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1

Yu, Jingxiong, Yuwan Chen, Jiangle Zhang, Shanjun Chen, Qiaolin Wang, Zhengbo Qin, and Zichao Tang. "Development of a miniature time-of-flight mass spectrometer coupled with an improved substrate-enhanced laser-induced acoustic desorption source (SE-LIAD/TOF-MS)." Analyst 146, no. 13 (2021): 4365–73. http://dx.doi.org/10.1039/d1an00696g.

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Jordan, Sina, Anja Junker, John D. Helmann, and Thorsten Mascher. "Regulation of LiaRS-Dependent Gene Expression in Bacillus subtilis: Identification of Inhibitor Proteins, Regulator Binding Sites, and Target Genes of a Conserved Cell Envelope Stress-Sensing Two-Component System." Journal of Bacteriology 188, no. 14 (July 15, 2006): 5153–66. http://dx.doi.org/10.1128/jb.00310-06.

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ABSTRACT The regulatory network of the cell envelope stress response in Bacillus subtilis involves both extracytoplasmic function σ-factors and two-component signal transducing systems. One such system, LiaRS, responds to cell wall antibiotics that interfere with the undecaprenol cycle and to perturbation of the cytoplasmic membrane. It is encoded by the last two genes of the liaIHGFSR locus. Here, we analyzed the expression of two LiaR-dependent operons, liaIHGFSR and yhcYZ-yhdA, and characterized a palindromic sequence required for LiaR-dependent activation. Since induction of the strong liaI promoter leads to both liaIH and liaIHGFRS transcripts, LiaR is positively autoregulated. Systematic deletion analysis of the liaI operon revealed that LiaF is a potent negative regulator of LiaR-dependent gene expression: a nonpolar liaF deletion led to constitutive activation of both characterized LiaR-dependent promoters. The liaF gene is conserved in both sequence and genomic context in the Firmicutes group of gram-positive bacteria, located directly upstream of liaSR orthologs. LiaH, a homolog of Escherichia coli phage shock protein A, also plays a more subtle role in negatively modulating the bacitracin-inducible expression from LiaR-dependent promoters. Our results support a model in which the LiaFRS module integrates both positive and negative feedback loops to transduce cell envelope stress signals.
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Ortiz-Velez, Laura C., Sandra L. Rincon, Jesse Degani, Yousif Shamoo, Truc T. Tran, Cesar A. Arias, and Diana Panesso. "599. LiaF is an Activator of the LiaR-Mediated Response Against Daptomycin and Antimicrobial Peptides in Multidrug-Resistant Enterococcus faecalis (Efs)." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S281. http://dx.doi.org/10.1093/ofid/ofz360.668.

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Abstract Background Daptomycin (DAP) is a key first-line agent for the treatment of vancomycin-resistant enterococcal infections. Resistance to DAP in enterococci is regulated by the liaFSR three-component regulatory system that consists of a histidine kinase sensor (LiaS), a response regulator (LiaR) and a transmembrane protein of unknown function (LiaF). Previous studies indicate that deletion of isoleucine in position 177 of LiaF results in DAP tolerance and is sufficient to change membrane architecture. Here, we dissect the role of LiaF in DAP resistance Methods We generated three liaF mutants in OG1RF, a DAP-susceptible laboratory strain of Efs (DAP MIC = 2 µg/mL): (i) a non-polar, C-terminal truncation of liaF (OG1RFliaF∆152), (ii) a null liaF mutant with a premature stop-codon (OG1RFliaF*11), and (iii) an isoleucine deletion at position 177 (OG1RFliaF177). We determined DAP MIC by Etest and characterized the localization of anionic phospholipids microdomains using 10-nonyl-acridine-orange (NAO). The expression of the liaXYZ (the main target of LiaR) and liaFSR clusters were evaluated by qRT-PCR and relative expression ratios (Log2 fold change) were calculated by normalizing to gyrB expression. We assessed activation of LiaFSR by evaluating surface exposure of LiaX by ELISA. We used the bacterial adenylate cyclase two-hybrid system (BACTH) to evaluate the protein-protein interaction between LiaF and LiaS. Results Full deletion of liaF or the C-terminal truncation of LiaF did not have any effect on DAP MICs, membrane architecture or a significant increase in LiaX surface exposure compared with parental strain OG1RF. In contrast, deletion of the codon encoding isoleucine in position 177 of LiaF caused a major increase (8-fold) in LiaX exposure and redistribution of anionic phospholipid microdomains away from the septum without changes in the actual DAP MIC. Transcriptional analyses indicated upregulation (>2 log2-fold) in the liaXYZ gene cluster indicating activation of the stress response. We also observed a positive interaction between LiaF and LiaS. Conclusion LiaF is likely a key activator of the LiaFSR stress response and the critical regulatory domain appears to be located in a stretch of four isoleucines toward the C-terminal of the protein. Disclosures All authors: No reported disclosures.
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4

Stewart, Matthew T., Taylor Nezich, Joyce M. Lee, Rebecca E. Hasson, and Natalie Colabianchi. "Using a Mobile Phone App to Analyze the Relationship Between Planned and Performed Physical Activity in University Students: Observational Study." JMIR mHealth and uHealth 9, no. 4 (April 29, 2021): e17581. http://dx.doi.org/10.2196/17581.

