Relevant bibliographies by topics / L-selectin

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  2. Dissertations / Theses
  3. Books
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Academic literature on the topic 'L-selectin'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "L-selectin"

1

Peng, Shuang, Shen-Bao Chen, Lin-Da Li, Chun-Fang Tong, Ning Li, Shou-Qin Lü, and Mian Long. "Impact of real-time shedding on binding kinetics of membrane-remaining L-selectin to PSGL-1." American Journal of Physiology-Cell Physiology 316, no. 5 (May 1, 2019): C678—C689. http://dx.doi.org/10.1152/ajpcell.00212.2018.

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L-selectin shedding induced by various cytokines is crucial in activating neutrophils (PMNs) in inflammatory cascade. While the real-time shedding in vivo lasts ~10 min after PMN activation, the impact of time-dependent shedding on binding kinetics of membrane-remaining L-selectins to its ligands is poorly understood at transient or steady state. Here, we developed an in vitro L-selectin shedding dynamics approach, together with competitive assays of cell adhesion, and proposed a theoretical model for quantifying the impact of real-time shedding on the binding kinetics of membrane-remaining L-selectins to P-selectin glycoprotein ligand-1 (PSGL-1). Our data indicated that the extent of L-selectin shedding on PMA activation is higher, but the terminating time is longer for Jurkat cells than those for human PMNs. Meanwhile, fMLF or IL-8 stimulation yields the longer terminating time than that on PMA stimulation but results in a similar shedding extent for PMNs. L-selectin shedding reduces L-selectin-PSGL-1-mediated cell adhesion in three ways: decreasing membrane-anchored L-selectins, increasing soluble L-selectins competitively binding to ligands, and presenting conformational alteration of membrane-remaining L-selectins themselves. Compared with those on intact cells, the binding affinities of membrane-remaining L-selectin-PSGL-1 pairs were all enhanced at initial and lowered at the late shedding phase for both PMN and Jurkat cells even with varied transition time points. The rolling velocities of both PMNs and Jurkat cells were increased following mechanically or biochemically induced shedding of L-selectin under shear flow. These findings help to further our understanding of the function of time-dependent L-selectin shedding during the inflammation cascade.
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Mattila, Polly E., Chad E. Green, Ulrich Schaff, Scott I. Simon, and Bruce Walcheck. "Cytoskeletal interactions regulate inducible L-selectin clustering." American Journal of Physiology-Cell Physiology 289, no. 2 (August 2005): C323—C332. http://dx.doi.org/10.1152/ajpcell.00603.2004.

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L-selectin (CD62L) amplifies neutrophil capture within the microvasculature at sites of inflammation. Activation by G protein-coupled stimuli or through ligation of L-selectin promotes clustering of L-selectin and serves to increase its adhesiveness, signaling, and colocalization with β2-integrins. Currently, little is known about the molecular process regulating the lateral mobility of L-selectin. On neutrophil stimulation, a progressive change takes place in the organization of its plasma membrane, resulting in membrane domains that are characteristically enriched in glycosyl phosphatidylinositol (GPI)-anchored proteins and exclude the transmembrane protein CD45. Clustering of L-selectin, facilitated by E-selectin engagement or antibody cross-linking, resulted in its colocalization with GPI-anchored CD55, but not with CD45 or CD11c. Disrupting microfilaments in neutrophils or removing a conserved cationic motif in the cytoplasmic domain of L-selectin increased its mobility and membrane domain localization in the plasma membrane. In addition, the conserved element was critical for L-selectin-dependent tethering under shear flow. Our data indicate that L-selectin’s lateral mobility is regulated by interactions with the actin cytoskeleton that in turn fortifies leukocyte tethering. We hypothesize that both membrane mobility and stabilization augment L-selectin’s effector functions and are regulated by dynamic associations with membrane domains and the actin cytoskeleton.
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Miles, Mary P., Sharyn K. Leach, William J. Kraemer, Keiichiro Dohi, Jill A. Bush, and Andrea M. Mastro. "Leukocyte adhesion molecule expression during intense resistance exercise." Journal of Applied Physiology 84, no. 5 (May 1, 1998): 1604–9. http://dx.doi.org/10.1152/jappl.1998.84.5.1604.

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We hypothesized that expression of L-selectin and very late antigen-4 (VLA-4) integrin adhesion molecules would influence cell type-specific redistribution during exercise. Women subjects performed six sets of 10-repetition maximum squats. L-selectin and VLA-4 integrin were measured by using flow cytometry pre- and postexercise on peripheral blood neutrophils and lymphocytes ( n = 29 subjects) and lymphocyte subsets ( n = 70 subjects), respectively. Neutrophil concentration increased 41.8% ( P < 0.001), whereas the percent expressing L-selectin was unchanged (79%). Lymphocyte concentration increased 61.8% ( P < 0.001). The percent of T cells expressing L-selectin decreased from 73.5 ± 8.9 to 68.2 ± 11.4% ( P < 0.001); the combined population of natural killer and B cells expressing L-selectin decreased from 80.4 ± 22.5 to 62.7 ± 25.8% ( P < 0.001). VLA-4 integrin was expressed by nearly all lymphocytes both pre- and postexercise. The proportional decrease in L-selectin positive cells could have resulted from 1) shedding of L-selectin, 2) selective entry of L-selectin-negative subsets, or 3) selective removal of L-selectin-positive subsets.
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Alon, R., R. C. Fuhlbrigge, E. B. Finger, and T. A. Springer. "Interactions through L-selectin between leukocytes and adherent leukocytes nucleate rolling adhesions on selectins and VCAM-1 in shear flow." Journal of Cell Biology 135, no. 3 (November 1, 1996): 849–65. http://dx.doi.org/10.1083/jcb.135.3.849.

