Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.

Thesis (doctoral)--Jāmiʻat al-Qāhirah, 1984. / Includes bibliographical references (p. 173-182).

Thesis (Ph. D.)--University of Chicago, Dept. of Economics, August 2002. / Includes bibliographical references. Also available on the Internet.

Thesis (Ph. D. in Biomedical Engineering)--Vanderbilt University, Dec. 2006. / Title from title screen. Includes bibliographical references.

Thesis (M.S.)--University of Oregon, 2004. / Includes bibliographical references (leaves 71-73).

Dissertation (Ph.D.)--Worcester Polytechnic Institute. / Keywords: fMRI; Segmentation; Registration; Rat Brain Atlas. Includes bibliographical references. (p.126-139)

Thesis (M.Pub.Health) - University of Queensland, 2006. / Includes bibliography.

Thesis (Ph. D.)--Georgia State University, 2006. / Marise B. Parent, committee chair; Timothy J. Bartness, Kim L. Huhman, Kyle J. Frantz, committee members. Electronic text (352 p. : ill.)) : digital, PDF file. Description based on contents viewed July 12, 2007. Includes bibliographical references (p. 307-352).

M.A. / As medical technology and procedures continue to improve, traumatically brain injured persons who previously would not have lived through their injuries are managing to survive. The traumatically brain-injured person must learn to cope with the profound physical, cognitive, emotional, and personality changes that are produced from brain trauma. Within the family system, the members reciprocally influence one another. Major events that occur within the family system have an immense effect on the family relationships, dynamics, roles, and expectations. A traumatic brain injury, with its sudden onset and the inherent uncertainty regarding recovery and rehabilitation, can have a devastating effect on the family as a whole, and upon its individual members. Research on the familial effects of a member’s traumatic brain injury portrays a bleak image of the family in the aftermath of TBI, and for years afterwards. Grief, anger, guilt, blame, loneliness, depression, and isolation are often reported in the literature. The literature focuses mainly on the primary caregiver, usually the spouse of the TBI person, or the parent of a TBI child. Limited research has been conducted regarding the psychological effects on the offspring of parents who sustain traumatic brain injuries. Surely, children and adolescents will feel the effects of a parent’s brain injury differently than a spouse would. However the actual experience as perceived by the offspring has been neglected in research thus far. Adolescents were the focus of the current study. Being in a time of transition between childhood and adulthood, it was thought that they would experience the effects of a parental brain injury differently than younger children or adults within the family would. The existential-phenomenological approach employed as the research methodology allowed for a rich, in depth understanding of the adolescents as beings-in-the-world interpreting their own experiences of having a traumatically brain-injured parent. Six adolescent offspring of traumatically brain-injured parents were sourced from Headway Gauteng, and interviewed for the study. The four interviews that were used for the intense phenomenological analysis were transcribed verbatim. Themes were derived from the experience of each participant, and then integrated and related to the relevant available literature and within the wider context of existential phenomenology, in order to arrive at an in-depth understanding of the adolescent experience of a parent’s traumatic brain injury. The phenomenon of parental traumatic brain injury in the lifeworlds of the adolescents was characterized by numerous themes. Adolescents experienced (to varying degrees) denial, anger, grief, guilt, and anxiety. There was a tendency towards overprotectiveness of the injured parent, resulting in the parentification of the adolescents. Loneliness and a sense that nobody could understand their feelings were particularly strong themes, perhaps exacerbated by the importance of conformity during the adolescent period. Furthermore, the adolescents experienced drastic changes in their lives following their parents’ traumatic brain injuries. Not only were family roles and dynamics affected, but also the adolescents reported extensive changes in themselves. There were sudden increases in their responsibilities alongside a sense that they were forced to mature sooner than their peers. The adolescents coped using both approach and avoidance styles of coping. Religion was a theme in the lives of all four adolescents. Despite the professed negative impact of the experience of having a traumatically brain-injured parent, the adolescents in the current study managed to find some degree of positive meaning in having to cope with such a traumatic event and its consequences. Professionals working with brain-injured clients and their families will find value in the present study. The in-depth description of the experience of adolescents with brain-injured parents will be helpful in planning support programmes and interventions following familial brain injuries. The findings of this study have also been the basis for recommendations for future empirical investigations.

Preliminary observations of the restricted regionalization of the enzyme 2' ,3'-cyclic nucleotide-3’ -phosphohydrolase led to an investigation of the subcellular regionalization of this enzyme in cerebral white matter. Since bovine corpus callosum contained eighteen times as much enzyme activity as grey matter, an association of the enzyme with myelin was suggested. Subsequent fractionation of bovine cerebral white matter by sucrose density gradient according to the procedure of Autilio, Norton, and Terry for the purification of myelin (1), showed that greater than 60% of the total activity was associated with the myelin rich fractions. In order to fractionate cerebral white matter more thoroughly, a modified De Robertis fractionation procedure was utilized allowing for separation of nuclear, mitochondrial, and microsomal pellets by differential centrffugation (2). Phosphohydrolase activity was distributed in all fractions, and electron microscopy demonstrated the presence of myelin in all of these fractions. Subsequent fractionation of these primary fractions on a discontinuous sucrose density gradient, showed essentially all of the phosphohydrolase activity in the lightest fraction at the top of each gradient. This band was comprised primarily of myelin figures as verified by electron microscopy. These studies indicated that the enzyme was associated with myelin. The foregoing result was further supported by a study of the increase in enzyme activity during myelination in rats. Myelination is known to occur early in the life of the rat, being initiated a few days after birth, entering a rapid phase of onset at about 10 days and being essentially complete after 50 days (3). Cholesterol was shown to increase in a corresponding manner indicating that myelination was indeed proceeding. Further evidence that the enzyme is associated with myelin came from an investigation of mutant mice. Quaking mice have been shown to be deficient in myelin, containing, according to Bauman and co-workers (4), only 62% of the normal galactolipid levels. Since galactolipids are presently accepted markers for myelin, and since adult quaking mice had 50% of the control enzyme activity, in agreement with the published galactolipid values, it was thought not unlikely that the two phenomena were related. This result also inferred an association of the enzyme with myelin. In attempt to further uncover the physiological role of the 2’,3'-cyclic nucleotide-3'-phosphqhydrolase, investigations have been directed towards elucidation of the substrate specificity of the enzyme. Uridine and guanosine-2’,3'-cyclic phosphothioates, kindly donated by Dr. Fritz Eckstein of the Max Planck Institut für Experimentelle Medizin, were hydrolyzed at rates of l.4 and l4.3% that of adenosine-2’,3'-cyclic phosphate. Cyclic inositol phosphate, synthesized from inositol-2-phosphate in the presence of dicyclohexylcarbodi-imide and pyridine, and glucose-l,2-cyclic phosphate, synthesized from (formula omitted)-D-glucose-l-phosphate, in a similar manner, were not hydrolyzed td any measureable extent. Preliminary results also show that ribose cyclic phosphates are not hydrolyzed, indicating a requirement for a purine or pyrimidine ring in the substrate molecule. These results are discussed with respect to their possible physiological significance. / Medicine, Faculty of / Biochemistry and Molecular Biology, Department of / Graduate