Entrevista a Jane Goodall, primatòloga

Va lluitar contra tot allò que l'impedia realitzar el seu somni a l'Àfrica, contra els estaments universitaris a Cambridge i ara lluita contra la desesperança del món actual. La primatòloga anglesa Jane Goodall va visitar la Universitat Autònoma de Barcelona per a una trobada internacional del Jane Goodall Institute. Aprofitant aquesta visita li vam fer una breu entrevista.Luchó contra todo lo que le impedía realizar su sueño en África, contra los estamentos universitarios en Cambridge y ahora lucha contra la desesperanza del mundo actual. La primatóloga Jane Goodall visitó la Universitat Autònoma de Barcelona para un encuentro internacional del Jane Goodall Institute. Aprovechando esta visita le hicimos una breve entrevista.She fought against all that prevented her from making her dreams in Africa come true, she fought against the establishment at Cambridge and now she is fighting against hopelessness in the world. Primatologist Jane Goodall visited Universitat Autònoma de Barcelona for an international meeting of the Jane Goodall Institutes. Taking advantage of her visit the university had the chance to interview her

Sharing the information with locals

It is rare for a journal to provide information not only about research and conservation of wildlife and wildlife habitats, but also about human development. The editors are to be congratulated, since my own experience in Africa makes it clear that long-term conservation can never be successful unless local people are taken into consideration. It is essential to raise the standard of living and education of the very poor, whilst ensuring that any development that results is environmentally sustainable. This journal thus provides a unique forum for the exchange of ideas and sharing of information between research, conservation and humanitarian organizations. There is no shortage of NGO´s in Madagascar, but many are working in isolation, unaware of others with similar concerns and projects: yet my experience suggests that when such organizations agree to cooperate, their effectiveness often increases dramatically. Madagascar, despite the damage inflicted on its island environment, is still stunningly beautiful with a rich diversity of flora and fauna. But unless everyone works together to save what is left and restore some crucially important habitats, whilst gaining the goodwill of the local people, many species will become extinct during this century. Thus I hope that, over the years, this journal will grow, both in scope and in its ability to reach ever more interest groups.Jane Goodall Ph.D., DB

Problems in combinatorics: Paths in graphs, partial orders of fixed width.

This thesis contains results in two areas, that is, graph theory and partial orders. (1) We consider graphs G with a specified subset W of vertices of large degree. We look for paths in G containing many vertices of W. The main results of the thesis are as follows. For G a graph on n vertices, and W of size w and minimum degree d, we show that there is always a path through at least vertices of W. We also prove some results for graphs in which only the degree sums of sets of independent vertices in W are known. (2) Let P = (X, ) be a poset on a set {lcub}1, 2,..., N{rcub}. Suppose X1 and X2 are a pair of disjoint chains in P whose union is X. Then P is a partial order of width two. A labelled poset is a partial order on a set {lcub}1, 2,..., N{rcub}. Suppose we have two labelled posets, P1 and P2, that are isomorphic. That is, there is a bijection between P1 and P2 which preserves all the order relations. Each isomorphism class of labelled posets corresponds to an unlabelled poset. (Abstract shortened by UMI.)

Jane Goodall Collection - Accession 1764

This collection consists mostly of memorabilia concerning Jane Goodall collected by Linda Driggers Williams (Winthrop Class of 1964, ‘69, ’82). Jane Goodall (b. 1934) is a conservationist and primatologist most known for her long-term study of wild chimpanzees in Tanzania and came to Rock Hill, SC in 1990 to lecture at Winthrop College and at the York County Museum. Contents include four books concerning Jane Goodall, three magazines concerning Jane Goodall, two photographs and three negatives of Jane Goodall, four newspaper articles concerning Jane Goodall, a Jane Goodall T-shirt, and a hard copy and digital copy of a talk given by Jane Goodall at the Museum of York County in 1990.https://digitalcommons.winthrop.edu/manuscriptcollection_findingaids/2778/thumbnail.jp