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We demonstrate an additional step and a positive feedback loop in leukocyte accumulation on inflamed endothelium. Leukocytes in shear flow bind to adherent leukocytes through L-selectin/ligand interactions and subsequently bind downstream and roll on inflamed endothelium, purified E-selectin, P-selectin, L-selectin, VCAM-1, or peripheral node addressin. Thus adherent leukocytes nucleate formation of strings of rolling cells and synergistically enhance leukocyte accumulation. Neutrophils, monocytes, and activated T cell lines, but not peripheral blood T lymphocytes, tether to each other through L-selectin. L-selectin is not involved in direct binding to either E- or P-selectin and is not a major counterreceptor of endothelial selectins. Leukocyte-leukocyte tethers are more tolerant to high shear than direct tethers to endothelial selectins and, like other L-selectin-mediated interactions, require a shear threshold. Synergism between leukocyte-leukocyte and leukocyte-endothelial interactions introduces novel regulatory mechanisms in recruitment of leukocytes in inflammation.
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Nelson, RM, O. Cecconi, WG Roberts, A. Aruffo, RJ Linhardt, and MP Bevilacqua. "Heparin oligosaccharides bind L- and P-selectin and inhibit acute inflammation." Blood 82, no. 11 (December 1, 1993): 3253–58. http://dx.doi.org/10.1182/blood.v82.11.3253.3253.

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Abstract Initial attachment of leukocytes to the vessel wall at sites of inflammation is supported by a family of carbohydrate-binding adhesion molecules called the selectins. Selectin ligands include sialyl-Lewis x (sLex, Neu5Ac alpha 2–3Gal beta 1–4[Fuc alpha 1–3]GlcNAc--) and related structures. We report here that defined heparin oligosaccharides interact with the selectins. Heparin chains containing four or more monosaccharide residues inhibited the function of L- and P-selectin, but not E-selectin, in vitro. In a competition enzyme-linked immunosorbent assay measuring inhibition of solution-phase selectin-Ig fusion proteins (selectin-Ig) binding to immobilized bovine serum albumin-sLex neoglycoprotein, a heparin-derived tetrasaccharide mixture inhibited 50% of L- and P-selectin-Ig binding (IC50) at 200 +/- 40 mumol/L and 850 +/- 110 mumol/L, respectively. A single hexasulfated tetrasaccharide (delta UA2S alpha 1–4GlcNS6S alpha 1–4IdoA2S alpha 1- 4GlcNS6S) was particularly active against L- and P-selectin-Ig (IC50 = 46 +/- 5 mumol/L and 341 +/- 24 mumol/L). By comparison, the tetrasaccharide sLex was not inhibitory at concentrations up to 1 mmol/L. In cell adhesion assays, heparin tetrasaccharides reduced binding of neutrophils to COS cells expressing P-selectin but not to COS cells expressing E-selectin. They also blocked colon cancer cell adhesion to L- and P-selectin but not E-selectin. In a model of acute inflammation, intravenously administered heparin tetrasaccharides diminished influx of neutrophils into the peritoneal cavities of thioglycollate-treated mice. We conclude that heparin oligosaccharides, including non-anticoagulant tetrasaccharides, are effective L- and P- selectin inhibitors in vitro and have anti-inflammatory activity in vivo.
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Nelson, RM, O. Cecconi, WG Roberts, A. Aruffo, RJ Linhardt, and MP Bevilacqua. "Heparin oligosaccharides bind L- and P-selectin and inhibit acute inflammation." Blood 82, no. 11 (December 1, 1993): 3253–58. http://dx.doi.org/10.1182/blood.v82.11.3253.bloodjournal82113253.

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Initial attachment of leukocytes to the vessel wall at sites of inflammation is supported by a family of carbohydrate-binding adhesion molecules called the selectins. Selectin ligands include sialyl-Lewis x (sLex, Neu5Ac alpha 2–3Gal beta 1–4[Fuc alpha 1–3]GlcNAc--) and related structures. We report here that defined heparin oligosaccharides interact with the selectins. Heparin chains containing four or more monosaccharide residues inhibited the function of L- and P-selectin, but not E-selectin, in vitro. In a competition enzyme-linked immunosorbent assay measuring inhibition of solution-phase selectin-Ig fusion proteins (selectin-Ig) binding to immobilized bovine serum albumin-sLex neoglycoprotein, a heparin-derived tetrasaccharide mixture inhibited 50% of L- and P-selectin-Ig binding (IC50) at 200 +/- 40 mumol/L and 850 +/- 110 mumol/L, respectively. A single hexasulfated tetrasaccharide (delta UA2S alpha 1–4GlcNS6S alpha 1–4IdoA2S alpha 1- 4GlcNS6S) was particularly active against L- and P-selectin-Ig (IC50 = 46 +/- 5 mumol/L and 341 +/- 24 mumol/L). By comparison, the tetrasaccharide sLex was not inhibitory at concentrations up to 1 mmol/L. In cell adhesion assays, heparin tetrasaccharides reduced binding of neutrophils to COS cells expressing P-selectin but not to COS cells expressing E-selectin. They also blocked colon cancer cell adhesion to L- and P-selectin but not E-selectin. In a model of acute inflammation, intravenously administered heparin tetrasaccharides diminished influx of neutrophils into the peritoneal cavities of thioglycollate-treated mice. We conclude that heparin oligosaccharides, including non-anticoagulant tetrasaccharides, are effective L- and P- selectin inhibitors in vitro and have anti-inflammatory activity in vivo.
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Matala, Erik, Shelia R. Alexander, Takashi K. Kishimoto, and Bruce Walcheck. "The Cytoplasmic Domain of L-Selectin Participates in Regulating L-Selectin Endoproteolysis." Journal of Immunology 167, no. 3 (August 1, 2001): 1617–23. http://dx.doi.org/10.4049/jimmunol.167.3.1617.

