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Journal articles on the topic 'Minnie Mouse'

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Published: 4 June 2021

Last updated: 5 February 2022

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1

Lavitt, Melissa R. "From Pippi Longstockings to Minnie Mouse: Reexamining Theories of Female Development." Journal of Baccalaureate Social Work 3, no. 1 (October 1, 1997): 17–30. http://dx.doi.org/10.18084/1084-7219.3.1.17.

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An awareness of the influence of sexism on the lives of women is typically evident in social work teaching and practice. The growth of scholarship on female psychological development makes fostering this awareness easier. This paper cautions against wholesale incorporation of the research findings on adolescent girls into the classroom or agency. Without such consideration, we are in danger of pathologizing female experience at adolescence, ignoring the concerns of younger girls, and decontextualizing human development. The feisty, self-assured nineyear-old Pippi Longstockings may not be an accurate picture just as the tentative 16-year-old Minnie Mouse may be limited in its generalizability. One must be cautious in claiming to discover yet another female problem. This paper summarizes and critically analyzes the current body of research; philosophical, theoretical and methodological concerns are described. Finally, recommendations for using the research in this area are outlined.

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Álvarez-Carrión, Luis, Irene Gutiérrez-Rojas, María Rosario Rodríguez-Ramos, Juan A. Ardura, and Verónica Alonso. "MINDIN Exerts Protumorigenic Actions on Primary Prostate Tumors via Downregulation of the Scaffold Protein NHERF-1." Cancers 13, no. 3 (January 24, 2021): 436. http://dx.doi.org/10.3390/cancers13030436.

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Advanced prostate cancer preferential metastasis to bone is associated with osteomimicry. MINDIN is a secreted matrix protein upregulated in prostate tumors that overexpresses bone-related genes during prostate cancer progression. Na+/H+ exchanger regulatory factor (NHERF-1) is a scaffold protein that has been involved both in tumor regulation and osteogenesis. We hypothesize that NHERF-1 modulation is a mechanism used by MINDIN to promote prostate cancer progression. We analyzed the expression of NHERF-1 and MINDIN in human prostate samples and in a premetastatic prostate cancer mouse model, based on the implantation of prostate adenocarcinoma TRAMP-C1 (transgenic adenocarcinoma of the mouse prostate) cells in immunocompetent C57BL/6 mice. The relationship between NHERF-1 and MINDIN and their effects on cell proliferation, migration, survival and osteomimicry were evaluated. Upregulation of MINDIN and downregulation of NHERF-1 expression were observed both in human prostate cancer samples and in the TRAMP-C1 model. MINDIN silencing restored NHERF-1 expression to control levels in the mouse model. Stimulation with MINDIN reduced NHERF-1 expression and triggered its mobilization from the plasma membrane to the cytoplasm in TRAMP-C1 cells. MINDIN-dependent downregulation of NHERF-1 promoted tumor cell migration and proliferation without affecting osteomimicry and adhesion. We propose that MINDIN downregulates NHERF-1 expression leading to promotion of processes involved in prostate cancer progression.

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3

Rambaruth, Neela, Sabine Jégouzo, Hayley Marlor, Maureen Taylor, and Kurt Drickamer. "Mouse Mincle: Characterization as a Model for Human Mincle and Evolutionary Implications." Molecules 20, no. 4 (April 15, 2015): 6670–82. http://dx.doi.org/10.3390/molecules20046670.

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4

van der Peet, Phillip L., Christian Gunawan, Shota Torigoe, Sho Yamasaki, and Spencer J. Williams. "Corynomycolic acid-containing glycolipids signal through the pattern recognition receptor Mincle." Chemical Communications 51, no. 24 (2015): 5100–5103. http://dx.doi.org/10.1039/c5cc00085h.

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Glucose monocorynomycolate is revealed to signal through both mouse and human Mincle. Glycerol monocorynomycolate is shown to selectively signal through human Mincle, with the activity residing predominantly in the 2′S-isomer.

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5

Shah, Sayali, Masahiro Nagata, Sho Yamasaki, and Spencer J. Williams. "Total synthesis of a cyclopropane-fatty acid α-glucosyl diglyceride from Lactobacillus plantarum and identification of its ability to signal through Mincle." Chemical Communications 52, no. 72 (2016): 10902–5. http://dx.doi.org/10.1039/c6cc05631h.