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Background The relationship between intention and behavior has been well researched, but most studies fail to capture dynamic, time-varying contextual factors. Ecological momentary assessment through mobile phone technology is an innovative method for collecting data in real time, including time-use data. However, only a limited number of studies have examined day-level plans to be physically active and subsequent physical activity behavior using real-time time-use data to better understand this relationship. Objective This study aims to examine whether plans to be physically active (recorded in advance on an electronic calendar) were associated with objectively assessed physical activity (accelerometry), to identify activities that replaced planned periods of physical activity by using the mobile app Life in a Day (LIAD), and to test the feasibility and acceptability of LIAD for collecting real-time time-use data. Methods The study included 48 university students who were randomly assigned to 1 of 3 protocols, which were defined by 1, 3, or 5 days of data collection. Participants were asked to record their planned activities on a Google Calendar and were provided with mobile phones with LIAD to complete time-use entries in real time for a set of categories (eg, exercise or sports, eating or cooking, school, or personal care). Participants were instructed to wear an accelerometer on their nondominant wrist during the protocol period. A total of 144 days of protocol data were collected from the 48 participants. Results Protocol data for 123 days were eligible for analysis. A Fisher exact test showed a statistically significant association between plans and physical activity behavior (P=.02). The congruence between plans and behavior was fair (Cohen κ=0.220; 95% CI 0.028-0.411). Most participants did not plan to be active, which occurred on 75.6% (93/123) of days. Of these 93 days, no physical activity occurred on 76 (81.7%) days, whereas some physical activity occurred on 17 (18.3%) days. On the remaining 24.4% (30/123) of days, some physical activity was planned. Of these 30 days, no physical activity occurred on 18 (60%) days, whereas some physical activity occurred on 12 (40%) days. LIAD data indicated that activities related to screen time most often replaced planned physical activity, whereas unplanned physical activity was often related to active transport. Feasibility analyses indicated little difficulty in using LIAD, and there were no significant differences in feasibility by protocol length. Conclusions Consistent with previous literature, physical activity plans and physical activity behaviors were linked, but not strongly linked. LIAD offers insight into the relationship between plans and behavior, highlighting the importance of active transport for physical activity and the influence of screen-related behaviors on insufficient physical activity. LIAD is a feasible and practical method for collecting time-use data in real time.
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Jeha, Julio. "A cidade asilo: crimes de guerra e crimes sociais." Arquivo Maaravi: Revista Digital de Estudos Judaicos da UFMG 9, no. 17 (November 25, 2015): 383–85. http://dx.doi.org/10.17851/1982-3053.9.17.383-385.

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Lin, Rongkun, Qiao Lu, Zheng Lin, Wei Hang, and Benli Huang. "Laser-induced acoustic desorption coupled with electrospray ionization mass spectrometry for rapid qualitative and quantitative analysis of glucocorticoids illegally added in creams." Analyst 145, no. 20 (2020): 6625–31. http://dx.doi.org/10.1039/d0an00962h.

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7

Mariotti, E., S. Atutov, M. Meucci, P. Bicchi, C. Marinelli, and L. Moi. "Dynamics of rubidium light-induced atom desorption (LIAD)." Chemical Physics 187, no. 1-2 (September 1994): 111–15. http://dx.doi.org/10.1016/0301-0104(94)00192-8.

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8

Calvert, C. R., O. Kelly, L. Belshaw, M. J. Duffy, R. B. King, I. D. Williams, and J. B. Greenwood. "LIAD-FS: A new technique for gas-phase studies of biomolecules." Journal of Physics: Conference Series 388, no. 3 (November 5, 2012): 032050. http://dx.doi.org/10.1088/1742-6596/388/3/032050.

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9

Wolf, Diana, Falk Kalamorz, Tina Wecke, Anna Juszczak, Ulrike Mäder, Georg Homuth, Sina Jordan, et al. "In-Depth Profiling of the LiaR Response of Bacillus subtilis." Journal of Bacteriology 192, no. 18 (July 16, 2010): 4680–93. http://dx.doi.org/10.1128/jb.00543-10.