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Jutila, M. A., G. Watts, B. Walcheck, and G. S. Kansas. "Characterization of a functionally important and evolutionarily well-conserved epitope mapped to the short consensus repeats of E-selectin and L-selectin." Journal of Experimental Medicine 175, no. 6 (June 1, 1992): 1565–73. http://dx.doi.org/10.1084/jem.175.6.1565.

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Selectins represent a new family of adhesion molecules, expressed by leukocytes and endothelial cells, that are involved in the regulation of leukocyte traffic. Here we have characterized a new monoclonal antibody (mAb) (EL-246) that recognizes both human leukocyte L-selectin (previously called LAM-1, LECAM-1, or gp90MEL-14) and endothelial cell E-selectin (previously called ELAM-1). EL-246 recognized a 110-kD protein expressed on cells transfected with E-selectin cDNA and stained many postcapillary venules in inflamed human tonsil. EL-246 also stained human peripheral blood leukocytes and showed identity with anti-L-selectin mAb in two-color flow cytometric analysis. The expression of the leukocyte EL-246 antigen was regulated in the same manner as L-selectin and EL-246 recognized anti-L-selectin mAb affinity-purified antigen in SDS/PAGE Western blot analysis. Further, L-selectin cDNA transfectants were specifically stained by EL-246. EL-246 blocked greater than 95% of lymphocyte adhesion to peripheral lymph node high endothelial venules and greater than 90% of neutrophil adhesion to E-selectin transfectants. In addition to the EL-246 epitope being expressed on two different human selectins, it was detected on L-selectin from a variety of different animals. Interestingly, domain mapping studies localized the EL-246 epitope to the short consensus repeat (SCR) domains of L-selectin. EL-246 is the first mAb that recognizes two different selectins and potentially defines a functional epitope encoded by the SCR domains. Inhibitors of selectin function targeted to this region would be expected to have the added advantage of simultaneously blocking the activity of two distinct adhesion proteins involved in inflammation.
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Alon, Ronen, Shuqi Chen, Kamal D. Puri, Erik B. Finger, and Timothy A. Springer. "The Kinetics of L-selectin Tethers and the Mechanics of Selectin-mediated Rolling." Journal of Cell Biology 138, no. 5 (September 8, 1997): 1169–80. http://dx.doi.org/10.1083/jcb.138.5.1169.

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Two mechanisms have been proposed for regulating rolling velocities on selectins. These are (a) the intrinsic kinetics of bond dissociation, and (b) the reactive compliance, i.e., the susceptibility of the bond dissociation reaction to applied force. To determine which of these mechanisms explains the 7.5–11.5-fold faster rolling of leukocytes on L-selectin than on E- and P-selectins, we have compared the three selectins by examining the dissociation of transient tethers. We find that the intrinsic kinetics for tether bond dissociation are 7–10-fold more rapid for L-selectin than for E- and P-selectins, and are proportional to the rolling velocities through these selectins. The durations of pauses during rolling correspond to the duration of transient tethers on low density substrates. Moreover, applied force increases dissociation kinetics less for L-selectin than for E- and P-selectins, demonstrating that reactive compliance is not responsible for the faster rolling through L-selectin. Further measurements provide a biochemical and biophysical framework for understanding the molecular basis of rolling. Displacements of tethered cells during flow reversal, and measurements of the distance between successive pauses during rolling provide estimates of the length of a tether and the length of the adhesive contact zone, and suggest that rolling occurs with as few as two tethers per contact zone. Tether bond lifetime is an exponential function of the force on the bond, and the upper limit for the tether bond spring constant is of the same order of magnitude as the estimated elastic spring constant of the lectin–EGF unit. Shear uniquely enhances the rate of L-selectin transient tether formation, and conversion of tethers to rolling adhesions, providing further understanding of the shear threshold requirement for rolling through L-selectin.
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Dwir, Oren, Geoffrey S. Kansas, and Ronen Alon. "Cytoplasmic anchorage of L-selectin controls leukocyte capture and rolling by increasing the mechanical stability of the selectin tether." Journal of Cell Biology 155, no. 1 (October 1, 2001): 145–56. http://dx.doi.org/10.1083/jcb.200103042.

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L-selectin is a leukocyte lectin that mediates leukocyte capture and rolling in the vasculature. The cytoplasmic domain of L-selectin has been shown to regulate leukocyte rolling. In this study, the regulatory mechanisms by which this domain controls L-selectin adhesiveness were investigated. We report that an L-selectin mutant generated by truncation of the COOH-terminal 11 residues of L-selectin tail, which impairs association with the cytoskeletal protein α-actinin, could capture leukocytes to glycoprotein L-selectin ligands under physiological shear flow. However, the conversion of initial tethers into rolling was impaired by this partial tail truncation, and was completely abolished by a further four-residue truncation of the L-selectin tail. Physical anchorage of both cell-free tail-truncated mutants within a substrate fully rescued their adhesive deficiencies. Microkinetic analysis of full-length and truncated L-selectin–mediated rolling at millisecond temporal resolution suggests that the lifetime of unstressed L-selectin tethers is unaffected by cytoplasmic tail truncation. However, cytoskeletal anchorage of L-selectin stabilizes the selectin tether by reducing the sensitivity of its dissociation rate to increasing shear forces. Low force sensitivity (reactive compliance) of tether lifetime is crucial for selectins to mediate leukocyte rolling under physiological shear stresses. This is the first demonstration that reduced reactive compliance of L-selectin tethers is regulated by cytoskeletal anchorage, in addition to intrinsic mechanical properties of the selectin–carbohydrate bond.
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Dissertations / Theses on the topic "L-selectin"

