A Neural Network Approach to Border Gateway Protocol Peer Failure Detection and Prediction

The size and speed of computer networks continue to expand at a rapid pace, as do the corresponding errors, failures, and faults inherent within such extensive networks. This thesis introduces a novel approach to interface Border Gateway Protocol (BGP) computer networks with neural networks to learn the precursor connectivity patterns that emerge prior to a node failure. Details of the design and construction of a framework that utilizes neural networks to learn and monitor BGP connection states as a means of detecting and predicting BGP peer node failure are presented. Moreover, this framework is used to monitor a BGP network and a suite of tests are conducted to establish that this neural network approach as a viable strategy for predicting BGP peer node failure. For all performed experiments both of the proposed neural network architectures succeed in memorizing and utilizing the network connectivity patterns. Lastly, a discussion of this framework\u27s generic design is presented to acknowledge how other types of networks and alternate machine learning techniques can be accommodated with relative ease

Bioenergetics and neuroimaging research: a neuropathophysiological linkage in the setting of cocaine use amongst persons with HIV

Despite innovations in antiretroviral therapy (ART) that have transformed HIV infection from an acute illness with high mortality risk into a chronic, largely manageable disease, the viral reservoir that persists in brain continues to pose a risk for neurocognitive impairment and other deleterious clinical outcomes. ART regimens can inhibit viral integration and suppress replication to nondetectable levels in plasma and cerebrospinal fluid (CSF) but do not eliminate viral reservoirs, including that in brain [1]. Moreover, HIV transcripts within CSF cells have been associated with brain injury despite suppressive ART [2]. Comorbid HIV and cocaine use exacerbates brain atrophy and neurocognitive decline despite viral suppression [3–5]. Intersecting factors disrupted by chronic cocaine use among people with HIV (PWH) contribute to HIV-associated neuropathology, including neurotransmitter signaling (particularly dopamine), neuroinflammation, blood–brain–barrier (BBB) integrity, and energy metabolism. Further, the neuropathological severity associated with HIV and cocaine is spatially heterogenous [6–8]. The healthy brain is energetically expensive and complex with region-specific, unique functional roles [9–11]. Further, compartmentalization of HIV infection in brain contributes to this heterogeneity [12]. Mechanistic links between HIV and cocaine require additional characterization to assess region-dependent contributions to develop therapeutic interventions for cocaine use disorder comorbid with HIV. Mamidi et al.[13] focused on associations between chronic cocaine use and HIV on glucose uptake. Using 18F-FDG PET/CT in a 2 × 2 experimental design with HIV (present/absent) and cocaine (present/absent) (N = 63), they showed the lowest uptake with both HIV and cocaine. One factor – HIV or cocaine – showed intermediate uptake, and neither factor showed the highest uptake. The pronounced impact of cocaine on HIV-associated neuropathology is, in part, due to disruption of dopaminergic neurotransmission. The dopamine system is linked to inflammation and immunological function. Brain regions with high basal dopamine levels, such as the striatum and substantia nigra, are amongst the most vulnerable to HIV [14]. Dopamine exposure to human macrophages results in elevated production of pro-inflammatory cytokines and chemokines [14]. Acutely, elevated dopamine concentrations due to cocaine use increase oxidative stress, exacerbated by Tat [15,16]. Chronically, cocaine use is associated with dopamine depletion, demonstrated by PET scanning research [17]. In addition, HIV itself is associated with dopamine depletion as well as neurocognitive impairment and depression [18] not investigated here. This constellation suggests a synergistic effect of HIV and cocaine on dopaminergic transmission. To the extent that dopaminergic neurotransmission impacts glucose uptake, only additive effects of HIV and cocaine were reported here. No interaction of HIV and cocaine was observed. A major hallmark of chronic HIV is elevated pro-inflammatory cytokine and chemokine production. Suppressed PWH still have elevated neuroinflammation in the parietal and occipital cortex and the globus pallidus. Neuroinflammation is associated with decreased neurocognitive performance and increased white matter damage supported by a PET study with [11C] PBR28 and neuropsychological testing [8]. Viral