Position and orientation correction for pipe profiling robots

Sewer pipelines are prevalent, important, valuable, unnoticed, and often in a state of disrepair. Pipeline inspection is essential for effective management of wastewater systems and is now mandated for many municipalities complying with the Governmental Accounting Standards Board Statement 34 and EPA regulations. Pipe inspection robots are routinely used to inspect underground pipelines for cracks, deformations, leaks, blockages and other anomalies to prevent catastrophic failure and to ensure cost effective maintenance and renewal. Most existing pipe inspection robots only collect video footage of pipe condition. Pipe profiling technology has recently been introduced to allow for measurement of the internal coordinate geometry of pipelines. Accurate radial measurements permit the calculation of several important pipe parameters which aid in the determination of pipe condition and prediction of time to failure. Significant research work has been completed in North America, Europe, Asia and Australia aimed at improving the accuracy and automation of the pipe inspection process. However, standard calibration, verification, reporting and analysis practices must be developed for pipe profilers if coordinate profiling data is to be effectively included in the long term management of pipeline assets. The objective of this research is to quantify the measurement error incurred by a pipe profiler\u27s misalignment with the pipe axis, present a new methodology to correct the measurement error, develop a prototype profiler to verify the equations derived herein, and to further the development of pipe profiler technology at the Trenchless Technology Center at Louisiana Tech University. Equations are derived for pipe ovality as a function of the robot\u27s position and orientation with respect to a pipe to demonstrate the magnitude of the error which is introduced by a robot\u27s misalignment with the pipe axis. A new technique is presented to estimate the position and orientation of a profiler using radial measurement devices at each of its ends. This technique is demonstrated by applying homogeneous coordinate transformations to simulated radial measurements based on mathematically generated data that would be obtained by incrementally rotating two parallel radial measuring devices in a perfectly cylindrical pipe. A prototype pipe profiling robot was developed to demonstrate the new position and orientation technique and to experimentally verify the measurement error caused by a robot\u27s misalignment with the pipe axis. This work improves the accuracy and automation of pipe profiling technology and makes a case for the development of industry standard calibration, verification, reporting and analysis practices

Parkinson-causing α-synuclein missense mutations shift native tetramers to monomers as a mechanism for disease initiation

β-Sheet-rich α-synuclein (αS) aggregates characterize Parkinson's disease (PD). αS was long believed to be a natively unfolded monomer, but recent work suggests it also occurs in α-helix-rich tetramers. Crosslinking traps principally tetrameric αS in intact normal neurons, but not after cell lysis, suggesting a dynamic equilibrium. Here we show that freshly biopsied normal human brain contains abundant αS tetramers. The PD-causing mutation A53T decreases tetramers in mouse brain. Neurons derived from an A53T patient have decreased tetramers. Neurons expressing E46K do also, and adding 1-2 E46K-like mutations into the canonical αS repeat motifs (KTKEGV) further reduces tetramers, decreases αS solubility and induces neurotoxicity and round inclusions. The other three fPD missense mutations likewise decrease tetramer:monomer ratios. The destabilization of physiological tetramers by PD-causing missense mutations and the neurotoxicity and inclusions induced by markedly decreasing tetramers suggest that decreased α-helical tetramers and increased unfolded monomers initiate pathogenesis. Tetramer-stabilizing compounds should prevent this

Imaging of bronchial pathology in antibody deficiency: Data from the European Chest CT Group

