Статті в журналах з теми "Winnie mouse"

The Winnie mouse, carrying a missense mutation in Muc2, is a model for chronic intestinal inflammation demonstrating symptoms closely resembling inflammatory bowel disease (IBD). Alterations to the immune environment, morphological structure, and innervation of Winnie mouse colon have been identified; however, analyses of intestinal transit and colonic functions have not been conducted. In this study, we investigated in vivo intestinal transit in radiographic studies and in vitro motility of the isolated colon in organ bath experiments. We compared neuromuscular transmission using conventional intracellular recording between distal colon of Winnie and C57BL/6 mice and smooth muscle contractions using force displacement transducers. Chronic inflammation in Winnie mice was confirmed by detection of lipocalin-2 in fecal samples over 4 wk and gross morphological damage to the colon. Colonic transit was faster in Winnie mice. Motility was altered including decreased frequency and increased speed of colonic migrating motor complexes and increased occurrence of short and fragmented contractions. The mechanisms underlying colon dysfunctions in Winnie mice included inhibition of excitatory and fast inhibitory junction potentials, diminished smooth muscle responses to cholinergic and nitrergic stimulation, and increased number of α-smooth muscle actin-immunoreactive cells. We conclude that diminished excitatory responses occur both prejunctionally and postjunctionally and reduced inhibitory purinergic responses are potentially a prejunctional event, while diminished nitrergic inhibitory responses are probably due to a postjunction mechanism in the Winnie mouse colon. Many of these changes are similar to disturbed motor functions in IBD patients indicating that the Winnie mouse is a model highly representative of human IBD. NEW & NOTEWORTHY This is the first study to provide analyses of intestinal transit and whole colon motility in an animal model of spontaneous chronic colitis. We found that cholinergic and purinergic neuromuscular transmission, as well as the smooth muscle cell responses to cholinergic and nitrergic stimulation, is altered in the chronically inflamed Winnie mouse colon. The changes to intestinal transit and colonic function we identified in the Winnie mouse are similar to those seen in inflammatory bowel disease patients.

Background: Colorectal cancer (CRC) is the third most common cancer worldwide, characterized by a multifactorial etiology including genetics, lifestyle, and environmental factors including microbiota composition. To address the role of microbial modulation in CRC, we used our recently established mouse model (the Winnie-APCMin/+) combining inflammation and genetics. Methods: Gut microbiota profiling was performed on 8-week-old Winnie-APCMin/+ mice and their littermates by 16S rDNA gene amplicon sequencing. Moreover, to study the impact of dysbiosis induced by the mother’s genetics in ACF development, the large intestines of APCMin/+ mice born from wild type mice were investigated by histological analysis at 8 weeks. Results: ACF development in 8-week-old Winnie-APCMin/+ mice was triggered by dysbiosis. Specifically, the onset of ACF in genetically predisposed mice may result from dysbiotic signatures in the gastrointestinal tract of the breeders. Additionally, fecal transplant from Winnie donors to APCMin/+ hosts leads to an increased rate of ACF development. Conclusions: The characterization of microbiota profiling supporting CRC development in genetically predisposed mice could help to design therapeutic strategies to prevent dysbiosis. The application of these strategies in mothers during pregnancy and lactation could also reduce the CRC risk in the offspring.

Background: The immune-modulator behaviour of the CCR6/CCL20 axis in multi -system pathophysiology and molecular signalling was investigated at two clinically significant time points, using a Ccr6—deficient mouse model of spontaneous colitis. Methods:Four groups of mice, (C57BL/6J, Ccr6−/− of C57BL/6J, Winnie × Ccr6−/− and Winnie) were utilized and (I) colonic clinical parameters (2) histology of colon, spleen, kidney and liver (3) T and B lymphocyte distribution in the spleen and MLN by flowcytometry (5) colonic CCL20, phosphorylated PI3K and phosphorylated Akt expression by immunohistochemistry and (6) colonic cytokine expression by RT-PCR were evaluated. Results: CCR6 deficiency was shown to attenuate inflammation in the spleen, liver and gut while renal histology remained unaffected. Marked focal lobular inflammation with reactive nuclear features were observed in hepatocytes and a significant neutrophil infiltration in red pulp with extra medullary hemopoiesis in the spleen existed in Winnie. These changes were considerably reduced in Winnie × Ccr6−/− with elevated goblet cell numbers and mucus production in the colonic epithelium. Conclusions: Results indicate that Ccr6-deficiency in the colitis model contributes towards resolution of disease. Our findings demonstrate an intricate networking role for CCR6 in immune activation, which is downregulated by Ccr6 deficiency, and could provide newer clinical therapies in colitis.

