. and Islam, Atiqul and Hasan, Nur A. and Nair, G. Balakrish and Watanabe, H. and Siddique, A. K. and Huq, Anwar and Sack, R. Bradley and Akhter, M. Z. and Grim, Christopher J. and Kam, K. M. and Luey, C. K. Y. and Endtz, Hubert P. and Cravioto, Alejandro and Rita R. Colwell} } @article {49676, title = {The draft genome of the transgenic tropical fruit tree papaya (Carica papaya Linnaeus).}, journal = {Nature}, volume = {452}, year = {2008}, month = {2008 Apr 24}, pages = {991-6}, abstract = {

Papaya, a fruit crop cultivated in tropical and subtropical regions, is known for its nutritional benefits and medicinal applications. Here we report a 3x draft genome sequence of {\textquoteright}SunUp{\textquoteright} papaya, the first commercial virus-resistant transgenic fruit tree to be sequenced. The papaya genome is three times the size of the Arabidopsis genome, but contains fewer genes, including significantly fewer disease-resistance gene analogues. Comparison of the five sequenced genomes suggests a minimal angiosperm gene set of 13,311. A lack of recent genome duplication, atypical of other angiosperm genomes sequenced so far, may account for the smaller papaya gene number in most functional groups. Nonetheless, striking amplifications in gene number within particular functional groups suggest roles in the evolution of tree-like habit, deposition and remobilization of starch reserves, attraction of seed dispersal agents, and adaptation to tropical daylengths. Transgenesis at three locations is closely associated with chloroplast insertions into the nuclear genome, and with topoisomerase I recognition sites. Papaya offers numerous advantages as a system for fruit-tree functional genomics, and this draft genome sequence provides the foundation for revealing the basis of Carica{\textquoteright}s distinguishing morpho-physiological, medicinal and nutritional properties.

}, keywords = {Arabidopsis, Carica, Contig Mapping, Databases, Genetic, Genes, Plant, Genome, Plant, Molecular Sequence Data, Plants, Genetically Modified, sequence alignment, Sequence Analysis, DNA, Transcription Factors, Tropical Climate}, issn = {1476-4687}, doi = {10.1038/nature06856}, author = {Ming, Ray and Hou, Shaobin and Feng, Yun and Yu, Qingyi and Dionne-Laporte, Alexandre and Saw, Jimmy H and Senin, Pavel and Wang, Wei and Ly, Benjamin V and Lewis, Kanako L T and Salzberg, Steven L and Feng, Lu and Jones, Meghan R and Skelton, Rachel L and Murray, Jan E and Chen, Cuixia and Qian, Wubin and Shen, Junguo and Du, Peng and Eustice, Moriah and Tong, Eric and Tang, Haibao and Lyons, Eric and Paull, Robert E and Michael, Todd P and Wall, Kerr and Rice, Danny W and Albert, Henrik and Wang, Ming-Li and Zhu, Yun J and Schatz, Michael and Nagarajan, Niranjan and Acob, Ricelle A and Guan, Peizhu and Blas, Andrea and Wai, Ching Man and Ackerman, Christine M and Ren, Yan and Liu, Chao and Wang, Jianmei and Wang, Jianping and Na, Jong-Kuk and Shakirov, Eugene V and Haas, Brian and Thimmapuram, Jyothi and Nelson, David and Wang, Xiyin and Bowers, John E and Gschwend, Andrea R and Delcher, Arthur L and Singh, Ratnesh and Suzuki, Jon Y and Tripathi, Savarni and Neupane, Kabi and Wei, Hairong and Irikura, Beth and Paidi, Maya and Jiang, Ning and Zhang, Wenli and Presting, Gernot and Windsor, Aaron and Navajas-P{\'e}rez, Rafael and Torres, Manuel J and Feltus, F Alex and Porter, Brad and Li, Yingjun and Burroughs, A Max and Luo, Ming-Cheng and Liu, Lei and Christopher, David A and Mount, Stephen M and Moore, Paul H and Sugimura, Tak and Jiang, Jiming and Schuler, Mary A and Friedman, Vikki and Mitchell-Olds, Thomas and Shippen, Dorothy E and dePamphilis, Claude W and Palmer, Jeffrey D and Freeling, Michael and Paterson, Andrew H and Gonsalves, Dennis and Wang, Lei and Alam, Maqsudul} } @article {38242, title = {Evolution of genes and genomes on the Drosophila phylogeny}, journal = {NatureNature}, volume = {450}, year = {2007}, note = {[szlig]}, type = {10.1038/nature06341}, abstract = {Comparative analysis of multiple genomes in a phylogenetic framework dramatically improves the precision and sensitivity of evolutionary inference, producing more robust results than single-genome analyses can provide. The genomes of 12 Drosophila species, ten of which are presented here for the first time (sechellia, simulans, yakuba, erecta, ananassae, persimilis, willistoni, mojavensis, virilis and grimshawi), illustrate how rates and patterns of sequence divergence across taxa can illuminate evolutionary processes on a genomic scale. These genome sequences augment the formidable genetic tools that have made Drosophila melanogaster a pre-eminent model for animal genetics, and will further catalyse fundamental research on mechanisms of development, cell biology, genetics, disease, neurobiology, behaviour, physiology and evolution. Despite remarkable similarities among these Drosophila species, we identified many putatively non-neutral changes in protein-coding genes, non-coding RNA genes, and cis-regulatory regions. These may prove to underlie differences in the ecology and behaviour of these diverse species.}, isbn = {0028-0836}, author = {Clark, Andrew G. and Eisen, Michael B. and Smith, Douglas R. and Bergman, Casey M. and Oliver, Brian and Markow, Therese A. and Kaufman, Thomas C. and Kellis, Manolis and Gelbart, William and Iyer, Venky N. and Pollard, Daniel A. and Sackton, Timothy B. and Larracuente, Amanda M. and Singh, Nadia D. and Abad, Jose P. and Abt, Dawn N. and Adryan, Boris and Aguade, Montserrat and Akashi, Hiroshi and Anderson, Wyatt W. and Aquadro, Charles F. and Ardell, David H. and Arguello, Roman and Artieri, Carlo G. and Barbash, Daniel A. and Barker, Daniel and Barsanti, Paolo and Batterham, Phil and Batzoglou, Serafim and Begun, Dave and Bhutkar, Arjun and Blanco, Enrico and Bosak, Stephanie A. and Bradley, Robert K. and Brand, Adrianne D. and Brent, Michael R. and Brooks, Angela N. and Brown, Randall H. and Butlin, Roger K. and Caggese, Corrado and Calvi, Brian R. and Carvalho, A. Bernardo de and Caspi, Anat and Castrezana, Sergio and Celniker, Susan