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Dias, Ana Carla da Silva Carvalho. "Efeito protetor da fucoidina, um inibidor de P e L-selectina, na resposta inflamatÃria sistÃmica e distÃrbios de motilidade gastrintestinal na pancreatite aguda experimental." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=10774.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
IntroduÃÃo e objetivos: Os neutrÃfilos desempenham importante papel na pancreatite aguda grave. InfiltraÃÃo de neutrÃfilos no pÃncreas à um processo complexo, coordenado por molÃculas de adesÃo especÃficas, tais como a P-selectina. Fucoidina à um polissacarÃdeo sulfatado que bloqueia a funÃÃo da L-e P-selectinas. No presente estudo avaliamos se o tratamento com fucoidina poderia impedir a infiltraÃÃo de neutrÃfilos e, assim, reverter a inflamaÃÃo sistÃmica e dismotilidades gastrintestinais associadas à pancreatite aguda grave. MÃtodos: A pancreatite aguda foi induzida em camundongos Swiss pela infusÃo retrÃgrada de Ãcido taurolitocÃlico (3,0%) (TLC-S) no ducto pancreÃtico ou por injeÃÃes intraperitoneais de ceruleÃna (50 Âg/kg/h). Os grupos experimentais receberam fucoidina (25 mg/kg, iv) antes da induÃÃo da pancreatite, e os grupos de controle receberam apenas soluÃÃo salina. ApÃs 24 horas, os nÃveis sÃricos de amilase, lipase, IL-1β, TNF-α, nitrito e de malondialdeÃdo (MDA) pancreÃtico foram medidos. AlÃm disso, a atividade de mieloperoxidase (MPO) (pulmÃo, pÃncreas, estÃmago e jejuno) e avaliaÃÃo histolÃgica (pÃncreas) foram determinadas. O esvaziamento gÃstrico e trÃnsito gastrintestinal foram medidos pelo mÃtodo de centro geomÃtrico. A contratilidade gastrintestinal in vitro foi registrada atravÃs de transdutores de forÃa conectados a sistema computadorizado de aquisiÃÃo de dados. Carbacol (0,01 ÂM - 30 ÂM), KCl 60 mM e estimulaÃÃo elÃctrica (0,5-8,0 Hz; 1ms, 40 V), foram aplicados sobre o fundo gÃstrico e jejuno dos animais 24 horas apÃs a pancreatite induzida por TLC-S. Resultados: Os nÃveis de MDA pancreÃtico, amilase, lipase, nitrito, TNF-α e IL-1β sÃricos, bem como MPO pancreÃtica e pulmonar estavam aumentados tanto no modelo de pancreatite aguda induzida por TLCS quanto no modelo ceruleÃna quando comparado aos grupos controle correspondentes. Fucoidina reduziu significativamente os nÃveis aumentados de amilase, lipase, MPO pancreÃtica e pulmonar, MDA, TNF-α, IL-1β e nitrito em ambos os modelos de pancreatite aguda. As mudanÃas histolÃgicas observadas no pÃncreas em ambos os modelos foram significativamente atenuadas pela fucoidina. O modelo de pancreatite aguda induzida por TLC-S induziu retardo no esvaziamento gÃstrico e trÃnsito gastrointestinal, aumento de MPO no estÃmago e no jejuno, alÃm de hipercontratilidade de jejuno in vitro. Fucoidina reverteu significativamente os distÃrbios gastrintestinais in vivo e in vitro e os nÃveis aumentados de MPO gÃstrica e jejunal induzidos pela injeÃÃo de TLC-S. ConclusÃo: Fucoidina reduziu a gravidade da pancreatite aguda experimental atravÃs da diminuiÃÃo da infiltraÃÃo de neutrÃfilos, inflamaÃÃo sistÃmica e dismotilidades gastrintestinais, sugerindo que a modulaÃÃo das selectinas, pode constituir uma abordagem terapÃutica promissora para pancreatite aguda.
Background & Aims: Neutrophils play a critical role in severe acute pancreatitis. Tissue infiltration of neutrophils in the pancreas is a multistep process, coordinated by specific adhesion molecules, such as P-selectin. Fucoidin is a sulphated fucosylated polysaccharide that binds to and blocks the function of L- and P-selectins, and the present study has evaluated whether fucoidin treatment could prevent neutrophil infiltration, and thereby reverse the systemic inflammation and gastrointestinal dysmotility associated with severe acute pancreatitis. Methods: Acute pancreatitis was induced in Swiss mice either by the retrograde infusion of taurolithocholic acid (3.0%) (TLC-S) into the pancreatic duct or by intraperitoneal injections of cerulein (50 Âg/kg/h). The experimental groups received fucoidan (25 mg/kg, i.v.) before pancreatitis induction whist control groups received only saline. After 24 hours, pancreatic malondialdehyde (MDA), serum amylase, lipase, IL-1β, TNF- and nitrite were measured. In addition, myeloperoxidase (MPO) activity (lung, pancreas, stomach and jejunum) and histological assessment (pancreas) were determined. Gastric emptying and gastrointestinal transit (using the geometric center method) were also measured. Gastrointestinal contractility in vitro was recorded through force transducers coupled to a computerized data acquisition system, carbachol (0,01 ÂM â 30 ÂM), KCl 60mM and electrical field stimulation (0.5-8.0 Hz; 1ms; 40 V), was applied on gastric fundus and jejunum of mice 24 hours after TLC-S induced pancreatitis. Results: Pancreatic MDA, serum amylase, lipase, nitrite, TNF- and IL-1β, pancreatic and lung MPO, were increased in both TLCS- and cerulein acute pancreatitis compared with respective control groups. Fucoidan significantly decreased the augmented levels of amylase, lipase, pancreatic and lung MPO, MDA, TNF-, IL-1β and nitrite in both acute pancreatitis models. Pancreas histological changes observed in both models were significantly attenuated by fucoidan. The acute pancreatitis model induced by TLC-S caused delayed gastric emptying and gastrointestinal transit, incresead gastric and jejunum MPO, and jejunum hypercontractility in vitro. Fucoidan significantly reversed the gastrointestinal disorders in vivo and in vitro and augmented levels of gastric and jejunum MPO induced by TLC-S. Conclusion: Fucoidan reduced the severity of acute pancreatitis in mice by decreasing neutrophil infiltration, systemic inflammation and gastrointestinal dysmotility, suggesting that modulation of selectins may constitute a promising therapeutic approach for acute pancreatitis.
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Fraser, Stuart Tallis. "Lectin - carbohydrate interactions in lympho-haemopoiesis: a study of L-selectin, ligands of L-selectin and CD24 inthe rat." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31236844.

