Haptic metal spinning

Sheet metal spinning is an incremental forming technique practiced for a long time only by experienced, skilled craftsmen. Over the last sixty years, attempts have been made to automate the process, but today the industrial practice still relies heavily on the skill of experienced operators. Complete analytical solutions to predict workpiece failure based on the path of the tool are not available, and finite element simulations of the process are too time-intensive to be of practical use for online toolpath correction. Therefore, today the design of toolpaths to avoid failure in spinning remains an art acquired by practice. In this paper, we approach the issue by designing an enhanced teach-in/playback system. We connect a haptic device to a CNC spinning machine; this device allows a human operator to control the working roller manually while feeling the force applied to the workpiece. Position, force and workpiece shape sensors allow collecting information on the toolpath followed by the operator and on its influence over the mechanics of the process. The opportunities offered by this system to derive rules for toolpath design are explored in two case studies on force control and wrinkling recovery, with new insights on the relationship between toolpaths and failure. A research agenda is outlined to exploit the full potential of haptic metal spinning

An evaluation of preference of delays to reinforcement on choice responding : a translational study

Delays to reinforcement are often a necessary component during treatments of challenging behavior (e.g., Functional Communication Training; FCT). In the absence of programmed delay training, the utility and generality of FCT may be limited. Despite the importance of delays to reinforcement during FCT, few studies have empirically isolated and investigated the parameters pertaining to the implementation of delays to reinforcement. Results from basic empirical studies have shown that variable delays, or bi-valued mixed delays to reinforcement, are preferred in humans and nonhuman studies. The current research examined response allocation between fixed and mixed delays to reinforcement using a concurrent schedule of reinforcement. Results showed preference for mixed delays to reinforcement with 4 out of 4 participants. Potential avenues of future research on the use of mixed delays to reinforcement, such as the application within FCT and maintenance of socially appropriate behaviors, are discussed.Special Educatio

All Rise, the Court Is in Session: What Judges Say About Court-Connected Mediation

Published in cooperation with the American Bar Association Section of Dispute Resolutio

Evaluating the Use of Competing Items in a Multiple Schedule During Reinforcement Schedule Thinning

Multiple schedules are schedules of reinforcement that are often used to facilitate more manageable rates of a replacement behavior such as a communication response following functional communication training as an intervention for destructive behavior. Commonly, reinforcement schedule thinning involves multiple fading steps that can take more than 100 sessions to achieve therapeutic goals. The purpose of this experiment was to evaluate a method for rapidly achieving fading steps in a multiple schedule by including competing items during the extinction interval. Four children diagnosed with autism successfully reached the terminal extinction interval with a ≥80% reduction in problem behavior. Two of the four participants reached the terminal extinction interval during a systematic assessment to identify an appropriate initial extinction interval. This study produced two important findings. First, the inclusion of competing items successfully and rapidly achieved the terminal extinction interval in a multiple schedule. Second, a novel use of a systematic assessment procedure identified participants for whom the competing items were unnecessary to rapidly achieve the terminal extinction interval

Cyfip1 haploinsufficient rats show white matter changes, myelin thinning, abnormal oligodendrocytes and behavioural inflexibility

The biological basis of the increased risk for psychiatric disorders seen in 15q11.2 copy number deletion is unknown. Previous work has shown disturbances in white matter tracts in human carriers of the deletion. Here, in a novel rat model, we recapitulated low dosage of the candidate risk gene CYFIP1 present within the 15q11.2 interval. Using diffusion tensor imaging, we first showed extensive white matter changes in Cyfip1 mutant rats, which were most pronounced in the corpus callosum and external capsule. Transmission electron microscopy showed that these changes were associated with thinning of the myelin sheath in the corpus callosum. Myelin thinning was independent of changes in axon number or diameter but was associated with effects on mature oligodendrocytes, including aberrant intracellular distribution of myelin basic protein. Finally, we demonstrated effects on cognitive phenotypes sensitive to both disruptions in myelin and callosal circuitry

Focal Spot, Winter 2009/2010

https://digitalcommons.wustl.edu/focal_spot_archives/1113/thumbnail.jp

Cortical circuit alterations precede motor impairments in Huntington's disease mice

Huntington's disease (HD) is a devastating hereditary movement disorder, characterized by degeneration of neurons in the striatum and cortex. Studies in human patients and mouse HD models suggest that disturbances of neuronal function in the neocortex play an important role in disease onset and progression. However, the precise nature and time course of cortical alterations in HD have remained elusive. Here, we use chronic in vivo two-photon calcium imaging to longitudinally monitor the activity of identified single neurons in layer 2/3 of the primary motor cortex in awake, behaving R6/2 transgenic HD mice and wildtype littermates. R6/2 mice show age-dependent changes in cortical network function, with an increase in activity that affects a large fraction of cells and occurs rather abruptly within one week, preceeding the onset of motor defects. Furthermore, quantitative proteomics demonstrate a pronounced downregulation of synaptic proteins in the cortex, and histological analyses in R6/2 mice and human HD autopsy cases reveal a reduction in perisomatic inhibitory synaptic contacts on layer 2/3 pyramidal cells. Taken together, our study provides a time-resolved description of cortical network dysfunction in behaving HD mice and points to disturbed excitation/inhibition balance as an important pathomechanism in HD

