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Search Results: 1 - 10 of 302653 matches for " Alan J Herron "
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Disrupting Circadian Homeostasis of Sympathetic Signaling Promotes Tumor Development in Mice
Susie Lee,Lawrence A. Donehower,Alan J. Herron,David D. Moore,Loning Fu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0010995
Abstract: Cell proliferation in all rapidly renewing mammalian tissues follows a circadian rhythm that is often disrupted in advanced-stage tumors. Epidemiologic studies have revealed a clear link between disruption of circadian rhythms and cancer development in humans. Mice lacking the circadian genes Period1 and 2 (Per) or Cryptochrome1 and 2 (Cry) are deficient in cell cycle regulation and Per2 mutant mice are cancer-prone. However, it remains unclear how circadian rhythm in cell proliferation is generated in vivo and why disruption of circadian rhythm may lead to tumorigenesis.
Scaffold attachment factor B1 (SAFB1) heterozygosity does not influence Wnt-1 or DMBA-induced tumorigenesis
Benny Kaipparettu, Klaudia M Dobrzycka, Ora Britton, Adrian V Lee, Alan J Herron, Yi Li, Michael T Lewis, Daniel Medina, Steffi Oesterreich
Molecular Cancer , 2009, DOI: 10.1186/1476-4598-8-15
Abstract: We crossed female SAFB1+/- (C57B6/129) mice with male MMTV-Wnt-1 (C57B6/SJL) mice to obtain SAFB1+/+/Wnt-1, SAFB1+/-/Wnt-1, and SAFB1+/- mice. For the chemical induced tumorigenesis study we treated 8 weeks old SAFB1+/- and SAFB+/+ BALB/c mice with 1 mg DMBA once per week for 6 weeks. Animals were monitored for tumor incidence and tumor growth. Tumors were characterized by performing H&E, and by staining for markers of proliferation and apoptosis.We did not detect significant differences in tumor incidence and growth between SAFB1+/+/Wnt-1 and SAFB1+/-/Wnt-1 mice, and between DMBA-treated SAFB1+/+ and SAFB1+/-mice. Histological evaluation of tumors showed that SAFB1 heterozygosity did not lead to changes in proliferation or apoptosis. There were, however, significant differences in the distribution of tumor histologies with an increase in papillary and cribriform tumors, and a decrease in squamous tumors in the SAFB1+/-/Wnt-1 compared to the SAFB1+/+/Wnt-1 tumors. Of note, DMBA treatment resulted in shortened survival of SAFB1+/- mice compared to their wildtype littermates, however this trend did not reach statistical significance.Our data show that SAFB1 heterozygosity does not influence Wnt-1 or DMBA-induced mammary tumorigenesis.Scaffold Attachment Factor B1 (SAFB1) is a multifunctional protein that is involved in RNA processing, transcriptional regulation, and stress response [1]. SAFB1 has previously been implicated in breast tumorigenesis. SAFB1 functions as an estrogen receptor α (ERα) corepressor [2], and its overexpression in cultured cells leads to growth inhibition. Importantly, SAFB1 mutations have been identified in microdissected breast tumors but not in the normal adjacent tissue, and SAFB1's chromosomal locus displays extremely high loss of heterozygocity LOH (78%) in invasive breast cancer [3]. There is no significant different in LOH frequencies between ER-positive and ER-negative tumors, and other in vitro observations [4] suggest that SAFB1 could
2001: a mouse genome odyssey
David R Beier, Bruce J Herron
Genome Biology , 2002, DOI: 10.1186/gb-2002-3-2-reports4005
Abstract: In a year notable for the completion of a draft human genome sequence, it was appropriate that a major topic at the 15th International Mouse Genome Conference was a discussion of the status of the mouse genome project. Details of the public-domain effort were presented by John McPherson (Washington University, St Louis, USA), Kerstin Lindblad-Toh (Whitehead Institute, Cambridge, USA), Shaying Zhao (The Institute for Genomic Research, Rockville, USA), Anne-Marie Mallon (Medical Research Council Mouse Genome Centre and Mammalian Genetics Unit (MRC MGU/MGC), Harwell, UK), and Jim Thomas (National Human Genome Research Institute, National Institutes of Health (NIH), Bethesda, USA). The approach being taken combines sequencing of bacterial artificial chromosomes (BACs) - this was the main method for sequencing the human genome - and whole-genome shotgun sequencing, which is advocated by investigators at Celera Genomics. A fingerprinted physical map of 300,000 BAC clones has been generated and aligned to the mouse radiation-hybrid map using sequence-tagged sites (STSs) derived from microsatellite sequences and expressed sequence tags (ESTs). The precise position of the BACs on the map is being refined with the help of the sequences of the ends of many of the BACs. Nearly threefold (3x) coverage of the genome using shotgun sequence has been completed and deposited in public domain databases.One aim of the public mouse genome-sequencing effort is to generate shotgun-sequence reads from different mouse strains, in order to identify single-nucleotide polymorphisms (SNPs). (As plans for this component are in development, we propose that the validation and characterization of SNPs in a large number of commonly used inbred strains is as important as SNP discovery itself, and urge that appropriate resources be devoted to it). An important part of genomics is the informatics required for data management and analysis; programs for organizing and annotating mouse genome sequence in
Association of Body Composition and Aerobic Fitness on Heart Rate Variability and Recovery in Young-Adult Black Men  [PDF]
Michael R. Esco, Robert L. Herron, Stephen J. Carter, Andrew A. Flatt
International Journal of Clinical Medicine (IJCM) , 2013, DOI: 10.4236/ijcm.2013.412092
Abstract:

