Human Activity Mediates a Trophic Cascade Caused by Wolves

Experimental evidence of trophic cascades initiated by large vertebrate predators is rare in terrestrial ecosystems. A serendipitous natural experiment provided an opportunity to test the trophic cascade hypothesis for wolves (Canis lupus) in Banff National Park, Canada. The first wolf pack recolonized the Bow Valley of Banff National Park in 1986. High human activity partially excluded wolves from one area of the Bow Valley (low-wolf area), whereas wolves made full use of an adjacent area (high-wolf area). We investigated the effects of differential wolf predation between these two areas on elk (Cervus elaphus) population density, adult female survival, and calf recruitment; aspen (Populus tremuloides) recruitment and browse intensity; willow (Salix spp.) production, browsing intensity, and net growth; beaver (Castor canadensis) density; and riparian songbird diversity, evenness, and abundance. We compared effects of recolonizing wolves on these response variables using the log response ratio between the low-wolf and high-wolf treatments. Elk population density diverged over time in the two treatments, such that elk were an order of magnitude more numerous in the low-wolf area compared to the high-wolf area at the end of the study. Annual survival of adult female elk was 62% in the high-wolf area vs. 89% in the low-wolf area. Annual recruitment of calves was 15% in the high-wolf area vs. 27% without wolves. Wolf exclusion decreased aspen recruitment, willow production, and increased willow and aspen browsing intensity. Beaver lodge density was negatively correlated to elk density, and elk herbivory had an indirect negative effect on riparian songbird diversity and abundance. These alternating patterns across trophic levels support the wolf-caused trophic cascade hypothesis. Human activity strongly mediated these cascade effects, through a depressing effect on habitat use by wolves. Thus, conservation strategies based on the trophic importance of large carnivores have increased support in terrestrial ecosystems. Read More: http://www.esajournals.org/doi/full/10.1890/04-126

Early life exposure to broccoli sprouts confers stronger protection against enterocolitis development in an immunological mouse model of inflammatory bowel disease

Crohn’s disease (CD) is a presentation of inflammatory bowel disease (IBD) that manifests in childhood and adolescence and involves chronic and severe enterocolitis, immune and gut microbial dysregulation, and other complications. Diet and gut-microbiota-produced metabolites are sources of anti-inflammatories that could ameliorate symptoms. However, questions remain on how IBD influences biogeographic patterns of microbial location and function in the gut, how early life transitional gut communities are affected by IBD and diet interventions, and how disruption to biogeography alters disease mediation by diet components or microbial metabolites. Many studies on diet and IBD use a chemically induced ulcerative colitis model, despite the availability of an immune-modulated CD model. Interleukin-10-knockout (IL-10-KO) mice on a C57BL/6 background, beginning at age 4 or 7 weeks, were fed a control diet or one containing 10% (wt/wt) raw broccoli sprouts, which was high in the sprout-sourced anti-inflammatory sulforaphane. Diets began 7 days prior to, and for 2 weeks after inoculation with Helicobacter hepaticus, which triggers Crohn’s-like symptoms in these immune-impaired mice. The broccoli sprout diet increased sulforaphane in plasma; decreased weight stagnation, fecal blood, and diarrhea associated; and increased microbiota richness in the gut, especially in younger mice. Sprout diets resulted in some anatomically specific bacteria in younger mice and reduced the prevalence and abundance of pathobiont bacteria which trigger inflammation in the IL-10-KO mouse, for example, Escherichia coli and Helicobacter. Overall, the IL-10-KO mouse model is responsive to a raw broccoli sprout diet and represents an opportunity for more diet-host-microbiome research

Country activities of Global Alliance against Chronic Respiratory Diseases (GARD): focus presentations at the 11th GARD General Meeting, Brussels

