Large scale distributed computing systems have been extensively utilized to host critical applications in the fields of national defense, finance, scientific research, commerce, etc. However, applications in distributed systems face the risk of service outages due to inevitable faults. Without proper fault management methods, faults can lead to significant revenue loss and degradation of Quality of Service (QoS). An ideal fault management solution should guarantee fast and accurate fault diagnosis, scalability in distributed systems, portability for a variety of systems, and the versatility of recovering different types of faults. This dissertation presents a model-based fault management structure which automatically recovers computing systems from faults. This structure can recover a system from common faults while minimizing the impact on the system’s QoS. It covers all stages of fault management including fault detection, identification and recovery. It also has the flexibility to incorporate various fault diagnosis methods. When faults occur, the approach identifies fault types and intensity, and it accordingly computes the optimal recovery plan with minimum performance degradation, based on a cost function that defines performance objectives and a predictive control algorithm. The fault management approach has been verified on a centralized Web application testbed and a distributed big data processing testbed with four types of simulated faults: memory leak, network congestion, CPU hog and disk failure. The feasibility of the fault recovery control algorithm is also verified. Simulation results show that our approach enabled effective automatic recovery from faults. Performance evaluation reveals that CPU and memory overhead of the fault management process is negligible. To let domain engineers conveniently apply the proposed fault management structure on their specific systems, a component-based modeling environment is developed. The meta-model of the fault management structure is developed with Unified Modeling Language as an abstract of a general fault recovery solution for computing systems. It defines the fundamental reusable components that comprise such a system, including the connections among them, attributes of each component and constraints. The meta-model can be interpreted into a userriendly graphic modeling environment for creating application models of practical domain specific systems and generating executable codes on them.

Advanced architectures for cluster-based services that have been recently proposed allow for service differentiation, server overload control and high utilization of resources. These systems, however, rely on centralized functions, which limit their ability to scale and to tolerate faults. In addition, they do not have built-in architectural support for automatic reconfiguration in case of failures or addition/removal of system components. Recent research in peer-to-peer systems and distributed management has demonstrated the potential benefits of decentralized over centralized designs: a decentralized design can reduce the configuration complexity of a system and increase its scalability and fault tolerance. This research focuses on introducing self-management capabilities into the design of cluster-based services. Its intended benefits are to make service platforms dynamically adapt to the needs of customers and to environment changes, while giving the service providers the capability to adjust operational policies at run-time. We have developed a decentralized design that efficiently allocates resources among multiple services inside a server cluster. The design combines the advantages of both centralized and decentralized architectures. It allows associating a set of QoS objectives with each service. In case of overload or failures, the quality of service degrades in a controllable manner. We have evaluated the performance of our design through extensive simulations. The results have been compared with performance characteristics of ideal systems. / QC 20101123

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<p>Results from this study show a moderate association between decentering and sBRS.</p> <p> Previous studies have associated decentering, a non-judgmental view of emotions, with lower arterial stiffness and better nocturnal blood pressure dipping in adults. It is unknown however if autonomic regulation of blood pressure is linked to decentering. Therefore, the purpose of this study was to determine if decentering was related to cardiovagal or sympathetic baroreflex sensitivity (sBRS). Thirty-three adults (age 25±6 years; BMI 25±3 kg/m2 ) with resting blood pressure ≥120/80 mmHg volunteered for this study. All participants had a BMI <30 kg/m2 , and had no history of smoking, diabetes, or prescriptions for blood pressure or cardiac function. Participants completed an 11-item experiences questionnaire to evaluate decentering, and then were equipped for a supine autonomic evaluation. The autonomic evaluation included continuous recording of heart rate via 3-lead ECG, muscle sympathetic nerve activity (MSNA) via microneurography, and beat-to-beat blood pressure via finger photoplethysmography. Cardiovagal baroreflex sensitivity (n=33) included estimation of vagal activation by evaluating up-up relationships between systolic arterial pressure (SAP) and R-R intervals of the ECG. Vagal withdrawal was also estimated via the down-down relationships between SAP and R-R intervals. Spontaneous sBRS (n=17) was evaluated by assessing the relationship between changes in diastolic arterial pressure (DAP) in 3 mmHg bins vs. changes in MSNA burst incidence (bursts / 100 heart beats) in those with DAP-MSNA correlations >0.70. Results from 2-tailed Pearson correlation analyses revealed that there was not a relationship between decentering and vagal activation (r=-0.07; p=0.71) or between decentering and vagal withdrawal (r=-0.28; p=0.12). There was a moderate, negative correlation between decentering and sBRS that lacked statistical significance (r= -0.35; p=0.17). Our findings suggest that there is not a clear link between decentering and autonomic regulation of blood pressure as estimated through cardiovagal 11 baroreflex sensitivity, but the moderate correlation between decentering and sBRS should be explored in a larger sample size. </p>

HRP applied to cut dorsal and ventral roots of the cat sacral spinal cord labeled afferent axons with swellings in close apposition to labeled preganglionic neurons (PGNs) in the sacral parasympathetic nucleus. Electron microscopy allowed characterization of synaptic contacts between afferents and PGNs. The results suggest that both the dorsal and ventral root afferents can directly activate autonomic preganglionic neurons.

