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Abstract Introduction: Previous research showed that comorbidities that are common in patients with Chronic Obstructive Pulmonary Disease (COPD) are anxiety and depression. Furthermore, stress can be associated with more depressive symptoms. Patients suffering from depression along with an additional medical condition, tend to have more severe symptoms in both depression and their medical illness.   Aim: The aim of this study was to investigate depression, anxiety, and stress among COPD patients, and also to examine if there was a difference in levels of depression, anxiety and stress between genders, and between COPD patients and patients with COPD together with comorbid chronic condition.   Method: This study had a descriptive and cross-sectional design with a quantitative method. The data collection took place at a respiratory ward at Cho Ray Hospital in Ho Chi Minh City, Vietnam. Sixty two COPD patients, both men and women, participated voluntarily by answering a questionnaire. Virginia Henderson´s nursing theory was used as a theoretical framework. Data analysis was conducted through using the statistical program SPSS.   Result: More than half of the COPD patients (88.8%) presented symptoms of depression, 93.5% presented symptoms of anxiety, and 54.8% presented symptoms of stress. There was a statistical significance between genders among COPD patients in anxiety, where all female participants (100%) showed extremely severe levels of anxiety. In levels of extreme severity, both patients with only COPD diagnosis and patients with COPD and comorbid chronic condition presented symptoms in both depression and anxiety, but not in levels of stress.     Conclusion: COPD patients in Ho Chi Minh City presented high levels of depression and anxiety. In addition, levels of stress were present, although not as high as depression and anxiety among this patient group. More information concerning psychological distress needs to be offered by healthcare professionals to COPD patients. Further research in this field is desirable. / Sammanfattning Introduktion: Tidigare forskning visar att depression och ångest är vanligt förekommande bland patienter med Kroniskt Obstruktiv Lungsjukdom (KOL). Stress kan associeras med flera depressiva symtom. Patienter som lider av depression tillsammans med annat mediciniskt tillstånd kan ha en tendens att utveckla svårare symptom i sin depression och sitt medicinska tillstånd.   Syfte: Syftet med denna studie var att undersöka depression, ångest och stress hos patienter med KOL och om skillnader fanns mellan kön. Vidare önskades skillnader undersökas mellan patienter med enbart KOL och patienter med KOL och annat kroniskt tillstånd.     Metod: Studien är en deskriptiv tvärsnittsstudie, med kvantitativ metod. Datainsamling utfördes på en respiratorisk avdelning på Cho Ray sjukhuset i Ho Chi Minh City, Vietnam. Sextio-två KOL-patienter, både män och kvinnor, deltog frivilligt genom att besvara en enkät. Virginia Hendersons omvårdnadsteori användes i detta arbete. Dataanalysen utfördes med hjälp av SPSS programmet.   Resultat: Mer än hälften (88,8 %) av KOL-patienterna visade symtom på depression, 93,5% för ångest, samt 54,8 % visade symtom för stress. Det fanns en statistisk signifikant skillnad mellan könen avseende ångest, där alla kvinnliga deltagare (100 %) visade extremt allvarliga nivåer av ångest. Patienter med enbart KOL-diagnos och patienter med KOL tillsammans med andra kroniska tillstånd uppvisade extremt allvarliga nivåer av både depression och ångest, dock inte av stress.   Slutsats: KOL-patienter i Ho Chi Minh City, Vietnam, uppvisar höga nivåer av depression och ångest. Höga stressnivåer bland deltagare kunde ses, dock inte i lika hög utsträckning som depression och ångest i denna patientgrupp. Mer studier i detta ämne är önskvärt.

