12,462 research outputs found

    Leadership and Ability of School Principals to Utilize an Asset-Based Approach as Learning Capital for Learning Based on Student Needs Based on School Potential (Literatur Review)

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    Educational transformation is a phenomenon that always occurs in the dynamics of educational development. This research aims to explore school strategies for overcoming obstacles to educational transformation in schools. The methods used were the critical method, dialectical method, and scholastic method. This research was included in library research. The author tried to find data, and theories related to the issues raised in various literature or references that the author found and then compared them using the method mentioned above. The research results showed that the leadership style and use of an asset-based community approach were prospective alternatives for overcoming obstacles, especially financial limitations that exist in schools. The distributed and learning leadership style was an alternative leadership style that was a solution because this style could change the mindset of the entire school community in overcoming the obstacles that the school had been experiencing. A community-based approach had a great opportunity to overcome financial constraints through the formation and empowerment of educational communities within the school environment

    COVID-19 Pandemic’s Effect on Occupational Therapy Students’ Time-Use and Occupational Engagement On Returning to In-Person Learning

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    The COVID-19 pandemic emotionally and physically impacted students in occupational therapy and occupational therapy assistant programs. College students lost autonomy and access to meaningful occupations and environments. As students returned to campus, they struggled to navigate and adapt to in-person occupations and how they use their time. This study uses a mixed method descriptive research design to understand how the pandemic affected occupational therapy students\u27 time-use and occupational engagement during the transition to in-person learning. Seventy-three students completed an online survey, while 12 of those students additionally participated in a follow-up time-use diary and interview. Eighty-three percent of the participants agreed or strongly agreed they learned more effectively in-person compared to online, while 65% agreed or strongly agreed to make time to participate in satisfying occupations. Three themes emerged after the thematic analysis of the qualitative data: time compression, lessons from adapting, and autonomy and choice. The findings provide perspectives on occupational therapy students\u27 ability to adapt and manage their time during this transition and offer insight into other transitions in their programs

    Discourses of COVID-19 Vaccination in China: Public Response to Government Domination and the Emergence of ‘Vaccine Citizenship’

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    Using online discourse-centred ethnography and focus group discussions, this paper explores evolving discourses of COVID-19 vaccination in China and corresponding public responded. In addition to the state’s intensive control of COVID-19 outbreaks, China initiated independent research and the development of vaccines from the spring of 2020. In line with the state’s emphasis on success in controlling the outbreaks, government propaganda aimed to shape and disseminate successful images of the vaccines developed. Correspondingly, the public showed a supportive attitude when the first two domestically produced vaccines received Emergency Use Authorisation (EUA) by China's authorities. In contrast, vaccine hesitancy emerged when the government claimed its initial success in pandemic control and tried to communicate the vaccine’s safety and effectiveness. Importantly, COVID-19 outbreaks have never disappeared in China. As new domestic outbreaks emerged and the administration started to promote vaccination more vigorously, more people were forced to accept vaccination. When the government endowed vaccine discourse with the responsibility of protecting the general population’s health, the implementation of the vaccination programme became even more constraining. This paper examines empirical data on the government’s and individuals’ discursive practices through a focus on subjectivity as part of China’s biopolitical governance of COVID-19 which presents vaccination as an individual ‘technology of the self’. In this complex context of top-down governance, I analyse how the exercise of biopower and a sense of governance emerged and changed during China’s efforts at COVID-19 control

