Relevant bibliographies by topics / LL37

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Academic literature on the topic 'LL37'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "LL37"

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Lande, Roberto, Immacolata Pietraforte, Anna Mennella, Raffaella Palazzo, Francesca Romana Spinelli, Konstantinos Giannakakis, Francesca Spadaro, et al. "Complementary Effects of Carbamylated and Citrullinated LL37 in Autoimmunity and Inflammation in Systemic Lupus Erythematosus." International Journal of Molecular Sciences 22, no. 4 (February 6, 2021): 1650. http://dx.doi.org/10.3390/ijms22041650.

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LL37 acts as T-cell/B-cell autoantigen in Systemic lupus erythematosus (SLE) and psoriatic disease. Moreover, when bound to “self” nucleic acids, LL37 acts as “danger signal,” leading to type I interferon (IFN-I)/pro-inflammatory factors production. T-cell epitopes derived from citrullinated-LL37 act as better antigens than unmodified LL37 epitopes in SLE, at least in selected HLA-backgrounds, included the SLE-associated HLA-DRB1*1501/HLA-DRB5*0101 backgrounds. Remarkably, while “fully-citrullinated” LL37 acts as better T-cell-stimulator, it loses DNA-binding ability and the associated “adjuvant-like” properties. Since LL37 undergoes a further irreversible post-translational modification, carbamylation and antibodies to carbamylated self-proteins other than LL37 are present in SLE, here we addressed the involvement of carbamylated-LL37 in autoimmunity and inflammation in SLE. We detected carbamylated-LL37 in SLE-affected tissues. Most importantly, carbamylated-LL37-specific antibodies and CD4 T-cells circulate in SLE and both correlate with disease activity. In contrast to “fully citrullinated-LL37,” “fully carbamylated-LL37” maintains both innate and adaptive immune-cells’ stimulatory abilities: in complex with DNA, carbamylated-LL37 stimulates plasmacytoid dendritic cell IFN-α production and B-cell maturation into plasma cells. Thus, we report a further example of how different post-translational modifications of a self-antigen exert complementary effects that sustain autoimmunity and inflammation, respectively. These data also show that T/B-cell responses to carbamylated-LL37 represent novel SLE disease biomarkers.
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Palazzo, Raffaella, Immacolata Pietraforte, Carlo Chizzolini, Roberto Lande, and Loredana Frasca. "RB139, RB140, RB141 and RB142 antibodies recognize human citrullinated LL37 by ELISA." Antibody Reports 3, no. 3 (May 26, 2020): e189. http://dx.doi.org/10.24450/journals/abrep.2020.e189.

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LL37 is a natural antibiotic, active against bacteria and fungi and some viruses. Here we show that three monoclonal antibodies (RB139, RB141, and RB142) are exclusively specific for citrullinated LL37, whereas RB140 recognizes both native LL37 and cit-LL37. None recognizes LL37 modified by carbamylation. These antibodies can represent previously unavailable tools to detect the presence of citrullinated LL37 in body fluids by ELISA in the course of autoimmune and infectious diseases.
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Lande, Roberto, Stefano Alivernini, Barbara Tolusso, Francesca Spadaro, Mario Falchi, Raffaella Palazzo, Immacolata Pietraforte, et al. "Monoclonal antibodies RB139 and RB142 recognize citrullinated LL37 by immunofluorescence in histological sections in Systemic lupus erythematosus (SLE) and Rheumatoid arthritis (RA)." Antibody Reports 3, no. 4 (July 27, 2020): e236. http://dx.doi.org/10.24450/journals/abrep.2020.e236.

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LL37 is a natural antibiotic, but is also a molecule with pleiotropic functions as well as an immune-modulator. LL37 is produced by epithelial cells and is present in neutrophils’ granules. LL37 alone, or in complex with DNA, can activate inflammatory pathways in psoriasis, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). In this work, we describe the capacity of two recombinant monoclonal antibodies, RB139 and RB142, previously shown to specifically recognize LL37 in its citrullinated form (cit-LL37) by ELISA, to detect LL37 by immunofluorescence in human inflamed tissues derived from SLE and RA patients. Such antibodies represent previously unavailable tools to detect the presence, the citrullinated state and the exact localization of cit-LL37 in human tissues in health and disease.
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Lande, Roberto, Stefano Alivernini, Barbara Tolusso, Francesca Spadaro, Mario Falchi, Raffaella Palazzo, Immacolata Pietraforte, et al. "RB137 recognizes LL37 in neutrophil-extracellular trap-like (NET) structures in systemic lupus erythematosus and rheumatoid arthritis inflamed tissues by immunofluorescence in histological sections." Antibody Reports 3, no. 4 (July 27, 2020): e235. http://dx.doi.org/10.24450/journals/abrep.2020.e235.

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Besides being a natural antibiotic, the human cathelicidin LL37, produced by epithelial cells and neutrophils, is an important immune-modulator. LL37 alone, or in complex with DNA, can activate inflammatory pathways in psoriasis, Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). In this work, we describe the capacity of the recombinant monoclonal antibody RB137, previously shown to specifically recognize LL37 in its native form by ELISA, to detect LL37 by immunofluorescence in human tissues derived from SLE and RA patients. In these tissues, LL37 decorates DNA filaments resembling neutrophil-extracellular-trap (NET) structures. This antibody represents a valuable tool to detect the presence, the native state and the exact localization of LL37 in human tissues in health and disease.
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Palazzo, Raffaella, Immacolata Pietraforte, Carlo Chizzolini, Roberto Lande, and Loredana Frasca. "RB137 and RB138 antibodies recognize human cathelicidin LL37 by ELISA." Antibody Reports 3, no. 3 (May 26, 2020): e188. http://dx.doi.org/10.24450/journals/abrep.2020.e188.

