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Добірка наукової літератури з теми "EVs trafficking"

Автор: Grafiati

Опубліковано: 14 березня 2023

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Статті в журналах з теми "EVs trafficking"

Maire, Cecile, Amanda Salviano-Silva, Katharina Kolbe, Manfred Westphal, Katrin Lamszus, and Franz Ricklefs. "TMIC-64. EXTRACELLULAR VESICLE TRAFFICKING IN GBM." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii285—vii286. http://dx.doi.org/10.1093/neuonc/noac209.1108.

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Abstract Extracellular vesicles (EVs) are secreted by all cell types, including tumor cells, and are found in increased numbers in the plasma of GBM patients. EVs may contain high-value genetic material that can be useful for tracking tumor development, as well as membrane proteins that affect other cells. This prompted us to investigate how tumor EVs might influence immune cells in glioma, and in primary and secondary lymphoid organs as well as in the circulation. To this end we used a syngeneic GBM mouse model and tracked tumor EVs from the brain to the meninges, cervical lymph nodes, plasma, bone marrow and spleen. Interestingly, we were able to identify tumor EVs mostly in the cervical lymph nodes by ImageStream imaging flow cytometry just 30min after tumor EV injection into the brain. However, when tumor EVs were produced by a large gliomas transfected with dTomato, we found them mainly in plasma, less frequently in bone marrow and never in the spleen. We confirmed these data by extracting DNA from EVs and detecting specific dTomato sequences using digital droplet PCR. In addition, we detected CD11b+ macrophages in the meninges that likely travel through the lymphatics that have taken up tumor EV or tumor material. We confirm that tumor EVs are capable of eliciting an immune response by activating T cells. However, prolonged contact and large number of EVs could also block antigen recognition by T cells and thus contribute to the propagation of an immunosuppressive environment in GBM.

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Kumar, Prashant, Fahad Zadjali, Ying Yao, Michael Köttgen, Alexis Hofherr, Kenneth W. Gross, Darshan Mehta, and John J. Bissler. "Single Gene Mutations in Pkd1 or Tsc2 Alter Extracellular Vesicle Production and Trafficking." Biology 11, no. 5 (May 6, 2022): 709. http://dx.doi.org/10.3390/biology11050709.

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Patients with autosomal dominant polycystic kidney disease (ADPKD) and tuberous sclerosis complex (TSC) are born with normal or near-normal kidneys that later develop cysts and prematurely lose function. Both renal cystic diseases appear to be mediated, at least in part, by disease-promoting extracellular vesicles (EVs) that induce genetically intact cells to participate in the renal disease process. We used centrifugation and size exclusion chromatography to isolate the EVs for study. We characterized the EVs using tunable resistive pulse sensing, dynamic light scattering, transmission electron microscopy, and Western blot analysis. We performed EV trafficking studies using a dye approach in both tissue culture and in vivo studies. We have previously reported that loss of the Tsc2 gene significantly increased EV production and here demonstrate that the loss of the Pkd1 gene also significantly increases EV production. Using a cell culture system, we also show that loss of either the Tsc2 or Pkd1 gene results in EVs that exhibit an enhanced uptake by renal epithelial cells and a prolonged half-life. Loss of the primary cilia significantly reduces EV production in renal collecting duct cells. Cells that have a disrupted Pkd1 gene produce EVs that have altered kinetics and a prolonged half-life, possibly impacting the duration of the EV cargo effect on the recipient cell. These results demonstrate the interplay between primary cilia and EVs and support a role for EVs in polycystic kidney disease pathogenesis.

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Santamaria, Sara, Maria Cristina Gagliani, Grazia Bellese, Silvia Marconi, Anastasia Lechiara, Martina Dameri, Cinzia Aiello, Erica Tagliatti, Patrizio Castagnola, and Katia Cortese. "Imaging of Endocytic Trafficking and Extracellular Vesicles Released Under Neratinib Treatment in ERBB2+ Breast Cancer Cells." Journal of Histochemistry & Cytochemistry 69, no. 7 (June 15, 2021): 461–73. http://dx.doi.org/10.1369/00221554211026297.

