Pest status and incidence of the honey bee tracheal mite in Finland

Selostus: Mehiläisen sisuspunkin aiheuttamat tuhot ja esiintyminen Suomessa

Kampen for livet i vemodets slør : å leve i spenningsfeltet mellom livets mulighet og dødens nødvendighet

The overallpurpose of this research is to develop knowledge about health and suffering in connection with serious cancer disease through the development of a contextual model describing how patients live their lives between the possibility of life and the necessity of death. The research takes its point of departure from a caring science perspective, and Gadamer's hermeneutical philosophy is chosen as the overall methodology. In addition to the caring science perspective, the existential philosophy of Kierkegaard constructs a framework of interpretation. The research consists of three empirical studies. In two of the studies 21 patients participated, whilst 8 nurses took part in the remaining study. The patients were seriously ill and the nurses had long experience of caring for seriously ill patients. Scientific conversations were used for data collection. The findings from the patient studies show that the relationship with one-self, others, God or the supernatural and nature, constitute the unit of meaning, in which the struggle between health and suffering takes place. This struggle takes the form of a dialectic movement between being delivered and being accommodated and confirmed. The patients strive, in their delivery, for health and integration, for being a self by being reconciled with one self. The patients are lonely in this struggle, as conversations related to existence and death seldom occurs with either the natural or the professional caregivers. Themes related to patients' death remain mainly unarticulated. The patients' life struggle appears on the existential level as a threefold struggle against time and annihilation, towards being accommodatedand confirmed and for restoration and reconciliation. Through the hermeneutic process the struggle at the ontological level appears as a struggle of the will between anxiety and love. The patients in this research experience their life's tragedy. A holistic interpretation of living under the pressure created between the possibility of life and the necessity of death appears to be a struggle for life in the veil of pensiveness. The nurses want to be involved in the patients' struggle, and they show a deep desire to support the dignity of the patients. The depth in the nurses' view of their responsibility for the patient as an entityof body, soul and spirit seems to be related to the nurses' understanding of life.

The role of cathepsin K in lung development and newborn chronic lung injury.

Chronic lung diseases, specifically bronchopulmonary dysplasia (BPD), are still causing mortality and morbidity amongst newborn infants. High protease activity has been suggested to have a deleterious role in oxygen-induced lung injuries. Cathepsin K (CatK) is a potent protease found in fetal lungs, degrading collagen and elastin. We hypothesized that CatK may be an important modulator of chronic lung injury in newborn infants and neonatal mice. First we measured CatK protein levels in repeated tracheal aspirate fluid samples from 13 intubated preterm infants during the first two weeks of life. The amount of CatK at 9-13 days was low in infants developing chronic lung disease. Consequently, we studied CatK mRNA expression in oxygen-exposed wild-type (WT) rats at postnatal day (PN) 14 and found decreased pulmonary mRNA expression of CatK in whole lung samples. Thereafter we demonstrated that CatK deficiency modifies lung development by accelerating the thinning of alveolar walls in newborn mice. In hyperoxia-exposed newborn mice CatK deficiency resulted in increased number of pulmonary foam cells, macrophages and amount of reduced glutathione in lung homogenates indicating intensified pulmonary oxidative stress and worse pulmonary outcome due to CatK deficiency. Conversely, transgenic overexpression of CatK caused slight enlargement of distal airspaces with increased alveolar chord length in room air in neonatal mice. While hyperoxic exposure inhibited alveolarization and resulted in enlarged airspaces in wild-type mice, these changes were significantly milder in CatK overexpressing mice at PN7. Finally, we showed that the expression of macrophage scavenger receptor 2 (MSR2) mRNA was down-regulated in oxygen-exposed CatK-deficient mice analyzed by microarray analysis. Our results demonstrate that CatK seems to participate in normal lung development and its expression is altered during pulmonary injury. In the presence of pulmonary risk factors, like high oxygen exposure, low amount of CatK may contribute to aggravated lung injury while sustained or slightly elevated amount of CatK may even protect the newborn lungs from excessive injury. Besides collagen degrading and antifibrotic function of CatK in the lungs, it is obvious that CatK may affect macrophage activity and modify oxidative stress response. In conclusion, pulmonary proteases, specifically CatK, have distinct roles in lung homeostasis and injury development, and although suggested, broad range inhibition of proteases may not be beneficial in newborn lung injury.