E. and Chang, Jean L. and Chapple, Charles and Chatterji, Sourav and Chinwalla, Asif and Civetta, Alberto and Clifton, Sandra W. and Comeron, Josep M. and Costello, James C. and Coyne, Jerry A. and Daub, Jennifer and David, Robert G. and Delcher, Arthur L. and Delehaunty, Kim and Do, Chuong B. and Ebling, Heather and Edwards, Kevin and Eickbush, Thomas and Evans, Jay D. and Filipski, Alan and Findei, and Sven and Freyhult, Eva and Fulton, Lucinda and Fulton, Robert and Garcia, Ana C. L. and Gardiner, Anastasia and Garfield, David A. and Garvin, Barry E. and Gibson, Greg and Gilbert, Don and Gnerre, Sante and Godfrey, Jennifer and Good, Robert and Gotea, Valer and Gravely, Brenton and Greenberg, Anthony J. and Griffiths-Jones, Sam and Gross, Samuel and Guigo, Roderic and Gustafson, Erik A. and Haerty, Wilfried and Hahn, Matthew W. and Halligan, Daniel L. and Halpern, Aaron L. and Halter, Gillian M. and Han, Mira V. and Heger, Andreas and Hillier, LaDeana and Hinrichs, Angie S. and Holmes, Ian and Hoskins, Roger A. and Hubisz, Melissa J. and Hultmark, Dan and Huntley, Melanie A. and Jaffe, David B. and Jagadeeshan, Santosh and Jeck, William R. and Johnson, Justin and Jones, Corbin D. and Jordan, William C. and Karpen, Gary H. and Kataoka, Eiko and Keightley, Peter D. and Kheradpour, Pouya and Kirkness, Ewen F. and Koerich, Leonardo B. and Kristiansen, Karsten and Kudrna, Dave and Kulathinal, Rob J. and Kumar, Sudhir and Kwok, Roberta and Lander, Eric and Langley, Charles H. and Lapoint, Richard and Lazzaro, Brian P. and Lee, So-Jeong and Levesque, Lisa and Li, Ruiqiang and Lin, Chiao-Feng and Lin, Michael F. and Lindblad-Toh, Kerstin and Llopart, Ana and Long, Manyuan and Low, Lloyd and Lozovsky, Elena and Lu, Jian and Luo, Meizhong and Machado, Carlos A. and Makalowski, Wojciech and Marzo, Mar and Matsuda, Muneo and Matzkin, Luciano and McAllister, Bryant and McBride, Carolyn S. and McKernan, Brendan and McKernan, Kevin and Mendez-Lago, Maria and Minx, Patrick and Mollenhauer, Michael U. and Montooth, Kristi and Stephen M. Mount and Mu, Xu and Myers, Eugene and Negre, Barbara and Newfeld, Stuart and Nielsen, Rasmus and Noor, Mohamed A. F. and O{\textquoteright}Grady, Patrick and Pachter, Lior and Papaceit, Montserrat and Parisi, Matthew J. and Parisi, Michael and Parts, Leopold and Pedersen, Jakob S. and Pesole, Graziano and Phillippy, Adam M. and Ponting, Chris P. and M. Pop and Porcelli, Damiano and Powell, Jeffrey R. and Prohaska, Sonja and Pruitt, Kim and Puig, Marta and Quesneville, Hadi and Ram, Kristipati Ravi and Rand, David and Rasmussen, Matthew D. and Reed, Laura K. and Reenan, Robert and Reily, Amy and Remington, Karin A. and Rieger, Tania T. and Ritchie, Michael G. and Robin, Charles and Rogers, Yu-Hui and Rohde, Claudia and Rozas, Julio and Rubenfield, Marc J. and Ruiz, Alfredo and Russo, Susan and Salzberg, Steven L. and Sanchez-Gracia, Alejandro and Saranga, David J. and Sato, Hajime and Schaeffer, Stephen W. and Schatz, Michael C. and Schlenke, Todd and Schwartz, Russell and Segarra, Carmen and Singh, Rama S. and Sirot, Laura and Sirota, Marina and Sisneros, Nicholas B. and Smith, Chris D. and Smith, Temple F. and Spieth, John and Stage, Deborah E. and Stark, Alexander and Stephan, Wolfgang and Strausberg, Robert L. and Strempel, Sebastian and Sturgill, David and Sutton, Granger and Sutton, Granger G. and Tao, Wei and Teichmann, Sarah and Tobari, Yoshiko N. and Tomimura, Yoshihiko and Tsolas, Jason M. and Valente, Vera L. S. and Venter, Eli and Venter, J. Craig and Vicario, Saverio and Vieira, Filipe G. and Vilella, Albert J. and Villasante, Alfredo and Walenz, Brian and Wang, Jun and Wasserman, Marvin and Watts, Thomas and Wilson, Derek and Wilson, Richard K. and Wing, Rod A. and Wolfner, Mariana F. and Wong, Alex and Wong, Gane Ka-Shu and Wu, Chung- I. and Wu, Gabriel and Yamamoto, Daisuke and Yang, Hsiao-Pei and Yang, Shiaw-Pyng and Yorke, James A. and Yoshida, Kiyohito and Zdobnov, Evgeny and Zhang, Peili and Zhang, Yu and Zimin, Aleksey V. and Baldwin, Jennifer and Abdouelleil, Amr and Abdulkadir, Jamal and Abebe, Adal and Abera, Brikti and Abreu, Justin and Acer, St Christophe and Aftuck, Lynne and Alexander, Allen and An, Peter and Anderson, Erica and Anderson, Scott and Arachi, Harindra and Azer, Marc and Bachantsang, Pasang and Barry, Andrew and Bayul, Tashi and Berlin, Aaron and Bessette, Daniel and Bloom, Toby and Blye, Jason and Boguslavskiy, Leonid and Bonnet, Claude and Boukhgalter, Boris and Bourzgui, Imane and Brown, Adam and Cahill, Patrick and Channer, Sheridon and Cheshatsang, Yama and Chuda, Lisa and Citroen, Mieke and Collymore, Alville and Cooke, Patrick and Costello, Maura and D{\textquoteright}Aco, Katie and Daza, Riza and Haan, Georgius De and DeGray, Stuart and DeMaso, Christina and Dhargay, Norbu and Dooley, Kimberly and Dooley, Erin and Doricent, Missole and Dorje, Passang and Dorjee, Kunsang and Dupes, Alan and Elong, Richard and Falk, Jill and Farina, Abderrahim and Faro, Susan and Ferguson, Diallo and Fisher, Sheila and Foley, Chelsea D. and Franke, Alicia and Friedrich, Dennis and Gadbois, Loryn and Gearin, Gary and Gearin, Christina R. and Giannoukos, Georgia and Goode, Tina and Graham, Joseph and Grandbois, Edward and Grewal, Sharleen and Gyaltsen, Kunsang and Hafez, Nabil and Hagos, Birhane and Hall, Jennifer and Henson, Charlotte and Hollinger, Andrew and Honan, Tracey and Huard, Monika D. and Hughes, Leanne and Hurhula, Brian and Husby, M. Erii and Kamat, Asha and Kanga, Ben and Kashin, Seva and Khazanovich, Dmitry and Kisner, Peter and Lance, Krista and Lara, Marcia and Lee, William and Lennon, Niall and Letendre, Frances and LeVine, Rosie and Lipovsky, Alex and Liu, Xiaohong and Liu, Jinlei and Liu, Shangtao and Lokyitsang, Tashi and Lokyitsang, Yeshi and Lubonja, Rakela and Lui, Annie and MacDonald, Pen and Magnisalis, Vasilia and Maru, Kebede and Matthews, Charles and McCusker, William and McDonough, Susan and Mehta, Teena and Meldrim, James and Meneus, Louis and Mihai, Oana and Mihalev, Atanas and Mihova, Tanya and Mittelman, Rachel and Mlenga, Valentine and