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University of Saskatchewan
1.
Givzad, Naseem.
Abnormal electrophysiological properties in sensory neurons from a swine model of cystic fibrosis.
Degree: 2020, University of Saskatchewan
URL: http://hdl.handle.net/10388/13009 
► Cystic fibrosis (CF) results from dysfunction of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) protein. CF has traditionally been considered a pediatric disease, but the…
(more)
▼ Cystic fibrosis (CF) results from dysfunction of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) protein. CF has traditionally been considered a pediatric disease, but the median predicted survival age in Canada is 55 years. As a result, patients are more likely to experience chronic complications of CF. One such complication is abnormal function of the peripheral nervous system, i.e., peripheral
neuropathy. Recent findings from a swine model of CF (CFTR-/-), shows these animals are born with peripheral
neuropathy. However, whether a lack of CFTR expression directly affects neuronal function remains to be explored. We hypothesize that the lack of functional CFTR in sensory neurons leads to electrophysiological abnormalities that contribute to the pathology of CF. We propose that malfunction in dorsal root ganglion (DRG) neurons innervating the GI tract contributes to gut-related complications. Using patch clamp electrophysiology, we found that DRG neurons from CFTR-/- (CF) swine had reduced generation of action potentials, compared to wild-type (WT) swine. Additionally, we observed a reduced percentage of neurons with T-type calcium currents in the CF swine, with respect to WT at postnatal day 7. Furthermore, our study showed that DRG neurons from CF swine, which displayed T-type calcium currents, had abnormal activation (G/Gmax) and inactivation () kinetics. Moreover, DRG neurons from CF swine showed a reduction in capsaicin-evoked currents with respect to WT, at both postnatal day 0 and 7. Taken together our data indicate that lack of CFTR expression in sensory neurons is linked to a depression of sensory function in DRG neurons in the first week postnatal. Our data strongly suggest that in
addition to the effects of CF in epithelial cells, impairments in sensory neurons may contribute to the pathology of CF.
Advisors/Committee Members: Campanucci, Veronica, Ianowski, Juan, Howland, John, Verge, Valerie, Mckinney, Martha.
Subjects/Keywords: cystic fibrosis; neuropathy
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APA (6th Edition):
Givzad, N. (2020). Abnormal electrophysiological properties in sensory neurons from a swine model of cystic fibrosis. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/13009
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Givzad, Naseem. “Abnormal electrophysiological properties in sensory neurons from a swine model of cystic fibrosis.” 2020. Thesis, University of Saskatchewan. Accessed March 09, 2021.
http://hdl.handle.net/10388/13009.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Givzad, Naseem. “Abnormal electrophysiological properties in sensory neurons from a swine model of cystic fibrosis.” 2020. Web. 09 Mar 2021.
Vancouver:
Givzad N. Abnormal electrophysiological properties in sensory neurons from a swine model of cystic fibrosis. [Internet] [Thesis]. University of Saskatchewan; 2020. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/10388/13009.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Givzad N. Abnormal electrophysiological properties in sensory neurons from a swine model of cystic fibrosis. [Thesis]. University of Saskatchewan; 2020. Available from: http://hdl.handle.net/10388/13009
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Illinois – Chicago
2.
Marangoni, Maria N.
Mechanism of Fast Axonal Transport Deficits in Diabetic Neuropathies.
Degree: 2012, University of Illinois – Chicago
URL: http://hdl.handle.net/10027/8642
► Diabetic neuropathy (DN) is one of the most common long-term complications of diabetes mellitus (DM) with no available therapies due to the lack of understanding…
(more)
▼ Diabetic
neuropathy (DN) is one of the most common long-term complications of diabetes mellitus (DM) with no available therapies due to the lack of understanding of pathogenic mechanisms for the disease. Impaired fast axonal transport (FAT) represents a candidate mechanism, but the molecular basis for transport changes in DN has never been explored. This work is the first report to describe a molecular mechanism for FAT deficits in DN.
The streptozotocin (STZ) model for induction of type 1 DM was optimized in the Fischer 344 rat strain. Behavioral, physiological and biochemical measurements were used to characterize development of DN. Putative mechanisms for FAT deficits were evaluated by measuring the activation state of kinases pertinent to FAT regulation and kinesin binding to microtubules (MT) in DM nerves.
This model developed sustained hyperglycemia typical of DM state. Moreover, this model consistently developed insensate
neuropathy co-presenting with cardiovascular autonomic
neuropathy in contrast to other DN animal models. Furthermore, this is the first report to elucidate a pattern of kinase activation relevant to FAT regulation consistent with deficient insulin signaling in both sciatic and vagus nerves. Further, STZ diabetic rats exhibited decreased kinesin binding to microtubules consistent with FAT deficits in DN.
Advisors/Committee Members: Piano, Mariann R. (advisor), Brady, Scott T. (committee member), LaDu, Mary J. (committee member), Unterman, Terry G. (committee member), Soliven, Betty (committee member).
Subjects/Keywords: diabetic neuropathy; axonal transport; kinases; sensory neuropathy; cardiovascular autonomic neuropathy; Fischer 344
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APA (6th Edition):
Marangoni, M. N. (2012). Mechanism of Fast Axonal Transport Deficits in Diabetic Neuropathies. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/8642
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Marangoni, Maria N. “Mechanism of Fast Axonal Transport Deficits in Diabetic Neuropathies.” 2012. Thesis, University of Illinois – Chicago. Accessed March 09, 2021.
http://hdl.handle.net/10027/8642.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Marangoni, Maria N. “Mechanism of Fast Axonal Transport Deficits in Diabetic Neuropathies.” 2012. Web. 09 Mar 2021.
Vancouver:
Marangoni MN. Mechanism of Fast Axonal Transport Deficits in Diabetic Neuropathies. [Internet] [Thesis]. University of Illinois – Chicago; 2012. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/10027/8642.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Marangoni MN. Mechanism of Fast Axonal Transport Deficits in Diabetic Neuropathies. [Thesis]. University of Illinois – Chicago; 2012. Available from: http://hdl.handle.net/10027/8642
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Manchester
3.
