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1
Pacumbaba, R. P., and R. O. Pacumbaba. "Growing Shiitake Mushroom on Hardwood Sawdust in the Greenhouse." HortTechnology 9, no. 1 (January 1999): 91–94. http://dx.doi.org/10.21273/horttech.9.1.91.
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Seven strains of shiitake mushroom [Lentinula edodes (Berk.) Pegler] produced spawn in culture vessels containing hardwood sawdust amended with YVMBS (yeast extract, multigrain oatmeal, brown sugar) broth within 35 to 45 days after mycelia inoculations. Under greenhouse conditions, shiitake basidiocarps (mushroom fruit) appeared from 1 to 3 months after spawn inoculations of the hardwood sawdust amended with YVMBS broth. The shiitake mushroom strains LE2, LE1, LE6, and LE5 had 10.4, 7.3, 2.5, and 1.6 times more fresh harvested basidiocarps, respectively, on the amended hardwood sawdust compared to the controls. The amount of basidiocarps produced by the shiitake strains LE3, LE4, and LE7 was the same on both hardwood sawdust treatments. The basidiocarps of LE1, LE2, LE3, LE4, and LE5 were averaged 5 inches (12.7 cm) in diameter, however, the basidiocarps of LE6 and LE7 were averaging only 2 inches (5.1 cm) in diameter. The only pests of the shiitake basidiocarps in the greenhouse were slugs, but they were easily controlled by applying table salt. The start up cost of inoculating 100 shiitake spawn blocks on hardwood sawdust on one bench in the greenhouse was $77. The start up cost of inoculating shiitake spawn on 100 logs was $1,329.75. In 1 year, shiitake strains LE1, LE2, LE5, and LE6 produced 19.5, 20.2, 7.9, and 4.5 lb (8.8, 9.2, 3.6, and 2.0 kg), respectively, of harvested fresh basidiocarps on amended hardwood sawdust in the greenhouse. The mushrooms retail for $3.20 to $4.20/lb ($7.05 to $9.26/kg). The use of the hardwood sawdust amended with YVMBS broth for shiitake production in the greenhouse has considerable economic potential for shiitake mushroom growers.
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Yamamoto, Takumi, Nana Yamamoto, Hidehiko Yoshimatsu, Mitsunaga Narushima, and Isao Koshima. "LEC Score." Annals of Plastic Surgery 70, no. 2 (February 2013): 227–30. http://dx.doi.org/10.1097/sap.0b013e3182380861.
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Chemani, Chanez, Anne Imberty, Sophie de Bentzmann, Maud Pierre, Michaela Wimmerová, Benoît P. Guery, and Karine Faure. "Role of LecA and LecB Lectins in Pseudomonas aeruginosa-Induced Lung Injury and Effect of Carbohydrate Ligands." Infection and Immunity 77, no. 5 (February 23, 2009): 2065–75. http://dx.doi.org/10.1128/iai.01204-08.
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ABSTRACT Pseudomonas aeruginosa is a frequently encountered pathogen that is involved in acute and chronic lung infections. Lectin-mediated bacterium-cell recognition and adhesion are critical steps in initiating P. aeruginosa pathogenesis. This study was designed to evaluate the contributions of LecA and LecB to the pathogenesis of P. aeruginosa-mediated acute lung injury. Using an in vitro model with A549 cells and an experimental in vivo murine model of acute lung injury, we compared the parental strain to lecA and lecB mutants. The effects of both LecA- and Lec B-specific lectin-inhibiting carbohydrates (α-methyl-galactoside and α-methyl-fucoside, respectively) were evaluated. In vitro, the parental strain was associated with increased cytotoxicity and adhesion on A549 cells compared to the lecA and lecB mutants. In vivo, the P. aeruginosa-induced increase in alveolar barrier permeability was reduced with both mutants. The bacterial burden and dissemination were decreased for both mutants compared with the parental strain. Coadministration of specific lectin inhibitors markedly reduced lung injury and mortality. Our results demonstrate that there is a relationship between lectins and the pathogenicity of P. aeruginosa. Inhibition of the lectins by specific carbohydrates may provide new therapeutic perspectives.
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Cohen, Jarish, Yang-Xin Fu, and Victor Engelhard. "Tolerogenic properties of lymphatic endothelial cells are controlled by the lymph node microenvironment (176.25)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 176.25. http://dx.doi.org/10.4049/jimmunol.188.supp.176.25.
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Abstract Lymphatic endothelial cells that reside in lymph nodes (LN-LEC) express peripheral tissue antigens, including the melanocyte differentiation protein tyrosinase, and induce deletional tolerance of tyrosinase-specific CD8 T cells. We have also recently shown that deletional tolerance is due to PD-L1 expressed by LN-LEC. To determine whether LEC from tissue lymphatic capillaries also have tolerogenic properties, we purified LEC from diaphragm (D-LEC) and colon (C-LEC). D-LEC and C-LEC express significantly less PD-L1 than LN-LEC, and express tyrosinase at levels insufficient to induce proliferation of tyrosinase-specific CD8 T cells in vitro. This suggested that cells and factors in the LN microenvironment induce the tolerogenic properties of LN-LEC. LEC from postnatal day 1 LN, which are severely lymphopenic, do not express PD-L1, but do so by day 7 when lymphocytes have colonized the LN. Adult LN contain 2 distinct LN-LEC subsets: PD-L1hi ICAM-1hi (LN-LEChi) and PD-L1int ICAM-1int (LN-LECint). Interestingly, tyrosinase expression and presentation is restricted to the LN-LEChi population. The representation and absolute number of LN-LEChi cells is reduced in Rag1-/- mice, µMT-/- (B cell-deficient) mice, and mice in which lymphotoxin β receptor (LtβR) signaling is blocked. Thus, LN-LEC are induced to express PD-L1 during the neonatal period, and B cells and LtβR signaling contribute to maintain a LN-LEC population that controls peripheral tolerance to tyrosinase.
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Vigato, Aryane A., Ian P. Machado, Matheus del Valle, Patricia A. da Ana, Anderson F. Sepulveda, Fabiano Yokaichiya, Margareth K. K. D. Franco, et al. "Monoketonic Curcuminoid-Lidocaine Co-Deliver Using Thermosensitive Organogels: From Drug Synthesis to Epidermis Structural Studies." Pharmaceutics 14, no. 2 (January 27, 2022): 293. http://dx.doi.org/10.3390/pharmaceutics14020293.
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Organogels (ORGs) are remarkable matrices due to their versatile chemical composition and straightforward preparation. This study proposes the development of ORGs as dual drug-carrier systems, considering the application of synthetic monoketonic curcuminoid (m-CUR) and lidocaine (LDC) to treat topical inflammatory lesions. The monoketone curcuminoid (m-CUR) was synthesized by using an innovative method via a NbCl5–acid catalysis. ORGs were prepared by associating an aqueous phase composed of Pluronic F127 and LDC hydrochloride with an organic phase comprising isopropyl myristate (IPM), soy lecithin (LEC), and the synthesized m-CUR. Physicochemical characterization was performed to evaluate the influence of the organic phase on the ORGs supramolecular organization, permeation profiles, cytotoxicity, and epidermis structural characteristics. The physico-chemical properties of the ORGs were shown to be strongly dependent on the oil phase constitution. Results revealed that the incorporation of LEC and m-CUR shifted the sol-gel transition temperature, and that the addition of LDC enhanced the rheological G′/G″ ratio to higher values compared to original ORGs. Consequently, highly structured gels lead to gradual and controlled LDC permeation profiles from the ORG formulations. Porcine ear skin epidermis was treated with ORGs and evaluated by infrared spectroscopy (FTIR), where the stratum corneum lipids were shown to transition from a hexagonal to a liquid crystal phase. Quantitative optical coherence tomography (OCT) analysis revealed that LEC and m-CUR additives modify skin structuring. Data from this study pointed ORGs as promising formulations for skin-delivery.
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Rouhani, Sherin, Eric Tewalt, Holly Davis, Lieping Chen, and Victor Engelhard. "Lymphatic endothelial cells induce anergy of β-galactosidase specific CD4 T cells by providing antigen to CD11c cells (P1147)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 50.16. http://dx.doi.org/10.4049/jimmunol.190.supp.50.16.
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Abstract Lymphatic endothelial cells (LEC) express a variety of peripheral tissue antigens (Ags) and induce deletional tolerance of tyrosinase-specific CD8 T cells. LEC express MHC II molecules, suggesting they may tolerize CD4 T cells. We expressed β-galactosidase (β-gal) selectively in LEC using Lyve-1cre x β-galflox mice to investigate the ability of LEC to tolerize β-gal specific CD4 and CD8 T cells (Bg2 and Bg1, respectively). Using in vitro co-cultures and MHC I-/- bone marrow chimeras, we demonstrated that Bg1 CD8 T cells undergo deletional tolerance after recognizing Ag presented by MHC I molecules on LEC. Peptide-pulsed LEC induce Bg2 CD4 T cell proliferation in vitro, indicating LEC express functional MHC II. However, Bg2 cells proliferate when co-cultured with CD11c cells but not with LEC from β-gal+ mice. When Ag presentation is restricted to LEC in MHC II-/- bone marrow chimeras, Bg2 cells do not proliferate or upregulate CD69, CD25 or CD44. However, Bg2 cells do proliferate when transferred into chimeras with MHC II+ β-galneg bone marrow, demonstrating that hematopoietic cells acquire and present Ag from LEC. Bg2 cells activated in vivo by hematopoietic presentation of LEC-derived Ag do not proliferate in response to subsequent rechallenge, demonstrating that they have become anergic. Thus, LEC show a diminished ability to directly present MHC II Ags, but play an important role in CD4 tolerance by serving as a reservoir of Ag used by hematopoietic cells to induce anergy.
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Howard, O. M. Zack, Hui Fang Dong, Aiko-Konno Shirakawa, and Joost J. Oppenheim. "LEC induces chemotaxis and adhesion by interacting with CCR1 and CCR8." Blood 96, no. 3 (August 1, 2000): 840–45. http://dx.doi.org/10.1182/blood.v96.3.840.
