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Trivalent M-related protein as a component of next generation group A streptococcal vaccines
Harry S. Courtney,Shannon E. Niedermeyer,Thomas A. Penfound,Claudia M. Hohn,Adam Greeley,James B. Dale 대한백신학회 2017 Clinical and Experimental Vaccine Research Vol.6 No.1
Purpose: There is a need to broaden protective coverage of M protein–based vaccines against group A streptococci (GAS) because coverage of the current 30-valent M protein vaccine does not extend to all emm types. An additional GAS antigen and virulence factor that could potentially extend vaccine coverage is M-related protein (Mrp). Previous work indicated that there are three structurally related families of Mrp (MrpI, MrpII, and MrpIII) and peptides of all three elicited bactericidal antibodies against multiple emm types. The purpose of this study was to determine if a recombinant form containing Mrp from the three families would evoke bactericidal antiserum and to determine if this antiserum could enhance the effectiveness of antisera to the 30-valent M protein vaccine. Materials and Methods: A trivalent recombinant Mrp (trMrp) protein containing N-terminal fragments from the three families (trMrp) was constructed, purified and used to immunize rabbits. Anti-trMrp sera contained high titers of antibodies against the trMrp immunogen and recombinant forms representing MrpI, MrpII, and MrpIII. Results: The antisera opsonized emm types of GAS representing each Mrp family and also opsonized emm types not covered by the 30-valent M protein–based vaccine. Importantly, a combination of trMrp and 30-valent M protein antiserum resulted in higher levels of opsonization of GAS than either antiserum alone. Conclusion: These findings suggest that trMrp may be an effective addition to future constructs of GAS vaccines.
Type VI secretion is a major virulence determinant in <i>Burkholderia mallei</i>
Schell, Mark A.,Ulrich, Ricky L.,Ribot, Wilson J.,Brueggemann, Ernst E.,Hines, Harry B.,Chen, Dan,Lipscomb, Lyla,Kim, H. Stanley,Mrá,zek, Jan,Nierman, William C.,DeShazer, David Blackwell Publishing Ltd 2007 Molecular microbiology Vol.64 No.6
<P><B>Summary</B></P><P> <I>Burkholderia mallei</I> is a host‐adapted pathogen and a category B biothreat agent. Although the <I>B. mallei</I> VirAG two‐component regulatory system is required for virulence in hamsters, the virulence genes it regulates are unknown. Here we show with expression profiling that overexpression of <I>virAG</I> resulted in transcriptional activation of ∼60 genes, including some involved in capsule production, actin‐based intracellular motility, and type VI secretion (T6S). The 15 genes encoding the major sugar component of the homopolymeric capsule were up‐expressed > 2.5‐fold, but capsule was still produced in the absence of <I>virAG</I>. Actin tail formation required <I>virAG</I> as well as <I>bimB</I>, <I>bimC</I> and <I>bimE</I>, three previously uncharacterized genes that were activated four‐ to 15‐fold when VirAG was overproduced. Surprisingly, actin polymerization was found to be dispensable for virulence in hamsters. In contrast, genes encoding a T6S system were up‐expressed as much as 30‐fold and mutations in this T6S gene cluster resulted in strains that were avirulent in hamsters. SDS‐PAGE and mass spectrometry demonstrated that BMAA0742 was secreted by the T6S system when <I>virAG</I> was overexpressed. Purified His‐tagged BMAA0742 was recognized by glanders antiserum from a horse, a human and mice, indicating that this Hcp‐family protein is produced <I>in vivo</I> during infection.</P>
( Harris A. Ahmad ),( James E. East ),( Remo Panaccione ),( Simon Travis ),( James B. Canavan ),( Keith Usiskin ),( Michael F. Byrne ) 대한장연구학회 2023 Intestinal Research Vol.21 No.3