Background: The primary purpose of this investigation was to determine the differences in resting heart rate variability and heart rate recovery between norm-referenced aerobic fitness groupings, independent of body composition, in Black men. Additionally, we sought to clarify the independent relationships that heart rate variability and heart rate recovery displayed with maximal aerobic fitness and selected body composition measures. Methods: Body mass index, waist circumference, and the sum of skinfold thickness were determined in forty Black men (23 ± 3 years). Each subject assumed a supine position while heart rate variability was analyzed for 5-minute and recorded as normalized high-frequency power and normalized low-frequency power to normalized high frequency ratio. A graded exercise treadmill protocol was performed to attain maximal aerobic fitness. Heart rate recovery was recorded at 1- and 2-minute of a cool-down period. Heart rate variability and heart rate recovery were compared across two groups whose maximal aerobic fitness was either below or above the normative mean value for the age group of men. Results: The results indicated that heart rate variability was higher in the group whose maximal aerobic fitness was above the normative mean value compared with the lower fit group (p < 0.05), but the differences disappeared when adjusting for body composition (p > 0.05). Regression analysis revealed that the sum of skinfolds accounted for the variation in normalized high frequency power (R2 = 0.20,

Graph-Theoretic Models of Mutations in the Nucleotide Binding Domain 1 of the Cystic Fibrosis Transmembrane Conductance Regulator
Debra J. Knisley,Jeff R. Knisley,Andrew Cade Herron
Computational Biology Journal , 2013, DOI: 10.1155/2013/938169
Abstract: Cystic fibrosis is one of the most common inherited diseases and is caused by a mutation in a membrane protein, the cystic fibrosis transmembrane conductance regulator (CFTR). This protein serves as a chloride channel and regulates the viscosity of mucus lining the ducts of a number of organs. Although much has been learned about the consequences of mutations on the energy landscape and the resulting disrupted folding pathway of CFTR, a level of understanding needed to correct the misfolding has not been achieved. The most common mutations of CFTR are located in one of two nucleotide binding domains, namely, the nucleotide binding domain 1 (NBD1). We model NBD1 using a nested graph model. The vertices in the lowest layer each represent an atom in the structure of an amino acid residue, while the vertices in the mid layer each represent the residue. The vertices in the top layer each represent a subdomain of the nucleotide binding domain. We use this model to quantify the effects of a single point mutation on the protein domain. We compare the wildtype structure with eight of the most common mutations. The graph-theoretic model provides insight into how a single point mutation can have such profound structural consequences. 1. Introduction Cystic fibrosis is the most common genetic disorder in the Caucasian population. Cystic fibrosis (CF) is caused by a single point mutation in the cystic fibrosis membrane conductance regulator (CFTR) protein [1–4]. CFTR is a chloride channel located in the apical membrane of epithelial cells and plays a fundamental role in transepithelial salt and water movement [5]. A mutation of this protein affects a number of organs in the body such as lungs, pancreas, reproductive organs, and colon. The viscosity of the mucus that lines the ducts of these organs is altered by the increased salt levels resulting in sticky mucus plugs that disrupt the normal function of these organs. A mutation in the CFTR protein occurs in approximately one in every twenty individuals in the Caucasian population and there are more than one thousand nine hundred different reported mutations of CFTR resulting in different levels of severity of clinical consequences [6]. Although there are a large number of reported mutations of CFTR, the deletion of phenylalanine at position 508 (ΔF508) occurs in more than 90% of the CF population [7]. The ΔF508 mutation prevents the correct folding of the protein and consequential degradation [7, 8]. Thus, this mutation results in one of the more severe phenotypes. Once considered a fatal disease, knowledge about
Automated measurement of the human corpus callosum using MRI
Timothy J. Herron,Xiaojian Kang,David L. Woods
Frontiers in Neuroinformatics , 2012, DOI: 10.3389/fninf.2012.00025
Abstract: The corpus callosum includes the majority of fibers that connect the two cortical hemispheres. Studies of cross-sectional callosal morphometry and area have revealed developmental, gender, and hemispheric differences in healthy populations and callosal deficits associated with neurodegenerative disease and brain injury. However, accurate quantification of the callosum using magnetic resonance imaging is complicated by intersubject variability in callosal size, shape, and location and often requires manual outlining of the callosum in order to achieve adequate performance. Here we describe an objective, fully automated protocol that utilizes voxel-based images to quantify the area and thickness both of the entire callosum and of different callosal compartments. We verify the method's accuracy, reliability, robustness, and multisite consistency and make comparisons with manual measurements using public brain-image databases. An analysis of age-related changes in the callosum showed increases in length and reductions in thickness and area with age. A comparison of older subjects with and without mild dementia revealed that reductions in anterior callosal area independently predicted poorer cognitive performance after factoring out Mini-Mental Status Examination scores and normalized whole brain volume. Open-source software implementing the algorithm is available at www.nitrc.org/projects/c8c8.