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Abstract Liver-expressed chemokine (LEC) is an unusually large CC chemokine, which is also known as LMC, HCC-4, NCC-4, and CCL16. Previously, LEC was shown to induce leukocyte migration but the responsible signaling receptors were not characterized. We report chemotaxis and competitive binding studies that show LEC binds to and activates CCR1 and CCR8 transfected HEK-293 cells. LEC induced maximal migration of CCR1 and CCR8 transfected cells at 89.3 nmol/L and cell adhesion at 5.6 nmol/L. The molar concentration of LEC required to induce maximum cell migration is 20- to 200-fold greater than that required for RANTES or I309, respectively. All 3 chemokines induced maximal static adhesion at 5 to 7 nmol/L. A neutralizing polyclonal antibody to LEC was developed to demonstrate that the unusually high concentration of LEC required to induce chemotaxis was a property of LEC and not as a result of an irrelevant protein contamination. This study suggests that LEC may be a more effective inducer of cell adhesion than cell migration.
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Howard, O. M. Zack, Hui Fang Dong, Aiko-Konno Shirakawa, and Joost J. Oppenheim. "LEC induces chemotaxis and adhesion by interacting with CCR1 and CCR8." Blood 96, no. 3 (August 1, 2000): 840–45. http://dx.doi.org/10.1182/blood.v96.3.840.015k32_840_845.
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Liver-expressed chemokine (LEC) is an unusually large CC chemokine, which is also known as LMC, HCC-4, NCC-4, and CCL16. Previously, LEC was shown to induce leukocyte migration but the responsible signaling receptors were not characterized. We report chemotaxis and competitive binding studies that show LEC binds to and activates CCR1 and CCR8 transfected HEK-293 cells. LEC induced maximal migration of CCR1 and CCR8 transfected cells at 89.3 nmol/L and cell adhesion at 5.6 nmol/L. The molar concentration of LEC required to induce maximum cell migration is 20- to 200-fold greater than that required for RANTES or I309, respectively. All 3 chemokines induced maximal static adhesion at 5 to 7 nmol/L. A neutralizing polyclonal antibody to LEC was developed to demonstrate that the unusually high concentration of LEC required to induce chemotaxis was a property of LEC and not as a result of an irrelevant protein contamination. This study suggests that LEC may be a more effective inducer of cell adhesion than cell migration.
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Grousset, René. "Lec MusÉe Cernuschi." Museum International (Edition Francaise) 1, no. 1-2 (April 24, 2009): 89–120. http://dx.doi.org/10.1111/j.1755-5825.1948.tb00266.x.
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Walusimbi, S. S., L. M. Wetzel, D. H. Townson, and J. L. Pate. "Isolation of luteal endothelial cells and functional interactions with T lymphocytes." Reproduction 153, no. 5 (May 2017): 519–33. http://dx.doi.org/10.1530/rep-16-0578.
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The objectives of this study were to optimize the isolation of luteal endothelial cells (LEC) and examine their functional interactions with autologous T lymphocytes. Analysis by flow cytometry showed that the purity of LEC isolated by filtration was nearly 90% as indicated byBandeiraea simplicifolia(BS)-1 lectin binding. LEC expressed mRNA for progesterone receptor (PGR), prostaglandin receptors (PTGFR, PTGER2 and 4, and PTGIR), tumor necrosis factor receptors (TNFRSF1A&B) and interleukin (IL) 1B receptors (IL1R1&2). LEC were pretreated with either vehicle, progesterone (P4; 0–20 µM), prostaglandin (PG) E2or PGF2α(0–0.2 µM), and further treated with or without TNF and IL1B (50 ng/mL each). LEC were then incubated with autologous T lymphocytes in an adhesion assay. Fewer lymphocytes adhered to LEC after exposure to high compared to low P4concentrations (cubic response;P < 0.05). In contrast, 0.2 µM PGE2and PGF2αeach increased T lymphocyte adhesion in the absence of cytokines (P < 0.05). LEC induced IL2 receptor alpha (CD25) expression and proliferation of T lymphocytes. In conclusion, filtration is an effective way of isolating large numbers of viable LEC. It is proposed that PGs and P4modulate the ability of endothelial cells to bind T lymphocytes, potentially regulating extravasation, and that LEC activate T lymphocytes migrating into or resident in the CL.
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Ono, Sawako, Hidenori Marunaka, Hiroyuki Yanai, Hotaka Kawai, Kiyofumi Takabatake, Kenji Nishida, Tomohiro Toji, Keisuke Nakano, Hitoshi Nagatsuka, and Tadashi Yoshino. "Lymphoepithelial Carcinoma in the Lateral Tongue: The Case Report." Reports 4, no. 3 (August 12, 2021): 24. http://dx.doi.org/10.3390/reports4030024.
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Lymphoepithelial carcinoma (LEC) of the tongue is a rare subtype of squamous cell carcinoma. Histologically, it is an undifferentiated carcinoma with rich lymphocyte and plasma cell infiltration. The most common location for LEC in the head and neck is the salivary glands, and LEC of the oral cavity is extremely rare. The second case report of LEC in the lateral tongue is presented. In addition, a review of the literature was performed, and the relationship between LEC and Epstein–Barr virus infection was considered.
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Tewalt, Eric, Jarish Cohen, Sherin Rouhani, Cynthia Guidi, Hui Qiao, Shawn Fahl, Timothy Bender, et al. "Peripheral tolerance induction by PD-L1+ lymphatic endothelial cell is due to deficient costimulation that leads to rapid, high-level expression of PD-1 on CD8 T cells (176.24)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 176.24. http://dx.doi.org/10.4049/jimmunol.188.supp.176.24.
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Abstract It has been shown that lymph node (LN) stromal cells directly present peripheral tissue antigens (PTA) leading to systemic peripheral tolerance. In particular, lymphatic endothelial cells (LEC) directly present an epitope from tyrosinase to CD8 T cells (TCD8). Here, we determined the roles of costimulatory and inhibitory pathways in the induction of LEC-mediated tolerance. LEC do not express costimulatory ligands but do express ligands for the PD-1, CD80, CD160, BTLA, and LAG-3 inhibitory pathways. Nonetheless, LEC-mediated deletion of tyrosinase-specific TCD8 is solely dependent on the PD-1:PD-L1 pathway. Based on radioresistance and the fact that LEC express the highest levels of any LN resident cell, we conclude that PD-L1 expressed by LEC is necessary and sufficient for tyrosinase-specific TCD8 deletion. Presentation of tyrosinase by LEC leads to deletion by inducing more rapid, high-level PD-1 expression on TCD8 than that induced by professional APC. This is due to lack of costimulation by LEC, and is correctable with agonistic anti-4-1BB and OX-40. Apoptosis of tyrosinase-specific TCD8 induced by PD-1 is a consequence of failure to upregulate the IL-2 receptor. Rescue of tyrosinase-specific TCD8 from LEC-mediated deletion by interference with PD-1:PD-L1 or provision of costimulatory signals leads to the induction of autoimmune vitiligo. As LEC express numerous PTA, this mechanism may be of general importance in the development of autoimmune diseases.
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Wright, Ann, and Sherie L. Morrison. "Effect of C2-Associated Carbohydrate Structure on Ig Effector Function: Studies with Chimeric Mouse-Human IgG1 Antibodies in Glycosylation Mutants of Chinese Hamster Ovary Cells." Journal of Immunology 160, no. 7 (April 1, 1998): 3393–402. http://dx.doi.org/10.4049/jimmunol.160.7.3393.
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Abstract The complex biantennary oligosaccharide at Asn297 of IgG is essential for some effector functions. To investigate the effect of carbohydrate structure on Ab function, we have now expressed mouse-human chimeric IgG1 Abs in Chinese hamster ovary (CHO) cells with defined defects in carbohydrate biosynthesis. We had previously shown that IgG1 Abs produced in the cell line Lec 1, which attaches a high-mannose intermediate carbohydrate, were severely deficient in complement activation, showed a slightly reduced affinity for FcγRI, and had a reduced in vivo half-life. We have extended these studies by producing the same dansyl-specific IgG1 in cell lines deficient in attachment of sialic acid (Lec 2) and galactose (Lec 8). IgG1-Lec 1, IgG1-Lec 2, and IgG1-Lec 8 all showed varying reactivity with a mAb specific for an epitope in the amino terminal region of CH2, suggesting that the conformations of these proteins were altered by the different carbohydrate structures. Functionally, IgG1-Lec 2 and IgG1-Lec 8 were comparable to wild type with respect to in vivo half-life, affinity for FcγRI, and capacity for complement-mediated hemolysis. While IgG1-Lec 2 was essentially identical to wild type in its capacity to interact with individual components of the classical complement activation pathway, IgG1-Lec 8 demonstrated equivalent maximal binding at lower concentrations and was preferentially bound by mannose-binding protein. Although IgG1-Lec 1 was deficient in activation of the classical pathway, it had a superior capacity to activate the alternative pathway. These studies demonstrate that Abs bearing CH2-linked carbohydrate of differing structures have different functional properties.
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McKenna, Nicole, Stella Berendam, Sherin Rouhani, Stephen Turner, Alex Koeppal, Kara Cummings, Rodney Dekoter, and Victor H. Engelhard. "Factors controlling the tolerogenic phenotype of lymphatic endothelial cells." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 212.11. http://dx.doi.org/10.4049/jimmunol.198.supp.212.11.
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Abstract The prevailing model of peripheral tolerance necessitates tissue-resident dendritic cells migrating to lymph nodes and cross presenting self-antigen to T cells, resulting in their deletion or anergy. Our lab has identified a novel mechanism of peripheral tolerance involving a subset of lymph node stromal cells called lymphatic endothelial cells (LEC). LEC in the lymph node induce peripheral tolerance by presenting epitopes derived from peripheral tissue antigens (PTAs) in conjunction with expression of PD-L1, leading to CD8 T cell deletion. However, PTAs and PD-L1 are not expressed on LEC in the colon or diaphragm. We performed RNAseq analysis on LEC from lymph node and diaphragm to identify differences in expression of transcription factors that might control expression of PD-L1 and PTA. We found that Spi-B is the most differentially expressed transcription factor in the lymph node compared to the diaphragm, with a fold change of over 500. Spi-B has been implicated in the development and function of medullary thymic epithelial cells, a key cell type in central tolerance. Lymph node LEC harvested from Spi-B deficient mice have a significant shift in markers associated with LEC tolerogenicity. Expression levels of PD-L1, ICAM-1, MAdCAM-1, and LTbR delineate different lymph node LEC subpopulations that vary in their ability to express PTAs and tolerize CD8 T cells. LEC from Spi-B deficient mice have decreased MAdCAM-1 expression and increased LTbR and ICAM-1 expression suggesting a population shift of non-tolerogenic lymph node LEC to tolerogenic lymph node LEC. This data suggests Spi-B may be involved in a negative feedback mechanism to limit the number of tolerogenic LEC during development.