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LL37 is a cationic antimicrobial peptide (AMP), which can undergo post-translational modifications (PTM), such as citrullination and carbamylation. We demonstrate here that recombinant antibodies RB137 and RB138 are specific for native LL37 and do not recognize modified LL37 (citrullinated and carbamylated). They thus represent tools to assess the presence of native, unmodified LL37 in body fluids by ELISA.
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Lande, Roberto, Raffaella Palazzo, Philippe Hammel, Immacolata Pietraforte, Isabelle Surbeck, Michel Gilliet, Carlo Chizzolini, and Loredana Frasca. "Generation of Monoclonal Antibodies Specific for Native LL37 and Citrullinated LL37 That Discriminate the Two LL37 Forms in the Skin and Circulation of Cutaneous/Systemic Lupus Erythematosus and Rheumatoid Arthritis Patients." Antibodies 9, no. 2 (May 11, 2020): 14. http://dx.doi.org/10.3390/antib9020014.

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Human cathelicidin LL37 is a cationic antimicrobial peptide active against bacteria and viruses and exerting immune modulatory functions. LL37 can be also a target of autoreactive B- and T-lymphocytes in autoimmune settings. Irreversible post-translational modifications, such as citrullination and carbamylation, mainly occurring at the level of cationic amino acids arginine and lysine, can affect the inflammatory properties and reduce antibacterial effects. Moreover, these modifications could be implicated in the rupture of immune tolerance to LL37 in chronic conditions such as psoriatic disease and cutaneous lupus (LE)/systemic lupus erythematosus (SLE). Here, we describe the generation and fine specificity of six recombinant antibodies (MRB137–MRB142), produced as a monovalent mouse antibody with the antigen-binding scFv portion fused to a mouse IgG2a Fc, and their ability to recognize either native or citrullinated LL37 (cit-LL37) and not cross-react to carbamylated LL37. By using these antibodies, we detected native LL37 or cit-LL37 in SLE and rheumatoid arthritis (RA) sera, and in LE skin, by ELISA and immunohistochemistry, respectively. Such antibodies represent previously unavailable and useful tools to address relationships between the presence of post-translational modified LL37 and the immune system status (in terms of innate/adaptive responses activation) and the clinical characteristics of patients affected by chronic immune-mediated diseases or infectious diseases.
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Ganguly, Dipyaman, Georgios Chamilos, Roberto Lande, Josh Gregorio, Stephan Meller, Valeria Facchinetti, Bernhard Homey, Franck J. Barrat, Tomasz Zal, and Michel Gilliet. "Self-RNA–antimicrobial peptide complexes activate human dendritic cells through TLR7 and TLR8." Journal of Experimental Medicine 206, no. 9 (August 24, 2009): 1983–94. http://dx.doi.org/10.1084/jem.20090480.

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Dendritic cell (DC) responses to extracellular self-DNA and self-RNA are prevented by the endosomal seclusion of nucleic acid–recognizing Toll-like receptors (TLRs). In psoriasis, however, plasmacytoid DCs (pDCs) sense self-DNA that is transported to endosomal TLR9 upon forming a complex with the antimicrobial peptide LL37. Whether LL37 also interacts with extracellular self-RNA and how this may contribute to DC activation in psoriasis is not known. Here, we report that LL37 can bind self-RNA released by dying cells, protect it from extracellular degradation, and transport it into endosomal compartments of DCs. In pDC, self-RNA–LL37 complexes activate TLR7 and, like self-DNA–LL37 complexes, trigger the secretion of IFN-α without inducing maturation or the production of IL-6 and TNF-α. In contrast to self-DNA–LL37 complexes, self-RNA–LL37 complexes also trigger the activation of classical myeloid DCs (mDCs). This occurs through TLR8 and leads to the production of TNF-α and IL-6, and the differentiation of mDCs into mature DCs. We also found that self-RNA–LL37 complexes are present in psoriatic skin lesions and are associated with mature mDCs in vivo. Our results demonstrate that the cationic antimicrobial peptide LL37 converts self-RNA into a trigger of TLR7 and TLR8 in human DCs, and provide new insights into the mechanism that drives the auto-inflammatory responses in psoriasis.
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Wu, Fan, and Cheemeng Tan. "Dead bacterial absorption of antimicrobial peptides underlies collective tolerance." Journal of The Royal Society Interface 16, no. 151 (February 2019): 20180701. http://dx.doi.org/10.1098/rsif.2018.0701.

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The collective tolerance towards antimicrobial peptides (APs) is thought to occur primarily through mechanisms associated with live bacterial cells. In contrast to the focus on live cells, we discover that the LL37 antimicrobial peptide kills a subpopulation of Escherichia coli , forming dead cells that absorb the remaining LL37 from the environment. Combining mathematical modelling with population and single-cell experiments, we show that bacteria absorb LL37 at a timing that coincides with the permeabilization of their cytoplasmic membranes. Furthermore, we show that one bacterial strain can absorb LL37 and protect another strain from killing by LL37. Finally, we demonstrate that the absorption of LL37 by dead bacteria can be reduced using a peptide adjuvant. In contrast to the known collective tolerance mechanisms, we show that the absorption of APs by dead bacteria is a dynamic process that leads to emergent population behaviour.
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Salamah, Maryam F., Divyashree Ravishankar, Xenia Kodji, Leonardo A. Moraes, Harry F. Williams, Thomas M. Vallance, Dina A. Albadawi, et al. "The endogenous antimicrobial cathelicidin LL37 induces platelet activation and augments thrombus formation." Blood Advances 2, no. 21 (November 9, 2018): 2973–85. http://dx.doi.org/10.1182/bloodadvances.2018021758.

