• Title/Summary/Keyword: HOST

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Short-Term Viral Evolution in Response to Passaging I. Consequences for Population Size

  • Park, Gyung-Soon;Steven E. Kelley;Hing, Jung-Lim
    • 한국생태학회:학술대회논문집
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    • 2002.08a
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    • pp.83-91
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    • 2002
  • The Red Queen hypothesis for the advantage of sex predicts that pathogens will evolve by increasing fitness with frequent encounters with specific host genotypes. In this study, BMV population size, measured as an indicator of fitness, was investigated during repeated passages through the same, or different host genotypes of the crop host, Hordeum vulgare (barley). Overall, mean BMV concentration within individual hosts was significantly higher in genetically homogeneous compared to heterogeneous host passage lines. In addition, BMV populations, passaged through a specific host variety, showed higher growth in that host variety compared to BMV passaged through varying varieties. These results supports the Red Queen hypothesis. However, the decrease in viral populations during passages contradicts the Red Queen. Nevertheless, the results found here show that even under simplified conditions, pathogens do not evolve in simple, predictable ways. Constraints on pathogen evolution may lead to counterintuitive results.

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Short-Term Viral Evolution in Response to Passaging I. Consequences for Population Size

  • Park, Gyung-Soon;Kelley, Steven E.;Hong, Jung-Lim
    • The Korean Journal of Ecology
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    • v.25 no.4
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    • pp.217-225
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    • 2002
  • The Red Queen hypothesis for the advantage of sex predicts that pathogens will evolve by increasing fitness with frequent encounters with specific host genotypes. In this study, BMV population size, measured as an indicator of fitness, was investigated during repeated passages through the same, or different host genotypes of the crop host, Hordeum vulgare (barley). Overall, mean BMV concentration within individual hosts was significantly higher in genetically homogeneous compared to heterogeneous host passage lines. In addition, BMV populations, passaged through a specific host variety, showed higher growth in that host variety compared to BMV passaged through varying varieties. These results supports the Red Queen hypothesis. However, the decrease in viral populations during passages contradicts the Red Queen. Nevertheless, the results found here show that even under simplified conditions, pathogens do not evolve in simple, predictable ways. Constraints on pathogen evolution may lead to counterintuitive results.

Remodeling of host glycoproteins during bacterial infection

  • Kim, Yeolhoe;Ko, Jeong Yeon;Yang, Won Ho
    • BMB Reports
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    • v.54 no.11
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    • pp.541-544
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    • 2021
  • Protein glycosylation is a common post-translational modification found in all living organisms. This modification in bacterial pathogens plays a pivotal role in their infectious processes including pathogenicity, immune evasion, and host-pathogen interactions. Importantly, many key proteins of host immune systems are also glycosylated and bacterial pathogens can notably modulate glycosylation of these host proteins to facilitate pathogenesis through the induction of abnormal host protein activity and abundance. In recent years, interest in studying the regulation of host protein glycosylation caused by bacterial pathogens is increasing to fully understand bacterial pathogenesis. In this review, we focus on how bacterial pathogens regulate remodeling of host glycoproteins during infections to promote the pathogenesis.

Host-Pathogen Interactions Operative during Mycobacteroides abscessus Infection

  • Eun-Jin Park;Prashanta Silwal;Eun-Kyeong Jo
    • IMMUNE NETWORK
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    • v.21 no.6
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    • pp.40.1-40.20
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    • 2021
  • Mycobacteroides abscessus (previously Mycobacterium abscessus; Mabc), one of rapidly growing nontuberculous mycobacteria (NTM), is an important pathogen of NTM pulmonary diseases (NTM-PDs) in both immunocompetent and immunocompromised individuals. Mabc infection is chronic and often challenging to treat due to drug resistance, motivating the development of new therapeutics. Despite this, there is a lack of understanding of the relationship between Mabc and the immune system. This review highlights recent progress in the molecular architecture of Mabc and host interactions. We discuss several microbial components that take advantage of host immune defenses, host defense pathways that can overcome Mabc pathogenesis, and how host-pathogen interactions determine the outcomes of Mabc infection. Understanding the molecular mechanisms underlying host-pathogen interactions during Mabc infection will enable the identification of biomarkers and/or drugs to control immune pathogenesis and protect against NTM infection.

Charge Trapping Host Structure for High Efficiency in Phosphorescent Organic Light-Emitting Diodes

  • Lee, Jun-Yeob
    • Journal of Information Display
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    • v.9 no.2
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    • pp.14-17
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    • 2008
  • A charge trapping host structure was developed to improve the light-emitting efficiency of green phosphorescent organic light-emitting diodes. N, N'-dicarbazolyl-3,5-benzene(mCP) and a spirobifluorene based triplet host(PHl) were co-deposited as hosts in the emitting layer and the device performance was examined according to the composition mCP and PH1. The results showed that the quantum efficiency could be improved by 30 % using a mixed host of mCP and PH1.