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Shabani, M. N., D. De Marzo, L. Esmailzadeh, A. Seidavi, V. Laudadio, and V. Tufarelli. "Early phase dietary supplementation of lipase and lecithin affects performance, haematology and immunology of broilers." South African Journal of Animal Science 51, no. 5 (May 10, 2022): 670–77. http://dx.doi.org/10.4314/sajas.v51i5.14.
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A total of 192 one-day-old Ross 308 chicks were weighed individually (42.0 ± 0.8 g live weight) and randomly assigned to four dietary groups, each with three replicates of 16 birds. One group was a control (CON) and fed a starter diet without supplementation. The other three groups were fed the same starter diet during the starter phase (1 - 10 days old) supplemented with lecithin (LEC) at 0.05 g/kg diet or lipase (LIP) at 0.05 g/kg, or a combination (LEC+LIP) at 0.05 + 0.05 g/kg. No significant effects of supplementation with LEC and LIP on feed intake of broilers were observed during the starter phase, whereas bodyweight gain increased after the combined addition of these supplemental ingredients. Thus, final bodyweight was greater in LEC+LIP broilers compared with the other groups. Dietary supplementation with LEC or LIP had a positive effect on final bodyweight. However, the effect was less than the simultaneous supplementation of LEC+LIP. Moreover, the feed conversion ratio in the LEC+LIP group improved (P <0.05) in the finisher phase (25 - 42 days old). Carcass traits and blood parameters were not influenced significantly by treatments, whereas supplementing LEC+LIP stimulated the immune system of broilers significantly. Thus, it can be concluded that supplementing LEC and LIP in early-stage broilers supported their performance and immune response positively up to finisher rearing phase.
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Schilsky, M. L., R. J. Stockert, and I. Sternlieb. "Pleiotropic effect of LEC mutation: a rodent model of Wilson's disease." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 5 (May 1, 1994): G907—G913. http://dx.doi.org/10.1152/ajpgi.1994.266.5.g907.
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Metabolic studies with 67Cu were undertaken to identify the site of the cellular defect in copper metabolism in the Long-Evans Cinnamon (LEC) rat. The apparent rate of copper uptake by LEC primary hepatocytes was increased [maximal velocity (Vmax) = 259 pmol.min-1.mg protein-1] compared with controls (Vmax = 161 pmol.min-1.mg protein-1); however, Michaelis-Menten constant (Km) values were comparable (11.8 and 12.7 microM, LEC and control, respectively). Efflux of copper from LEC and control hepatocytes was similar from 0 to 15 min, but was reduced from 15 to 60 min in the former. Although hepatic copper contents were markedly elevated in LEC rats compared with controls (658 +/- 199 vs. 21.5 +/- 6.6 micrograms/g dry wt), biliary copper concentration was reduced in LEC rats compared with controls (0.187 vs. 1.39 +/- 0.66 microgram/ml). Subcellular fractionation of LEC liver homogenates revealed approximately 75% of copper to be present in cytosol, with gradients of copper concentration from cytosol to either lysosome or microsomal subcellular fractions. LEC rat bile and hepatic microsome and lysosome fractions contained smaller fractions of 67Cu administered intravenously as cupric acetate compared with control rats. However, recovery of 67Cu in bile and in lysosomal subcellular fractions were similar for LEC and controls following administration of 67Cu-labeled asialoceruloplasmin, which is targeted to lysosomes. This discordance suggests a possible defect in the entry of copper into lysosomes but normal delivery of lysosomal copper to bile. Based on these findings, we conclude that the mutation in LEC rats alters copper transport at more than one cellular site.
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Xu, Hong, Shoji Sakakibara, Masashi Morifuji, Quazi Salamatulla, and Yoritaka Aoyama. "Excess dietary histidine decreases the liver copper level and serum alanine aminotransferase activity in Long-Evans Cinnamon rats." British Journal of Nutrition 90, no. 3 (September 2003): 573–79. http://dx.doi.org/10.1079/bjn2003939.
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Long-Evans Cinnamon (LEC) rats spontaneously develop fulminant hepatitis, associated with excess Cu accumulation in the liver: thus, they are considered an animal model of Wilson's disease. In the present study, we investigated the ability of excess dietary histidine to reduce the excess accumulation of liver Cu in LEC rats by comparing them with Fischer rats. The results clearly showed that the excess-histidine diet markedly stimulated the Cu excretion in urine, and significantly decreased the liver Cu content in LEC rats by 47·5%. The serum Cu content in LEC rats was not influenced by excess dietary histidine. We also compared the effects of excess dietary histidine on some liver antioxidant enzyme activities, liver and serum lipid levels and serum alanine aminotransferase activity of LEC and Fischer rats. Dietary histidine decreased the activities of total and Cu, Zn-superoxide dismutase in the liver of both strains. In LEC rats, the liver cholesterol content decreased, and serum cholesterol and phospholipids levels increased on feeding the excess-histidine diet. When fed on the basal diet, the serum alanine aminotransferase activity was higher in LEC rats than in Fischer rats, but a significant decrease in serum alanine aminotransferase activity of LEC rats was observed on feeding the excess-histidine diet. These results suggest that excess dietary histidine is effective in removing Cu ions from the liver of LEC rats. Thus, it may be of benefit in the prevention or treatment of liver injury in LEC rats and in patients with Wilson's disease.
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Nacef, L., H. Ferjani, H. Riahi, Y. Mabrouk, E. Labbene, K. Maatallah, D. Kaffel, M. Bouaziz, and W. Hamdi. "AB0191 ON WHICH FACTOR TO ACT TO REDUCE CARDIOVASCULAR RISK IN PATIENTS WITH RHEUMATOID ARTHRITIS?" Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1119.3–1120. http://dx.doi.org/10.1136/annrheumdis-2021-eular.4183.
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Background:Patients with rheumatoid arthritis (RA) are at higher cardiovascular risk (CVR) than the general population due to chronic inflammation. Several factors, both modifiable and non-modifiable, can increase this risk. Intima-media thickness (IMT) was considered as a marker for atherosclerosis.Objectives:This study aimed to identify predictor factors of increasing IMT.Methods:The prospective study was carried out on patients with RA who met the 2010 American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) classification criteria. These patients were followed in the rheumatology department of the Kassab Institute. The socio-demographic data, biological and immunological parameters were collected.Framingham’s score quantified the cardiovascular risk at 10-years. Carotid Ultrasonography (US) using a high resolution B mode carotid measured intima-media thickness (IMT) as a subclinical marker of atherosclerosis. Carotid US was performed in the supine position, according to American Society of Echocardiography guidelines. IMT was measured in the left (LCC) and right (RCC) common carotid arteries, the left (LIC) and right (RIC) internal carotid arteries, and the left (LEC) and right (RIC) internal carotid arteries. An increased IMT was defined as ≥0.9 mm.We analyzed data by the SPSS statistical package. A p-value <0.05 was considered significant.Results:Of the 47 patients surveyed, 78.7% were female. The mean age was 52.5 ±11.06 [32-76]. The duration disease was 86.25 ±63 months [5-288] and was erosive in 81.6% of cases. The rheumatoid factor (RF) was positive in 57.8% of patients, and citrullinated antipeptide antibodies (ACPA) were present in 62.2%. Eight patients had a previous CV history (hypertension, diabetes or dyslipidemia) and 16.4% were active smokers. Among women, 43.6% were postmenopausal. ITM was significantly higher in men at LIC (0.037) and LEC (0.025). Older age was associated with increased ITM in LIC (p=0.046; r=0.295), LEC (p=0.05; r=0.412), RCC (p=0.034; r=0.317), and REC (p=0.009; r=0.382). The ITM for LCC, LIC, LEC, RCC, RIC, and REC was higher in postmenopausal women, with no significant difference (p=0.782, p=0.208, p=0.877, r=0.734, p=0.808, p=0.437, respectively).Among the modifiable factors, active smoking was associated with a higher ITM at the REC level (p=0.047). However, weight was not associated with an increased ITM (LCC: p=0.092; LIC: p=0.985; LEC: p=0.952; RCC: p=0.744; RIC: p=0.210; REC: p=0.510). In our study, there was no significant association between DAS28 disease activity or inflammatory marks and ITM (LCC: p=0.784; LIC: p=0.316; LEC: p=0.420; RCC: p=0.784; RIC: p=0.484; REC: p=0.754).Conclusion:In our study, the non-modifiable factors associated with increased ITM were advanced age and male gender. The modifiable factor impacting ITM was primarily active smoking. Surprisingly, disease activity and biological inflammation did not influence ITM.References:[1]S. Gunter and al. Arterial wave reflection and subclinical atherosclerosis in rheumatoid arthritis. Clinical and experimental rheumatology 2018; 36: clinical e.xperimental.[2]Aslan and al. Assessment of local carotid stiffness in seronegative and seropositive rheumatoid Arthritis. Scandinavian cardiovascular journal, 2017.[3]Martin i. Wah-suarez and al, carotid ultrasound findings in rheumatoid arthritis and control subjects: a case-control study. Int j rheum dis. 2018;1–7.Disclosure of Interests:None declared
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Galletti, Cosimo, Cristina Pizzimenti, Vittorio Cavallari, and Bruno Galletti. "Larynx lymphoepithelial carcinoma: surgical management." BMJ Case Reports 14, no. 7 (July 2021): e241460. http://dx.doi.org/10.1136/bcr-2020-241460.