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6

Ardura, Juan A., Irene Gutiérrez-Rojas, Luis Álvarez-Carrión, M. Rosario Rodríguez-Ramos, José M. Pozuelo, and Verónica Alonso. "The secreted matrix protein mindin increases prostate tumor progression and tumor-bone crosstalk via ERK 1/2 regulation." Carcinogenesis 40, no. 7 (June 5, 2019): 828–39. http://dx.doi.org/10.1093/carcin/bgz105.

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Abstract Advanced prostate cancer cells preferentially metastasize to bone by acquiring a bone phenotype that allows metastatic cells to thrive in the skeletal environment. Identification of factors that promote the expression of ectopic bone genes—process known as osteomimicry—leading to tumor progression is crucial to prevent and treat metastatic prostate cancer and prolong life expectancy for patients. Here, we identify the extracelular matrix protein mindin in the secretome of prostate adenocarcinoma cells and show that mindin overexpression in human and mouse TRAMP-C1-induced prostate tumors correlates with upregulated levels of bone-related genes in the tumorigenic prostate tissues. Moreover, mindin silencing decreased osteomimicry in adenocarcinoma cells and in the prostate tumor mice model, as well as reduced tumor cell proliferation, migration and adhesion to bone cells. Inhibition of the extracellular signal-regulated kinase 1/2 (ERK 1/2) phosphorylation decreased the proliferative, migratory and pro-adhesion actions of mindin on prostate tumor cells. In addition, conditioned media obtained by crosstalk stimulation of either osteocytes or osteoblasts with the secretome of TRAMP-C1 cells promoted osteomimicry in prostate tumor cells; an effect inhibited by mindin silencing of TRAMP-C1 cells. In vivo, tibiae of primary tumor-bearing mice overexpressed the pro-angiogenic and pro-metastattic factor vascular endothelial growth factor receptor 2 (VEGFR2) in a mindin-dependent manner. Our findings indicate that mindin is a novel regulator of osteomimicry in prostate tumors and potentially mediates tumor-bone cell crosstalk, suggesting its promising role as a target to inhibit bone metastases.

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Bugarcic, A., K. Hitchens, A. G. Beckhouse, C. A. Wells, R. B. Ashman, and H. Blanchard. "Human and mouse macrophage-inducible C-type lectin (Mincle) bind Candida albicans." Glycobiology 18, no. 9 (June 25, 2008): 679–85. http://dx.doi.org/10.1093/glycob/cwn046.

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8

Carlson, David R. "Essays on Ricardian Literature in Honour of J. A. Burrow by A.J. Minnis, Charlotte C. Morse and Thorlac Turville-Petre." Arthuriana 9, no. 1 (1999): 155–57. http://dx.doi.org/10.1353/art.1999.0025.

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9

Hattori, Yuki, Daisuke Morita, Nagatoshi Fujiwara, Daiki Mori, Takashi Nakamura, Hideyoshi Harashima, Sho Yamasaki, and Masahiko Sugita. "Glycerol Monomycolate Is a Novel Ligand for the Human, but Not Mouse Macrophage Inducible C-type Lectin, Mincle." Journal of Biological Chemistry 289, no. 22 (April 13, 2014): 15405–12. http://dx.doi.org/10.1074/jbc.m114.566489.

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10

Kerscher, Bernhard, Gillian J. Wilson, Delyth M. Reid, Daiki Mori, Julie A. Taylor, Gurdyal S. Besra, Sho Yamasaki, Janet A. Willment, and Gordon D. Brown. "Mycobacterial receptor, Clec4d (CLECSF8, MCL), is coregulated with Mincle and upregulated on mouse myeloid cells following microbial challenge." European Journal of Immunology 46, no. 2 (December 8, 2015): 381–89. http://dx.doi.org/10.1002/eji.201545858.

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11

Trivedi, Nikita H., Jieh-Juen Yu, Chiung-Yu Hung, Richard P. Doelger, Christopher S. Navara, Lisa Y. Armitige, Janakiram Seshu, et al. "Microbial co-infection alters macrophage polarization, phagosomal escape, and microbial killing." Innate Immunity 24, no. 3 (February 26, 2018): 152–62. http://dx.doi.org/10.1177/1753425918760180.