Quantitative volumetric study of brain in chronic striatolenticular stroke

Perforating branches of the middle cerebral artery, namely the striato-lenticular arteries provide the majority of blood supply for the striatum and posterior limb of the internal capsules. Occlusions of these arteries cause a small stroke but have a devastating effect on patients’ functions. Previous studies showed that the anterior two thirds of the internal capsule is occupied by the prefrontal tracts with the posterior one third by connection to/from sensorimotor, temporal and posterior parietal cortices. In this study, we aimed to examine the long-term effect of infarction in the striato-capsular region on cerebral cortex thickness and also its association with stroke volume and different functional tests. We hypothesized that because of extensive connections of striatum and internal capsule with the cerebral cortex, infarction of this area results in an extensive cortical thickness degeneration which could in turn cause low fictional measurement scores. High resolution T1 weighted MRI was obtained from 21 patients with ischemic stroke in the striatum/posterior limb of the internal capsule region. Subjects were carefully selected from a pool of 140 stroke cases recruited for the Northstar Stroke Project. 63 healthy volunteers (30 male), matched for age and gender were also chosen to form the control group from the OASIS database. Patients and normal subjects were right handed except for 3 patients who have the stroke in the left side of the brain. Patients were defined as left-sided stroke and right-sided stroke depending on the side of the stroke in brain. MRI scans were done 6 months to 2 years after the stroke. To measure cortical thickness, we used Freesurfer software. Vertexwise group comparison was carried out using General Linear Models (GLM). With the Significance level set at 0.05. Population maps of stroke lesions showed that the majority of strokes were located in the striatum and posterior internal capsule. Cortical thickness reduction was greater in the ipsilateral hemisphere. Vertex-wise group comparison between leftsided stroke patients and controls group showed significant reduction in the cortical II thickness in the dorsal and medial prefrontal, premotor, posterior parietal, precuneus, and temporal cortex which survived after correction for multiple comparison using false discovery rate at Freesurfer. Similar comparison for rightsided stroke showed a similar pattern of cortical thinning, however the extent of cortical thinning was much less than in that of the left-sided stroke patients but the ROI analysis showed the main effect of side was significant (f (1, 19) =6.909, p=0.017), which showed that the left hemisphere stroke side group had a thicker cortex (mean=2.463, sd= 0.020) on average compare to the right hemisphere stroke side (mean=2.372, sd= 0.028). Primary motor cortex was surprisingly spared in both stroke groups. In addition, volume of the corpus callosum increased significantly in the stroke group. The differences between motor cortex (M1) thickness in left-hemispheric stroke patients versus controls (t=1.24, n=14, p>0.05) and right-hemispheric stroke patients versus controls (t=-0.511, n=7, p>0.05) were not significant. There was a negative correlation between the volume of the stroke lesions and the affected M1 thickness. There was no correlation between the stroke volume and functional tests in patients and also no correlation between the motor cortex thickness and functional tests in patients. Regarding normal subjects, comparison between two sides of the brain showed that the both hemispheres are symmetrical. In addition, correlation between age and cortical thickness showed a negative significant correlation (1-tailed, p<0.0007, manual correction for multiple comparisons) in M1, superior frontal, lingual cortex at both side of the brain and also negative significant correlation in superior temporal cortex and isthmus cingulated cortex on the left side of brain and supramarginal cortex on the right side of brain but there was no significant difference in cortical thickness between males and females. The finding from this study suggests that the size of the lesion can be a predictor of further M1 cortex reduction. The correlation of M1 thickness with stroke volume showed that secondary cortical degeneration may be mainly depends on the size of neuronal loss in strital-capsular stroke. From normal subject study it can be concluded that generally cortical thickness will decrease with ageing but gender does not have an effect on the cortical thickness. III Furthermore, the lack of behavioural correlation with M1 thickness and stroke volume and also the non significant M1 cortex reduction versus control group may suggest that the long-term functional disability after capsular-striatal stroke may not be entirely dependent on primary motor cortex and secondary motor cortex and primary somatosensory cortex could have an important role as well. These results may help to understand why relatively small subcortical infarcts often cause severe disability that is relatively resistant to recovery in the long term

Detecting and tracking early neurodegeneration in familial Alzheimer’s disease

Alzheimer’s disease (AD) is recognized to have a long presymptomatic period, with initial deposition of extracellular amyloid and intracellular tau, followed by downstream neurodegeneration and cognitive decline. There is great interest in testing potential disease-modifying treatments for AD prior to the onset of symptoms, when minimal neuronal loss has occurred. To facilitate this, robust and sensitive methods are needed to identify at-risk individuals, stage their disease, and track progression. Familial Alzheimer’s disease (FAD) shares many features, clinically, radiologically, and neurophysiologically, with the more common sporadic form of disease. Carriers of autosomal dominantly inherited mutations in the presenilin 1, presenilin 2, and amyloid precursor protein genes have relatively predictable ages at symptom onset, based on family history. Study of FAD mutation carriers therefore provides the opportunity for the prospective study of asymptomatic individuals with known underlying AD pathology prior to the onset of clinical disease. The studies presented herein aim to improve the identification and characterization of early FAD neurodegenerative change and its earliest downstream cognitive effects. A multimodal approach is taken, with both presymptomatic and mildly symptomatic individuals included. Chapter one provides an introduction to AD and methods for measuring early neurodegeneration. Chapter two then outlines the general methodological approach across the different studies. Chapters three and four present results of magnetic resonance imaging studies of macrostructural (cortical thickness) and microstructural (diffusion-weighted imaging) cortical change. Chapter five reports results for a new blood-based biomarker of neurodegeneration – serum neurofilamentlight. Chapter six investigates a novel approach to presymptomatic cognitive testing – 6 assessing accelerated long-term forgetting. In all studies, significant differences between mutation carriers and non-carrier controls are detectable during the presymptomatic period. The thesis draws together these different approaches and discusses how they advance our understanding of the neurobiology of AD and their potential utility in both clinical assessment and presymptomatic therapeutic trials