115 research outputs found
Small_Scale_Fishery_ Fish2Sustainability _Data_2023
No full text<p><strong>Dataset name -</strong> World_ IRD_ Small_Scale_Fishery_Data_2023</p>
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<p><strong>Title:</strong> Qualitative Data on 61 Small-Scale Fisheries: A socio-ecological rapid appraisal applied to cases from Colombia, Ecuador, France, Kenya, Madagascar, Mexico, and Nigeria.</p>
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<p><strong>Description</strong></p>
<p>This dataset was created for the Fish2Sustainability research project, which aims to evaluate how small-scale fisheries (SSF) contribute to Sustainable Development Goals (SDGs). The dataset includes 61 case studies across seven countries and was developed using a rapid appraisal framework. The framework includes a four-step process:</p>
<ol>
<li>Identifying specific SDG targets influenced by SSF;</li>
<li>Extracting relevant variables from UN indicators;</li>
<li>Gathering expert input via a questionnaire to score these variables;</li>
<li>Creating composite indicators to measure SSF performance against SDGs.</li>
</ol>
<p>The dataset contains raw data from step 3, case study details, variable scores, and comments from data collectors (contributing authors). The dataset is valuable for researchers interested in small-scale fisheries and socio-ecological systems. By incorporating expert judgments from individuals with expertise in SSF, particularly in data-poor contexts, the dataset offers a wealth of knowledge for conducting comparative analyses across different contexts.</p>
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<p><strong>Authors</strong></p>
<p>Léopold, M.<sup>1</sup>, Bitoun, R.E.<sup>2</sup>, Chuenpagdee, R.<sup>3</sup>, Fondo, E.N.<sup>4</sup>, Akintola, S.L.<sup>5</sup>, Bach, P.<sup>6</sup>, Frangoudes, K.<sup>7</sup>, Gaibor, N.<sup>8</sup>, Gutierrez-Cala, L.<sup>9</sup>, Massey, Y.<sup>6</sup>, Randrianandrasana, R.<sup>10</sup>, Razanakoto, T.<sup>10</sup>, Saavedra-Díaz, L.M.<sup>9</sup>, Salas, S.<sup>11</sup>, Devillers, R.<sup>2, 3</sup></p>
<p><strong>Affiliations</strong></p>
<p><sup>1</sup> ENTROPIE (IRD, University of La Reunion, CNRS, University of New Caledonia, Ifremer), c/o IUEM, Plouzané, France</p>
<p><sup>2</sup> Espace-Dev (IRD, Univ. Montpellier, Univ. Guyane, Univ. La Réunion, Univ. Antilles, Univ. Nouvelle Calédonie), Montpellier, France</p>
<p><sup>3</sup> Department of Geography, Memorial University of Newfoundland, St. John’s, NL, Canada</p>
<p><sup>4</sup> Kenya Marine and Fisheries Research Institute (KMFRI), Mombasa, Kenya</p>
<p><sup>5</sup> Department of Fisheries, Faculty of Science, Lagos State University, Lagos, Nigeria</p>
<p><sup>6 </sup>MARBEC (University of Montpellier, CNRS, Ifremer, IRD), Sète, France</p>
<p><sup>7</sup> Université de Bretagne Occidentale, Brest, France</p>
<p><sup>8</sup> Instituto Público de Investigación de Acuicultura y Pesca (IPIAP), Universidad del Pacifico (UPAC), Guayaquil, Ecuador</p>
<p><sup>9</sup> Grupo de Investigación en Sistemas Socioecológicos para el Bienestar Humano (GISSBH), Programa de Biología, Universidad del Magdalena, Colombia</p>
<p><sup>10</sup> Centre d’Etudes et de Recherches Economiques pour le Développement (CERED), Université d’Antananarivo, Madagascar</p>
<p><sup>11</sup> Centro de Investigación y de Estudios Avanzados (CINVESTAV), IPN, Unidad Mérida, Mexico</p>
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<p><strong>Method</strong></p>
<p>Case studies were selected in seven countries by national SSF experts, based on specific criteria and research priorities. Case studies were not selected to represent the full diversity of SSF globally or even nationally. Instead, they were chosen to capture a range of fisheries that could showcase different contributions to SDGs. SSFs were defined based on various characteristics, such as resources harvested, gear used, and location of the fishery.</p>
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<p><strong>Geographical Coverage</strong></p>
<p>61 small-scale fisheries located in seven countries are documented in the data:</p>
<ul>
<li>Colombia (4 case studies) – Caribe: La Guajira, San Andrés y Providencia; Pacifico: Chocó, Cauca, Valle del Cauca, Nariño.</li>
<li>Ecuador (3) – Region: Esmeraldas, Manabi, Guayas, El Oro.</li>
<li>France (2) – Region: Bretagne, Occitanie.</li>