A probiotic and prebiotic food ingredient combination was tested for synergistic functioning in modulation of the colonic microbiome and remediation of the gastrointestinal immune and inflammatory responses in a spontaneous colitic mouse model. Bacillus coagulans MTCC5856 spores with capability to metabolise complex plant polysaccharides were supplemented with complex whole-plant prebiotic sugarcane fibre (PSCF). The combined and individual efficacies were tested for their influence on the outcomes of chronic inflammation in Muc2 mutant colitic Winnie mice. The mice were fed normal chow diet supplemented with either ingredient or a combination for 21 days. Synbiotic combined supplementation ameliorated clinical symptoms and histological colonic damage scores more effectively than either B. coagulans or PSCF alone. PSCF and B. coagulans alone also induced considerable immunomodulatory effects. Synbiotic supplementation however was the most efficacious in modulating the overall immune profile compared to the unsupplemented Winnie-control. The augmented synbiotic effect could potentially be due to a combination of increased levels of fermentation products, direct immune-modulating abilities of the components, their capability to reduce colonic epithelial damage and/or modulation of the microbiota. The beneficial effects of the supplementation with a complex plant fibre and a fibre-degrading probiotic parallel the effects seen in human microbiota with high plant fibre diets.

Sustained endoplasmic reticular stress (ERS) is implicated in aggressive metastasis of cancer cells and increased tumor cell proliferation. Cancer cells activate the unfolded protein response (UPR), which aids in cellular survival and adaptation to harsh conditions. Inhibition of apoptosis, in contrast, is a mechanism adopted by cancer cells with the help of the inhibitor of an apoptosis (IAP) class of proteins such as Survivin to evade cell death and gain a proliferative advantage. In this study, we aimed to reveal the interrelation between ERS and Survivin. We initially verified the expression of Survivin in Winnie (a mouse model of chronic ERS) colon tissues by using immunohistochemistry (IHC) and immunofluorescence (IF) in comparison with wild type Blk6 mice. Additionally, we isolated the goblet cells and determined the expression of Survivin by IF and protein validation. Tunicamycin was utilized at a concentration of 10 µg/mL to induce ERS in the LS174T cell line and the gene expression of the ERS markers was measured. This was followed by determination of inflammatory cytokines. Inhibition of ERS was carried out by 4Phenyl Butyric acid (4PBA) at a concentration of 10 mM to assess whether there was a reciprocation effect. The downstream cell death assays including caspase 3/7, Annexin V, and poly(ADP-ribose) polymerase (PARP) cleavage were evaluated in the presence of ERS and absence of ERS, which was followed by a proliferative assay (EdU click) with and without ERS. Correspondingly, we inhibited Survivin by YM155 at a concentration of 100 nM and observed the succeeding ERS markers and inflammatory markers. We also verified the caspase 3/7 assay. Our results demonstrate that ERS inhibition not only significantly reduced the UPR genes (Grp78, ATF6, PERKandXBP1) along with Survivin but also downregulated the inflammatory markers such as IL8, IL4, and IL6, which suggests a positive correlation between ERS and the inhibition of apoptosis. Furthermore, we provided evidence that ERS inhibition promoted apoptosis in LS174T cells and shortened the proliferation rate. Moreover, Survivin inhibition by YM155 led to a comparable effect as that of ERS inhibition, which includes attenuation of ERS genes and inflammatory markers as well as the promotion of programmed cell death via the caspase 3/7 pathway. Together, our results propose the interrelation between ERS and inhibition of apoptosis assigning a molecular and therapeutic target for cancer treatment.