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ABSTRACT The Lia system, a cell envelope stress response module of Bacillus subtilis, is comprised of the LiaRS two-component system and a membrane-anchored inhibitor protein, LiaF. It is highly conserved in the Firmicutes bacteria, and all orthologs investigated so far are activated by cell wall antibiotics. In response to envelope stress, the systems in Firmicutes cocci induce the expression of a number of genes that are involved in conferring resistance against its inducers. In contrast, a complete picture of the LiaR regulon of B. subtilis is still missing and no phenotypes could be associated with mutants lacking LiaRS. Here, we performed genome-wide transcriptomic, proteomic, and in-depth phenotypic profiling of constitutive “Lia ON” and “Lia OFF” mutants to obtain a comprehensive picture of the Lia response of Bacillus subtilis. In addition to the known targets liaIH and yhcYZ-yhdA, we identified ydhE as a novel gene affected by LiaR-dependent regulation. The results of detailed follow-up gene expression studies, together with proteomic analysis, demonstrate that the liaIH operon represents the only relevant LiaR target locus in vivo. It encodes a small membrane protein (LiaI) and a phage shock protein homolog (LiaH). LiaH forms large oligomeric rings reminiscent of those described for Escherichia coli PspA or Arabidopsis thaliana Vipp1. The results of comprehensive phenotype studies demonstrated that the gene products of the liaIH operon are involved in protecting the cell against oxidative stress and some cell wall antibiotics. Our data suggest that the LiaFSR system of B. subtilis and, presumably, other Firmicutes bacilli coordinates a phage shock protein-like response.
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Bayan Imsamran. "The construction of war texts in the Chinese chronicle literature “Liad Kok”." JOURNAL OF KOREAN ASSOCIATION OF THAI STUDIES 23, no. 1 (August 2016): 169–202. http://dx.doi.org/10.22473/kats.2016.23.1.005.

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Niazi, M. S., V. Timo Meinders, H. H. Wisselink, C. H. L. J. ten Horn, Gerrit Klaseboer, and A. H. van den Boogaard. "A Plasticity Induced Anisotropic Damage Model for Sheet Forming Processes." Key Engineering Materials 554-557 (June 2013): 1245–51. http://dx.doi.org/10.4028/www.scientific.net/kem.554-557.1245.

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The global fuel crisis and increasing public safety concerns are driving the automotive industry to design high strength and low weight vehicles. The development of Dual Phase (DP) steels has been a big step forward in achieving this goal. DP steels are used in many automotive body-in-white structural components such as A and B pillar reinforcements, longitudinal members and crash structure parts. DP steels are also used in other industrial sectors such as precision tubes, train seats and Liquid Petroleum Gas (LPG) cylinders. Although the ductility of DP steel is higher than classical high strength steels, it is lower than that of classical deep drawing steels it has to replace. The low ductility of DP steels is attributed to damage development. Damage not only weakens the material but also reduces the ductility by formation of meso-cracks due to interacting micro defects. Damage in a material usually refers to presence of micro defects in the material. It is a known fact that plastic deformation induces damage in DP steels. Therefore damage development in these steels have to be included in the simulation of the forming process. In ductile metals, damage leads to crack initiation. A crack is anisotropic which makes damage anisotropic in nature. However, most researchers assume damage to be an isotropic phenomenon. For correct and accurate simulation results, damage shall be considered as anisotropic, especially if the results are used to determine the crack propagation direction. This paper presents an efficient plasticity induced anisotropic damage model to simulate complex failure mechanisms and accurately predict failure in macro-scale sheet forming processes. Anisotropy in damage can be categorized based on the cause which induces the anisotropy, i.e. the loading state and the material microstructure. According to the Load Induced Anisotropic Damage (LIAD) model, if the material is deformed in one direction then damage will be higher in this direction compared to the other two orthogonal directions, irrespective of the microstructure of the material. According to Material Induced Anisotropic Damage (MIAD) model, if there is an anisotropy in shape or distribution of the particles responsible for damage (hard second phase particles, inclusions or impurities) then the material will have different damage characteristics for different orientations in the sheet material. The LIAD part of the damage model is a modification of Lemaitre’s (ML) anisotropic damage model. Modifications are made for damage development under compression state and influence of strain rate on damage, and are presented in this paper. Viscoplastic regularization is used to avoid pathological mesh dependency. The MIAD part of the model is an extension of the LIAD model. Experimental evidence is given of the MIAD phenomenon in DP600 steel. The experimental analysis is carried out using tensile tests, optical strain measurement system (ARAMIS) and scanning electron microscopy. The extension to incorporate MIAD in the ML anisotropic damage model is presented in this paper as well. The paper concludes with a validation of the anisotropic damage model for different applications. The MIAD part of the model is validated by experimental cylindrical cup drawing wheras the LIAD part of the model is validated by the cross die drawing process.
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Morillo, Pedro, José J. Navarro-Pérez, Juan M. Orduña, and Marcos Fernández. "Evaluation of an Intervention Program Based on Mobile Apps to Learn Sexism Prevention in Teenagers." ACM Transactions on Multimedia Computing, Communications, and Applications 18, no. 2 (May 31, 2022): 1–20. http://dx.doi.org/10.1145/3471139.

