Neck-shoulder pain (NSP) is a highly prevalent musculoskeletal disorder with unclear causes, and effective prevention and treatment require a further understanding of the underlying mechanisms. Aberrant autonomic nervous system (ANS) regulation is a hypothesized causal element in the development and maintenance of chronic muscle pain. The overall aim of this thesis was to investigate possible differences in ANS regulation between chronic NSP and healthy control (CON) groups using both laboratory assessment and ambulatory monitoring in daily life. Four papers are included in this thesis, based on data from three groups with chronic NSP. Autonomic responses to laboratory stressors were assessed using heart rate variability (HRV), blood pressure, trapezius muscle activity and blood flow measurements (Study І) in NSP and CON. Long-term ambulatory monitoring of HRV, physical activity and perceived symptoms were assessed in Studies ІІ and IV to investigate group differences in real-life conditions. Finally, the effects of a ten-week intervention (using individually adjusted HRV biofeedback) to reinstating ANS balance in subjects with chronic NSP were evaluated using self-reported symptoms and health ratings, as well as autonomic regulation testing (i.e., evaluating HRV at rest and in response to stress) (Study ІІІ). The main findings from the four studies demonstrated aberrant ANS regulation in the NSP group compared to CON, which was predominantly characterized by diminished parasympathetic cardiac activity during rest and sleep, and altered sympathetic reactivity to laboratory stressors (Studies І, ІІ and IV). Different patterns in physical activity were observed between the NSP and CON groups, with reduced physical activity during leisure time in the NSP group (Studies ІІ and IV). Physical activity was found to be positively associated with HRV. Positive effects of HRV-biofeedback were found on perceived health, including social function, vitality and bodily pain, and improved HRV (Study ІІІ). In conclusion, imbalanced ANS regulation was demonstrated among persons with chronic NSP at both the systemic and local levels. Diminished parasympathetic activity in NSP was modulated by lower levels of physical activity in leisure time. Interventions targeting ANS functions might benefit persons with chronic NSP.

No description available.

名古屋大学博士学位論文 学位の種類 : 博士(医学)(論文) 学位授与年月日:平成5年1月28日 平山正昭氏の博士論文として提出された

Animal research has elucidated the neurobiological substrates and environmental determinants of pain modulation. Despite these advances, relatively little is known about how psychological processes activate pain modulatory systems. One psychological process that is thought to play an important role in regulating pain sensitivity is emotion. In addition, previous research into the human menstrual cycle and the animal estrous cycle have determined that either the presence of certain gonadal hormones or the fluctuations of these hormones may lead to changes in how females perceive pain, regulate emotion, and modulate pain. The present study examines both the role of emotion and the human menstrual cycle in pain modulation. Participants were 39 female undergraduate students with a mean age of 18.7 years (SD=1.46). Results are consistent with prior studies indicating that progesterone has antiinflammatory effects. Specifically, significant effects were observed primarily in the luteal phase. Subjects in the luteal phase demonstrated less sympathetic arousal during the experiment but greater autonomic arousal during the noise stressor. Participants in the luteal phase also demonstrated an analgesic/anti-inflammatory response evidenced by an observed decrease in secondary hyperalgesia for those that did not receive the noise stressor. No such changes in pain perception were discovered in the ovulation and follicular phases. Finally, in response to the noise stressor, an inhibition of the analgesic/anti-inflammatory effects was observed in the luteal phase. No such evidence of stress-induced pain modulation was discovered in the ovulation and follicular phases. Although the specific mechanisms of this action still remain unclear, prior evidence points to the role of centrally-mediated pain modulation. It is likely that the stressor worked to inhibit the anti-inflammatory effects commonly observed in the luteal phase to persistent inflammatory pain through centrally-mediated pain modulatory mechanisms. It is hypothesized that hormone-mediated effects at the level of the amygdala influenced the impact of affective pain modulation.

Thesis (M. Phil.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 87-102).