In the mature mouse lung, the proximal-distal (P-D) axis is delineated by two distinct epithelial subpopulations: the proximal bronchiolar epithelium and the distal respiratory epithelium. Little is known about the signaling molecules that pattern the lung along the P-D axis. One candidate is Bone Morphogenetic Protein 4 (Bmp4), which is expressed in a dynamic pattern in the epithelial cells in the tips of growing lung buds. Previous studies in which Bmp4 was overexpressed in the lung endoderm (Bellusci, S., Henderson, R., Winnier, G., Oikawa, T. and Hogan, B. L. M. (1996) Development 122, 1693–1702) suggested that this factor plays an important role in lung morphogenesis. To further investigate this question, two complementary approaches were utilized to inhibit Bmp signaling in vivo. The Bmp antagonist Xnoggin and, independently, a dominant negative Bmp receptor (dnAlk6), were overexpressed using the surfactant protein C (Sp-C) promoter/enhancer. Inhibiting Bmp signaling results in a severe reduction in distal epithelial cell types and a concurrent increase in proximal cell types, as indicated by morphology and expression of marker genes, including the proximally expressed hepatocyte nuclear factor/forkhead homologue 4 (Hfh4) and Clara cell marker CC10, and the distal marker Sp-C. In addition, electron microscopy demonstrates the presence of ciliated cells, a proximal cell type, in the most peripheral regions of the transgenic lungs. We propose a model in which Bmp4 is a component of an apical signaling center controlling P-D patterning. Endodermal cells at the periphery of the lung, which are exposed to high levels of Bmp4, maintain or adopt a distal character, while cells receiving little or no Bmp4 signal initiate a proximal differentiation program.

Sonic hedgehog (Shh) signaling patterns many vertebrate tissues. shh mutations dramatically affect mouse ventral forebrain and floor plate but produce minor defects in zebrafish. Zebrafish have two mammalian Shh orthologs, sonic hedgehog and tiggy-winkle hedgehog, and another gene, echidna hedgehog, that could have overlapping functions. To examine the role of Hedgehog signaling in zebrafish, we have characterized slow muscle omitted (smu) mutants. We show that smu encodes a zebrafish ortholog of Smoothened that transduces Hedgehog signals. Zebrafish smoothened is expressed maternally and zygotically and supports specification of motoneurons, pituitary cells and ventral forebrain. We propose that smoothened is required for induction of lateral floor plate and a subpopulation of hypothalamic cells and for maintenance of medial floor plate and hypothalamic cells.

Abstract Background: Hepatocellular carcinoma (HCC) is a major clinical challenge because of increasing rates of incidence and mortality, and high resistance to standard radio- and chemotherapy. Identification of novel molecules regulating HCC facilitates development of targeted therapies having a lasting impact on HCC patient survival. The oncogene MDA-9/SDCBP promotes tumorigenesis and metastasis in many cancers. In The Cancer Genome Atlas (TCGA), 8% of HCC patients show amplification of MDA-9 gene. However, the role of MDA-9 in regulating HCC has not been well-studied. Objective: To unravel the function of MDA-9 in HCC using a transgenic mouse model with hepatocyte-specific overexpression of MDA-9 (Alb/MDA-9). Study design: Alb/MDA-9 mice were generated in B6/CBA background by using the mouse albumin promoter/enhancer element to drive human MDA-9 expression. N-nitrosodiethylamine (DEN)/phenobarbital (PB) was used for induction of HCC. Tumor immune profile was analyzed by Opal multiplex staining and flow cytometry. RNA-sequencing (RNA-seq) was performed to analyze MDA-9-mediated gene regulation. Results: At 18 months of age, none of the WT mice developed liver tumor, while one male and one female Alb/MDA-9 mice (n = 11) developed one isolated tumor each, suggesting that MDA-9 may not be a strong driver oncogene, rather it