Montmayeur, Anna and Mulrain, Leonidas and Navidi, Adam and Naylor, Jerome and Negash, Tamrat and Nguyen, Thu and Nguyen, Nga and Nicol, Robert and Norbu, Choe and Norbu, Nyima and Novod, Nathaniel and O{\textquoteright}Neill, Barry and Osman, Sahal and Markiewicz, Eva and Oyono, Otero L. and Patti, Christopher and Phunkhang, Pema and Pierre, Fritz and Priest, Margaret and Raghuraman, Sujaa and Rege, Filip and Reyes, Rebecca and Rise, Cecil and Rogov, Peter and Ross, Keenan and Ryan, Elizabeth and Settipalli, Sampath and Shea, Terry and Sherpa, Ngawang and Shi, Lu and Shih, Diana and Sparrow, Todd and Spaulding, Jessica and Stalker, John and Stange-Thomann, Nicole and Stavropoulos, Sharon and Stone, Catherine and Strader, Christopher and Tesfaye, Senait and Thomson, Talene and Thoulutsang, Yama and Thoulutsang, Dawa and Topham, Kerri and Topping, Ira and Tsamla, Tsamla and Vassiliev, Helen and Vo, Andy and Wangchuk, Tsering and Wangdi, Tsering and Weiand, Michael and Wilkinson, Jane and Wilson, Adam and Yadav, Shailendra and Young, Geneva and Yu, Qing and Zembek, Lisa and Zhong, Danni and Zimmer, Andrew and Zwirko, Zac and Jaffe, David B. and Alvarez, Pablo and Brockman, Will and Butler, Jonathan and Chin, CheeWhye and Gnerre, Sante and Grabherr, Manfred and Kleber, Michael and Mauceli, Evan and MacCallum, Iain} } @article {49677, title = {Evolution of genes and genomes on the Drosophila phylogeny.}, journal = {Nature}, volume = {450}, year = {2007}, month = {2007 Nov 8}, pages = {203-18}, abstract = {

Comparative analysis of multiple genomes in a phylogenetic framework dramatically improves the precision and sensitivity of evolutionary inference, producing more robust results than single-genome analyses can provide. The genomes of 12 Drosophila species, ten of which are presented here for the first time (sechellia, simulans, yakuba, erecta, ananassae, persimilis, willistoni, mojavensis, virilis and grimshawi), illustrate how rates and patterns of sequence divergence across taxa can illuminate evolutionary processes on a genomic scale. These genome sequences augment the formidable genetic tools that have made Drosophila melanogaster a pre-eminent model for animal genetics, and will further catalyse fundamental research on mechanisms of development, cell biology, genetics, disease, neurobiology, behaviour, physiology and evolution. Despite remarkable similarities among these Drosophila species, we identified many putatively non-neutral changes in protein-coding genes, non-coding RNA genes, and cis-regulatory regions. These may prove to underlie differences in the ecology and behaviour of these diverse species.

}, keywords = {Animals, Codon, DNA Transposable Elements, Drosophila, Drosophila Proteins, Evolution, Molecular, Gene Order, Genes, Insect, Genome, Insect, Genome, Mitochondrial, Genomics, Immunity, Multigene Family, Phylogeny, Reproduction, RNA, Untranslated, sequence alignment, Sequence Analysis, DNA, Synteny}, issn = {1476-4687}, doi = {10.1038/nature06341}, author = {Clark, Andrew G and Eisen, Michael B and Smith, Douglas R and Bergman, Casey M and Oliver, Brian and Markow, Therese A and Kaufman, Thomas C and Kellis, Manolis and Gelbart, William and Iyer, Venky N and Pollard, Daniel A and Sackton, Timothy B and Larracuente, Amanda M and Singh, Nadia D and Abad, Jose P and Abt, Dawn N and Adryan, Boris and Aguade, Montserrat and Akashi, Hiroshi and Anderson, Wyatt W and Aquadro, Charles F and Ardell, David H and Arguello, Roman and Artieri, Carlo G and Barbash, Daniel A and Barker, Daniel and Barsanti, Paolo and Batterham, Phil and Batzoglou, Serafim and Begun, Dave and Bhutkar, Arjun and Blanco, Enrico and Bosak, Stephanie A and Bradley, Robert K and Brand, Adrianne D and Brent, Michael R and Brooks, Angela N and Brown, Randall H and Butlin, Roger K and Caggese, Corrado and Calvi, Brian R and Bernardo de Carvalho, A and Caspi, Anat and Castrezana, Sergio and Celniker, Susan E and Chang, Jean L and Chapple, Charles and Chatterji, Sourav and Chinwalla, Asif and Civetta, Alberto and Clifton, Sandra W and Comeron, Josep M and Costello, James C and Coyne, Jerry A and Daub, Jennifer and David, Robert G and Delcher, Arthur L and Delehaunty, Kim and Do, Chuong B and Ebling, Heather and Edwards, Kevin and Eickbush, Thomas and Evans, Jay D and Filipski, Alan and Findeiss, Sven and Freyhult, Eva and Fulton, Lucinda and Fulton, Robert and Garcia, Ana C L and Gardiner, Anastasia and Garfield, David A and Garvin, Barry E and Gibson, Greg and Gilbert, Don and Gnerre, Sante and Godfrey, Jennifer and Good, Robert and Gotea, Valer and Gravely, Brenton and Greenberg, Anthony J and Griffiths-Jones, Sam and Gross, Samuel and Guigo, Roderic and Gustafson, Erik A and Haerty, Wilfried and Hahn, Matthew W and Halligan, Daniel L and Halpern, Aaron L and Halter, Gillian M and Han, Mira V and Heger, Andreas and Hillier, LaDeana and Hinrichs, Angie S and Holmes, Ian and Hoskins, Roger A and Hubisz, Melissa J and Hultmark, Dan and Huntley, Melanie A and Jaffe, David B and Jagadeeshan, Santosh and Jeck, William R and Johnson, Justin and Jones, Corbin D and Jordan, William C and Karpen, Gary H and Kataoka, Eiko and Keightley, Peter D and Kheradpour, Pouya and Kirkness, Ewen F and Koerich, Leonardo B and Kristiansen, Karsten and Kudrna, Dave and Kulathinal, Rob J and Kumar, Sudhir and Kwok, Roberta and Lander, Eric and Langley, Charles H and Lapoint, Richard and Lazzaro, Brian P and Lee, So-Jeong and Levesque, Lisa and Li, Ruiqiang and Lin, Chiao-Feng and Lin, Michael F and Lindblad-Toh, Kerstin and Llopart, Ana and Long, Manyuan and Low, Lloyd and Lozovsky, Elena and Lu, Jian and Luo, Meizhong and Machado, Carlos A and Makalowski, Wojciech and Marzo, Mar and Matsuda, Muneo and Matzkin, Luciano and McAllister, Bryant and McBride, Carolyn S and McKernan, Brendan and McKernan, Kevin and Mendez-Lago, Maria and Minx, Patrick and Mollenhauer, Michael U and Montooth, Kristi and Mount, Stephen M and Mu, Xu and Myers, Eugene and Negre, Barbara and Newfeld, Stuart and Nielsen, Rasmus and Noor, Mohamed A F and O{\textquoteright}Grady, Patrick and Pachter, Lior