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Abstract Platelet-associated complications including thrombosis, thrombocytopenia, and hemorrhage are commonly observed during various inflammatory diseases such as sepsis, inflammatory bowel disease, and psoriasis. Despite the reported evidence on numerous mechanisms/molecules that may contribute to the dysfunction of platelets, the primary mechanisms that underpin platelet-associated complications during inflammatory diseases are not fully established. Here, we report the discovery of formyl peptide receptor 2, FPR2/ALX, in platelets and its primary role in the development of platelet-associated complications via ligation with its ligand, LL37. LL37 acts as a powerful endogenous antimicrobial peptide, but it also regulates innate immune responses. We demonstrate the impact of LL37 in the modulation of platelet reactivity, hemostasis, and thrombosis. LL37 activates a range of platelet functions, enhances thrombus formation, and shortens the tail bleeding time in mice. By utilizing a pharmacological inhibitor and Fpr2/3 (an ortholog of human FPR2/ALX)–deficient mice, the functional dependence of LL37 on FPR2/ALX was determined. Because the level of LL37 is increased in numerous inflammatory diseases, these results point toward a critical role for LL37 and FPR2/ALX in the development of platelet-related complications in such diseases. Hence, a better understanding of the clinical relevance of LL37 and FPR2/ALX in diverse pathophysiological settings will pave the way for the development of improved therapeutic strategies for a range of thromboinflammatory diseases.
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Chang, Hao-Teng, Pei-Wen Tsai, Hsin-Hui Huang, Yu-Shu Liu, Tzu-Shan Chien, and Chung-Yu Lan. "LL37 and hBD-3 elevate the β-1,3-exoglucanase activity of Candida albicans Xog1p, resulting in reduced fungal adhesion to plastic." Biochemical Journal 441, no. 3 (January 16, 2012): 963–70. http://dx.doi.org/10.1042/bj20111454.

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The opportunistic fungus Candida albicans causes oral thrush and vaginal candidiasis, as well as candidaemia in immunocompromised patients including those undergoing cancer chemotherapy, organ transplant and those with AIDS. We previously found that the AMPs (antimicrobial peptides) LL37 and hBD-3 (human β-defensin-3) inhibited C. albicans viability and its adhesion to plastic. For the present study, the mechanism by which LL37 and hBD-3 reduced C. albicans adhesion was investigated. After AMP treatment, C. albicans adhesion to plastic was reduced by up to ~60% and was dose-dependent. Our previous study indicated that LL37 might interact with the cell-wall β-1,3-exoglucanase Xog1p, which is involved in cell-wall β-glucan metabolism, and consequently the binding of LL37 or hBD-3 to Xog1p might cause the decrease in adhesion. For the present study, Xog1p(41–438)-6H, an N-terminally truncated, active, recombinant construct of Xog1p and Xog1p fragments were produced and used in pull-down assays and ELISA in vitro, which demonstrated that all constructs interacted with both AMPs. Enzymatic analyses showed that LL37 and hBD-3 enhanced the β-1,3-exoglucanase activity of Xog1p(41–438)-6H approximately 2-fold. Therefore elevated Xog1p activity might compromise cell-wall integrity and decrease C. albicans adhesion. To test this hypothesis, C. albicans was treated with 1.3 μM Xog1p(41–438)-6H and C. albicans adhesion to plastic decreased 47.7%. Taken together, the evidence suggests that Xog1p is one of the LL37/hBD-3 targets, and elevated β-1,3-exoglucanase activity reduces C. albicans adhesion to plastic.
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Dissertations / Theses on the topic "LL37"

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Lozeau, Lindsay Dawn. "Design and Study of Collagen-Tethered LL37 for Chronic Wound Healing." Digital WPI, 2018. https://digitalcommons.wpi.edu/etd-dissertations/536.

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As society draws closer to the post-antibiotic era and the pipeline for alternatives dries, there is an urgent need for the development of novel antimicrobial therapies that do not promote bacterial resistance, particularly for immunocompromised chronic wound patients. Antimicrobial peptides (AMPs), including human-derived LL37, show considerable promise as broad spectrum alternatives that also have wound healing properties; however, few have been clinically implemented as novel antimicrobials due to their cytotoxicity stemming from a poor understanding of their mechanisms and low stability in vivo. It has been suggested that tethering, or attaching AMPs onto surfaces, is a viable strategy of delivering bioactive AMPs to surfaces while reducing cytotoxicity and improving stability. Thus, we designed new chimeric versions of LL37 with collagen-binding domains (CBD), derived from collagenase (cCBD-LL37) and fibronectin (fCBD-LL37) for non-covalent tethering onto collagen, a prevalent biopolymer in commercially available wound dressings and scaffolds. Our overall hypothesis was that CBDs would mediate stable tethering of broadly active, non-cytotoxic CBD-LL37 onto collagen-based scaffolds. We first studied the loading, release and bioactivities (e.g. antimicrobial activity and cytotoxicity) of each CBD-LL37 on commercially available 100% collagen type I PURACOL® wound scaffolds. We found that both cCBD-LL37 and fCBD-LL37 bound highly to collagen, were active against relevant wound pathogens, demonstrated stable activity after 14 days of release, and were not cytotoxic to human fibroblasts. The addition of different CBDs onto LL37 also markedly altered their soluble bioactivities. Using similar methods, we then studied the loading, release and bioactivity of each CBD-LL37 on a commercially available FIBRACOL® wound scaffolds, comprised of 90% collagen type I and 10% calcium alginate biopolymers. We found that both cCBD-LL37 and fCBD-LL37 also bound highly to and retained on collagen for 14 days, but were only active against Gram-negative P. aeruginosa. This suggested that the presence other biopolymers in addition to collagen, which is common among commercial wound dressings, could cause significant differences in binding, retention and bioactivities of CBD-LL37. To better understand how CBD modification affected CBD-LL37 structure leading to different bioactivities, we studied the CBD sequence-, peptide structure-, concentration-, time-, and bilayer composition-dependent interactions of soluble CBD-LL37 and compared these findings with the properties of unmodified LL37. Using Molecular Dynamics (MD) simulations, circular dichroism (CD) spectroscopy, quartz crystal microbalance with dissipation (QCM-D), and fluorescent bilayer imaging we determined the structural basis behind CBD alterations in bioactivities. MD and CD, in addition to other intrinsic CBD properties (helicity, amphiphilicity, charge) we hypothesized that cCBD-LL37 utilized similar mechanisms as unmodified LL37 while fCBD-LL37 demonstrated based primarily on surface adsorption. We used QCM-D and Voigt-Kelvin viscoelastic modeling to determine the time- and concentration-dependent interactions of unmodified LL37 with model mammalian lipid bilayers, the mechanisms of which are still controversial in literature despite being widely studied. These results were used to propose a model for the interaction mechanism of LL37 with zwitterionic bilayers that aligned with its bioactive concentrations. LL37 adsorbed at concentrations where it is immunomodulatory until reaching a threshold which corresponded with its antimicrobial concentrations. The threshold was correlated to lipid bilayer saturation, after which LL37 formed transmembrane pores. We observed collapse of the bilayer into a rigid proteolipid film at concentrations higher than the reported cytotoxic threshold of LL37. The mechanistic and structural information for each CBD-LL37 and unmodified LL37 provided a baseline for QCM-D and Voigt-Kelvin viscoelastic modeling to further elucidate the time-, concentration-, lipid composition- and CBD sequence-dependent basis behind the observed bioactivities of cCBD-LL37 and fCBD-LL37. We found that similar to LL37, cCBD-LL37 demonstrated pore formation mechanisms likely due to their similar charges, structural content and amphiphilicity. fCBD-LL37 demonstrated time-dependent, adsorption-based mechanism likely due to its anchoring aromatic residues, low charge, and low amphiphilicity. Knowledge gained from this study allowed mechanistic predictions of two newly designed hypothetical CBD-LL37 peptides. Results from this study contribute to a better understanding of a new class of antimicrobial, non-cytotoxic therapies based on collagen-tethered CBD-LL37, bringing it closer to clinical implementation in chronic wound applications and demonstrate the viability of biopolymer tethering as a platform toward using AMPs to quench the resistance crisis.
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Heilborn, Johan. "The human antimicrobial protein hCAP18/LL37 in wound healing and cell proliferation /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-432-5/.

