Background: Chronic cough is a common health problem with variable success rates to standardized treatment. Psychologic symptoms of depression, anxiety, and stress have been reported in association with chronic cough. The purpose of this study was to examine changes in the psychologic symptoms of depression, anxiety, and stress in adults with chronic cough 3 months after management using the ACCP cough treatment guidelines. Methods: This study used a descriptive longitudinal observation design. The major tenets associated with the Theory of Unpleasant Symptoms were examined. Intervention fidelity to the study components was measured. Results: A sample of 80 consecutive patients with chronic cough of greater than 8 weeks duration was recruited from one cough specialty clinic. Mean age of subjects was 58.54 years; 68.7% were female; 98.7% were white, and 97.5% were non-smokers. Mean cough duration was 85.99 months and mean cough severity was 6.11 (possible 0 –10; higher scores equal greater cough severity). Cough severity improved post treatment (n=65, M=2.32, (SE =.291), t (64) =7.98, p=.000); cough-specific quality-of-life also improved (n=65, M=9.17, (SE=1.30), t (64) =7.02, p=.000). Physiologic (urge-to-cough r=.360, ability to speak r=.469) and psychologic factors (depression r=.512, anxiety r=.507, stress r=.484) were significantly related to cough-specific quality-of-life and to cough severity (urge-to-cough r=.643, ability to speak r=.674 and depression r=.356, anxiety r=.419, stress r=.323) (all r, p=.01); social support and number of diagnoses were not related to either variable. Those experiencing greater financial strain had worse cough severity. Women, those experiencing financial strain, and those taking self-prescribed therapy had worse cough-specific quality-of-life. Intervention fidelity to the study plan was rated as high according to observation, participant receipt, and patient/physician concordance. Qualitative review identified potential areas of variability with intervention fidelity. Conclusions: By measuring the factors related to the major tenets of the Theory of Unpleasant Symptoms, this theory has helped to explain why those with chronic cough may have symptoms of depression, anxiety, and stress and why these symptoms improve as cough severity and cough-specific quality-of-life improve. Moreover, by measuring intervention fidelity, it may be possible to determine why cough guidelines may not be yielding consistently favorable results.

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Since February 2020, the world is in a COVID-19 pandemic [1]. Researchers around the globe are pitching in to develop a fast reliable, non-invasive testing methodology to solve this problem and one of the key directions of research is to utilize coughs and their corresponding vocal biomarkers for diagnosis of COVID-19. In this thesis, we propose a fast, real-time cough detection pipeline that can be used to detect and localize coughs from audio samples. The core of the pipeline utilizes the yolo-v3 model [2] from vision domain to localize coughs in the audio spectrograms by treating them as objects. This outcome is transformed to localize the boundaries of cough utterances in the input signal. The system to detect coughs from CoughVid dataset [3] is then evaluated. Furthermore, the pipeline is compared with other existing algorithms like tinyyolo-v3 to test for better localization and classification. Average precision(AP@0.5) of yolo-v3 and tinyyolo-v3 model are 0.67 and 0.78 respectively. Based on the AP values, tinyyolo-v3 performs better than yolo-v3 by atleast 10% and based on its computational advantage, its inference time was also found to be 2.4 times faster than yolo-v3 model in our experiments. This work is considered to be novel and significant in detection and localization of cough in an audio stream. In the end, the resulting cough events are used to extract MFCC features from it and classifiers were trained to predict whether a cough has COVID-19 or not. The performance of different classifiers were compared and it was observed that random forest outperformed other models with a precision of 83.04%. It can also be inferred from the results that the classifier looks promising, however, in future this model has to be trained using clinically approved dataset and tested for its reliability in using this model in a clinical setup. / Sedan februari 2020 är världen inne i en COVID-19-pandemi [1]. Forskare runt om i världen satsar på att utveckla en snabb tillförlitlig, icke-invasiv testmetodik för att lösa detta problem och en av de viktigaste forskningsriktningarna är att använda hosta och deras motsvarande vokala biomarkörer för diagnos av COVID-19. I denna avhandling föreslår vi en snabb pipeline för hostdetektering i realtid som kan användas för att upptäcka och lokalisera hosta från ljudprover. Kärnan i rörledningen använder yolo-v3-modellen [2] från syndomänen för att lokalisera hosta i ljudspektrogrammen genom att behandla dem som objekt. Detta resultat transformeras för att lokalisera gränserna för hosta yttranden i insignalen. Systemet för att upptäcka hosta från CoughVid dataset [3] utvärderas sedan. Dessutom jämförs rörledningen med andra befintliga algoritmer som tinyyolo-v3 för att testa för bättre lokalisering och klassificering. Genomsnittlig precision (AP@0.5) för modellen yolo-v3 och tinyyolo-v3 är 0,67 respektive 0,78. Baserat på AP-värdena fungerar tinyyolo-v3 bättre än yolo-v3 med minst 10% och baserat på dess beräkningsfördel befanns dess inferenstid också vara 2,4 gånger snabbare än yolo-v3- modellen i våra experiment. Detta arbete anses vara nytt och viktigt för att upptäcka och lokalisera hosta i en ljudström. I slutändan används de resulterande hosthändel-serna för att extrahera MFCC-funktioner från det och klassificerare utbildades för att förutsäga om en hosta har COVID-19 eller inte. Prestanda för olika klassificerare jämfördes och det observerades att slumpmässig skog överträffade andra modeller med en precision på 83.04%. Av resultaten kan man också dra slutsatsen att klassificeraren ser lovande ut, men i framtiden måste denna modell utbildas med hjälp av kliniskt godkänd dataset och testas med avseende på dess tillförlitlighet vid användning av denna modell i ett kliniskt upplägg.