and Papaceit, Montserrat and Parisi, Matthew J and Parisi, Michael and Parts, Leopold and Pedersen, Jakob S and Pesole, Graziano and Phillippy, Adam M and Ponting, Chris P and Pop, Mihai and Porcelli, Damiano and Powell, Jeffrey R and Prohaska, Sonja and Pruitt, Kim and Puig, Marta and Quesneville, Hadi and Ram, Kristipati Ravi and Rand, David and Rasmussen, Matthew D and Reed, Laura K and Reenan, Robert and Reily, Amy and Remington, Karin A and Rieger, Tania T and Ritchie, Michael G and Robin, Charles and Rogers, Yu-Hui and Rohde, Claudia and Rozas, Julio and Rubenfield, Marc J and Ruiz, Alfredo and Russo, Susan and Salzberg, Steven L and Sanchez-Gracia, Alejandro and Saranga, David J and Sato, Hajime and Schaeffer, Stephen W and Schatz, Michael C and Schlenke, Todd and Schwartz, Russell and Segarra, Carmen and Singh, Rama S and Sirot, Laura and Sirota, Marina and Sisneros, Nicholas B and Smith, Chris D and Smith, Temple F and Spieth, John and Stage, Deborah E and Stark, Alexander and Stephan, Wolfgang and Strausberg, Robert L and Strempel, Sebastian and Sturgill, David and Sutton, Granger and Sutton, Granger G and Tao, Wei and Teichmann, Sarah and Tobari, Yoshiko N and Tomimura, Yoshihiko and Tsolas, Jason M and Valente, Vera L S and Venter, Eli and Venter, J Craig and Vicario, Saverio and Vieira, Filipe G and Vilella, Albert J and Villasante, Alfredo and Walenz, Brian and Wang, Jun and Wasserman, Marvin and Watts, Thomas and Wilson, Derek and Wilson, Richard K and Wing, Rod A and Wolfner, Mariana F and Wong, Alex and Wong, Gane Ka-Shu and Wu, Chung-I and Wu, Gabriel and Yamamoto, Daisuke and Yang, Hsiao-Pei and Yang, Shiaw-Pyng and Yorke, James A and Yoshida, Kiyohito and Zdobnov, Evgeny and Zhang, Peili and Zhang, Yu and Zimin, Aleksey V and Baldwin, Jennifer and Abdouelleil, Amr and Abdulkadir, Jamal and Abebe, Adal and Abera, Brikti and Abreu, Justin and Acer, St Christophe and Aftuck, Lynne and Alexander, Allen and An, Peter and Anderson, Erica and Anderson, Scott and Arachi, Harindra and Azer, Marc and Bachantsang, Pasang and Barry, Andrew and Bayul, Tashi and Berlin, Aaron and Bessette, Daniel and Bloom, Toby and Blye, Jason and Boguslavskiy, Leonid and Bonnet, Claude and Boukhgalter, Boris and Bourzgui, Imane and Brown, Adam and Cahill, Patrick and Channer, Sheridon and Cheshatsang, Yama and Chuda, Lisa and Citroen, Mieke and Collymore, Alville and Cooke, Patrick and Costello, Maura and D{\textquoteright}Aco, Katie and Daza, Riza and De Haan, Georgius and DeGray, Stuart and DeMaso, Christina and Dhargay, Norbu and Dooley, Kimberly and Dooley, Erin and Doricent, Missole and Dorje, Passang and Dorjee, Kunsang and Dupes, Alan and Elong, Richard and Falk, Jill and Farina, Abderrahim and Faro, Susan and Ferguson, Diallo and Fisher, Sheila and Foley, Chelsea D and Franke, Alicia and Friedrich, Dennis and Gadbois, Loryn and Gearin, Gary and Gearin, Christina R and Giannoukos, Georgia and Goode, Tina and Graham, Joseph and Grandbois, Edward and Grewal, Sharleen and Gyaltsen, Kunsang and Hafez, Nabil and Hagos, Birhane and Hall, Jennifer and Henson, Charlotte and Hollinger, Andrew and Honan, Tracey and Huard, Monika D and Hughes, Leanne and Hurhula, Brian and Husby, M Erii and Kamat, Asha and Kanga, Ben and Kashin, Seva and Khazanovich, Dmitry and Kisner, Peter and Lance, Krista and Lara, Marcia and Lee, William and Lennon, Niall and Letendre, Frances and LeVine, Rosie and Lipovsky, Alex and Liu, Xiaohong and Liu, Jinlei and Liu, Shangtao and Lokyitsang, Tashi and Lokyitsang, Yeshi and Lubonja, Rakela and Lui, Annie and MacDonald, Pen and Magnisalis, Vasilia and Maru, Kebede and Matthews, Charles and McCusker, William and McDonough, Susan and Mehta, Teena and Meldrim, James and Meneus, Louis and Mihai, Oana and Mihalev, Atanas and Mihova, Tanya and Mittelman, Rachel and Mlenga, Valentine and Montmayeur, Anna and Mulrain, Leonidas and Navidi, Adam and Naylor, Jerome and Negash, Tamrat and Nguyen, Thu and Nguyen, Nga and Nicol, Robert and Norbu, Choe and Norbu, Nyima and Novod, Nathaniel and O{\textquoteright}Neill, Barry and Osman, Sahal and Markiewicz, Eva and Oyono, Otero L and Patti, Christopher and Phunkhang, Pema and Pierre, Fritz and Priest, Margaret and Raghuraman, Sujaa and Rege, Filip and Reyes, Rebecca and Rise, Cecil and Rogov, Peter and Ross, Keenan and Ryan, Elizabeth and Settipalli, Sampath and Shea, Terry and Sherpa, Ngawang and Shi, Lu and Shih, Diana and Sparrow, Todd and Spaulding, Jessica and Stalker, John and Stange-Thomann, Nicole and Stavropoulos, Sharon and Stone, Catherine and Strader, Christopher and Tesfaye, Senait and Thomson, Talene and Thoulutsang, Yama and Thoulutsang, Dawa and Topham, Kerri and Topping, Ira and Tsamla, Tsamla and Vassiliev, Helen and Vo, Andy and Wangchuk, Tsering and Wangdi, Tsering and Weiand, Michael and Wilkinson, Jane and Wilson, Adam and Yadav, Shailendra and Young, Geneva and Yu, Qing and Zembek, Lisa and Zhong, Danni and Zimmer, Andrew and Zwirko, Zac and Jaffe, David B and Alvarez, Pablo and Brockman, Will and Butler, Jonathan and Chin, CheeWhye and Gnerre, Sante and Grabherr, Manfred and Kleber, Michael and Mauceli, Evan and MacCallum, Iain} } @article {38205, title = {Differential Transcriptional Response to Nonassociative and Associative Components of Classical Fear Conditioning in the Amygdala and Hippocampus}, journal = {Learning \& MemoryLearn. Mem.Learning \& MemoryLearn. Mem.}, volume = {13}, year = {2006}, type = {10.1101/lm.86906}, abstract = {Classical fear conditioning requires the recognition of conditioned stimuli (CS) and the association of the CS with an aversive stimulus. We used Affymetrix oligonucleotide microarrays to characterize changes in gene expression compared to naive mice in both the amygdala and the hippocampus 30 min after classical fear conditioning and 30 min after exposure to the CS in the absence of an aversive stimulus. We found that in the hippocampus, levels of gene regulation induced by classical fear conditioning were not significantly greater than those induced by CS alone, whereas in the amygdala, classical fear conditioning did induce significantly greater levels of gene regulation compared to the CS. Computational studies suggest that transcriptional changes in the hippocampus and amygdala are mediated by large and overlapping but distinct combinations of molecular events. Our results demonstrate that an increase in gene regulation in the amygdala was partially correlated to associative learning and partially correlated to nonassociative components of the task, while gene regulation in the hippocampus was correlated to nonassociative components of classical fear conditioning, including configural learning.