Automated Semmes Weinstein monofilament examination replication using optical imaging and mechanical probe assembly

The World Health Organization reports more than 135 million people globally suffer from diabetes, with 25% developing peripheral neuropathy and estimates the numbers living with diabetes will reach over 300 million by 2025. Peripheral neuropathy is a term used to describe the loss of feeling in the peripheral limbs. If not properly managed, amputation of the lower limbs can be the result. Regular screening is required for this condition so as to avoid further deterioration. This paper describes an automated peripheral neuropathy testing device replicating the widely accepted Semmes Weinstein Monofilament Examination. In this paper a patient’s foot is scanned optically and the subsequent image processing and grid information algorithms presented reliably identify the plantar surface sensory neuropathy pressure points on a given patient’s foot. Then, these coordinates are relayed to an automated mechanical probe driven by a microcontroller where it randomly applies the accepted 98mN (10g) of force to those pressure points

Functional and Skeletal Muscle Impairments In Progressive Diabetic CKD

1-in-3 persons with type 2 diabetes (T2DM) develop chronic kidney disease (CKD), which is characterized by progressive renal dysfunction leading to end-stage renal disease. In response to elevated blood glucose and systemic inflammation of diabetes, a process of active thickening of the renal glomerular basement membrane ensues with concomitant damage to the structural supports (podocytes) of the kidneyճ filtration barrier. This results in impaired renal filtration. The metabolic sequelea of T2DM and CKD also, synergistically, alter skeletal muscleճ degradative pathways, satellite cell function (muscle reparative cells), and mitochondrial health (muscle energetic machinery) -- resulting in muscle breakdown, poor muscle quality, and exercise intolerance, and immobility that exacerbates CKD. The temporal nature and extent of these changes in CKD, however, remains unknown. With mandates from the Center for Disease Control (CDC) urging avenues of treatment that impede the progression of CKD, it is critical now, more than ever, to gain a better understanding of the factors that contribute to disease progression. This will inform more effective targeted interventions. We therefore aim to determine how renal dysfunction dictates the activity of muscle degredative pathways, the status of muscle reparative cells, and the energetic production of muscle, to ultimately influence muscle quality, performance and physical mobility. This will be determined across stages of CKD. In chapter 1, we examine how CKD progression in T2DM, impacts muscle performance and physical function. Our results suggest that muscle performance of the lower extremity, particularly the quadriceps, and physical function decline in-parallel with progression of CKD in T2DM, with these declines becoming clinically evident in stage 3. Moreover, we find that CKD-stage, and renal filtration/function (eGFR) are both significant predictors of overall physical function, with increasing CKD stage/worsening kidney filtration predicting worse functional mobility. In chapter 2, we examine the CKD-stage specific functional status of skeletal muscle mitochondrial ATP production, and electron transport chain kinetics, as these are critical cellular processes to fuel muscle cross-bridge cycling, contraction and movement. We find that intrinsic skeletal muscle mitochondrial electron transport chain function is reduced with progression of CKD, with significant reductions in ATP-production capacity emerging as early as stage 3 CKD. Moreover, these changes may derive from transcriptome-level alterations in gene networks governing muscle mitochondrial health and function. In Chapter 3, we examine muscle regenerative and maintenance capacity in relationship to CKD progression. We find the muscle-resident satellite cell pool to decline significantly with CKD progression, and exhibit impaired myogenic capacity with altered gene activation patterns, that relate strongly to findings of poor muscle quality with progressive CKD stage. Using transcriptomics, we report significant dowregulation in gene networks that influence muscle SC behavior and myogenesis. Overall, our data suggests that the progression of diabetes-induced chronic kidney disease, is paralleled by impairments in skeletal muscle ATP-producing capacity, and these energetic deficits are accompanied by CKD-associated reductions in muscle SC abundance, and reparative function. Both changes perhaps stem from alterations in gene pathway expression that is imparted by the altered uremic environment. These impairments may promote the development of poor muscle quality and performance that ultimately impairs functional capacity, even in middle-stage CKD

Abstracts on Radio Direction Finding (1899 - 1995)

The files on this record represent the various databases that originally composed the CD-ROM issue of "Abstracts on Radio Direction Finding" database, which is now part of the Dudley Knox Library's Abstracts and Selected Full Text Documents on Radio Direction Finding (1899 - 1995) Collection. (See Calhoun record https://calhoun.nps.edu/handle/10945/57364 for further information on this collection and the bibliography). Due to issues of technological obsolescence preventing current and future audiences from accessing the bibliography, DKL exported and converted into the three files on this record the various databases contained in the CD-ROM. The contents of these files are: 1) RDFA_CompleteBibliography_xls.zip [RDFA_CompleteBibliography.xls: Metadata for the complete bibliography, in Excel 97-2003 Workbook format; RDFA_Glossary.xls: Glossary of terms, in Excel 97-2003 Workbookformat; RDFA_Biographies.xls: Biographies of leading figures, in Excel 97-2003 Workbook format]; 2) RDFA_CompleteBibliography_csv.zip [RDFA_CompleteBibliography.TXT: Metadata for the complete bibliography, in CSV format; RDFA_Glossary.TXT: Glossary of terms, in CSV format; RDFA_Biographies.TXT: Biographies of leading figures, in CSV format]; 3) RDFA_CompleteBibliography.pdf: A human readable display of the bibliographic data, as a means of double-checking any possible deviations due to conversion

Mechanisms of Vascular Disease: A Reference Book for Vascular Specialists

New updated edition first published with Cambridge University Press. This new edition includes 29 chapters on topics as diverse as pathophysiology of atherosclerosis, vascular haemodynamics, haemostasis, thrombophilia and post-amputation pain syndromes