Autonomic Computing is an approach to designing systems that are capable of self-management. Fundamental to the autonomic ideal is a software's awareness of and ability to tune parameters that affect metrics like performance and security. Traditionally, these parameters are tuned by human experts with extensive knowledge of parameter names and effects---existing software was not designed to be self-tuning. Efforts to automate the isolation and tuning of parameters have yielded encouraging results. However, the parameters are identified manually. This thesis proposes the adaptation of reverse engineering techniques for automating the recovery of software tuning parameters. Tuning parameters from several industrially relevant applications are studied for patterns of use. These patterns are used to classify the parameters into a taxonomy, and to develop a metamodel of the source code elements and relationships needed to express them. An extractor is then built to obtain instances of the relationships from source code. The relationships are represented as graphs, which are manipulated and queried for instances of tuning parameter patterns. The recovery is implemented as a tool for finding tuning parameters in applications. Experimental results show that the approach is effective at recovering documented tuning parameters, as well as other undocumented ones. The results also indicate that the tuning parameter patterns are not specific to a particular application, or application domain. / Thesis (Master, Computing) -- Queen's University, 2008-06-28 19:36:43.291

In today’s database server environments, multiple types of workloads, such as on-line transaction processing, business intelligence and administrative utilities, can be present in a system simultaneously. Workloads may have different levels of business importance and distinct performance objectives. When the workloads execute concurrently on a database server, interference may occur and result in the workloads failing to meet the performance objectives and the database server suffering severe performance degradation. To evaluate and classify the existing workload management systems and techniques, we develop a taxonomy of workload management techniques. The taxonomy categorizes workload management techniques into multiple classes and illustrates a workload management process. We propose a general framework for autonomic workload management for database management systems (DBMSs) to dynamically monitor and control the flow of the workloads and help DBMSs achieve the performance objectives without human intervention. Our framework consists of multiple workload management techniques and performance monitor functions, and implements the monitor–analyze–plan–execute loop suggested in autonomic computing principles. When a performance issue arises, our framework provides the ability to dynamically detect the issue and to initiate and coordinate the workload management techniques. To detect severe performance degradation in database systems, we propose the use of indicators. We demonstrate a learning-based approach to identify a set of internal DBMS monitor metrics that best indicate the problem. We illustrate and validate our framework and approaches using a prototype system implemented on top of IBM DB2 Workload Manager. Our prototype system leverages the existing workload management facilities and implements a set of corresponding controllers to adapt to dynamic and mixed workloads while protecting DBMSs against severe performance degradation. / Thesis (Ph.D, Computing) -- Queen's University, 2014-05-07 13:35:42.858

This thesis examined Autonomic Nervous System activity evoked by postural instability. Autonomic reactions were assessed using measures of electrodermal activity at the surface of the skin. Perturbation-evoked electrodermal responses (EDRs) were consistently observed in conjunction with both upper and lower limb postural reactions. These autonomic responses were sensitive to perturbation amplitude, as well as experimental manipulations which did not influence the perturbation itself but which affected response execution. In particular, stimulus predictability and movement challenge modulated EDRs, although purely cognitive manipulations did not significantly affect autonomic responses. Probes examining the potential role of such autonomic potentials in compensatory balance control revealed that EDRs evoked during compensatory postural reactions were larger and more consistent than potentials evoked by purely motor or sensory stimuli, suggesting that evoked autonomic activity plays a role in compensatory behavior. While the specific role of autonomic contributions in compensatory balance control require further study, speculative models for autonomic contributions propose either feedback-based pathways for detection of instability to initiate the postural reaction, and/ or an adaptive role to higher centers important for establishing sensorimotor gain in future conditions. This thesis presents new evidence regarding basic neural mechanisms engaged in the recognition and response to postural instability, and future work may extend these findings in clinical populations with high fall incidence and offer clues as to alternative causes for falls and fall prevention.