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The fight against sexism is nowadays one of the flagship social movements in western countries. Adolescence is a crucial period, and some empirical studies have focused on the socialization of teenagers, proving that the socialization with the surrounding environment prevent sexist practices. In a previous work, we developed and tested the effectiveness of a mobile app, called Liad@s , with the goals of helping teenagers to prevent sexism and build healthy couple relationships. In this article, we carry out a study where (using a real situation) we compare the effectiveness of the Liad@s app in front of traditional interventions like a workshop about sexism for teenagers. Also, we evaluate the usability of the app and the user satisfaction with this application. In this study, our primary hypothesis is that the effectiveness of using our mobile application, in terms of knowledge acquired about sexism, would be at least as good as attending the workshop. Our secondary hypothesis is that the user satisfaction with the mobile application would be higher than the one with the workshop, causing a preference for the app. The results of this study show significant differences in learning appeared between gender and between the two different procedures when separately evaluating the data collected from both hostile sexism (HS) and benevolent sexism (BS) questionnaires. These results validate our primary hypothesis. Also, most of the population under study preferred the mobile app in front of the traditional workshop, validating also our secondary hypothesis.
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Calvert, C. R., L. Belshaw, M. J. Duffy, O. Kelly, R. B. King, A. G. Smyth, T. J. Kelly, et al. "LIAD-fs scheme for studies of ultrafast laser interactions with gas phase biomolecules." Physical Chemistry Chemical Physics 14, no. 18 (2012): 6289. http://dx.doi.org/10.1039/c2cp23840c.

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Little, J. P. "Review: Simone Weil's 'The "liad"; or, The Poem of Force': A Critical Edition." French Studies 58, no. 3 (July 1, 2004): 437–38. http://dx.doi.org/10.1093/fs/58.3.437.

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Calvert, C. R., O. Kelly, M. J. Duffy, L. Belshaw, R. B. King, I. D. Williams, and J. B. Greenwood. "LIAD-fs: A novel method for studies of ultrafast processes in gas phase neutral biomolecules." Journal of Physics: Conference Series 388, no. 1 (November 5, 2012): 012032. http://dx.doi.org/10.1088/1742-6596/388/1/012032.

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Fritsch, Frederike, Norman Mauder, Tatjana Williams, Julia Weiser, Markus Oberle, and Dagmar Beier. "The cell envelope stress response mediated by the LiaFSR Lm three-component system of Listeria monocytogenes is controlled via the phosphatase activity of the bifunctional histidine kinase LiaS Lm." Microbiology 157, no. 2 (February 1, 2011): 373–86. http://dx.doi.org/10.1099/mic.0.044776-0.

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Most members of the phylum Firmicutes harbour a two-component system (TCS), LiaSR, which is involved in the response to cell envelope stress elicited most notably by inhibitors of the lipid II cycle. In all LiaSR systems studied in detail, LiaSR-mediated signal transduction has been shown to be negatively controlled by a membrane protein, LiaF, encoded upstream of liaSR. In this study we have analysed the LiaSR orthologue of Listeria monocytogenes (LiaSR Lm ). Whole-genome transcriptional profiling indicated that activation of LiaSR Lm results in a remodelling of the cell envelope via the massive upregulation of membrane-associated and extracytoplasmic proteins in the presence of inducing stimuli. As shown for other LiaSR TCSs, LiaSR Lm is activated by cell wall-active antibiotics. We demonstrate that the level of phosphorylated LiaR Lm , which is required for the induction of the LiaSR Lm regulon, is controlled by the interplay between the histidine kinase and phosphatase activities of the bifunctional sensor protein LiaS Lm . Our data suggest that the phosphatase activity of LiaS Lm is stimulated by LiaF Lm in the absence of cell envelope stress.
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Yu, Jingxiong, Fanggang Liu, Zefeng Deng, Zaifa Shi, Jiangle Zhang, Qiaolin Wang, Jing Yang, Haoquan Hu, Zhengbo Qin, and Zichao Tang. "Insights into a Low-Rank Naomaohu Coal Structural Information by Multistage Fractions Coupled with LIAD-VUVPI-TOFMS." ACS Omega 7, no. 8 (February 17, 2022): 6935–43. http://dx.doi.org/10.1021/acsomega.1c06619.

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Chang, Ben-Jye, Shu-Yu Lin, and Jun-Yu Jin. "LIAD: Adaptive bandwidth prediction based Logarithmic Increase Adaptive Decrease for TCP congestion control in heterogeneous wireless networks." Computer Networks 53, no. 14 (September 2009): 2566–85. http://dx.doi.org/10.1016/j.comnet.2009.05.010.

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Nguyen, April, Truc T. Tran, Diana Panesso, Ayesha Khan, Eugenia Mileykovskaya, Heidi Vitrac, and Cesar A. Arias. "602. Mechanism of LiaY-Mediated Daptomycin Resistance in Enterococcus faecalis." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S282. http://dx.doi.org/10.1093/ofid/ofz360.671.

