Evaluation of the color image and video processing chain and visual quality management for consumer systems

With the advent of novel digital display technologies, color processing is increasingly becoming a key aspect in consumer video applications. Today’s state-of-the-art displays require sophisticated color and image reproduction techniques in order to achieve larger screen size, higher luminance and higher resolution than ever before. However, from color science perspective, there are clearly opportunities for improvement in the color reproduction capabilities of various emerging and conventional display technologies. This research seeks to identify potential areas for improvement in color processing in a video processing chain. As part of this research, various processes involved in a typical video processing chain in consumer video applications were reviewed. Several published color and contrast enhancement algorithms were evaluated, and a novel algorithm was developed to enhance color and contrast in images and videos in an effective and coordinated manner. Further, a psychophysical technique was developed and implemented for performing visual evaluation of color image and consumer video quality. Based on the performance analysis and visual experiments involving various algorithms, guidelines were proposed for the development of an effective color and contrast enhancement method for images and video applications. It is hoped that the knowledge gained from this research will help build a better understanding of color processing and color quality management methods in consumer video

Imaging of cognitive outcomes in patients with autoimmune encephalitis

Die Autoimmunenzephalitis ist eine kürzlich beschriebene entzündliche Erkrankung des zentralen Nervensystems, die Gedächtnisdefizite, Psychosen, oder epileptische Anfälle hervorrufen kann. Derzeit ist hingegen noch nicht ausreichend verstanden, welche pathologischen Veränderungen zu den kognitiven Defiziten führen und welche neuropsychologischen und bildgebenden Langzeitoutcomes zu erwarten sind. Anhand von strukturellen und funktionellen Bildgebungsanalysen zeigt diese Dissertation, dass kognitive Defizite auch nach der akuten Phase der Autoimmunenzephalitis fortbestehen können. Bei der LGI1-Enzephalitis gehen Gedächtnisdefizite mit fokalen strukturellen Läsionen im Hippocampus einher. Durch eine funktionelle Störung der Resting-State-Konnektivität des Default-Mode- und Salienznetzwerkes beeinträchtigen diese Hippocampusläsionen auch Hirnregionen außerhalb des limbischen Systems. Bei Patient:innen mit NMDA-Rezeptor-Enzephalitis finden sich in der longitudinalen neuropsychologischen Untersuchung trotz guter allgemeiner Genesung auch noch mehrere Jahre nach der Akutphase persistierende Defizite des Gedächtnisses und exekutiver Funktionen. Zuletzt zeigt eine transdiagnostische Analyse, dass der anteriore Hippocampus eine erhöhte Vulnerabilität gegenüber immunvermittelten pathologischen Prozessen aufweist. Diese Ergebnisse legen nahe, dass kognitive Symptome auch noch nach der Entlassung aus der stationären Behandlung fortbestehen können. Sowohl umschriebene strukturelle Hippocampusläsionen als auch Veränderungen in makroskopischen funktionellen Hirnnetzwerken tragen zur pathophysiologischen Erklärung dieser Symptome bei. Zudem erlauben diese Ergebnisse einen Einblick in neuroplastische Veränderungen des Gehirns und haben weitreichende Implikationen für die Langzeitversorgung und das Design zukünftiger klinischer Studien.Autoimmune encephalitis is a recently described inflammatory disease of the central nervous system that can cause memory deficits, psychosis, or seizures. The trajectory of cognitive dysfunction and the underlying long-term imaging correlates are, however, not yet fully understood. By using advanced structural and functional neuroimaging, this thesis shows that cognitive deficits persist beyond the acute phase. In LGI1 encephalitis, MRI postprocessing revealed that memory deficits are related to focal structural hippocampal lesions. These hippocampal lesions propagate to brain areas outside the limbic system through aberrant resting-state connectivity of the default mode network (DMN) and the salience network. In NMDA receptor encephalitis, a longitudinal analysis of neuropsychological data describes persistent cognitive deficits, especially in the memory and executive domains, despite good physical recovery several years after the acute disease. Lastly, a transdiagnostic analysis reveals that the anterior hippocampus is particularly vulnerable to immune-mediated damage. In conclusion, these results demonstrate that cognitive symptoms in autoimmune encephalitis can persist beyond discharge from neurological care. Both discrete structural hippocampal damage and changes in macroscopic functional networks shed light on the pathophysiological basis of these symptoms. These findings help to explain how the brain responds to pathological damage and have substantial implications for long-term patient care and the design of future clinical studies