might promote HCC progression once tumor is initiated. Indeed, at 32 weeks after induction of HCC using DEN/PB, tumor burden in the livers of Alb/MDA-9 mice was significantly higher compared to WT. These tumors showed loss of hepatic architecture and hepatocyte ballooning, features of HCC. Increased staining for the proliferation marker PCNA, HCC markers AFP and cytokeratin, and angiogenesis marker CD31 in tumor sections, and significantly increased levels of serum liver enzymes, AST and ALT, were observed in Alb/MDA-9 mice vs WT. Macrophage-mediated inflammation plays a central role in HCC. Compared to WT, Alb/MDA-9 tumors showed marked infiltration of CD11b+ myeloid cells, FoxP3+ T regulatory cells and F4/80+ macrophages. RNA-seq in naïve WT and Alb/MDA-9 hepatocytes identified activation of signaling pathways associated with invasion, angiogenesis and inflammation. Conclusions: MDA-9 overexpression in hepatocytes promotes HCC by stimulating inflammation, angiogenesis and immune modulation. Studies are ongoing to obtain in-depth understanding of the molecular mechanisms by which MDA-9 exerts these pleiotropic effects. This study was supported by NIH/NCI Grant 1R01CA244993-01 (DS and PBF). Citation Format: Debashri Manna, Saranya Chidambaranathan Reghupaty, Rachel Gredler Mendoza, Maria Del Camarena, Mark A. Subler, Jennifer Koblinski, Rebecca Martin, Mikhail G. Dozmorov, Swadesh K. Das, Jolene J. Windle, Paul B. Fisher, Devanand Sarkar. Melanoma differentiation associated gene-9/syndecan binding protein (mda-9/sdcbp): A positive regulator of hepatocellular carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 920.

Abstract Background The autonomic nervous system (ANS) is thought to play a critical role in the anti-inflammatory reflex pathway in acute colitis via its interaction with the spleen and colon. Inflammation in the intestine is associated with a blunting of vagal signaling and increased sympathetic activity. As a corollary, methods to restore sympatho-vagal balance are being investigated as therapeutic strategies for the treatment of intestinal inflammation. Nevertheless, it is indefinite whether these autonomic signaling adaptations in colitis are detrimental or beneficial to controlling intestinal inflammation. In this study, models of moderate and severe chronic colitis are utilized to resolve the correlations between sympatho-vagal signaling and the severity of intestinal inflammation. Methods Spleens and colons were collected from Winnie (moderate colitis), Winnie-Prolapse (severe colitis), and control C57BL/6 mice. Changes to the size and histomorphology of spleens were evaluated. Flow cytometry was used to determine the expression of adrenergic and cholinergic signaling proteins in splenic B and T lymphocytes. The inflammatory profile of the spleen and colon was determined using a RT-PCR gene array. Blood pressure, heart rate, splanchnic sympathetic nerve and vagus nerve activity were recorded. Results Spleens and colons from Winnie and Winnie-Prolapse mice exhibited gross abnormalities by histopathology. Genes associated with a pro-inflammatory response were upregulated in the colons from Winnie and further augmented in colons from Winnie-Prolapse mice. Conversely, many pro-inflammatory markers were downregulated in the spleens from Winnie-Prolapse mice. Heightened activity of the splanchnic nerve was observed in Winnie but not Winnie-Prolapse mice. Conversely, vagal nerve activity was greater in Winnie-Prolapse mice compared with Winnie mice. Splenic lymphocytes expressing α1 and β2 adrenoreceptors were reduced, but those expressing α7 nAChR and producing acetylcholine were increased in Winnie and Winnie-Prolapse mice. Conclusions Sympathetic activity may correlate with an adaptive mechanism to reduce the severity of chronic colitis. The Winnie and Winnie-Prolapse mouse models of moderate and severe chronic colitis are well suited to examine the pathophysiology of progressive chronic intestinal inflammation.