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Fraser, Stuart Tallis. "Lectin - carbohydrate interactions in lympho-haemopoiesis : a study of L-selectin, ligands of L-selectin and CD24 in the rat /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20667450.

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Newman, Andrew. "The regulation of L-selectin activity by proteolysis." Thesis, Cardiff University, 2017. http://orca.cf.ac.uk/103855/.

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L-selectin (CD62L) is a type I transmembrane protein expressed by lymphocytes which directs their migration from the bloodstream into lymph nodes and infected tissues. Stimulation of the T cell receptor (TCR) activates the enzyme A Disintegrin and Metalloproteinase 17 (ADAM 17), which cleaves L-selectin at the ectodomain generating a metalloproteinase product (MP product) comprising of a transmembrane region and a 17-amino acid intracellular domain (ICD). ϒ-secretase is a multi-subunit protease that cleaves up to 90 identified type I transmembrane proteins in the intramembrane region following ectodomain proteolysis by metalloproteinases. Presenilin (PS), the catalytic component of γ-secretase is activated during an intramolecular cleavage called endoproteolysis separating the carboxy (C) and amino (N) termini. The catalytically active C-terminal fragment of PS then induces intramembrane proteolysis of substrates. The aim of my thesis was to firstly determine whether the MP product of L-selectin was a substrate for PS. Subsequently, I analysed whether stimulation of the TCR activates PS, inducing intramembrane proteolysis of the MP product releasing the ICD into the intracellular region. My data showed for the first time that in a resting T-cell, L-selectin forms a multi-component complex with both ADAM 17 and PS. TCR-activation induces ADAM 17 dependent proteolysis of L-selectin generating an MP product. Stimulation of the TCR also causes endoproteolysis of PS, where activated PS then cleaves the bound MP product. After PS cleavage, the released ICD was unstable and therefore difficult to detect, however I was able to block its formation using either PS inhibitor treatment or generating I351W mutated L-selectin, which was resistant to intramembrane proteolysis.
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Killock, David James. "Molecular characterisation of L-selectin-dependent adhesion and signalling." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.512055.

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Tanousis, Kyriakos Michael. "The role of L-selectin shedding in regulating lymphocyte migration." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368043.

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Smith, Tracy L. "The Effect of Anticoagulants on White Blood Cell L-selectin Levels." Youngstown State University / OhioLINK, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=ysu997725968.

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Nicholson, Martin William Michael. "Molecular analysis of the leukocyte cell-surface adhesion protein L-selectin." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260752.

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Gräfe, Michael. "Die Bedeutung entzündlicher Reaktionen für die Pathogenese der Arteriosklerose." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2001. http://dx.doi.org/10.18452/13763.

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Während die zellulären Mechanismen der Pathogenese der Arteriosklerose intensiv untersucht worden sind, ist über die Mechanismen, die zu einer bevorzugten Lokalisation arteriosklerotischer Läsionen in bestimmten Gefäßarealen führen, weniger bekannt. Zur Untersuchung dieser Mechanismen wurden Endothelzellen aus menschlichen Koronararterien, einem Gefäßbereich, in dem häufig arteriosklerotische Läsionen beobachtete werden, isoliert und kultiviert. Endothelzellen der Mikrozirkulation menschlicher Herzen wurden unter gleichen Bedingungen kultiviert und die Reaktionen beider Zellarten verglichen. Inkubation der Zellen mit den in Bezug auf die Bildung arteriosklerotischer Plaques besonders pathogenen oxidierten LDL induzierte in makrovaskulären koronaren Endothelzellen eine stärkere Zunahme der PAI-1 Aktivität (182%, p
While the cellular mechanisms of atherosclerosis have been intensively studied, the mechanisms leading to preferential localization of atherosclerotic lesions are less well understood. To further define these mechanisms, endothelial cells from coronary arteries, i.e. vessels with frequent atherosclerotic lesions, were isolated and grown in vitro. In order to compare the reactions of both cell types, endothelial cells derived from microvessels of human hearts were isolated and cultured under identical conditions. Incubation of endothelial cells with oxidized LDL (75 µg/ml protein) induced a significant increase in PAI-1 activity (182 %, p
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Kilian, Karin. "Identification of novel interaction partners for the leukocyte adhesion molecule L-selectin." [S.l. : s.n.], 2002. http://www.diss.fu-berlin.de/2002/295/index.html.

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Books on the topic "L-selectin"

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Natural selection and social theory: Selected papers of Robert L. Trivers. New York: Oxford University Press, 2002.

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Lowry, L. S. L. S. Lowry R. A. (1887-1976): A selection of masterpieces. London: Crane Kalman Gallery, 1994.

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Philadelphia, Athenaeum of. A splendid array: Selections from the Robert L. Raley collection. Philadelphia, PA: Athenaeum of Philadelphia, 2001.