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Lymphoepithelial carcinoma (LEC) is an entity mostly frequent in the nasopharynx, which represents 40% of all neoplasms. The incidence’s not exclusive of a geographic area; however, it has an endemic distribution in Southeast Asia and Eskimos. LEC is not exclusive of the nasopharynx, has also been reported in other anatomical areas, such as the sinonasal tract, nasolacrimal duct, oral cavity, oropharynx, salivary glands, thymus, hypopharynx, oesophagus, stomach, trachea, lung and others. Non-nasopharyngeal and nasopharyngeal LEC have the same microscopic features, but the nasopharyngeal is more likely associated with Epstein-Barr virus. LEC has been approved by the WHO. LEC located in the larynx is quite rare and worthy of attention for its implication in the treatment and prognosis. We present a case of LEC treated in our ENT department in a middle-aged man.
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Bekkers, R. L. M., K. G. G. Keyser, J. Bulten, A. G. J. M. Hanselaar, C. P. T. Schijf, H. Boonstra, and L. F. A. G. Massuger. "The value of loop electrosurgical conization in the treatment of stage IA1 microinvasive carcinoma of the uterine cervix." International Journal of Gynecologic Cancer 12, no. 5 (2002): 485–89. http://dx.doi.org/10.1136/ijgc-00009577-200209000-00013.
Full textAbstract:
The objective of this study is to assess the value of Loop Electrosurgical Conization (LEC) in the treatment of stage IA1 microinvasive squamous cell carcinoma (MIC) of the uterine cervix. Retrospectively, 82 patients with FIGO stage IA1 MIC, primarily treated with LEC on see and treat basis, were analyzed.After the initial LEC, 16 patients received cytologic and colposcopic follow-up only, 66 patients underwent a second procedure (repeat LEC, Cold Knife Conization (CKC), or hysterectomy), and four patients underwent a third procedure (hysterectomy). In 63 patients (77%) no residual CIN 3 or MIC was present after the initial LEC. Treatment of residual CIN 3 or MIC was equally effective with a repeat LEC as with CKC. One patient defaulted follow-up and developed a recurrence in the vaginal vault and was treated with a radical hysterectomy.LEC can be used as an alternative for CKC in treatment of patients with stage IA1 MIC. The advantage of LEC is that it can be performed as an outpatient procedure in addition to a diagnostic colposcopy and does not require a major anesthetic. Only a small number of patients will need a more extensive procedure.
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Takeda, Daisuke, Manabu Shigeoka, Tenyu Sugano, Nanae Yatagai, Takumi Hasegawa, and Masaya Akashi. "A Case Report of Tongue Lymphoepithelial Carcinoma with a Histological Diagnostic Dilemma." Diagnostics 11, no. 6 (June 4, 2021): 1039. http://dx.doi.org/10.3390/diagnostics11061039.
Full textAbstract:
Most head and neck lymphoepithelial carcinomas (LECs) arise in the nasopharynx and harbor Epstein–Barr virus (EBV). LEC is also a rare subtype of the oral squamous cell carcinoma (SCC). Morphologically, LEC is defined as resembling non-keratinizing nasopharyngeal carcinoma, undifferentiated subtype. The histological features and pathogenesis of oral LEC are not established. We describe a case of tongue LEC with histopathological diagnostic difficulties. A 72-year-old Japanese female presented with a whitish change on her left-side tongue. The diagnosis was atypical epithelium; neoplastic change could not be ruled out by a biopsy. Although the lesion was monitored at our hospital per her request, invasive carcinoma was detected 11 months later. Microscopically, conventional SCC was observed with the characteristic features as LEC confined to the deep part of the lesion. We briefly discuss this unusual histological finding and make a novel proposal for distinguishing oral LEC from LECs in other regions based on these histological findings.
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Alemán, Ailén, Selene Pérez-García, Pilar Fernández de Palencia, María Pilar Montero, and María del Carmen Gómez-Guillén. "Physicochemical, Antioxidant, and Anti-Inflammatory Properties of Rapeseed Lecithin Liposomes Loading a Chia (Salvia hispanica L.) Seed Extract." Antioxidants 10, no. 5 (April 28, 2021): 693. http://dx.doi.org/10.3390/antiox10050693.
Full textAbstract:
Vegetal waste materials were used to produce liposomes with both antioxidant and anti-inflammatory properties. Differences in the chemical composition of rapeseed lecithin (LEC) and a partially purified phospholipid fraction (PPL) were studied in terms of fatty acids (neutral lipids, free fatty acids, and phospholipids), sterols, tocopherols, and amino acid composition. Neutral lipids, campesterol, β-sitosterol, and γ-tocopherol were the most depleted compounds in PPL. Qualitative differences between LEC and PPL were revealed by infrared spectroscopy and differential scanning calorimetry. An ethanol/water antioxidant extract from chia seeds (ChE), with a high content in rosmarinic acid and rosmarinic acid 3-O-glucoside, along with other minor phenolic acids determined by HPLC-MS, was encapsulated in liposomes made of LEC (L-LEC) and PPL (L-PPL) with an entrapment efficiency of 61.3% and 69.3%, respectively. L-PPL suspensions showed smaller particle size and lower ζ potential than their L-LEC counterparts, along with noticeable particle destabilization after 7 days of storage. Antioxidant properties were greater in L-LEC than in L-PPL suspensions. L-LEC, ChE, and lecithin empty liposomes (L-E) showed no cytotoxic effect in either Caco-2 or THP-1 cells and induced downregulation of the inflammation response.
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OHTA, A., T. MATSUBAYASHI, Y. SONE, and S. NAKAYAMA. "PIXE DETERMINATION ON THE CHANGES IN THE COPPER CONTENT IN LIVERS OF LONG-EVANS CINNAMON (LEC) RATS FOLLOWING SUPPLEMENT WITH IRON AND CALCIUM." International Journal of PIXE 08, no. 04 (January 1998): 267–74. http://dx.doi.org/10.1142/s0129083598000297.
Full textAbstract:
The analysis of copper, iron, calcium, and other elements in livers of Long-Evans Cinnamon(LEC) rats by PIXE determination is described. The copper contents in the livers of LEC rats which were supplemented with 1g/100g, in the food of calcium chloride dihydrate and iron(II) chloride n-hydrate, respectively, for 5 weeks were determined before and after supplement by PIXE. The experimental results showed that after supplement of the calcium- and iron-fortified food the copper content in the livers of LEC rats decreased with the supplement. The present data suggest that supplement of iron or calcium can be responsible for copper homeostasis in livers of LEC rats, and that the excessive accumulation of copper in livers of LEC rats can readily remove when high load of iron or calcium are supplemented.
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Sone, Michihiko, Tsutomu Nakashima, Testuro Nagasaka, Akihide Itoh, and Noriyuki Yanagita. "Lymphoepithelioma-like carcinoma of the larynx associated with an Epstein-Barr viral infection." Otolaryngology–Head and Neck Surgery 119, no. 1 (July 1998): 134–37. http://dx.doi.org/10.1016/s0194-5998(98)70185-8.
Full textAbstract:
L ymphoepithelioma is a term used to describe undifferentiated squamous cell carcinoma variants of nasopharyngeal neoplasms (WHO type 3). Correlations between lymphoepithelioma and Epstein-Barr virus (EBV) have been investigated with serologic1 and pathologic evaluation. 2 , 3 Recently, nonnasopharyngeal neoplasms, which have morphologic features identical to those of lymphoepithelioma, called lymphoepithelioma-like carcinoma (LEC), have been reported in other anatomic sites. 4 – 10 Seven cases of laryngeal LEC have been reported in the English literature to date, but EBV has yet to be detected in laryngeal LEC. In this article, LEC in the epiglottis of the larynx is described with cellular localization of EBV-encoded immediate-early RNAs (BHLF) in the tumor cells of the larynx. This case report is the first to show laryngeal LEC associated with an EBV infection.
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Masuda, R., M. C. Yoshida, M. Sasaki, K. Dempo, and M. Mori. "Hereditary hepatitis of LEC rats is controlled by a single autosomal recessive gene." Laboratory Animals 22, no. 2 (April 1, 1988): 166–69. http://dx.doi.org/10.1258/002367788780864402.
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The natural history of hereditary hepatitis in long-survived LEC rats was reported. Among 56 (female: male, 28:28) LEC rats of F30, 16 (8:8) (29%) died of fulminant hepatitis approximately four months after birth. The remaining 40 (20:20) rats that survived more than one year developed chronic hepatitis and subsequent hepatic lesions including hepatocellular carcinomas. Further study made with 32 F31 rats killed at the age of five months revealed that hepatitis occurred in all of these rats. Genetic analysis performed by various crosses of LEC and LEJ rats confirmed the previous result that hereditary hepatitis was caused by a single autosomal recessive gene. F1 hybrid rats never developed hepatitis, showing normal histology of the liver. Histological features of hepatitis in F2 (F1×1) and backcross (F1×LEC) rats were the same as those observed in the LEC rats. The preneoplastic foci also appeared in some of these hybrid rats at the age of eight months. We propose a gene symbol hts to designate the present hepatitis which is assumed to be homozygous in LEC strain rats.
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Bingöl, Fatih, Hilal Balta, Buket Özel Bingöl, Recai Muhammet Mazlumoğlu, and Korhan Kılıç. "Lymphoepithelial Cyst in the Palatine Tonsil." Case Reports in Otolaryngology 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/6296840.
Full textAbstract:
Lymphoepithelial cyst (LEC) is the most commonly encountered congenital neck pathology in the lateral part of the neck. A 66-year-old woman presented to the ENT clinic due to difficulty in swallowing persisting for approximately 1 year. Magnetic resonance imaging revealed a cystic mass at right tonsil. Surgery was performed due to this unilateral tonsillar mass, which was excised together with the right tonsil. LEC was diagnosed at histopathological examination. LEC in the palatine tonsil is rare, and only a few cases have been reported in the literature. We report a rare case of LEC in the palatine tonsil.
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Kuruvilla, Maneesh V., David I. G. Wilson, and James A. Ainge. "Lateral entorhinal cortex lesions impair both egocentric and allocentric object–place associations." Brain and Neuroscience Advances 4 (January 2020): 239821282093946. http://dx.doi.org/10.1177/2398212820939463.
