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Search Results: 1 - 10 of 153454 matches for " Marcus B. Jones "
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Exogenous Interferon-α and Interferon-γ Increase Lethality of Murine Inhalational Anthrax
Jeffrey A. Gold, Yoshihiko Hoshino, Marcus B. Jones, Satomi Hoshino, Anna Nolan, Michael D. Weiden
PLOS ONE , 2007, DOI: 10.1371/journal.pone.0000736
Abstract: Background Bacillus anthracis, the etiologic agent of inhalational anthrax, is a facultative intracellular pathogen. Despite appropriate antimicrobial therapy, the mortality from inhalational anthrax approaches 45%, underscoring the need for better adjuvant therapies. The variable latency between exposure and development of disease suggests an important role for the host's innate immune response. Type I and Type II Interferons (IFN) are prominent members of the host innate immune response and are required for control of intracellular pathogens. We have previously described a protective role for exogenous Type I and Type II IFNs in attenuating intracellular B.anthracis germination and macrophage cell death in vitro. Methodology and Principal Findings We sought to extend these findings in an in vivo model of inhalational anthrax, utilizing the Sterne strain (34F2) of B.anthracis. Mice devoid of STAT1, a component of IFN-α and IFN-γ signaling, had a trend towards increased mortality, bacterial germination and extrapulmonary spread of B.anthracis at 24 hrs. This was associated with impaired IL-6, IL-10 and IL-12 production. However, administration of exogenous IFN-γ, and to a lesser extent IFN-α, at the time of infection, markedly increased lethality. While IFNs were able to reduce the fraction of germinated spores within the lung, they increased both the local and systemic inflammatory response manifest by increases in IL-12 and reductions in IL-10. This was associated with an increase in extrapulmonary dissemination. The mechanism of IFN mediated inflammation appears to be in part due to STAT1 independent signaling. Conclusions In conclusion, while endogenous IFNs are essential for control of B.anthracis germination and lethality, administration of exogenous IFNs appear to increase the local inflammatory response, thereby increasing mortality.
Differential Gene Expression to Investigate the Effects of Low-level Electrochemical Currents on Bacillus subtilis
Robert Szkotak, Tagbo H R Niepa, Nikhil Jawrani, Jeremy L Gilbert, Marcus B Jones, Dacheng Ren
AMB Express , 2011, DOI: 10.1186/2191-0855-1-39
Abstract: The rapid development and spread of multidrug resistant infections present an increasing challenge to public health and disease therapy (Alekshun and Levy 2003). As an intrinsic mechanism of drug resistance, biofilm formation renders bacteria up to 1000 times less susceptible to antibiotics than their planktonic (free-swimming) counterparts of the same genotype (Costerton et al. 1994). Such intrinsic mechanisms also facilitate the development of resistance through acquired mechanisms that are based on genetic mutations or drug resistance genes. Consistently, excessive antibiotic treatment of biofilm infections at sublethal concentrations has been shown to generate antibiotic-tolerant strains (Narisawa et al. 2008). Biofilms are responsible for at least 65% of human bacterial infections (Costerton et al. 2003). For example, it is estimated that in the United States 25% of urinary catheters become infected with a biofilm within one week of a hospital stay, with a cumulative 5% chance each subsequent day (Maki and Tambyah 2001). Biofilms are also detected on implanted devices and are a major cause of implant surgical removal (Hetrick and Schoenfisch 2006; Norowski and Bumgardner 2009). Orthopedic implants showed a 4.3% infection rate, or approximately 112,000 infections per year in the U.S. (Hetrick and Schoenfisch 2006). This rate increases to 7.4% for cardiovascular implants (Hetrick and Schoenfisch 2006), and anywhere from 5%-11% for dental implants (Norowski and Bumgardner 2009).In the biofilm state, bacteria undergo significant changes in gene expression leading to phenotypic changes that serve to enhance their ability to survive in challenging environments. Although not completely understood, the tolerance to antibiotic treatments is thought to arise from a combination of limited antibiotic diffusion through the extracellular polymeric substances (EPS), decreased growth rate of biofilm cells, and increased expression of antibiotic tolerance genes in biofilm cells
Dendritic and spine alterations in areas 9 and 17 in schizophrenia and Huntington chorea and the role of neuroleptic exposure  [PDF]
Latchman Somenarain, Liesl B. Jones
Open Journal of Psychiatry (OJPsych) , 2012, DOI: 10.4236/ojpsych.2012.23032
Abstract: Recent morphological studies in schizophrenia suggest atrophic changes in the neuropil of the prefrontal cortex. Most recently, we showed a schizophrenia-associated decrease in MAP2 in schizophrenia, which we believed is not due to neuroleptic exposure. MAP2 is a very important protein in the assembly of micro-tubule in neurons; therefore, it plays a major role in neuronal processes like dendrites, spines and synapses. Additionally, recent studies from our lab showed decreases in dendrites in area 32 and area 9. In this study we examined the dendrites and spines in area 9 and 17 to determine if neuroleptic drugs play a role. Huntington’s patients take neuroleptics similar to schizophrenics; therefore, by comparing the two groups to controls we can determine if neuroleptics play a role in the deficits reported in schizophrenia. Our results showed a significant decrease in both basal dendrites and spines for both layers III and V in area 9 in schizophrenia compared to controls. The Huntington’s brains, on the other hand, showed no significant difference compared to controls. In area 17, there was also no significant difference when comparing the three groups. The data suggest that neuroleptic drugs may not be responsible for the changes observed in schizophrenia.