Nótula acêrca de "O que em mim 'stá pensando"
Robert Herron
Alfa : Revista de Linguística , 2001,
Abstract:
Segregation of Seizure Traits in C57 Black Mouse Substrains Using the Repeated-Flurothyl Model
Sridhar B. Kadiyala, Dominick Papandrea, Bruce J. Herron, Russell J. Ferland
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0090506
Abstract: Identifying the genetic basis of epilepsy in humans is difficult due to its complexity, thereby underlying the need for preclinical models with specific aspects of seizure susceptibility that are tractable to genetic analyses. In the repeated-flurothyl model, mice are given 8 flurothyl-induced seizures, once per day (the induction phase), followed by a 28-day rest period (incubation phase) and final flurothyl challenge. This paradigm allows for the tracking of multiple phenotypes including: initial generalized seizure threshold, decreases in generalized seizure threshold with repeated flurothyl exposures, and changes in the complexity of seizures over time. Given the responses we previously reported in C57BL/6J mice, we analyzed substrains of the C57BL lineage to determine if any of these phenotypes segregated in these substrains. We found that the generalized seizure thresholds of C57BL/10SNJ and C57BL/10J mice were similar to C57BL/6J mice, whereas C57BL/6NJ and C57BLKS/J mice showed lower generalized seizure thresholds. In addition, C57BL/6J mice had the largest decreases in generalized seizure thresholds over the induction phase, while the other substrains were less pronounced. Notably, we observed only clonic seizures during the induction phase in all substrains, but when rechallenged with flurothyl after a 28-day incubation phase, ~80% of C57BL/6J and 25% of C57BL/10SNJ and C57BL/10J mice expressed more complex seizures with tonic manifestations with none of the C57BL/6NJ and C57BLKS/J mice having complex seizures with tonic manifestations. These data indicate that while closely related, the C57BL lineage has significant diversity in aspects of epilepsy that are genetically controlled. Such differences further highlight the importance of genetic background in assessing the effects of targeted deletions of genes in preclinical epilepsy models.
Using the GLOBE Program to Educate Students on the Interdependence of Our Planet and People  [PDF]
Sherry S. Herron, Jennifer L. Robertson
Creative Education (CE) , 2013, DOI: 10.4236/ce.2013.44A005
Abstract:
We present how we have used GLOBE protocols and programs in a college undergraduate English course for science and non-science majors, Writing in the Sciences, and in a graduate-level field course for in-service teachers. Collecting land cover data and determining biomass in conjunction with a series of writing assignments allowed the English students to connect their work to research done in ecosystems throughout the world, and to specific environmental concerns such as carbon sequestration, biodiversity, and the impact of controlled burning on ecosystems. Teachers demonstrated increased knowledge of ecology, natural histories of various organisms, and awareness of environmental resources. A study conducted the following summer revealed that teachers valued the course and felt that their experiences helped them be more effective teachers. Six of the eight teachers had conducted field activities with their students, but also reported significant challenges associated with the effort.
Molecular Correlates of Host Specialization in Staphylococcus aureus
Lisa Herron-Olson, J. Ross Fitzgerald, James M. Musser, Vivek Kapur
PLOS ONE , 2007, DOI: 10.1371/journal.pone.0001120
Abstract: Background The majority of Staphylococcus aureus isolates that are recovered from either serious infections in humans or from mastitis in cattle represent genetically distinct sets of clonal groups. Moreover, population genetic analyses have provided strong evidence of host specialization among S. aureus clonal groups associated with human and ruminant infection. However, the molecular basis of host specialization in S. aureus is not understood. Methodology/Principal Findings We sequenced the genome of strain ET3-1, a representative isolate of a common bovine mastitis-causing S. aureus clone. Strain ET3-1 encodes several genomic elements that have not been previously identified in S. aureus, including homologs of virulence factors from other Gram-positive pathogens. Relative to the other sequenced S. aureus associated with human infection, allelic variation in ET3-1 was high among virulence and surface-associated genes involved in host colonization, toxin production, iron metabolism, antibiotic resistance, and gene regulation. Interestingly, a number of well-characterized S. aureus virulence factors, including protein A and clumping factor A, exist as pseudogenes in ET3-1. Whole-genome DNA microarray hybridization revealed considerable similarity in the gene content of highly successful S. aureus clones associated with bovine mastitis, but not among those clones that are only infrequently recovered from bovine hosts. Conclusions/Significance Whole genome sequencing and comparative genomic analyses revealed a set of molecular genetic features that distinguish clones of highly successful bovine-associated S. aureus optimized for mastitis pathogenesis in cattle from those that infect human hosts or are only infrequently recovered from bovine sources. Further, the results suggest that modern bovine specialist clones diverged from a common ancestor resembling human-associated S. aureus clones through a combination of foreign DNA acquisition and gene decay.
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