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Röbke, Christina [Verfasser]. "Synthetische Derivate des humanen Cathelicidins hCAP18/LL37 sind potentielle, antitumorale Medikamente / Christina Röbke." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2011. http://d-nb.info/1014152011/34.

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Jacob, Rebecca. "Lipid bilayers and their interactions with the antimicrobial peptide LL37: a TIR Raman study." Thesis, KTH, Skolan för kemivetenskap (CHE), 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-207018.

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As a direct consequence of the misuse of antibiotics since its first discovery, bacteria have developed extensive resistance mechanisms making them once again potential lethal threats. This eventuality has triggered a vast research effort from scientists worldwide to find solutions to mitigate antimicrobial resistance. One such option is the identification of new potential antimicrobial agents, like for example antimicrobial peptides (AMPs). Various methods have been applied to evaluate the properties and determine the complex mechanism of AMPs. However, the details of the mechanism remain unknown and hence the work in this project seeks to examine the suitability of using TIR Raman, a vibrational spectroscopy technique which is sufficiently surface sensitive to study the interaction of AMPs in contact with lipid bilayers, which are just a few nanometres thick. In order to evaluate the information that could be extracted from TIR Raman, measurement of solid supported lipid bilayers in the absence of peptides were first carried out. In particular, the lipid DMPC with a phase transition close to room temperature, was measured at various temperatures to determine spectral changes associated with the transition. For the peptide-membrane interactions, the AMP LL37 was put into contact with solid supported lipid bilayers modelling the cell membranes of bacteria (DOPE, DOPG) or humans (DOPC) respectively. The data clearly indicates that the membrane composition, and specifically the lipid head group charge, play an important role in the peptide-membrane interactions. In the bilayers mimicking bacteria cell membranes, the peptide either absorbed onto or inserted into the bilayer. In contrast, for the bilayer modelling a human cell membrane, no significant variations were detected, indicating no interaction with LL37. The findings presented in this work generally coincide with similar research of LL37 using other techniques. At hand of the herein presented data, TIR Raman has proven suitable and effective in detecting effects of antimicrobial peptides in contact with model lipid bilayers, and hence can be recommended for further studies.
Som en direkt följd av missbruket av antibiotika sedan det först upptäcktes, har bakterier utvecklat omfattande resistensmekanismer vilket föranlett dem att återigen utgöra potentiellt dödlig hot. Denna situation har manat fram en väsentlig forskningsinsats från forskare världen över att hitta lösningar för att minska antimikrobiell resistens. Ett sådant alternativ har varit identifieringen av nya potentiella antimikrobiella substanser, så som till exempel antimikrobiella peptider. Ett flertal metoder har använts för att både evaluera peptiders egenskaper och fastställa deras komplexa mekanism. Detta till trots förblir de exakta detaljerna i mekanismen okända, vilket föranlett arbetet i detta projekt att undersöka lämpligheten i att använda TIR Raman, en vibrational-spektroskopisk metod som är tillräckligt ytkänslig för att studera interaktionen hos antimikrobiella peptider i kontakt med lipidmembran, vilka endast är några få nanometer tjocka. För att evaluera informationen som kan utvinnas med TIR Raman, utfördes först mätningar av lipidmembran, skapade på ett solitt underlag, utan tillägg av peptider. Mer noggrant, har lipiden DMPC med en fasövergång nära vid rumstemperatur, mätts vid olika temperaturer för att fastställa spektrala variationer associerade till övergången. För peptid-membran interaktionerna, sattes den antimikrobiella peptiden LL37 i kontakt med lipidmembran som modellerar cellmembranet hos bakterier (DOPE, DOPG) respektive människor (DOPC). Mätdatan indikerar tydligt att membrankompositionen, och där specifikt laddningen av lipidens huvudgrupp, spelar en viktig roll i membran-peptid interaktionerna. För lipidmembranen som imiterar bakteriella cellmembran, adsorberade peptiden till membranet eller integrerades in i det. Till skillnad från detta, kunde inga signifikanta variationer detekteras för lipidmembranet som modellerade ett mänskligt membran vilket indikerar att det inte interagerar med peptiden LL37. Upptäckterna som presenteras i detta arbete sammanfaller generellt med andra, liknande studier där andra instrument använts för att undersöka LL37. Det kan ur materialet som presenterats här utläsas att TIR Raman visat sig lämpligt och effektivt i detekteringen av antimikrobiella peptider i kontakt med modeller av lipidmembran, och kan därav rekommenderas för fortsatta studier.
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Herster, Franziska [Verfasser], and Alexander N. R. [Akademischer Betreuer] Weber. "PMNs, naRNA-LL37 complexes and platelets - a vicious inflammatory 'trio' in psoriasis / Franziska Herster ; Akademischer Betreuer: Alexander N. R. Weber." Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1213763045/34.