Ferdousi, Maryam.
ASSESSMENT OF CORNEAL PATHOLOGY USING CORNEAL CONFOCAL
MICROSCOPY IN PERIPHERAL NEUROPATHIES.
Degree: 2016, University of Manchester
URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:303675
► The validity of corneal confocal microscopy (CCM) in assessing peripheral neuropathy has been studied extensively in several studies with a large cohort of subjects with…
(more)
▼ The validity of corneal confocal microscopy (CCM)
in assessing peripheral
neuropathy has been studied extensively in
several studies with a large cohort of subjects with diabetes and
in a handful of studies with small sample sizes in subjects with
other systemic conditions. The non-invasive nature of this
technique as well as its high reproducibility, moderate to high
sensitivity and specificity, and ease of use make it an ideal
biomarker for diagnosing onset, severity and progression of
peripheral
neuropathy. This thesis aims to further investigate the
potential of CCM by evaluating abnormalities in the corneal
sub-basal nerve plexus, Langerhans Cells (LCs) and epithelial cells
in
neuropathy related to diabetes and cancer. This thesis has
established that evaluating the sub-basal nerve plexus in the
centre and at the inferior whorl increases the diagnostic
performance of CCM. In addition to diagnosing clinical and
subclinical
neuropathy in children and adults with diabetes CCM can
also identify sub-clinical nerve damage in patients with upper
gastrointestinal cancer and assess the effects of chemotherapy. CCM
also identifies differences in small fibre pathology between
diabetic patients with and without painful
neuropathy. Although
there was an increased prevalence and severity of dry eye and LCs’
density, this was not related to an abnormality of corneal nerves
in diabetic patients with no or mild
neuropathy. Epithelial cell
morphology was not associated with corneal nerve damage and did not
alter in patients with Type 1 diabetes. In conclusion, CCM has been
shown to be an ideal marker for quantifying early small fibre
pathology and assessing peripheral neuropathies.
Advisors/Committee Members: MALIK, RAYAZ RA, TAVAKOLI, MITRA M, Boulton, Andrew, Malik, Rayaz, Tavakoli, Mitra.
Subjects/Keywords: Corneal Confocal Microscopy; Peripheral neuropathy
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APA (6th Edition):
Ferdousi, M. (2016). ASSESSMENT OF CORNEAL PATHOLOGY USING CORNEAL CONFOCAL
MICROSCOPY IN PERIPHERAL NEUROPATHIES. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:303675
Chicago Manual of Style (16th Edition):
Ferdousi, Maryam. “ASSESSMENT OF CORNEAL PATHOLOGY USING CORNEAL CONFOCAL
MICROSCOPY IN PERIPHERAL NEUROPATHIES.” 2016. Doctoral Dissertation, University of Manchester. Accessed March 09, 2021.
http://www.manchester.ac.uk/escholar/uk-ac-man-scw:303675.
MLA Handbook (7th Edition):
Ferdousi, Maryam. “ASSESSMENT OF CORNEAL PATHOLOGY USING CORNEAL CONFOCAL
MICROSCOPY IN PERIPHERAL NEUROPATHIES.” 2016. Web. 09 Mar 2021.
Vancouver:
Ferdousi M. ASSESSMENT OF CORNEAL PATHOLOGY USING CORNEAL CONFOCAL
MICROSCOPY IN PERIPHERAL NEUROPATHIES. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Mar 09].
Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:303675.
Council of Science Editors:
Ferdousi M. ASSESSMENT OF CORNEAL PATHOLOGY USING CORNEAL CONFOCAL
MICROSCOPY IN PERIPHERAL NEUROPATHIES. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:303675
University of Manchester
4.
Azmi, Shazli.
LONGITUDINAL STUDIES IN METABOLIC NEUROPATHIES:
DEVELOPMENT OF IMAGING BIOMARKERS.
Degree: 2017, University of Manchester
URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:308004
► Corneal Confocal Microscopy (CCM) is a non-invasive imaging technique to quantify small nerve fibre structure in patients with diabetic somatic and autonomic neuropathy and increasingly…
(more)
▼ Corneal Confocal Microscopy (CCM) is a non-invasive
imaging technique to quantify small nerve fibre structure in
patients with diabetic somatic and autonomic
neuropathy and
increasingly other metabolic, hereditary, toxic and inflammatory
peripheral neuropathies.This thesis establishes that CCM is indeed
a powerful imaging technique which can identify early small fibre
degeneration and regeneration in relation to the clinical phenotype
of subjects with obesity, impaired glucose tolerance and Type1/2
diabetes.We demonstrate a precise relationship between small fibre
neuropathy and erectile dysfunction in subjects with Type 1
diabetes. We also demonstrate the utility of CCM in demonstrating
relative protection from small fibre damage in Type 1 patients with
extreme duration diabetes (medallists) at baseline and over 3 years
and repair in patients undergoing simultaneous pancreas and kidney
transplantation.This thesis provides further evidence for the
utility of CCM as a marker of early small fibre
neuropathy by
demonstrating nerve damage in subjects with morbid obesity with and
without diabetes and explore the mechanisms underlying nerve damage
at baseline and repair following bariatric surgery.We also show
that CCM can track dynamic changes in small fibre degeneration and
regeneration in subjects with impaired glucose tolerance in
relation to change in glucose tolerance status and following
continuous subcutaneous insulin infusion in subjects with Type 1
diabetes.
Advisors/Committee Members: MALIK, RAYAZ RA, Jeziorska, Maria, Malik, Rayaz.