}, isbn = {1072-0502, 1549-5485}, author = {Keeley, Michael B. and Wood, Marcelo A. and Isiegas, Carolina and Stein, Joel and Hellman, Kevin and Sridhar Hannenhalli and Abel, Ted} } @article {49751, title = {How A.I. and multi-robot systems research will accelerate our understanding of social animal behavior}, volume = {94}, year = {2006}, pages = {1445-1463}, author = {Tucker Balch and Frank Dellaert and Adam Feldman and Andrew Guillory and Charles Isbell and Zia Khan and Andrew Stein and Hank Wilde} } @article {49561, title = {How Multirobot Systems Research will Accelerate our Understanding of Social Animal Behavior}, volume = {94}, year = {2006}, month = {Jan-07-2006}, pages = {1445 - 1463}, issn = {0018-9219}, doi = {10.1109/JPROC.2006.876969}, url = {http://ieeexplore.ieee.org/lpdocs/epic03/wrapper.htm?arnumber=1677955}, author = {Balch, T. and Dellaert, F. and Feldman, A. and Guillory, A. and Isbell, C.L. and Khan, Z. and Pratt, S.C. and Stein, A.N. and Wilde, H.} } @article {38162, title = {Comparative Genomics of Trypanosomatid Parasitic Protozoa}, journal = {ScienceScience}, volume = {309}, year = {2005}, type = {10.1126/science.1112181}, abstract = {A comparison of gene content and genome architecture of Trypanosoma brucei, Trypanosoma cruzi, and Leishmania major, three related pathogens with different life cycles and disease pathology, revealed a conserved core proteome of about 6200 genes in large syntenic polycistronic gene clusters. Many species-specific genes, especially large surface antigen families, occur at nonsyntenic chromosome-internal and subtelomeric regions. Retroelements, structural RNAs, and gene family expansion are often associated with syntenic discontinuities that{\textemdash}along with gene divergence, acquisition and loss, and rearrangement within the syntenic regions{\textemdash}have shaped the genomes of each parasite. Contrary to recent reports, our analyses reveal no evidence that these species are descended from an ancestor that contained a photosynthetic endosymbiont.}, author = {Najib M. El-Sayed and Myler, Peter J. and Blandin, Ga{\"e}lle and Berriman, Matthew and Crabtree, Jonathan and Aggarwal, Gautam and Caler, Elisabet and Renauld, Hubert and Worthey, Elizabeth A. and Hertz-Fowler, Christiane and Ghedin, Elodie and Peacock, Christopher and Bartholomeu, Daniella C. and Haas, Brian J. and Tran, Anh-Nhi and Wortman, Jennifer R. and Alsmark, U. Cecilia M. and Angiuoli, Samuel and Anupama, Atashi and Badger, Jonathan and Bringaud, Frederic and Cadag, Eithon and Carlton, Jane M. and Cerqueira, Gustavo C. and Creasy, Todd and Delcher, Arthur L. and Djikeng, Appolinaire and Embley, T. Martin and Hauser, Christopher and Ivens, Alasdair C. and Kummerfeld, Sarah K. and Pereira-Leal, Jose B. and Nilsson, Daniel and Peterson, Jeremy and Salzberg, Steven L. and Shallom, Joshua and Silva, Joana C. and Sundaram, Jaideep and Westenberger, Scott and White, Owen and Melville, Sara E. and Donelson, John E. and Andersson, Bj{\"o}rn and Stuart, Kenneth D. and Hall, Neil} } @article {38104, title = {Advances in schistosome genomics}, journal = {Trends in ParasitologyTrends in Parasitology}, volume = {20}, year = {2004}, type = {16/j.pt.2004.02.002}, abstract = {In Spring 2004, the first draft of the 270~Mb genome of Schistosoma mansoni will be released. This sequence is based on the assembly and annotation of a >7.5-fold coverage, shotgun sequencing project. The key stages involved in the international collaborative efforts that have led to the generation of these sequencing data for the parasite S. mansoni are discussed here.}, isbn = {1471-4922}, author = {Najib M. El-Sayed and Bartholomeu, Daniella and Ivens, Alasdair and Johnston, David A. and LoVerde, Philip T.} } @article {38149, title = {CHARACTERIZATION OF< i> Ath17, A QUANTITATIVE TRAIT LOCUS FOR ATHEROSCLEROSIS SUSCEPTIBILITY BETWEEN C57BL/6J AND 129S1/SvImJ; SINGLE-NUCLEOTIDE POLYMORPHISMS HAVE IMPORTANT IMPLICATIONS ON IDENTIFYING ATHEROSCLEROSIS MODIFIER GENES}, journal = {Cardiovascular PathologyCardiovascular Pathology}, volume = {13}, year = {2004}, publisher = {Elsevier}, author = {Ishimori, N. and Walsh, K. and Zheng, X. and Lu, F. and Sridhar Hannenhalli and Nusskern, D. and Mural, R. and Paigen, B.} } @article {49635, title = {Gene synteny and evolution of genome architecture in trypanosomatids.}, journal = {Mol Biochem Parasitol}, volume = {134}, year = {2004}, month = {2004 Apr}, pages = {183-91}, abstract = {

The trypanosomatid protozoa Trypanosoma brucei, Trypanosoma cruzi and Leishmania major are related human pathogens that cause markedly distinct diseases. Using information from genome sequencing projects currently underway, we have compared the sequences of large chromosomal fragments from each species. Despite high levels of divergence at the sequence level, these three species exhibit a striking conservation of gene order, suggesting that selection has maintained gene order among the trypanosomatids over hundreds of millions of years of evolution. The few sites of genome rearrangement between these species are marked by the presence of retrotransposon-like elements, suggesting that retrotransposons may have played an important role in shaping trypanosomatid genome organization. A degenerate retroelement was identified in L. major by examining the regions near breakage points of the synteny. This is the first such element found in L. major suggesting that retroelements were found in the common ancestor of all three species.