Inflammatory bowel disease encompasses Crohn’s disease and ulcerative colitis and is characterized by uncontrolled, relapsing, and remitting course of inflammation in the gastrointestinal tract. Artificial intelligence represents a new era within the field of gastroenterology, and the amount of research surrounding artificial intelligence in patients with inflammatory bowel disease is on the rise. As clinical trial outcomes and treatment targets evolve in inflammatory bowel disease, artificial intelligence may prove as a valuable tool for providing accurate, consistent, and reproducible evaluations of endoscopic appearance and histologic activity, thereby optimizing the diagnosis process and identifying disease severity. Furthermore, as the applications of artificial intelligence for inflammatory bowel disease continue to expand, they may present an ideal opportunity for improving disease management by predicting treatment response to biologic therapies and for refining the standard of care by setting the basis for future treatment personalization and cost reduction. The purpose of this review is to provide an overview of the unmet needs in the management of inflammatory bowel disease in clinical practice and how artificial intelligence tools can address these gaps to transform patient care. (Intest Res 2023;21:283-294)
Spiral spin structures and origin of the magnetoelectric coupling inYMn2O5
Kim, J.-H.,Lee, S.-H.,Park, S. I.,Kenzelmann, M.,Harris, A. B.,Schefer, J.,Chung, J.-H.,Majkrzak, C. F.,Takeda, M.,Wakimoto, S.,Park, S. Y.,Cheong, S-W.,Matsuda, M.,Kimura, H.,Noda, Y.,Kakurai, K. American Physical Society 2008 Physical review. B, Condensed matter and materials Vol.78 No.24
Membrane-wrapped nanoparticles for photothermal cancer therapy
Aboeleneen Sara B.,Scully Mackenzie A.,Harris Jenna C.,Sterin Eric H.,Day Emily S. 나노기술연구협의회 2022 Nano Convergence Vol.9 No.37
Cancer is a global health problem that needs effective treatment strategies. Conventional treatments for solid-tumor cancers are unsatisfactory because they cause unintended harm to healthy tissues and are susceptible to cancer cell resistance. Nanoparticle-mediated photothermal therapy is a minimally invasive treatment for solid-tumor cancers that has immense promise as a standalone therapy or adjuvant to other treatments like chemotherapy, immunotherapy, or radiotherapy. To maximize the success of photothermal therapy, light-responsive nanoparticles can be camouflaged with cell membranes to endow them with unique biointerfacing capabilities that reduce opsonization, prolong systemic circulation, and improve tumor delivery through enhanced passive accumulation or homotypic targeting. This ensures a sufficient dose of photoresponsive nanoparticles arrives at tumor sites to enable their complete thermal ablation. This review summarizes the state-of-the-art in cell membrane camouflaged nanoparticles for photothermal cancer therapy and provides insights to the path forward for clinical translation.
Localization Length Exponent in Quantum Percolation
Chang ,Iksoo,Lev, Zvi,Harris, A.B.,Adler, Joan,Aharony, Amnon 부산대학교 기초과학연구소 1995 부산대학교 기초과학연구소 연구논문집 Vol.15 No.-
Connecting perfect one-dimensional leads to sites i and j on the quantum percolation (QP) model, we calculate the transmission coefficient T_(ij)(E) atan energy E near the band center and the averages of ∑_(ij)T_(ij),∑_(ij)r²_(ij)T_(ij), and ∑_(ij)r⁴_(ij)T_(ij) to tenth order in the concentration p. In three dimensions, all three seried diverge at P_(q)=0.36^(+0.01)_(-0.02), with exponents τ=0.82^(+0.10)_(-0.15), τ+2ν. and τ+4ν. We find ν=0.38 ±0.07, differing from "usual" Anderson localization and violationg the bound ν ≥ 2/d of Chayer et al. [Phys. Rev. Lett. 57, 2999(1986)]. Thus, QP belongs to a new universality class.
