Καταστροφές και Κρίσεις σε Τουριστικούς Προορισμούς. Η Διαχείριση Διακινδύνευσης Καταστροφών στις Τουριστικές Επιχειρήσεις της Κέρκυρας.

Ο τουρισμός αποτελεί βασικό στοιχείο της οικονομικής δραστηριότητας στην Ελλάδα, ωστόσο είναι ένας ευάλωτος τομέας που διαμορφώνεται και από διάφορους εξωγενείς παράγοντες. Οι φυσικές καταστροφές και οι κρίσεις που μπορεί να εκδηλωθούν οπουδήποτε στον κόσμο, είναι χαρακτηριστικά παραδείγματα τέτοιων καθοριστικών παραγόντων που ενδέχεται να προκαλέσουν σοβαρές ζημιές επηρεάζοντας αρνητικά το αίσθημα ασφάλειας των τουριστών και την οικονομία ενός προορισμού. Ο τουρισμός στην Κέρκυρα είναι ο κυρίαρχος κλάδος της τοπικής οικονομίας και απασχόλησης με τις τουριστικές επιχειρήσεις να αποτελούν τη βάση και προϋπόθεση για την τοπική ανάπτυξη. Σκοπός της παρούσας διπλωματικής εργασίας είναι να γίνει προσέγγιση θεμάτων που αφορούν στη διαχείριση της διακινδύνευσης καταστροφών στις τουριστικές επιχειρήσεις της Κέρκυρας. Για να ολοκληρωθεί αυτή η μελέτη πραγματοποιήθηκε βιβλιογραφική επισκόπηση και συλλογή πληροφοριών, ενώ διεξήχθη και πρωτογενής έρευνα. Το πρώτο μέρος της έρευνας συγκεντρώνει πληροφορίες βασισμένες στην αντίληψη, τις γνώσεις και τις εμπειρίες των επισκεπτών της Κέρκυρας σε σχέση με τις φυσικές καταστροφές που ενδεχομένως να πλήξουν το νησί κατά τη διάρκεια των διακοπών τους. Στο πλαίσιο αυτό δημιουργήθηκαν ερωτηματολόγια τα οποία διανεμήθηκαν σε τουρίστες. Το δεύτερο μέρος της έρευνας εξετάζει τον βαθμό ετοιμότητας των τοπικών τουριστικών επιχειρήσεων έναντι των φυσικών καταστροφών σε όλα τα στάδια (πρόληψη, ετοιμότητα, απόκριση και αποκατάσταση). Η έρευνα αυτή πραγματοποιήθηκε μέσω συνεντεύξεων. Στο τέλος παρουσιάζονται τα αποτελέσματα της έρευνας, τα συμπεράσματα, καθώς και προτάσεις σχετικές με την αποτελεσματική διαχείριση καταστροφών και κρίσεων, που πιθανόν να συμβάλλουν θετικά στην αναβάθμιση του τουριστικού προϊόντος του νησιού.Tourism is a key element of economic activity in Greece; however it is a vulnerable sector that is shaped by various external factors. Natural disasters and crises that can occur anywhere in the world are typical examples of such factors that can cause serious damages, affecting in a negative way the sense of security of tourists and the economy of a destination. Tourism in Corfu is the dominant sector of the local economy and employment with tourism enterprises being the basis of the local growth. The purpose of this master Thesis is to approach the disaster risk management in Corfu tourist enterprises. In order to complete this study, a bibliographic review and information collection was carried out, while primary research was conducted. The first part of the research is gathering information based on the perception, knowledge and experiences that visitors of Corfu have, in relation to the natural disasters that may affect the island during their holidays. In this context, questionnaires were created and distributed to tourists. The second part of the research examines the degree of readiness of local tourist companies in the face of natural disasters in all stages (prevention, preparedness, response and rehabilitation). This research was conducted through interviews. At the end the results and the conclusions of the research are presented, as well as proposals related to the effective management of disasters and crises, which might have a positive contribution in upgrading the tourist product of the island