    Signaling Mechanisms Behind the Benefits of Sleep

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    Hintergrund: Schlaf ist ein streng regulierter Zustand körperlicher Ruhe und reduzierten Bewusstseins, der evolutionĂ€r im ganzen Tierreich konserviert ist. Schlafmangel ist in der modernen Gesellschaft weit verbreitet und betrifft 10 – 30 % der Erwachsenen. Dies stellt ein ernstes gesundheitliches Problem dar, da Schlafmangel mit vielen Krankheiten assoziiert ist, darunter Depressionen, Krebs und Herz-Kreislauf-Erkrankungen. Umgekehrt beeinflussen auch Krankheiten und das Immunsystem das Schlafverhalten. Trotz der fundamentalen Rolle dieser Wechselbeziehung sind grundlegende molekulare Mechanismen, die Funktionen des Immunsystems und Schlafkontrolle verbinden, bisher kaum verstanden. Da die Schlafregulation in SĂ€ugetieren sehr komplex ist, ist es sinnvoll konservierte Mechanismen zuerst in einfacheren Modellorganismen zu untersuchen. Der Rundwurm C. elegans ist ein solcher etablierter, simpler und vielseitiger Modellorganismus fĂŒr die Schlafforschung. Er schlĂ€ft sowohl im Rhythmus seiner Larvenentwicklung immer jeweils wĂ€hrend des Lethargus kurz vor der HĂ€utung, als auch nach besonderem Stress, wie zum Beispiel Hunger oder Hitze. C. elegans besitzt ein invariantes Nervensystem, in dem eine rapide Depolarisation des einzelnen RIS-Interneurons genĂŒgt, um Schlaf zu induzieren. Eine Mutation des AP2 Transkriptionsfaktors APTF-1 verhindert die Expression von FLP-11, dem schlafinduzierenden Neuropeptid von RIS. Dies fĂŒhrt praktisch zu völliger Schlaflosigkeit, die in C. elegans in der Regel nicht tödlich ist, und deshalb ein nĂŒtzliches Modell fĂŒr genetisch-chronischen Schlafmangel darstellt. Unser Labor fand heraus, dass eine Gain-of-function-Mutation in der Kollagenase NAS-38 ĂŒber Signalwege der angeborenen ImmunitĂ€t und RIS-Aktivierung zu vermehrtem Schlaf wĂ€hrend des Lethargus fĂŒhrt. Gleichzeitig wird dabei die Expression einer ganzen Familie antimikrobieller Peptide (AMP) hochreguliert. Derselbe Signalweg, einschließlich der AMP, sowie das Schlafverhalten werden auch durch Verletzungen induziert. Interessanterweise sterben nicht-schlafende WĂŒrmer nach einer Verletzung hĂ€ufiger. Insgesamt deutet dies darauf hin, dass AMP als SignalmolekĂŒle fungieren könnten, die Schlaf als Teil einer globalen Schutzreaktion vom peripheren Gewebe zum Nervensystem signalisieren. FĂŒr diese Hypothese fehlten bisher jedoch die Beweise. Fragestellungen und Hypothesen: Mein Ziel war es, den molekularen Mechanismus zu entschlĂŒsseln, durch den verschiedene Reize der angeborenen ImmunitĂ€t, das heißt NAS-38 sowie epidermale Verletzungen, Schlaf induzieren. Zwei Fragen habe ich hierbei im Speziellen adressiert: Welche DomĂ€nen des NAS 38-Proteins sind an der Schlafregulation beteiligt? Da die Astacin-DomĂ€ne als aktive ProteasedomĂ€ne von NAS-38 angesehen wird, erwartete ich eine SchlĂŒsselrolle dieser DomĂ€ne auch in der Schlafinduktion. Zweitens, welche Rolle spielen AMP bei der Signalisierung von immunitĂ€tsinduziertem Schlaf? Da gezeigt wurde, dass AMP wĂ€hrend des NAS-38 Schlafes und auch nach Verwundung hochreguliert sind, erwartete ich, dass AMP an der Signalisierung von Schlaf von der Epidermis zum Nervensystem beteiligt sind. In einem zweiten Schritt untersuchte ich die molekularen Mechanismen, die den Vorteilen von Schlaf fĂŒr das Überleben von Verletzungen zugrunde liegen. Auch hier habe ich speziell zwei Fragestellungen untersucht: VerĂ€ndert genetischer Schlafentzug die transkriptionelle Reaktion auf epidermale Verletzungen? Da Schlaf fĂŒr viele fundamentale Prozesse wichtig ist und Schlaflosigkeit die Sterblichkeit nach Verletzungen erhöht, vermutete ich, dass genetischer Schlafentzug die transkriptionelle Reaktion auf Verletzungen beeintrĂ€chtigt. Zweitens, ist Schlaf wichtig fĂŒr die Entwicklung von Robustheit, um im Falle einer Verletzung weniger Schaden zu nehmen? WĂ€hrend der Larvenentwicklung fĂ€llt die Cuticula-Synthese mit Schlaf zeitlich zusammen. Daher stellte ich die Hypothese auf, dass Schlafentzug die korrekte Bildung einer Cuticula beeintrĂ€chtigt. Methoden: Zur Analyse der Signalmechanismen, durch die sowohl NAS-38 als auch Verletzungen Schlaf induzieren, filmte ich das Schlafverhalten von C. elegans mittels Langzeit-Bildgebung in Agarose-Mikrokammern. So fĂŒhrte ich eine Struktur-Funktions-Analyse