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Breast cancers (BCa) with ERBB2 amplification show rapid tumor growth, increased disease progression, and lower survival rate. Deregulated intracellular trafficking and extracellular vesicle (EVs) release are mechanisms that support cancer progression and resistance to treatments. Neratinib (NE) is a Food and Drug Administration–approved pan-ERBB inhibitor employed for the treatment of ERBB2+ BCa that blocks signaling and causes survival inhibition. However, the effects of NE on ERBB2 internalization, its trafficking to multivesicular bodies (MVBs), and the release of EVs that originate from these organelles remain poorly studied. By confocal and electron microscopy, we observed that low nanomolar doses of NE induced a modest ERBB2 internalization along with an increase of clathrin-mediated endocytosis and of the CD63+ MVB compartment in SKBR-3 cells. Furthermore, we showed in the culture supernatant two distinct EV subsets, based on their size and ERBB2 positivity: small (30–100 nm) ERBB2− EVs and large (>100 nm) ERBB2+ EVs. In particular, we found that NE increased the overall release of EVs, which displayed a reduced ERBB2 positivity compared with controls. Taken together, these results provide novel insight into the effects of NE on ERBB2+ BCa cells that may lead to a reduction of ERBB2 potentially transferred to distant target cells by EVs:

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Baxter, Amy A. "Stoking the Fire: How Dying Cells Propagate Inflammatory Signalling through Extracellular Vesicle Trafficking." International Journal of Molecular Sciences 21, no. 19 (October 1, 2020): 7256. http://dx.doi.org/10.3390/ijms21197256.

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Communication between dying cells and their environment is a critical process that promotes tissue homeostasis during normal cellular turnover, whilst during disease settings, it can contribute to inflammation through the release of intracellular factors. Extracellular vesicles (EVs) are a heterogeneous class of membrane-bound cell-derived structures that can engage in intercellular communication via the trafficking of bioactive molecules between cells and tissues. In addition to the well-described functions of EVs derived from living cells, the ability of dying cells to release EVs capable of mediating functions on target cells or tissues is also of significant interest. In particular, during inflammatory settings such as acute tissue injury, infection and autoimmunity, the EV-mediated transfer of proinflammatory cargo from dying cells is an important process that can elicit profound proinflammatory effects in recipient cells and tissues. Furthermore, the biogenesis of EVs via unique cell-death-associated pathways has also been recently described, highlighting an emerging niche in EV biology. This review outlines the mechanisms and functions of dying-cell-derived EVs and their ability to drive inflammation during various modes of cell death, whilst reflecting on the challenges and knowledge gaps in investigating this subgenre of extracellular vesicles research.

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Roberts-Dalton, H. D., A. Cocks, J. M. Falcon-Perez, E. J. Sayers, J. P. Webber, P. Watson, A. Clayton, and A. T. Jones. "Fluorescence labelling of extracellular vesicles using a novel thiol-based strategy for quantitative analysis of cellular delivery and intracellular traffic." Nanoscale 9, no. 36 (2017): 13693–706. http://dx.doi.org/10.1039/c7nr04128d.

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Ortega, Miguel A., Oscar Fraile-Martinez, Cielo Garcia-Montero, Miguel Angel Alvarez-Mon, Ana Maria Gomez-Lahoz, Agustin Albillos, Guillermo Lahera, et al. "An Updated View of the Importance of Vesicular Trafficking and Transport and Their Role in Immune-Mediated Diseases: Potential Therapeutic Interventions." Membranes 12, no. 6 (May 25, 2022): 552. http://dx.doi.org/10.3390/membranes12060552.