Subjects/Keywords: Neuropathy; Diabetes Mellitus; Obesity
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APA (6th Edition):
Azmi, S. (2017). LONGITUDINAL STUDIES IN METABOLIC NEUROPATHIES:
DEVELOPMENT OF IMAGING BIOMARKERS. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:308004
Chicago Manual of Style (16th Edition):
Azmi, Shazli. “LONGITUDINAL STUDIES IN METABOLIC NEUROPATHIES:
DEVELOPMENT OF IMAGING BIOMARKERS.” 2017. Doctoral Dissertation, University of Manchester. Accessed March 09, 2021.
http://www.manchester.ac.uk/escholar/uk-ac-man-scw:308004.
MLA Handbook (7th Edition):
Azmi, Shazli. “LONGITUDINAL STUDIES IN METABOLIC NEUROPATHIES:
DEVELOPMENT OF IMAGING BIOMARKERS.” 2017. Web. 09 Mar 2021.
Vancouver:
Azmi S. LONGITUDINAL STUDIES IN METABOLIC NEUROPATHIES:
DEVELOPMENT OF IMAGING BIOMARKERS. [Internet] [Doctoral dissertation]. University of Manchester; 2017. [cited 2021 Mar 09].
Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:308004.
Council of Science Editors:
Azmi S. LONGITUDINAL STUDIES IN METABOLIC NEUROPATHIES:
DEVELOPMENT OF IMAGING BIOMARKERS. [Doctoral Dissertation]. University of Manchester; 2017. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:308004
5.
Lumbwe, Chishimba M.
Autonomic neuropathy and impotence in Zambian diabetics.
Degree: 2013, University of Zimbabwe
URL: http://dspace.unza.zm/handle/123456789/2014
► A Study was carried out among male diabetic subjects over a period of six months to determine the prevalences of both autonomic neuropathy and impotence…
(more)
▼ A Study was carried out among male diabetic subjects over a period of six months to determine the prevalences of both autonomic neuropathy and impotence in diabetics in Zambia. The subjects of the study group were from those diabetics attending the diabetic outpatient clinic at the University Teaching Hospital, Lusaka, Zambia, Three tests were used to diagnose autonomic neuropathy;
1.A fall in systolic blood pressure of more than 30 mmHg from supine to erect.
2.An abnormal heart rate response to standing measured on an electro cardiogram.
3.An abnormal heart rate response to deep breathing, measured on an electro cardiogram, expressed as Expiratory : Inspiratory (E:l) ratio.The normal E:l ratios had previously been determined in healthy male Zambians.Autonomic neuropathy was considered to be present if any one of the above tests were abnormal.Out of a total of forty two diabetic subjects admitted to the study fifteen (35.7%) had autonomic neuropathy; impotence was present in fourteen subjects (33.3%). The prevalence of autonomic neuropathy in impotent diabetics was 64.3%.These findings are comparable to results where. As symptomatic autonomic neuropathy carries a grave prognosis, this complication should be kept in mind and looked for in all diabetic patients.
Subjects/Keywords: Neuropathy- -Zambia; Diabetic Neuropathies
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APA (6th Edition):
Lumbwe, C. M. (2013). Autonomic neuropathy and impotence in Zambian diabetics. (Thesis). University of Zimbabwe. Retrieved from http://dspace.unza.zm/handle/123456789/2014
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Lumbwe, Chishimba M. “Autonomic neuropathy and impotence in Zambian diabetics.” 2013. Thesis, University of Zimbabwe. Accessed March 09, 2021.
http://dspace.unza.zm/handle/123456789/2014.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lumbwe, Chishimba M. “Autonomic neuropathy and impotence in Zambian diabetics.” 2013. Web. 09 Mar 2021.
Vancouver:
Lumbwe CM. Autonomic neuropathy and impotence in Zambian diabetics. [Internet] [Thesis]. University of Zimbabwe; 2013. [cited 2021 Mar 09].
Available from: http://dspace.unza.zm/handle/123456789/2014.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lumbwe CM. Autonomic neuropathy and impotence in Zambian diabetics. [Thesis]. University of Zimbabwe; 2013. Available from: http://dspace.unza.zm/handle/123456789/2014
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
6.
Davies, Ben.
Painful diabetic neuropathy : exploring management options.
Degree: PhD, 2017, University of the West of England, Bristol
URL: https://uwe-repository.worktribe.com/output/881421
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.723174
► Painful diabetic neuropathy (PDN) is one microvascular complication of diabetes mellitus (DM) and the focus of this thesis. PDN is a neuropathic pain condition characterised…
(more)
▼ Painful diabetic neuropathy (PDN) is one microvascular complication of diabetes mellitus (DM) and the focus of this thesis. PDN is a neuropathic pain condition characterised by severe burning pain in the feet and sometimes hands. It has significant impacts on peoples’ mobility, sleep quality and overall quality of life. The personal and societal burden associated with DM and PDN is predicated to rise as prevalence rates increase. Pharmacological management of PDN is often less than optimal, and people are left with few strategies to cope. Multidisciplinary pain management programmes (PMPs) use physical activity and psychological coping strategies to help people live better with persistent pain, yet people with PDN are rarely referred. It is unknown whether these strategies would be appropriate to help people live with PDN. This thesis aimed to: 1) locate and appraise all literature relating to physical activity and psychological coping strategies in PDN; 2) interview people with PDN and explore how PDN impacted on their lives; 3) explore the perspectives of patients and clinicians on the relevance of PMP approaches; and 4) explore patients’ treatment priorities and whether these might be addressed by PMP strategies. To address these aims, firstly a systematic literature review was conducted. The review identified a paucity of studies investigating physical activity or psychological coping strategies for PDN. Two interview studies were conducted, and data were analysed using thematic analysis (TA). A study with patients (n=23) found the impacts of PDN were wide ranging, people had experimented with many coping strategies unsuccessfully and there was some scepticism that PMP strategies were relevant to PDN, though few participants had direct experience of them. The second study interviewed specialist diabetes and pain clinicians and representatives from primary care (n=19). Clinicians relied primarily on medication strategies and did not have alternatives when these failed. Diabetes clinicians highlighted that people with PDN were medically complex patients and were at risk of tissue damage from too much physical activity. Pain clinicians felt PMP strategies could be adapted to suit the population with PDN. Informed by the patient interview study, an Internet survey was developed to explore the management priorities of people with PDN (n=63 respondents). Sleep disturbance was the top priority in all subgroups analysed. There were six impacts most frequently prioritised by respondents, which did not include pain. Potential clinical management strategies for these impacts have been described, and suggestions made for future research. This thesis has shown a scarcity of existing evidence for non-pharmacological strategies in the management of PDN. PMP strategies were not necessarily viewed as appropriate by patient participants. The impacts prioritized by people with PDN could however be matched to management strategies from other conditions where persistent pain is common. There is no a priori reason why these strategies…
Subjects/Keywords: 616.4; Diabetes; Neuropathy; Pain; Rehabilitation
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APA (6th Edition):
Davies, B. (2017). Painful diabetic neuropathy : exploring management options. (Doctoral Dissertation). University of the West of England, Bristol. Retrieved from https://uwe-repository.worktribe.com/output/881421 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.723174
Chicago Manual of Style (16th Edition):
Davies, Ben. “Painful diabetic neuropathy : exploring management options.” 2017. Doctoral Dissertation, University of the West of England, Bristol. Accessed March 09, 2021.