Recent publications from the Alzheimer's Disease Neuroimaging Initiative: Reviewing progress toward improved AD clinical trials

INTRODUCTION: The Alzheimer's Disease Neuroimaging Initiative (ADNI) has continued development and standardization of methodologies for biomarkers and has provided an increased depth and breadth of data available to qualified researchers. This review summarizes the over 400 publications using ADNI data during 2014 and 2015. METHODS: We used standard searches to find publications using ADNI data. RESULTS: (1) Structural and functional changes, including subtle changes to hippocampal shape and texture, atrophy in areas outside of hippocampus, and disruption to functional networks, are detectable in presymptomatic subjects before hippocampal atrophy; (2) In subjects with abnormal β-amyloid deposition (Aβ+), biomarkers become abnormal in the order predicted by the amyloid cascade hypothesis; (3) Cognitive decline is more closely linked to tau than Aβ deposition; (4) Cerebrovascular risk factors may interact with Aβ to increase white-matter (WM) abnormalities which may accelerate Alzheimer's disease (AD) progression in conjunction with tau abnormalities; (5) Different patterns of atrophy are associated with impairment of memory and executive function and may underlie psychiatric symptoms; (6) Structural, functional, and metabolic network connectivities are disrupted as AD progresses. Models of prion-like spreading of Aβ pathology along WM tracts predict known patterns of cortical Aβ deposition and declines in glucose metabolism; (7) New AD risk and protective gene loci have been identified using biologically informed approaches; (8) Cognitively normal and mild cognitive impairment (MCI) subjects are heterogeneous and include groups typified not only by "classic" AD pathology but also by normal biomarkers, accelerated decline, and suspected non-Alzheimer's pathology; (9) Selection of subjects at risk of imminent decline on the basis of one or more pathologies improves the power of clinical trials; (10) Sensitivity of cognitive outcome measures to early changes in cognition has been improved and surrogate outcome measures using longitudinal structural magnetic resonance imaging may further reduce clinical trial cost and duration; (11) Advances in machine learning techniques such as neural networks have improved diagnostic and prognostic accuracy especially in challenges involving MCI subjects; and (12) Network connectivity measures and genetic variants show promise in multimodal classification and some classifiers using single modalities are rivaling multimodal classifiers. DISCUSSION: Taken together, these studies fundamentally deepen our understanding of AD progression and its underlying genetic basis, which in turn informs and improves clinical trial desig

Advancing automation and robotics technology for the Space Station and for the US economy, volume 2

In response to Public Law 98-371, dated July 18, 1984, the NASA Advanced Technology Advisory Committee has studied automation and robotics for use in the Space Station. The Technical Report, Volume 2, provides background information on automation and robotics technologies and their potential and documents: the relevant aspects of Space Station design; representative examples of automation and robotics; applications; the state of the technology and advances needed; and considerations for technology transfer to U.S. industry and for space commercialization

Testing Spatial Cognition in Mild Cognitive Impairment Using Immersive Virtual Reality

The prodromal stage of dementia is known as mild cognitive impairment (MCI). Currently, cognitive tests are unable to correctly characterize the MCI type, and specifically, whether it will develop into Alzheimer's disease (AD). This means that cognitive deficits are detected long after the onset of pathological changes. More sensitive and specific tests, which can non-invasively detect the subtle, early signs of AD in MCI, would facilitate investigation of its early development and potentially permit early treatments. This thesis aims to develop a diagnostic tool to target the cognitive functions – and engage the corresponding brain regions – typically affected during the prodromal stages of AD. Pathological changes start in the hippocampal formation, a critical area for episodic memory and navigation. The tasks are developed from previous work demonstrating hippocampal dependence and make use of recent advances in immersive virtual reality, providing an ecologically valid improvement on standard tests of cognitive function. The first experimental chapter presents a test of navigation by path integration, a function specifically associated with processing by grid cells in the medial entorhinal cortex (mEC). The second experiment presents a test of object-location memory, believed to involve place cells in the hippocampus proper, combining inputs from mEC and object-identity information from the lateral entorhinal cortex (lEC). The third experiment tests object-location memory in a way that enables the contribution of self-motion to be assessed. Results show that the immersive virtual reality paradigms developed to test spatial cognition in prodromal AD are able to differentiate MCI patients from healthy age-matched older controls. Additionally, in combination with CSF biomarkers, navigation testing has proven the ability to stratify between MCI with different levels of biomarkers, identifying the patients who are most likely going to develop the disease. Finally, the last experiment, in an attempt to summarize different aspects of spatial cognition tested in the previous experiments, can detect subtle changes starting from ageing that may further decline with the onset of cognitive decline due to AD neuropathology. In conclusion within this thesis, we demonstrated the use of immersive virtual reality tests as an ecological valid tool for assessing the behavioural changes associated with the early progression of AD