Full textAbstract:
During navigation, landmark processing is critical either for generating an allocentric-based cognitive map or in facilitating egocentric-based strategies. Increasing evidence from manipulation and single-unit recording studies has highlighted the role of the entorhinal cortex in processing landmarks. In particular, the lateral (LEC) and medial (MEC) sub-regions of the entorhinal cortex have been shown to attend to proximal and distal landmarks, respectively. Recent studies have identified a further dissociation in cue processing between the LEC and MEC based on spatial frames of reference. Neurons in the LEC preferentially encode egocentric cues while those in the MEC encode allocentric cues. In this study, we assessed the impact of disrupting the LEC on landmark-based spatial memory in both egocentric and allocentric reference frames. Animals that received excitotoxic lesions of the LEC were significantly impaired, relative to controls, on both egocentric and allocentric versions of an object–place association task. Notably, LEC lesioned animals performed at chance on the egocentric version but above chance on the allocentric version. There was no significant difference in performance between the two groups on an object recognition and spatial T-maze task. Taken together, these results indicate that the LEC plays a role in feature integration more broadly and in specifically processing spatial information within an egocentric reference frame.
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Pacheco, Amanda Rossetto, Miguel Stancare Neto, Gustavo Henrique Gravatim Costa, Marcelo da Fossa Paz, and Marcos Vinicius Bohrer Monteiro Siqueira. "Desenvolvimento do amendoim-bravo (Pterogyne nitens Tul.) sob lâminas de água e composições de substratos." Journal of Biotechnology and Biodiversity 9, no. 4 (November 16, 2021): 359–68. http://dx.doi.org/10.20873/jbb.uft.cemaf.v9n4.pacheco.
Full textAbstract:
O amendoim-bravo (Pterogyne nitens Tul.) é considerado uma espécie rústica e adaptável a várias regiões do território nacional, e indicada para silvicultura, plantios em áreas degradas e reposição de matas ciliares. O objetivo deste trabalho foi avaliar o desenvolvimento das mudas de amendoim-bravo sob concentrações de lodo de esgoto compostado (LEC), substrato comercial (SC) e lâminas de água. O delineamento experimental foi composto por 240 mudas, divididas em cinco tratamentos diferentes: S1 (100% LEC), S2 (75% LEC + 25% SC), S3 (50% LEC + 50% SC), S4 (25% LEC + 75% SC) e S5 (100% SC). O experimento contou com três lâminas de irrigação, quatro vezes ao dia: L1 (6 minutos), L2 (9 minutos) e L3 (12 minutos). Foram avaliadas as seguintes características: altura da parte aérea, diâmetro do coleto, número de folhas, peso da massa seca e o Índice de Qualidade de Dickson. Os dados foram submetidos a análise de variância e as medidas comparadas pelo teste de Tukey. Tratamentos com 75% a 100% de LEC apresentaram resultados superiores nos parâmetros avaliados em relação ao SC. Para o regime hídrico, não houve influência significativa das lâminas de água sobre as características morfológicas das mudas.
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Seo, Yeon S., Jung H. Kwon, Usman Yaqoob, Liu Yang, Thiago M. De Assuncao, Douglas A. Simonetto, Vikas K. Verma, and Vijay H. Shah. "HMGB1 recruits hepatic stellate cells and liver endothelial cells to sites of ethanol-induced parenchymal cell injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 11 (December 1, 2013): G838—G848. http://dx.doi.org/10.1152/ajpgi.00151.2013.
Full textAbstract:
Hepatic stellate cells (HSC) and liver endothelial cells (LEC) migrate to sites of injury and perpetuate alcohol-induced liver injury. High-mobility group box 1 (HMGB1) is a protein released from the nucleus of injured cells that has been implicated as a proinflammatory mediator. We hypothesized that HMGB1 may be released from ethanol-stimulated liver parenchymal cells and contribute to HSC and LEC recruitment. Ethanol stimulation of rat hepatocytes and HepG2 cells resulted in translocation of HMGB1 from the nucleus as assessed by Western blot. HMGB1 protein levels were increased in the supernatant of ethanol-treated hepatocytes compared with vehicle-treated cells. Migration of both HSC and LEC was increased in response to conditioned medium for ethanol-stimulated hepatocytes (CMEtOH) compared with vehicle-stimulated hepatocytes (CMVEH) ( P < 0.05). However, the effect of CMEtOH on migration was almost entirely reversed by treatment with HMGB1-neutralizing antibody or when HepG2 cells were pretransfected with HMGB1-siRNA compared with control siRNA-transfected HepG2 cells ( P < 0.05). Recombinant HMGB1 (100 ng/ml) also stimulated migration of HSC and LEC compared with vehicle stimulation ( P < 0.05 for both HSC and LEC). HMGB1 stimulation of HSC increased the phosphorylation of Src and Erk and HMGB1-induced HSC migration was blocked by the Src inhibitor PP2 and the Erk inhibitor U0126. Hepatocytes release HMGB1 in response to ethanol with subsequent recruitment of HSC and LEC. This pathway has implications for HSC and LEC recruitment to sites of ethanol-induced liver injury.
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Ma, Wanshu, Hyea Jin Gil, Xiaolei Liu, Lauren P. Diebold, Marc A. Morgan, Michael J. Oxendine-Burns, Peng Gao, Navdeep S. Chandel, and Guillermo Oliver. "Mitochondrial respiration controls the Prox1-Vegfr3 feedback loop during lymphatic endothelial cell fate specification and maintenance." Science Advances 7, no. 18 (April 2021): eabe7359. http://dx.doi.org/10.1126/sciadv.abe7359.
Full textAbstract:
Recent findings indicate that mitochondrial respiration regulates blood endothelial cell proliferation; however, its role in differentiating lymphatic endothelial cells (LECs) is unknown. We hypothesized that mitochondria could work as a sensor of LECs’ metabolic specific needs by determining their functional requirements according to their differentiation status and local tissue microenvironment. Accordingly, we conditionally deleted the QPC subunit of mitochondrial complex III in differentiating LECs of mouse embryos. Unexpectedly, mutant mice were devoid of a lymphatic vasculature by mid-gestation, a consequence of the specific down-regulation of main LEC fate regulators, particularly Vegfr3, leading to the loss of LEC fate. Mechanistically, this is a result of reduced H3K4me3 and H3K27ac in the genomic locus of key LEC fate controllers (e.g., Vegfr3 and Prox1). Our findings indicate that by sensing the LEC differentiation status and microenvironmental metabolic conditions, mitochondrial complex III regulates the critical Prox1-Vegfr3 feedback loop and, therefore, LEC fate specification and maintenance.
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Matsubayashi, Hiroyuki, Yoshiko Aikawa, Teiichi Sugiura, Keiko Sasaki, Kinichi Hotta, and Hiroyuki Ono. "Pancreatic Lymphoepithelial Cyst Showing Multiple Floating Ball-like Appearances." Journal of Gastrointestinal and Liver Diseases 25, no. 2 (June 1, 2016): 239–42. http://dx.doi.org/10.15403/jgld.2014.1121.252.lym.
Full textAbstract:
A lymphoepithelial cyst (LEC) is a rare pancreatic lesion, histologically showing squamous epithelia, dense lymphoid tissues, and a keratin substance. Cross-section images of the pancreatic LEC typically show a well demarcated unilocular or multilocular cyst without a solid component. Here we report a rare case of pancreatic LEC in which multiple floating ball-like components were depicted via endoscopic ultrasound. The ball-like components were also depicted by various imaging methods such as computed tomography (CT) showing low-density components, T1-weighted magnetic resonance imaging (MRI) and diffusion-weighted imaging (DWI) showing high-intensity components, and T2-weighted MRI showing low-intensity components. The ball-like components in all images were not well enhanced. Laparotomic cyst resection was performed, and the surgical material revealed keratin balls inside the pancreatic LEC. Keratin components of a pancreatic LEC can take a liquid, sludge, or solid form. Clinicians must be aware of the variations in imaging to facilitate the differentiation and management of pancreatic cystic lesions.
Abbreviations: CA 19-9: carbohydrate antigen 19-9; CEA: carcinoembryonic antigen; DWI: diffusion-weighted image; LEC: lymphoepithelial cyst; IPMN: intraductal papillary neoplasm; MCN: mucinous cystic neoplasm.
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East, Brett S., Lauren R. Brady, and Jennifer J. Quinn. "Differential Effects of Lateral and Medial Entorhinal Cortex Lesions on Trace, Delay and Contextual Fear Memories." Brain Sciences 12, no. 1 (December 28, 2021): 34. http://dx.doi.org/10.3390/brainsci12010034.
Full textAbstract:
The entorhinal cortex (EC), with connections to the hippocampus, amygdala, and neocortex, is a critical, yet still underexplored, contributor to fear memory. Previous research suggests possible heterogeneity of function among its lateral (LEC) and medial (MEC) subregions. However, it is not well established what unique roles these subregions serve as the literature has shown mixed results depending on target of manipulation and type of conditioning used. Few studies have manipulated both the LEC and MEC within the same experiment. The present experiment systematically manipulated LEC and MEC function to examine their potential roles in fear memory expression. Long-Evans rats were trained using either trace or delay fear conditioning. The following day, rats received an N-methyl-D-aspartate (NMDA)-induced lesion to the LEC or MEC or received a sham surgery. Following recovery, rats were given an 8-min context test in the original context. The next day, rats were tested for tone freezing in a novel context with three discrete tone presentations. Further, rats were tested for hyperactivity in an open field under both dark and bright light gradient conditions. Results: Following either LEC or MEC lesion, freezing to context was significantly reduced in both trace and delay conditioned rats. LEC-lesioned rats consistently showed significantly less freezing following tone-offset (trace interval, or equivalent, and intertrial interval) in both trace and delay fear conditioned rats. Conclusions: These data suggest that the LEC may play a role in the expression of a conjunctive representation between the tone and context that mediates the maintenance of post-tone freezing.
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Gavrilovskaya, Irina N., Elena E. Gorbunova, and Erich R. Mackow. "Andes Virus Infection of Lymphatic Endothelial Cells Causes Giant Cell and Enhanced Permeability Responses That Are Rapamycin and Vascular Endothelial Growth Factor C Sensitive." Journal of Virology 86, no. 16 (June 13, 2012): 8765–72. http://dx.doi.org/10.1128/jvi.00817-12.