The growing connectivity of cyber-physical systems (CPSes) has led to an increased concern over the ability of cyber-attacks to inflict physical damage. Current cybersecurity measures focus on preventing attacks from penetrating control supervisory networks. These reactive techniques, however, are often plagued with vulnerabilities and zero-day exploits. Embedded processors in CPS field devices often possess little security of their own, and are easily exploited once the network is penetrated. In response, researchers at Georgia Tech and Virginia Tech have proposed a Trustworthy Autonomic Interface Guardian Architecture (TAIGA), which monitors communication between the embedded controller and physical process. This autonomic architecture provides the physical process with a last line of defense against cyber-attacks by switching process control to a trusted backup controller if an attack causes a system specification violation. This thesis focuses on classifying the effects of cyberattacks on embedded controllers, evaluating TAIGA’s resilience against these attacks, and determining the applicability of TAIGA to other CPSes. This thesis identifies four possible outcomes of a cyber-attack on a CPS embedded processor. We then evaluate TAIGA’s mechanisms to defend against those attack outcomes, and verify TAIGA satisfies the listed trust requirements. Next, we discuss an implementation and the experimental results of TAIGA on a hazardous cargo transportation robot. Then, by making various modifications to the setup configuration, we are able to explore TAIGA’s ability to provide security and process protection to other CPSes with varying levels of autonomy or distributed components.

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

published_or_final_version / Biochemistry / Master / Master of Philosophy

Theory and research suggests a link between self-esteem and cardiac vagal tone (parasympathetic nervous system influence on the heart). A literature review suggests that vagal tone protects the body against physiological threat responding (e.g., sympathetic responding) and that vagal tone is highest when we feel secure. Terror management theory posits that humans, who live in a largely symbolic world, derive feelings of security and protection from threat by way of acquiring and maintaining self-esteem. Thus we hypothesized that if vagal tone provides physiological security, and we derive a sense of security through symbolic means by way of self-esteem, then high or increased self-esteem should lead to high or increased vagal tone. To test this hypothesis we conducted two studies in which we manipulated self-esteem by giving participants positive or negative feedback. We predicted that positive feedback would lead to higher vagal tone than negative feedback. Consistent with these predictions, in both studies we found indications that positive feedback increased vagal tone relative to negative feedback. In Study 2, to more fully test our theoretical perspective we induced threat by leading participants to believe they would receive electric shocks. We predicted that both self-esteem and vagal tone would buffer against sympathetic threat responding. Consistent with our model we found that the positive feedback eliminated the sympathetic response to threat of shock that was elicited in the negative feedback condition. Also consistent with our model, higher vagal tone predicted lower sympathetic responding to threat of shock. We discuss future directions for this research and implications for physical health.

Adiponectin regulates feeding behavior, energy expenditure and autonomic function through the activation of two receptors present in nuclei throughout the central nervous system, however much remains unknown about the mechanisms mediating these effects. Here I investigate the actions of adiponectin in autonomic centers of the hypothalamus (the paraventricular nucleus) and brainstem (the nucleus of the solitary tract) through examining molecular, electrical, hormonal and physiological consequences of peptidergic signalling. RT-PCR and in situ hybridization experiments demonstrate the presence of AdipoR1 and AdipoR2 mRNA in the paraventricular nucleus. Investigation of the electrical consequences following receptor activation in the paraventricular nucleus indicates that magnocellular-oxytocin cells are homogeneously inhibited while magnocellular-vasopressin neurons display mixed responses. Single cell RT-PCR analysis shows oxytocin neurons express both receptors while vasopressin neurons express either both receptors or one receptor. Co-expressing oxytocin and vasopressin neurons express neither receptor and are not affected by adiponectin. Median eminence projecting corticotropin releasing hormone neurons, brainstem projecting oxytocin neurons, and thyrotropin releasing hormone neurons are all depolarized by adiponectin. Plasma adrenocorticotropin hormone concentration is increased following intracerebroventricular injections of adiponectin. I demonstrate that the nucleus of the solitary tract, the primary cardiovascular regulation site of the medulla, expresses mRNA for AdipoR1 and AdipoR2 and mediates adiponectin induced hypotension. Adiponectin has electrical effects on a majority of medial solitary tract neurons and depolarizes those expressing mRNA for the hypotensive neuropeptide Y, revealing a central mechanism to modulate blood pressure. Finally, I show that adiponectin controls paraventricular nucleus neuron excitability by either inhibiting a tetraethyl ammonium-sensitive potassium current thereby depolarizing neurons or activating a glibenclamide-sensitive voltage independent potassium current hyperpolarizing neurons. Therefore, adiponectin differentially modulates potassium current to confer its central effects. These results are the first to show the physiological and electrical actions of adiponectin on individual neurons in blood brain barrier protected central autonomic nuclei. This thesis provides a framework for how adiponectin acts centrally to coordinate whole body energy homeostasis and feeding behavior in the rat. / Thesis (Ph.D, Physiology) -- Queen's University, 2009-09-15 16:50:13.933