The Extended Environment of M17: A Star Formation History

M17 is one of the youngest and most massive nearby star-formation regions in the Galaxy. It features a bright H II region erupting as a blister from the side of a giant molecular cloud (GMC). Combining photometry from the Spitzer GLIMPSE survey with complementary infrared (IR) surveys, we identify candidate young stellar objects (YSOs) throughout a 1.5 deg x 1 deg field that includes the M17 complex. The long sightline through the Galaxy behind M17 creates significant contamination in our YSO sample from unassociated sources with similar IR colors. Removing contaminants, we produce a highly-reliable catalog of 96 candidate YSOs with a high probability of association with the M17 complex. We fit model spectral energy distributions to these sources and constrain their physical properties. Extrapolating the mass function of 62 intermediate-mass YSOs (M >3 Msun), we estimate that >1000 stars are in the process of forming in the extended outer regions of M17. From IR survey images from IRAS and GLIMPSE, we find that M17 lies on the rim of a large shell structure ~0.5 deg in diameter (~20 pc at 2.1 kpc). We present new maps of CO and 13CO (J=2-1) emission, which show that the shell is a coherent, kinematic structure associated with M17 at v = 19 km/s. The shell is an extended bubble outlining the photodissociation region of a faint, diffuse H II region several Myr old. We provide evidence that massive star formation has been triggered by the expansion of the bubble. The formation of the massive cluster ionizing the M17 H II region itself may have been similarly triggered. We conclude that the star formation history in the extended environment of M17 has been punctuated by successive waves of massive star formation propagating through a GMC complex.Comment: 31 pages, 15 figures, accepted for publication in ApJ. For a version with higher-quality figures, see http://www.astro.wisc.edu/glimpse/Povich2009_M17.pd

Space programs summary no. 37-58, volume 3 for the period 1 June - 31 July 1969. Supporting research and advanced development

Review of developments in current engineering and scientific work at JP

Cerebrovascular Dysfunction and Degeneration in Alzheimer’s Disease Pathophysiology