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Nicolaeva, Nicoletta [Verfasser]. "Die Rolle der Gliazellen in der funktionalen Expression des antimikrobiellen Peptids LL37, Cathelicidin-Related Antimicrobial Peptide (CRAMP) im zentralen Nervensystem der Ratte / Nicoletta Nicolaeva." Kiel : Universitätsbibliothek Kiel, 2013. http://d-nb.info/1031667059/34.

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Wu, Yang. "Accélération de la simulation logique : architecture et algorithmes de LL3T." Phd thesis, Grenoble INPG, 1990. http://tel.archives-ouvertes.fr/tel-00338790.

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Cette thèse présente la conception d'un accélérateur matériel dédié à la simulation de circuits intégrés. Sur cet accélérateur sont développés un ensemble de logiciels constituant un environnement intégré de simulation. Nous y discutons tout d'abord des concepts de base de la modélisation des circuits intégrés, de la simulation logico-fonctionnelle, de la simulation de pannes, des langages de description du matériel, ainsi que des techniques d'accélération de la simulation de circuits intégrés. Nous présentons ensuite la structure générale de l'accélérateur. Il est basé sur une architecture parallèle : un réseau en anneau sur lequel sont disposées des unités de simulation, où chaque unité de simulation est composée de trois microprocesseurs exécutant trois tâches respectivement. l'ensemble des logiciels implémentés sur cet accélérateur est présenté. Le simulateur réalise ainsi la simulation multi-niveaux (porte logique, fonctionnel et interrupteur) et la simulation de pannes. Des outils de compilation permettent l'utilisation des langages de description du matériel pour modéliser les circuits intégrés de manière structurelle et fonctionnelle. Enfin, différentes stratégies de parallélisation de la simulation ainsi que plusieurs algorithmes de simulation adaptés aux différents niveaux d'abstraction sont étudiés
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Wu, Yang Mazaré Guy Verjus Jean-Pierre Borrione Dominique. "Accélération de la simulation logique architecture et algorithmes de LL3T /." S.l. : Université Grenoble 1, 2008. http://tel.archives-ouvertes.fr/tel-00338790.

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Huang, Feng-Ju, and 黃鳳茹. "Effects of cathelicidin (LL37) on human dental pulp cells." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/50254443235330120502.

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碩士
國立陽明大學
口腔生物研究所
101
Dental caries is one of the most common infectious diseases which may cause demineralization and destruction of the hard tissues and pulp inflammation. With the discovery of regenerative potential of the dental pulp, there is a shift on the treatment of pulpal inflammation to a more conservative approach. The antimicrobial peptide LL37 (cathelicidin), which is part of the innate immune system, has been suggested for the regenerative procedures due to the ability to defense against pathogens and regulate wound healing. However, little was known about the expression of LL37 in dental pulp tissue. In this study, the expressions and functions of LL37 in human dental pulp were studied. The results showed that the expression levels of LL37 were up-regulated in carious dental pulps comparing to the healthy controls. In addition, LL37 enhanced cell proliferation and the expression of collagen in human dental pulp cells. On the other hand, the Escherichia coli (E. coli) lipopolysaccharide (LPS) - induced expressions of IL-1β (interleukin-1β), IL-6 (interleukin-6), IL-8 (interleukin-8), TNF-α (tumor necrosis factor-α) and MCP-1 (monocyte chemoattractant protein-1) were suppressed by the treatment of LL-37. LL37 was shown to neutralize LPS and therefore inhibited LPS-induced NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) translocation. The results of the present study showed the future potential of LL37, which could be used in vital pulp therapy to facilitate pulp healing.
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Comune, Michela. "Wound healing and pro-angiogenic properties of LL37-conjugated nanoparticles." Doctoral thesis, 2016. http://hdl.handle.net/10316/30202.