La mise au point de médicaments ciblant la neuroinflammation, une composante importante de la physiopathologie des maladies neurodégénératives, fait l’objet de nombreuses recherches. Dans ce travail de thèse, nous avons étudié les effets de deux molécules potentiellement anti-inflammatoires et neuroprotectrices : l’hémine, un inducteur de l’hème oxygénase 1(HO-1) et ; le C16, un inhibiteur de la protéine kinase activée par l’ARN (PKR) dans un modèle de neuroinflammation in vivo par injection intrastriatale d’acide quinolinique (AQ) chez le rat. Nos résultats ont montré que l’induction de la HO-1 produit des effets délétères tandis que l’inhibition de la PKR induit des effets neuroprotecteurs et antiapoptotiques. Ce travail a par ailleurs permis de décrire l’évolution cinétique de la neuroinflammation sur 90 jours dans le modèle AQ, la capacité du tissu cérébral à se régénérer après la lésion et l’intérêt de ce modèle dans l’étude des effets d’agents neuroprotecteurs administrés au long cours. / Neuroinflammation is a key part of the physiopathology of neurodegenerative diseases and is an interesting target in their treatment. In this PhD work, we studied the effects of two potentially anti-inflammatory and neuroprotective molecules, hemin and C16, in an in vivo rat model of neuroinflammation by intrastriatal injection of quinolinic acid (QA). We showed that heme oxygenase 1 (HO-1) induction by hemin has deleterious effects whereas inhibition of the protein kinase RNA activated (PKR) by C16 treatment induced neuroprotective and anti-inflammatory effects. Concurrently, we evaluated longitudinal evolution of neuroinflammation in our model. Results showed the kinetic of the inflammatory phenomena; the ability of cerebral tissue to recover integrity and the capability of this model to evaluate potential neuroprotective and anti-inflammatory drugs in a long-time study.

The diploma thesis titled "Political developments in Vietnam from 1954 to the present" focuses on the political development of Vietnam after the war in Indochina until present days. It describes what led Ho Chi Minh to adopt communism, after what and by whom he was inspired and why communism has nowadays still a strong position in Vietnam. The main attention is devoted to the reforms of Doi Moi, that have lifted the country's economy. It outlines the positive and negative aspects following the introduction of these reforms.

Ein wesentliches Merkmal der Immundepression ist eine Monozytendeaktivierung mit verminderter Antigenpräsentation und Sekretion proinflammatorischer Zytokine. Infolge dessen sind Patienten mit Immundepression besonders anfällig gegenüber Infektionen. Als mögliche Mediatoren werden antiinflammatorische Zytokin wie IL10 und TGF-beta diskutiert, deren immunhemmende Wirkung allerdings nach Ihrem Entfernen schnell reversibel ist. An der Entwicklung einer langanhaltenden Immundepression müssen demnach weitere Mediatoren beteiligt sein. Eine Studie mit Patienten nach Herz-Operationen zeigte eine Korrelation zwischen einer erhöhten Anfälligkeit gegenüber Infektionen und einer Überexpression des Hitzeschockproteins Hämoxygenase-1 (HO-1) in peripheren Blutleukozyten, dem in vielen Studien eine antiinflammatorische und cytoprotektive Wirkung zugeschrieben wird. Eine Porphyrin-induzierte HO-1 Überexpression in humanen Monozyten korreliert mit einer verminderten MHC-II Expression. Allerdings kann eine Hemmung der HO-1-Expression diesen Effekt nicht aufheben, so dass die verwendeten Porphyrine die Antigenpräsentation durch HO-1-unabhängige Mechanismen beeinflussen müssen. Während sich die Hemmung der IFN-Gamma-induzierten MHC-II Expression durch eine gleichzeitig verminderte STAT-1-Phosphorylierung erklären lässt, ist die Porphyrin-induzierte Hemmung der konstitutiven MHC-II-Expression unabhängig von STAT-1. Zudem konnte weder eine Abhängigkeit von STAT-3, noch von einer verstärkten Histonacetylierung oder PKA-Aktivierung gezeigt werden. Die Ergebnisse deuten zudem darauf hin, dass die Porphyrin-Effekte nicht über eine Interaktion mit dem Hämoglobin-Scavenger Rezeptor CD163 induziert werden. Eine Porphyrin-Behandlung von Monozyten in vitro resultiert in einem ähnlichen Phänotyp, wie er in Monozyten von immundepressiven Patienten beobachtet wird, so dass ein verbessertes Wissen über die beeinflussten Signalwege neue Ansätze zur frühzeitigen Behandlung einer Immundepression liefern kann. / A long lasting immunodepression is characterised by a deactivation of the function of monocytes with decreased antigen presentation and decreased secretion of pro-inflammatory cytokines. This may predispose patients with immunodepression to infectious complications. Although anti-inflammatory cytokines as IL-10 and TGF-beta are discussed, the mechanism that induces and sustains this long lasting immunodepression is still incompletely understood. A previous study with patients after cardiac surgery could show a correlation between over expression of heme oxygenase-1 (HO-1) in peripheral blood leukocytes and an increased susceptibility to infection related complications. HO-1 is a stress-inducible heat shock protein with potent anti-inflammatory and cytoprotective properties. A porphyrin-induced HO-1 overexpression in human monocytes correlates with decreased MHC-II expression. However, inhibition of HO-1 expression does not abrogate this effect. According to this, porphyrins must affect the antigen presentation by HO-1-independent mechanisms. While the inhibition of IFN-Gamma-induced MHC-II expression could be explained by a simultaneously decreased STAT-1 phosphorylation, the porphyrin-induced inhibition of the constitutive MHC-II expression is independent of STAT-1. Moreover, neither STAT-3 activity, nor an increased histone acetylation or PKA activation is clearly involved in porphyrin mediated inhibition of MHC-II. The results further suggest that the porphyrin-effects are not induced by an interaction with the hemoglobin scavenger receptor CD163. Nevertheless a porphyrin-treatment of monocytes in vitro results in a similar phenotype, as observed in monocytes from patients with immunodepression. Therefore, better understanding of the involved pathways could reveal new approaches for the early treatment of patients with immunodepression.