The invention of the vaccine has been one of the greatest public health triumphs of the modern world. Each new vaccine has saved thousands - even millions - of lives worldwide, but this success has been fraught with controversy over the safety and even the effectiveness of vaccines. Vaccines have not always had a spotless safety record, but today’s vaccines are incredibly safe and continue to protect millions of people against diseases that have significantly declined or nearly disappeared from the developing world. It is this very success that has led many people to forget, or never discover, what those diseases are and how destructive they can be. This report tells the story of several families whose lives were deeply affected by vaccine-preventable diseases, accompanied with images that help tell their story. Following these stories is a broader discussion of the issues related to vaccines, the misunderstandings and misinformation that often circulate about them, a brief mention of their safety and efficacy, and a general discussion of many of the diseases they can prevent. / text

The original work presented in this thesis investigates some of the mechanisms that may be responsible for the aetiology of altitude-related cough. Particular attention is paid to its relationship to the long recognised, but poorly understood, changes in lung volumes that occur on ascent to altitude. The literature relevant to this thesis is reviewed in Chapter 1.<p><p>Widespread reports have long existed of a debilitating cough affecting visitors to high altitude that can incapacitate the sufferer and, on occasions, be severe enough to cause rib fractures (22, 34, 35). The prevalence of cough at altitude has been estimated to be between 22 and 42% at between 4200 and 4900 m in the Everest region of Nepal (10, 29). Traditionally the cough was attributed to the inspiration of the cold, dry air characteristic of the high altitude environment (37) but no attempts were made to confirm this aetiology. In the first formal study of cough at high altitude, nocturnal cough frequency was found to increase with increasing altitude during a trek to Everest Base Camp (5300 m) and massively so in 3 climbers on whom recordings were made up to 7000 m on Everest (8). After 9 days at 5300 m the citric acid cough threshold, a measure of the sensitivity of the cough reflex arc, was significantly reduced compared with both sea level and arrival at 5300 m.<p><p>During Operation Everest II, a simulated climb of Mount Everest in a hypobaric chamber, the majority of the subjects were troubled above 7000 m by pain and dryness in the throat and an irritating cough despite the chamber being maintained at a relative humidity of between 72 and 82% and a temperature of 23ºC (18). This argued against the widely held view that altitude-related cough was due to the inspiration of cold, dry air. <p><p>In the next major hypobaric chamber study, Operation Everest III, nocturnal cough frequency and citric acid cough threshold were measured on the 8 subjects in the study. The chamber temperature was maintained between 18 and 24ºC and relative humidity between 30 and 60% (24). This work is presented in Chapter 2 and, demonstrated an increase in nocturnal cough frequency with increasing altitude which immediately returned to control values on descent to sea level. Citric acid cough threshold was reduced at 8000 m compared to both sea level and 5000 m values. Changes in citric acid cough threshold at lower altitudes may not have been detected because of the constraints on subject numbers in the chamber. The study still however demonstrated an increase in clinical cough and a reduction in the citric acid cough threshold at extreme altitude, despite controlled environmental conditions, and thus refuted the long held belief that altitude-related cough is solely due to the inspiration of cold, dry air. <p><p>If altitude-related cough is not simply due to the inspiration of cold, dry air, other possible aetiologies are:<p>•\ / Doctorat en Sciences médicales / info:eu-repo/semantics/nonPublished