Home-Field Advantage: Why Host-Specificity is Important for Therapeutic Microbial Engraftment

  • Tyler J. Long
    • Microbiology and Biotechnology Letters
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    • v.51 no.1
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    • pp.124-127
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    • 2023
  • Among certain animals, gut microbiomes demonstrate species-specific patterns of beta diversity. This host-specificity is a potent driver of exogenous microbial exclusion. To overcome persistent translational limitations, translational microbiome research and therapeutic development must account for host-specific patterns of microbial engraftment. This commentary seeks to highlight the important implications of host-specificity for microbial ecology, Fecal Microbiota Transplantation (FMT), next-generation probiotics, and translational microbiota research.

OPTIMAL CONTROL PROBLEM FOR HOST-PATHOGEN MODEL

  • P. T. Sowndarrajan
    • Nonlinear Functional Analysis and Applications
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    • v.28 no.3
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    • pp.659-670
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    • 2023
  • In this paper, we study the distributed optimal control problem of a coupled system of the host-pathogen model. The system consists of the density of the susceptible host, the density of the infected host, and the density of pathogen particles. Our main goal is to minimize the infected density and also to decrease the cost of the drugs administered. First, we prove the existence and uniqueness of solutions for the proposed problem. Then, the existence of the optimal control is established and necessary optimality conditions are also derived.

Performance Improvement of Lazy Scheme for an Efficient Failure Recovery of Mobile Host (이동 호스트의 효율적 결함 복구를 위한 Lazy 기법의 성능 개선)

  • Kwon, Won-Seok;Kim, Sung-Soo;Kim, Jai-Hoon
    • The Transactions of the Korea Information Processing Society
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    • v.7 no.9
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    • pp.2969-2979
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    • 2000
  • A mobile host has failure causes such as failure of the mobile host, disconnection of the mobile host, and wireless link failure that have not been seen in traditional computing environments. So far there have been few studies on fault tolerance of a mobile host in mobile computing environments. The Lazy scheme, a failure recovery technique of the mobile host, is a cost-effective one. However, this scheme has a defect that the mobile host cannot be recovered from failure of the base station with acheckpoint of the mobile host. In this paper, we propose and evaluate the Redundant Lazy scheme for performance improvement of the Lazy scheme.

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Bcl-2 Knockdown Accelerates T Cell Receptor-Triggered Activation-Induced Cell Death in Jurkat T Cells

  • Lee, Yun-Jung;Won, Tae Joon;Hyung, Kyeong Eun;Lee, Mi Ji;Moon, Young-Hye;Lee, Ik Hee;Go, Byung Sung;Hwang, Kwang Woo
    • The Korean Journal of Physiology and Pharmacology
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    • v.18 no.1
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    • pp.73-78
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    • 2014
  • Cell death and survival are tightly controlled through the highly coordinated activation/inhibition of diverse signal transduction pathways to insure normal development and physiology. Imbalance between cell death and survival often leads to autoimmune diseases and cancer. Death receptors sense extracellular signals to induce caspase-mediated apoptosis. Acting upstream of CED-3 family proteases, such as caspase-3, Bcl-2 prevents apoptosis. Using short hairpin RNAs (shRNAs), we suppressed Bcl-2 expression in Jurkat T cells, and this increased TCR-triggered AICD and enhanced TNFR gene expression. Also, knockdown of Bcl-2 in Jurkat T cells suppressed the gene expression of FLIP, TNF receptor-associated factors 3 (TRAF3) and TRAF4. Furthermore, suppressed Bcl-2 expression increased caspase-3 and diminished nuclear factor kappa B (NF-${\kappa}B$) translocation.

Variation of Inclusion Selectivities of the Cadmium Host Complexes with Ammonium Oniums for Aromatic Guest Molecules (암모니움 이온을 가진 카드뮴 호스트 착물의 방향족 게스트 분자에 대한 포접선택성 변화)

  • Kim, Chong-Hyeak;Lee, Sueg-Geun
    • Analytical Science and Technology
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    • v.17 no.3
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    • pp.282-288
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    • 2004
  • Inclusion selectivities of the cyanocadmate host complexes with ammonium oniums, $[Cd_x(CN)_{2x}][onium{\cdot}zG]$ (onium = $NMe_3Et^+$, $NMeEt{_3}^+$ and $NEt{_4}^+$, G = guest), have been investigated for $C_6H_6$ (B), PhMe (T), PhEt (E), ortho (O), meta (M), and para (P) isomers of $C_6H_4Me_2$ as the aromatic guest molecules. From the binary, ternary, quaternary and quinary mixed guests of B, T, E, O, M and P, the order of preference in the $NMe_3Et+$-host is $B{\gg}$T>P${\fallingdotseq}O{\fallingdotseq}M$ and E>O${\gg}P{\fallingdotseq}M$; in the $NMeEt{_3}^+$-host is T>B>P${\gg}O{\fallingdotseq}M$ and E>P${\gg}$M>O; in the $NEt{_4}^+$-host is $B{\gg}T{\fallingdotseq}O{\fallingdotseq}M{\fallingdotseq}P$. However, the $NEt{_4}^+$-host complexes of E, O, M and P mixed-guests were not obtained. These inclusion selectivities were compared to our previous results of the $NMe{_4}^+$-host; T>B>P${\gg}$M>O and E>P${\gg}$M>O.