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- 저자 : Hassett, (검색결과 5 건)
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STABILITY COMPUTATION VIA GROBNER BASIS
Hassett, Brendan,Hyeon, Dong-Hoon,Lee, Yong-Nam Korean Mathematical Society 2010 대한수학회지 Vol.47 No.1
In this article, we discuss a Grobner basis algorithm related to the stability of algebraic varieties in the sense of Geometric Invariant Theory. We implement the algorithm with Macaulay 2 and use it to prove the stability of certain curves that play an important role in the log minimal model program for the moduli space of curves.
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STABILITY COMPUTATION VIA GR¨OBNER BASIS
Brendan Hassett,David Donghoon Hyeon,이용남 대한수학회 2010 대한수학회지 Vol.47 No.1
In this article, we discuss a Gr¨obner basis algorithm related to the stability of algebraic varieties in the sense of Geometric Invariant Theory. We implement the algorithm with Macaulay 2 and use it to prove the stability of certain curves that play an important role in the log minimal model program for the moduli space of curves.
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Daniel J. Hassett,Michael T. Borchers,Ralph J. Panos 한국미생물학회 2014 The journal of microbiology Vol.52 No.3
Chronic obstructive pulmonary disease (COPD), a diseasemanifested by significantly impaired airflow, afflicts ~14.2million cases in the United States alone with an estimated63 million people world-wide. Although there are a numberof causes, the predominant cause is excessive tobacco smoke. In fact, in China, there have been estimates of 315,000,000people that smoke. Other less frequent causes are associatedwith indirect cigarette smoke, air pollutants, biomass fuels,and genetic mutations. COPD is often associated with heartdisease, lung cancer, osteoporosis and conditions can worsenin patients with sudden falls. COPD also affects both innateand adaptive immune processes. Cigarette smoke increasesthe expression of matrix metalloproteases and proinflammatorychemokines and increases lung titers of natural killercells and neutrophils. Yet, neutrophil reactive oxygen species(ROS) mediated by the phagocytic respiratory burst andphagocytosis is impaired by nicotine. In contrast to innateimmunity in COPD, dendritic cells represent leukocytes recruitedto the lung that link the innate immune responsesto adaptive immune responses by activating naïve T cellsthrough antigen presentation. The autoimmune process thatis also a significant part of inflammation associated withCOPD. Moreover, coupled with restricted FEV1 values, arethe prevalence of patients with single or multiple infectionsby bacteria, viruses and fungi. Finally, we focus on one ofthe more problematic infectious agents, the Gram-negativeopportunistic pathogenic bacterium, Pseudomonas aeruginosa. Specifically, we delve into the development of highlyproblematic biofilm infections that are highly refractory toconventional antibiotic therapies in COPD. We offer a nonconventional,biocidal treatment that may be effective forCOPD airway infections as well as with combinations ofcurrent antibiotic regimens for more effective treatment outcomes outcomes and relief for patients with COPD.
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Heo, Yun-Jeong,Chung, In-Young,Cho, Wan-Je,Lee, Bo-Young,Kim, Jung-Hoon,Choi, Kyoung-Hee,Lee, Jin-Won,Hassett, Daniel J.,Cho, You-Hee American Society for Microbiology 2010 Journal of Bacteriology Vol.192 No.2
<B>ABSTRACT</B><P>The adaptive response to hydrogen peroxide (H2O2) in <I>Pseudomonas aeruginosa</I> involves the major catalase, KatA, and OxyR. However, neither the molecular basis nor the relationship between the aforementioned proteins has been established. Here, we demonstrate that the transcriptional activation of the <I>katA</I> promoter (<I>katAp</I>) in response to H2O2 was abrogated in the <I>P. aeruginosa</I> PA14 <I>oxyR</I> null mutant. Promoter deletion analyses revealed that H2O2-mediated induction was dependent on a region of DNA −76 to −36 upstream of the H2O2-responsive transcriptional start site. This region harbored the potential operator sites (OxyR-responsive element [ORE]) of the <I>Escherichia coli</I> OxyR binding consensus. Deletion of the entire ORE not only abolished H2O2-mediated induction but also elevated the basal transcription, suggesting the involvement of OxyR and the ORE in both transcriptional activation and repression. OxyR bound to the ORE both <I>in vivo</I> and <I>in vitro</I>, demonstrating that OxyR directly regulates the <I>katAp</I>. Three distinct mobility species of oxidized OxyR were observed in response to 1 mM H2O2, as assessed by free thiol trapping using 4-acetamido-4′-maleimidylstilbene-2,2′-disulfonic acid. These oxidized species were not observed for the double mutants with mutations in the conserved cysteine (Cys) residues (C199 and C208). The uninduced transcription of <I>katAp</I> was elevated in an <I>oxyR</I> mutant with a mutation of Cys to serine at 199 (C199S) and even higher in the <I>oxyR</I> mutant with a mutation of Cys to alanine at 199 (C199A) but not in <I>oxyR</I> mutants with mutations in C208 (C208S and C208A). In both the C199S and the C208S mutant, however, <I>katAp</I> transcription was still induced by H2O2 treatment, unlike in the <I>oxyR</I> null mutant and the C199A mutant. The double mutants with mutations in both Cys residues (C199S C208S and C199A C208S) did not differ from the C199A mutant. Taken together, our results suggest that <I>P. aeruginosa</I> OxyR is a bona fide transcriptional regulator of the <I>katA</I> gene, sensing H2O2 based on the conserved Cys residues, involving more than one oxidation as well as activation state <I>in vivo</I>.</P>
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