Abstract Background Osteoporosis is a common extraintestinal manifestation of inflammatory bowel disease (IBD). However, studies have been scarce, mainly because of the lack of an appropriate animal model of colitis-associated bone loss. In this study, we aimed to decipher skeletal manifestations in the Winnie mouse model of spontaneous chronic colitis, which carries a MUC2 gene mutation and closely replicates ulcerative colitis. In our study, Winnie mice, prior to the colitis onset at 6 weeks old and progression at 14 and 24 weeks old, were compared with age-matched C57BL/6 controls. We studied several possible mechanisms involved in colitis-associated bone loss. Methods We assessed for bone quality (eg, microcomputed tomography [micro-CT], static and dynamic histomorphometry, 3-point bending, and ex vivo bone marrow analysis) and associated mechanisms (eg, electrochemical recordings for gut-derived serotonin levels, real-time polymerase chain reaction [qRT-PCR], double immunofluorescence microscopy, intestinal inflammation levels by lipocalin-2 assay, serum levels of calcium, phosphorus, and vitamin D) from Winnie (6–24 weeks) and age-matched C57BL6 mice. Results Deterioration in trabecular and cortical bone microarchitecture, reductions in bone formation, mineral apposition rate, bone volume/total volume, osteoid volume/bone surface, and bone strength were observed in Winnie mice compared with controls. Decreased osteoblast and increased osteoclast numbers were prominent in Winnie mice compared with controls. Upregulation of 5-HTR1B gene and increased association of FOXO1 with ATF4 complex were identified as associated mechanisms concomitant to overt inflammation and high levels of gut-derived serotonin in 14-week and 24-week Winnie mice. Conclusions Skeletal phenotype of the Winnie mouse model of spontaneous chronic colitis closely represents manifestations of IBD-associated osteoporosis/osteopenia. The onset and progression of intestinal inflammation are associated with increased gut-derived serotonin level, increased bone resorption, and decreased bone formation.

Abstract Winnie, a mouse carrying a missense mutation in the MUC2 mucin gene, is a valuable model for inflammatory bowel disease (IBD) with signs and symptoms that have multiple similarities with those observed in patients with ulcerative colitis. MUC2 mucin is present in Winnie, but is not firmly compacted in a tight inner layer. Indeed, these mice develop chronic intestinal inflammation due to the primary epithelial defect with signs of mucosal damage, including thickening of muscle and mucosal layers, goblet cell loss, increased intestinal permeability, enhanced susceptibility to luminal inflammation-inducing toxins, and alteration of innervation in the distal colon. In this study, we show that the intestinal environment of the Winnie mouse, genetically determined by MUC2 mutation, selects an intestinal microbial community characterized by specific pro-inflammatory, genotoxic, and metabolic features that could imply a direct involvement in the pathogenesis of chronic intestinal inflammation. We report results obtained by using a variety of in vitro approaches for fecal microbiota functional characterization. These approaches include Caco-2 cell cultures and Caco-2/THP-1 cell co-culture models for evaluation of geno-cytotoxic and pro-inflammatory properties using a panel of 43 marker RNAs assayed by RT-qPCR, and cell-based phenotypic testing for metabolic profiling of the intestinal microbial communities by Biolog EcoPlates. While adding a further step towards understanding the etiopathogenetic mechanisms underlying IBD, the results of this study provide a reliable method for phenotyping gut microbial communities, which can complement their structural characterization by providing novel functional information.

Abstract Background Inflammatory bowel disease (IBD) associates with damage to the enteric nervous system (ENS), leading to gastrointestinal (GI) dysfunction. Oxidative stress is important for the pathophysiology of inflammation-induced enteric neuropathy and GI dysfunction. Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) is a dual functioning protein that is an essential regulator of the cellular response to oxidative stress. In this study, we aimed to determine whether an APE1/Ref-1 redox domain inhibitor, APX3330, alleviates inflammation-induced oxidative stress that leads to enteric neuropathy in the Winnie murine model of spontaneous chronic colitis. Methods Winnie mice received APX3330 or vehicle via intraperitoneal injections over 2 weeks and were compared with C57BL/6 controls. In vivo disease activity and GI transit were evaluated. Ex vivo experiments were performed to assess functional parameters of colonic motility, immune cell infiltration, and changes to the ENS. Results Targeting APE1/Ref-1 redox activity with APX3330 improved disease severity, reduced immune cell infiltration, restored GI function ,and provided neuroprotective effects to the enteric nervous system. Inhibition of APE1/Ref-1 redox signaling leading to reduced mitochondrial superoxide production, oxidative DNA damage, and translocation of high mobility group box 1 protein (HMGB1) was involved in neuroprotective effects of APX3330 in enteric neurons. Conclusions This study is the first to investigate inhibition of APE1/Ref-1’s redox activity via APX3330 in an animal model of chronic intestinal inflammation. Inhibition of the redox function of APE1/Ref-1 is a novel strategy that might lead to a possible application of APX3330 for the treatment of IBD.