proteins, Tat and gp120, both facilitate the production of pro-inflammatory cytokine and chemokines that decrease BBB tight junction protein expression and are directly neurotoxic [19]. Loss of BBB integrity allows free virus and HIV-infected monocytes to enter brain, exacerbating neuronal damage [20]. Similarly, cocaine increases neuroinflammatory markers by activating microglial cells and disrupting BBB integrity – decreasing tight junction protein expression in human pericytes [21]. When measuring chronic cocaine-induced microglial activation in vivo, rhesus macaques displayed increased TSPO PET expression in dopamine-rich regions via [3H] PK-11195 [6,7]. However, humans with a history of chronic cocaine use assessed with TSPO PET via [11C] PBR28 displayed no significant changes [6,22]. Of note, increased TSPO expression using current tracers does not distinguish between microglial and astrocytic activation. Further, there are other limitations with the utility of both PK-11195 and PBR28 tracers. Hence, PET scanning studies are currently inconclusive, though studies using other methodologies support neuroinflammatory effects associated with cocaine. Cocaine has been linked with increased TNF-α expression and is well known to stimulate HIV replication through induction of NF-κB and activation of transcription through the HIV LTR. The increased expression of TNF-α induced by HIV might exacerbate that by cocaine. Pro-inflammatory cytokine production has been associated with dopamine depletion outside of HIV infection. This suggests an intrinsic link between chronic HIV despite suppression, ongoing neuroinflammation, and persistent dopamine depletion, which is associated with depression and neurocognitive symptoms. This linkage may also reflect the results reported here and suggests the possible clinical utility of TNF-α inhibitors and dopaminergic agonists for the treatment of depressive and neurocognitive symptoms in virally suppressed PWH, supporting normalization of brain glucose uptake. In adults, the brain\u27s immense energetic demands require roughly 20% of all glucose and constitute approximately the same proportion of total oxygen consumption during resting conditions [23,24]. Maintenance of brain metabolic homeostasis is particularly sensitive to metabolic coupling between types of brain cells that contribute to clinical disorders when disrupted [25–27]. Viral–host interactions after an infection like HIV shift bioenergetics for incompletely understood reasons. Changes in energetic metabolism have been reported to occur in vitro using cultured astrocytes, neurons, and microglia due to Tat and gp120 [28–30], cytokines and chemokines [31], oxidative stress [32], and ART [33]. In vivo, virally suppressed PWH display decreased glucose uptake in the frontal cortex and the anterior cingulate cortex via FDG-PET [34,35]. Altogether, these changes suggest a shift from metabolism of primarily glucose to other oxidative substrates. Moreover, in vitro, cocaine is associated with a similar metabolic shift [29]. As suggested above, energetic demands vary across brain regions. Recent studies suggest that the brain also uses other substrates, such as fatty acids, lactate, pyruvate, glutamate, glutamine, and ketone bodies, more frequently than previously considered [10,11,36]. The composition of substrates used may shift under various factors such as age, diet, brain activity or injury, cognitive reserve, and the presence of viral infections like HIV [26,37]. Hence, future studies should expand from the general study of glucose uptake as the primary substrate to other substrates and associated changes in oxidative stress and mitochondrial function. Clinical research suggests the importance of associated interacting comorbidities, such as cardiovascular disease, with HIV [38] and cocaine [39]. It should be noted that age, ethnicity, and education and concomitant opioid use were not able to be separately analyzed here. Of note, older age is also associated with dopamine depletion, suggesting a more prominent effect amongst older PWH. In addition to future studies examining other energy substrate outcome measures; improved control of extraneous factors; and integration of clinical outcomes of cocaine use among PWH, neuroimaging studies can be particularly helpful in examining spatial heterogeneity in energetic effects induced by toxic HIV protein and transcript burden as well as pro-inflammatory cytokine secretion associated with cocaine use. Yet, these methods incompletely capture metabolic changes in brain. It can be concluded that there remains much to explore as to how the bioenergetic shifts occurring due to HIV and cocaine may be mechanistically linked to clinical outcomes