mit verschiedenen nas-38 Mutanten durch, in denen jeweils eine andere NAS-38 DomĂ€ne deletiert war. DarĂŒber hinaus testete ich verschiedene Suppressoren fĂŒr immunvermittelten Schlaf, der durch NAS 38 oder Verletzungen induziert war. Die Redundanz des Suppressionseffektes der verschiedenen Mitglieder der AMP-Familie auf immunvermittelten Schlaf testete ich, indem ich den SuppressionsphĂ€notyp einer CRISPR/Cas9-editierten Multi-Knockout-Mutante analysierte, in der insgesamt 19 AMP deletiert waren. Um Effektoren zu identifizieren, die den AMP nachgeschaltet sind, induzierte ich Schlaf durch Überexpression des AMP NLP 29 unter der Kontrolle eines Hitzeschock-Promotors und analysierte die Sschlafsuppression durch verschiedene Knockout-Mutanten. Im zweiten Projekt beschĂ€ftigte ich mich mit der Frage, wie genau Schlaf das Überleben nach Verletzungen unterstĂŒtzt. Ich verglich die Expression von literaturbekannten Reportern fĂŒr verschiedene Aspekte der Verwundungsreaktion mittels Langzeit-Fluoreszenzmikroskopie im Wildtyp sowie dem Modell fĂŒr chronisch-genetischen Schlafmangel. DarĂŒber hinaus habe ich die Transkriptome zwischen jeweils adulten verwundeten und unverwundeten Wildtypen und schlaflosen Mutanten verglichen. Um die Struktur der Cuticula des Wildtyps und der schlaflosen Mutante zu vergleichen, analysierte ich außerdem rasterelektronen-mikroskopische Aufnahmen. Ergebnisse: Im ersten Projekt konnte ich zeigen, dass NAS-38 Schlaf durch seine Astacin-DomĂ€ne verlĂ€ngert. Dieser Prozess wird moderiert durch die TSP-1-DomĂ€ne. Weiterhin konnte ich zeigen, dass viele AMP redundant wirken um immunvermittelten Schlaf, verursacht durch NAS-38 oder Verletzungen, zu signalisieren. Ich konnte zeigen, dass das AMP NLP-29 ĂŒber den Neuropeptidrezeptor NPR-12 wirkt. Dieser kann NLP-29-induzierten Schlaf vermitteln, wenn er in einem neuronalen Netzwerk exprimiert wird, welches nachweislich RIS aktiviert. Interessanterweise fand ich außerdem heraus, dass fĂŒr NLP-29-vermittelten Schlaf der EGFR Signalweg notwendig ist. Im zweiten Projekt entdeckte ich, dass Schlaflosigkeit die transkriptionelle Reaktion auf Verletzungen nicht dramatisch verĂ€ndert. Allerdings ist das Transkriptionsprofil bereits in der unverletzten schlaflosen Mutante verĂ€ndert. Dies betraf unter anderem eine Gruppe oszillierender Gene, die Cuticula-assoziierte Proteine codieren, und deren Expression normalerweise ihren Höhepunkt gegen Ende des Lethargus erreicht. Da angenommen wird, dass der Zeitpunkt der Kollagenexpression entscheidend fĂŒr eine fehlerfreie Cuticula-Bildung ist, analysierte ich die Cuticula der schlaflosen Mutante. Ich konnte zeigen, dass die Cuticula des adulten Tieres tatsĂ€chlich einen strukturellen Defekt aufweist. Dieser betrifft speziell Furchen in der Region nahe den Alae und könnte möglicherweise die StrapazierfĂ€higkeit der Cuticula gegenĂŒber bestimmten Belastungen verringern. Daher könnte Schlaf erforderlich sein, Robustheit in Form einer strukturierten Cuticula zu fördern. Schlussfolgerungen: In diesem Dissertationsprojekt vollendete ich die Charakterisierung eines neuentdeckten Mechanismus in C. elegans, durch den Verwundungen Schlaf als Teil der Immunantwort aus der Peripherie zum Nervensystem signalisieren. Ich konnte zeigen, dass AMP gewebeĂŒbergreifend Signale von der Epidermis an ein neuronales Netz vermitteln, welches wiederum RIS aktiviert und dadurch Schlaf induziert. Da Komponenten dieses Signalweges konserviert sind, könnten AMP auch in anderen Tieren, einschließlich des Menschen, Schlaf zur Genesung fördern. DarĂŒber hinaus habe ich die Grundlagen fĂŒr die Analyse molekularer Mechanismen geschaffen, die den essentiellen Funktionen des Schlafes fĂŒr Heilung und Überleben zugrunde liegen. Obwohl Schlaflosigkeit die transkriptionelle Reaktion auf Verletzungen nicht drastisch zu verĂ€ndern scheint, deuten meine Ergebnisse auf eine Rolle des Schlafes bei der richtigen Cuticula-Bildung und möglicherweise sogar auf eine vielfĂ€ltigere Rolle bei der zeitlichen Regulierung der Genexpression hin.:Summary I Zusammenfassung IV Contents VII List of Figures XII List of Tables XIV Abbreviations XV 1. Introduction 1 1.1. Sleep is fascinating 1 1.1.1. The origin and basic features of sleep 1 1.1.2. Regulation of sleep in higher animals 3 1.1.2.1. Neuronal control of sleep 3 1.1.2.2. Molecular control of sleep 5 1.1.3. The functions of