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Abstract Background Daptomycin (DAP) is a lipopeptide antibiotic that targets the cell membrane (CM) at the division septum. DAP resistance (DAP-R) in E. faecalis (Efs) has been linked to mutations in genes encoding the LiaFSR stress response system and lipid biosynthetic enzymes, including cardiolipin synthase (Cls). The signature phenotype of DAP-R is redistribution of CM anionic phospholipid (APL) microdomains. Using a genetic approach, we have identified a transmembrane protein (LiaY) as a major mediator of cell membrane APL redistribution associated with DAP-R. Here, we explore the mechanism of LiaY-mediated changes in the CM under the hypothesis that CM remodeling occurs through interactions with Cls. Methods Efs encodes two cls genes (cls1 and cls2). Deletion mutants of both cls genes were generated using the Crispr/cas9 system in the daptomycin-sensitive strain Efs OG117 and Efs OG117∆liaX (a DAP-R derivative of OG117). DAP minimum inhibitory concentration (MIC) was determined using E-test on Mueller–Hinton II agar. Visualization of APL microdomains was performed by staining mid-logarithmic phase cells with 1 µM of 10-N-nonyl-acridine orange (NAO) and fluorescence microscopy. Bacterial two-hybrid system was used to study interactions between LiaY with Cls1 or Cls2. Results Single or double deletion of cls1 or cls2 in Efs OG117 did not affect DAP MIC, and no changes in CM architecture were seen by NAO staining. In contrast,deletion of cls1 (alone or in conjunction with a deletion of cls2) in a DAP-R derivative of OG117 OG117∆liaX, resulted in a marked decrease in DAP MIC, and NAO staining of Efs OG117∆liaX∆cls1∆cls2 shows a restoration of septal APL microdomain localization.In the same DAP-R background, deletion of cls2 alone did not have any effect on DAP MIC or APL microdomain distribution. Additionally, bacterial two-hybrid assays showed a positive interaction of LiaY with Cls1 but not with Cls2. Conclusion We have identified the biochemical basis for DAP-R associated CM remodeling. In a proposed model, the LiaR-mediated activation of the LiaY triggers specific interactions with Cls1 displacing the protein away from the septum, resulting in local generation of APL microdomains that prevents DAP-mediated damage to the CM. Disclosures All authors: No reported disclosures.
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Butcher, Bronwyn G., Yi-Pin Lin, and John D. Helmann. "The yydFGHIJ Operon of Bacillus subtilis Encodes a Peptide That Induces the LiaRS Two-Component System." Journal of Bacteriology 189, no. 23 (October 5, 2007): 8616–25. http://dx.doi.org/10.1128/jb.01181-07.

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ABSTRACT The Bacillus subtilis LiaRS two-component system (TCS) responds to perturbations of the cell envelope induced by lipid II-interacting antibiotics, such as vancomycin, ramoplanin, nisin, and bacitracin. Here, we characterize Tn7-generated mutations that induce the liaRS TCS. In addition to insertions in liaF, a known negative regulator of the LiaRS TCS, we identified two disruptions in the last two genes of the yydFGHIJ operon. This operon is predicted to encode a 49-amino-acid peptide (YydF), a modification enzyme (YydG), a membrane-embedded protease (YydH), and an ATP-binding cassette (ABC) transporter (YydIJ). Genome sequence comparisons suggest that the yydFGHIJ operon may have been acquired by horizontal transfer. Inactivation of the YydIJ transporter resulted in increased expression from the LiaR-dependent P liaI promoter only in the presence of the yydFGH genes. Cells harboring the complete yydFGHIJ operon induced LiaR activity in cocultured cells lacking either this transporter or the complete operon. These results suggest that this operon is involved in the synthesis and export of a modified peptide (YydF*) that elicits cell envelope stress sensed by the LiaRS TCS.
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Chong, Patrick, Laura Drake, and Indranil Biswas. "LiaS Regulates Virulence Factor Expression in Streptococcus mutans." Infection and Immunity 76, no. 7 (May 5, 2008): 3093–99. http://dx.doi.org/10.1128/iai.01627-07.

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ABSTRACT Streptococcus mutans, a major oral pathogen responsible for dental caries formation, possesses a variety of mechanisms for survival in the human oral cavity, where the conditions of the external environment are diverse and in a constant state of flux. The formation of biofilms, survival under conditions of acidic pH, and production of mutacins are considered to be important virulence determinants displayed by this organism. Biofilm formation is facilitated by the production of GbpC, an important cell surface-associated protein that binds to glucan, an adhesive polysaccharide produced by the organism itself. To better understand the nature of the environmental cues that induce GbpC production, we examined the roles of 14 sensor kinases in the expression of gbpC in S. mutans strain UA159. We found that only the LiaS sensor kinase regulates gbpC expression, while the other sensor kinases had little or no effect on gbpC expression. We also found that while LiaS negatively regulates gbpC expression, the inactivation of its cognate response regulator, LiaR, does not appear to affect the expression of gbpC. Since both gbpC expression and mutacin IV production are regulated by a common regulatory network, we also tested the effect of the liaS mutation on mutacin production and found that LiaS positively regulates mutacin IV production. Furthermore, reverse transcription-PCR analysis suggests that LiaS does so by regulating the expression of nlmA, which encodes a peptide component of mutacin IV, and nlmT, which encodes an ABC transporter. As with the expression of gbpC, LiaR did not have any apparent effect on mutacin IV production. Based on the results of our study, we speculate that LiaS is engaged in cross talk with one or more response regulators belonging to the same family as LiaR, enabling LiaS to regulate the expression of several genes coding for virulence factors.
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Axell-House, Dierdre B., Ayesha Khan, Samuel A. Shelburne, Yousif Shamoo, Truc T. Tran, and Cesar A. Arias. "650. LiaX as a Surrogate Marker of Daptomycin Susceptibility in Multidrug-Resistant Enterococcus faecium." Open Forum Infectious Diseases 8, Supplement_1 (November 1, 2021): S427. http://dx.doi.org/10.1093/ofid/ofab466.847.