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Cellular trafficking is the set of processes of distributing different macromolecules by the cell. This process is highly regulated in cells, involving a system of organelles (endomembranous system), among which are a great variety of vesicles that can be secreted from the cell, giving rise to different types of extracellular vesicles (EVs) that can be captured by other cells to modulate their function. The cells of the immune system are especially sensitive to this cellular traffic, producing and releasing different classes of EVs, especially in disease states. There is growing interest in this field due to the therapeutic and translational possibilities it offers. Different ways of taking advantage of the understanding of cell trafficking and EVs are being investigated, and their use as biomarkers or therapeutic targets is being investigated. The objective of this review is to collect the latest results and knowledge in this area with a specific focus on immune-mediated diseases. Although some promising results have been obtained, further knowledge is still needed, at both the basic and translational levels, to understand and modulate cellular traffic and EVs for better clinical management of these patients.

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Cruz Camacho, Abel, Daniel Alfandari, Ewa Kozela, and Neta Regev-Rudzki. "Biogenesis of extracellular vesicles in protozoan parasites: The ESCRT complex in the trafficking fast lane?" PLOS Pathogens 19, no. 2 (February 23, 2023): e1011140. http://dx.doi.org/10.1371/journal.ppat.1011140.

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Extracellular vesicles (EVs) provide a central mechanism of cell–cell communication. While EVs are found in most organisms, their pathogenesis-promoting roles in parasites are of particular interest given the potential for medical insight and consequential therapeutic intervention. Yet, a key feature of EVs in human parasitic protozoa remains elusive: their mechanisms of biogenesis. Here, we survey the current knowledge on the biogenesis pathways of EVs secreted by the four main clades of human parasitic protozoa: apicomplexans, trypanosomatids, flagellates, and amoebae. In particular, we shine a light on findings pertaining to the Endosomal Sorting Complex Required for Transport (ESCRT) machinery, as in mammals it plays important roles in EV biogenesis. This review highlights the diversity in EV biogenesis in protozoa, as well as the related involvement of the ESCRT system in these unique organisms.

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Zhang, Pan, Su Bin Lim, Kuan Jiang, Ti Weng Chew, Boon Chuan Low, and Chwee Teck Lim. "Distinct mRNAs in Cancer Extracellular Vesicles Activate Angiogenesis and Alter Transcriptome of Vascular Endothelial Cells." Cancers 13, no. 9 (April 22, 2021): 2009. http://dx.doi.org/10.3390/cancers13092009.

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Cancer-derived extracellular vesicles (EVs) have been demonstrated to be implicated in various processes of cancer development, with most of the EV-induced changes attributed to EV-proteins and EV-microRNAs. However, the knowledge about the abundance of cancer EV-mRNAs and their contribution to cancer development remain elusive. Here, we show that mRNAs prevail in cancer EVs as compared with normal EVs, and cancer EVs that carry abundant angiogenic mRNAs activate angiogenesis in human umbilical vein endothelial cells (HUVECs). Specifically, of a gene panel comprising 61 hypoxia-targeted oncogenes, a larger proportion is harbored by cancer EVs (>40%) than normal EVs (14.8%). Fluorescent trafficking indicates cancer EVs deliver translatable mRNAs such as VEGFA to HUVECs, contributing to the activation of VEGFR-dependent angiogenesis and the upregulation of epithelial-mesenchymal transition-related and metabolism-related genes. Overall, our findings provide novel insights into EV-mRNAs and their role in angiogenesis, and has potential for diagnostic and therapeutic applications.

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Auger, Clément, Aude Brunel, Tiffany Darbas, Hussein Akil, Aurélie Perraud, Gaëlle Bégaud, Barbara Bessette, Niki Christou, and Mireille Verdier. "Extracellular Vesicle Measurements with Nanoparticle Tracking Analysis: A Different Appreciation of Up and Down Secretion." International Journal of Molecular Sciences 23, no. 4 (February 19, 2022): 2310. http://dx.doi.org/10.3390/ijms23042310.