sleep 6 1.2. The immune system and its relationship to sleep 7 1.3. Wound healing and its relationship to sleep 10 1.4. Caenorhabditis elegans is a well-studied model organism 12 1.4.1. Sleep in C. elegans 15 1.4.2. The C. elegans cuticle 18 1.4.3. Immunity in C. elegans 19 1.4.4. Wound healing response in C. elegans 22 2. Previous results 25 2.1. A strong gain-of-function mutation in the astacin metallo-proteinase NAS 38 increases lethargus duration and movement quiescence in C. elegans 25 2.2. NAS-38 increases sleep mostly through the RIS neuron 25 2.3. NAS-38 is expressed in the epidermis and oscillates with the developmental rhythm 25 2.4. nas-38(ok3407) acts via innate immunity pathways to increase lethargus duration and AMP expression 27 2.5. Overexpression of AMPs induces RIS dependent quiescence 30 2.6. Epidermal wounding induces RIS-dependent sleep, which is beneficial for survival 31 3. Thesis Aims 34 3.1. Aim 1 – Characterizing the molecular mechanism through which NAS-38, innate immunity, and wounding induce sleep 34 3.2. Aim 2 – Analyzing how sleep promotes survival after wounding 35 4. Materials and Methods 36 4.1. C. elegans maintenance 36 4.2. C. elegans crossing and genotyping 41 4.3. Creation of transgenic animals 45 4.3.1. Creating the npr-12 rescue in nmr-1 expressing neurons 45 4.3.2. Microparticle bombardment 45 4.3.3. CRISPR/Cas9 system 46 4.4. Synchronizing worm cultures by hypochlorite treatment 48 4.5. Imaging 49 4.5.1. Imaging setups 49 4.5.2. DIC Imaging of worm development, lethargus, and sleep behavior 50 4.5.2.1. Imaging of heterozygous mutants 50 4.5.3. DIC imaging in the temperature control device 51 4.5.4. Fluorescent imaging experiments 51 4.5.4.1. nas-38p::d1GFP and nlp-29p::GFP during L1 development 51 4.5.4.2. nlp-29p::GFP in L4 larvae 52 4.5.4.3. nlp-29p::GFP after heat shock-induced lin-3 overexpression 52 4.5.4.4. Imaging fluorescent markers in (wounded) young adults 52 4.5.4.5. Functional Ca2+ imaging in young adults 52 4.5.4.6. Fluorescence imaging across the whole developmental time 54 4.5.4.7. Nuclear decompaction assays 55 4.5.4.8. Transcription factor localization with spinning disc confocal microscopy 55 4.5.4.9. Imaging DPY-13::mKate2 in young adults 56 4.6. Image analysis 56 4.6.1. Assessment of developmental time and lethargus detection 56 4.6.2. Sleep detection in DIC mode 56 4.6.3. Analyzing functional Ca2+ images 57 4.6.4. Fluorescent reporter analysis during long-term imaging 57 4.7. RNAi-by-feeding 58 4.8. Transcriptome analysis 59 4.8.1. Analysis of the nas-38(ok3407) transcriptome 59 4.8.2. Analysis of the wounding transcriptome 59 4.9. Epidermal wounding 62 4.9.1. Laser wounding 62 4.9.2. Needle wounding 62 4.9.3. Survival assay 63 4.10. Scanning Electron Microscopy (SEM) 63 4.11. Histamine-inducible hyperpolarization of RIS 64 4.12. Cuticle integrity test with Sodium hypochlorite 64 4.13. NPR-12 receptor modeling 64 4.14. Quantification and statistical analysis 65 5. Results 66 5.1. Aim 1 – Characterizing the pathway through which NAS 38, wounding and innate immunity induce sleep 66 5.1.1. The loss of function mutation nas-38(tm2655) shows the opposite phenotype to the gain of function mutation nas-38(ok3407) 66 5.1.2. nas-38 gain-of-function mutants act through their astacin protease domain and are semi-dominant 66 5.1.3. Transcriptome analysis of nas-38(ok3407) reveals upregulation of genes associated with secretion, innate immunity and cuticle formation 69 5.1.4. nas-38(knu568) increased movement quiescence can be suppressed by mutations of innate immunity pathways 72 5.1.5. Multiple NLPs and CNCs act in parallel to mediate nas-38(ok3407) induced sleep 75 5.1.6. Wounding-induced sleep requires RIS, ALA, EGFR and immune signaling 77 5.1.7. NLP-29 signals via the NPR-12 receptor in neurons upstream of RIS 80 5.1.8. NLP-29 requires neuronal EGFR signaling to induce sleep 81 5.1.9. Simple in silico models suggest that many different NLPs can bind to NPR-12 83 5.1.10. AMPs contribute to the survival after wounding 85 5.2. Aim 2 – Identifying the advantages sleep provides that help to survive harmful conditions 87 5.2.1. Wounding decreases the lifespan in the wild type and the aptf 1(gk794) mutant 87 5.2.2. Histamine-inducible RIS hyperpolarization suppresses wounding sleep 87 5.2.3. Genetic sleep deprivation decreases translocation of DAF-16 into the nucleus immediately