}, keywords = {Animals, Computational Biology, Evolution, Molecular, Gene Order, Genome, Protozoan, Genomics, Leishmania major, Multigene Family, Recombination, Genetic, Retroelements, Selection, Genetic, Synteny, Trypanosoma brucei brucei, Trypanosoma cruzi, Trypanosomatina}, issn = {0166-6851}, doi = {10.1016/j.molbiopara.2003.11.012}, author = {Ghedin, Elodie and Bringaud, Frederic and Peterson, Jeremy and Myler, Peter and Berriman, Matthew and Ivens, Alasdair and Andersson, Bj{\"o}rn and Bontempi, Esteban and Eisen, Jonathan and Angiuoli, Sam and Wanless, David and Von Arx, Anna and Murphy, Lee and Lennard, Nicola and Salzberg, Steven and Adams, Mark D and White, Owen and Hall, Neil and Stuart, Kenneth and Fraser, Claire M and el-Sayed, Najib M A} } @article {38418, title = {Pandemic strains of O3:K6 Vibrio parahaemolyticus in the aquatic environment of Bangladesh}, journal = {Canadian Journal of MicrobiologyCanadian Journal of Microbiology}, volume = {50}, year = {2004}, abstract = {A total of 1500 environmental strains of Vibrio parahaemolyticus, isolated from the aquatic environment of Bangladesh, were screened for the presence of a major V. parahaemolyticus virulence factor, the thermostable direct haemolysin (tdh) gene, by the colony blot hybridization method using a digoxigenin-labeled tdh gene probe. Of 1500 strains, 5 carried the tdh sequence, which was further confirmed by PCR using primers specific for the tdh gene. Examination by PCR confirmed that the 5 strains were V. parahamolyticus and lacked the thermostable direct haemolysin-related haemolysin (trh) gene, the alternative major virulence gene known to be absent in pandemic strains. All 5 strains gave positive Kanagawa phenomenon reaction with characteristic beta-haemolysis on Wagatsuma agar medium. Southern blot analysis of the HindIII-digested chromosomal DNA demonstrated, in all 5 strains, the presence of 2 tdh genes common to strains positive for Kanagawa phenomenon. However, the 5 strains were found to belong to 3 different serotypes (O3:K29, O4:K37, and O3:K6). The 2 with pandemic serotype O3:K6 gave positive results in group-specific PCR and ORF8 PCR assays, characteristics unique to the pandemic clone. Clonal variations among the 5 isolates were analyzed by comparing RAPD and ribotyping patterns. Results showed different patterns for the 3 serotypes, but the pattern was identical among the O3:K6 strains. This is the first report on the isolation of pandemic O3:K6 strains of V. parahaemolyticus from the aquatic environment of Bangladesh.}, author = {Islam, M. S. and Tasmin, Rizwana and Khan, Sirajul I. s l a m and Bakht, Habibul B. M. and Mahmood, Zahid H. a y a t and Rahman, M. Z. i a u r and Bhuiyan, Nurul A. m i n and Nishibuchi, Mitsuaki and Nair, G. B. a l a k r i s h and Sack, R. B. r a d l e y and Huq, Anwar and Rita R. Colwell and Sack, David A.} } @article {38562, title = {Variation of toxigenic Vibrio cholerae O1 in the aquatic environment of Bangladesh and its correlation with the clinical strains}, journal = {Microbiology and immunologyMicrobiology and Immunology}, volume = {48}, year = {2004}, author = {Islam, M. S. and Talukder, K. A. and Khan, N. H. and Mahmud, Z. H. and Rahman, M. Z. and Nair, G. B. and Siddique, A. K. M. and Yunus, M. and Sack, D. A. and Sack, R. B. and Rita R. Colwell} } @article {38576, title = {Whole-genome shotgun assembly and comparison of human genome assemblies}, journal = {Proceedings of the National Academy of Sciences of the United States of AmericaProceedings of the National Academy of Sciences of the United States of America}, volume = {101}, year = {2004}, publisher = {National Acad Sciences}, author = {Istrail, S. and Sutton, G. G. and Florea, L. and Halpern, A. L. and Mobarry, C. M. and Lippert, R. and Walenz, B. and Shatkay, H. and Dew, I. and Miller, J. R. and others,} } @article {38098, title = {A 4-Year Study of the Epidemiology of Vibrio Cholerae in Four Rural Areas of Bangladesh}, journal = {Journal of Infectious DiseasesJ Infect Dis.Journal of Infectious DiseasesJ Infect Dis.}, volume = {187}, year = {2003}, type = {10.1086/345865}, abstract = {How Vibrio cholerae spreads around the world and what determines its seasonal peaks in endemic areas are not known. These features of cholera have been hypothesized to be primarily the result of environmental factors associated with aquatic habitats that can now be identified. Since 1997, fortnightly surveillance in 4 widely separated geographic locations in Bangladesh has been performed to identify patients with cholera and to collect environmental data. A total of 5670 patients (53\% <5 years of age) have been studied; 14.3\% had cholera (10.4\% due to V. cholerae O1 El Tor, 3.8\% due to O139). Both serogroups were found in all locations; outbreaks were seasonal and often occurred simultaneously. Water-use patterns showed that bathing and washing clothes in tube-well water was significantly protective in two of the sites. These data will be correlated with environmental factors, to develop a model for prediction of cholera outbreaks}, isbn = {0022-1899, 1537-6613}, author = {Sack, R. Bradley and Siddique, A. Kasem and Longini, Ira M. and Nizam, Azhar and Yunus, Md and M. Sirajul Islam and Morris and Ali, Afsar and Huq, Anwar and Nair, G. Balakrish and Qadri, Firdausi and Faruque, Shah M. and Sack, David A. and Rita R. Colwell} } @article {38458, title = {Reduction of Cholera in Bangladeshi Villages by Simple Filtration}, journal = {Proceedings of the National Academy of SciencesPNASProceedings of the National Academy of SciencesPNAS}, volume = {100}, year = {2003}, type = {10.1073/pnas.0237386100}, abstract = {Based on results of ecological studies demonstrating that Vibrio cholerae, the etiological agent of epidemic cholera, is commensal to zooplankton, notably copepods, a simple filtration procedure was developed whereby zooplankton, most phytoplankton, and particulates >20 μm were removed from water before use. Effective deployment of this filtration procedure, from September 1999 through July 2002 in 65 villages of rural Bangladesh, of which the total population for the entire study comprised ≈133,000 individuals, yielded a 48\% reduction in cholera (P < 0.005) compared with the control.}, isbn = {0027-8424, 1091-6490}, author = {Rita R. Colwell and Huq, Anwar and M. Sirajul Islam and K. M. A. Aziz and Yunus, M. and N. Huda Khan and A. Mahmud and Sack, R. Bradley and Nair, G. B. and J. Chakraborty and Sack, David A. and E. Russek-Cohen} } @article {38148, title = {Characterization of Pseudoalteromonas citrea and P. nigrifaciens Isolated from Different Ecological Habitats Based on REP-PCR Genomic Fingerprints}, journal = {Systematic and Applied MicrobiologySystematic and Applied Microbiology}, volume = {25}, year = {2002}, type = {10.1078/0723-2020-00103}, abstract = {SummaryDNA primers corresponding to conserved repetitive interspersed genomic motifs and PCR were used to show that REP, ERIC and BOX-like DNA sequences are present in marine, oxidative, Gram-negative Pseudoalteromonas strains. REP, ERIC and BOX-PCR were used for rapid molecular characterization of both the type species of the genus and environmental strains isolated from samples collected in different geographical areas. PCR-generated genomic fingerprint patterns were found to be both complex and strain specific. Analysis of the genotypic structure of phenotypically diverse P. citrea revealed a geographic clustering of Far Eastern brown-pigmented, agar-digesting strains of this species. Marine isolates of P. nigrifaciens with 67{\textendash}70\% DNA relatedness generated genomic patterns different from those of the type strain and formed a separate cluster. It is concluded that REP, ERIC and BOX-PCR are effective in generating strain specific patterns that can be used to elucidate geographic distribution, with these genomic patterns providing a valuable biogeographic criterion.}, keywords = {biogeography, BOX-PCR, ERIC, Pseudoalteromonas, REP}, isbn = {0723-2020}, author = {Ivanova, Elena P. and Matte, Glavur R. and Matte, Maria H. and Coenye, Tom and Huq, Anwarul and Rita R. Colwell} } @article {49687, title = {The draft genome of Ciona intestinalis: insights into chordate and vertebrate origins.}, journal = {Science}, volume = {298}, year = {2002}, month = {2002 Dec 13}, pages = {2157-67}, abstract = {

The first chordates appear in the fossil record at the time of the Cambrian explosion, nearly 550 million years ago. The modern ascidian tadpole represents a plausible approximation to these ancestral chordates. To illuminate the origins of chordate and vertebrates, we generated a draft of the protein-coding portion of the genome of the most studied ascidian, Ciona intestinalis. The Ciona genome contains approximately 16,000 protein-coding genes, similar to the number in other invertebrates, but only half that found in vertebrates. Vertebrate gene families are typically found in simplified form in Ciona, suggesting that ascidians contain the basic ancestral complement of genes involved in cell signaling and development. The ascidian genome has also acquired a number of lineage-specific innovations, including a group of genes engaged in cellulose metabolism that are related to those in bacteria and fungi.