https://uwe-repository.worktribe.com/output/881421 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.723174.
MLA Handbook (7th Edition):
Davies, Ben. “Painful diabetic neuropathy : exploring management options.” 2017. Web. 09 Mar 2021.
Vancouver:
Davies B. Painful diabetic neuropathy : exploring management options. [Internet] [Doctoral dissertation]. University of the West of England, Bristol; 2017. [cited 2021 Mar 09].
Available from: https://uwe-repository.worktribe.com/output/881421 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.723174.
Council of Science Editors:
Davies B. Painful diabetic neuropathy : exploring management options. [Doctoral Dissertation]. University of the West of England, Bristol; 2017. Available from: https://uwe-repository.worktribe.com/output/881421 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.723174
Colorado State University
7.
Scott, Ernie.
Long term stability of sensation thresholds from 10 millisecond pulses of 2.01 micrometer laser light.
Degree: MS(M.S.), Environmental and Radiological Health Sciences, 2013, Colorado State University
URL: http://hdl.handle.net/10217/80309
► Current methods for diagnosing and evaluating efficacy for treatment of diabetic neuropathy either give only subjective data or are invasive. However, the use of laser…
(more)
▼ Current methods for diagnosing and evaluating efficacy for treatment of diabetic
neuropathy either give only subjective data or are invasive. However, the use of laser induced sensations to evaluate threshold sensations gives precisely quantifiable and reproducible stimulus and is 100% non-invasive. In this study we evaluated whether or not laser sensation thresholds were stable in 12 human subjects over a four month period of time. Subjects' hands and feet were exposed over eight different exposure sessions to 10 ms pulses of laser light produced by a 50 W Tm: YAG laser system. Sensation threshold values (in mJ/mm2) were determined for each session and compared by regression analysis. The results showed an upward trend in sensation thresholds over time in the majority of the
subject's hands and feet, indicating that laser sensation thresholds are not stable over time.
Subject desensitization to the sensation over time combined with too short a time between exposures, or variations in baseline skin temperature of the exposure site due to changes in weather are discussed as possible causes of the upward trend. Finally, suggestions are made for future studies to include a study over a longer period of time with more time between exposure sessions and more subjects as well as a study where the exposure sites are heated/cooled to a standardized baseline temperature prior to each exposure session.
Advisors/Committee Members: Johnson, Thomas (advisor), Brandl, Alex (committee member), Walrond, John (committee member).
Subjects/Keywords: laser; thresholds; sensation; neuropathy
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APA ·
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Manager
APA (6th Edition):
Scott, E. (2013). Long term stability of sensation thresholds from 10 millisecond pulses of 2.01 micrometer laser light. (Masters Thesis). Colorado State University. Retrieved from http://hdl.handle.net/10217/80309
Chicago Manual of Style (16th Edition):
Scott, Ernie. “Long term stability of sensation thresholds from 10 millisecond pulses of 2.01 micrometer laser light.” 2013. Masters Thesis, Colorado State University. Accessed March 09, 2021.
http://hdl.handle.net/10217/80309.
MLA Handbook (7th Edition):
Scott, Ernie. “Long term stability of sensation thresholds from 10 millisecond pulses of 2.01 micrometer laser light.” 2013. Web. 09 Mar 2021.
Vancouver:
Scott E. Long term stability of sensation thresholds from 10 millisecond pulses of 2.01 micrometer laser light. [Internet] [Masters thesis]. Colorado State University; 2013. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/10217/80309.
Council of Science Editors:
Scott E. Long term stability of sensation thresholds from 10 millisecond pulses of 2.01 micrometer laser light. [Masters Thesis]. Colorado State University; 2013. Available from: http://hdl.handle.net/10217/80309
University of Manitoba
8.
Habash, Tarek.
Interleukin-17A (IL-17A) enhances axonal regeneration and mitochondrial function of normal and diabetic sensory neurons.