after wounding 89 5.2.4. Genetic sleep deprivation hardly changes the transcriptional wounding response 95 5.2.5. Genetic sleep deprivation and wounding increase nuclear PHA 4 101 5.2.6. Oscillating genes and genes associated with the cuticle and the unfolded protein response are upregulated in young adult aptf 1(gk794) mutants 106 5.2.7. Genetic sleep deprivation leads to a malformation of cuticular furrows 109 5.2.8. Genetic sleep deprivation leads to an increased transcription of lethargus specific oscillating genes in young adults 114 5.2.9. Genetic sleep deprivation does not significantly affect development time or body size 120 5.2.10. Expression of fluorescent reporters of oscillating genes is not phase-shifted in the aptf-1(gk794) mutant 122 6. Discussion and Outlook 128 6.1. NAS-38 acts through its astacin domain to increase sleep via innate immunity pathways 128 6.2. NAS-38 during larval lethargus and epidermal wounding in the adult signal sleep via many AMPs as part of a peripheral immune response 130 6.3. Epidermal AMPs activate a neuronal circuit to induce sleep 131 6.4. Genetically sleep deprived worms can mount a proper wounding response in many ways, except for DAF-16/FOXO regulation 132 6.5. Genetic sleep deprivation alters cuticle formation 135 6.6. The role of PHA-4/FOXA in genetically sleep-deprived animals 137 6.7. Conclusion 139 7. References 140 8. Acknowledgements 163 9. Appendix 166 9.1. Standard reagents 166 9.2. Sequence summary of PHX3754 167 9.3. MATLAB script to analyze the intensity of fluorescent reporters over time 171 9.4. Permissions to reprint figures 174 9.5. Experimental author contributions 175 9.6. Predicted interactions between the NPR-12 receptor and peptides of the nlp and cnc families 176 9.7. Overlap of the adult wounding transcriptome with other data sets 179 9.8. Curriculum Vitae – Marina Patricia Sinner 181Background: Sleep is a tightly regulated state of behavioral quiescence and reduced consciousness, which is conserved throughout the animal kingdom. In modern societies 10 – 30 % of the adult population suffer from insufficient sleep, which poses a serious health problem as sleep deprivation is associated with a variety of diseases including depression, cancer, and cardiovascular diseases. Conversely, sickness and the immune system also influence sleep patterns. Despite the important role of this interrelationship between sleep and immunity, basic molecular mechanisms that link both vital functions are only poorly understood yet. As sleep regulation is complex in mammals and is thus difficult to address experimentally, it is reasonable to investigate its basic conserved mechanisms in simpler models first. The nematode C. elegans is such a well-established, simple, and powerful model organism for sleep research. It displays stress-induced sleep, for example upon starvation or heat shock, but also developmentally-timed sleep during lethargus prior to each larval molt. C. elegans possesses an invariant nervous system in which rapid depolarization of the single RIS interneuron is sufficient to induce sleep. Mutation of the AP2 transcription factor APTF 1 deprives RIS of its sleep-inducing neuropeptide FLP-11 and thus virtually abolishes sleep. This is not per se lethal in C. elegans, thereby presenting a powerful model for genetic sleep deprivation. Our lab found that a gain-of-function mutation in the collagenase NAS-38 strongly increases RIS-dependent sleep during lethargus with a concomitant upregulation of a large family of antimicrobial peptides (AMPs) via immunity pathways. Epidermal wounding also triggers AMP expression via immune signaling and induces sleep in the adult worm. Moreover, genetic sleep deprivation increases mortality upon epidermal injury. Together, this suggests AMPs to act as somnogens from peripheral tissues to the nervous system as part of a protective response. This hypothesis, however, was hitherto lacking final evidence and pathway components. Research questions and hypotheses: I aimed to characterize the molecular mechanism by which separate triggers of innate immunity, i. e. NAS-38 and wounding, induce sleep. I specifically addressed two questions: Firstly, which domains of the NAS-38 protein are involved in sleep regulation? As the astacin domain is predicted to be the active protease domain of NAS-38, I expected a role for it also in sleep