From a "Student" to a Lifelong "Consumer" : Constructions of Educability in Adult Students' Narrative Life Histories

The focus of this study was to examine the constructions of the educable subject of the lifelong learning (LLL) narrative in the narrative life histories of adult students at general upper secondary school for adults (GUSSA). In this study lifelong learning has been defined as a cultural narrative on education, “a system of political thinking” that is not internally consistent, but has contradictory themes embedded within it (Billig et al., 1988). As earlier research has shown and this study also confirms, the LLL narrative creates differences between those who are included and those who fall behind and are excluded from the learning society ideal. Educability expresses socially constructed interpretations on who benefit from education and who should be educated and how. The presupposition in this study has been that contradictions between the LLL narrative and the so-called traditional constructions of educability are likely to be constructed as the former relies on the all-inclusive interpretation of educability and the latter on the meritocratic model of educating individuals based on their innate abilities. The school system continues to uphold the institutionalized ethos of educability that ranks students into the categories “bright”, “mediocre”, and “poor” (Räty & Snellman, 1998) on the basis of their abilities, including gender-related differences as well as differences based on social class. Traditional age-related norms also persist, for example general upper secondary education is normatively completed in youth and not in adulthood, and the formal learning context continues to outweigh both non-formal and informal learning. Moreover, in this study the construction of social differences in relation to educability and, thereafter unequal access to education has been examined in relation to age, social class, and gender. The biographical work of the research participants forms a peephole that permits the examination of the dilemmatic nature of the constructions of educability in this study. Formal general upper secondary education in adulthood is situated on the border between the traditional and the LLL narratives on educability: participation in GUSSA inevitably means that one’s ability and competence as a student and learner becomes reassessed through the assessment criteria maintained by schools, whereas according to the principles of LLL everyone is educable; everyone is encouraged to learn throughout their lives regardless of age, social class, or gender. This study is situated in the field of adult education, sociology of education, and social psychological research on educability, having also been informed by feminist studies. Moreover, this study contributes to narrative life history research combining the structural analysis of narratives (Labov & Waletzky, 1997), i.e. mini-stories within life history, with the analysis of the life histories as structural and thematic wholes and the creation of coherence in them; thus, permitting both micro and macro analyses. On accounting for the discontinuity created by participation in general upper secondary school study in adulthood and not normatively in youth, the GUSSA students construct coherence in relation to their ability and competence as students and learners. The seven case studies illuminate the social differences constructed in relation to educability, i.e. social class, gender, age, and the “new category of student and learner”. In the data of this study, i.e. 20 general upper secondary school adult graduates’ narrative life histories primarily generated through interviews, two main coherence patterns of the adult educable subject emerge. The first performance-oriented pattern displays qualities that are closely related to the principles of LLL. Contrary to the principles of lifewide learning, however, the documentation of one’s competence through formal qualifications outweighs non-formal and informal learning in preparation for future change and the competition for further education, professional careers, and higher social positions. The second flexible learning pattern calls into question the status of formal, especially theoretical and academically oriented education; inner development is seen as more important than such external signs of development — grades and certificates. Studying and learning is constructed as a hobby and as a means to a more satisfactory life as opposed to a socially and culturally valued serious occupation leading to further education and career development. Consequently, as a curious, active, and independent learner, this educable but not readily employable subject is pushed into the periphery of lifelong learning. These two coherence patterns of the adult educable subject illuminate who is to be educated and how. The educable and readily employable LLL subject is to participate in formal education in order to achieve qualifications for working life, whereas the educable but not employable subject may utilize lifewide learning for her/his own pleasure. Key words: adult education, general upper secondary school for adults, educability, lifelong learning, narrative life history

Mitochondrial Malfunction in Tumor Formation and Neuromuscular Diseases : Consequences of defects in fumarate hydratase and in the respiratory chain