Degree: Pharmacology and Therapeutics, 2014, University of Manitoba
URL: http://hdl.handle.net/1993/23900
► Rationale and hypothesis: Diabetic neuropathy involves dying back of nerve endings that reflects impairment in axonal plasticity and regenerative nerve growth. Metabolic changes in diabetes…
(more)
▼ Rationale and hypothesis: Diabetic
neuropathy involves dying back of nerve endings that reflects impairment in axonal plasticity and regenerative nerve growth. Metabolic changes in diabetes can lead to a dysregulation of hormonal mediators, such as cytokines. Thus I studied the effect of interleukin-17A (IL-17A), a proinflammatory cytokine produced by T-cells, on the phenotype of sensory neurons derived from control or diabetic rats. I hypothesized that IL-17A induces neurite outgrowth in sensory neurons through signaling pathways that enhance mitochondrial function. IL-17A can also reverse impaired nerve regeneration associated with diabetes
Objectives: Determine the ability of IL-17A to enhance neurite outgrowth in cultured sensory neurons. Investigate the signalling pathways activated by IL-17A and mechanistically link to neurite outgrowth. Study the ability of IL-17A to improve mitochondrial function of sensory neurons (since axon outgrowth consumes high levels of ATP).
Methodology: Cultured adult dorsal root ganglia (DRG) sensory neurons derived from age matched control or streptozotocin (STZ)-induced type 1 diabetic rats were fixed and stained for fluorescent imaging to determine total neurite outgrowth. Western blotting determined the levels of MAPK and PI-3K activation by IL-17A and for measuring levels of proteins of mitochondrial oxidative phosphorylation pathway. Mitochondrial bioenergetic function was tested in cultured DRG neurons using the Seahorse XF Analyzer.
Results: I found that IL-17A (10 ng/ml; P<0.05) significantly increased total neurite outgrowth in cultures derived from both control and STZ-diabetic rat models. This enhancement was mediated by IL-17A-dependent activation of MAPK and PI-3K pathways with maximal effect at 15 minutes (P<0.05). Pharmacological blockade of one of these activated pathways led to total inhibition of neurite outgrowth. IL-17A improved mitochondrial bioenergetic function of sensory neurons. Bioenergetics function was associated with augmented expression of proteins of mitochondrial oxidative phosphorylation.
Conclusion: IL-17A enhanced axonal plasticity through activation of MAPK and PI-3K pathways and was associated with augmented mitochondrial bioenergetics function in sensory neurons
Advisors/Committee Members: Fernyhough, Paul (Pharmacology and Therapeutics) (supervisor), Albensi, Benedict (Pharmacology and Therapeutics) Czubryt, Michael (Physiology) (examiningcommittee).
Subjects/Keywords: Diabetes; Neuropathy; Sensory; Neurons; Mitochondria
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APA (6th Edition):
Habash, T. (2014). Interleukin-17A (IL-17A) enhances axonal regeneration and mitochondrial function of normal and diabetic sensory neurons. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/23900
Chicago Manual of Style (16th Edition):
Habash, Tarek. “Interleukin-17A (IL-17A) enhances axonal regeneration and mitochondrial function of normal and diabetic sensory neurons.” 2014. Masters Thesis, University of Manitoba. Accessed March 09, 2021.
http://hdl.handle.net/1993/23900.
MLA Handbook (7th Edition):
Habash, Tarek. “Interleukin-17A (IL-17A) enhances axonal regeneration and mitochondrial function of normal and diabetic sensory neurons.” 2014. Web. 09 Mar 2021.
Vancouver:
Habash T. Interleukin-17A (IL-17A) enhances axonal regeneration and mitochondrial function of normal and diabetic sensory neurons. [Internet] [Masters thesis]. University of Manitoba; 2014. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/1993/23900.
Council of Science Editors:
Habash T. Interleukin-17A (IL-17A) enhances axonal regeneration and mitochondrial function of normal and diabetic sensory neurons. [Masters Thesis]. University of Manitoba; 2014. Available from: http://hdl.handle.net/1993/23900
9.
Azmi, Shazli.
Longitudinal studies in metabolic neuropathies : development of imaging biomarkers.
Degree: PhD, 2017, University of Manchester
URL: https://www.research.manchester.ac.uk/portal/en/theses/longitudinal-studies-in-metabolic-neuropathies-development-of-imaging-biomarkers(6913e957-0e81-4af8-a544-f943f0105b8c).html
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.713593
► Corneal Confocal Microscopy (CCM) is a non-invasive imaging technique to quantify small nerve fibre structure in patients with diabetic somatic and autonomic neuropathy and increasingly…
(more)
▼ Corneal Confocal Microscopy (CCM) is a non-invasive imaging technique to quantify small nerve fibre structure in patients with diabetic somatic and autonomic neuropathy and increasingly other metabolic, hereditary, toxic and inflammatory peripheral neuropathies. This thesis establishes that CCM is indeed a powerful imaging technique which can identify early small fibre degeneration and regeneration in relation to the clinical phenotype of subjects with obesity, impaired glucose tolerance and Type1/2 diabetes. We demonstrate a precise relationship between small fibre neuropathy and erectile dysfunction in subjects with Type 1 diabetes. We also demonstrate the utility of CCM in demonstrating relative protection from small fibre damage in Type 1 patients with extreme duration diabetes (medallists) at baseline and over 3 years and repair in patients undergoing simultaneous pancreas and kidney transplantation. This thesis provides further evidence for the utility of CCM as a marker of early small fibre neuropathy by demonstrating nerve damage in subjects with morbid obesity with and without diabetes and explore the mechanisms underlying nerve damage at baseline and repair following bariatric surgery. We also show that CCM can track dynamic changes in small fibre degeneration and regeneration in subjects with impaired glucose tolerance in relation to change in glucose tolerance status and following continuous subcutaneous insulin infusion in subjects with Type 1 diabetes.
Subjects/Keywords: 616.4; Diabetes Mellitus; Neuropathy; Obesity
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APA (6th Edition):
Azmi, S. (2017). Longitudinal studies in metabolic neuropathies : development of imaging biomarkers. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/longitudinal-studies-in-metabolic-neuropathies-development-of-imaging-biomarkers(6913e957-0e81-4af8-a544-f943f0105b8c).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.713593
Chicago Manual of Style (16th Edition):
Azmi, Shazli. “Longitudinal studies in metabolic neuropathies : development of imaging biomarkers.” 2017. Doctoral Dissertation, University of Manchester. Accessed March 09, 2021.
https://www.research.manchester.ac.uk/portal/en/theses/longitudinal-studies-in-metabolic-neuropathies-development-of-imaging-biomarkers(6913e957-0e81-4af8-a544-f943f0105b8c).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.713593.