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As is the case with most eucaryotic cells, cancer cells are able to secrete extracellular vesicles (EVs) as a communication means towards their environment and surrounding cells. EVs are represented by microvesicles and smaller vesicles called exosomes, which are known for their involvement in cancer aggressiveness. The release of such EVs requires the intervention of trafficking-associated proteins, mostly represented by the RAB-GTPases family. In particular, RAB27A is known for its role in addressing EVs-to-be secreted towards the the plasma membrane. In this study, shRNAs targeting RAB27A were used in colorectal (CRC) and glioblastoma (GB) cell lines in order to alter EVs secretion. To study and monitor EVs secretion in cell lines’ supernatants, nanoparticle tracking analysis (NTA) was used through the NanoSight NS300 device. Since it appeared that NanoSight failed to detect the decrease in the EVs secretion, we performed another approach to drop EVs secretion (RAB27A-siRNA, indomethacin, Nexihnib20). Similar results were obtained i.e., no variation in EVs concentration. Conversely, NTA allowed us to monitor EVs up-secretion following rotenone treatment or hypoxia conditions. Therefore, our data seemed to point out the insufficiency of using only this technique for the assessment of EVs secretion decrease.

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Lipinski, Simone, and Katharina Tiemann. "Extracellular Vesicles and Their Role in the Spatial and Temporal Expansion of Tumor–Immune Interactions." International Journal of Molecular Sciences 22, no. 7 (March 25, 2021): 3374. http://dx.doi.org/10.3390/ijms22073374.

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Extracellular vesicles (EVs) serve as trafficking vehicles and intercellular communication tools. Their cargo molecules directly reflect characteristics of their parental cell. This includes information on cell identity and specific cellular conditions, ranging from normal to pathological states. In cancer, the content of EVs derived from tumor cells is altered and can induce oncogenic reprogramming of target cells. As a result, tumor-derived EVs compromise antitumor immunity and promote cancer progression and spreading. However, this pro-oncogenic phenotype is constantly being challenged by EVs derived from the local tumor microenvironment and from remote sources. Here, we summarize the role of EVs in the tumor–immune cross-talk that includes, but is not limited to, immune cells in the tumor microenvironment. We discuss the potential of remotely released EVs from the microbiome and during physical activity to shape the tumor–immune cross-talk, directly or indirectly, and confer antitumor activity. We further discuss the role of proinflammatory EVs in the temporal development of the tumor–immune interactions and their potential use for cancer diagnostics.

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Більше джерел

Дисертації з теми "EVs trafficking"

TOTI, ALESSANDRA. "TUMOUR MICROENVIRONMENT: PROTEIN MEDIATORS OF INTERCELLULAR CROSSTALK." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1070249.

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Tumor progression is not only due to the aggressiveness of cancer cells but also to the support given by tumour reactive stroma; reason why the study of stromal cell involvement in tumor microenvironment has become extremely important in the last decades. Tumor mass is a complex network of cancer and stromal cells, and fibroblasts are the main component. Under the influence of tumor cells, fibroblasts engage a transdifferentiation program converting them into their active form (myofibroblast), the so called cancer associated fibroblasts (CAFs), that, in turn, are able to enhance tumor cells growth, migration and invasion. This crosstalk is mediated by soluble factors, cell–cell contacts and extracellular vesicles (EVs) trafficking. Our work is focused in particular on cellular interaction based on EVs trafficking. Two types of Evs has been described, ectosomes (with a diameter from 100 nm to 1 μm) and exosomes (from 30 to 100 nm) that show differences in size, biogenesis and composition. It has been discovered by my research group that a transfer of proteins and lipids between CAFs and cancer cells mediated by ectosomes exists and that this is, essentially unidirectional from CAFs to cancer cells. We have identified about two hundreds proteins that are specifically transferred to cancer cells by this type of cargo. One of the most interesting proteins, considering its role in cancer progression is Galectin-1 We have found that Galectin-1 silencing in CAFs reduce the migration of cancer cells, revealing a novel mechanism by which tumor stroma contribute to cancer progression. These results are important because Galectin-1 has been highlighted as a good target in both cancer and fibroblast cells, increasing the possibilities to counteract cancer aggressiveness by reducing Galectin- 1 action through specific inhibitors. In the second part of my thesis the role of low molecular weight protein tyrosine phosphatase (LMW-PTP) in fibroblasts during their activation has been investigated for the first time. It is known that LMW-PTP expression in cancer increases with the staging of tumor and that it is implicated in several biological processes. Our findings show that the activation induces in CAFs an increase of LMW-PTP expression that is associated to cytoskeletal rearrangement. As a consequence CAFs show a more invasive phenotype that is reversed when LMW-PTP is silenced. Additionally our results suggest the LMW-PTP involvement in cell metabolism. The increase of LMW- PTP induces a more gycolytic metabolism and its silencing causes the induction of a more OXPHOS behaviour. We hypothesize that LMW-PTP could drive fibroblast infiltration and migration during tumor progression. These findings, taken together, contribute to highlight the role of CAFs within tumor microenvironment in sustaining tumors.