Alzheimer’s disease (AD) is a terminal illness and the most common form of dementia, which disproportionately affects the aged population. The pathophysiology of AD is characterized by neurodegeneration that slowly progresses, affecting regions of the brain that are involved in learning, memory, language, and executive function. In patients with the disease, early symptoms include non-disruptive forgetfulness that evolves into the inability to form new memories and ultimately the loss of autonomy at late stages. Histopathological hallmarks in the brain from patients with AD is the presence of amyloid-β (Aβ)-plaques and neurofibrillary tangles (NFT) deposited in the parenchyma. Since the discovery of these hallmarks, the majority of AD research has disproportionately focused on Aβ -plaques and NFT. Although the etiology of AD remains unknown, considerable advances have been made describing the cellular, molecular, and genetic contributions to the disease. Aging is the important risk factor for the development of AD, many other factors that increase the risk of developing AD later in life are vascular in nature. The function of the cardiovascular system is known to decline during healthy aging, and the same is true for the cerebrovasculature. Empirical evidence has demonstrated a decline cerebrovascular function in AD that exceeds the decline that occurs in healthy aging. Cerebrovascular dysfunction is the major contributor to the development of hypoperfusion and hypometabolism in patients diagnosed with AD. Cerebral amyloid angiopathy (CAA) is a neuropathological condition defined by the abnormal accumulation of Aβ on the walls of the cerebrovasculature. CAA occurs in as many as 90% of patients with AD and is implicated in the weakening of the walls of cerebral blood vessels. The occurrence of microhemorrhages, aneurysms, and microinfarctions are pathological manifestations associated with weakened walls of cerebral blood vessels in the brains of patients with confirmed AD. Noteworthy, cerebrovascular dysfunction, hypoperfusion, and hypometabolism occur before the onset of Aβ-plaque and NFT deposition in the brain of patients and animal models with AD. These findings provide a compelling basis that suggest a prominent role of dysfunctional cerebrovasculature in the etiology and for the progression of AD. Although the overwhelming evidence that implicates cerebrovascular dysfunction in AD, a thorough account of the changes that occur to the cerebrovasculature nor the mechanisms that drive these changes during the development and progression of AD has not been previously reported. The overarching goal(s) of this work are to; (1) provide a thorough description of the changes that occur to the cerebrovasculature during age and the progression of AD; (2) describe the mechanisms involved in cerebrovascular damage in AD; and (3) characterize the degeneration that results from cerebrovascular hypoperfusion. These overarching goals were achieved by completing five separate studies. Described in study 1, we investigated the effects of hypoxia on astrocytic mitochondria by assessing mitochondrial fission-fusion dynamics, reactive oxygen species production, synthesis of ATP, and mitophagy. Overall, we found a drastic mitochondrial network change that is triggered by metabolic crisis during hypoxia; these changes are followed by mitochondrial degradation and retraction of astrocytic extensions during reoxygenation. In study 2, we provide a novel model for the gradual development of cerebrovascular hypoperfusion in mice. Cerebrovascular hypoperfusion developed over 34-days by inserting an ameroid constrictor ring and microcoil bilaterally around the external carotid arteries. We investigated the neurodegenerative effects of hypoperfusion in mice by assessing both gray and white matter pathology. Histopathological analyses of the brain revealed neuronal and axonal degeneration as well as necrotic lesions. The most severely affected regions were located in the hippocampus and corpus callosum. Described in study 3, we performed a series of experiments to investigate the effects of Aβ on cerebrovascular endothelial cells. In this study, we focused on characterizing the changes to mitochondrial oxidative phosphorylation, superoxide production, mitochondrial calcium, ATP synthesis, and endothelial cell death. These results describe a mechanism for mitochondrial degeneration caused by the production of mitochondrial superoxide, which was driven by increased mitochondrial Ca2+ uptake. We found that persistent superoxide production injures mitochondria and disrupts electron transport in cerebrovascular endothelial cells. In study 4, we developed a method to evaluate the cerebrovasculature of the whole-brain and constructed analyses to assess the angioarchitecture. We used vascular corrosion casting method to replicate the cerebrovasculature in adult mice and used MicroCT to acquire volumetric imaging data of the cerebrovascular network at a resolution required to investigate the microvasculature. Our analyses of the cerebrovasculature evaluated the morphology, topology, and organization of the angioarchitecture. With these developments, we investigated the effects of age and progression of disease on the cerebrovasculature in wild type mice and the triple transgenic mouse model of AD. Study 5 provides data describing degenerative changes to the microvascular network that progress with age in the triple transgenic mouse model of AD. These changes to the microvasculature occurred early, before the onset of Aβ-plaque deposition and NFT development. Overall, this body of work provides evidence of an early cerebrovascular disruption in the etiology of AD that progresses with age. Aβ mediates early cerebrovascular damage through direct interaction with vascular endothelial cells. Microvascular degeneration can lead to hypoperfusion which damages both gray and white matter. Hypoperfusion-associated hypoxia may mediate parenchymal damage by disrupting mitochondrial fission-fusion dynamics and enhancing mitophagy. These data provide a basis for the development of novel therapeutic strategies that target the changes to the cerebrovasculature for the treatment of AD. These observations may substantiate a prophylactic strategy for the treatment of AD by preventing the initial factors that lead to compromised cerebrovasculature

The Telecommunications and Data Acquisition Report

Developments in space communications, radio navigation, radio science, ground-base radio astronomy, reports on the Deep Space Network (DSN) and its Ground Communications Facility (GCF), and applications of radio interferometry at microwave frequencies are discussed