}, keywords = {Alleles, Animals, Apoptosis, Base Sequence, Cellulose, Central Nervous System, Ciona intestinalis, Computational Biology, Endocrine System, Gene Dosage, Gene Duplication, genes, Genes, Homeobox, Genome, Heart, Immunity, Molecular Sequence Data, Multigene Family, Muscle Proteins, Organizers, Embryonic, Phylogeny, Polymorphism, Genetic, Proteins, Sequence Analysis, DNA, Sequence Homology, Nucleic Acid, Species Specificity, Thyroid Gland, Urochordata, Vertebrates}, issn = {1095-9203}, doi = {10.1126/science.1080049}, author = {Dehal, Paramvir and Satou, Yutaka and Campbell, Robert K and Chapman, Jarrod and Degnan, Bernard and De Tomaso, Anthony and Davidson, Brad and Di Gregorio, Anna and Gelpke, Maarten and Goodstein, David M and Harafuji, Naoe and Hastings, Kenneth E M and Ho, Isaac and Hotta, Kohji and Huang, Wayne and Kawashima, Takeshi and Lemaire, Patrick and Martinez, Diego and Meinertzhagen, Ian A and Necula, Simona and Nonaka, Masaru and Putnam, Nik and Rash, Sam and Saiga, Hidetoshi and Satake, Masanobu and Terry, Astrid and Yamada, Lixy and Wang, Hong-Gang and Awazu, Satoko and Azumi, Kaoru and Boore, Jeffrey and Branno, Margherita and Chin-Bow, Stephen and DeSantis, Rosaria and Doyle, Sharon and Francino, Pilar and Keys, David N and Haga, Shinobu and Hayashi, Hiroko and Hino, Kyosuke and Imai, Kaoru S and Inaba, Kazuo and Kano, Shungo and Kobayashi, Kenji and Kobayashi, Mari and Lee, Byung-In and Makabe, Kazuhiro W and Manohar, Chitra and Matassi, Giorgio and Medina, Monica and Mochizuki, Yasuaki and Mount, Steve and Morishita, Tomomi and Miura, Sachiko and Nakayama, Akie and Nishizaka, Satoko and Nomoto, Hisayo and Ohta, Fumiko and Oishi, Kazuko and Rigoutsos, Isidore and Sano, Masako and Sasaki, Akane and Sasakura, Yasunori and Shoguchi, Eiichi and Shin-i, Tadasu and Spagnuolo, Antoinetta and Stainier, Didier and Suzuki, Miho M and Tassy, Olivier and Takatori, Naohito and Tokuoka, Miki and Yagi, Kasumi and Yoshizaki, Fumiko and Wada, Shuichi and Zhang, Cindy and Hyatt, P Douglas and Larimer, Frank and Detter, Chris and Doggett, Norman and Glavina, Tijana and Hawkins, Trevor and Richardson, Paul and Lucas, Susan and Kohara, Yuji and Levine, Michael and Satoh, Nori and Rokhsar, Daniel S} } @article {38317, title = {Genomic profiles of clinical and environmental isolates of Vibrio cholerae O1 in cholera-endemic areas of Bangladesh}, journal = {Proceedings of the National Academy of SciencesProceedings of the National Academy of Sciences}, volume = {99}, year = {2002}, type = {10.1073/pnas.192426499}, abstract = {Diversity, relatedness, and ecological interactions of toxigenic Vibrio cholerae O1 populations in two distinctive habitats, the human intestine and the aquatic environment, were analyzed. Twenty environmental isolates and 42 clinical isolates were selected for study by matching serotype, geographic location of isolation in Bangladesh, and season of isolation. Genetic profiling was done by enterobacterial repetitive intergenic consensus sequence{\textendash}PCR, optimized for profiling by using the fully sequenced V. cholerae El Tor N16961 genome. Five significant clonal clusters of haplotypes were found from 57 electrophoretic types. Isolates from different areas or habitats intermingled in two of the five significant clusters. Frequencies of haplotypes differed significantly only between the environmental populations (exact test; P < 0.05). Analysis of molecular variance yielded a population genetic structure reflecting the differentiating effects of geographic area, habitat, and sampling time. Although a parameter confounding the latter differences explained 9\% of the total molecular variance in the entire population (P < 0.01), the net effect of habitat and time could not be separated because of the small number of environmental isolates included in the study. Five subpopulations from a single area were determined, and from these we were able to estimate a relative differentiating effect of habitat, which was small compared with the effect of temporal change. In conclusion, the resulting population structure supports the hypothesis that spatial and temporal fluctuations in the composition of toxigenic V. cholerae populations in the aquatic environment can cause shifts in the dynamics of the disease.}, isbn = {0027-8424, 1091-6490}, author = {Zo, Y. G. and Rivera, I. N. G. and E. Russek-Cohen and Islam, M. S. and Siddique, A. K. and Yunus, M. and Sack, R. B. and Huq, A. and Rita R. Colwell} } @article {38449, title = {Proceedings of the sixth annual international conference on Computational biology}, year = {2002}, publisher = {ACM}, author = {Myers, G. and Sridhar Hannenhalli and Sankoff, D. and Istrail, S. and Pevzner, P. and Waterman, M.} } @article {49692, title = {The genome sequence of Drosophila melanogaster.}, journal = {Science}, volume = {287}, year = {2000}, month = {2000 Mar 24}, pages = {2185-95}, abstract = {

The fly Drosophila melanogaster is one of the most intensively studied organisms in biology and serves as a model system for the investigation of many developmental and cellular processes common to higher eukaryotes, including humans. We have determined the nucleotide sequence of nearly all of the approximately 120-megabase euchromatic portion of the Drosophila genome using a whole-genome shotgun sequencing strategy supported by extensive clone-based sequence and a high-quality bacterial artificial chromosome physical map. Efforts are under way to close the remaining gaps; however, the sequence is of sufficient accuracy and contiguity to be declared substantially complete and to support an initial analysis of genome structure and preliminary gene annotation and interpretation. The genome encodes approximately 13,600 genes, somewhat fewer than the smaller Caenorhabditis elegans genome, but with comparable functional diversity.