RCFA for Recurring Impeller Failures in a 4

LectureA Root Cause Failure Analysis (RCFA) for repeated impeller blade failures in a five stage centrifugal propane compressor is described. The initial failure occurred in June 2007 with a large crack found in one blade on the third impeller and two large pieces released from adjacent blades on the fourth impeller. An RCFA was performed to determine the cause of the failures. The failure mechanism was identified to be high cycle fatigue. Several potential causes related to the design, manufacture, and operation of the compressor were examined. The RCFA concluded that the design and manufacture were sound and there were no conclusive issues with respect to operation. A specific root cause was never identified. In June 2009, a second case of blade cracking occurred with a piece once again released from a single blade on the fourth impeller. Due to the commonality with the previous instance this was identified as a repeat failure. Specifically, both cases had occurred in the same compressor whereas, two compressors operating in identical service in Copyright © 2011 by Turbomachinery Laboratory, Texas A&M University adjacent Liquefied natural Gas (LNG) trains had not encountered the problem. A second RCFA was accordingly launched with the ultimate objective of preventing further repeated failures. Both RCFA teams were established comprising of engineers from the End User (RasGas), the OEM (Elliott Group) and an independent consultancy (Southwest Research Institute). The scope of the current investigation included a detailed metallurgical assessment, impeller modal frequency assessment, steady and unsteady computational fluid dynamics (CFD) assessment, finite element analyses (FEA), fluid structure interaction (FSI) assessment, operating history assessment and a comparison change analysis. By the process of elimination, the most probable causes were found to be associated with: · vane wake excitation of either the impeller 1-diameter cover/blades modal frequency or the blade leading edge modal frequency from mistuning · mist carry over from third side load upstream scrubber · end of curve operation in the compressor rear sectio

Hedonic Price Indexes for Personal Computer Operating Systems and Productivity Suites

Results of hedonic price regressions for personal computer operating systems and productivity suites advertised in PC World magazine by retail vendors during the time period 1984 to 2000 are reported. Among the quality attribute variables we use are new measures capturing the presence of network effects in personal computer operating systems, such as connectivity and compatibility, and product integration among components of productivity suites. Average annual growth rates of quality-adjusted prices of personal computer operating systems range from -15 to -18 percent, while those for productivity suites generally range between -13 and -16 percent. Price declines are generally greater in the latter half of the samples.

Understanding Lipid Catabolism and Homeostasis in the Mammalian Brain

Neurologic dysfunction in humans including depression and autism spectrum disorders have been associated with genetic errors in fatty acid oxidation (FAO) enzymes. Furthermore, dietary changes that increase circulating fatty acids, including ketogenic diet (high-fat, low-carbohydrate) and intermittent fasting, have historically been used therapeutically. Despite this evidence, the contributions of brain fatty acid catabolism and mechanisms of regulating brain lipid homeostasis in response to metabolic cues, that when altered renders the brain vulnerable to impairment, are not well defined. The brain is one of the most lipid-rich tissues in the body and has a unique lipid distribution compared to peripheral tissues. Oxidation of radiolabeled fatty acids, 14C-palmitate or 14C-oleate has previously been observed in vitro using isolated brain tissue. Still, the existence, capacity, and relevance for FAO in the brain itself remain highly controversial. I evaluated the capacity for FAO in vivo using mice with brain-specific loss of FAO by conditional deletion of carnitine palmitoyltransferase 2 (CPT2B-/-). Most notably, I determined that acylcarnitines, an intermediate of FAO, are highly enriched in CPT2B-/- indicating that they are being mobilized for oxidation to a greater extent in normal brains than previously considered. Mechanisms of regulating brain lipid homeostasis in response to metabolic cues are not well characterized. Ethanolamine phosphate phospholyase (Etnppl) is an enzyme that has previously been associated with mood disorders and found to catabolize phosphoethanolamine, an amino acid commonly found as a component of many complex lipids. I determined that the Etnppl gene was regulated by overnight fasting specifically in astrocytes. I used a constitutive knockout mouse of Etnppl to evaluate its contributions to brain lipid homeostasis. Etnppl was developmentally regulated with a high increase in expression in early postnatal life in the brain. Etnppl was also induced after exposure to glucocorticoids. Furthermore, Etnppl loss resulted in elevated total abundance of the phospholipid phosphatidylethanolamine and altered abundances of species of multiple phospholipids in brain and liver indicating that it has a role in maintaining brain lipid homeostasis. Overall, understanding lipid catabolism and the regulation of lipid homeostasis in the brain is critical to understanding the contributions of metabolism to neurologic function

An Introductory Analysis to Nonverbal Communication in the Workplace

While engaged in conversation with anyone, humans judge the speaker not only through what they are saying, but also through nonverbal artifacts. These artifacts have a wide range of what they say about the person. One such nonverbal artifact that is seen commonly for females in today’s culture is makeup. This leads to the question of makeup and how it makes an individual be viewed within the professional work environment. A member of our group was used to demonstrate different levels of makeup applications, from no makeup to a heavy application, and then photographed. These photographs were later used for visual evidence in a survey given to professional S.T.E.M. (Science, Technology Engineering, and Mathematical) companies. Thanks to numerous responses, this question has been evaluated to its full extent on many different faucets, such as both negative and positive characteristics the individual seems to display. These results were then complied and analyzed statistically to fully understand the implications of this artifact on women in the professional work environment