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Abstract Background Vancomycin-resistant Enterococcus faecium (VREfm) are important causes of bloodstream infections (BSI) in patients (pts) with cancer, liver disease, and foreign bodies. Daptomycin (DAP) is commonly used to treat VRE BSI, but DAP resistance (DAP-R) is increasing. Current methods to determine DAP minimum inhibitory concentrations (MICs) have poor reproducibility. DAP triggers the LiaFSR cell membrane stress response pathway, resulting in the extracellular release of LiaX, a protein that functions as a sentinel molecule for DAP, and controls the cell membrane response. Methods We used 6 reference Efm isolates to optimize a whole-cell enzyme-linked immunosorbent assay (ELISA) method for LiaX detection. We then assessed 86 clinical Efm BSI isolates recovered from 3 hospitals in Houston and Detroit for DAP MICs and used whole genome sequencing to assess for substitutions in LiaFSR/LiaXYZ proteins. We collected patient and microbiological data by chart review. Results All DAP-R reference strains had increased detection of LiaX compared to DAP-S strains (p< 0.0001). Of the 86 pts with Efm BSI, 73.2% had malignancy, 9.3% had liver disease, and 76.7% had foreign bodies. The source of 52.3% of BSIs was determined to be gastrointestinal. Two of the 86 isolates were DAP-R by CLSI breakpoints. The LiaX test and DAP MICs had a categorical agreement in 62.8% of isolates. All isolates with discordant ELISA/MIC results had DAP-S MIC (median 2, IQR 1-3)but increased LiaX. Using the genomic information, we identified 41 sites of amino acid (AA) changes in the LiaFSR/XYZ proteins of the ELISA/MIC discordant isolates. The substitutions LiaR S19F and LiaS E153K/D251E were associated with discordancy (p=0.0036 and p=0.0018, respectively). Conclusion Detection of LiaX is likely to indicate activation of the DAP-mediated cell membrane response in Efm and may be an indicator of DAP-R. Important discrepancies between LiaX and standard DAP MIC determination were found, highlighting the limitation of MIC determination. Further characterization of the discrepant isolates by time-kill assays and evaluation of patient clinical outcomes are warranted to fully validate the performance and clinical utility of the LiaX ELISA. Disclosures Truc T. Tran, PharmD, Merck (Grant/Research Support) Cesar A. Arias, M.D., MSc, Ph.D., FIDSA, Entasis Therapeutics (Grant/Research Support)MeMed Diagnostics (Grant/Research Support)Merk (Grant/Research Support)
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Khan, Ayesha, Milya Davlieva, Diana Panesso, Sandra Rincon, William R. Miller, Lorena Diaz, Jinnethe Reyes, et al. "Antimicrobial sensing coupled with cell membrane remodeling mediates antibiotic resistance and virulence inEnterococcus faecalis." Proceedings of the National Academy of Sciences 116, no. 52 (December 9, 2019): 26925–32. http://dx.doi.org/10.1073/pnas.1916037116.

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Bacteria have developed several evolutionary strategies to protect their cell membranes (CMs) from the attack of antibiotics and antimicrobial peptides (AMPs) produced by the innate immune system, including remodeling of phospholipid content and localization. Multidrug-resistantEnterococcus faecalis,an opportunistic human pathogen, evolves resistance to the lipopeptide daptomycin and AMPs by diverting the antibiotic away from critical septal targets using CM anionic phospholipid redistribution. The LiaFSR stress response system regulates this CM remodeling via the LiaR response regulator by a previously unknown mechanism. Here, we characterize a LiaR-regulated protein, LiaX, that senses daptomycin or AMPs and triggers protective CM remodeling. LiaX is surface exposed, and in daptomycin-resistant clinical strains, both LiaX and the N-terminal domain alone are released into the extracellular milieu. The N-terminal domain of LiaX binds daptomycin and AMPs (such as human LL-37) and functions as an extracellular sentinel that activates the cell envelope stress response. The C-terminal domain of LiaX plays a role in inhibiting the LiaFSR system, and when this domain is absent, it leads to activation of anionic phospholipid redistribution. Strains that exhibit LiaX-mediated CM remodeling and AMP resistance show enhanced virulence in theCaenorhabditis elegansmodel, an effect that is abolished in animals lacking an innate immune pathway crucial for producing AMPs. In conclusion, we report a mechanism of antibiotic and AMP resistance that couples bacterial stress sensing to major changes in CM architecture, ultimately also affecting host–pathogen interactions.
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Dawadi, Babu Ram, Subarna Shakya, and Rajendra Paudyal. "CoMMoN: The Real-Time Container and Migration Monitoring as a Service in the Cloud." Journal of the Institute of Engineering 12, no. 1 (March 6, 2017): 51–62. http://dx.doi.org/10.3126/jie.v12i1.16770.