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Brenner, Christiane. "Dissecting peptidoglycan trafficking and transport(ers) in human cells." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB240.

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Les fragments du peptidoglycane, les muropeptides muramyl-triDAP (MTP) et le muramyl dipeptide (MDP) sont détectés spécifiquement par les récepteurs cytosoliques du système immunitaire inné, Nod1 et Nod2, respectivement. Mais à ce jour, l’internalisation cellulaire de ces fragments, et plus particulièrement dans les cellules du colon humain, reste mal connue. Dans le but de mieux comprendre ce processus d’internalisation cellulaire, une lignée de cellules humaines du colon HT-29 a été utilisée comme modèle. Les deux récepteurs, Nod1 et Nod2 ont été décrits comme étant exprimés dans cette lignée cellulaire, ainsi que la famille du “Solute Carrier 15A“ (SLC15A) connue pour être impliquée dans le transport des MDP et MTP dans d’autres systèmes cellulaires, mais ce qui ne semble pas être le cas dans notre lignée modèle. A titre d’exemples, SLC15A1 (PEPT1) et SLC15A2 (PEPT2) sont exprimés à l’apex des cellules et transportent, en général, des di-et tripeptides dans les cellules intestinales et rénales. Les transporteurs SLC15A3 (PHT2) et SLC15A4 (PHT1) quant à eux, seraient responsables du transport des MDP et MTP, respectivement, dans les endosomes et les lysosomes. L’objectif de cette thèse était d’identifier le mécanisme d’internalisation du MDP dans les cellules HT-29. Ainsi, différents inhibiteurs des voies d’endocytose ont été utilisés dans des expériences de microscopie. Nos résultats suggèrent que la voie d’internalisation est différente de celle utilisée par la transferrine. En effet, l’internalisation du MDP est partiellement dépendante de la dynamine, une GTPase, et des protéines Rac1/Cdc42, deux Rho GTPases. Ces trois protéines sont impliquées dans l’endocytose et Rac1 joue également un rôle dans l’immunité innée. En parallèle, nous avons inactivé le gène MFSD3 par la technique CRISPR-Cas9. Ce dernier est l’homologue du gène ampG d’Escherichia coli qui transporte spécifiquement les muropeptides anhydres. MFSD3 a été proposé comme un autre transporteur de muropeptides, comme le MTP, permettant leur accès à Nod1 et Nod2. Ainsi, nous avons étudié la fonction de MFSD3. Les cellules déplétées pour MFSD3 étaient affectées dans leur prolifération et dans l’accumulation d’Acetyl-CoA. Une étude protéomique a montré l’implication de MFSD3 dans plusieurs voies de signalisation, suggérant son rôle important dans le métabolisme et, plus largement, dans l’immunité
In the past it has been found that the peptidoglycan fragments muramyl dipeptide (MDP) and muramyl-triDAP (MTP) are specifically recognized by the cytosolic immune receptors Nod2 and Nod1, respectively. However, it is not clear, especially in intestinal and colon epithelial cells, how these fragments are internalized. HT-29, a human cell line from the colon has been stimulated with MDP-Rhodamine to decipher its uptake mechanism. HT-29 poses an interesting model for studying since it is a colonic cell line and both NOD1 and NOD2 are endogenously expressed, while the Solute Carrier Family SLC15A, that has been associated in the past with internalization of both MDP and MTP, seems to be expressed within these cells, however the transporters do not seem to have a role in transport of these fragments in this cell model. SLC15A1 (PEPT1) and SLC15A2 (PEPT2) are expressed at the apical side of cell membranes and mediate the uptake of di- and tripeptides into intestinal and renal cells, while SLC15A3 (PHT1) and SLC15A4 (PHT1) are assumed to be transporting MDP and MTP, respectively, from the early endosome and from the lysosome. One aim of this thesis was to identify the uptake-mechanism for MDP within these cells. By using different inhibitors of endocytosis in combination with microscopy, it has been found that MDP conjugated to Rhodamine is partly endocytosed by an uptake mechanism dependent on Dynamin and Rac1, two Rho GTPases. These two proteins are both involved in endocytosis and vesicular trafficking. Rac1 many different cellular processes such as gene transcription, vesicle trafficking and cytoskeleton architecture, as well as immune signaling. In addition, CRISPR-Cas9 was applied by a collaboration of the lab to knock-down MFSD3, the human homologue of the AmpG gene in E. coli that has been found to recycle murein tripeptide and transport anhydrous muropeptides required to have the disaccharide N-acetylglucosamine-N-acetylmuramic acid (GlcNac-MurNAc). It was suggested in the literature that MFSD3 thus could be another likely candidate to transport ligands to NOD1. Therefore, it was investigated what the substrate, and in general the function of MFSD3 could be. A proteomics approach was carried out and by this several interesting signaling pathways could be identified that suggest that the gene is likely to be important in metabolism and immunity