MLA Handbook (7th Edition):
Azmi, Shazli. “Longitudinal studies in metabolic neuropathies : development of imaging biomarkers.” 2017. Web. 09 Mar 2021.
Vancouver:
Azmi S. Longitudinal studies in metabolic neuropathies : development of imaging biomarkers. [Internet] [Doctoral dissertation]. University of Manchester; 2017. [cited 2021 Mar 09].
Available from: https://www.research.manchester.ac.uk/portal/en/theses/longitudinal-studies-in-metabolic-neuropathies-development-of-imaging-biomarkers(6913e957-0e81-4af8-a544-f943f0105b8c).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.713593.
Council of Science Editors:
Azmi S. Longitudinal studies in metabolic neuropathies : development of imaging biomarkers. [Doctoral Dissertation]. University of Manchester; 2017. Available from: https://www.research.manchester.ac.uk/portal/en/theses/longitudinal-studies-in-metabolic-neuropathies-development-of-imaging-biomarkers(6913e957-0e81-4af8-a544-f943f0105b8c).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.713593
10.
Harris, Hannah Marie.
Cannabinoid Modulation Of Cisplatin Induced Neuropathy.
Degree: MA, Psychology, 2015, University of Mississippi
URL: https://egrove.olemiss.edu/etd/1142
► Endocannabinoid modulation of cancer-related pain is well-documented. Sativex, a cannabinoid extract with a 1:1 ratio of tetrahydrocannabinol (thc) and cannabidiol (cbd) has been shown to…
(more)
▼ Endocannabinoid modulation of cancer-related pain is well-documented. Sativex, a cannabinoid extract with a 1:1 ratio of tetrahydrocannabinol (thc) and cannabidiol (cbd) has been shown to alleviate neuropathic pain associated with chemotherapy. This research examined whether thc or cbd alone is effective in attenuating or preventing tactile allodynia associated with cisplatin-administration. Mice (c57bl/6) were given eight doses of 2.3 mg/kg cisplatin or saline solution ip every second day to induce tactile allodynia (ringers on alternate days). Tactile responses to hind-paws were quantified in g of force using an electric von frey (evf) prior to (baseline) and after the cisplatin administration protocol. Separate groups of mice were then given vehicle, 100 mg/kg gabapentin, 2 mg/kg thc or 2 mg/kg cbd ip and tested 60 m later on evf. In the prevention studies, cbd (0.0, 0.5,1.0, and 2.0 mg/kg) or thc (0.0, 0.5,1.0, and 2.0 mg/kg) was given ip 30 m prior to cisplatin administration (2.3 or 1.0 mg/kg) utilizing a six-dose alternate day protocol. As before, tactile response was measured using evf prior to and after cisplatin dosings. Cisplatin produced a reduction in g of force indicative of
neuropathy in each study. Gabapentin, thc, and cbd did not alter tactile responses in control mice. Cisplatin allodynia was attenuated by gabapentin, thc, and cbd but was not prevented by either cannabinoid tested. These data demonstrate that thc and cbd administered alone, unlike that in sativex, can achieve analgesic effects in this murine model of cisplatin
neuropathy.
Advisors/Committee Members: Kenneth J. Sufka, Todd A. Smitherman, Michael T. Allen.
Subjects/Keywords: Cannabinoids; Cisplatin; Neuropathy; Biological Psychology
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APA (6th Edition):
Harris, H. M. (2015). Cannabinoid Modulation Of Cisplatin Induced Neuropathy. (Masters Thesis). University of Mississippi. Retrieved from https://egrove.olemiss.edu/etd/1142
Chicago Manual of Style (16th Edition):
Harris, Hannah Marie. “Cannabinoid Modulation Of Cisplatin Induced Neuropathy.” 2015. Masters Thesis, University of Mississippi. Accessed March 09, 2021.
https://egrove.olemiss.edu/etd/1142.
MLA Handbook (7th Edition):
Harris, Hannah Marie. “Cannabinoid Modulation Of Cisplatin Induced Neuropathy.” 2015. Web. 09 Mar 2021.
Vancouver:
Harris HM. Cannabinoid Modulation Of Cisplatin Induced Neuropathy. [Internet] [Masters thesis]. University of Mississippi; 2015. [cited 2021 Mar 09].
Available from: https://egrove.olemiss.edu/etd/1142.
Council of Science Editors:
Harris HM. Cannabinoid Modulation Of Cisplatin Induced Neuropathy. [Masters Thesis]. University of Mississippi; 2015. Available from: https://egrove.olemiss.edu/etd/1142
University of Manchester
11.
Fadavi, Hassan.
The mechanistic basis of vascular and neural dysfunction
in patients with diabetes:The role of ethnic differences.
Degree: 2014, University of Manchester
URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:241425
► The University of ManchesterAbstract of thesis submitted by Hassan Fadavi for the degree of Doctor of Philosophy and titled:The mechanistic basis of vascular and neural…
(more)
▼ The University of ManchesterAbstract of thesis
submitted by Hassan Fadavi for the degree of Doctor of Philosophy
and titled:The mechanistic basis of vascular and neural dysfunction
in patients with diabetes: The role of ethnic differencesMay
2014AbstractNeuropathy is one of the main long term complications
of diabetes affecting 30-50% of patients. It is the major
contributing factor for foot ulceration with a life time risk which
may be as high as 25%. Hence
neuropathy leads to reduced pain and
pressure perception, anatomic deformities and an impaired
microcirculation. More specifically, unperceived minor trauma
results in cutaneous injury which when combined with an inadequate
pressure induced vasodilator response leads to tissue breakdown and
ulceration. Once ulcers form, healing may be delayed or difficult
to achieve, particularly if infection occurs in the deeper tissues
and bone which can then lead to amputation. In the UK, South Asians
(people originating from India, Pakistan and Bangladesh) have an
excess mortality for coronary artery disease (CAD), stroke and
end-stage renal disease when compared to white Europeans. However,
it has been shown that South Asian people with type 2 diabetes in
the UK are only one third as likely to have a foot ulcer compared
with White European diabetic patients. This has been attributed to
lower levels of peripheral
neuropathy in Asians, but has not been
systematically explored in detail. In the present study, both
neurological and vascular deficits in a group of South Asian and
European patients with type II diabetes have been assessed. The
results demonstrate that: • South Asian diabetic patients have
poorer glycaemic control, but paradoxically lower triglycerides.
