21,541 research outputs found
Protecting Animals 36: Author Witi Ihimaera
No full textIn this very special episode of Knowing Animals I am joined by beloved New Zealand author Witi Ihimaera. Witi has written many books featuring nonhuman animals. He offers us a non-colonial lens through which to think about the human/nonhuman relationship
I Think I Am Philip K. Dick
No full textFor years, noted writer Laurence A. Rickels often found himself compared to novelist Philip K. Dickthough in fact Rickels had never read any of the science fiction writers work. When he finally read his first Philip K. Dick novel, while researching for his recent book The Devil Notebooks , it prompted a prolonged immersion in Dicks writing as well as a recognition of Rickelss own long-documented intellectual pursuits. The result of this engagement is I Think I Am: Philip K. Dick , a profound thought experiment that charts the wide relevance of the pulp sci-fi author and paranoid visionary. I Think I Am: Philip K. Dick explores the science fiction authors meditations on psychic reality and psychosis, Christian mysticism, Eastern religion, and modern spiritualism. Covering all of Dicks science fiction, Rickels corrects the lack of scholarly interest in the legendary Californian author and, ultimately, makes a compelling case for the philosophical and psychoanalytic significance of Philip K. Dicks popular and influential science fiction.Intro -- Contents -- Introjection -- Part I -- Endopsychic Allegories -- Schreber Guardian -- Belief System Surveillance -- Part II -- Deeper Problems -- Veil of Tears -- Go West -- Dick Manfred -- Timing -- Glimmung -- Part III -- Spiritualism Analogy -- Imitating the Dead -- Indexical Layer -- Ilse -- Hammers and Things -- Crucifictions -- Over There -- Martyrology -- Can't Live, Can't Live -- Lola -- Umwelt, Mitwelt, and Eigenwelt -- Outer Race -- The German Introject -- Part IV -- Materialism, Idealism, and Cybernetics -- Startling Stories -- A Couple of Years -- Android Empathy -- Homunculus and Robot -- ALL OF YOU ARE DEAD. I AM ALIVE. -- Go with the Flow -- Part V -- Room for Thought -- Caduceus -- Jump -- Still -- A Wake -- Spätwerk -- Let the Dead Be -- Play Bally -- Das Hund -- Notes -- BibliographyFor years, noted writer Laurence A. Rickels often found himself compared to novelist Philip K. Dickthough in fact Rickels had never read any of the science fiction writers work. When he finally read his first Philip K. Dick novel, while researching for his recent book The Devil Notebooks , it prompted a prolonged immersion in Dicks writing as well as a recognition of Rickelss own long-documented intellectual pursuits. The result of this engagement is I Think I Am: Philip K. Dick , a profound thought experiment that charts the wide relevance of the pulp sci-fi author and paranoid visionary. I Think I Am: Philip K. Dick explores the science fiction authors meditations on psychic reality and psychosis, Christian mysticism, Eastern religion, and modern spiritualism. Covering all of Dicks science fiction, Rickels corrects the lack of scholarly interest in the legendary Californian author and, ultimately, makes a compelling case for the philosophical and psychoanalytic significance of Philip K. Dicks popular and influential science fiction.Description based on publisher supplied metadata and other sources.Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, YYYY. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries
