M.Sc. / Heat shock proteins (HSP) are a group of highly conserved proteins induced in pro- and eukaryotes by a wide variety of environmental stresses such as heat shock (HS) and oxidative injury. HSP are classified into families according to their apparent molecular mass and respective inducers. Induction of HSP is primarily regulated on transcriptional level through multiple copies of a conserved cis-acting heat shock element (HSE) in the promoter region of all hsp genes to which the heat shock transcription factor (HSF) binds. Members of the HSP family function collectively as molecular chaperone systems, and fulfil essential roles under normal conditions and provide protection and adaptation during and following stress. The induction of HSP following stress and the subsequent protection confer HSP the potential application in stress therapy and in biomarking of stress. During a previous study in which the effect of Mycobacterium tuberculosis (M.tb) on the stress response of peripheral blood moncytes (PBM) from different donors was investigated, it was observed that different individuals from different South African populations showed differential a HSP synthesis in response to M.tb. This compelled us to investigate the following: Variation in HSP synthesis in peripheral blood monocytes (PBM) from different individuals in response to the classical HSP inducer, HS. The most appropriate technique to study HSP expression on protein level. HSP synthesis was studied in PBM from 36 individuals (European (E): n=22; non-Europeans (nE): n=14) using biometabolic labelling. Three techniques were compared in the determination of HSP expression in six donors in terms of HSP synthesis, which is measured by biometabolic labelling, and accumulation of hsp70 that were measured by Western blot analysis and flow cytometry. Results obtained are : European (E) and non-European (nE) populations differed significantly (p < 0.05) from each other in spite of a prominent variation in HSP synthesis within donors ; Flow cytometry is the technique of choice for the analysis of HSP levels, since it allows fast and safe measurement of HSP levels in single cel populations within a mixed population. Data from flow cytometry correlate with Western blot analysis, but not with biometabolic labelling. The means and ranges for different HSP synthesis in different populations reported in this study, set a standard for the use of HSP as biomarker of pa environmental stress for populations inhabiting southern Africa. Efficient measurement of HSP expression as biomarker of stress can therefore be implemented in routine analysis of environmental stress, as well as investigations concerning the implications of HSP in pathology.

Liu Ming Ju. / "June 2003." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2003. / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

by Angela Mara Bentes de Souza. / "June 2003." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (p. 176-200). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

The success of endoluminal stent-graft treatment for abdominal aortic aneurysm relies on maintenance of an effective seal when the stent expands into the healthy artery. Clinical observation of aortic neck dilation following endoluminal grafting has led to the hypothesis that excessive stent expansion forces may cause remodelling and dilation of the artery to accommodate the strong forces. This may lead to failure of the seal, hence so-called endoleak. In this research, we analysed the force field generated by aortic stent-grafts and investigated in vitro approaches for studying the effects of these forces on cells within the vascular wall. The pressure-deformation behaviour of ovine arteries was examined experimentally and was found to vary with artery type. A finite element model of abdominal aorta (AA) characterised by Mooney-Rivlin hyperelastic material properties was validated. The property inputs were derived from the polynomial form of the strain energy density function proposed by Patel and Vaishnav. Stent-artery contact simulations revealed stresses 1.2-19 times higher than within a normal vessel at 120 mmHg when contacted by a zig-zag, square cross-section stent that expanded the AA by 3-16%. Streses 1.3-23 times normal were predicted for circular cross-section stents at the same range of expansions. The stress distribution was determined to be concentrated at the contacting surface and within the inner region of the aortic wall. These results confirmed that the forces within the vessel wall are likely to place unnatural physiological demands on the cells within. We then developed an in vitro system for studying the impact of this mechanical stress on cells within a three dimensional (3D) structure. A 20 wt% poly(vinyl alcohol) (PVA) - 5 wt% collagen tubular construct was developed to support cells, and was shown to sustain physiological blood pressures. Two cell-seeding techniques were examined, direct cell encapsulation and surface cell-seeding. Both demonstrated the capability of entrapping viable cells within the construct that remained viable for up to 4 days. In conclusion, stent contact does create abnormal stress concentrations within the vessel wall with a magnitude severely higher than physiological levels. A feasible tubular construct and an in vitro system were developed, enabling further assessments on the effects of these abnormality on the cells.