© Journal of Thoracic Disease. All rights reserved.The Global Alliance against Chronic Respiratory Diseases (GARD) is a voluntary network of national and international organizations, institutions and agencies led by the World Health Organization (WHO), working towards the vision of a world where all people breathe freely (1). GARD is supporting WHO in successfully implementing the WHO’s Global Action Plan for the Prevention and Control of Noncommunicable Diseases (NCDs) 2013–2020. The GARD report on GARD activities is published on a regular basis. Collaboration among GARD countries is critical for sharing experiences and providing technical assistance to developing countries based on each country’s needs (2). The annual GARD meeting is a unique opportunity for assembling all of the GARD participants from developed and developing countries: European countries, North and South American Countries, China, Vietnam as well as Eastern Mediterranean, and African countries. Coordinator for Management of NCDs in the WHO Department for Management of Noncommunicable Diseases, Disability, Violence and Injury Prevention (Cherian Varghese) is present at this meeting. The annual meeting of GARD is a forum for exchanging opinions in order to improve care for chronic respiratory diseases (CRDs) and to achieve the GARD goal—a world where all people breathe freely. Experts—in collaboration with WHO—are helping developing countries to achieve their projects regarding teaching, research and programming for CRD. Each year, there is a poster presentation session on country activities. Each participant is able to present his/her country activities that have been achieved since the last meeting. This is followed by discussion. In this paper, we summarize the posters presented during the 11th GARD general meeting. We hope that this will give readers of the GARD section an opportunity to learn for their countries. We can find all posters on the link: https://gard-breathefreely.org/resources-poster/.info:eu-repo/semantics/publishedVersio

Epsin 1 Promotes Synaptic Growth by Enhancing BMP Signal Levels in Motoneuron Nuclei

We thank Carl-Henrik Heldin (Uppsala University, Sweden) for his generous gift of the PS1 pMad antibody, Hugo Bellen, Corey Goodman, Janis Fischer, Graeme Davis, Guillermo Marques, Michael O'Connor, Kate O'Connor-Giles, and the Bloomington Drosophila Stock Center for flies strains, the Developmental Studies Hybridoma Bank at the University of Iowa for antibodies to Wit and CSP; Marie Phillips for advice on membrane fractionation; Avital Rodal, Kate O'Connor-Giles, Ela Serpe, Kristi Wharton, Mojgan Padash-Barmchi for discussions or comments on the manuscript. We also thank Jody Summers at OUHSC for her generosity in letting us to use her confocal microscope.Conceived and designed the experiments: PAV TRF LRC BZ. Performed the experiments: PAV TRF LRC SMR HB NER BZ. Analyzed the data: PAV TRF LRC SMR HB NER BZ. Wrote the paper: PAV TRF BZ.Bone morphogenetic protein (BMP) retrograde signaling is crucial for neuronal development and synaptic plasticity. However, how the BMP effector phospho-Mother against decapentaplegic (pMad) is processed following receptor activation remains poorly understood. Here we show that Drosophila Epsin1/Liquid facets (Lqf) positively regulates synaptic growth through post-endocytotic processing of pMad signaling complex. Lqf and the BMP receptor Wishful thinking (Wit) interact genetically and biochemically. lqf loss of function (LOF) reduces bouton number whereas overexpression of lqf stimulates bouton growth. Lqf-stimulated synaptic overgrowth is suppressed by genetic reduction of wit. Further, synaptic pMad fails to accumulate inside the motoneuron nuclei in lqf mutants and lqf suppresses synaptic overgrowth in spinster (spin) mutants with enhanced BMP signaling by reducing accumulation of nuclear pMad. Interestingly, lqf mutations reduce nuclear pMad levels without causing an apparent blockage of axonal transport itself. Finally, overexpression of Lqf significantly increases the number of multivesicular bodies (MVBs) in the synapse whereas lqf LOF reduces MVB formation, indicating that Lqf may function in signaling endosome recycling or maturation. Based on these observations, we propose that Lqf plays a novel endosomal role to ensure efficient retrograde transport of BMP signaling endosomes into motoneuron nuclei.Yeshttp://www.plosone.org/static/editorial#pee

Incorporating critical pedagogy into the scholarship of teaching and learning: making the journey alongside our students

In this paper we draw on our teaching and learning experiences in the management classroom, to illustrate how reflective teaching practices and experiential learning can be used to incorporate critical pedagogy into the SoTL. The exercise described within is one which, at first glance, appears very simple and straight forward, and is perhaps the most basic example of all our experiential practices. However, we found this simple exercise to have powerful learning and reflection effects for both the students and ourselves. This experience, and our subsequent pedagogical reflection, reaffirms the need for educators to remain present in the classroom, and reflective about the impacts of their teaching practices on students

Estratégia global para o diagnóstico, manejo e prevenção da Doença Pulmonar Obstrutiva Crónica