Full textAbstract:
Hantaviruses primarily infect endothelial cells (ECs) and nonlytically cause vascular changes that result in hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Acute pulmonary edema during HPS may be caused by capillary leakage and failure of lymphatic vessels to clear fluids. Uniquely regulated lymphatic ECs (LECs) control fluid clearance, although roles for lymphatics in hantavirus disease remain undetermined. Here we report that hantaviruses productively infect LECs and that LEC infection by HPS causing Andes virus (ANDV) and HFRS causing Hantaan virus (HTNV) are inhibited by αvβ3integrin antibodies. Although αvβ3integrins regulate permeabilizing responses directed by vascular endothelial growth factor receptor 2 (VEGFR2), we found that only ANDV-infected LECs were hyperpermeabilized by the addition of VEGF-A. However, VEGF-C activation of LEC-specific VEGFR3 receptors blocked ANDV- and VEGF-A-induced LEC permeability. In addition, ∼75% of ANDV-infected LECs became viable mononuclear giant cells, >4 times larger than normal, in response to VEGF-A. Giant cells are associated with constitutive mammalian target of rapamycin (mTOR) activation, and we found that both giant LECs and LEC permeability were sensitive to rapamycin, an mTOR inhibitor, and VEGF-C addition. These findings indicate that ANDV uniquely alters VEGFR2-mTOR signaling responses of LECs, resulting in giant cell and LEC permeability responses. This suggests that ANDV infection alters normal LEC and lymphatic vessel functions which may contribute to edematous fluid accumulation during HPS. Moreover, the ability of VEGF-C and rapamycin to normalize LEC responses suggests a potential therapeutic approach for reducing pulmonary edema and the severity of HPS following ANDV infection.
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Emfietzoglou, Rodopi, Efstathios Pettas, Maria Georgaki, Erofili Papadopoulou, Vasileios Ionas Theofilou, Nikolaos Papadogeorgakis, Evangelia Piperi, Marcio Ajudarte Lopes, and Nikolaos G. Nikitakis. "Lymphoepithelial Subtype of Oral Squamous Cell Carcinoma: Report of an EBV-Negative Case and Literature Review." Dentistry Journal 10, no. 9 (September 5, 2022): 165. http://dx.doi.org/10.3390/dj10090165.
Full textAbstract:
Lymphoepithelial carcinoma (LEC) of the oral mucosa is a rare histopathologic subtype of squamous cell carcinoma (SCC), which shares morphologic similarities with nasopharyngeal carcinoma (NPC), non-keratinizing undifferentiated subtype. The admixture of neoplastic epithelial tumor cells and a dense lymphoplasmacytic infiltrate makes microscopic diagnosis challenging. LEC etiopathogenesis has been variably associated with Epstein–Barr virus (EBV) infection, depending on the specific anatomic location and racial predilection, with a higher incidence in endemic populations. Although described in several subsites of the head and neck region, including the major salivary glands, the oral mucosa is considered an infrequent location for LEC development, deriving either from minor salivary glands (MSGs) or the surface epithelium. Herein, we report a rare case of an EBV-negative LEC arising from the oral surface epithelium, presenting as gingival swelling, and review the pertinent English-language literature, which revealed only 26 previously reported oral LECs. Our case is only the fourth oral LEC originating from the surface epithelium and the first one to affect the gingiva.
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Chen, Jia-Mei, Bo Luo, Ru Ma, Xi-Xi Luo, Yong-Shun Chen, and Yan Li. "Lymphatic Endothelial Markers and Tumor Lymphangiogenesis Assessment in Human Breast Cancer." Diagnostics 12, no. 1 (December 21, 2021): 4. http://dx.doi.org/10.3390/diagnostics12010004.
Full textAbstract:
Metastasis via lymphatic vessels or blood vessels is the leading cause of death for breast cancer, and lymphangiogenesis and angiogenesis are critical prerequisites for the tumor invasion–metastasis cascade. The research progress for tumor lymphangiogenesis has tended to lag behind that for angiogenesis due to the lack of specific markers. With the discovery of lymphatic endothelial cell (LEC) markers, growing evidence demonstrates that the LEC plays an active role in lymphatic formation and remodeling, tumor cell growth, invasion and intravasation, tumor–microenvironment remodeling, and antitumor immunity. However, some studies have drawn controversial conclusions due to the variation in the LEC markers and lymphangiogenesis assessments used. In this study, we review recent findings on tumor lymphangiogenesis, the most commonly used LEC markers, and parameters for lymphangiogenesis assessments, such as the lymphatic vessel density and lymphatic vessel invasion in human breast cancer. An in-depth understanding of tumor lymphangiogenesis and LEC markers can help to illustrate the mechanisms and distinct roles of lymphangiogenesis in breast cancer progression, which will help in exploring novel potential predictive biomarkers and therapeutic targets for breast cancer.
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Cardier, José E., and Jack Dempsey. "Thrombopoietin and Its Receptor, c-mpl, Are Constitutively Expressed by Mouse Liver Endothelial Cells: Evidence of Thrombopoietin as a Growth Factor for Liver Endothelial Cells." Blood 91, no. 3 (February 1, 1998): 923–29. http://dx.doi.org/10.1182/blood.v91.3.923.
Full textAbstract:
Abstract Present data suggest that the primary site of thrombopoietin (TPO) mRNA is the liver. Previously, we reported that specific murine liver endothelial cells (LEC-1) located in the hepatic sinusoids support in vitro megakaryocytopoiesis from murine hematopoietic stem cells suggesting that these cells may be a source of TPO. We report here that TPO and its receptor, c-mpl, are coexpressed on cloned LEC-1. Enzyme-linked immunosorbent assay (ELISA), biological assay, and flow cytometry studies confirmed the expression of both TPO and its receptor, respectively, at the protein level. TPO activity was enhanced in supernatants from LEC-1 treated with tumor necrosis factor (TNF)-α and γ-interferon (INF). Our results show that TPO through its receptor stimulated the growth of LEC-1 in vitro. These observations establish LEC-1 as a novel source of TPO in the liver. To our knowledge, this is the first report that liver endothelial cells express both TPO and its receptor, c-mpl, and our findings indicate that this cytokine constitutes a growth factor for liver endothelial cells in vitro.
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Cardier, José E., and Jack Dempsey. "Thrombopoietin and Its Receptor, c-mpl, Are Constitutively Expressed by Mouse Liver Endothelial Cells: Evidence of Thrombopoietin as a Growth Factor for Liver Endothelial Cells." Blood 91, no. 3 (February 1, 1998): 923–29. http://dx.doi.org/10.1182/blood.v91.3.923.923_923_929.
Full textAbstract:
Present data suggest that the primary site of thrombopoietin (TPO) mRNA is the liver. Previously, we reported that specific murine liver endothelial cells (LEC-1) located in the hepatic sinusoids support in vitro megakaryocytopoiesis from murine hematopoietic stem cells suggesting that these cells may be a source of TPO. We report here that TPO and its receptor, c-mpl, are coexpressed on cloned LEC-1. Enzyme-linked immunosorbent assay (ELISA), biological assay, and flow cytometry studies confirmed the expression of both TPO and its receptor, respectively, at the protein level. TPO activity was enhanced in supernatants from LEC-1 treated with tumor necrosis factor (TNF)-α and γ-interferon (INF). Our results show that TPO through its receptor stimulated the growth of LEC-1 in vitro. These observations establish LEC-1 as a novel source of TPO in the liver. To our knowledge, this is the first report that liver endothelial cells express both TPO and its receptor, c-mpl, and our findings indicate that this cytokine constitutes a growth factor for liver endothelial cells in vitro.
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Wright, A., and S. L. Morrison. "Effect of altered CH2-associated carbohydrate structure on the functional properties and in vivo fate of chimeric mouse-human immunoglobulin G1." Journal of Experimental Medicine 180, no. 3 (September 1, 1994): 1087–96. http://dx.doi.org/10.1084/jem.180.3.1087.
Full textAbstract:
Immunoglobulin G (IgG) molecules are glycosylated in CH2 at Asn297; the N-linked carbohydrates attached there have been shown to contribute to antibody (Ab) stability and various effector functions. The carbohydrate attached to the IgG constant region is a complex biantennary structure. Alterations in the structure of oligosaccharide have been associated with human diseases such as rheumatoid arthritis and osteoarthritis. To study the effects of altered carbohydrate structure on Ab effector function, we have used gene transfection techniques to produce mouse-human chimeric IgG1 Abs in the Chinese hamster ovary (CHO) cell line Lec 1, which is incapable of processing the high-mannose intermediate through the terminal glycosylation steps. We also produced IgG1 Abs in Pro-5, the wild-type CHO cell line that is the parent of Lec 1. The Pro-5-produced Ab (IgG1-Pro-5) was similar to IgG1-My 1, a myeloma-produced IgG1 Ab of the same specificity, in its biologic properties such as serum half-life, ability to effect complement-mediated cytolysis, and affinity for Fc gamma RI. Although the Lec 1-produced Ab, IgG1-Lec 1, was properly assembled and retained antigen specificity, it was incapable of complement-mediated hemolysis and was substantially deficient in complement consumption, C1q binding, and C1 activation. IgG1-Lec 1 also showed reduced but significant affinity for Fc gamma R1 receptors. The in vivo half-life of IgG1-Lec 1 was shorter than that of either the myeloma- or Pro-5-produced counterpart, with more being cleared during the alpha-phase and with more rapid clearance during the beta-phase. Clearance of IgG1-Lec 1 could be inhibited by the administration of yeast-derived mannan. Thus the uptake of IgG1-Lec 1 appears to be accelerated by the presence of terminally mannosylated oligosaccharide. Therefore, certain Ab functions as well as the in vivo fate of the protein are dramatically affected by altered carbohydrate structure. Expression of Igs in cell lines with defined glycosylation mutations is shown to be a useful technique for investigating the contribution of carbohydrate structure to Ab function.
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Nemoto-Sasaki, Yoko, Ko Hayama, Hiroyuki Ohya, Yoichiro Arata, Mika Kato Kaneko, Naruya Saitou, Jun Hirabayashi, and Ken-ichi Kasai. "Caenorhabditis elegans galectins LEC-1–LEC-11: Structural features and sugar-binding properties." Biochimica et Biophysica Acta (BBA) - General Subjects 1780, no. 10 (October 2008): 1131–42. http://dx.doi.org/10.1016/j.bbagen.2008.07.003.