Transcriptional Regulation of Multi-Drug Tolerance and Antibiotic-Induced Responses by the Histone-Like Protein Lsr2 in M. tuberculosis
Roberto Colangeli ,Danica Helb,Catherine Vilchèze,Manzour Hernando Hazbón,Chee-Gun Lee,Hassan Safi,Brendan Sayers,Irene Sardone,Marcus B Jones,Robert D Fleischmann,Scott N Peterson,William R Jacobs Jr.,David Alland
PLOS Pathogens , 2007, DOI: 10.1371/journal.ppat.0030087
Abstract: Multi-drug tolerance is a key phenotypic property that complicates the sterilization of mammals infected with Mycobacterium tuberculosis. Previous studies have established that iniBAC, an operon that confers multi-drug tolerance to M. bovis BCG through an associated pump-like activity, is induced by the antibiotics isoniazid (INH) and ethambutol (EMB). An improved understanding of the functional role of antibiotic-induced genes and the regulation of drug tolerance may be gained by studying the factors that regulate antibiotic-mediated gene expression. An M. smegmatis strain containing a lacZ gene fused to the promoter of M. tuberculosis iniBAC (PiniBAC) was subjected to transposon mutagenesis. Mutants with constitutive expression and increased EMB-mediated induction of PiniBAC::lacZ mapped to the lsr2 gene (MSMEG6065), a small basic protein of unknown function that is highly conserved among mycobacteria. These mutants had a marked change in colony morphology and generated a new polar lipid. Complementation with multi-copy M. tuberculosis lsr2 (Rv3597c) returned PiniBAC expression to baseline, reversed the observed morphological and lipid changes, and repressed PiniBAC induction by EMB to below that of the control M. smegmatis strain. Microarray analysis of an lsr2 knockout confirmed upregulation of M. smegmatis iniA and demonstrated upregulation of genes involved in cell wall and metabolic functions. Fully 121 of 584 genes induced by EMB treatment in wild-type M. smegmatis were upregulated (“hyperinduced”) to even higher levels by EMB in the M. smegmatis lsr2 knockout. The most highly upregulated genes and gene clusters had adenine-thymine (AT)–rich 5-prime untranslated regions. In M. tuberculosis, overexpression of lsr2 repressed INH-mediated induction of all three iniBAC genes, as well as another annotated pump, efpA. The low molecular weight and basic properties of Lsr2 (pI 10.69) suggested that it was a histone-like protein, although it did not exhibit sequence homology with other proteins in this class. Consistent with other histone-like proteins, Lsr2 bound DNA with a preference for circular DNA, forming large oligomers, inhibited DNase I activity, and introduced a modest degree of supercoiling into relaxed plasmids. Lsr2 also inhibited in vitro transcription and topoisomerase I activity. Lsr2 represents a novel class of histone-like proteins that inhibit a wide variety of DNA-interacting enzymes. Lsr2 appears to regulate several important pathways in mycobacteria by preferentially binding to AT-rich sequences, including genes induced by
AML presenting as a mediastinal mass and right ventricular failure  [PDF]
Jeremy B. Moad, Kellie R. Jones
Case Reports in Clinical Medicine (CRCM) , 2013, DOI: 10.4236/crcm.2013.21010

Extrinsic compression of the pulmonary arteries by mediastinal masses, while rare, is the most common cause of non-congenital peripheral pulmonary artery stenosis. Granulocytic myeloid sarcomas are an extramedullary manifestation of acute myeloid leukemia, with a wide variability in their presentation. They can present either de novo as soft tissue masses or in conjunction with acute myeloid leukemia. Myeloid sarcomas are uncommon and their prognosis is generally considered poor when present in patients with acute myeloid leukemia (AML). We present a case of a granulocytic myeloid sarcoma causing pulmonary artery stenosis and right ventricular failure. This case represents a unique cause of pulmonary arterial stenosis.