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Abstract:
Tese de doutoramento em Biociências na especialidade de Biotecnologia, apresentada ao Departamento de Ciências da Vida da Faculdade de Ciências e Tecnologia da Universidade de Coimbra
Problemas de cicatrização de feridas e suas complicações médicas continuam a ser um dos problemas de saúde mais prevalentes e economicamente onerosos do mundo. Nos Estados Unidos, as feridas crónicas afectam 6.5 milhões de pacientes. Mais de 25 bilhões de dólares são gastos anualmente em tratamento de feridas crónicas e a despesa irá crescer rapidamente devido ao aumento dos custos de saúde, o envelhecimento da população e um aumento acentuado na incidência de diabetes e obesidade em todo o mundo. Dados recentes indicam que 11.7% da população Portuguesa é diabética. Uma das complicações mais graves e debilitantes da diabetes é o desenvolvimento de feridas crónicas e não cicatrizantes. Nos últimos anos, tem havido esforços para se desenvolver terapias avançadas para a cicatrização de feridas crónicas, incluindo o uso tópico de factores de crescimentos ou terapias celulares. Infelizmente, em muitos casos, a eficácia terapêutica é baixa, as terapias são caras, requerem aplicação clínica e não possuem actividade antimicrobiana. Portanto, é imperativo o desenvolvimento de novas terapêuticas para responder a esta necessidade clínica. Os péptidos antimicrobianos (AMPs) sintetizados na pele podem constituir futuras terapias já que são moléculas que formam uma barreira à infecção e alguns deles são muito importantes para a regeneração da pele (4). O péptido LL37 é o AMP mais importante na pele, actuando como primeira linha de defesa contra bactérias, vírus, fungos e desempenha um papel importante na imunomodulação, angiogénese e cicatrização de feridas. Recentemente, foram publicados os resultados de um ensaio clínico fase I / II com o péptido LL37 que demonstram a sua eficácia terapêutica em feridas crónicas; no entanto, foram necessárias múltiplas administrações tópicas. O objectivo principal desta tese foi desenvolver uma formulação de nanopartículas conjugadas com LL37 de forma a possuir maior actividade de cicatrização da pele que o péptido livre (não imobilizado). A formulação de nanopartículas foi preparada por uma nova metodologia na qual foi utilizado o péptido LL37 com um terminal tiol, actuando o péptido como agente de revestimento durante a formação da nanopartícula. Esta formulação tem um núcleo de ouro (Au) e um escudo formado pelo péptido catiónico LL37. Durante esta tese seleccionámos nanopartículas de ouro porque é relativamente fácil a imobilização de altas concentrações de LL37 por unidade de superfície, a modificação das suas propriedades (incluindo tamanho, carga e morfologia), e pelo facto destas nanopartículas terem sido utilizadas na prática clínica há muitos anos. Estas nanopartículas possuem um tamanho controlado (21 nm), baixa polidispersão, um potencial zeta positivo (15 mV), alta densidade de LL37 (250 μg de péptido por mg de nanopartícula) e alta estabilidade em soluções aquosas e meios de cultura celular. As nanopartículas mostraram actividade antimicrobiana contra E. coli e elevada actividade biológica contra células de mamíferos, ou seja, actividade pró-angiogénica em células endoteliais e actividade pró-migratória em queratinócitos. Surpreendentemente, as nanopartículas conjugadas com LL37 possuem menor citotoxicidade que o péptido LL37 livre. Os nossos resultados mostram ainda que as nanopartículas são internalizadas pelos queratinócitos e células endoteliais, e no caso de queratinócitos, o processo de internalização é mediado principalmente pelo receptor scavenger. As nanopartículas internalizadas tendem a se acumular no compartimento endolisomal dos queratinócitos, mas conseguem escapar o compartimento endolisomal em células endoteliais. Em ambos os modelos celulares, as nanopartículas induzem a transactivação do EGFR. No caso dos queratinócitos, o processo é iniciado pela activação de receptores P2X que levam a uma prolongada fosforilação de EGFR e de ERK. Isto leva a que os queratinócitos possuam maiores propriedades migratórias. Os resultados in vivo mostram que nanopartículas conjugadas com LL37 têm melhores propriedades cicatrizantes de feridas comparativamente ao péptido livre. No caso de células endoteliais, o péptido LL37, mas não as nanopartículas conjugadas com LL37, levam à activação do receptor FPRL-1, à acumulação de cálcio intracelular e à secreção de VEGF165. No entanto, tanto o péptido LL37 como as nanopartículas conjugadas com LL37 têm elevada actividade pró-angiogénica, demonstrado num ensaio de membrana corioalantóica (CAM). É provável que a actividade pró-angiogénica das nanopartículas conjugadas com LL37 seja mediada pela transactivação de EGFR, mas mais estudos são necessários para responder a esta questão. Os resultados apresentados nesta tese são um primeiro passo para o desenvolvimento de terapias baseadas em nanomedicina à base de péptidos antimicrobianos. Esta é a primeira terapia que combina propriedades de cicatrização de feridas e actividade antimicrobiana na mesma formulação, é mais barata do que as terapias avançadas actuais, e pode ser administrada uma única vez. Impaired wound healing and its medical complications remain one of the most prevalent and economically burdensome healthcare issues in the world. In the United States alone, chronic wounds affect 6.5 million patients. More than US$25 billion is spent annually on treatment of chronic wounds and the burden is growing rapidly due to increasing health care costs, an aging population and a sharp rise in the incidence of diabetes and obesity worldwide. Recent data indicate that 11.7% of the Portuguese population is diabetic. One of the most serious and debilitating complications of diabetes is the development of chronic non-healing wounds. In recent years, there have been efforts to develop new advanced methodologies to heal chronic wounds including the use of topic growth factors or cell-based thera- pies. Unfortunately, in many cases, the therapeutic efficacy is low, the therapies are expensive and require application in a clinical facility, and they have no antimicro- bial activity. Therefore, development of new therapeutics is absolutely necessary and important to satisfy the unmet clinical need. Antimicrobial peptides (AMPs) synthesized in the skin provide a barrier to infection and some of them are very im- portant for the regeneration of skin. LL37 is the most important AMP in skin, acts as first line of defense against bacteria, virus, fungi and plays an important role in im- munomodulation, angiogenesis and wound healing properties. Recently, phase I/II clinical trials have demonstrated its therapeutic efficacy in chronic wounds; how- ever, multiple topical administrations were required. The main goal of this the- sis was to develop a LL37 nanoparticulate formulation with higher wound healing properties than the free peptide. The nanoparticulate formulation was prepared by a novel methodology in which thiol-terminated LL37 acts as capping agent during NP formation. This formulation has a gold (Au) core and a hydrophilic cationic LL37 peptide shell. We have selected Au NPs because it is relatively easy the immo- bilization of high concentrations of LL37 per surface area, the modification of their properties (including size, charge and morphology), and they have been used in the clinic for many years. LL37-Au NPs have controlled size (21 nm), low polydisper- sity, positive zeta potential (15 mV), high density of LL37 (250 μ g of peptide per mg of NP) and high stability in aqueous solutions and cell culture media. They showed antimicrobial activity against E . coli and high biological activity against mammalian cells, namely pro-angiogenic activity against endothelial cells and pro-migratory activity against keratinocytes. Remarkably, LL37-Au NPs have lower cytotoxicity than LL37 peptide. Our results further show that LL37-Au NPs are internalized by keratinocytes and endothelial cells, and in case of keratinocytes, the internalization process is mostly mediated by scavenger receptors. The internalized LL37-Au NPs tend to accumulate in the endolysomal compartment in keratinocytes while escape the endolysomal compartment in endothelial cells. In both cell models, LL37-Au NPs induce the transactivation of EGFR. In case of keratinocytes, the process is ini- tiated by the activation of P2X receptors that leads to a long-lasting phosphorylation of EGFR and ERK. This results in enhanced migratory properties of keratinocytes. In vivo results show that LL37-Au NPs have superior wound healing properties than LL37 peptide in a splinted mouse full thickness excisional model. In case of endothelial cells, LL37 peptide but not LL37-Au NPs activate FPRL-1, intracellular accumulation of Ca 2 + and secretion of VEGF165. Yet, both LL37 and LL37-Au NPs have high pro-angiogenic activity as demonstrated in a chorioallantoic membrane (CAM) assay. It is likely that the pro-angiogenic activity of LL37-Au NPs is medi- ated by the transactivation of EGFR but further studies are needed to address this issue. The results presented here are an exciting first step toward the development of antimicrobial peptide-based nanotherapeutics for skin disorders paving the way for additional studies in more complex animal models. It is the first skin therapy that combines wound-healing efficacy and antimicrobial activity in the same for- mulation, it is cheaper than the actual advanced therapies, and may be administered only one time.
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Books on the topic "LL37"