The mitochondrion is an organelle of outmost importance, and the mitochondrial network performs an array of functions that go well beyond ATP synthesis. Defects in mitochondrial performance lead to diseases, often affecting nervous system and muscle. Although many of these mitochondrial diseases have been linked to defects in specific genes, the molecular mechanisms underlying the pathologies remain unclear. The work in this thesis aims to determine how defects in mitochondria are communicated within - and interpreted by - the cells, and how this contributes to disease phenotypes. Fumarate hydratase (FH) is an enzyme of the citrate cycle. Recessive defects in FH lead to infantile mitochondrial encephalopathies, while dominant mutations predispose to tumor formation. Defects in succinate dehydrogenase (SDH), the enzyme that precedes FH in the citrate cycle, have also been described. Mutations in SDH subunits SDHB, SDHC and SDHD are associated with tumor predisposition, while mutations in SDHA lead to a characteristic mitochondrial encephalopathy of childhood. Thus, the citrate cycle, via FH and SDH, seems to have essential roles in mitochondrial function, as well as in the regulation of processes such as cell proliferation, differentiation or death. Tumor predisposition is not a typical feature of mitochondrial energy deficiency diseases. However, defects in citrate cycle enzymes also affect mitochondrial energy metabolism. It is therefore necessary to distinguish what is specific for defects in citrate cycle, and thus possibly associated with the tumor phenotype, from the generic consequences of defects in mitochondrial aerobic metabolism. We used primary fibroblasts from patients with recessive FH defects to study the cellular consequences of FH-deficiency (FH-). Similarly to the tumors observed in FH- patients, these fibroblasts have very low FH activity. The use of primary cells has the advantage that they are diploid, in contrast with the aneuploid tumor cells, thereby enabling the study of the early consequences of FH- in diploid background, before tumorigenesis and aneuploidy. To distinguish the specific consequences of FH- from typical consequences of defects in mitochondrial aerobic metabolism, we used primary fibroblasts from patients with MELAS (mitochondrial encephalopathy with lactic acidosis and stroke-like episodes) and from patients with NARP (neuropathy, ataxia and retinitis pigmentosa). These diseases also affect mitochondrial aerobic metabolism but are not known to predispose to tumor formation. To study in vivo the systemic consequences of defects in mitochondrial aerobic metabolism, we used a transgenic mouse model of late-onset mitochondrial myopathy. The mouse contains a transgene with an in-frame duplication of a segment of Twinkle, the mitochondrial replicative helicase, whose defects underlie the human disease progressive external ophthalmoplegia. This mouse model replicates the phenotype in the patients, particularly neuronal degeneration, mitochondrial myopathy, and subtle decrease of respiratory chain activity associated with mtDNA deletions. Due to the accumulation of mtDNA deletions, the mouse was named deletor. We first studied the consequences of FH- and of respiratory chain defects for energy metabolism in primary fibroblasts. To further characterize the effects of FH- and respiratory chain malfunction in primary fibroblasts at transcriptional level, we used expression microarrays. In order to understand the in vivo consequences of respiratory chain defects in vivo, we also studied the transcriptional consequences of Twinkle defects in deletor mice skeletal muscle, cerebellum and hippocampus. Fumarate accumulated in the FH- homozygous cells, but not in the compound heterozygous lines. However, virtually all FH- lines lacked cytoplasmic FH. Induction of glycolysis was common to FH-, MELAS and NARP fibroblasts. In deletor muscle glycolysis seemed to be upregulated. This was in contrast with deletor cerebellum and hippocampus, where mitochondrial biogenesis was in progress. Despite sharing a glycolytic pattern in energy metabolism, FH- and respiratory chain defects led to opposite consequences in redox environment. FH- was associated with reduced redox environment, while MELAS and NARP displayed evidences of oxidative stress. The deletor cerebellum had transcriptional induction of antioxidant defenses, suggesting increased production of reactive oxygen species. Since the fibroblasts do not represent the tissues where the tumors appear in FH- patients, we compared the fibroblast array data with the data from FH- leiomyomas and normal myometrium. This allowed the determination of the pathways and networks affected by FH-deficiency in primary cells that are also relevant for myoma formation. A key pathway regulating smooth muscle differentiation, SRF (serum response factor)-FOS-JUNB, was found to be downregulated in FH- cells and in myomas. While in the deletor mouse many pathways were affected in a tissue-specific basis, like FGF21 induction in the deletor muscle, others were systemic, such as the downregulation of ALAS2-linked heme synthesis in all deletor tissues analyzed. However, interestingly, even a tissue-specific response of FGF21 excretion could elicit a global starvation response. The work presented in this thesis has contributed to a better understanding of mitochondrial stress signalling and of pathways interpreting and transducing it to human pathology.

TCP Performance in Heterogeneous Wireless Networks

The TCP protocol is used by most Internet applications today, including the recent mobile wireless terminals that use TCP for their World-Wide Web, E-mail and other traffic. The recent wireless network technologies, such as GPRS, are known to cause delay spikes in packet transfer. This causes unnecessary TCP retransmission timeouts. This dissertation proposes a mechanism, Forward RTO-Recovery (F-RTO) for detecting the unnecessary TCP retransmission timeouts and thus allow TCP to take appropriate follow-up actions. We analyze a Linux F-RTO implementation in various network scenarios and investigate different alternatives to the basic algorithm. The second part of this dissertation is focused on quickly adapting the TCP's transmission rate when the underlying link characteristics change suddenly. This can happen, for example, due to vertical hand-offs between GPRS and WLAN wireless technologies. We investigate the Quick-Start algorithm that, in collaboration with the network routers, aims to quickly probe the available bandwidth on a network path, and allow TCP's congestion control algorithms to use that information. By extensive simulations we study the different router algorithms and parameters for Quick-Start, and discuss the challenges Quick-Start faces in the current Internet. We also study the performance of Quick-Start when applied to vertical hand-offs between different wireless link technologies.

