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Search Results: 1 - 10 of 2857 matches for " Baribault Carl "
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A Metastate HMM with Application to Gene Structure Identification in Eukaryotes
Winters-Hilt Stephen,Baribault Carl
EURASIP Journal on Advances in Signal Processing , 2010,
Abstract: We introduce a generalized-clique hidden Markov model (HMM) and apply it to gene finding in eukaryotes (C. elegans). We demonstrate a HMM structure identification platform that is novel and robustly-performing in a number of ways. The generalized clique HMM begins by enlarging the primitive hidden states associated with the individual base labels (as exon, intron, or junk) to substrings of primitive hidden states, or footprint states, having a minimal length greater than the footprint state length. The emissions are likewise expanded to higher order in the fundamental joint probability that is the basis of the generalized-clique, or "metastate", HMM. We then consider application to eukaryotic gene finding and show how such a metastate HMM improves the strength of coding/noncoding-transition contributions to gene-structure identification. We will describe situations where the coding/noncoding-transition modeling can effectively recapture the exon and intron heavy tail distribution modeling capability as well as manage the exon-start needle-in-the-haystack problem. In analysis of the C. elegans genome we show that the sensitivity and specificity (SN,SP) results for both the individual-state and full-exon predictions are greatly enhanced over the standard HMM when using the generalized-clique HMM.
A Metastate HMM with Application to Gene Structure Identification in Eukaryotes
Stephen Winters-Hilt,Carl Baribault
EURASIP Journal on Advances in Signal Processing , 2010, DOI: 10.1155/2010/581373
Abstract:
RNA CoMPASS: A Dual Approach for Pathogen and Host Transcriptome Analysis of RNA-Seq Datasets
Guorong Xu, Michael J. Strong, Michelle R. Lacey, Carl Baribault, Erik K. Flemington, Christopher M. Taylor
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0089445
Abstract: High-throughput RNA sequencing (RNA-seq) has become an instrumental assay for the analysis of multiple aspects of an organism's transcriptome. Further, the analysis of a biological specimen's associated microbiome can also be performed using RNA-seq data and this application is gaining interest in the scientific community. There are many existing bioinformatics tools designed for analysis and visualization of transcriptome data. Despite the availability of an array of next generation sequencing (NGS) analysis tools, the analysis of RNA-seq data sets poses a challenge for many biomedical researchers who are not familiar with command-line tools. Here we present RNA CoMPASS, a comprehensive RNA-seq analysis pipeline for the simultaneous analysis of transcriptomes and metatranscriptomes from diverse biological specimens. RNA CoMPASS leverages existing tools and parallel computing technology to facilitate the analysis of even very large datasets. RNA CoMPASS has a web-based graphical user interface with intrinsic queuing to control a distributed computational pipeline. RNA CoMPASS was evaluated by analyzing RNA-seq data sets from 45 B-cell samples. Twenty-two of these samples were derived from lymphoblastoid cell lines (LCLs) generated by the infection of na?ve B-cells with the Epstein Barr virus (EBV), while another 23 samples were derived from Burkitt's lymphomas (BL), some of which arose in part through infection with EBV. Appropriately, RNA CoMPASS identified EBV in all LCLs and in a fraction of the BLs. Cluster analysis of the human transcriptome component of the RNA CoMPASS output clearly separated the BLs (which have a germinal center-like phenotype) from the LCLs (which have a blast-like phenotype) with evidence of activated MYC signaling and lower interferon and NF-kB signaling in the BLs. Together, this analysis illustrates the utility of RNA CoMPASS in the simultaneous analysis of transcriptome and metatranscriptome data. RNA CoMPASS is freely available at http://rnacompass.sourceforge.net/.