Dysregulation of the autonomic cardiovascular control is a complication of diseases including diabetes, hypertension, sleep apnea, and aging. A common factor in these conditions is an increase in reactive oxygen species (ROS) in neural, cardiac, and endothelial tissues. Cu/Zn superoxide dismutase (SOD1) is an intracellular anti-oxidant enzyme that catalyzes dismutation of the superoxide anion (O2.-) to hydrogen peroxide (H2O2). Expression and function of this enzyme are diminished in pathologies that impair cardiovascular autonomic control. This study employed mice overexpressing a transgene for human SOD1 (hSOD1) to determine if its overexpression would alter autonomic regulation of BP, HR, and BRS in healthy animals, and if this animal line (C57B6SJL-Tg (SOD1)2 Gur/J) could be used in future studies to determine if hSOD1 overexpression can preserve cardiac autonomic function in disease models. To accomplish this aim, using anesthetized SOD1 and C57 (control) mice, we recorded HR, and aortic depressor nerve (ADN) activity changes in response to pharmacologically-induced BP changes in order to measure baroreflex and baroreceptor sensitivity, respectively. In order to identify any alterations in central, efferent, and cardiac components of the baroreflex arc, we electrically stimulated the left ADN and left cervical vagus and compared the reductions in BP and HR between the C57 and SOD1 mice. Time- and frequency-domain analysis of heart rate variability (HRV) was performed using pulse pressure recordings prior to pharmacologic or surgical procedures. We found that hSOD1 overexpression in the SOD1 mouse line, in comparison to C57 controls did not significantly affect resting HR (C57: 558 ± 8 vs. SOD1:553 ± 13 beats-per-minute) or blood pressure (C57: 88.8 ± 2.9 vs.SOD1: 85.8 ± 2.1 mmHg). hSOD1 overexpression did not affect the decrease in average mean arterial pressure (MAP) following injection of sodium nitroprusside (SNP) (C57: 38.7 ± 1.4 vs. SOD1: 39.5 ± 1.3 mmHg) or increase in average MAP (C57: 135.8 ± 3.1 vs. SOD1: 136.6 ± 3.5 mmHg) following injection of phenylephrine (PE). BRS, as measured by the averaged regression lines for ΔHR/ΔMAP for the SNP-induced tachycardic baroreflex (C57: 0.57 ± 0.06 bpm/mmHg, SOD1: 0.61 ± 0.08 bpm/mmHg)) and the PE-induced bradycardic baroreflex (C57: -2.9 ± 0.57 bmp/mmHg, SOD1: -4.3 ± 0.84 bpm/mmHg) are not significantly different between C57 and SOD1. Baroreceptor activation showed a significant increase in gain (C57: 5.4 ± 0.3 vs. SOD1: 7.4 ± 0.5 %/mmHg, P < 0.01) in the SOD1 transgenic mice. Heart rate depression in response to electrical stimulation of the left ADN and cervical vagus was comparable between C57 and SOD1, though MAP reduction in response to ADN stimulation is slightly, but significantly increased at 50 Hz in SOD1 animals. Time- domain analysis of HRV did not reveal any significant difference in beat-to-beat variability between SOD1 and C57 (SDNN: C57: 2.78 ± 0.20, SOD1: 2.89 ± 0.27), although frequency-domain analysis uncovered a significant reduction in the low-frequency power component of the HRV power spectral distribution (C57: 1.19 ± 0.11, SOD1: 0.35 ± 0.06, P < 0.001). This study shows that although hSOD1 overexpression does not affect overall baroreflex function, it does potentiate baroreceptor sensitivity and brain stem control of arterial pressure, and reduces low-frequency beat-to-beat variations in HR, without affecting total HRV.