Spinal cord injury can result in partial or complete loss of supraspinal control of sympathetic outflow below the lesion. Despite the importance of the sympathetic nervous system in autonomic dysreflexia and orthostatic hypotension, its integrity is not currently assessed in the clinical determination of lesion level - only motor and sensory pathways are examined. The aim of this thesis was to develop non-invasive means of assessing the integrity of sympathetic pathways following human spinal cord injury. Brief innocuous electrical stimuli applied to the forehead evoked cutaneous vasoconstrictor and sudomotor responses in the fingers and toes of able-bodied subjects, which were abolished by complete spinal lesions. Application of these same stimuli to the abdominal wall (below lesion) generated long-lasting cutaneous vasoconstriction (but not sweat release) and significant increases in blood pressure that accumulated with repeated stimuli. Moreover, the magnitude and duration of these spinal somatosympathetic reflexes did not depend on the number of impulses or duration of the sensory input, suggesting that only the initial part of the sensory barrage elicits reflex responses. This work has shown that cutaneous vascoconstriction provides a more robust measure of the integrity of sympathetic pathways than does sweat release. This was confirmed during natural stimulation of somatic afferents during vibroejaculation, which caused marked increases in blood pressure and marked cutaneous vasoconstriction but negligible sweat release below lesion. Muscle vasoconstrictor function below lesion was assessed by asking subjects to perform a maximal inspiratory breath-hold, which is known to cause a sustained activation of muscle vasoconstrictor neurones that counteracts the fall in blood pressure in able-bodied subjects. Blood pressure remained low in paraplegics and, especially, quadriplegics during this manouevre; importantly, heart rate showed a linear increase only in the spinal patients. In the absence of blood pressure measurements, the latter infers an interruption of descending muscle vasoconstrictor pathways. In conclusion, this thesis has demonstrated simple, non-invasive techniques that can be utilised to assess the function of the sympathetic nervous system in spinal cord injury, and highlighted the need to assess the injury in terms of the integrity of the sympathetic nervous system below the lesion level.

Spinal cord injury can result in partial or complete loss of supraspinal control of sympathetic outflow below the lesion. Despite the importance of the sympathetic nervous system in autonomic dysreflexia and orthostatic hypotension, its integrity is not currently assessed in the clinical determination of lesion level - only motor and sensory pathways are examined. The aim of this thesis was to develop non-invasive means of assessing the integrity of sympathetic pathways following human spinal cord injury. Brief innocuous electrical stimuli applied to the forehead evoked cutaneous vasoconstrictor and sudomotor responses in the fingers and toes of able-bodied subjects, which were abolished by complete spinal lesions. Application of these same stimuli to the abdominal wall (below lesion) generated long-lasting cutaneous vasoconstriction (but not sweat release) and significant increases in blood pressure that accumulated with repeated stimuli. Moreover, the magnitude and duration of these spinal somatosympathetic reflexes did not depend on the number of impulses or duration of the sensory input, suggesting that only the initial part of the sensory barrage elicits reflex responses. This work has shown that cutaneous vascoconstriction provides a more robust measure of the integrity of sympathetic pathways than does sweat release. This was confirmed during natural stimulation of somatic afferents during vibroejaculation, which caused marked increases in blood pressure and marked cutaneous vasoconstriction but negligible sweat release below lesion. Muscle vasoconstrictor function below lesion was assessed by asking subjects to perform a maximal inspiratory breath-hold, which is known to cause a sustained activation of muscle vasoconstrictor neurones that counteracts the fall in blood pressure in able-bodied subjects. Blood pressure remained low in paraplegics and, especially, quadriplegics during this manouevre; importantly, heart rate showed a linear increase only in the spinal patients. In the absence of blood pressure measurements, the latter infers an interruption of descending muscle vasoconstrictor pathways. In conclusion, this thesis has demonstrated simple, non-invasive techniques that can be utilised to assess the function of the sympathetic nervous system in spinal cord injury, and highlighted the need to assess the injury in terms of the integrity of the sympathetic nervous system below the lesion level.

HSCR has been felt to be a polygeneic disease on the basis of an incompletely penetrant sex modified transmission, which may be either autosomal dominant or recessive in different kindred. During the 1990's several of the genes involved in this transmission have come to light. Other genes remain to be discovered.

Thesis (Ph.D.)--Drexel University, 2007. / Includes abstract and vita. Includes bibliographical references (leaves 105-110).

Thesis (PhD)--Montana State University--Bozeman, 2008. / Typescript. Chairperson, Graduate Committee: John Paxton. Includes bibliographical references (leaves 107-114).

Thesis (Ph. D.)--Ohio State University, 2003. / Title from first page of PDF file. Document formatted into pages; contains xiii, 127 p.; also includes graphics Includes bibliographical references (p. 91-105). Available online via OhioLINK's ETD Center

Thesis (Ph. D.)--University of Wisconsin--Madison, 1965. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 72-80).