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Arumugam, Prabhu, Natalie Fletcher, Charis Kyriakides, Lisa Mears, and Hemant M. Kocher. "Lymphoepithelial Cyst of the Pancreas." Case Reports in Gastroenterology 10, no. 1 (May 19, 2016): 186–97. http://dx.doi.org/10.1159/000445373.
Full textAbstract:
Lymphoepithelial cyst (LEC) of the pancreas is an extremely rare, benign pancreatic cystic lesion that is difficult to differentiate preoperatively from other cystic pancreatic lesions. LEC may have malignant potential. Here, we describe a case of LEC of the pancreas – initially suspected to be a mucinous cyst neoplasm – in an elderly man presenting with abdominal pain, who went on to have a distal pancreatectomy and splenectomy. We also review the relevant literature and discuss implications for the diagnosis and management of this rare lesion.
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Manning, G., L. G. Fuller, R. G. Eilers, and I. Florinsky. "Soil moisture and nutrient variation within an undulating Manitoba landscape." Canadian Journal of Soil Science 81, no. 4 (August 1, 2001): 449–58. http://dx.doi.org/10.4141/s00-058.
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The use of discrete management units for variable-rate N fertilization requires that factors influencing grain yield response to N fertilizer are adequately characterized by delineating landscapes into such management units. The objective of this study was to compare the use of topographically derived landform element complexes (LEC) and the use of individual soil series as management units. Soil volumetric moisture content, nitrate-N, exchangeable ammonium-N, extractable phosphorus, exchangeable potassium, and sulphate-sulphur were studied in 10 intensively sampled transects in an undulating glacial till landscape near Miniota, Manitoba. The study site was delineated into upper, mid and lower LEC using a digital elevation model derived from relative elevation data. The LEC were useful in capturing gross variability at a manageable landscape scale. Among LEC there was a general trend of lower > mid > upper for median values of soil moisture, nitrate, phosphate, potassium and sulphate, as these attributes generally increased with convergent landscape character. Differences among LEC were often statistically significant, and relative distributions exhibited temporal persistence. The site was also stratified by soil series, including Newdale, Varcoe and Angusville soils (Black Chernozems), which were identified by examination of individual soil cores at each sample point. Stratifying the site into management units using soil genetic information, which is reflective of historical moisture conditions and biomass production, was expected to be superior. There was little advantage, however, in using soil series rather than LEC. Spatial distributions of the most agronomically relevant attributes (soil moisture and nitrate) were expressed at a landscape scale broader than that at which soil series occurred within the site. While there were important differences among soil series with respect to nutrients such as phosphate and sulphate, the site was better stratified by LEC with respect to soil moisture and nitrate. Key words: Soil-landscape, soil series, soil moisture, soil residual nitrate, extractable phosphorus
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Kawai, Yoshiko, Yumiko Yokoyama, Maki Kaidoh, and Toshio Ohhashi. "Shear stress-induced ATP-mediated endothelial constitutive nitric oxide synthase expression in human lymphatic endothelial cells." American Journal of Physiology-Cell Physiology 298, no. 3 (March 2010): C647—C655. http://dx.doi.org/10.1152/ajpcell.00249.2009.
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To clarify the roles of lymphatic endothelial cells (LEC) in the regulation of endothelial constitutive nitric oxide synthase (ecNOS) expression, we examined the effects of shear stress on ecNOS immunohistochemical staining and mRNA and protein expression in human LEC as well as on ATP release from these cells. Shear stress at 0.5 or 1.0 dyn/cm2 increased ecNOS immunohistochemical staining and ecNOS mRNA and protein expression in cultured LEC. The same strength of shear stress produced a significant release of ATP from the LEC. Exogenous ATP ranging in concentration from 10−9 to 10−6 M produced a significant increase in ecNOS immunohistochemical expression in a dose-dependent manner. The increase in ecNOS expression mediated by 10−6M ATP was significantly reduced by 10−5 M suramin. Suramin (10−5 M) caused a significant reduction in the shear stress-mediated increases in ecNOS immunohistochemical staining and mRNA expression. The shear stress-mediated increases in ecNOS expression were significantly reduced by 3 mM tetraethylammonium, 10−4 M apamin, 10−9 M iberiotoxin, 10−5 M 2-aminoethoxydephenyl borate, or 10−5M xestospongin C, but not 10−5 M glybenclamide or 10−5 M nifedipine. The shear stress-mediated increases in ecNOS expression were significantly potentiated by pinacidil or NS1619 in a dose-dependent manner. The immunohistochemical expression of small- (SKCa) and big-conductance (BKCa) Ca2+-activated K+ channels was confirmed on the surfaces of human LEC. These findings suggest that shear stress produces a significant release of ATP from LEC, which activates the purinergic P2X/2Y receptor, thereby facilitating ecNOS mRNA and protein expression through inositol 1,4,5-trisphosphate-mediated release of intracellular Ca2+ ions and the activation of Ca2+-activated K+ channels in LEC.
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Piao, Wenji, Lushen Li, vikas saxena, Keli Hippen, Blazar Bruce, Leonardo Riella, and jonathan bromberg. "PD-1 licenses activated Treg for lymphatic migration." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 105.04. http://dx.doi.org/10.4049/jimmunol.208.supp.105.04.
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Abstract Rather than serving as fluid transport conduits, the lymphatic vessels have been proved to be critical portals for immune cell migration. As non-immune cell, the lymphatic endothelial cell (LEC) constitutively express high level of programmed death-1 (PD-1) ligand (PD-L1), known as an immune checkpoint protein. We hypothesized that LECs use PD-L1 to regulate PD-1-expressing immune cells during transendothelial migration (TEM). Activated T cells expressed substantially elevated levels of both PD-1 and PD-L1. For human and mouse Tregs PD-1 was in excess of PD-L1, while effector CD4 T cells (Teffs) expressed PD-L1 in excess of PD-1. PD-1−/− but not PD-L1−/− Tregs had reduced migration and motility compared to WT. Engagement by PD-L1 Fc induced rapid activation of Akt but suppressed classical NFkB-P65 signaling in Tregs. WT LECs constitutively expressed high level of surface PD-L1. PD-L1−/− LEC or lymphatic vessels (LV) had increased adhesion and junction proteins VCAM-1 and zonulin-1, and had more zipper junctions. PD-1 triggered PD-L1 signaling in LEC result in strong PI3K/Akt and NFkB-p65 responses that regulated endothelial structure and enhanced TEM. Similar changes to LEC junctions were observed when PD-1high Tregs migrated across LEC layers, resulting in rapidly induced NFkB-p65 translocation into the LEC nucleus. PD-1-induced PD-L1 signaling decreased VE-cadherin expression, which was restored by blocking ERK and PI3K/Akt. Importantly, PD-1-blockade of intra-tumoral Tregs reduced tumor egress and the detained Tregs converted to IFN-g-producing Th1Tregs. These data demonstrate novel roles for Treg PD-1 and LEC PD-L1 in regulation of lymphatic migration and ultimately Treg suppressive function. Supported by grants from NIH (2R37AI062765-17A1)
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Mehta, Padmaja, Kamala D. Patel, Thomas M. Laue, Harold P. Erickson, and Rodger P. McEver. "Soluble Monomeric P-Selectin Containing Only the Lectin and Epidermal Growth Factor Domains Binds to P-Selectin Glycoprotein Ligand-1 on Leukocytes." Blood 90, no. 6 (September 15, 1997): 2381–89. http://dx.doi.org/10.1182/blood.v90.6.2381.
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Abstract Under shear stress, leukocytes use P-selectin glycoprotein ligand-1 (PSGL-1) to tether to and roll on P-selectin expressed on activated platelets or endothelial cells. P-selectin has an NH2-terminal lectin domain, an epidermal growth factor (EGF)-like motif, nine consensus repeats (CRs), a transmembrane domain, and a cytoplasmic tail. To determine whether the CRs are required for P-selectin to bind PSGL-1, we expressed a soluble protein (Lec-EGF) that contained only the lectin and EGF domains, plus a short C-terminal epitope tag. Electron microscopy and hydrodynamic analysis confirmed that Lec-EGF was monomeric, as previously shown for soluble P-selectin (sPS) that contained the lectin and EGF domains plus all nine CRs. Fluid-phase Lec-EGF or sPS inhibited binding of oligomeric125I-labeled membrane-derived P-selectin (mPS) to PSGL-1 on neutrophils and binding of 125I-PSGL-1 to immobilized mPS. The IC50 for inhibiting binding of mPS to neutrophils was fivefold greater for Lec-EGF than for sPS, whereas the IC50 for inhibiting binding of mPS to purified PSGL-1 was indistinguishable for Lec-EGF and sPS. Under static or shear conditions, neutrophils used PSGL-1 to tether to or roll on Lec-EGF that was captured by an immobilized monoclonal antibody to the C-terminal epitope. These data show that P-selectin requires only the lectin and EGF domains to bind to PSGL-1.
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Mehta, Padmaja, Kamala D. Patel, Thomas M. Laue, Harold P. Erickson, and Rodger P. McEver. "Soluble Monomeric P-Selectin Containing Only the Lectin and Epidermal Growth Factor Domains Binds to P-Selectin Glycoprotein Ligand-1 on Leukocytes." Blood 90, no. 6 (September 15, 1997): 2381–89. http://dx.doi.org/10.1182/blood.v90.6.2381.2381_2381_2389.