induction by NAS-38. Secondly, what is the role of AMPs in signaling immunity-induced sleep? As they have been shown to be upregulated during times of increased sleep in the nas-38 mutant and after wounding, I expected AMPs to be involved in signaling sleep from the epidermis to the nervous system. In a second step, I investigated the molecular mechanisms underlying the benefits of sleep for surviving injury. Again, I addressed two questions: Firstly, does genetic sleep deprivation alter the transcriptional wounding response? As sleep has a role in many fundamental processes and sleeplessness increases mortality upon wounding, I hypothesized that genetic sleep deprivation impairs wounding-induced changes of transcriptional activity. Secondly, does sleep help building robustness before encountering injury? During larval development the synthesis of a new cuticle coincides with sleep. Thus, I hypothesized that genetic sleep deprivation impairs proper cuticle formation. Methods: To dissect the signaling mechanisms by which NAS-38 and wounding induced sleep, I followed sleep behavior of C. elegans by long-term imaging in agarose microchambers. I performed a structure-function analysis with different nas-38 mutants, each carrying a deletion of a different domain. Moreover, I screened for suppressors of sleep induced by NAS 38 or wounding. To test for redundancy of the AMP family, I investigated the suppression-phenotype of a CRISPR/Cas9 edited multi-knockout mutant lacking 19 AMPs. To identify downstream effectors of the AMP NLP 29, I induced sleep by overexpressing NLP 29 from a heat-shock promoter and analyzed the suppression-phenotype of different knockout mutants. For the second project, I addressed the question how sleep aids recovery from injury. I followed fluorescent reporters of previously described wounding response pathways by fluorescent long-term imaging in wild-type and genetically sleep-deprived animals. Moreover, I compared the transcriptomes of adult wild-type and genetically sleep-deprived worms both wounded and unwounded. To investigate the structure of the cuticle, I analyzed scanning electron microscopy images. Results: In the first project, I could show that NAS-38 indeed increases sleep via its astacin domain in a process that is modulated by the TSP-1 domain. Moreover, I could show that many AMPs act redundantly in mediating immunity-induced sleep downstream of NAS-38 and after wounding. I demonstrated that the AMP NLP-29 signals sleep via the neuropeptide receptor NPR 12. This receptor can mediate sleep when it is specifically expressed in command interneurons of a circuit that has been shown to activate RIS. Interestingly, I also found that EGFR signaling is required to mediate NLP-29-induced sleep. In the second project, I found that sleeplessness does not dramatically alter the transcriptional wounding response. However, I could show that transcription is altered already in the unwounded non-sleeping mutant. This affects, among others, a specific subset of oscillating collagen-coding genes, whose expression usually peaks around the end of lethargus. As the timing of expression of collagens is thought to be highly important for proper cuticle formation, I characterized the cuticle of the aptf-1(gk794) mutant. I could show that young adult aptf 1(gk794) worms indeed have a structural defect affecting cuticular furrows in the region adjacent to the alae, which could potentially decrease specific aspects of resilience of the cuticle. Thus, sleep might be required to build robustness in the form of a properly structured cuticle. Conclusion: In this PhD project, I completed the characterization of a novel mechanism by which wounding signals sleep from the periphery to the nervous system as part of the immune response in C. elegans. I could show that AMPs act as cross-tissue signals from the epidermis to a neuronal RIS-controlling circuit that ultimately leads to sleep induction. As components of this molecular pathway are highly conserved, AMPs might also induce sleep to promote recovery from injury in other organisms, including humans. Moreover, I laid the foundations for dissecting the molecular mechanisms behind the functions of sleep for healing and survival. Even though the disability to sleep did not seem to drastically change the transcriptional response to wounding, my results indicate a role for