Systems biology applications to study mechanisms of human immunodeficiency virus latency and reactivation

Eradication of human immunodeficiency virus (HIV) in infected individuals is currently not possible because of the presence of the persistent cellular reservoir of latent infection. The identification of HIV latency biomarkers and a better understanding of the molecular mechanisms contributing to regulation of HIV expression might provide essential tools to eliminate these latently infected cells. This review aims at summarizing gene expression profiling and systems biology applications to studies of HIV latency and eradication. Studies comparing gene expression in latently infected and uninfected cells identify candidate latency biomarkers and novel mechanisms of latency control. Studies that profiled gene expression changes induced by existing latency reversing agents (LRAs) highlight uniting themes driving HIV reactivation and novel mechanisms that contribute to regulation of HIV expression by different LRAs. Among the reviewed gene expression studies, the common approaches included identification of differentially expressed genes and gene functional category assessment. Integration of transcriptomic data with other biological data types is presently scarce, and the field would benefit from increased adoption of these methods in future studies. In addition, designing prospective studies that use the same methods of data acquisition and statistical analyses will facilitate a more reliable identification of latency biomarkers using different model systems and the comparison of the effects of different LRAs on host factors with a role in HIV reactivation. The results from such studies would have the potential to significantly impact the process by which candidate drugs are selected and combined for future evaluations and advancement to clinical trials

Towards water literacy: an interdisciplinary analysis of standards for teaching and learning about humans and Water

Water is critical to sustain human existence. Water literacy involves understanding the interactions within and between natural and human dimensions of water systems to support informed decision-making, an important outcome for learners of all ages. It is therefore critical to foster water literacy in today’s global citizens, particularly through formal education. The purpose of this study, in tandem with a parallel study focusing on natural dimensions of water systems (Mostacedo-Marasovic et al., in press), is to examine water-related K-12 standards for teaching and learning about human dimensions of water systems to develop a comprehensive and transdisciplinary perspective on water education. Our overarching question is, “What do disciplinary standards specify as outcomes for students’ learning about water and humans?”. Our research questions are: i) “To what extent do these water-related standards address recognized domains of learning?” and ii) “What thematic outcomes for students’ learning are apparent across grades in these water-related standards?”. We use chi-square statistics and a conventional qualitative content analysis method complemented by processes from grounded theory to analyze water-related education standards (N = 341) from 12 education-oriented, governmental and non-governmental organizations based in the United States. Our results indicate that first, water-related standards emphasize the cognitive domain, including declarative and procedural knowledge. The affective domain and its social and emotional components are much less prevalent. Second, the water-related standards illustrate five categories which encompass human dimensions of water spanning K-12 grade bands, including human settlements; the nexus between water, food, and energy; public health; impacts of human activities on water quality and quantity; and water resources management. Overall, the study contributes to a more holistic and comprehensive perspective of water and human systems that can help inform teaching and learning to cultivate water literacy, including curriculum development and classroom pedagogy

Assessing Social-Emotional Abilities of Preschool-Aged Children Within a Social-Emotional Learning Framework

During the past decade, there has been an increasing amount of research demonstrating a positive relationship between early childhood social-emotional abilities and later life outcomes. As such, practitioners who work with preschool-aged children are called to understand the social-emotional abilities that constitute healthy development. Doing so provides practitioners with a social-emotional framework from which to work so that they may efficiently assess and intervene in these abilities. This manuscript grounds social-emotional abilities within the Collaborative for Academic, Social, and Emotional Learning’s (CASEL) Framework for Social-Emotional Learning (SEL). We describe the need for a multi-method, multi-sourced, multi-setting comprehensive social-emotional assessment of preschool-aged children and describe a rating scale that can be used as a part of the assessment process. The manuscript concludes with a discussion regarding the importance of intervening early to prepare preschool-aged children for future academic and life success

Unmasking Cost Growth Behavior: A Longitudinal Study

This article examines how cost growth factors (CGF) change over a program’s acquisition life cycle for 36 Department of Defense aircraft programs. Starting from Milestone B, the authors examine CGFs at five gateways: Critical Design Review, First Flight (FF), the end of Developmental Test and Evaluation (DT&E), Initial Operational Capability, and Full Operational Capability. Each CGF is assigned a color rating based upon the program’s cost growth: Green (low), Amber (moderate), or Red (high). Significant findings include dependencies among similar CGF color ratings and cost growth occurring primarily between FF and the end of DT&E during a program’s life cycle