Validation of the German Revised Addenbrooke's Cognitive Examination for Detecting Mild Cognitive Impairment, Mild Dementia in Alzheimer's Disease and Frontotemporal Lobar Degeneration
No full textBackground/Aims: The diagnostic accuracy of the German version of the revised Addenbrooke's Cognitive Examination (ACE-R) in identifying mild cognitive impairment (MCI), mild dementia in Alzheimer's disease (AD) and mild dementia in frontotemporal lobar degeneration (FTLD) in comparison with the conventional Mini Mental State Examination (MMSE) was assessed. Methods: The study encompasses 76 cognitively healthy elderly individuals, 75 patients with MCI, 56 with AD and 22 with FTLD. ACE-R and MMSE were validated against an expert diagnosis based on a comprehensive diagnostic procedure. Statistical analysis was performed using the receiver operating characteristic method and regression analyses. Results: The optimal cut-off score for the ACE-R for detecting MCI, AD, and FTLD was 86/87, 82/83 and 83/84, respectively. ACE-R was superior to MMSE only in the detection of patients with FTLD {[}area under the curve (AUC): 0.97 vs. 0.92], whilst the accuracy of the two instruments did not differ in identifying MCI and AD. The ratio of the scores of the memory ACE-R subtest to verbal fluency subtest contributed significantly to the discrimination between AD and FTLD (optimal cut-off score: 2.30/2.31, AUC: 0.77), whereas the MMSE and ACE-R total scores did not. Conclusion: The German ACE-R is superior to the most commonly employed MMSE in detecting mild dementia in FTLD and in the differential diagnosis between AD and FTLD. Thus it might serve as a valuable instrument as part of a comprehensive diagnostic workup in specialist centres/clinics contributing to the diagnosis and differential diagnosis of the cause of dementia. Copyright (C) 2010 S. Karger AG, Base
Liftings for noncomplete probability spaces
No full textThe current state of knowledge concerning liftings for noncomplete probability spaces is discussed. This is a somewhat expanded version of the author's talk given at the 1991 Summer Conference on General Topology and Applications in Honor of Mary Ellen Rudin and Her Work.PT: S; CR: BURKE MR, IN PRESS P AM MATH S BURKE MR, 1991, ISRAEL J MATH, V73, P33 BURKE MR, 1992, ISRAEL J MATH, V79, P289 CARLSON T, THEOREM LIFTING CHRISTENSEN JPR, 1974, TOPOLOGY BOREL STRUC FREMLIN DH, 1989, HDB BOOLEAN ALGEBRAS, P877 INOESCUTULCEA A, 1966, 5TH P BERK S MATH ST, V2 IONESCUTULCEA A, 1967, CONTRIBUTIONS PROB 1, P63 IONESCUTULCEA A, 1969, TOPICS THEORY LIFTIN JECH TJ, 1978, SET THEORY JOHNSON RA, 1980, P AM MATH SOC, V80, P234 JUST W, IN PRESS T AM MATH S KUPKA J, 1983, INDIANA U MATH J, V32, P717 LOSERT V, 1983, LNM, V1080, P95 MAHARAM D, 1958, P AM MATH SOC, V9, P987 SHELAH S, 1983, ISRAEL J MATH, V45, P90 TALAGRAND M, 1982, P AM MATH SOC, V84, P379 VONNEUMANN J, 1931, CRELLES J MATH, V165, P109; NR: 18; TC: 0; J9: ANN N Y ACAD SCI; PG: 4; GA: BZ86BSource type: Electronic(1
Cerebral atrophy in mild cognitive impairment and Alzheimer disease: rates and acceleration.