This finding may be relevant to the finding that they have a lower
incidence of
neuropathy, as triglycerides have been related to
neuropathy and foot ulceration. • South Asians compared to
Europeans have better small fibre function and a trend for better
structure (Intra epidermal nerve fibre density and corneal nerve
morphology) and large fibre function assessed with nerve conduction
studies. • South Asians have higher foot skin oxygenation and
hyperaemic blood flow response to heating. • South Asians have a
thicker epidermis and a trend for a better capillary density.
Therefore these alterations may protect South Asians from the
development of foot ulceration.
Advisors/Committee Members: JEZIORSKA, MARIA M, ABBOTT, CAROLINE CA, Malik, Rayaz, Jeziorska, Maria, Abbott, Caroline.
Subjects/Keywords: Diabetic neuropathy; foot ulcer; ethnicity
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Manager
APA (6th Edition):
Fadavi, H. (2014). The mechanistic basis of vascular and neural dysfunction
in patients with diabetes:The role of ethnic differences. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:241425
Chicago Manual of Style (16th Edition):
Fadavi, Hassan. “The mechanistic basis of vascular and neural dysfunction
in patients with diabetes:The role of ethnic differences.” 2014. Doctoral Dissertation, University of Manchester. Accessed March 09, 2021.
http://www.manchester.ac.uk/escholar/uk-ac-man-scw:241425.
MLA Handbook (7th Edition):
Fadavi, Hassan. “The mechanistic basis of vascular and neural dysfunction
in patients with diabetes:The role of ethnic differences.” 2014. Web. 09 Mar 2021.
Vancouver:
Fadavi H. The mechanistic basis of vascular and neural dysfunction
in patients with diabetes:The role of ethnic differences. [Internet] [Doctoral dissertation]. University of Manchester; 2014. [cited 2021 Mar 09].
Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:241425.
Council of Science Editors:
Fadavi H. The mechanistic basis of vascular and neural dysfunction
in patients with diabetes:The role of ethnic differences. [Doctoral Dissertation]. University of Manchester; 2014. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:241425
University of Sydney
12.
Boland-Freitas, Robert.
Muscle And Nerve Excitability In Myotonic Dystrophy.
Degree: 2019, University of Sydney
URL: http://hdl.handle.net/2123/21289
► Abstract: Myotonic dystrophy is the most common form of muscular dystrophy in adults. Both subtypes, Type 1 (DM1) and Type 2 (DM2), affect multiple body…
(more)
▼ Abstract: Myotonic dystrophy is the most common form of muscular dystrophy in adults. Both subtypes, Type 1 (DM1) and Type 2 (DM2), affect multiple body systems. Myotonia and muscle atrophy are common to DM1 and DM2 and contribute to morbidity. The main purpose of this thesis was to elucidate aspects of muscle and nerve function in these conditions. To do this, the neurophysiological techniques of skeletal muscle and axonal excitability assessment, in addition to quantitative sensory thermal thresholds testing were used. Given that relationships between serum electrolyte levels and muscle excitability measures have been found in disease states, in this thesis their assessment was undertaken in healthy individuals. The inter-rater reliability of thermal threshold assessment was also examined, as this method was used to assess small nerve fibre function in DM1 and DM2. Significant muscle excitability differences were found between persons with advanced DM1 and healthy individuals, consistent with sodium-potassium pump dysfunction. Additionally, chloride channel dysfunction was demonstrated in both advanced DM1 and in DM2. It is concluded the technique may merit use as a disease biomarker and aid in diagnosis. Serum electrolyte concentration variation between disease groups and healthy individuals is concluded to be unlikely to account for differences observed between muscle disease and normal groups, despite significant correlations being demonstrated between some measures and ions. Increases in inward rectification, possibly reflecting neural adaptation to muscle weakness, and nodal sodium currents we found on advanced DM1 motor axon excitability. Sensory nerve excitability was not altered, though larger studies of lower limb nerves could increase sensitivity. Perception of thermal change was found to be abnormal in the upper and lower extremities in DM1, consistent with small fibre sensory neuropathy that precedes or occurs in isolation from large fibre nerve dysfunction.
Subjects/Keywords: myotonic dystrophy; muscle excitability; neuropathy.
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APA (6th Edition):
Boland-Freitas, R. (2019). Muscle And Nerve Excitability In Myotonic Dystrophy.
(Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/21289
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Boland-Freitas, Robert. “Muscle And Nerve Excitability In Myotonic Dystrophy.
” 2019. Thesis, University of Sydney. Accessed March 09, 2021.
http://hdl.handle.net/2123/21289.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Boland-Freitas, Robert. “Muscle And Nerve Excitability In Myotonic Dystrophy.
” 2019. Web. 09 Mar 2021.
Vancouver:
Boland-Freitas R. Muscle And Nerve Excitability In Myotonic Dystrophy.
[Internet] [Thesis]. University of Sydney; 2019. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/2123/21289.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Boland-Freitas R. Muscle And Nerve Excitability In Myotonic Dystrophy.
[Thesis]. University of Sydney; 2019. Available from: http://hdl.handle.net/2123/21289
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Sydney
13.