Full textAbstract:
Under shear stress, leukocytes use P-selectin glycoprotein ligand-1 (PSGL-1) to tether to and roll on P-selectin expressed on activated platelets or endothelial cells. P-selectin has an NH2-terminal lectin domain, an epidermal growth factor (EGF)-like motif, nine consensus repeats (CRs), a transmembrane domain, and a cytoplasmic tail. To determine whether the CRs are required for P-selectin to bind PSGL-1, we expressed a soluble protein (Lec-EGF) that contained only the lectin and EGF domains, plus a short C-terminal epitope tag. Electron microscopy and hydrodynamic analysis confirmed that Lec-EGF was monomeric, as previously shown for soluble P-selectin (sPS) that contained the lectin and EGF domains plus all nine CRs. Fluid-phase Lec-EGF or sPS inhibited binding of oligomeric125I-labeled membrane-derived P-selectin (mPS) to PSGL-1 on neutrophils and binding of 125I-PSGL-1 to immobilized mPS. The IC50 for inhibiting binding of mPS to neutrophils was fivefold greater for Lec-EGF than for sPS, whereas the IC50 for inhibiting binding of mPS to purified PSGL-1 was indistinguishable for Lec-EGF and sPS. Under static or shear conditions, neutrophils used PSGL-1 to tether to or roll on Lec-EGF that was captured by an immobilized monoclonal antibody to the C-terminal epitope. These data show that P-selectin requires only the lectin and EGF domains to bind to PSGL-1.
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Dobrochaeva, Kira, Nailya Khasbiullina, Nadezhda Shilova, Nadezhda Antipova, Polina Obukhova, Oxana Galanina, Mikhail Gorbach, et al. "Human Natural Antibodies Recognizing Glycan Galβ1-3GlcNAc (LeC)." International Journal of Molecular Sciences 21, no. 18 (September 5, 2020): 6511. http://dx.doi.org/10.3390/ijms21186511.
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The level of human natural antibodies of immunoglobulin M isotype against LeC in patients with breast cancer is lower than in healthy women. The epitope specificity of these antibodies has been characterized using a printed glycan array and enzyme-linked immunosorbent assay (ELISA), the antibodies being isolated from donors’ blood using LeC-Sepharose (LeC is Galβ1-3GlcNAcβ). The isolated antibodies recognize the disaccharide but do not bind to glycans terminated with LeC, which implies the impossibility of binding to regular glycoproteins of non-malignant cells. The avidity (as dissociation constant value) of antibodies probed with a multivalent disaccharide is 10−9 M; the nanomolar level indicates that the concentration is sufficient for physiological binding to the cognate antigen. Testing of several breast cancer cell lines showed the strongest binding to ZR 75-1. Interestingly, only 7% of the cells were positive in a monolayer with a low density, increasing up to 96% at highest density. The enhanced interaction (instead of the expected inhibition) of antibodies with ZR 75-1 cells in the presence of Galβ1-3GlcNAcβ disaccharide, indicates that the target epitope of anti-LeC antibodies is a molecular pattern with a carbohydrate constituent rather than a glycan.
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Jiang, Shuguang, Alexis S. Bailey, John R. Swain, Erin M. Hewett, Melissa H. Wong, Philip R. Streeter, and William H. Fleming. "Hematopoietic Stem Cells Contribute to Lymphatic Endothelium." Blood 108, no. 11 (November 16, 2006): 1658. http://dx.doi.org/10.1182/blood.v108.11.1658.1658.
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Abstract The lymphatic system plays an important physiological role in vascular and immune homeostasis. Lymphatic vessel function is implicated in a number of pathological conditions including tumor metastasis and impaired wound healing. The identity and origin of lymphatic endothelial precursors is poorly understood. Previously we have shown that adult bone marrow-derived, hematopoietic stem cells (HSCs, c-kit+, Sca-1+, lineage−) can differentiate into functional blood vascular endothelial cells. Given the close relationship between the blood and lymphatic vascular systems, we have investigated whether HSCs also give rise to lymphatic endothelial cells (LEC). GFP+ HSCs were transplanted into lethally irradiated (1200 cGy) recipient mice. Donor-derived LEC expressing lymphatic endothelial markers including LYVE-1 and VEGFR3 were clearly distinguished from hematopoietic cells by the absence of CD45 and F4/80 expression. Deconvolution microscopy confirmed the co-localization of donor and LEC marker expression in individual cells. Transplanted HSCs gave rise to LEC in the liver, gut, gastric and kidney. Donor-derived LEC were detected in 2.4% of liver lymphatic vessels at 4 weeks and persisted for at least 12 months (mean of 3.4%). The self-renewal capacity of HSC-derived lymphatic progenitor cells was demonstrated by serial transplantation. The contribution of these progenitors to tumor lymphatics was evaluated. Transplantation of HSCs into young Min−/− mice resulted in the incorporation of donor-derived LEC into the lymphatics of intestinal adenomas that spontaneously develop in these mice. In addition, CD45+F4/80+ leukocytes were detected in the vessel lumens indicating that these are functional tumor lymphatic vessels. Finally, to determine if LEC progenitors contribute to lymphatic vessels in the absence of radiation injury or tumorigenesis, a parabiosis model was evaluated. Donor-derived LEC were detected in parabiotic mice at a frequency similar to that observed for donor-derived blood vascular endothelial cells. This finding suggests that circulating progenitor cells contribute to lymphangiogenesis during steady-state conditions. Our results indicate that hematopoietic stem cells have the potential to contribute to lymphatic endothelium and therefore HSC-derived progenitors may be potential therapeutic targets for hematopoietic and lymphatic disease.
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Evans, Colin E. "Hypoxia-Inducible Factor Signaling in Inflammatory Lung Injury and Repair." Cells 11, no. 2 (January 6, 2022): 183. http://dx.doi.org/10.3390/cells11020183.
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Inflammatory lung injury is characterized by lung endothelial cell (LEC) death, alveolar epithelial cell (AEC) death, LEC–LEC junction weakening, and leukocyte infiltration, which together disrupt nutrient and oxygen transport. Subsequently, lung vascular repair is characterized by LEC and AEC regeneration and LEC–LEC junction re-annealing, which restores nutrient and oxygen delivery to the injured tissue. Pulmonary hypoxia is a characteristic feature of several inflammatory lung conditions, including acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and severe coronavirus disease 2019 (COVID-19). The vascular response to hypoxia is controlled primarily by the hypoxia-inducible transcription factors (HIFs) 1 and 2. These transcription factors control the expression of a wide variety of target genes, which in turn mediate key pathophysiological processes including cell survival, differentiation, migration, and proliferation. HIF signaling in pulmonary cell types such as LECs and AECs, as well as infiltrating leukocytes, tightly regulates inflammatory lung injury and repair, in a manner that is dependent upon HIF isoform, cell type, and injury stimulus. The aim of this review is to describe the HIF-dependent regulation of inflammatory lung injury and vascular repair. The review will also discuss potential areas for future study and highlight putative targets for inflammatory lung conditions such as ALI/ARDS and severe COVID-19. In the development of HIF-targeted therapies to reduce inflammatory lung injury and/or enhance pulmonary vascular repair, it will be vital to consider HIF isoform- and cell-specificity, off-target side-effects, and the timing and delivery strategy of the therapeutic intervention.
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Irwin, D. C., M. C. Tissot van Patot, A. Tucker, and R. Bowen. "Direct ANP inhibition of hypoxia-induced inflammatory pathways in pulmonary microvascular and macrovascular endothelial monolayers." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 5 (May 2005): L849—L859. http://dx.doi.org/10.1152/ajplung.00294.2004.
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Atrial natriuretic peptide (ANP) has been shown to reduce hypoxia-induced pulmonary vascular leak in vivo, but no explanation of a mechanism has been offered other than its vasodilatory and natriuretic actions. Recently, data have shown that ANP can protect endothelial barrier functions in TNF-α-stimulated human umbilical vein endothelial cells. Therefore, we hypothesized that ANP actions would inhibit pulmonary vascular leak by inhibition of TNF-α secretion and F-actin formation. Bovine pulmonary microvascular (MVEC) and macrovascular endothelial cell (LEC) monolayers were stimulated with hypoxia, TNF-α, or bacterial endotoxin (LPS) in the presence or absence of ANP, and albumin flux, NF-κB activation, TNF-α secretion, p38 mitogen-activated protein kinase (MAPK), and F-actin (stress fiber) formation were assessed. In Transwell cultures, ANP reduced hypoxia-induced permeability in MVEC and TNF-α-induced permeability in MVEC and LEC. ANP inhibited hypoxia and LPS increased NF-κB activation and TNF-α synthesis in MVEC and LEC. Hypoxia decreased activation of p38 MAPK in MVEC but increased activation of p38 MAPK and stress fiber formation in LEC; TNF-α had the opposite effect. ANP inhibited an activation of p38 MAPK in MVEC or LEC. These data indicate that in endothelial cell monolayers, hypoxia activates a signal cascade analogous to that initiated by inflammatory agents, and ANP has a direct cytoprotective effect on the pulmonary endothelium other than its vasodilatory and natriuretic properties. Furthermore, our data show that MVEC and LEC respond differently to hypoxia, TNF-α-stimulation, and ANP treatment.
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Dolka, Izabella, Marek Tomaszewski, Daria Wola, Michał Czopowicz, and Jarosław Kaba. "Lymphoepithelial Cyst of the Salivary Gland in a Small Ruminant Lentivirus-Positive Goat." Animals 10, no. 9 (September 1, 2020): 1545. http://dx.doi.org/10.3390/ani10091545.
Full textAbstract:
The lymphoepithelial cyst (LEC) of the major salivary gland is a rare lesion described in medical literature. It is found in human immunodeficiency virus (HIV)-infected patients and considered an early manifestation of this infection. Despite the variety of theories, the origin of this lesion remains controversial. No veterinary studies on LEC have been published so far. This study is the first-ever that aims to describe histopathological, histochemical, and immunohistochemical features of a LEC located adjacent to the salivary gland of a goat. The goat proved seropositive for the small ruminant lentivirus, showed clinical signs of caprine arthritis-encephalitis, and had caprine arthritis-encephalitis virus (CAEV)-infected cells in the lung. The histopathology revealed a cystic lesion lined mainly with squamous epithelium surrounded by a lymphoid component, containing a mucus-negative material and a few nonbirefringent structures corresponding to amylase crystalloids. Using immunohistochemistry, CAEV-positive cells were detected in macrophages, LEC epithelial cells, and the salivary gland. The B cells were mainly in the germinal centres, the intraepithelial lymphocytes expressed CD3 and Bcl-2, and the proliferative activity was low. This study showed that LEC had many similar histological and immunohistochemical features to those seen in humans. However, further studies are required in this respect.