Gene expression during normal and FSHD myogenesis
Koji Tsumagari, Shao-Chi Chang, Michelle Lacey, Carl Baribault, Sridar V Chittur, Janet Sowden, Rabi Tawil, Gregory E Crawford, Melanie Ehrlich
BMC Medical Genomics , 2011, DOI: 10.1186/1755-8794-4-67
Abstract: Using exon-based microarrays, the expression profiles of myogenic precursor cells were determined. Both undifferentiated myoblasts and myoblasts differentiated to myotubes derived from FSHD patients and controls were studied after immunocytochemical verification of the quality of the cultures. To further our understanding of FSHD and normal myogenesis, the expression profiles obtained were compared to those of 19 non-muscle cell types analyzed by identical methods.Many of the ~17,000 examined genes were differentially expressed (> 2-fold, p < 0.01) in control myoblasts or myotubes vs. non-muscle cells (2185 and 3006, respectively) or in FSHD vs. control myoblasts or myotubes (295 and 797, respectively). Surprisingly, despite the morphologically normal differentiation of FSHD myoblasts to myotubes, most of the disease-related dysregulation was seen as dampening of normal myogenesis-specific expression changes, including in genes for muscle structure, mitochondrial function, stress responses, and signal transduction. Other classes of genes, including those encoding extracellular matrix or pro-inflammatory proteins, were upregulated in FSHD myogenic cells independent of an inverse myogenesis association. Importantly, the disease-linked DUX4 RNA isoform was detected by RT-PCR in FSHD myoblast and myotube preparations only at extremely low levels. Unique insights into myogenesis-specific gene expression were also obtained. For example, all four Argonaute genes involved in RNA-silencing were significantly upregulated during normal (but not FSHD) myogenesis relative to non-muscle cell types.DUX4's pathogenic effect in FSHD may occur transiently at or before the stage of myoblast formation to establish a cascade of gene dysregulation. This contrasts with the current emphasis on toxic effects of experimentally upregulated DUX4 expression at the myoblast or myotube stages. Our model could explain why DUX4's inappropriate expression was barely detectable in myoblasts and myotu
Differences in Gastric Carcinoma Microenvironment Stratify According to EBV Infection Intensity: Implications for Possible Immune Adjuvant Therapy
Michael J. Strong equal contributor,Guorong Xu equal contributor,Joseph Coco,Carl Baribault,Dass S. Vinay,Michelle R. Lacey,Amy L. Strong,Teresa A. Lehman,Michael B. Seddon,Zhen Lin,Monica Concha,Melody Baddoo,MaryBeth Ferris,Kenneth F. Swan,Deborah E. Sullivan,Matthew E. Burow,Christopher M. Taylor ,Erik K. Flemington
PLOS Pathogens , 2013, DOI: 10.1371/journal.ppat.1003341
Abstract: Epstein-Barr virus (EBV) is associated with roughly 10% of gastric carcinomas worldwide (EBVaGC). Although previous investigations provide a strong link between EBV and gastric carcinomas, these studies were performed using selected EBV gene probes. Using a cohort of gastric carcinoma RNA-seq data sets from The Cancer Genome Atlas (TCGA), we performed a quantitative and global assessment of EBV gene expression in gastric carcinomas and assessed EBV associated cellular pathway alterations. EBV transcripts were detected in 17% of samples but these samples varied significantly in EBV coverage depth. In four samples with the highest EBV coverage (hiEBVaGC – high EBV associated gastric carcinoma), transcripts from the BamHI A region comprised the majority of EBV reads. Expression of LMP2, and to a lesser extent, LMP1 were also observed as was evidence of abortive lytic replication. Analysis of cellular gene expression indicated significant immune cell infiltration and a predominant IFNG response in samples expressing high levels of EBV transcripts relative to samples expressing low or no EBV transcripts. Despite the apparent immune cell infiltration, high levels of the cytotoxic T-cell (CTL) and natural killer (NK) cell inhibitor, IDO1, was observed in the hiEBVaGCs samples suggesting an active tolerance inducing pathway in this subgroup. These results were confirmed in a separate cohort of 21 Vietnamese gastric carcinoma samples using qRT-PCR and on tissue samples using in situ hybridization and immunohistochemistry. Lastly, a panel of tumor suppressors and candidate oncogenes were expressed at lower levels in hiEBVaGC versus EBV-low and EBV-negative gastric cancers suggesting the direct regulation of tumor pathways by EBV.
Keratins provide virus-dependent protection or predisposition to injury in coxsackievirus-induced pancreatitis
DM Toivola, SE Ostrowski, H Baribault, et al
Cell Health and Cytoskeleton , 2009, DOI: http://dx.doi.org/10.2147/CHC.S5792
Abstract: atins provide virus-dependent protection or predisposition to injury in coxsackievirus-induced pancreatitis Original Research (4039) Total Article Views Authors: DM Toivola, SE Ostrowski, H Baribault, et al Published Date August 2009 Volume 2009:1 Pages 51 - 65 DOI: http://dx.doi.org/10.2147/CHC.S5792 DM Toivola1, SE Ostrowski2, H Baribault3, TM Magin4, AI Ramsingh2, MB Omary5 1 bo Akademi University, Dept. Biology, BioCity, Turku, Finland and Stanford University School of Medicine and Digestive Disease Center; 2New York State Department of Health, Albany, NY, USA; 3Amgen, South San Francisco, CA, USA; 4University of Bonn, Bonn, Germany; 5Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Mi, USA Abstract: Keratins 8 and 18 (K8/K18) are the two major intermediate filament proteins in hepatocytes and pancreatic acinar cells. Acinar cell keratins are organized as cytoplasmic and apicolateral filaments. An important role of hepatocyte K8/K18 is to maintain cellular integrity, while this cytoprotective function of K8/K18 is not evident in the pancreas since keratin-deficient mice cope well with pancreatitis models. To further study the roles of keratins in the exocrine pancreas, we used coxsackievirus B4-models, CVB4-V and CVB4-P, to induce severe acute/chronic pancreatitis and acute pancreatitis, respectively, in K8-null (which lack acinar keratins) and K18-null (which lack cytoplasmic keratins) mice. Despite similar virus titers in all mice, CVB4-V resulted in 40% mortality of the K8-null mice 14 days post-infection compared to no lethality of WT and K18-null mice. In contrast, K8-null mice were far less susceptible to CVB4-P-induced damage as determined by histology and serology analysis, and they recover faster than WT and K18-null mice. After CVB4 virus infection, keratins aggregated during acinar degranulation, and K8/K18 site-specific phosphorylation was observed during degranulation and recovery. Hence, keratins significantly affect CVB4 virulence, positively or negatively, depending on the virus subtype and keratin makeup, in a virus replication-independent manner.