Studies of chest computed tomography (CT) in patients with primary antibody deficiency syndromes (ADS) suggest a broad range of bronchial pathology. However, there are as yet no multicentre studies to assess the variety of bronchial pathology in this patient group. One of the underlying reasons is the lack of a consensus methodology, a prerequisite to jointly document chest CT findings. We aimed to establish an international platform for the evaluation of bronchial pathology as assessed by chest CT and to describe the range of bronchial pathologies in patients with antibody deficiency. Ffteen immunodeficiency centres from 9 countries evaluated chest CT scans of patients with ADS using a predefined list of potential findings including an extent score for bronchiectasis. Data of 282 patients with ADS were collected. Patients with common variable immunodeficiency disorders (CVID) comprised the largest subgroup (232 patients, 82.3%). Eighty percent of CVID patients had radiological evidence of bronchial pathology including bronchiectasis in 61%, bronchial wall thickening in 44% and mucus plugging in 29%. Bronchiectasis was detected in 44% of CVID patients aged less than 20 years. Cough was a better predictor for bronchiectasis than spirometry values. Delay of diagnosis as well as duration of disease correlated positively with presence of bronchiectasis. The use of consensus diagnostic criteria and a pre-defined list of bronchial pathologies allows for comparison of chest CT data in multicentre studies. Our data suggest a high prevalence of bronchial pathology in CVID due to late diagnosis or duration of disease

Distinct clinical and neuropathological features of G51D SNCA mutation cases compared with SNCA duplication and H50Q mutation

Background: We and others have described the neurodegenerative disorder caused by G51D SNCA mutation which shares characteristics of Parkinson’s disease (PD) and multiple system atrophy (MSA). The objective of this investigation was to extend the description of the clinical and neuropathological hallmarks of G51D mutant SNCA-associated disease by the study of two additional cases from a further G51D SNCA kindred and to compare the features of this group with a SNCA duplication case and a H50Q SNCA mutation case. Results: All three G51D patients were clinically characterised by parkinsonism, dementia, visual hallucinations, autonomic dysfunction and pyramidal signs with variable age at disease onset and levodopa response. The H50Q SNCA mutation case had a clinical picture that mimicked late-onset idiopathic PD with a good and sustained levodopa response. The SNCA duplication case presented with a clinical phenotype of frontotemporal dementia with marked behavioural changes, pyramidal signs, postural hypotension and transiently levodopa responsive parkinsonism. Detailed post-mortem neuropathological analysis was performed in all cases. All three G51D cases had abundant α-synuclein pathology with characteristics of both PD and MSA. These included widespread cortical and subcortical neuronal α-synuclein inclusions together with small numbers of inclusions resembling glial cytoplasmic inclusions (GCIs) in oligodendrocytes. In contrast the H50Q and SNCA duplication cases, had α-synuclein pathology resembling idiopathic PD without GCIs. Phosphorylated α-synuclein was present in all inclusions types in G51D cases but was more restricted in SNCA duplication and H50Q mutation. Inclusions were also immunoreactive for the 5G4 antibody indicating their highly aggregated and likely fibrillar state. Conclusions: Our characterisation of the clinical and neuropathological features of the present small series of G51D SNCA mutation cases should aid the recognition of this clinico-pathological entity. The neuropathological features of these cases consistently share characteristics of PD and MSA and are distinct from PD patients carrying the H50Q or SNCA duplication

Correction to: Imaging of Bronchial Pathology in Antibody Deficiency: Data from the European Chest CT Group.

In the original version of this article unfortunately two authors were missing: Dr. Jürgen Weidemann and Dr. Daniel Berthold. The correct list of authors is presented above

Contributions of dynamic systems theory to cognitive development

We examine the contributions of dynamic systems theory to the field of cognitive development, focusing on modeling using dynamic neural fields. After introducing central concepts of dynamic field theory (DFT), we probe empirical predictions and findings around two examples—the DFT of infant perseverative reaching that explains Piaget's A-not-B error and the DFT of spatial memory that explain changes in spatial cognition in early development. Review of the literature around these examples reveals that computational modeling is having an impact on empirical research in cognitive development; however, this impact does not extend to neural and clinical research. Moreover, there is a tendency for researchers to interpret models narrowly, anchoring them to specific tasks. We conclude on an optimistic note, encouraging both theoreticians and experimentalists to work toward a more theory-driven future