Passive and active heat loading causes cardiovascular strain, which can have diverse and substantial effects. Thus, cardiovascular function is integral to work and heat stress tolerance, but recent hyperthermia and exercise literature has not emphasised this relationship, instead focusing on the roles of upper �critical� core temperature or rate of heat storage as primary mechanisms of fatigue. Therefore, the aim of this thesis was to examine some potential causes and effects of cardiovascular strain under heat stress, including potential strategies for attenuating that strain. Body precooling before exercise increases heat storage capacity; the primary mechanism by which attenuations in thermal and cardiovascular strain, and improved work capacity is thought to occur. However, no precooling study has utilised realistic airflow in the laboratory, possibly inflating its purported benefits. Therefore, Study One examined the cardiovascular, thermal, psychophysical and ergogenic effects of precooling with and without airflow in the heat (30�C, 50% rh). Ten males completed four trials in balanced order, comprising 60- min immersion in thermoneutral (35�C) or cool (24�C) water before cycling at 95% ventilatory threshold with airflow (~4.8 m�s⁻�) or no airflow, until exhaustion. Heart rate and mean core, body, and skin temperatures were attenuated for 15 min into cycling after precooling. Endurance time was extended by 30 � 23 min with airflow, and 16 � 15 min with precooling relative to control (28 � 12 min) but not further extended with strategies combined (29 � 21 min). Precooling removed 784 � 223 kJ�m⁻� (calorimetrically); less than the effect of airflow alone (1323 � 1128 kJ�m⁻�). Competition for blood between tissues is pronounced during exercise in the heat: skin and gut have marked increases and decreases, respectively. Gut ischemia affects epithelial tight junction integrity, allowing lippopolysaccharide ingress and immune responses. Bovine colostrum may attenuate gut permeability. Study Two (double-blind, placebo controlled) investigated the effects of aerobic fitness (7 highly fit, 8 moderately fit) and bovine colostrum on physiological and perceived strain, and performance during mixed-mode exercise; cycle 15 min at 50% maximal heart rate range (HRR), run 30 min at 80% HRR then 30 min self-selected paced before another 15 min cycle at the same work-rate. Airflow was graded to running speed. During the last cycle, blood pressure, stroke volume and total peripheral resistance were lower, heart rate and skin blood flow increased, and skin temperature was unchanged compared to the first cycle. Indices of fever response (IL-1β, TNF-α) were not evident during exercise, nor were those of blood-brain barrier permeability (S100β) or cognitive impairment (Stroop test). Neither bovine colostrum, nor higher fitness modified these measures. Moving to upright posture is orthostatically stressful and can initially decrease cerebral perfusion. Compression garments are used to assist venous return; while their effectiveness is unknown, they could reduce heat or orthostatic-induced hypoperfusion. Study Three investigated the cardiovascular and cerebrovascular responses to orthostatic stress with and without passive heating (+0.5�C). Fifteen participants completed two trials (compression v placebo garments) in balanced order. Cerebral autoregulation was assessed via 3-min stand, and via thigh cuff inflation. All participants experienced initial orthostatic hypotension upon standing in one or more trials, with 4/15 individuals experiencing presyncopal symptoms, aborting the standing protocol. In those who "fainted", reductions in blood pressure and partial pressure of end-tidal CO₂ reduced middle cerebral artery velocity. Neither training status nor compression trousers modified the responses. Collectively, cardiovascular strain to heat stress is attenuated when realistic airflow is provided. Increased cardiovascular strain does not inevitably result in clinical outcomes to heat stress. Higher fitness does not necessarily attenuate cardiovascular responses or higher tolerance to heat stress.

Thesis (Ph. D.)--Rutgers University, 2009. / "Graduate Program in Psychology." Includes bibliographical references (p. 102-115).

Thesis (Ph. D.)--West Virginia University, 2002. / Title from document title page. Document formatted into pages; contains viii, 135 p. : ill. Vita. Includes abstract. Includes bibliographical references.

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (p. 255-271).

Thesis--Massachusetts Institute of Technology. / This report was prepared for the Manpower Administration, U.S. Department of Labor, under research and development contract (grant) no. 91-25-75-17-1. Available from the National Technical Information Center, Springfield, Va. Includes bibliographical references (leaves 300-311).

published_or_final_version / Anatomy / Master / Master of Medical Sciences