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Macrophages are important innate immune cells that respond to microbial insults. In response to multi-bacterial infection, the macrophage activation state may change upon exposure to nascent mediators, which results in different bacterial killing mechanism(s). In this study, we utilized two respiratory bacterial pathogens, Mycobacterium bovis (Bacillus Calmette Guẻrin, BCG) and Francisella tularensis live vaccine strain (LVS) with different phagocyte evasion mechanisms, as model microbes to assess the influence of initial bacterial infection on the macrophage response to secondary infection. Non-activated (M0) macrophages or activated M2-polarized cells (J774 cells transfected with the mouse IL-4 gene) were first infected with BCG for 24–48 h, subsequently challenged with LVS, and the results of inhibition of LVS replication in the macrophages was assessed. BCG infection in M0 macrophages activated TLR2-MyD88 and Mincle-CARD9 signaling pathways, stimulating nitric oxide (NO) production and enhanced killing of LVS. BCG infection had little effect on LVS escape from phagosomes into the cytosol in M0 macrophages. In contrast, M2-polarized macrophages exhibited enhanced endosomal acidification, as well as inhibiting LVS replication. Pre-infection with BCG did not induce NO production and thus did not further reduce LVS replication. This study provides a model for studies of the complexity of macrophage activation in response to multi-bacterial infection.

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Thoennissen, Nils Heinrich, Tadayuki Akagi, Jee Hoon Song, Gabriela B. Iwanski, and H. Phillip Koeffler. "In Vivo Deficiency of Both Transcription Factors, C/EBPbeta and C/EBPepsilon, Results in Lack of Cytokine Response and a High Susceptibility for Overwhelming Infections." Blood 114, no. 22 (November 20, 2009): 3641. http://dx.doi.org/10.1182/blood.v114.22.3641.3641.

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Abstract Abstract 3641 Poster Board III-577 Transcription factors including the CCAAT/enhancer binding protein (C/EBP) family are essential for hematopoietic cell development including myelopoiesis. In response to cytokines and/or infection, C/EBPbeta is important for emergent neutrophil production, whereas C/EBPepsilon induces terminal differentiation of granulocytes. We recently generated C/EBPbeta and C/EBPepsilon double-knockout (KO) mice and demonstrated the dependence of the hematopoietic system on both transcription factors. In order to study inflammatory response of this transgenic in vivo model, bone marrow-derived macrophages from wild-type (WT), single- as well as double-KO mice were cultured either with or without 100 ng/mL LPS and 100 ng/mL mIFNgamma as activating stimuli. After 24 hours of exposure, RNA was extracted, and gene expression difference was interrogated by whole genome microarray (Affymetrix®, mouse genome 430 2.0). The probes were normalized with the MAS 5.0 software for processing Affymetrix oligonucleotide array data, and genes were considered to be differentially expressed with a fold change level of at least 2. Remarkably, we found more than 75 genes which were up to 20-fold downregulated in the stimulated macrophages of the double-KO mice compared to either single KO or WT mice. A pathway-based analysis indicated that these deregulated genes formed networks associated with development and function of the hematopoietic system, inflammatory response and cell-cell signaling. We confirmed the expression for some of the most highly decreased genes by RT-PCR; for example, interleukin-(IL)1beta, IL-12beta, CD38, macrophage mannose receptor (Mrc-1), toll-like receptor-2 (TLR-2), C-type lectin receptor Mincle, and insulin-like growth factor (IGF-1) were almost not detectable in the activated macrophages of the double-KO mice compared to either single-deficient or WT mice. Lacking these and other important regulators of appropriate immune responses and hematopoiesis, the double KO died between 2 - 3 months of age due to systemic infections including formation of hepatic, peritoneal and lung abscesses with Streptococcus viridians, Enterococcus species and Escherichia coli. In conclusion, phentotype as well as expression pattern of mediators of inflammatory response and hematopoiesis of the double-KO mice was distinct from either the C/EBPbeta- or C/EBPepsilon-KO mice, demonstrating that each transcription factor is important in cytokine expression and host defense, but can in part compensate for each other in the single knockout genotype. Disclosures: No relevant conflicts of interest to declare.