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B, Helzel Florence, and Judah L. Magnes Memorial Museum., eds. The Jewish illustrated book: A selection from the Judah L. Magnes Museum. Berkeley, Calif: The Museum, 1986.

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Scott, Paeth, Breitenberg E. Harold 1955-, and Lee Hak Joon 1958-, eds. Shaping public theology: Selections from the writings of Max L. Stackhouse. Grand Rapids, Michigan: William B. Eerdmans Pub. Company, 2014.

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Vuokko, Risto. Species selection for the afforestation of 'Imperata cylindrica (L.) Beauv.' grasslands in Indonesia. Dublin: University College Dublin, 1996.

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Lane, Simon John. Selection of feeding sites by overwintering dark-bellied brent geese branta bernicla bernicla (L.). Norwich: University of East Anglia, 1994.

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Balke, Ralf. Israel. München: Beck, 2000.

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Latham, Dorian Miles. The terrestrial habitat selection and utilisation by the common toad (Bufo bufo L.) in agricultural landscapes. Leicester: De Montfort University, 1997.

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Helzel, Florence B. Witnesses to history: The Jewish poster, 1770-1985 : a selection from the Judah L. Magnes Museum. Berkeley, Calif: The Museum, 1989.

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Book chapters on the topic "L-selectin"

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Gupta, G. S. "L-Selectin (CD62L) and Its Ligands." In Animal Lectins: Form, Function and Clinical Applications, 553–74. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-1065-2_26.

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Steeber, Douglas A., Hariharan Subramanian, Jamison J. Grailer, Rochelle M. Conway, and Traci J. Storey. "L-selectin-mediated leukocyte adhesion and migration." In Adhesion Molecules: Function and Inhibition, 27–70. Basel: Birkhäuser Basel, 2007. http://dx.doi.org/10.1007/978-3-7643-7975-9_2.

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Kishimoto, Takashi K., Julius Kahn, Grace Migaki, Elizabeth Mainolfi, Francine Shirley, Richard Ingraham, and Robert Rothlein. "Regulation of L-Selectin Expression by Membrane Proximal Proteolysis." In Inflammation: Mechanisms and Therapeutics, 121–34. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7343-7_11.

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Kawashima, Hiroto. "Analysis of L-Selectin-Mediated Cellular Interactions Under Flow Conditions." In Methods in Molecular Biology, 401–12. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1292-6_35.

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Walcheck, Bruce, and Mark A. Jutila. "The Contribution of L-Selectin to Leukocyte Trafficking In Vivo." In Structure, Function, and Regulation of Molecules Involved in Leukocyte Adhesion, 182–90. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9266-8_14.

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Tedder, Thomas F., Anjun Chen, and Pablo Engel. "L-Selectin Regulation of Lymphocyte Homing and Leukocyte Rolling and Migration." In Cardiovascular Disease 2, 173–84. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1959-1_22.

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Girard, Jean-Philippe, and François Amalric. "Biosynthesis of Sulfated L-Selectin Ligands in Human High Endothelial Venules (HEV)." In Advances in Experimental Medicine and Biology, 55–62. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5383-0_6.

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Renkonen, Risto. "Endothelial Sialyl Lewis X as a Crucial Glycan Decoration on L-Selectin Ligands." In Advances in Experimental Medicine and Biology, 63–73. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5383-0_7.

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Farstad, Inger Nina, Trond S. Halstensen, Dag Kvalel, Olav Fausa, and Per Brandtzaeg. "Expression of VLA-4 and L-Selectin in Human Gut-Associated Lymphoid Tissue (GALT)." In Advances in Experimental Medicine and Biology, 91–96. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1941-6_16.

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Jensen, G. S., J. L. Po, P. Huerta, and C. Shustik. "Circulating B-Ceils in Follicular Non-Hodgkin’s Lymphoma Show Variant Expression of L-Selectin Epitopes." In Current Topics in Microbiology and Immunology, 171–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_21.

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Conference papers on the topic "L-selectin"

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Cellars, Nicholas J., Ariel L. Lanier, and Monica M. Burdick. "Abstract 63: Breast and colon cancer cells express L-selectin ligands that interact with L-selectin on white blood cells under flow conditions." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-63.

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Cellars, Nicholas J., Ariel L. Lanier, and Monica M. Burdick. "Abstract 63: Breast and colon cancer cells express L-selectin ligands that interact with L-selectin on white blood cells under flow conditions." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-63.

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bergantini, laura, Miriana D'Alessandro, Paolo Cameli, Alfonso Carleo, Piersante Sestini, and Elena Bargagli. "Regulatory T cells and L-selectin in severe asthmatic patients treated with mepolizumab." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2667.

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Kuret, T., K. Lakota, P. igon, M. Ogric, S. Sodin-Šemrl, R. Ješe, S. Cucnik, M. Tomšic, and A. Hocevar. "P053 Serum amyloid a can modulate neutrophil surface expression of l-selectin and integrin alpha m." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.72.

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YOON, HO IL, S. F. Man, Bartolome Celli, NR Anthonisen, D. P. Tashkin, J. R. Connett, R. A. Wise, and D. D. Sin. "Soluble L-Selectin Level Is Associated With Lower Mortality In Patients With Chronic Obstructive Lung Disease." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3012.

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Patterson, Dillon G., Christopher D. Scharer, Tian Mi, Madeline J. Price, Sakeenah L. Hicks, and Jeremy M. Boss. "Abstract A74: Loss of L-selectin distinguishes activated B cells destined to differentiate to plasma cells." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a74.

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Gupta, Vijay K., and Charles D. Eggleton. "A 3-D Computational Model of L-Selectin-PSGL-1 Dependent Homotypic Leukocyte Binding and Rupture in Shear Flow." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80862.