I giocattoli con tratti fisici non antropomorfizzati in letteratura, specie quando rivolta a un pubblico infantile, si rivelano come un utile strumento per riflettere sulla distinzione tra ‘umano’ e ‘non umano’. Il corpo artificiale del giocattolo e la caratterizzazione animale incarnano, infatti, in modo evidente il concetto di alterità rispetto all’idea stereotipica di umanità. Ispirati dalle vicende narrate, i giovani lettori possono trarre degli essenziali insegnamenti, quali le capacità di empatia e di resilienza ai traumi di piccola o grande entità che ciascuno può incontrare nel corso della vita. L’introduzione critica a queste riflessioni è completata dall’analisi letteraria circa la caratterizzazione dei giocattoli in alcuni testi per l’infanzia: il giocattolo-coniglio in The Velveteen Rabbit (1922) di Margery Williams, i giocattoli-topi in The Mouse and His Child (1967) di Russell Hoban e il giocattolo-orso in Winnie-the-Pooh (1926) di A. A. Milne.

AWARDSSome major international children’s literature awards have just been announced as I compile the news for this issue. Several of these have Canadian connections.2016 ALSC (Association for Library Service to Children) Book & Media Award WinnersJohn Newbery Medal"Last Stop on Market Street,” written by Matt de la Peña, illustrated by Christian Robinson and published by G. P. Putnam’s Sons, an imprint of Penguin Books (USA) LLC Newbery Honor Books"The War that Saved My Life," written by Kimberly Brubaker Bradley and published by Dial Books for Young Readers, an imprint of Penguin Books (USA) LLC“Roller Girl,” written and illustrated by Victoria Jamieson and published by Dial Books for Young Readers, an imprint of Penguin Books (USA) LLC“Echo,” written by Pam Muñoz Ryan and published by Scholastic Press, an imprint of Scholastic Inc.Randolph Caldecott Medal"Finding Winnie: The True Story of the World’s Most Famous Bear," illustrated by Sophie Blackall, written by Lindsay Mattick and published by Little, Brown and Company, a division of Hachette Book Group, Inc.Caldecott Honor Books"Trombone Shorty," illustrated by Bryan Collier, written by Troy Andrews and published by Abrams Books for Young Readers, an imprint of ABRAMS“Waiting,” illustrated and written by Kevin Henkes, published by Greenwillow Books, an imprint of HarperCollins Publishers“Voice of Freedom Fannie Lou Hamer Spirit of the Civil Rights Movement,” illustrated by Ekua Holmes, written by Carole Boston Weatherford and published by Candlewick Press“Last Stop on Market Street,” illustrated by Christian Robinson, written by Matt de le Peña and published by G. P. Putnam’s Sons, an imprint of Penguin Books (USA) LLC Laura Ingalls Wilder AwardJerry Pinkney -- His award-winning works include “The Lion and the Mouse,” recipient of the Caldecott Award in 2010. In addition, Pinkney has received five Caldecott Honor Awards, five Coretta Scott King Illustrator Awards, and four Coretta Scott King Illustrator Honors. 2017 May Hill Arbuthnot Honor Lecture AwardJacqueline Woodson will deliver the 2017 May Hill Arbuthnot Honor Lecture. Woodson is the 2014 National Book Award winner for her New York Times bestselling memoir, “Brown Girl Dreaming.” Mildred L. Batchelder Award“The Wonderful Fluffy Little Squishy,” published by Enchanted Lion Books, written and illustrated by Beatrice Alemagna, and translated from the French by Claudia Zoe BedrickBatchelder Honor Books“Adam and Thomas,” published by Seven Stories Press, written by Aharon Appelfeld, iIllustrated by Philippe Dumas and translated from the Hebrew by Jeffrey M. Green“Grandma Lives in a Perfume Village,” published by NorthSouth Books, an imprint of Nordsüd Verlag AG, written by Fang Suzhen, iIllustrated by Sonja Danowski and translated from the Chinese by Huang Xiumin“Written and Drawn by Henrietta,” published by TOON Books, an imprint of RAW Junior, LLC and written, illustrated, and