<li>Kenya (24) – County: Kilifi, Kwale, Lamu, Mombasa, Tana River.</li>
<li>Madagascar (20) – Region: Analanjirofo, Anosy, Atsimo Andrefana, Boeny, Diana, Menabe, Vatovavy Fitovinany.</li>
<li>Mexico (2) – State: Baja California Sur, Campeche, Yucatan.</li>
<li>Nigeria (6) – State: Bayelsa, Cross River, Lagos, Ondo, Ogun.</li>
</ul>
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<p><strong>Data Collection</strong></p>
<p>Data collection took place from November 30, 2022, to July 3, 2023, spanning approximately seven months. The data presented serve as a snapshot of the conditions within a specific small-scale fishery during the assessment period. To consider the evolution of trends such as exports, economic growth, and income, we considered any relevant variables over the past decade.</p>
<p>Data collection approaches varied depending on the context, and data collectors received training to ensure survey consistency. We used primary data sources such as interviews, observations, and measurements whenever possible. In cases where resources were limited, we preferred secondary sources such as existing datasets and literature. Our methods were standardized, but data collectors could adjust them based on their resources. We primarily used direct observation, focus groups, and interviews to collect data. Scoring in interviews and focus groups was done directly or through group analysis by interviewers. Disagreements were resolved through additional interviews or group discussions, with secondary data used if needed.</p>
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<p><strong>Ethics</strong></p>
<p>Participants had the option to join of their own accord, were fully briefed on the research goals, and were given the opportunity to review interview guidelines before proceeding. Depending on the circumstances, interviews could last 45 minutes to 4.5 hours. Participants were guaranteed confidentiality and anonymity in the handling and reporting of their data.</p>
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<p><strong>Suggested citation</strong></p>
<p>Léopold, M., Bitoun, R.E., Chuenpagdee, R., Fondo, E.N., Akintola, S.L., Bach, P., Frangoudes, K., Gaibor, N., Gutierrez-Cala, L., Massey, Y., Randrianandrasana, R., Razanakoto, T., Saavedra-Díaz, L.M., Salas, S., Devillers, R. (2023). World_ IRD_ Small_Scale_Fishery_Data_2023 [Data set]. DOI: 10.5281/zenodo.8321911</p>
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<p><strong>Data Files</strong></p>
<p>The dataset includes the following:</p>
<ul>
<li>The raw dataset (.xls format).</li>
<li>A data dictionary describing and defining each dataset column (.xls format).</li>
</ul>
Molecular mechanisms involved in the transduction efficiency of AAV vectors in dystrophic muscle
No full textLa Dystrophie Musculaire de Duchenne (DMD) est une maladie génétique causée par l’absence de dystrophine et provoquant une dégénérescence musculaire sévère. Aucun traitement curatif n’existe aujourd’hui mais la thérapie génique par vecteur AAV est l’une des stratégies les plus prometteuses pour traiter la DMD. Malgré l’efficacité bien établie de l’AAV de sérotype 8 (AAV8) pour le transfert de gène dans le muscle, de fortes doses de vecteurs sont nécessaires pour obtenir une efficacité thérapeutique dans des modèles animaux de la DMD. Dans ce contexte, j’ai étudié les mécanismes qui peuvent limiter l’efficacité de transduction du vecteur AAV8 dans le muscle dystrophique. Pour cela, j’ai étudié le devenir du vecteur AAV dans le muscle DMD puis caractérisé le système endosomal, essentiel au transport et la maturation des vecteurs AAV, dans différents modèles de la DMD. Mes résultats ont montré que l’efficacité de transduction de l’AAV8 est plus faible dans les cellules musculaires DMD comparées aux contrôles. De plus, la dérégulation du système endosomal dans la DMD peut impacter le transfert de gène par vecteur AAV dans ces cellules. Par ailleurs, l'amélioration de l'efficacité des vecteurs AAV en thérapie génique nécessite aussi une meilleure connaissance des protéines cellulaires qui interagissent avec le génome viral et qui régulent son expression. Dans ce contexte, nous avons montré que les facteurs de transcription RFX1 et RFX3 sont capables d’interagir avec la région ITR du génome viral et de moduler l’expression des vecteurs AAV.Duchenne Muscular Dystrophy (DMD) is a genetic disorder caused by the absence of dystrophin and causing severe