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Schotte, Remko, Julien Villaudy, Greta De Jong, Viviana Neviani, Wouter Pos, Sophie E. Levie, Daniel M. Go, et al. "Preclinical Development of AT1412, a Patient Derived CD9 Antibody That Does Not Induce Thrombosis for Treatment of B ALL." Blood 136, Supplement 1 (November 5, 2020): 41–42. http://dx.doi.org/10.1182/blood-2020-134088.

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Despite recent advances in treatment of B-acute lymphoblastic leukemia (B-ALL) there is still a need for novel targeted therapies. The tetraspanin CD9 is expressed in 60-80% of B-ALL and correlates with adverse prognosis. Recently, the mouse CD9 antibody ALB6 was shown to induce leukemia rejection in NOD/SCID mice. However, clinical development of ALB6 and other CD9-targeting antibodies was hampered by their CD9 mediated induction of platelet aggregation. It is known that CD9 is still expressed on tumor cells after treatment with chemotherapy or blinatumomab (Leung, 2019; Linder, 2016). AT1412 is a fully human antibody isolated from B cells of a patient that was cured from stage IV metastatic melanoma (Verdegaal, 2011). AT1412 targets CD9, without inducing platelet aggregation in vitro or thrombosis in cynomolgus monkeys after intravenous administration at therapeutic dose levels. By crystallography AT1412 was shown to bind a unique epitope preventing homodimerization of CD9, distinctly different from other CD9 antibodies. AT1412 binds a majority of patient B-ALL samples, but not T-ALL and induces ADCC and ADCP of CD9 positive B-ALL primary cells and the level of cytotoxicity significantly correlated with that of AT1412 binding. In both NSG and immunodeficient mice harboring a human immune system (HIS mice) AT1412 demonstrated a strong, dose-dependent tumor rejection of B-ALL, most pronounced in the extramedullary sites. In HIS mice AT1412 treatment led to an accumulation of T cells and CD14+ myeloid cells at the tumor sites. To support clinical development, pre-clinical safety of AT1412 was evaluated in cynomolgus monkeys. AT1412 demonstrated a half-life of 8.5 days, supporting 2-3 weekly administration in humans. Besides transient thrombocytopenia no other pathological deviations were observed. No effect on coagulation parameters, bruising or bleeding were observed macro- or microscopically. The thrombocytopenia is reversible, and its recovery accelerated in those animals developing anti-drug antibodies. Taken together, we demonstrate that CD9 on B-ALL cells can be successfully targeted by AT1412. AT1412 targets a unique epitope and does not induce thrombosis. Pre-clinical safety assessment is supporting that AT1412 can be safely administered. A First in Human clinical study is scheduled to start early 2021 in human solid tumors to determine safety and efficacy. AT1412 efficacy will be evaluated in B-ALL in expansion cohorts. Leung, K.T., Zhang, C., Chan, K.Y.Y., Li, K., Cheung, J.T.K., Ng, M.H.L., Zhang, X.-B., Sit, T., Lee, W.Y.W., Kang, W., et al. (2019). CD9 blockade suppresses disease progression of high-risk pediatric B-cell precursor acute lymphoblastic leukemia and enhances chemosensitivity. Leukemia. Linder, K., Gandhiraj, D., Hanmantgad, M., Seiter, K., and Liu, D. (2016). Complete remission after single agent blinatumomab in a patient with pre-B acute lymphoid leukemia relapsed and refractory to three prior regimens: HyperCVAD, high dose cytarabine mitoxantrone and CLAG. Exp. Hematol. Oncol. 5, 5-8. Verdegaal, E.M.E., Visser, M., Ramwadhdoebé, T.H., van der Minne, C.E., van Steijn, J. a Q.M.J., Kapiteijn, E., Haanen, J.B. a G., van der Burg, S.H., Nortier, J.W.R., and Osanto, S. (2011). Successful treatment of metastatic melanoma by adoptive transfer of blood-derived polyclonal tumor-specific CD4+ and CD8+ T cells in combination with low-dose interferon-alpha. Cancer Immunol. Immunother. 60, 953-963. Disclosures Schotte: AIMM Therapeutics: Current Employment, Current equity holder in private company. Villaudy:AIMM Therapeutics: Current Employment, Current equity holder in private company. Levie:AIMM Therapeutics: Current Employment, Current equity holder in private company. Go:AIMM Therapeutics: Current Employment, Current equity holder in private company. Yasuda:AIMM Therapeutics: Current Employment, Current equity holder in private company. Frankin:AIMM Therapeutics: Current Employment, Current equity holder in private company. Cercel:AIMM Therapeutics: Current Employment, Current equity holder in private company. van Hal-van Veen:AIMM Therapeutics: Current Employment, Current equity holder in private company. van de Berg:AIMM Therapeutics: Current Employment, Current equity holder in private company. Fatmawati:AIMM Therapeutics: Current Employment, Current equity holder in private company. Kedde:AIMM Therapeutics: Current Employment, Current equity holder in private company. Claassen:AIMM Therapeutics: Current Employment, Current equity holder in private company. Rijneveld:Amgen: Research Funding; Servier: Research Funding. Spits:AIMM Therapeutics: Current equity holder in private company, Ended employment in the past 24 months, Membership on an entity's Board of Directors or advisory committees. van Eenennaam:AIMM Therapeutics: Current Employment, Current equity holder in private company.