Role of thrombin in coronary artery bypass grafting

Thrombin is a multifunctional protease, which has a central role in the development and progression of coronary atherosclerotic lesions and it is a possible mediator of myocardial ischemia-reperfusion injury. Its generation and procoagulant activity are greatly upregulated during cardiopulmonary bypass (CPB). On the other hand, activated protein C, a physiologic anticoagulant that is activated by thrombomodulin-bound thrombin, has been beneficial in various models of ischemia-reperfusion. Therefore, our aim in this study was to test whether thrombin generation or protein C activation during coronary artery bypass grafting (CABG) associate with postoperative myocardial damage or hemodynamic changes. To further investigate the regulation of thrombin during CABG, we tested whether preoperative thrombophilic factors associate with increased CPB-related generation of thrombin or its procoagulant activity. We also measured the anticoagulant effects of heparin during CPB with a novel coagulation test, prothrombinase-induced clotting time (PiCT), and compared the performance of this test with the present standard of laboratory-based anticoagulation monitoring. One hundred patients undergoing elective on-pump CABG were studied prospectively. A progressive increase in markers of thrombin generation (F1+2), fibrinolysis (D-dimer), and fibrin formation (soluble fibrin monomer complexes) was observed during CPB, which was further distinctly propagated by reperfusion after myocardial ischemia, and continued to peak after the neutralization of heparin with protamine. Thrombin generation during reperfusion after CABG associated with postoperative myocardial damage and increased pulmonary vascular resistance. Activated protein C levels increased only slightly during CPB before the release of the aortic clamp, but reperfusion and more significantly heparin neutralization caused a massive increase in activated protein C levels. Protein C activation was clearly delayed in relation to both thrombin generation and fibrin formation. Even though activated protein C associated dynamically with postoperative hemodynamic performance, it did not associate with postoperative myocardial damage. Preoperative thrombophilic variables did not associate with perioperative thrombin generation or its procoagulant activity. Therefore, our results do not favor routine thrombophilia screening before CABG. There was poor agreement between PiCT and other measurements of heparin effects in the setting of CPB. However, lower heparin levels during CPB associated with inferior thrombin control and high heparin levels during CPB associated with fewer perioperative transfusions of blood products. Overall, our results suggest that hypercoagulation after CABG, especially during reperfusion, might be clinically important.

The relationships between work stressors and organizational performance in long-term care for elderly residents

This study investigates the relationships between work stressors and organizational performance in terms of the quality of care provided by the long-term care facilities. Work stressors are first examined in relation to the unit's structural factors, resident characteristics, and to the unit specialization. The study is completed by an investigation into the associations of work stressors such as job demands or time pressure, role ambiguity, resident-related stress, and procedural injustice to organizational performance. Also the moderating effect of job control in the job demands organizational performance relationship is examined. The study was carried out in the National Research and Development Centre for Welfare and Health (STAKES). Survey data were drawn from 1194 nursing employees in 107 residential-home and health-center inpatient units in 1999 and from 977 employees in 91 units in 2002. Information on the unit resident characteristics and the quality of care was provided by the Resident Assessment Instrument (RAI). The results showed that large unit size or lower staffing levels were not consistently related to work stressors, whereas the impairments in residents' physical functioning in particular initiated stressful working conditions for employees. However, unit specialization into dementia and psychiatric residents was found to buffer the effects that the resident characteristics had on employee appraisals of work stressors, in that a high proportion of behavioral problems was related to less time pressure and role conflicts for employees in specialized units. Unit specialization was also related to improved team climates and the organizational commitment of employees. Work stressors associated with problems in care quality. Time pressure explained most of the differences between units in how the employees perceived the quality of physical and psychosocial care they provide for the residents. A high level of job demands in the unit was also found to be related to some increases in all clinical quality problems. High job control buffered the effects of job demands on the quality of care in terms of the use of restraints on elderly residents. Physical restraint and especially antipsychotic drug use were less prevalent in units that combined both high job demands and high control for employees. In contrast, in high strain units where heavy job demands coincided with a lack of control for employees, quality was poor in terms of the frequent use of physical restraints. In addition, procedural injustice was related to the frequent use of antianxiety of hypnotic drugs for elderly residents. The results suggest that both job control and procedural justice may have improved employees' abilities to cope when caring for the elderly residents, resulting in better organizational performance.