muscle degeneration. No curative treatment exists today but AAV-based gene therapy is one of the most promising strategies for treating DMD. Despite the well-established efficacy of AAV serotype 8 (AAV8) for gene transfer into muscle, high doses of vectors are required to achieve therapeutic efficacy in DMD animal models. In this context, I aimed at investigating the mechanisms that may limit the transduction efficiency of the AAV8 vector in dystrophic muscle. For this, I studied the fate of the AAV vector in the DMD muscle and then characterized the endosomal system, essential for the transport and maturation of AAV vectors, in different models of DMD. We have shown that the transduction efficiency of AAV8 is lower in DMD muscle cells compared to controls. The dysfunction of the endosomal system identified in this study may impact AAV vector gene transfer into these cells. Moreover, improving the efficiency of AAV vectors in gene therapy also requires a better understanding of cellular proteins that interact with the viral genome and regulate its expression. In this context, we have shown that the transcription factors RFX1 and RFX3 are able to interact with the ITR region of the viral genome and to modulate the expression of AAV vectors
La myopathie centronucléaire liée au gène de la dynamine 2
No full textLa myopathie centronucléaire autosomique dominante (AD-CNM) est une myopathie congénitale rare caractérisée par une faiblesse musculaire et par la présence de noyaux centraux dans les fibres musculaires en absence de tout processus de régénération. L’AD-CNM est due à des mutations du gène DNM2 codant la dynamine 2 (DNM2), une volumineuse GTPase impliquée dans le trafic membranaire intracellulaire et un régulateur des cytosquelettes d’actine et de microtubules. Les mutations de la DNM2 sont associées à un large éventail clinique allant de formes sévères néonatales à des formes moins graves à début plus tardif. La signature histopathologique inclut une centralisation nucléaire, une prédominance et une atrophie des fibres lentes, ainsi que des travées sarcoplasmiques en rayons de roue. Pour expliquer la dysfonction musculaire, plusieurs mécanismes physiopathologiques affectant des étapes clés de l’homéostasie musculaire ont été identifiés. Ils incluent des défauts du couplage excitation-contraction, de la régénération musculaire, des mitochondries ou de l’autophagie. Plusieurs approches thérapeutiques sont en développement, en particulier la modulation de l’expression de la DNM2 pan-allélique ou ne ciblant que l’allèle muté, ouvrant ainsi la porte à des essais cliniques dans cette pathologie
Netherton syndrome showing a large clinical overlap with generalized inflammatory peeling skin syndrome
No full text[No abstract available]Bitoun E, 2003, HUM MOL GENET, V12, P2417, DOI 10.1093-hmg-ddg247; Bitoun E, 2002, J INVEST DERMATOL, V118, P352, DOI 10.1046-j.1523-1747.2002.01603.x; Chavanas S, 2000, NAT GENET, V25, P141; Levy-Nissenbaum E, 2003, NAT GENET, V34, P151, DOI 10.1038-ng1163; Oji V, 2010, AM J HUM GENET, V87, P274, DOI 10.1016-j.ajhg.2010.07.005; Yang T, 2004, GENE DEV, V18, P2354, DOI 10.1101-gad.123210411
A review of Dynamin 2 involvement in cancers highlights a promising therapeutic target
No full textInternational audienceDynamin 2 (DNM2) is an ubiquitously expressed large GTPase well known for its role in vesicle formation in endocytosis and intracellular membrane trafficking also acting as a regulator of cytoskeletons. During the last two decades, DNM2 involvement, through mutations or overexpression, emerged in an increasing number of cancers and often associated with poor prognosis. A wide panel of DNM2-dependent processes was described in cancer cells which explains DNM2 contribution to cancer pathomechanisms. First, DNM2 dysfunction may promote cell migration, invasion and metastasis. Second, DNM2 acts on intracellular signaling pathways fostering tumor cell proliferation and survival. Relative to these roles, DNM2 was demonstrated as a therapeutic target able to reduce cell proliferation, induce apoptosis, and reduce the invasive phenotype in a wide range of cancer cells in vitro. Moreover, proofs of concept of therapy by modulation of DNM2 expression was also achieved in vivo in several animal models. Consequently, DNM2 appears as a promising molecular target for the development of anti-invasive agents and the already provided proofs of concept in animal models represent an important step of preclinical development