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Janas, Eva [Verfasser]. "Intracellular peptide trafficking in yeast / vorgelegt von Eva Janas." 2003. http://d-nb.info/968931669/34.

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Книги з теми "EVs trafficking"

Biaudet, Eva. Speech by Eva Biaudet, Special Representative and Co-ordinator for Combating Trafficking in Human Beings, at the Permanent Council meeting of November 22, 2007. Vienna: OSCE, 2007.

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Biaudet, Eva. Talking points of Ms. Eva Biaudet, OSCE Special Representative and Co-ordinator for Combating Trafficking in Human Beings: Alliance Against Trafficking in Persons Conference : assistance to trafficked persons : we can do better, Vienna, Hofburg, 10-11 September 2007. [Vienna]: OSCE, 2008.

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Biaudet, Eva. Concluding statement by the OSCE Special Representative and Co-ordinator for Combating Trafficking in Human Beings, Ms. Eva Biaudet, at the Vilnius conference " Preventing trafficking in human beings: Challenges and solutions, Vilnius, 26 October 2007. Vienna: OSCE, 2007.

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Biaudet, Eva. Presentation by Ms. Eva Biaudet, OSCE Special Representative and Co-ordinator for Combating Trafficking in Human Beings: Alliance Against Trafficking in Persons Conference, Vienna, 26-27 May 2008 : Child trafficking : responses and challenges at local level. Vienna]: OSCE, 2008.

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Biaudet, Eva. Opening remards by Ms. Eva Biaudet, OSCE Special Representative and Co-ordinator for Combating Trafficking in Human Beings: Supplementary Human Dimension Meeting on Combating Sexual Exploitation of Children, 18th October 2007, Hofburg, Vienna. [Vienna]: OSCE, 2007.

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Catholic Church. Baraza la Maaskofu Katoliki wa Tanzania, ed. The church and civil society: Building social conscience for democratic participation. Mount Pleasant, Harare, Zimbabwe: African Forum for Catholic Social Teaching, 2009.

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Council of Europe Convention on Action Against Trafficking in Human Beings Ets 197. Council of Europe, 2005.