A model for best practice HTA

The aims of this paper are: to review and describe different approaches to HTA used in Australia and in other countries and to identify the features of best practice in HTA, particularly those likely to be most relevant to HTA at a local (ie state/regional) level. There are a number of well-developed models of HTA at the national and local levels. Most information about the operation of these models, particularly about the type and number of evaluations conducted, the recommendations/decisions made and the reasons for these is available for national processes, but there is much less readily available documentation about local level HTA. Most HTA processes that operate nationally and internationally can be categorised in one of three ways: guidance (provides structured information about appropriate technologies), mandatory (provides mandatory information about technologies to be implemented) and funding and implementation (provides structured evidence-based advice about which technologies should be implemented, the level of funding required to implement them and the source of these funds). The main factors which distinguish a high quality HTA process are that i) it is efficient in terms of setting priorities, the scope of the technologies to be assessed, avoidance of duplication and overall cost of the process, ii) the overall impact on utilisation and health budget is calculated as part of the HTA and iii) procedural justice occurs and is seen to occur; iv) it includes a comprehensive assessment of the impact on issues such as workforce, credentialing of providers and the ethical dimension of the technology; v) it influences decision making by being communicated appropriately and using trusted methods; vi) it influences adoption and diffusion of technology by ensuring that there is no diffusion prior to HTA, the results are incorporated into guidelines or recommendations, funding is linked to the decision, and remuneration arrangements and other characteristics of the HS facilitate the appropriate adoption and diffusion and vii) it influences health outcomes/efficiency/equity by ensuring that the methods and/or results are available and able to be used at a local level. Firm recommendations for an ideal system for HTA at the local level are not possible as much of the necessary information and evidence is not available about the strengths and weaknesses of HTA practices and processes currently in use. However, it is likely that the operation of a successful model of HTA at a local level would require the development of a central organizational unit, a process for implementing the results of HTA and, crucially, the building of capacity to support both types of activities. Additional expertise and skills will be required for both providers of HTA evaluations and for the commissioners and users of HTA.health technology assessment, Australia, review

What are the barriers and enablers to trauma-informed emergency departments? A scoping review protocol

Introduction There is a high prevalence of psychological trauma among the population. Such people are more likely to have poorer health outcomes and these factors may contribute to increased use of the emergency department. There has been some attempt to implement a trauma-informed approach across public services, especially in health and social care. However, it is unclear how this concept applies to the challenging and high-demand emergency department context. The review aims to locate, examine and describe the literature on trauma-informed care in the unique and challenging healthcare delivery context that is the emergency department. The review aims to identify the barriers and enablers that may facilitate trauma-informed care in the emergency department context. Methods and analysis This scoping review will use the Joanna Briggs Institute methodology for scoping reviews. Systematic searches of relevant databases (CINAHL, MEDLINE, PsycINFO, EMBASE, Knowledge Network and Web of Science) will be conducted. Empirical studies of any methodological approach, published in English between January 2001 and September 2023 will be included. The 'grey' literature will also be accessed. Two reviewers will independently screen all studies. Data will be extracted, collated and charted to summarise all the relevant methods, outcomes and key findings in the articles. Ethics and dissemination Formal ethical approval is not required. The findings of this study will be disseminated through peer-reviewed publications, conference presentations and condensed summaries for key stakeholders in the field. The data generated will be used to inform a programme of work related to trauma-informed care.</p

Tslp Production by Dendritic Cells Is Modulated by IL-1β and Components of the Endoplasmic Reticulum Stress Response

Thymic stromal lymphopoietin (TSLP) produced by epithelial cells acts on dendritic cells (DCs) to drive differentiation of TH2-cells, and is therefore important in allergic disease pathogenesis. However, DCs themselves make significant amounts of TSLP in response to microbial products, but little is known about the key downstream signals that induce and modulate this TSLP secretion from human DCs. We show that human monocyte derived DC (mDC) secretion of TSLP in response to Candida albicans and β-glucans requires dectin-1, Syk, NF-κB, and p38 MAPK signaling. In addition, TSLP production by mDCs is greatly enhanced by IL-1β, but not TNF-α, in contrast to epithelial cells. Furthermore, TSLP secretion is significantly increased by signals emanating from the endoplasmic reticulum (ER) stress response, specifically the unfolded protein response sensors, inositol-requiring transmembrane kinase/endonuclease 1 and protein kinase R-like ER kinase, which are activated by dectin-1 stimulation. Thus, TSLP production by mDCs requires the integration of signals from dectin-1, the IL-1 receptor, and ER stress signaling pathways. Autocrine TSLP production is likely to play a role in mDC-controlled immune responses at sites removed from epithelial cell production of the cytokine, such as lymphoid tissue

Necrotic Cell Sensor Clec4e Promotes a Proatherogenic Macrophage Phenotype Through Activation of the Unfolded Protein Response.