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Selleck, Dorothy. Ysgol y Friog, Y Friog, Gwynedd, LL38 2RQ: Arolygiad dan adran 9 o Ddeddf Addysg (Ysgolion) 1992 : rhif ysgol: 573/2216 : dyddiad yr arolygiad: Chwefror 27-29, 1996 = Ysgol y Friog, Y Friog, Gwynedd, LL38 2RQ : inspection under section 9 of the Education (Schools) Act 1992 : date of inspection: 27-29 February, 1996. Cardiff: Welsh Office, 1996.

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Morris, Dorothy. Ysgol Abercaseg, Bethesda, Gwynedd LL57 3PL: Inspection under section 10 of the Schools Inspections Act 1996 : school number: 661/2126 : date of inspection: 4-5 April, 2000 = Ysgol Abercaseg, Bethesda, Gwynedd LL57 3PL : arolygiad dan adran 10 o Ddeddf Arolygiadau Ysgolion 1996 : rhif yr ysgol: 661/2126 : dyddiad yr arolygiad: 4-5 Ebrill, 2000. Cardiff: Estyn, 2000.

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Cray, D. M. Ysgol Corn Hir, Llangefni, Ynys Môn, LL77 7JB: Arolygiad o dan Adran 10 Deddf Arolygiadau Ysgolion 1996 : rhif yr ysgol: 660/2226 : dyddiad yr arolygiad: 18-21 Mehefin 2001 = Ysgol Corn Hir, Llangefni, Ynys Môn LL77 7JB : inspection under Section 10 of the Schools Inspections Act 1996 : school number: 660/2226 : date of inspection: 18-21 June 2001. Cardiff: Estyn, 2001.

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Thomas, Meurig. Ysgol Gymuned Bodffordd, Bodffordd, Anglesey LL77 7LZ: Inspection under section 10 of the School Inspections Act 1996 : school number: 660/2133 : date of inspection: 3-4 March 2003 = Ysgol Gymuned Bodffordd, Bodffordd, Ynys Môn LL77 7LZ : arolygiad dan adran 10 o'r Ddeddf Arolygu Ysgolion 1996 : rhif ysgol: 660/2133 : dyddiad yr arolwg: 3-5 Mawrth 2003. Cardiff: Estyn, 2003.

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Marshall, Jean. Ysgol Maelgwn, Broad Street, Llandudno Junction, Conwy LL31 9HG: Inspection under section 10 of the Schools Inspections Act 1996 : school number: 662/2064 : date of inspection: 10-13 December 2001 = Ysgol Maelgwn, Broad Street, Cyffordd Llandudno Conwy LL31 9HG : arolygiad dan adran 10 Deddf Arolygu Ysgolion 1996 : rhif yr ysgol: 662/2064 : dyddiad arolygiad: 10-13 Rhagfyr 2001. Cardiff: Estyn, 2002.

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Thomas, M. Ysgol Gynradd Corn Hir, Llangefni, Ynys Môn, Gwynedd, LL77 7JB: Archwiliad dan adran 9 Deddf Addysg (Ysgolion) 1992 : rhif ysgol: 573/2226 : dyddiad yr archwiliad: 23-25 Ionawr 1996 = Ysgol Gynradd Corn Hir, Llangefni, Ynys Môn, Gwynedd, LL77 7JB : inspectionunder section 9 of the Education (Schools) Act 1992 : school number: 573/2226 : date of inspection: 23-25 January 1996. Cardiff: Welsh Office, 1996.

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Jones, Gareth Davies. Ysgol Pen-y-Bryn, Bethesda, Gwynedd LL57 3BE: Inspection under section 10 of the Schools Inspections Act 1996 : school number: 661/2028 : date of inspection: 7-9 February, 2000 = Ysgol Pen-y-Bryn, Bethesda, Gwynedd LL57 3BE : arolygiad dan adran 10 o Ddeddf Arolygiadau Ysgolion 1996 : rhif yr ysgol: 661/2028 : dyddiad yr arolygiad: 7-9 Chwefror, 2000. Cardiff: Estyn, 2000.

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Selleck, Dorothy. Ysgol Gynradd Llanegryn, Llanegryn, Tywyn, Gwynedd, LL36 9SS: Arolygiad dan adran 9 o Ddeddf Addysg (Ysgolion) 1992 : rhif ysgol: 573/2196 : dyddiad yr arolygiad: Hydref 30 - Tachwedd 2, 1995 = Ysgol Gynradd Llanegryn, Llanegryn, Tywyn, Gwynedd, LL36 9SS : inspection under section 9 of the Education (Schools) Act 1992 : school number: 573/2196 : date of inspection: 30 October - 2 November, 1995. Cardiff: Welsh Office, 1996.