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14

KITLV, Redactie. "Book Reviews." New West Indian Guide / Nieuwe West-Indische Gids 72, no. 1-2 (January 1, 1998): 125–99. http://dx.doi.org/10.1163/13822373-90002604.

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-Valerie I.J. Flint, Margarita Zamora, Reading Columbus. Berkeley: University of California Press, 1993. xvi + 247 pp.-Riva Berleant-Schiller, Historie Naturelle des Indes: The Drake manuscript in the Pierpont Morgan Library. New York: Norton, 1996. xxii + 272 pp.-Neil L. Whitehead, Charles Nicholl, The creature in the map: A journey to Eldorado. London: Jonathan Cape, 1995. 398 pp.-William F. Keegan, Ramón Dacal Moure ,Art and archaeology of pre-Columbian Cuba. Pittsburgh: University of Pittsburgh Press, 1996. xxiv + 134 pp., Manuel Rivero de la Calle (eds)-Michael Mullin, Stephan Palmié, Slave cultures and the cultures of slavery. Knoxville: University of Tennessee Press, 1995. xlvii + 283 pp.-Bill Maurer, Karen Fog Olwig, Small islands, large questions: Society, culture and resistance in the post-emancipation Caribbean. London: Frank Cass, 1995. viii + 200 pp.-David M. Stark, Laird W. Bergad ,The Cuban slave market, 1790-1880. Cambridge: Cambridge University Press, 1995. xxi + 245 pp., Fe Iglesias García, María Del Carmen Barcia (eds)-Susan Fernández, Tom Chaffin, Fatal glory: Narciso López and the first clandestine U.S. war against Cuba. Charlottesville: University Press of Virginia, 1996. xxii + 282 pp.-Damian J. Fernández, María Cristina García, Havana USA: Cuban exiles and Cuban Americans in South Florida, 1959-1994. Berkeley: University of California Press, 1996. xiii + 290 pp.-Myrna García-Calderón, Carmen Luisa Justiniano, Con valor y a cómo dé lugar: Memorias de una jíbara puertorriqueña. Río Piedras: Editorial de la Universidad de Puerto Rico, 1994. 538 pp.-Jorge Pérez-Rolon, Ruth Glasser, My music is my flag: Puerto Rican musicians and their New York communities , 1917-1940. Los Angeles: University of California Press, 1995. xxiv + 253 pp.-Lauren Derby, Emelio Betances, State and society in the Dominican Republic. Boulder CO: Westview Press, 1995. xix + 162 pp.-Michiel Baud, Bernardo Vega, Trujillo y Haiti, Volumen II (1937-1938). Santo Domingo: Fundación Cultural Dominicana, 1995. 427 pp.-Danielle Bégot, Elborg Forster ,Sugar and slavery, family and race: The letters and diary of Pierre Dessalles, Planter in Martinique, 1808-1856. Elborg & Robert Forster (eds. and trans.). Baltimore: John Hopkins University Press, 1996. 322 pp., Robert Forster (eds)-Catherine Benoit, Richard D.E. Burton, La famille coloniale: La Martinique et la mère patrie, 1789-1992. Paris: L'Harmattan, 1994. 308 pp.-Roderick A. McDonald, Kathleen Mary Butler, The economics of emancipation: Jamaica & Barbados, 1823-1843. Chapel Hill: University of North Carolina Press, 1995. xviii + 198 pp.-K.O. Laurence, David Chanderbali, A portrait of Paternalism: Governor Henry Light of British Guiana, 1838-48. Turkeyen, Guyana: Dr. David Chanderbali, Department of History, University of Guyana, 1994. xiii + 277 pp.