Chevauchement génétique entre neuropathies et myopathies : vers une convergence des deux entités
No full textLes neuropathies et les myopathies ont longtemps été étudiées séparément, avec peu ou pas de recouvrement décrit entre les deux entités. Toutefois, l’avènement de la biologie moléculaire à haut débit au cours des 20 dernières années a permis de découvrir des mutations d’un même gène causant myopathies et neuropathies héréditaires. Si ce chevauchement est bien connu pour les gènes mitochondriaux, il est plus inattendu pour des gènes tels que BAG3, DES et CRYAB, mutés à la fois dans les myopathies myofibrillaires et dans des neuropathies pouvant être isolées ou associées à des atteintes musculaires. Plus récemment, des gènes impliqués dans des protéinopathies multi-systémiques, tels que VCP, MATR3, SQTMS1 et TIA1 ont également été associés à diverses combinaisons de lésions nerveuses, cérébrales, musculaires et osseuses. D’autre part, des gènes comme HSPB8 ou SPTAN1, connus pour être responsables de neuropathie motrice distale, ont été impliqués dans la myopathie distale et/ou axiale ou dans un tableau mixte combinant des composantes neurogène et myogène, à la fois électromyographiquement et histologiquement. Au fur et à mesure que les techniques de séquençage progressent, des corrélations génotype-phénotype inattendues apparaissent, impliquant un gène de myopathie dans une neuropathie périphérique et vice versa, conduisant à réévaluer le chevauchement existant entre ces deux entités
Gene Expression of Taurine Transporter and Taurine Biosynthetic Enzymes in Hyperosmotic States
No full textOn D-modules related to the b-function and Hamiltonian flow
No full textLet f be a quasi-homogeneous polynomial with an isolated singularity in Cn . We compute the length of the D -modules Df/Df+1 generated by complex powers of f in terms of the Hodge filtration on the top cohomology of the Milnor fiber. When =−1 we obtain one more than the reduced genus of the singularity ( dimHn−2(Z,OZ) for Z the exceptional fiber of a resolution of singularities). We conjecture that this holds without the quasi-homogeneous assumption. We also deduce that the quotient Df/Df+1 is nonzero when is a root of the b -function of f (which Saito recently showed fails to hold in the inhomogeneous case). We obtain these results by comparing these D -modules to those defined by Etingof and the second author which represent invariants under Hamiltonian flow
Calcium homeostasis alterations in a mouse model of the Dynamin 2-related centronuclear myopathy
No full textInternational audienceAutosomal dominant centronuclear myopathy (CNM) is a rare congenital myopathy characterized by centrally located nuclei in muscle fibers. CNM results from mutations in the gene encoding dynamin 2 (DNM2), a large GTPase involved in endocytosis, intracellular membrane trafficking, and cytoskeleton regulation. We developed a knock-in mouse model expressing the most frequent DNM2-CNM mutation; i.e. the KI-Dnm2 R465W model. Heterozygous (HTZ) KI-Dnm2 mice progressively develop muscle atrophy, impairment of contractile properties, histopathological abnormalities, and elevated cytosolic calcium concentration. Here, we aim at better characterizing the calcium homeostasis impairment in extensor digitorum longus (EDL) and soleus muscles from adult HTZ KI-Dnm2 mice. We demonstrate abnormal contractile properties and cytosolic Ca 2+ concentration in EDL but not soleus muscles showing that calcium impairment is correlated with muscle weakness and might be a determinant factor of the spatial muscle involvement. In addition, the elevated cytosolic Ca 2+ concentration in EDL muscles is associated with an increased sarcolemmal permeability to Ca 2+ and releasable Ca 2+ content from the sarcoplasmic reticulum. However, amplitude and kinetics characteristics of the calcium transient appear unchanged. This suggests that calcium defect is probably not a primary cause of decreased force generation by compromised sarcomere shortening but may be involved in long-term deleterious consequences on muscle physiology. Our results highlight the first pathomechanism which may explain the spatial muscle involvement occurring in DNM2-related CNM and open the way toward development of a therapeutic approach to normalize calcium content
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