Haichang Xin,Linda A. Harris,Inmaculada B. Aban,Gary Cutter 대한신경과학회 2019 Journal of Clinical Neurology Vol.15 No.3
Background and Purpose Patients with refractory myasthenia gravis (MG) experience ongoing disease burden that might be reflected in their healthcare utilization. Here we examine the impact of refractory MG on healthcare utilization. Methods The 825 included participants were aged 18–64 years, enrolled in the Myasthenia Gravis Foundation of America Patient Registry between July 2013 and February 2018, and had been diagnosed with MG ≥2 years previously. Results Participants comprised 76 (9.2%) with refractory MG and 749 (90.8%) with nonrefractory MG. During the 6 months before enrollment, participants with refractory MG were significantly more likely than those with nonrefractory MG to have experienced at least one exacerbation [67.1% vs. 52.0%, respectively, p=0.01; odds ratio (OR)=1.882, 95% confidence interval (CI)=1.141–3.104], visited an emergency room at least once [43.4% vs. 27.1%, p<0.01; OR=2.065, 95% CI=1.276–3.343], been hospitalized overnight at least once (32.9% vs. 20.5%, p=0.01; OR=1.900, 95% CI=1.140–3.165), ever been admitted to an intensive care unit (ICU) (61.8% vs. 33.4%, p<0.01; OR=3.233, 95% CI=1.985–5.266), or ever required a feeding tube (21.1% vs. 9.1%, p<0.01; OR=2.671, 95% CI=1.457–4.896). A total of 75.8% younger females with refractory disease (<51 years, n=33) experienced at least one exacerbation, 69.7% had been admitted to an ICU, and 30.3% had required a feeding tube. For older females with refractory disease (≥51 years, n=33), 60.6%, 54.6%, and 6.1% experienced these outcomes, respectively (between-group differences were not significant). Conclusions Refractory MG is associated with higher disease burden and healthcare utilization than nonrefractory MG.
Precise Manipulation of Chromosomes in Vivo Enables Genome-Wide Codon Replacement
Isaacs, Farren J.,Carr, Peter A.,Wang, Harris H.,Lajoie, Marc J.,Sterling, Bram,Kraal, Laurens,Tolonen, Andrew C.,Gianoulis, Tara A.,Goodman, Daniel B.,Reppas, Nikos B.,Emig, Christopher J.,Bang, Duhe American Association for the Advancement of Scienc 2011 Science Vol.333 No.6040
<P>We present genome engineering technologies that are capable of fundamentally reengineering genomes from the nucleotide to the megabase scale. We used multiplex automated genome engineering (MAGE) to site-specifically replace all 314 TAG stop codons with synonymous TAA codons in parallel across 32 Escherichia coli strains. This approach allowed us to measure individual recombination frequencies, confirm viability for each modification, and identify associated phenotypes. We developed hierarchical conjugative assembly genome engineering (CAGE) to merge these sets of codon modifications into genomes with 80 precise changes, which demonstrate that these synonymous codon substitutions can be combined into higher-order strains without synthetic lethal effects. Our methods treat the chromosome as both an editable and an evolvable template, permitting the exploration of vast genetic landscapes.</P>
Ruchi Bansal,Shigeki Nakagawa,Saleh Yazdani,Joop van Baarlen,Anu Venkatesh,Anna P Koh,송원민,Nicolas Goossens,Hideo Watanabe,Mary B Beasley,Charles A Powell,Gert Storm,Naftali Kaminski,Harry van Goor,Sco 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Tissue fibrosis, characterized by excessive accumulation of aberrant extracellular matrix (ECM) produced by myofibroblasts, is a growing cause of mortality worldwide. Understanding the factors that induce myofibroblastic differentiation is paramount to prevent or reverse the fibrogenic process. Integrin-mediated interaction between the ECM and cytoskeleton promotes myofibroblast differentiation. In the present study, we explored the significance of integrin alpha 11 (ITGA11), the integrin alpha subunit that selectively binds to type I collagen during tissue fibrosis in the liver, lungs and kidneys. We showed that ITGA11 was co-localized with α-smooth muscle actin-positive myofibroblasts and was correlatively induced with increasing fibrogenesis in mouse models and human fibrotic organs. Furthermore, transcriptome and protein expression analysis revealed that ITGA11 knockdown in hepatic stellate cells (liver-specific myofibroblasts) markedly reduced transforming growth factor β-induced differentiation and fibrotic parameters. Moreover, ITGA11 knockdown dramatically altered the myofibroblast phenotype, as indicated by the loss of protrusions, attenuated adhesion and migration, and impaired contractility of collagen I matrices. Furthermore, we demonstrated that ITGA11 was regulated by the hedgehog signaling pathway, and inhibition of the hedgehog pathway reduced ITGA11 expression and fibrotic parameters in human hepatic stellate cells in vitro, in liver fibrosis mouse model in vivo and in human liver slices ex vivo. Therefore, we speculated that ITGA11 might be involved in fibrogenic signaling and might act downstream of the hedgehog signaling pathway. These findings highlight the significance of the ITGA11 receptor as a highly promising therapeutic target in organ fibrosis.