A Search for Gamma-Ray Bursts and Pulsars, and the Application of Kalman Filters to Gamma-Ray Reconstruction
B. B. Jones
Physics , 2002,
Abstract: Part I describes the analysis of periodic and transient signals in EGRET data. A method to search for the transient flux from gamma-ray bursts independent of triggers from other gamma-ray instruments is developed. Several known gamma-ray bursts were independently detected, and there is evidence for a previously unknown gamma-ray burst candidate. Statistical methods using maximum likelihood and Bayesian inference are developed and implemented to extract periodic signals from gamma-ray sources in the presence of significant astrophysical background radiation. The analysis was performed on six pulsars and three pulsar candidates. The three brightest pulsars, Crab, Vela, and Geminga, were readily identified, and would have been detected independently in the EGRET data without knowledge of the pulse period. No significant pulsation was detected in the three pulsar candidates. Eighteen X-ray binaries were examined. None showed any evidence of periodicity. In addition, methods for calculating the detection threshold of periodic flux modulation were developed. The future hopes of gamma-ray astronomy lie in the development of the Gamma-ray Large Area Space Telescope, or GLAST. Part II describes the development and results of the particle track reconstruction software for a GLAST science prototype instrument beam test. The Kalman filtering method of track reconstruction is introduced and implemented. Monte Carlo simulations, very similar to those used for the full GLAST instrument, were performed to predict the instrumental response of the prototype. The prototype was tested in a gamma-ray beam at SLAC. The reconstruction software was used to determine the incident gamma-ray direction. It was found that the simulations did an excellent job of representing the actual instrument response.
Desenvolvimento de metodologia otimiza a determina o de substancia precursora do Tamiflu e reduz impacto ambiental Método rápido y de bajo impacto ambiental facilita la determinación del precursor del Tamiflu Research cooperation leads to improving method to determine the level of endogenous shikimic acid in several plant species
Marcus B. Matallo
Planta Daninha , 2009,
Marcus E. B. Fernandes
Boletim do Museu Paraense Emílio Goeldi : Ciências Naturais , 2006,
Osteosarcomagenesis: Modeling Cancer Initiation in the Mouse
Kevin B. Jones
Sarcoma , 2011, DOI: 10.1155/2011/694136
Abstract: Osteosarcoma remains a deadly malignancy afflicting adolescents and young adults. The lack of a precursor and the panoply of genetic aberrations present in identified osteosarcomas makes study of its initiation difficult. A number of candidate hypotheses have been tested in the mouse, a species with a higher background incidence of osteosarcoma. Chemical carcinogens, external beam radiation, and bone-seeking heavy metal radioisotopes have all proven to be osteosarcomagenic in wild-type mice. A number of oncogenes, introduced via integrating viruses or aberrantly activated from heritable genetic loci, participate in and can individually drive osteosarcomagenesis. Germline and conditional gene ablations in the form of some but not all aneuploidy-inducing genes, conventional tumor suppressors, and factors that function normally in mesenchymal differentiation have also proven osteosarcomagenic, especially in combinations that silence the Rb1 and p53 pathways. This paper reviews the rich history of mouse models of osteosarcomagenesis, what they have taught us about the human disease, and what future mouse experiments yet promise to teach.
Social parasitism in mammals with particular reference to neotropical primates
Jones,Clara B.;
Mastozoolog?-a neotropical , 2005,
Abstract: organisms often respond in ways that appear to benefit others rather than themselves. this phenomenon is consistent with the views of darwin (1859) and dawkins (1999) that individuals may exploit the responses of others. this phenomenon, "social parasitism", has been extensively investigated in social insects, particularly, ants. other empirical studies have demonstrated social parasitism in fish, birds, and mammals. this paper reviews several possible examples of mammalian social parasitism, with an emphasis upon intraspecific social parasitism (isp) in neotropical primates. social parasitism is discussed as a life history feature of long-lived, social organisms such as many primates, including humans. a simple mathematical model, applied to social parasitism, is presented linking parasite transmission to a parasite’s influence on its host. phenotypic manipulation is assessed as a mechanism of social parasitism, and possible examples from the literature on neotropical primates are provided. social parasitism is discussed in relation to the evolution of higher grades of sociality (eusociality, cooperative breeding), manipulation success (infectivity), and the evolution of virulence (e.g., aggression, punishment). it is proposed that an understanding of variations in virulence and infectivity by social parasites is likely to reveal important evolutionary dynamics for an integrated view of social evolution.
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