Parainfluenza virus 5 genomes are located in viral cytoplasmic bodies whilst the virus dismantles the interferon-induced antiviral state of cells

Although the replication cycle of parainfluenza virus type 5 (PIV5) is initially severely impaired in cells in an interferon (IFN)-induced antiviral state, the virus still targets STAT1 for degradation. As a consequence, the cells can no longer respond to IFN and after 24−48 h, they go out of the antiviral state and normal virus replication is established. Following infection of cells in an IFN-induced antiviral state, viral nucleocapsid proteins are initially localized within small cytoplasmic bodies, and appearance of these cytoplasmic bodies correlates with the loss of STAT1 from infected cells. In situ hybridization, using probes specific for the NP and L genes, demonstrated the presence of virus genomes within these cytoplasmic bodies. These viral cytoplasmic bodies do not co-localize with cellular markers for stress granules, cytoplasmic P-bodies or autophagosomes. Furthermore, they are not large insoluble aggregates of viral proteins and/or nucleocapsids, as they can simply and easily be dispersed by ‘cold-shocking’ live cells, a process that disrupts the cytoskeleton. Given that during in vivo infections, PIV5 will inevitably infect cells in an IFN-induced antiviral state, we suggest that these cytoplasmic bodies are areas in which PIV5 genomes reside whilst the virus dismantles the antiviral state of the cells. Consequently, viral cytoplasmic bodies may play an important part in the strategy that PIV5 uses to circumvent the IFN system

Influenza vaccination induces NK-cell-mediated type-II IFN response that regulates humoral immunity in an IL-6-dependent manner

The role of natural killer (NK) cells in the immune response against vaccines is not fully understood. Here, we examine the function of infiltrated NK cells in the initiation of the inflammatory response triggered by inactivated influenza virus vaccine in the draining lymph node (LN). We observed that, following vaccination, NK cells are recruited to the interfollicular and medullary areas of the LN and become activated by type I interferons (IFNs) produced by LN macrophages. The activation of NK cells leads to their early production of IFNγ, which in turn regulates the recruitment of IL-6+ CD11b+ dendritic cells. Finally, we demonstrate that the interleukin-6 (IL-6)-mediated inflammation is important for the development of an effective humoral response against influenza virus in the draining LN

RNA-Containing Cytoplasmic Inclusion Bodies in Ciliated Bronchial Epithelium Months to Years after Acute Kawasaki Disease

Kawasaki Disease (KD) is the most common cause of acquired heart disease in children in developed nations. The KD etiologic agent is unknown but likely to be a ubiquitous microbe that usually causes asymptomatic childhood infection, resulting in KD only in genetically susceptible individuals. KD synthetic antibodies made from prevalent IgA gene sequences in KD arterial tissue detect intracytoplasmic inclusion bodies (ICI) resembling viral ICI in acute KD but not control infant ciliated bronchial epithelium. The prevalence of ICI in late-stage KD fatalities and in older individuals with non-KD illness should be low, unless persistent infection is common.Lung tissue from late-stage KD fatalities and non-infant controls was examined by light microscopy for the presence of ICI. Nucleic acid stains and transmission electron microscopy (TEM) were performed on tissues that were strongly positive for ICI. ICI were present in ciliated bronchial epithelium in 6/7 (86%) late-stage KD fatalities and 7/27 (26%) controls ages 9-84 years (p = 0.01). Nucleic acid stains revealed RNA but not DNA within the ICI. ICI were also identified in lung macrophages in some KD cases. TEM of bronchial epithelium and macrophages from KD cases revealed finely granular homogeneous ICI.These findings are consistent with a previously unidentified, ubiquitous RNA virus that forms ICI and can result in persistent infection in bronchial epithelium and macrophages as the etiologic agent of KD

Macrophage death following influenza vaccination initiates the inflammatory response that promotes dendritic cell function in the draining lymph node