}, keywords = {Animals, Biological Transport, Chromatin, Cloning, Molecular, Computational Biology, Contig Mapping, Cytochrome P-450 Enzyme System, DNA Repair, DNA Replication, Drosophila melanogaster, Euchromatin, Gene Library, Genes, Insect, Genome, Heterochromatin, Insect Proteins, Nuclear Proteins, Protein Biosynthesis, Sequence Analysis, DNA, Transcription, Genetic}, issn = {0036-8075}, author = {Adams, M D and Celniker, S E and Holt, R A and Evans, C A and Gocayne, J D and Amanatides, P G and Scherer, S E and Li, P W and Hoskins, R A and Galle, R F and George, R A and Lewis, S E and Richards, S and Ashburner, M and Henderson, S N and Sutton, G G and Wortman, J R and Yandell, M D and Zhang, Q and Chen, L X and Brandon, R C and Rogers, Y H and Blazej, R G and Champe, M and Pfeiffer, B D and Wan, K H and Doyle, C and Baxter, E G and Helt, G and Nelson, C R and Gabor, G L and Abril, J F and Agbayani, A and An, H J and Andrews-Pfannkoch, C and Baldwin, D and Ballew, R M and Basu, A and Baxendale, J and Bayraktaroglu, L and Beasley, E M and Beeson, K Y and Benos, P V and Berman, B P and Bhandari, D and Bolshakov, S and Borkova, D and Botchan, M R and Bouck, J and Brokstein, P and Brottier, P and Burtis, K C and Busam, D A and Butler, H and Cadieu, E and Center, A and Chandra, I and Cherry, J M and Cawley, S and Dahlke, C and Davenport, L B and Davies, P and de Pablos, B and Delcher, A and Deng, Z and Mays, A D and Dew, I and Dietz, S M and Dodson, K and Doup, L E and Downes, M and Dugan-Rocha, S and Dunkov, B C and Dunn, P and Durbin, K J and Evangelista, C C and Ferraz, C and Ferriera, S and Fleischmann, W and Fosler, C and Gabrielian, A E and Garg, N S and Gelbart, W M and Glasser, K and Glodek, A and Gong, F and Gorrell, J H and Gu, Z and Guan, P and Harris, M and Harris, N L and Harvey, D and Heiman, T J and Hernandez, J R and Houck, J and Hostin, D and Houston, K A and Howland, T J and Wei, M H and Ibegwam, C and Jalali, M and Kalush, F and Karpen, G H and Ke, Z and Kennison, J A and Ketchum, K A and Kimmel, B E and Kodira, C D and Kraft, C and Kravitz, S and Kulp, D and Lai, Z and Lasko, P and Lei, Y and Levitsky, A A and Li, J and Li, Z and Liang, Y and Lin, X and Liu, X and Mattei, B and McIntosh, T C and McLeod, M P and McPherson, D and Merkulov, G and Milshina, N V and Mobarry, C and Morris, J and Moshrefi, A and Mount, S M and Moy, M and Murphy, B and Murphy, L and Muzny, D M and Nelson, D L and Nelson, D R and Nelson, K A and Nixon, K and Nusskern, D R and Pacleb, J M and Palazzolo, M and Pittman, G S and Pan, S and Pollard, J and Puri, V and Reese, M G and Reinert, K and Remington, K and Saunders, R D and Scheeler, F and Shen, H and Shue, B C and Sid{\'e}n-Kiamos, I and Simpson, M and Skupski, M P and Smith, T and Spier, E and Spradling, A C and Stapleton, M and Strong, R and Sun, E and Svirskas, R and Tector, C and Turner, R and Venter, E and Wang, A H and Wang, X and Wang, Z Y and Wassarman, D A and Weinstock, G M and Weissenbach, J and Williams, S M and Worley, K C and Wu, D and Yang, S and Yao, Q A and Ye, J and Yeh, R F and Zaveri, J S and Zhan, M and Zhang, G and Zhao, Q and Zheng, L and Zheng, X H and Zhong, F N and Zhong, W and Zhou, X and Zhu, S and Zhu, X and Smith, H O and Gibbs, R A and Myers, E W and Rubin, G M and Venter, J C} } @article {49627, title = {Genetic nomenclature for Trypanosoma and Leishmania.}, journal = {Mol Biochem Parasitol}, volume = {97}, year = {1998}, month = {1998 Nov 30}, pages = {221-4}, keywords = {Animals, Leishmania, Terminology as Topic, Trypanosoma}, issn = {0166-6851}, author = {Clayton, C and Adams, M and Almeida, R and Baltz, T and Barrett, M and Bastien, P and Belli, S and Beverley, S and Biteau, N and Blackwell, J and Blaineau, C and Boshart, M and Bringaud, F and Cross, G and Cruz, A and Degrave, W and Donelson, J and El-Sayed, N and Fu, G and Ersfeld, K and Gibson, W and Gull, K and Ivens, A and Kelly, J and Vanhamme, L} } @proceedings {38502, title = {A SIMD solution to the sequence comparison problem on the MGAP}, year = {1994}, month = {1994}, publisher = {IEEE}, type = {10.1109/ASAP.1994.331791}, abstract = {Molecular biologists frequently compare an unknown biosequence with a set of other known biosequences to find the sequence which is maximally similar, with the hope that what is true of one sequence, either physically or functionally, could be true of its analogue. Even though efficient dynamic programming algorithms exist for the problem, when the size of the database is large, the time required is quite long, even for moderate length sequences. In this paper, we present an efficient pipelined SIMD solution to the sequence alignment problem on the Micro-Grain Array Processor (MGAP), a fine-grained massively parallel array of processors with nearest-neighbor connections. The algorithm compares K sequences of length O(M) with the actual sequence of length N, in O(M+N+K) time with O(MN) processors, which is AT-optimal. The implementation on the MGAP computes at the rate of about 0.1 million comparisons per second for sequences of length 128}, keywords = {AT-optimal algorithm, Biological information theory, biology computing, biosequence comparison problem, computational complexity, Computer science, Costs, database size, Databases, DNA computing, dynamic programming, dynamic programming algorithms, fine-grained massively parallel processor array, Genetics, Heuristic algorithms, maximally similar sequence, MGAP parallel computer, Micro-Grain Array Processor, Military computing, molecular biology, molecular biophysics, Nearest neighbor searches, nearest-neighbor connections, Parallel algorithms, pipeline processing, pipelined SIMD solution, sequence alignment problem, sequences}, isbn = {0-8186-6517-3}, author = {Borah, M. and Bajwa, R. S. and Sridhar Hannenhalli and Irwin, M. J.} }