BACKGROUND: Atherosclerotic lesion expansion is characterized by the development of a lipid-rich necrotic core known to be associated with the occurrence of complications. Abnormal lipid handling, inflammation, and alteration of cell survival or proliferation contribute to necrotic core formation, but the molecular mechanisms involved in this process are not properly understood. C-type lectin receptor 4e (Clec4e) recognizes the cord factor of Mycobacterium tuberculosis but also senses molecular patterns released by necrotic cells and drives inflammation. METHODS: We hypothesized that activation of Clec4e signaling by necrosis is causally involved in atherogenesis. We addressed the impact of Clec4e activation on macrophage functions in vitro and on the development of atherosclerosis using low-density lipoprotein receptor-deficient (Ldlr-/-) mice in vivo. RESULTS: We show that Clec4e is expressed within human and mouse atherosclerotic lesions and is activated by necrotic lesion extracts. Clec4e signaling in macrophages inhibits cholesterol efflux and induces a Syk-mediated endoplasmic reticulum stress response, leading to the induction of proinflammatory mediators and growth factors. Chop and Ire1a deficiencies significantly limit Clec4e-dependent effects, whereas Atf3 deficiency aggravates Clec4e-mediated inflammation and alteration of cholesterol efflux. Repopulation of Ldlr-/- mice with Clec4e-/- bone marrow reduces lipid accumulation, endoplasmic reticulum stress, and macrophage inflammation and proliferation within the developing arterial lesions and significantly limits atherosclerosis. CONCLUSIONS: Our results identify a nonredundant role for Clec4e in coordinating major biological pathways involved in atherosclerosis and suggest that it may play similar roles in other chronic inflammatory diseases.This work was supported by a European Research Council grant (to Z.M.), and by the British Heart Foundation (Z. M.).This is the author accepted manuscript. The final version is available from the American Heart Association via https://doi.org/10.1161/CIRCULATIONAHA.116.02266

Necrotic Cell Sensor Clec4e Promotes a Proatherogenic Macrophage Phenotype Through Activation of the Unfolded Protein Response

$\textbf{Background}$: Atherosclerotic lesion expansion is characterized by the development of a lipid-rich necrotic core known to be associated with the occurrence of complications. Abnormal lipid handling, inflammation, and alteration of cell survival or proliferation contribute to necrotic core formation, but the molecular mechanisms involved in this process are not properly understood. C-type lectin receptor 4e (Clec4e) recognizes the cord factor of Mycobacterium $\textit{tuberculosis}$ but also senses molecular patterns released by necrotic cells and drives inflammation. $\textbf{Methods}$: We hypothesized that activation of Clec4e signaling by necrosis is causally involved in atherogenesis. We addressed the impact of Clec4e activation on macrophage functions in vitro and on the development of atherosclerosis using low-density lipoprotein receptor–deficient ($\textit{Ldlr}$$^{−/−}$) mice in vivo. $\textbf{Results}$: We show that Clec4e is expressed within human and mouse atherosclerotic lesions and is activated by necrotic lesion extracts. Clec4e signaling in macrophages inhibits cholesterol efflux and induces a Syk-mediated endoplasmic reticulum stress response, leading to the induction of proinflammatory mediators and growth factors. $\textit{Chop }$and $\textit{Ire1a}$ deficiencies significantly limit Clec4e-dependent effects, whereas $\textit{Atf}$3 deficiency aggravates Clec4e-mediated inflammation and alteration of cholesterol efflux. Repopulation of $\textit{Ldlr}$$^{−/−}$ mice with $\textit{Clec4e}$$^{−/−}$ bone marrow reduces lipid accumulation, endoplasmic reticulum stress, and macrophage inflammation and proliferation within the developing arterial lesions and significantly limits atherosclerosis. $\textbf{Conclusions}$: Our results identify a nonredundant role for Clec4e in coordinating major biological pathways involved in atherosclerosis and suggest that it may play similar roles in other chronic inflammatory diseases.This work was supported by a European Research Council grant (to Z.M.), and by the British Heart Foundation (Z. M.).This is the author accepted manuscript. The final version is available from the American Heart Association via https://doi.org/10.1161/CIRCULATIONAHA.116.02266

IL-1α cleavage by inflammatory caspases of the noncanonical inflammasome controls the senescence-associated secretory phenotype.

Interleukin-1 alpha (IL-1α) is a powerful cytokine that modulates immunity, and requires canonical cleavage by calpain for full activity. Mature IL-1α is produced after inflammasome activation and during cell senescence, but the protease cleaving IL-1α in these contexts is unknown. We show IL-1α is activated by caspase-5 or caspase-11 cleavage at a conserved site. Caspase-5 drives cleaved IL-1α release after human macrophage inflammasome activation, while IL-1α secretion from murine macrophages only requires caspase-11, with IL-1β release needing caspase-11 and caspase-1. Importantly, senescent human cells require caspase-5 for the IL-1α-dependent senescence-associated secretory phenotype (SASP) in vitro, while senescent mouse hepatocytes need caspase-11 for the SASP-driven immune surveillance of senescent cells in vivo. Together, we identify IL-1α as a novel substrate of noncanonical inflammatory caspases and finally provide a mechanism for how IL-1α is activated during senescence. Thus, targeting caspase-5 may reduce inflammation and limit the deleterious effects of accumulated senescent cells during disease and Aging.Work was funded by British Heart Foundation grants FS/13/3/30038, FS/18/19/33371 and RG/16/8/32388 (MC); Cancer Research UK Cambridge Institute Core Grant C14303/A17197, Medical Research Council grants MR/M013049/1 and MR/R010013/1 (MN); and the Cambridge NIHR Biomedical Research Centre