The mechanism by which inflammation influences the adaptive response to vaccines is not fully understood. Here, we examine the role of lymph node macrophages (LNMs) in the induction of the cytokine storm triggered by inactivated influenza virus vaccine. Following vaccination, LNMs undergo inflammasome-independent necrosis-like death that is reliant on MyD88 and Toll-like receptor 7 (TLR7) expression and releases pre-stored interleukin-1α (IL-1α). Furthermore, activated medullary macrophages produce interferon-β (IFN-β) that induces the autocrine secretion of IL-1α. We also found that macrophage depletion promotes lymph node-resident dendritic cell (LNDC) relocation and affects the capacity of CD11b+ LNDCs to capture virus and express co-stimulatory molecules. Inhibition of the IL-1α-induced inflammatory cascade reduced B cell responses, while co-administration of recombinant IL-1α increased the humoral response. Stimulation of the IL-1α inflammatory pathway might therefore represent a strategy to enhance antigen presentation by LNDCs and improve the humoral response against influenza vaccines

Avidity engineering of human heavy-chain-only antibodies mitigates neutralization resistance of SARS-CoV-2 variants

Emerging SARS-CoV-2 variants have accrued mutations within the spike protein rendering most therapeutic monoclonal antibodies against COVID-19 ineffective. Hence there is an unmet need for broad-spectrum mAb treatments for COVID-19 that are more resistant to antigenically drifted SARS-CoV-2 variants. Here we describe the design of a biparatopic heavy-chain-only antibody consisting of six antigen binding sites recognizing two distinct epitopes in the spike protein NTD and RBD. The hexavalent antibody showed potent neutralizing activity against SARS-CoV-2 and variants of concern, including the Omicron sub-lineages BA.1, BA.2, BA.4 and BA.5, whereas the parental components had lost Omicron neutralization potency. We demonstrate that the tethered design mitigates the substantial decrease in spike trimer affinity seen for escape mutations for the hexamer components. The hexavalent antibody protected against SARS-CoV-2 infection in a hamster model. This work provides a framework for designing therapeutic antibodies to overcome antibody neutralization escape of emerging SARS-CoV-2 variants

A broad-spectrum macrocyclic peptide inhibitor of the SARS-CoV-2 spike protein

The ongoing COVID-19 pandemic has had great societal and health consequences. Despite the availability of vaccines, infection rates remain high due to immune evasive Omicron sublineages. Broad-spectrum antivirals are needed to safeguard against emerging variants and future pandemics. We used mRNA display under a reprogrammed genetic code to find a spike-targeting macrocyclic peptide that inhibits SARS-CoV-2 Wuhan strain infection and pseudoviruses containing spike proteins of SARS-CoV-2 variants or related sarbecoviruses. Structural and bioinformatic analyses reveal a conserved binding pocket between the receptor binding domain, N-terminal domain and S2 region, distal to the ACE2 receptor-interaction site. Our data reveal a hitherto unexplored site of vulnerability in sarbecoviruses that peptides and potentially other drug-like molecules can target

A broad-spectrum macrocyclic peptide inhibitor of the SARS-CoV-2 spike protein

The ongoing COVID-19 pandemic has had great societal and health consequences. Despite the availability of vaccines, infection rates remain high due to immune evasive Omicron sublineages. Broad-spectrum antivirals are needed to safeguard against emerging variants and future pandemics. We used messenger RNA (mRNA) display under a reprogrammed genetic code to find a spike-targeting macrocyclic peptide that inhibits SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) Wuhan strain infection and pseudoviruses containing spike proteins of SARS-CoV-2 variants or related sarbecoviruses. Structural and bioinformatic analyses reveal a conserved binding pocket between the receptor-binding domain, N-terminal domain, and S2 region, distal to the angiotensin-converting enzyme 2 receptor-interaction site. Our data reveal a hitherto unexplored site of vulnerability in sarbecoviruses that peptides and potentially other drug-like molecules can target