-Mindie Lazarus-Black, Brian L. Moore, Cultural power, resistance and pluralism: Colonial Guyana 1838-1900. Montreal & Kingston: McGill-Queen's University Press; Mona, Kingston: The Press-University of the West Indies, 1995. xv + 376 pp.-Madhavi Kale, K.O. Laurence, A question of labour: Indentured immigration into Trinidad and British Guiana, 1875-1917. Kingston: Ian Randle; London: James Currey, 1994. ix + 648 pp.-Franklin W. Knight, O. Nigel Bolland, On the March: Labour rebellions in the British Caribbean, 1934-39. Kingston: Ian Randle; London: James Currey, 1995. viii + 216 pp.-Linden Lewis, Kevin A. Yelvington, Producing power: Ethnicity, gender, and class in a Caribbean workplace. Philadelphia: Temple University Press, 1995. xv + 286 pp.-Consuelo López Springfield, Alta-Gracia Ortíz, Puerto Rican women and work: Bridges in transnational labor. Philadelphia: Temple University Press, 1996. xi + 249 pp.-Peta Henderson, Irma McClaurin, Women of Belize: Gender and change in Central America. New Brunswick NJ: Rutgers University Press, 1996. x + 218 pp.-Bonham C. Richardson, David M. Bush ,Living with the Puerto Rico Shore. José Gonzalez Liboy & William J. Neal. Durham: Duke University Press, 1995. xx + 193 pp., Richard M.T. Webb, Lisbeth Hyman (eds)-Bonham C. Richardson, David Barker ,Environment and development in the Caribbean: Geographical perspectives. Mona, Kingston: The Press-University of the West Indies, 1995. xv + 304 pp., Duncan F.M. McGregor (eds)-Alma H. Young, Anthony T. Bryan ,Distant cousins: The Caribbean-Latin American relationship. Miami: North-South-Center Press, 1996. iii + 132 pp., Andrés Serbin (eds)-Alma H. Young, Ian Boxill, Ideology and Caribbean integration. Mona, Kingston: The Press-University of the West Indies, 1993. xiii + 128 pp.-Stephen D. Glazier, Howard Gregory, Caribbean theology: Preparing for the challenges ahead. Mona, Kingston: Canoe Press, University of the West Indies, 1995. xx + 118 pp.-Lise Winer, Richard Allsopp, Dictionary of Caribbean English usage. With a French and Spanish supplement edited by Jeanette Allsopp. Oxford: Oxford University Press, 1996. lxxviii + 697 pp.-Geneviève Escure, Jacques Arends ,Pidgins and Creoles: An introduction. Amsterdam/Philadelphia: John Benjamins, 1995. xiv + 412 pp., Pieter Muysken, Norval Smith (eds)-Jacques Arends, Angela Bartens, Die iberoromanisch-basierten Kreolsprachen: Ansätze der linguistischen Beschreibung. Frankfurt am Main: Peter Lang, 1995. vii + 345 pp.-J. Michael Dash, Richard D.E. Burton, Le roman marron: Études sur la littérature martiniquaise contemporaine. Paris: L'Harmattan. 1997. 282 pp.

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15

Lv, Lin-Li, Cui Wang, Zuo-Lin Li, Jing-Yuan Cao, Xin Zhong, Ye Feng, Jun Chen, et al. "SAP130 released by damaged tubule drives necroinflammation via miRNA-219c/Mincle signaling in acute kidney injury." Cell Death & Disease 12, no. 10 (September 23, 2021). http://dx.doi.org/10.1038/s41419-021-04131-7.