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With the advancement of computing technologies, the modern cloud computing and virtualization system is highly distributed by the invention of better and light weight distributed applications packaging toolkit over the cloud environment, called the container technology. Cloud containers feature the management of applications with easy plug and play ability, migration, replication, relocation, upgrading et cetera in the real time. Such containers running different applications over the cloud infrastructure may consume different resources that require real time monitoring. Docker is an open source platform independent tool to create, deploy, and run applications by using Containers. Billions of applications for the end users and SMEs running over the cloud require efficient management, monitoring and operations to achieve better SLAs for cloud service providers. With this research, a Docker Container and Migration Monitoring System (CoMMoN) has been developed in which a customer running its application in a Container shall monitor its application in the real-time as well as take decision for the migration of Container to another network by service provider for liad balancing or by the customer under the violation of SLA. Once the customer registers its Container to the monitoring system, the monitoring probe collects different monitoring metrics and sends those parameters to remote monitoring system. The system which stores the monitoring metrics into InFluxDB, a time series database, also monitors the real-time migration of the Containers among the network.Journal of the Institute of Engineering, 2016, 12(1): 51-62
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25

Xiao, Huagang, Shikui Dong, and Tao Gao. "Electronic structure and laser cooling of LiAg and LiAu molecules." Chemical Physics Letters 793 (April 2022): 139407. http://dx.doi.org/10.1016/j.cplett.2022.139407.

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26

REHBOCK, THEDA. "Don’t Lie! . . . Why Not?" Cambridge Quarterly of Healthcare Ethics 21, no. 2 (February 29, 2012): 177–87. http://dx.doi.org/10.1017/s0963180111000685.

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You have lied! You are a liar! This is one of the most serious moral offences one can be blamed for. Augustine even regards lying as the fundamental moral offence and identifies it with sin and evil in general. For Augustine and Kant, lying is in itself morally reprehensible and not justifiable at all.
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27

Suntharalingam, Prashanth, M. D. Senadheera, Richard W. Mair, Céline M. Lévesque, and Dennis G. Cvitkovitch. "The LiaFSR System Regulates the Cell Envelope Stress Response in Streptococcus mutans." Journal of Bacteriology 191, no. 9 (February 27, 2009): 2973–84. http://dx.doi.org/10.1128/jb.01563-08.

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ABSTRACT Maintaining cell envelope integrity is critical for bacterial survival, including bacteria living in a complex and dynamic environment such as the human oral cavity. Streptococcus mutans, a major etiological agent of dental caries, uses two-component signal transduction systems (TCSTSs) to monitor and respond to various environmental stimuli. Previous studies have shown that the LiaSR TCSTS in S. mutans regulates virulence traits such as acid tolerance and biofilm formation. Although not examined in streptococci, homologs of LiaSR are widely disseminated in Firmicutes and function as part of the cell envelope stress response network. We describe here liaSR and its upstream liaF gene in the cell envelope stress tolerance of S. mutans strain UA159. Transcriptional analysis established liaSR as part of the pentacistronic liaFSR-ppiB-pnpB operon. A survey of cell envelope antimicrobials revealed that mutants deficient in one or all of the liaFSR genes were susceptible to Lipid II cycle interfering antibiotics and to chemicals that perturbed the cell membrane integrity. These compounds induced liaR transcription in a concentration-dependent manner. Notably, under bacitracin stress conditions, the LiaFSR signaling system was shown to induce transcription of several genes involved in membrane protein synthesis, peptidoglycan biosynthesis, envelope chaperone/proteases, and transcriptional regulators. In the absence of an inducer such as bacitracin, LiaF repressed LiaR-regulated expression, whereas supplementing cultures with bacitracin resulted in derepression of liaSR. While LiaF appears to be an integral component of the LiaSR signaling cascade, taken collectively, we report a novel role for LiaFSR in sensing cell envelope stress and preserving envelope integrity in S. mutans.
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28

Frantz, Simon. "Liar liar." Nature Reviews Molecular Cell Biology 3, no. 2 (February 2002): 3–4. http://dx.doi.org/10.1038/nrm725.

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29

Carson, Thomas. "Liar Liar." International Journal of Applied Philosophy 22, no. 2 (2008): 189–210. http://dx.doi.org/10.5840/ijap200822215.