The sympathetic (SNS) and parasympathetic (PSNS) branches of the autonomic nervous system (ANS) innervate the heart, exerting excitatory and inhibitory influences (respectively) over cardiac functions (heart rate, AV conduction velocity, and contractility). However, the distribution and structure of SNS and PSNS innervation has not yet been well studied. Detailed characterization of the distributional organization and structural morphology of the SNS and PSNS in normal states is essential to the study of pathological autonomic remodeling. The present study utilized double immunohistochemical labeling techniques to examine tyrosine hydroxylase (TH) immunoreactive (IR) SNS and vesicular acetylcholine transporter (VAChT) IR PSNS axons and terminal structures in whole-mount atria of C57BL/6 mice. We found that: (1) The atria contain a dense network of ANS axons. TH-IR, VAChT-IR, and dual cholinergic/dopaminergic TH+VAChT-IR axons travel together in bundles on the epicardium before branching into differentiated terminal structures. (2) Parallel TH-IR and VAChT-IR axons often diverge from epicardial bundles and travel in parallel (less than 1μm apart) before forming terminal structures in the epicardium and myocardium. Such parallel SNS/PSNS axons interdigitize and have large alternating varicosities along their length adjacent to one other, suggesting possible antagonistic communication between both branches of the ANS at the prejunctional level. (3) Intrinsic cardiac ganglia (ICG) are targets for extrinsic sympathetic nerves which travel through ICG without forming large synaptic varicosities around cardiac principal neurons (PNs). (4) Small intensely fluorescent (SIF) cells (presumably chemoreceptors and/or interneurons) exist near SNS bundles, inside ICG, and in the epicardium unaccompanied by ganglia and nerve bundles. (5) The subpopulation of TH+VAChT-IR PNs within ICG form loose terminals in the atria and do not project to other PNs. (6) Both TH-IR and VAChT-IR axons innervate atrial vasculature. (7) TH-IR axons innervate fat pads adjacent to the heart. (8) SNS/PSNS parallelism is not exclusive to the atria. Similar structures exist in the esophagus, right ventricle, and small intestine. This study provides a novel and overall view of the innervation and interaction of the SNS and PSNS in the atria. This will underlie a foundation for future physiological, pharmacological, and anatomical studies of SNS/PSNS innervation, interaction, and remodeling in pathological states (such as aging, intermittent hypoxia and diabetes).

The relationship between autonomic dysfunction and primary headache disorders has been established in the adult population. The aim of this retrospective study was to elucidate if there was a similar association in the pediatric primary headache population. Three groups were compared - migraine patients, tension-type headache patients and idiopathic scoliosis patients as a control group. Utilizing clinical data collected during patients' initial visits, prevalence of autonomic dysfunction symptoms were quantified. The headache groups also filled out the Functional Disability Index (FDI) as well as the Children's Depression Inventory (CDI) to help elucidate if there was a relationship between function disability, psychiatric state and primary headaches and/or autonomic dysfunction symptoms. It was found that the headache groups had significantly greater dysautonomia as compared to the control group. Only slight differences were found between the migraine and tension-type patients in regards to dysautonomia. No significant differences were found in total FDI or CDI scores. These results illuminate a relationship between autonomic nervous system dysfunction and primary headache disorders in the pediatric population studied. Prospective studies and the development of standardized dysautonomia questionnaires will allow a more detailed autonomic dysfunction profile to be built for this population.

Vor dem Hintergrund, dass die ALS zunehmend als Multisystem- denn als reine Motoneuronerkrankung verstanden wird, stellt nicht-motorische Symptomatik bei ALS-Patienten ein Forschungsgebiet von Interesse dar. Eine genauere Kenntnis darüber kann Diagnostik, adäquate Therapie sowie das pathogenetische Verständnis der ALS verbessern. Ziel der vorliegenden monozentrischen Querschnittsstudie war, nicht-motorischer Symptomatik, konkret der Symptomatik autonomer Dysfunktion bei ALS-Patienten anhand eines multimodalen Ansatzes nachzugehen. Dazu erhoben wir zur Beurteilung klinisch relevanter Symptome einen Fragebogen zu nicht-motorischer Symptomatik (NMSS), einen hieraus abgeleiteten autonomen Subscore sowie ein kognitives Assessment (MoCA), führten eine Herzfrequenzvariabilitäts-Messung zur Beurteilung des kardioautonomen Systems durch und evaluierten die sonographische Querschnittsfläche des Vagusnerven auf Höhe der Schilddrüse als strukturelles Korrelat des autonomen Nervensystems und des Medianusnerven als peripherer Kontrollnerv bei 37 ALS-Patienten und 40 gesunden Kontrollen, rekrutiert zwischen September 2017 und September 2020. Mithilfe der verwendeten Methoden ließ sich keine spezifische, klinisch relevante Beeinträchtigung des autonomen Nervensystems bei ALS-Patienten erheben. Die Scores des Fragebogens zur nicht-motorischen Symptomatik fielen bei ALS-Patienten signifikant höher aus, vorwiegend jedoch aufgrund von Symptomen eigentlich motorischer Art. Bereits wissenschaftlich anerkannte nicht-motorische Symptomatik kognitiver Art ließ sich durch signifikant niedrigere Gesamtpunktzahlen im MoCA von ALS-Patienten im Vergleich zu Kontrollpatienten reproduzieren, was die Bedeutung von nicht-motorischen Symptomen neuropsychiatrischer Art erneut unterstreicht. Der Vagus-Nerv zeigte sich im Vergleich zum Kontrollkollektiv im ALS-Kollektiv sonographisch nicht größenverändert. Beobachtete erhöhte Ruhe-Herzfrequenzen in der Herzfrequenzvariabilitätsmessung können zur weiteren Evaluierung einer postulierten sympathischen Überaktivität bei ALS-Patienten anregen. Multizentrische, longitudinale Studien größerer Fallzahlen sowie methodische Spezifizierungen sind von Nöten, um Symptomen autonomer Dysfunktion bei ALS-Patienten weiter nachzugehen sowie um Testverfahren mit ausreichender Reliabilität und Validität zu generieren.

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