Hidden Markov Model with Duration Side Information for Novel HMMD Derivation, with Application to Eukaryotic Gene Finding
Winters-Hilt S,Jiang Z,Baribault C
EURASIP Journal on Advances in Signal Processing , 2010,
Abstract: We describe a new method to introduce duration into an HMM using side information that can be put in the form of a martingale series. Our method makes use of ratios of duration cumulant probabilities in a manner that meshes with the column-level dynamic programming construction. Other information that could be incorporated, via ratios of sequence matches, includes an EST and homology information. A familiar occurrence of a martingale in HMM-based efforts is the sequence-likelihood ratio classification. Our method suggests a general procedure for piggybacking other side information as ratios of side information probabilities, in association (e.g., one-to-one) with the duration-probability ratios. Using our method, the HMM can be fully informed by the side information available during its dynamic table optimization—in Viterbi path calculations in particular.
Hidden Markov Model with Duration Side Information for Novel HMMD Derivation, with Application to Eukaryotic Gene Finding
S. Winters-Hilt,Z. Jiang,C. Baribault
EURASIP Journal on Advances in Signal Processing , 2010, DOI: 10.1155/2010/761360
Abstract:
Keratins provide virus-dependent protection or predisposition to injury in coxsackievirus-induced pancreatitis
DM Toivola, SE Ostrowski,H Baribault,et al
Cell Health and Cytoskeleton , 2009,
Abstract: DM Toivola1, SE Ostrowski2, H Baribault3, TM Magin4, AI Ramsingh2, MB Omary51 bo Akademi University, Dept. Biology, BioCity, Turku, Finland and Stanford University School of Medicine and Digestive Disease Center; 2New York State Department of Health, Albany, NY, USA; 3Amgen, South San Francisco, CA, USA; 4University of Bonn, Bonn, Germany; 5Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Mi, USAAbstract: Keratins 8 and 18 (K8/K18) are the two major intermediate filament proteins in hepatocytes and pancreatic acinar cells. Acinar cell keratins are organized as cytoplasmic and apicolateral filaments. An important role of hepatocyte K8/K18 is to maintain cellular integrity, while this cytoprotective function of K8/K18 is not evident in the pancreas since keratin-deficient mice cope well with pancreatitis models. To further study the roles of keratins in the exocrine pancreas, we used coxsackievirus B4-models, CVB4-V and CVB4-P, to induce severe acute/chronic pancreatitis and acute pancreatitis, respectively, in K8-null (which lack acinar keratins) and K18-null (which lack cytoplasmic keratins) mice. Despite similar virus titers in all mice, CVB4-V resulted in 40% mortality of the K8-null mice 14 days post-infection compared to no lethality of WT and K18-null mice. In contrast, K8-null mice were far less susceptible to CVB4-P-induced damage as determined by histology and serology analysis, and they recover faster than WT and K18-null mice. After CVB4 virus infection, keratins aggregated during acinar degranulation, and K8/K18 site-specific phosphorylation was observed during degranulation and recovery. Hence, keratins significantly affect CVB4 virulence, positively or negatively, depending on the virus subtype and keratin makeup, in a virus replication-independent manner.Keywords: keratin, pancreatitis, coxsackievirus
Cerebrospinal Fluid Magnesium Level in Different Neurological Disorders  [PDF]
Carl-Albrecht Haensch
Neuroscience & Medicine (NM) , 2010, DOI: 10.4236/nm.2010.12009
Abstract: Magnesium (Mg) is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. The aim of the present study was to determine the CSF concentration of Mg in various neurological disorders (n = 72) and in healthy subjects (n = 75). The control group included 35 males and 40 females, aged 16-89 years (mean age 53 years) who were subjected to a lumbar puncture for diagnostic reasons. The CSF examination was normal mainly as concerns the macroscopically examination, the leukocyte count and the protein level. The determination of Mg was performed with xylidyl-blue photometry. Our normal CSF Mg mean value was 0.97 ± 0.08 mmol/l (range 0.6-1.4 mmol/l). In the group of patients (n = 11) with convulsive seizures a slightly but significantly lower Mg were revealed (0.92 ± 0.03 mmol/l; p = 0.001; paired two-tailed Student’s t-tests). No statistically significant change of CSF Mg levels was noted in patients suffering from alcohol withdrawal syndrome, multiple sclerosis or Bell’s palsy. Our results indi-cate that magnesium deficiency may play a role for seizure manifestation even in patients with a moderate low Mg without neurological signs. Low CSF magnesium is associated with epilepsy, further studies may determine the influ-ence of anti-epileptic drug therapy on CSF magnesium levels.
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