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Cell adhesion plays a pivotal role in diverse biological processes, including inflammation, tumor metastasis, arteriosclerosis, and thrombosis. Changes in cell adhesion can be the defining event in a wide range of diseases, including cancer, atherosclerosis, osteoporosis, and arthritis. Cells are exposed constantly to hemodynamic/hydrodynamic forces and the balance between the dispersive hydrodynamic forces and the adhesive forces generated by the interactions of membrane-bound receptors and their ligands determines cell adhesion. Therefore to develop novel tissue engineering based approaches for therapeutic interventions in thrombotic disorders, inflammatory, and a wide range of other diseases, it is crucial to understand the complex interplay among blood flow, cell adhesion, and vascular biology at the molecular level. In response to tissue injury or infection, polymorphonuclear (PMN) leukocytes are recruited from the bloodstream to the site of inflammation through interactions between cell surface receptors and complementary ligands expressed on the surface of the endothelium [1]. PMN-PMN interactions also contribute to the process of recruitment. It has been shown that PMNs rolling on activated endothelium cells can mediate secondary capture of PMNs flowing in the free blood stream through homotypic interactions [2]. This is mediated by L-selectin (ligand) binding to PSGL-1 (receptor) between a free-stream PMN and one already adherent to the endothelium cells [3]. Both PSGL-1 and L-selectin adhesion molecules are concentrated on tips of PMN microvilli [4]. Homotypic PMN aggregation in vivo or in vitro is supported by multiple L-selectin–PSGL-1 bondings between pairs of microvilli. The ultimate objective of our work is to develop software that can simulate the adhesion of cells colliding under hydrodynamic forces that can be used to investigate the complex interplay among the physical mechanisms and scales involved in the adhesion process. However, cell-cell adhesion is a complex phenomenon involving the interplay of bond kinetics and hydrodynamics. Hence, as a first step we recently developed a 3-D computational model based on the Immersed Boundary Method to simulate adhesion-detachment of two PMN cells in quiescent conditions and the exposing the cells to external pulling forces and shear flow in order to investigate the behavior of the nano-scale molecular bonds to forces applied at the cellular scale [5]. Our simulations predicted that the total number of bonds formed is dependent on the number of available receptors (PSGL-1) when ligands (L-selectin) are in excess, while the excess amount of ligands controls the rate of bond formation [5]. Increasing equilibrium bond length causes an increased intercellular contact area hence results in a higher number of receptor-ligand bonds [5]. Off-rates control the average number of bonds by modulating bond lifetimes while On-rate constants determine the rate of bond formation [5]. An applied external pulling force leads to time-dependent on- and off-rates and causes bond rupture [5]. It was shown that the time required for bond rupture in response to an applied external force is inversely proportional to the applied external force and decreases with increasing offrate [5]. Fig. 1 shows the time evolution of the total number of bonds formed for various values of NRmv (number of receptor) and NLmv (number of ligand). As expected, the total number of bonds formed at equilibrium is dependent on NRmv when NLmv is in excess. In this particular case study since two pairs (or four) microvilli each with NRmv are involved in adhesion hence the equilibrium bond number is approximately 4NRmv. It is noticed that for NRmv = 50, as we vary NLmv the mean value of the total number of bonds at equilibrium does not change appreciably. However, it can be noticed from Fig. 1 that for NRmv = 50, as the excess number of ligands (NLmv) increases there is a slight increase in the rate of bond formation due to the increase in probability of bond formation. Having developed confidence in the ability of the numerical method to simulate the adhesion of two cells that can form up to 200 bonds, we apply the method to study the effect of shear rate on the detachment of two cells. In particular, we first would like to establish the minimum shear rate needed for the two cells to detach for a given number of bonds between them. Fig. 2 shows the variation of force per bond at no rupture with number of bonds for various shear rates indicated. It is seen that at a given shear rate as the number of bonds increases the force per bond at no rupture decreases. This is attributed to the fact that force caused by shear flow is shared equally among the existing bonds. Further, it is seen that a given number of bonds as the shear rate increases the force per bond at no rupture increases. This is due to the fact that at a given number of bonds between the cells as we increase the shear rate the force caused by the flow increases hence the force per bond increases. We further notice that at shear rate = 3000 s−1 cells attached either by a single bond or by two bonds detach while they don’t for higher (> 2) number of bonds. This clearly demonstrate that there is a minimum shear rate needed to detach cells adhered by a given number of bonds. The higher the number of bonds, the higher the minimum shear rate for complete detachment of cells. For example, from Fig. 2 is it clear that for the cells adhered by two and five bonds the minimum shear rate needed for complete detachment of these two cells are 3000 s−1 and 6000 s−1, respectively.
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Choudhary, Dharamainder, Poornima Hegde, Shilpa Choudhary, Kevin Claffey, Pramod Srivastava, Carol C. Pilbeam, and John Arthur Taylor. "Abstract 53: Increased expression of L-selectin (CD62L) in high grade bladder cancer: a potential biomarker for lymph node metastasis." 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.am2014-53.

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Carlson, Grady E., Venktesh S. Shirure, Vicente A. Resto, Ramiro Malgor, Douglas J. Goetz, and Monica M. Burdick. "Abstract 203: Dynamic biochemical tissue analysis provides a unique method to detect functional in situ L-selectin ligands and unveils intercellular heterogeneity in colon cancer tissues." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-203.

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Shupletsova, O. N. "Obtaining barley genotypes in selective in vitro systems with complex resistance to soil stress factors." In CURRENT STATE, PROBLEMS AND PROSPECTS OF THE DEVELOPMENT OF AGRARIAN SCIENCE. Federal State Budget Scientific Institution “Research Institute of Agriculture of Crimea”, 2020. http://dx.doi.org/10.33952/2542-0720-2020-5-9-10-99.