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AbstractTubules injury and immune cell activation are the common pathogenic mechanisms in acute kidney injury (AKI). However, the exact modes of immune cell activation following tubule damage are not fully understood. Here we uncovered that the release of cytoplasmic spliceosome associated protein 130 (SAP130) from the damaged tubular cells mediated necroinflammation by triggering macrophage activation via miRNA-219c(miR-219c)/Mincle-dependent mechanism in unilateral ureteral obstruction (UUO) and cisplatin-induced AKI mouse models, and in patients with acute tubule necrosis (ATN). In the AKI kidneys, we found that Mincle expression was tightly correlated to the necrotic tubular epithelial cells (TECs) with higher expression of SAP130, a damaged associated molecule pattern (DAMP), suggesting that SAP130 released from damaged tubular cells may trigger macrophage activation and necroinflammation. This was confirmed in vivo in which administration of SAP130-rich supernatant from dead TECs or recombinant SAP130 promoted Mincle expression and macrophage accumulation which became worsen with profound tubulointerstitial inflammation in LPS-primed Mincle WT mice but not in Mincle deficient mice. Further studies identified that Mincle was negatively regulated via miR-219c-3p in macrophages as miR-219c-3p bound Mincle 3′-UTR to inhibit Mincle translation. Besides, lentivirus-mediated renal miR-219c-3p overexpression blunted Mincle and proinflammatory cytokine expression as well as macrophage infiltration in the inflamed kidney of UUO mice. In conclusion, SAP130 is released by damaged tubules which elicit Mincle activation on macrophages and renal necroinflammation via the miR-219c-3p-dependent mechanism. Results from this study suggest that targeting miR-219c-3p/Mincle signaling may represent a novel therapy for AKI.

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Rui-Zhi, Tan, Diao Hui, Li Jian-Chun, Zhong Xia, Wang Xiao-Jia, Wen Dan, Fan Jun-Ming, and Wang Li. "Astragalus mongholicus Bunge and Panax Notoginseng Formula (A&P) Combined With Bifidobacterium Contribute a Renoprotective Effect in Chronic Kidney Disease Through Inhibiting Macrophage Inflammatory Response in Kidney and Intestine." Frontiers in Physiology 11 (November 27, 2020). http://dx.doi.org/10.3389/fphys.2020.583668.

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There is increasing evidence that Chronic Kidney Disease (CKD) can cause intestinal dysfunction, which in turn aggravates the progression of kidney disease. Studies have shown that the immune response of macrophage plays an important role in promoting inflammation in kidney and intestine of CKD. Astragalus mongholicus Bunge and Panax notoginseng formula (A&P) is a widely used traditional medicine for the treatment of CKD in China, however, the underlying mechanism is largely unclear. In this study, we aimed to explore the role of A&P and Bifidobacterium combination treatment in regulation of inflammatory response of macrophage in kidney and intestine of CKD mouse, as well as the potential molecular mechanism. We established a CKD mouse model with 5/6 nephrectomy and a macrophage inflammatory cellular model with LPS and urotoxin in vivo and in vitro. The results showed that A&P combined with Bifidobacterium significantly reduced the expression and secretion of IL-1β, IL-6, TNFα, and MCP-1 in kidney and blood, as well as in inflammatory macrophage. Interestingly, A&P combined with Bifidobacterium strongly improved the intestinal flora and protected the intestinal barrier. Notably, the maintainer of macrophage polarization, Mincle, was activated in kidney and intestine of CKD mouse as well as in urotoxin stimulated macrophage, that was effectively inhibited by the treatment of A&P and Bifidobacterium combination. Overexpression of Mincle by genetic modification can abolish the inhibitory effects of A&P combined with Bifidobacterium on inflammation in urotoxin stimulated RAW264.7 cells. In summary, these findings demonstrated that A&P combined with Bifidobacterium can protect kidney against CKD by down-regulating macrophage inflammatory response in kidney and intestine via suppressing Mincle signaling, which provides a new insight in the treatment of CKD with traditional medicine.

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17

Hupfer, Thomas, Judith Schick, Katrin Jozefowski, David Voehringer, Jenny Ostrop, and Roland Lang. "Stat6-Dependent Inhibition of Mincle Expression in Mouse and Human Antigen-Presenting Cells by the Th2 Cytokine IL-4." Frontiers in Immunology 7 (October 14, 2016). http://dx.doi.org/10.3389/fimmu.2016.00423.

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18

"A. J. Minnis, Charlotte C. Morse, and Thorlac Turville-Petre, eds., Essays on Ricardian Literature: In Honour of J. A. Burrow. Oxford: Clarendon Press; New York: Oxford University Press, 1997. Pp. xv, 358 plus black-and-white frontispiece portrait. $85." Speculum 74, no. 03 (July 1999): 874. http://dx.doi.org/10.1017/s0038713400200237.

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