    Spartan Daily, March 21, 2023

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    Volume 160, Issue 23https://scholarworks.sjsu.edu/spartan_daily_2023/1022/thumbnail.jp

    Mizzou, volume 111, number 3 (2023 Spring)

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    Softening Corners: How a Carefully Considered Hospitality Operation Impacted an Educational Institution

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    Enter quickly, as I am afraid of my happiness! (Derrida, 2000, p.131) This research project is an attempt to bridge the gap between the philosophical ideals of hospitality and the hospitality industry, by examining how a carefully considered hospitality operation impacted an educational institution over the course of eight years. The aim of this study is to demonstrate that the application of the philosophical ideals to a commercial hospitality setting yielded profoundly positive results. The primary research was compiled by the author conducting a case study of her own food business, Luncheonette which was located in the National College of Art and Design in Dublin. A strong motivation behind this thesis is to present an alternative model for hospitality in an institutional setting which could be useful to others. The term Softening Corners, used in the title refers to the additional yielding layer of humanity which thoughtful hospitality can bring to harsh space. This research has been informed by the literature surrounding the philosophy, sociology, etymology and historic origins of hospitality. A qualitative approach was adopted to collect primary research. Nine semi-structured interviews were conducted with students, staff and visitors to the college. The interviews were juxtaposed with a collection of autoethnographic research compiled by the author, outlining the experience, knowledge and skills gained by operating a college canteen which had an unforeseen impact on the institution it served. These two sources of data are treated to a thematic analysis and arranged into seven themes, each one acting as a response to the directive: How to Soften Corners. The findings of this research study reveal that the influence and legacy that this active hospitality practice had on this educational institution was profoundly positive and far beyond any expectations of what an institutional catering operation could achieve

    The Lumberjack, November 08, 2023

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    The student newspaper of Humboldt State University.https://digitalcommons.humboldt.edu/studentnewspaper/3224/thumbnail.jp

    Symphony No. V: Elements (Julie Giroux, 2018); An Overview Of Programmatic Elements and Performance Devices

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    Julie Giroux is a multi-faceted composer who has been writing for the wind band since the 1980s. Having composed and arranged over 125 works for wind band, Giroux has dedicated her compositional career to furthering the development of the wind band repertoire while simultaneously working to establish the wind band genre as an area of serious artistic merit. Giroux is in constant demand as a commissioned composer. Her projects are often commissioned by distinguished ensembles, both in the United States and around the world, and many of her pieces receive performances at significant events such as The Midwest Clinic Band and Orchestra Conference in Chicago, Illinois. A composer of programmatic music, Giroux has brought to life the stories of many people, places, organizations, and current issues in society. Among her works are six symphonies. Each symphony portrays its own ideas through a skillful use of the wind ensemble. The purpose of this study is to explore the programmatic elements and performance devices of Julie Giroux’s Symphony No. V: Elements (2018). This study addresses compositional intent through technique and analysis. To better understand the components employed by Giroux in her fifth symphony, a brief look at her first four symphonies is explored. Through an exploration of her symphonies, specifically Symphony No. V: Elements, the compositional techniques of Julie Giroux are dissected to reveal how the composer portrays the ideas she is depicting through music
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