La toxine de pertussis (PTX) est une A-B protéine considérée comme l’un des principaux facteurs de virulence de Bordetella pertussis, l’agent bactérien responsable de la coqueluche. Aujourd’hui, cette maladie représente encore un réel danger pour les nouveaux-nés et les<p>nourrissons non ou partiellement immunisés. Actuellement, la coqueluche provoque encore la<p>mort d’environ 350.000 individus par an. La toxicité de la PTX est liée à l’activité<p>enzymatique de sa sous-unité A capable d’inhiber les voies de signalisation associées aux<p>protéines Gi. La partie B, quant à elle, permet l’entrée de cette sous-unité A dans le<p>cytoplasme des cellules cibles en se liant spécifiquement à son ou ses récepteurs<p>membranaires toujours inconnus de nos jours.<p><p>Des études réalisées chez la souris et chez l’homme ont montré que les vaccins anticoquelucheux combinés à différents antigènes vaccinaux étaient capables de moduler<p>leurs réponses humorales spécifiques. Par ailleurs, la PTX est couramment qualifiée d’agent<p>immunostimulant. En effet, des modèles murins de vaccination permirent d’identifier des<p>propriétés adjuvantes de la PTX coadministrée avec des antigènes non relevants.<p><p>Le travail développé dans ce manuscrit étudie les effets de la PTX sur 2 types cellulaires<p>primordiaux sollicités lors d’une vaccination :la cellule dendritique (DC) et le lymphocyte T<p>CD4+ naïf.<p><p>Les DC sont les seules cellules présentatrices d’antigènes aptes à initier une réponse immune<p>primaire. Dans un premier temps, nous avons montré que la PTX était capable d’activer des<p>DC générées in vitro à partir de monocytes. En effet, elles acquièrent un phénotype mature<p>caractérisé par une augmentation de l’expression membranaire des molécules costimulatrices<p>et du CMH de classe II, démontrant un effet direct et spécifique de la PTX sur les DC<p>myéloïdes. Parallèlement, ces DC produisent du TNF-a, de l’IL-12p40 et de l’IL-12p70 et<p>activent NF-kappaB, un facteur de transcription essentiel au processus de maturation. Nous<p>avons obtenu des résultats similaires avec une toxine génétiquement modifiée qui est<p>enzymatiquement inactive. A partir de sang total incubé avec la PTX, nous avons par ailleurs<p>observé que les DC circulantes du nouveau-né étaient déficientes dans leur maturation et leur<p>sécrétion d’IL-12p70 comparées aux DC de l’adulte.<p><p>D’autre part, il a été décrit précédemment que la PTX exerçait des effets mitogènes sur les<p>lymphocytes T humains et murins. Cependant, le rôle qu’elle joue sur la population des<p>lymphocytes T CD4 naïfs reste peu connu. A l’issue de notre second travail, nous pouvons<p>dès lors affirmer que la PTX est également capable d’activer des lymphocytes T<p>CD4+CD45RA+ naïfs isolés à partir des cellules mononuclées du sang périphérique, et ce<p>indépendamment de son activité enzymatique. En effet, ces lymphocytes T CD4+ naïfs stimulés par la PTX prolifèrent, synthétisent des quantités non négligeables d'ARN messagers<p>codant pour l’IL-2 et le TNF-a, augmentent l’expression membranaire des molécules CD40L,<p>CD69 et CD25 et expriment la protéine Foxp3. Cette activation s’accompagne de la translocation nucléaire de NF-kappaB et NFAT. Parallèlement à l’adulte, la PTX active les lymphocytes T CD4 néonataux. Néanmoins, ceux-ci prolifèrent moins bien et expriment plus faiblement le CD40L à leur surface.<p><p>Enfin, la PTX induit la sécrétion de taux importants d’IFN-g par des T CD4+CD45RA+ naïfs<p>adultes mis en présence de DC autologues.<p><p>Nous terminerons en proposant l’hypothèse suivante :La PTX pourrait exercer ses propriétés<p>adjuvantes par l’intermédiaire de différents mécanismes comprenant notamment la maturation<p>des DC d’origine myéloïde et l’activation des lymphocytes T CD4+CD45RA+ naïfs. Ces 2 populations cellulaires sont en effet les principaux protagonistes impliqués dans la réponse<p>immune primaire. / Doctorat en sciences pharmaceutiques / info:eu-repo/semantics/nonPublished

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