translated from the Spanish by Liniers.Pura Belpre (Author) Award“Enchanted Air: Two Cultures, Two Wings: A Memoir," written by Margarita Engle and published by Atheneum Books for Young Readers, an imprint of Simon & Schuster Children’s Publishing DivisionBelpre (Author) Honor Books"The Smoking Mirror," written by David Bowles and published by IFWG Publishing, Inc."Mango, Abuela, and Me," written by Meg Medina, illustrated by Angela Dominguez and published by Candlewick PressPura Belpre (Illustrator) Award"The Drum Dream Girl," illustrated by Rafael López, written by Margarita Engle and published by Houghton Mifflin HarcourtBelpre (Illustrator) Honor Books"My Tata’s Remedies = Los remedios de mi tata,” iIllustrated by Antonio Castro L., written by Roni Capin Rivera-Ashford and published by Cinco Puntos Press“Mango, Abuela, and Me,” illustrated by Angela Dominguez, written by Meg Medina and published by Candlewick Press“Funny Bones: Posada and His Day of the Dead Calaveras,” illustrated and written by Duncan Tonatiuh and published by Abrams Books for Young Readers, an imprint of ABRAMSAndrew Carnegie Medal "That Is NOT a Good Idea," produced by Weston Woods Studios, Inc.Theodor Seuss Geisel Award"Don’t Throw It to Mo!" written by David A. Adler, illustrated by Sam Ricks and published by Penguin Young Readers, and imprint of Penguin Group (USA), LLCGeisel Honor Books "A Pig, a Fox, and a Box," written and illustrated by Jonathan Fenske and published by Penguin Young Readers, an Imprint of Penguin Group (USA) LLC"Supertruck," written and illustrated by Stephen Savage and published by A Neal Porter Book published by Roaring Brook Press, a division of Holtzbrinck Publishing Holdings Limited Partnership"Waiting," written and illustrated by Kevin Henkes and published by Greenwillow Books, an imprint of HarperCollins Publishers.Odyssey Award"The War that Saved My Life," produced by Listening Library, an imprint of the Penguin Random House Audio Publishing Group, written by Kimberly Brubaker Bradley and narrated by Jayne EntwistleOdyssey Honor Audiobook"Echo," produced by Scholastic Audio / Paul R. Gagne, written by Pam Munoz Ryan and narrated by Mark Bramhall, David De Vries, MacLeod Andrews and Rebecca SolerRobert F. Sibert Informational Book Medal"Funny Bones: Posada and His Day of the Dead Calaveras,” written and illustrated by Duncan Tonatiuh and published by Abrams Books for Young Readers, an imprint of ABRAMSSibert Honor Books"Drowned City: Hurricane Katrina and New Orleans," written and illustrated by Don Brown and published by Houghton Mifflin Harcourt"The Boys Who Challenged Hitler: Knud Pedersen and the Churchill Club," by Phillip Hoose and published by Farrar Straus Giroux Books for Young Readers"Turning 15 on the Road to Freedom: My Story of the 1965 Selma Voting Rights March," written by Lynda Blackmon Lowery as told to Elspeth Leacock and Susan Buckley, illustrated by PJ Loughran and published by Dial Books, an imprint of Penguin Group (USA) LLC"Voice of Freedom: Fannie Lou Hamer, Spirit of the Civil Rights Movement," written by Carole Boston Weatherford, illustrated by Ekua Holmes and published by Candlewick PressCONFERENCES & EVENTSThis 2016 is shaping up to be a busy year for those of us involved with Canadian children’s literature. To tantalize your appetite (and encourage you to get involved) here are some highlights:January:Vancouver Children’s Literature Roundtable event: A Celebration of BC’s Award Children’s Authors and Illustrators with special guests Rachel Hartman and the Children’s Literature Roundtables of Canada 2015 Information Book Award winners Margriet Ruurs & Katherine Gibson, January 27, 2016, 7 – 9 pm. Creekside Community Centre, 1 Athletes Way, Vancouver. Free to members and students.April:Wordpower programs from the Young Alberta Book Society feature teams of Albertan children’s literary artists