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Ischaemia/Reperfusion Injury (IRI) is the most common cause of acute kidney injury- a devastating clinical problem lacking any specific treatments to promote renal recovery. Macrophages (Mφ) are pleiotropic cells of the innate immune system, with roles spanning host defence, cytotoxicity, clearance of apoptotic cells and promotion of tissue repair. Mφ are also known to be important mediators of renal injury in other experimental models of renal disease including transplantation, obstruction and glomerulonephritis. This work sought to examine the role of Mφ in mediating renal IRI. Conditional renal Mφ and monocyte depletion prior to experimental IRI was achieved by administering diphtheria toxin to the CD11b-DTR transgenic animal. This had no impact on either renal function or structural injury. In contrast liposomal clodronate mediated Mφ depletion provided functional and structural protection from injury. Administration of exogenous apoptotic cells also protected renal function if delivered 24h prior to IRI. Immunodeficient SCID mice exhibited a protected injury phenotype after IRI, however derived no additional protection from the administration of either liposomal clodronate or i.v. apoptotic cells. These findings suggest that the protective phenotype must involve either lymphocyte populations or circulating antibody. Preliminary work demonstrates that SCID mice lack IgM natural antibody which deposits in the kidney in the first 30 minutes after IRI. It was also demonstrated that apoptotic cells bind IgM natural antibody present within the circulation. The potential for the key antioxidant enzyme Heme oxygenase-1 (HO-1) to protect renal function was also examined in aged mice using hemearginate (HA) - a potent HO-1 inducer. Echoing epidemiological studies in humans aged mice had increased susceptibility to IRI, whilst failing to induce medullary HO-1. The main site of medullary HO-1 induction by HA was in medullary Mφ, and the protective phenotype was abolished by Mφ ablation, implicating Mφ as the key mediators of HA induced protection in renal IRI. Final studies employed adenoviral transduction to overexpress HO-1 within bone marrow derived Mφ, leading to a modified phenotype with increased IL- 10 and phagocytosis, and reduced TNFα and NO production. When these were introduced in vivo after IRI renal function was improved, potentially due to accelerated clearance of renal platelet deposition.

The purpose of this paper is to create an easily understandable version of the Ho-Lee interest rate model. The first part analyzes the model in detail, and the second part calibrates it to demonstrate how it can be applied to real market data.

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

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