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Roberts, Huw Alun. Ysgol Tryfan, Lôn Powys, Bangor, Gwynedd, LL57 2TU: Arolygiad dan adran 9 o Ddeddf Addysg (Ysgolion) 1992 : rhif ysgol: 573/4037 : dyddiad yr arolygiad: Chwefror 26 - Mawrth 1, 1996 = Ysgol Tryfan, Lôn Powys, Bangor, Gwynedd, LL57 2TU : inspection under section 9 of the Education (Schools) Act 1992 : school number: 573/4037 : date of inspection: 26 February - 1 March, 1996. Cardiff: Welsh Office, 1996.

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Mostert, Phil. Ysgol Dolgarrog, Conwy, Gwynedd, LL32 8QE: Inspection under section 9 of the Education (Schools) Act 1992 : school number: 573/2002 : date of inspection: 4-6 December 1995. Cardiff: Welsh Office, 1996.

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Book chapters on the topic "LL37"

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Felgueiras, Helena P., Marta A. Teixeira, and M. Teresa P. Amorim. "Potentialities of LL37 for Wound Healing Applications: Study of Its Activity in Synergy with Biodegradable Composites Made of PVA and CA." In IFMBE Proceedings, 1223–26. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-31635-8_148.

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"ll6-ll7." In Cationic Surfactants, 76–112. CRC Press, 1990. http://dx.doi.org/10.1201/9781482293302-5.

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"ll3 The Ambiguity of Modern Disability Welfare: Success Story or Political Fiasco?" In Welfare in an Idle Society?, 408–27. Routledge, 2017. http://dx.doi.org/10.4324/9781315234229-22.

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Conference papers on the topic "LL37"

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Frasca, L., R. Palazzo, M. S. Chimenti, E. Botti, S. E. Auteri, F. Spadaro, S. Alivernini, et al. "SAT0039 Ll37 up-regulation and anti-ll37 reactivity are shared by psoriasis and psoriatic arthritis patients." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5725.

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Valencia, Yeny Y. P., Gabriel C. A. da Hora, and Thereza A. Soares. "SIMULAÇÃO COMPUTACIONAL DE AGREGADOS DE POPG NA PRESENÇA DO PEPTÍDEO ANTIMICROBIANO LL37." In Encontro Anual da Biofísica 2018. São Paulo: Editora Blucher, 2018. http://dx.doi.org/10.5151/biofisica2018-06.

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Vey, Nelly, Elena Blanc, Vanja Sisirak, Sandra Thys, Céline Le Beux, Nadège Goutagny, Isabelle Treilleux, et al. "Abstract 1109: The antimicrobial peptide LL37 activates plasmacytoid dendritic cells in breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1109.

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Felgueiras, Helena P., Marta A. Teixeira, Tânia D. Tavares, Natália C. Homem, Marta S. Teixeira, Andrea Zille, Joana C. Antunes, and M. Teresa P. Amorim. "Flexible, biodegradable LL37-anchored poly(vinyl alcohol)/cellulose acetate films for enhanced infection control." In 2nd Coatings and Interfaces Web Conference. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ciwc2020-06807.

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Pouwels, Simon, Nick Ten Hacken, Jaap Lubbers, Antoon Van Oosterhout, Martijn Nawijn, and Irene Heijink. "The human cathelicidin LL37 and mitochondrial DAMPs induce airway inflammation in epithelial cells and mice." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa5115.

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Lo, Jiang-Wei, Chin-An Lin, and Jr-Hau He. "Enhanced 1540 nm emission from Er-doped ZnO nanorod arrays via coupling with localized surface plasmon of Au island film." In 2008 MRS Fall Meetin. Materials Research Society, 2008. http://dx.doi.org/10.1557/proc-1144-ll07-09.

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Kway, Wayne L., H. W. Newkirk, and L. L. Chase. "Growth and Characterization of LiCaAIF6:Cr3+ for Solid State Laser Applications." In Advanced Solid State Lasers. Washington, D.C.: OSA, 1989. http://dx.doi.org/10.1364/assl.1989.ll3.

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Balembois, François, Patrick Georges, François Salin, Gérard Roger, Alain Brun, and Jean Luc Tapié. "High Repetition Rate CW Pumped Cr:LiSAF Femtosecond Regenerative Amplifier." In Advanced Solid State Lasers. Washington, D.C.: OSA, 1993. http://dx.doi.org/10.1364/assl.1993.ll3.

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Balembois, François, Patrick Georges, François Salin, Gérard Roger, and Alain Brun. "Tunable Blue Light Source by Intracavity Frequency Doubling of a Cr-Doped LiSAF Laser." In Advanced Solid State Lasers. Washington, D.C.: OSA, 1993. http://dx.doi.org/10.1364/assl.1993.ll7.

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Reports on the topic "LL37"

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Roberts, R. S., J. Goforth, A. Perkins, and E. Twarog. LL17-GEOVIS-PD3SS_Final_Report. Office of Scientific and Technical Information (OSTI), October 2019. http://dx.doi.org/10.2172/1573159.

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Roberts, R. S. FY19Q3 LL17-GEOVIS-PD3SS. Office of Scientific and Technical Information (OSTI), July 2019. http://dx.doi.org/10.2172/1573153.

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Bernstein, A. LL17-extended range Antineutrino-PD3RB - Q3 FY19. Office of Scientific and Technical Information (OSTI), January 2020. http://dx.doi.org/10.2172/1597581.

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Bernstein, A. LL17-extended range Antineutrino-PD3RB - Q4 FY19. Office of Scientific and Technical Information (OSTI), January 2020. http://dx.doi.org/10.2172/1597621.

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