RESUMO: A consciência da importância em termos de saúde da DPOC levou à discussão prolongada e à publicação deste documento, no sentido de propor uma actuação que possa inverter a actual crescente morbilidade e mortalidade desta doença. Nos Estados Unidos é já a 4ª causa de morte e estima-se que em 2020 seja a 5ª causa de morte a nível mundial.à semelhança do projecto GINA desenvolvido para a asma, o GOLD propõe uma definição actual de DPOC, os critérios de gravidade, quais os factores de risco mais frequentes e um plano de actuação dividido em 4 componentes. A DPOC é definida como uma entidade caracterizada por limitação do fluxo aéreo que não é completamente reversível. Esta limitação é habitualmente progressiva e associada a uma resposta inflamatória anormal dos pulmões a partículas tóxicas ou gases. O diagnóstico deve ser considerado num doente com sintomas de tosse, expectoração, ou dispneia, e/ou com história de exposição a factores de risco para a doença (tabagismo, químicos ou poeiras ocupacionais e fumo gerado por combustíveis nas habitações). O diagnóstico é confirmado por espirometria. A presença, após broncodilatador, de um VEMS80% â Estádio II (DPOC moderada) - sintomas eIIA- VEMS entre 80 e 50%IIB- VEMS entre 50 e 30 % â Estádio III (DPOC grave) - com VEMS<30% ou presença de insuficiência respiratória ou cardíaca direita. Os 4 componentes de actuação propostos são: â Componente 1 â diagnóstico, avaliação da gravidade e monitorização da evolução da doença. â Componente 2 â redução dos factores de risco através da prevenção e cessação tabágica (esta medida é considerada como a principal a realizar na prevenção da DPOC na fase pré-clínica da doença), redução da exposição ocupacional e da poluição 'indoor/outdoor'. â Componente 3 â manejo da DPOC estável. â tratamento farmacológico: broncodilatadores e corticóides inalados, estes em especial a partir do Estádio II, se houver boa resposta clínica ou funcional, mas no Estádio IIB devem ser usados para diminuir o número e a gravidade das exacerbações. â tratamento não-farmacológico que pode incluir a reabilitação, a oxigenoterapia e o suporte ventilatório e o tratamento cirúrgico (bulectomia, cirurgia de redução de volume e transplante pulmonar). â Componente 4 â manejo das exacerbações. Neste componente, para além das medidas farmacológicas, são propostos critérios de internamento hospitalar, admissão à unidade de cuidados intensivos, orientações para a instituição de ventilação não-invasiva e suas contra-indicações, e indicações para a ventilação mecânica invasiva. São ainda referidos os critérios da alta hospitalar e do seguimento nas semanas seguintes após a exacerbação. A finalizar, o GOLD aponta áreas de investigação futura para uma melhor compreensão e tratamento da DPOC. COMENTÃRIO: Qualquer comentário a este documento de profunda solidez científica será desajustado, inoportuno e pretensioso. Constitui de facto uma das mais importantes e a mais recente 'bíblia' em que nos devemos basear para tratar os doentes com DPOC. No entanto, assisti à discussão pública nos últimos anos, nas mais importantes reuniões pneumológicas internacionais, e penso que ficaram algumas questões por responder.à do conhecimento geral que existem doentes com critérios clínicos e funcionais de DPOC que não apresentam os factores de risco acima mencionados. Deverse-á por esse motivo considerar o estudo funcional respiratório como um exame de rotina?à sabido que os factores de agudização mais frequentes são as infecções respiratórias e que a flora envolvida depende da gravidade clínica e funcional dos doentes. Não seria de propor também uma antibioterapia diferenciada e baseada nos critérios de gravidade, associada ao tratamento segundo a gravidade, e que essencialmente refere os broncodilatadores e corticóides inalados? Uma vez que a DPOC é considerada uma doença inflamatória diferente da asma, por que não considerar um tratamento anti-inflamatório nos doentes graves não agudizados com corticóides orais e/ou imunossupressores?Todos os que têm experiência em ventilação não-invasiva, e confrontados com as dificuldades em instituir esta terapêutica em grande número de doentes, não concordarão com a afirmação de que esta modalidade de tratamento não está indicada no doente grave e estável, como eventual terapêutica de base como acontece com a oxigenoterapia, mas apenas nas exacerbações dos mesmos doentes graves. Por fim, é de lamentar a ausência de um português no comité científico do Projecto GOLD.Convém recordar que em 1997 foi terminado em Portugal um enorme estudo epidemiológico (Projecto PNEUMOBIL) que avaliou mais de 12 000 indivíduos e que permitiu calcular que em Portugal existem mais de 33 000 doentes no agora definido Estádio IIA, cerca de 10 000 no Estádio IIB e cerca de 8 000 no Estádio III. Esta difícil realidade epidemiológica, económica e humana também nos toca a nós.REV PORT PNEUMOL VII(4):39