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The aim of the work was to develop selective in vitro systems and obtain on their basis the initial breeding material of spring barley adapted to adverse soil conditions – increased acidity, toxicity of aluminum and heavy metals, drought. In the process of research, optimal patterns for selecting callus lines on selective media using various combinations of stress factors were identified: Al3 + (20–40 mg/l), H+ (4.0–6.0 pH units), Cd2 + (10-20 mg/l), Mn2 + (100–250 mg/l) and osmotic (10–20 % polyethyleneglycol). In the proposed in vitro selective systems, more than a thousand regenerated plants were obtained. Varieties created on the basis of regenerants exceed the standard in yield, have high productive tillering (29.0–67.5 % higher than the standard) and dense spike (4.5–6.6 % higher than the standard). Their advantage is due to resistance to lodging, a high level of survival, germination and environment-forming activity of the root system.
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Reports on the topic "L-selectin"

1

Noble, Linda J., Christopher J. Sontag, Alpa Mahuvakar, Thomas Fandel, and Aida F. Martinez. Targeting L-Selectin to Improve Neurologic and Urologic Function After Spinal Cord Injury. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599594.

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Mudge, Christopher, and Kurt Getsinger. Comparison of generic and proprietary aquatic herbicides for control of invasive vegetation; part 3 : submersed plants. Engineer Research and Development Center (U.S.), September 2021. http://dx.doi.org/10.21079/11681/42061.

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Herbicide selection is key to efficiently managing nuisance vegetation in our nation’s waterways. After selecting the active ingredient, there still remains multiple proprietary and generic products to choose from. Recent small-scale research has been conducted to compare the efficacy of these herbicides against floating and emergent species. Therefore, a series of mesocosm and growth chamber trials were conducted to evaluate subsurface applications of the following herbicides against submersed plants: diquat versus coontail (Ceratophyllum demersum L.), hydrilla (Hydrilla verticillata L.f. Royle), southern naiad (Najas guadalupensis (Sprengel) Magnus), and Eurasian watermilfoil (Myriophyllum spicatum L.); flumioxazin versus coontail, hydrilla, and Eurasian watermilfoil; and triclopyr against Eurasian watermilfoil. All active ingredients were applied at concentrations commonly used to manage these species in public waters. Visually, all herbicides within a particular active ingredient performed similarly with regard to the onset and severity of injury symptoms throughout the trials. All trials, except diquat versus Eurasian watermilfoil, resulted in no differences in efficacy among the 14 proprietary and generic herbicides tested, and all herbicides provided 43%–100% control, regardless of active ingredient and trial. Under mesocosm and growth chamber conditions, the majority of the generic and proprietary herbicides evaluated against submersed plants provided similar control.
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Parker, L. E. L-ALLIANCE: a mechanism for adaptive action selection in heterogeneous multi-robot teams. Office of Scientific and Technical Information (OSTI), November 1995. http://dx.doi.org/10.2172/211400.

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Sibener, Steven J. Fundamental Studies of Molecule-Surface Encounters Relevant to Molecular Adsorption, Size and Chemically Selective Collection, and Trace Identification/C and L (CBT). Fort Belvoir, VA: Defense Technical Information Center, March 2011. http://dx.doi.org/10.21236/ada545390.

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Chandra, Shailesh, Mehran Rahmani, Timothy Thai, Vivek Mishra, and Jacqueline Camacho. Evaluating Financing Mechanisms and Economic Benefits to Fund Grade Separation Projects. Mineta Transportation Institute, January 2021. http://dx.doi.org/10.31979/mti.2020.1926.

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Investment in transportation infrastructure projects generates benefits, both direct and indirect. While emissions reductions, crash reductions, and travel time savings are prominent direct benefits, there are indirect benefits in the form of real estate enhancements that could pay off debt or loan incurred in the improvement of the infrastructure itself. Studies have shown that improvements associated with rail transportation (such as station upgrades) trigger an increase in the surrounding real estate values, increasing both the opportunity for monetary gains and, ultimately, property tax collections. There is plenty of available guidance that provides blueprints for benefits calculations for operational improvements in rail transportation. However, resources are quite limited in the analysis of benefits that accrue from the separation of railroad at-grade crossings. Understanding the impact of separation in a neighborhood with high employment or population could generate revenues through increased tax collections. In California, the research need is further amplified by a lack of guidance from the California Public Utilities Commission (CPUC) on at-grade crossing for separation based on revenue generated. There is a critical need to understand whether grade separation projects could impact neighboring real estate values that could potentially be used to fund such separations. With COVID-19, as current infrastructure spending in California is experiencing a reboot, an approach more oriented to benefits and costs for railroad at-grade separation should be explored. Thus, this research uses a robust benefits-to-cost analysis (BCA) to probe the economic impacts of railroad at-grade separation projects. The investigation is carried out across twelve railroad-highway at-grade crossings in California. These crossings are located at Francisquito Ave., Willowbrook/Rosa Parks Station, Sassafras St., Palm St., Civic Center Dr., L St., Spring St. (North), J St., E St., H St., Parkmoor West, and Nursery Ave. The authors found that a majority of the selected at-grade crossings analyzed accrue high benefits-to-cost (BC) ratios from travel time savings, safety improvements, emissions reductions, and potential revenue generated if property taxes are collected and used to fund such separation projects. The analysis shows that with the estimated BC ratios, the railroad crossing at Nursery Ave. in Fremont, Palm St. in San Diego, and H St. in Chula Vista could be ideal candidates for separation. The methodology presented in this research could serve as a handy reference for decision-makers selecting one or more at-grade crossings for the separation considering economic outputs and costs.
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