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1. An augmented reality approach for ADL support in Alzheimer’s disease: a crossover trial

Author

Nina Rohrbach, Philipp Gulde, Alan Robert Armstrong, Linda Hartig, Anas Abdelrazeq, Stefan Schröder, Johanne Neuse, Timo Grimmer, Janine Diehl-Schmid, and Joachim Hermsdörfer

Subjects
ADL, Augmented reality, Alzheimer’s disease, Usability, Assistive technology, Mixed methods, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

Abstract Background Dementia of the Alzheimer’s type can impair the performance of activities of daily living and therefore severely impact independent living. Assistive technologies can support such patients when carrying out daily tasks. Methods In this crossover study, we used an augmented reality approach using a Microsoft HoloLens to support patients in a tea making task. During task execution, subjects received three-dimensional dynamic holograms of the sub-steps necessary to complete the task. Ten patients suffering from Alzheimer’s disease were tested and post-hoc semi-structured interviews were conducted to assess usability. Results The patients committed errors when executing the task with and without holographic assistance. No differences in success rates or error frequencies were observed (psuccess = .250, perrors = .887). Patients revealed prolonged trial durations (Glass’ Δ = 1.475) when wearing the augmented reality headset. A model of multiple linear regression (R2 adjusted = .958) revealed an influence of the errors in the control condition and a moderation by the errors in the experimental condition. Patients with more severe problems in the natural performance of the task showed lower increases in trial durations when wearing the HoloLens. Conclusions We assume that the application was a secondary task requesting its own resources and impairing performance on its own. The regression suggests however that the given assistance was compensating these additional costs in patients with stronger needs of support. Interview data on usability revealed an overall positive feedback towards the application although the hardware was considered uncomfortable and too large. We conclude that the approach proved feasible and the acceptability was overall high, although advances in hardware and the patient-interface are necessary to assist patients suffering from Alzheimer’s disease in daily activities. Trial registration DRKS, DRKS00014870. Registered 11 June 2018 - Retrospectively registered, TrialID = DRKS00014870.

Published
2019
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2. Aberrant Collagenase Expression in Chronic Idiopathic Myelofibrosis Is Related to the Stage of Disease but Not to the JAK2 Mutation Status

Author

Kais Hussein, Johanne Neuse, Oliver Bock, Thomas Buhr, Guntram Buesche, Kai Brakensiek, Birgitt Wiese, and Hans Kreipe

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Bone Marrow Cells, Matrix metalloproteinase, Pathology and Forensic Medicine, Fibrosis, Proto-Oncogene Proteins, medicine, Humans, Collagenases, RNA, Messenger, Myelofibrosis, Aged, Aged, 80 and over, Janus kinase 2, biology, Neutrophil collagenase, Endothelial Cells, Tissue Inhibitor of Metalloproteinases, Janus Kinase 2, Middle Aged, Protein-Tyrosine Kinases, medicine.disease, Matrix Metalloproteinases, Hematopoiesis, Up-Regulation, Haematopoiesis, Protein Transport, Primary Myelofibrosis, Mutation, Collagenase, biology.protein, Disease Progression, Interstitial collagenase, Female, Megakaryocytes, medicine.drug, Regular Articles
Abstract

Bone marrow fibrosis in chronic idiopathic myelofibrosis (cIMF) most likely represents an imbalance between synthesis and turnover of collagen fibers. Because the JAK-STAT signaling pathway is involved in the regulation of genes encoding matrix metalloproteinases (MMPs), we examined the expression of MMPs, their tissue inhibitors (TIMPs), and collagen types in relation to the JAK2 status (V617F mutation versus wild-type) in cIMF (n = 64). Whereas no correlation was found between the JAK2 status and MMP gene products, there was an evident association with the stage of disease. Membrane type 1-MMP (MMP-14) was overexpressed by up to 80-fold in advanced stages that progressed to fibrosis (P < 0.001), and megakaryocytes and endothelial cells were unmasked as the major cellular source. By contrast, a significantly higher expression of neutrophil collagenase (MMP-8) was encountered in the prefibrotic stages of cIMF (P < 0.001). Altogether, the stepwise progress of myelofibrosis in cIMF was associated with expression of a defined subset of target genes as shown in sequential trephine biopsies of cIMF patients. We conclude that the expression of matrix-modeling genes in cIMF is not influenced by the JAK2 mutation status but is predominantly related to the stage of disease.

Published
2006

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