touring to schools in rural areas. Thanks to the generous sponsorship of Cenovus Energy, schools unable to book artist visits due to prohibitive travel costs are able to participate.April 4-8: Wordpower South will send 8 artist teams to communities roughly between Drumheller and Medicine Hat. Artists include Karen Bass, Lorna Shultz-Nicholson, Bethany Ellis, Marty Chan, Mary Hays, Sigmund Brouwer, Carolyn Fisher, Natasha DeenApril 25-29: Wordpower North will have a team of 8 artists traveling among communities in north-eastern Alberta such as Fort MacKay, Conklin, Wabasca, Lac La Biche, Cold Lake, and Bonnyville. The artists include Kathy Jessup, Lois Donovan, Deborah Miller, David Poulsen, Gail de Vos, Karen Spafford-Fitz, Hazel Hutchins, Georgia Graham May: COMICS AND CONTEMPORARY LITERACY: May 2, 2016; 8:30am - 4:30pm at the Rozsa Centre, University of Calgary. This is a one day conference featuring presentations and a workshop by leading authors, scholars, and illustrators from the world of comics and graphic novels. This conference is the 5th in the annual 'Linguistic Diversity and Language Policy' series sponsored by the Chair, English as an Additional Language, Werklund School of Education, University of Calgary. Tom Ricento is the current Chair-holder. The conference is free and lunch is provided. Seating is limited, so register early. The four presenters are:Jillian Tamaki, illustrator for This One Summer, and winner of the Governor General's Award for children's illustration.Richard van Camp, best-selling author of The Lesser Blessed and Three Feathers, and member of the Dogrib Nation.Dr. Nick Sousanis, post-doctoral scholar, teacher and creator of the philosophical comic Unflattening.Dr. Bart Beaty, University of Calgary professor, acclaimed comics scholar and author of Comics vs. Art TD Canadian Children’s Book Week 2016. In 2016, the Canadian Children's Book Centre celebrates 40 years of bringing great Canadian children's books to young readers across the country and the annual TD Canadian Children’s Book Week will be occurring this May across Canada. The theme this year is the celebration of these 40 years of great books written, illustrated and published in Canada as well as stories that have been told over the years. The 2016 tour of storytellers, authors and illustrators and their area of travel are as follows:Alberta: Bob Graham, storyteller; Kate Jaimet, authorBritish Columbia (Interior region) Lisa Dalrymple, author; (Lower Mainland region) Graham Ross, illustrator; (Vancouver Island region) Wesley King, author; (Northern region, Rebecca Bender, author & illustrator.Manitoba: Angela Misri, author; Allison Van Diepen, authorNew Brunswick: Mary Ann Lippiatt, storytellerNewfoundland: Maureen Fergus, authorLabrador: Sharon Jennings, authorNorthwest Territories: Geneviève Després, illustratorNova Scotia: Judith Graves, authorNunavut: Gabrielle Grimard, illustratorOntario: Karen Autio, author; Marty Chan, author; Danika Dinsmore, author; Kallie George, author; Doretta Groenendyk, author & illustrator; Alison Hughes, author; Margriet Ruurs, author.Prince Edward Island: Wallace Edwards, author & illustratorQuebec (English-language tour): LM Falcone, author; Simon Rose, author; Kean Soo, author & illustrator; Robin Stevenson, author; and Tiffany Stone, author/poet.Saskatchewan: (Saskatoon and northern area) Donna Dudinsky, storyteller; (Moose Jaw/Regina and southern area) Sarah Ellis, authorYukon: Vicki Grant, author-----Gail de Vos is an adjunct professor who teaches courses on Canadian children's literature, young adult literature, and comic books & graphic novels at the School of Library and Information Studies (SLIS) at the University of Alberta. She is the author of nine books on storytelling and folklore. Gail is also a professional storyteller who has taught the storytelling course at SLIS for over two decades.