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Частини книг з теми "EVs trafficking"

Tonn Eisinger, Katherine R., Paul G. Mermelstein, and John Meitzen. "Estrogen Receptors at the Membrane." In Estrogens and Memory, 24–37. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190645908.003.0003.

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Recent research has established that modified versions of classical estrogen receptors (ERs) act at the membrane to influence neuronal function. Specifically, palmitoylated ERα‎ and ERβ‎ stimulate signal transduction pathways from the membrane through transactivation of metabotropic glutamate receptors (mGluRs). Caveolin (Cav) proteins assemble mGluR and ER into functional signaling microdomains, with the pairing of specific mGluR and ER varying by brain region and Cav isoform. Palmitoylation regulates the trafficking, localization, and interaction of these proteins by allowing association with membrane lipid rafts. This chapter outlines the discovery that the same ERs responsible for nuclear signaling act at the plasma membrane to exert a wide array of effects. Membrane-associated ER signaling affects molecular, structural, and physiological states, leading to system-level changes in circuit dynamics and, ultimately, behavior.

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N. Winter, Steven, Gillian Eastwood, and Manuel A. Barrios-Izás. "Drugs and Biodiversity Loss: Narcotraffic-Linked Landscape Change in Guatemala." In Sustainable Development. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.107152.

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Characteristic of the Anthropocene, human impacts have resulted in worldwide losses in forested land cover, which can directly and indirectly drive biodiversity loss. The global illicit drug trade is one source of deforestation directly implicated with habitat loss in Central America, typically for drug trafficking and livestock production for money laundering. Given reports of deforestation in Central America linked to narcotraffic, we explored vegetation changes within Guatemala’s highly biodiverse Maya Biosphere Reserve by examining trends suggestive of deforestation in a protected area. As such, we collected satellite-derived data in the form of enhanced vegetation index (EVI), as well as history of burned areas, published human-“footprint” data, official population density, and artificial light activity in Laguna del Tigre National Park from 2002 to 2020 for descriptive analysis. We found consistent reductions in EVI and trends of anomalous losses of vegetation despite a baseline accounting for variation within the park. Analyses revealed weak correlations (R2 ≤ 0.26) between EVI losses and official sources of anthropogenic data, which may be attributable to the data’s limited spatial and temporal resolution. Alarmingly, simple analyses identified vegetation losses within a protected area, thus emphasizing the need for additional monitoring and science-based, but interdisciplinary policies to protect this biodiversity hotspot.

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Musu, Costanza. "Cultural Heritage Protection, Illicit Antiquities, and the International Fight Against Terrorism Financing." In NATO Science for Peace and Security Series - E: Human and Societal Dynamics. IOS Press, 2021. http://dx.doi.org/10.3233/nhsdp210029.

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This paper examines the issue of illicit trade in antiquities and its connection to conflict and terrorism financing. The focus is on the Middle East, and particularly Syria and Iraq, as a “source region” of the artifacts, and on the efforts of the United States and the European Union to fight this illicit trade through national initiatives and international cooperation. The paper concentrates on changes in the political response to this problem since 2001, when evidence started accumulating of the importance of the ‘blood antiquities-terrorism’ nexus, which increases the impact of negative externalities of the trade transforming illicit art trafficking into a major threat to international security.(A more detailed version of this paper appears in the following edited volume: Saskia Hufnagel, Michelle Fabiani and Kate Melody Burmon (eds.), Cultural Property Crime and the Law, Routledge, 2022.)

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Тези доповідей конференцій з теми "EVs trafficking"

Ikezoe, Kohei, Toru Oga, Tetsuya Honda, Mariko Hara-Chikuma, Xiaojun Ma, Tatsuaki Tsuruyama, Kazuko Uno, et al. "Aquaporin-3 potentiates murine asthma through mediating T-cell trafficking and chemokine production." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa1104.

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Rutherford, E., D. Van Den Boomen, K. Lim, P. Lehner, E. Rawlins, S. Marciniak, and J. Dickens. "Using forward genetic screens and novel human alveolar organoid models to study surfactant protein C trafficking in heath and disease." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1772.

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