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30

Wilson, Rick K., and Jane Sell. "“Liar, Liar... ”." Journal of Conflict Resolution 41, no. 5 (October 1997): 695–717. http://dx.doi.org/10.1177/0022002797041005005.

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31

Quinn, Elizabeth. "Child behaviour LIAR LIAR." Early Years Educator 1, no. 1 (May 1999): 53–54. http://dx.doi.org/10.12968/eyed.1999.1.1.15831.

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32

Quealy-Gainer, Kate. "Liar, Liar (review)." Bulletin of the Center for Children's Books 64, no. 7 (2011): 342–43. http://dx.doi.org/10.1353/bcc.2011.0211.

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33

Horvath, B. "Liar! Liar! Jack Kerouac--Novelist." American Literature 73, no. 1 (March 1, 2001): 210–11. http://dx.doi.org/10.1215/00029831-73-1-210.

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34

White, Christopher J. "Liar, liar, pants on fire." Catheterization and Cardiovascular Interventions 72, no. 3 (August 26, 2008): 430–31. http://dx.doi.org/10.1002/ccd.21721.

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35

Schutte, Sabine, Manfred Sievritts, and Peter Muhlbauer. "Lied, Song, Chanson. Bd. 2: Politisch Lied, ein garstig Lied?" Jahrbuch für Volksliedforschung 32 (1987): 142. http://dx.doi.org/10.2307/849430.

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36

ZHANG, Yunzhao. "Lied." National History 1, no. 1 (January 2008): nh20070602a1. http://dx.doi.org/10.3128/nh20070602a1.

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37

O'Connor, Seán. "Liam." Comhar 62, no. 7 (2002): 11. http://dx.doi.org/10.2307/25574420.

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38

Harris, Mark. "Liar!" IEEE Spectrum 47, no. 8 (August 2010): 40–53. http://dx.doi.org/10.1109/mspec.2010.5520628.

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39

Webber, J. "Liar!" Analysis 73, no. 4 (October 1, 2013): 651–59. http://dx.doi.org/10.1093/analys/ant081.

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40

Chen, Huanyin, and Marjan Abdolyousefi. "Generalized cline’s formula for g-Drazin inverse in a ring." Filomat 35, no. 8 (2021): 2573–83. http://dx.doi.org/10.2298/fil2108573c.

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In this paper, we give a generalized Cline?s formula for the generalized Drazin inverse. Let R be a ring, and let a, b, c, d ? R satisfying (ac)2 = (db)(ac), (db)2 = (ac)(db), b(ac)a = b(db)a, c(ac)d = c(db)d. Then ac ? Rd if and only if bd ? Rd. In this case, (bd)d = b((ac)d)2d: We also present generalized Cline?s formulas for Drazin and group inverses. Some weaker conditions in a Banach algebra are also investigated. These extend the main results of Cline?s formula on g-Drazin inverse of Liao, Chen and Cui (Bull. Malays. Math. Soc., 37(2014), 37-42), Lian and Zeng (Turk. J. Math., 40(2016), 161-165) and Miller and Zguitti (Rend. Circ. Mat. Palermo, II. Ser., 67(2018), 105-114). As an application, new common spectral property of bounded linear operators over Banach spaces is obtained.
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41

Varga von Kibéd, Matthias, and Elke Brendel. "The Liar." Grazer Philosophische Studien 39 (1991): 165–94. http://dx.doi.org/10.5840/gps19913933.

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42

Fields, Keota. "Intensional Liar." Philosophical Topics 45, no. 2 (2017): 21–32. http://dx.doi.org/10.5840/philtopics201745212.

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43

Wilson, Anthony. "German Lied." Musical Times 136, no. 1826 (April 1995): 196. http://dx.doi.org/10.2307/1004176.

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44

Drange, T. M. "Liar syllogisms." Analysis 50, no. 1 (January 1, 1990): 1–7. http://dx.doi.org/10.1093/analys/50.1.1.

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45

Ince, Susan. "Ronglih Liao." Circulation Research 118, no. 10 (May 13, 2016): 1464–67. http://dx.doi.org/10.1161/circresaha.116.308912.

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46

Holmstrom, Sven-Eric. "Khrushchev Lied." Socialism and Democracy 26, no. 2 (July 2012): 119–24. http://dx.doi.org/10.1080/08854300.2012.686278.

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47

Snaider, Javier, and Stan Franklin. "Vector LIDA." Procedia Computer Science 41 (2014): 188–203. http://dx.doi.org/10.1016/j.procs.2014.11.103.

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48

Dolan, Liam. "Liam Dolan." Current Biology 26, no. 3 (February 2016): R85—R86. http://dx.doi.org/10.1016/j.cub.2015.12.059.

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49

Faletar, Sanjica. "LIDA 2004." Library Hi Tech News 21, no. 7 (August 2004): 3–4. http://dx.doi.org/10.1108/07419050410.

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50

Lahman, Maria. "Mother Liar." Qualitative Inquiry 15, no. 9 (July 31, 2009): 1452–54. http://dx.doi.org/10.1177/1077800409343078.

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