No full textOBJECTIVE: To quantify the regional and global cerebral atrophy rates and assess acceleration rates in healthy controls, subjects with mild cognitive impairment (MCI), and subjects with mild Alzheimer disease (AD). METHODS: Using 0-, 6-, 12-, 18-, 24-, and 36-month MRI scans of controls and subjects with MCI and AD from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, we calculated volume change of whole brain, hippocampus, and ventricles between all pairs of scans using the boundary shift integral. RESULTS: We found no evidence of acceleration in whole-brain atrophy rates in any group. There was evidence that hippocampal atrophy rates in MCI subjects accelerate by 0.22%/year2 on average (p = 0.037). There was evidence of acceleration in rates of ventricular enlargement in subjects with MCI (p = 0.001) and AD (p < 0.001), with rates estimated to increase by 0.27 mL/year2 (95% confidence interval 0.12, 0.43) and 0.88 mL/year2 (95% confidence interval 0.47, 1.29), respectively. A post hoc analysis suggested that the acceleration of hippocampal loss in MCI subjects was mainly driven by the MCI subjects that were observed to progress to clinical AD within 3 years of baseline, with this group showing hippocampal atrophy rate acceleration of 0.50%/year2 (p = 0.003). CONCLUSIONS: The small acceleration rates suggest a long period of transition to the pathologic losses seen in clinical AD. The acceleration in hippocampal atrophy rates in MCI subjects in the ADNI seems to be driven by those MCI subjects who concurrently progressed to a clinical diagnosis of AD
A Clinical and In Vitro Study of the Distal Hereditary Motor Neuropathies
No full textThe hereditary motor neuropathies (HMN) encompass diseases of motor axons and neurons and range from the progressive, length dependent distal hereditary motor neuropathies (dHMN) to the developmental, non-progressive dominant congenital spinal muscular atrophies (DCSMA). In this Thesis I have investigated the pathomechanisms of HMN and undertaken a natural history study of patients with dHMN. In Chapter 2 I investigated the pathomechanism of dHMN due to homozygous mutations in the heat shock protein HSJ1, using primary motor neurons (MNs) from HSJ1 knockout mice. Using live cell confocal imaging I examined mitochondrial axonal transport and ER calcium levels, but found no evidence of axonal transport deficits or ER stress. In Chapter 3 I examined the pathomechanism of dHMN due to a novel mutation in FBXO38. FBXO38 modulates the transcriptional activity of KLF7; a transcription factor with a role in neuronal development and repair. I therefore examined neurite outgrowth in lentivirus-infected primary MNs and demonstrated a reduction in neurite outgrowth in mutant FBXO38 infected MNs. In Chapter 4, I identified a mutation in a new disease gene, BICD2, in a family with a form of DCSMA termed lower extremity dominant SMA. BICD2 is a dynein adaptor protein and using immunoprecipitation I found that two disease mutations in BICD2 increase dynein binding affinity. In Chapter 5, I performed a genetic study of the HMNs and showed that mutations in HSPB1 are the most common cause of dHMN. I also evaluated plasma neurofilament heavy chain (NFH) as a biomarker of disease activity in the inherited neuropathies but was unable to detect a difference between patients and healthy volunteers. This would suggest that plasma NFH levels are not a suitable biomarker of disease activity in the inherited neuropathies
The AM Canum Venaticorum binary SDSS J173047.59+554518.5
No full textThe AM Canum Venaticorum (AM CVn) binaries are a rare group of hydrogen-deficient, ultrashort period, mass-transferring white dwarf binaries and are possible progenitors of Type Ia supernovae. We present time-resolved spectroscopy of the recently discovered AM CVn binary SDSS J173047.59+554518.5. The average spectrum shows strong double-peaked helium emission lines, as well as a variety of metal lines, including neon; this is the second detection of neon in an AM CVn binary, after the much brighter system GP Com. We detect no calcium in the accretion disc, a puzzling feature that has been noted in many of the longer period AM CVn binaries. We measure an orbital period, from the radial velocities of the emission lines, of 35.2 ± 0.2 min, confirming the ultracompact binary nature of the system. The emission lines seen in SDSS J1730 are very narrow, although double-peaked, implying a low-inclination, face-on accretion disc; using the measured velocities of the line peaks, we estimate i ≤ 11°. This low inclination makes SDSS J1730 an excellent system for the identification of emission lines
Neologistic jargon aphasia and agraphia in primary progressive aphasia
No full textThe terms 'jargon aphasia' and 'jargon agraphia' describe the production of incomprehensible language containing frequent phonological, semantic or neologistic errors in speech and writing, respectively. Here we describe two patients with primary progressive aphasia (PPA) who produced neologistic jargon either in speech or writing. We suggest that involvement of the posterior superior temporal-inferior parietal region may lead to a disconnection between stored lexical representations and language output pathways leading to aberrant activation of phonemes in neologistic jargon. Parietal lobe involvement is relatively unusual in PPA, perhaps accounting for the comparative rarity of jargon early in the course of these diseases. (C) 2008 Elsevier B.V. All rights reserved
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