Garg, Nidhi.
Mechanisms Of Nerve Dysfunction Across The Spectrum Of Immunemediated Neuropathies
.
Degree: 2018, University of Sydney
URL: http://hdl.handle.net/2123/20260
► This thesis explores mechanisms of nerve dysfunction in the autoimmune neuropathies chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy (MMN) and the neuropathy associated with…
(more)
▼ This thesis explores mechanisms of nerve dysfunction in the autoimmune neuropathies chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy (MMN) and the neuropathy associated with IgM antibodies against myelin-associated glycoprotein (MAG). Initially, the frequency of autoantibodies to nodal and paranodal proteins was established via serum assays. The clinical and neurophysiological features of patients with neurofascin-155 IgG4 antibodies were examined. In antibody-negative patients, axonal excitability studies revealed marked differences between CIDP and MMN patients with conduction block. CIDP with block was associated with paranodal dysfunction – evidenced by the excitability profile and serum binding to paranodes in teased nerve fibres. Excitability changes in MMN suggested a reduction in ion channel density along axons, potentially due to enlargement of motor units, prompting the subsequent study aimed at assessing motor unit properties in MMN. This study confirmed striking enlargement of motor units due to reinnervation, masking severe axonal loss and highlighting that assessment of motor unit numbers and size are critical in disease monitoring. Finally, studies in patients with anti-MAG neuropathy revealed a characteristic axonal excitability profile, consistent with an increase in juxtaparanodal fast potassium channel conductance, suggesting that nerve function may be improved by blockade of fast potassium channels. In summary, this thesis has demonstrated significant differences in molecular mechanisms across the immune-mediated neuropathies and provided new insights and tools to guide treatment approaches and monitor disease progression.
Subjects/Keywords: Neuropathy;
Neurophysiology;
CIDP;
MMN;
Immunology
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APA (6th Edition):
Garg, N. (2018). Mechanisms Of Nerve Dysfunction Across The Spectrum Of Immunemediated Neuropathies
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/20260
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Garg, Nidhi. “Mechanisms Of Nerve Dysfunction Across The Spectrum Of Immunemediated Neuropathies
.” 2018. Thesis, University of Sydney. Accessed March 09, 2021.
http://hdl.handle.net/2123/20260.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Garg, Nidhi. “Mechanisms Of Nerve Dysfunction Across The Spectrum Of Immunemediated Neuropathies
.” 2018. Web. 09 Mar 2021.
Vancouver:
Garg N. Mechanisms Of Nerve Dysfunction Across The Spectrum Of Immunemediated Neuropathies
. [Internet] [Thesis]. University of Sydney; 2018. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/2123/20260.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Garg N. Mechanisms Of Nerve Dysfunction Across The Spectrum Of Immunemediated Neuropathies
. [Thesis]. University of Sydney; 2018. Available from: http://hdl.handle.net/2123/20260
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Manchester
14.
Alam, Uazman.
Vitamin D and diabetic neuropathy.
Degree: PhD, 2013, University of Manchester
URL: https://www.research.manchester.ac.uk/portal/en/theses/vitamin-d-and-diabetic-neuropathy(325ec59d-7fdd-40c3-a9d1-2db32162eb79).html
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607117
► The accurate assessment of human diabetic somatic polyneuropathy (DSPN) is important to define at risk patients, predict deterioration, and assess the efficacy of pathogenetic treatments.…
(more)
▼ The accurate assessment of human diabetic somatic polyneuropathy (DSPN) is important to define at risk patients, predict deterioration, and assess the efficacy of pathogenetic treatments. Corneal confocal microscopy (CCM) has been proposed as a surrogate endpoint for DSPN. Approximately 50% of patients with DSPN experience neuropathic pain or symptoms and the underlying reasons are not clearly elucidated. Vitamin D deficiency has been associated with diabetic complications including DSPN and diabetic retinopathy (DR). However there is a paucity of data regarding the interaction of vitamin D status with diabetic complications. This thesis shows that CCM can readily detect small fibre neuropathy prior to large fibre involvement and assess rapidly progressive nerve fibre loss prior to conventional thermal threshold testing. CCM has a superior diagnostic capabilities compared to intra-epidermal nerve fibres and correlates better with nerve conduction studies. Patients with LADA have a greater prevalence of small fibre neuropathy compared to matched patients with type 2 diabetes. Vitamin D deficiency is highly prevalent in patients with diabetes and despite relatively aggressive replacement regimens are inadequate in raising vitamin D levels in a significant proportion of patients. Vitamin D deficiency is not associated with DR but there is a strong association between painful DSPN and vitamin D insufficiency and more so with overt deficiency.
Subjects/Keywords: 616.4; Vitamin D; Diabetic Neuropathy; Painful Diabetic Neuropathy; Diabetic Retinopathy
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Manager
APA (6th Edition):
Alam, U. (2013). Vitamin D and diabetic neuropathy. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/vitamin-d-and-diabetic-neuropathy(325ec59d-7fdd-40c3-a9d1-2db32162eb79).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607117
Chicago Manual of Style (16th Edition):
Alam, Uazman. “Vitamin D and diabetic neuropathy.” 2013. Doctoral Dissertation, University of Manchester. Accessed March 09, 2021.
https://www.research.manchester.ac.uk/portal/en/theses/vitamin-d-and-diabetic-neuropathy(325ec59d-7fdd-40c3-a9d1-2db32162eb79).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607117.
MLA Handbook (7th Edition):
Alam, Uazman. “Vitamin D and diabetic neuropathy.” 2013. Web. 09 Mar 2021.
Vancouver:
Alam U. Vitamin D and diabetic neuropathy. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2021 Mar 09].
Available from: https://www.research.manchester.ac.uk/portal/en/theses/vitamin-d-and-diabetic-neuropathy(325ec59d-7fdd-40c3-a9d1-2db32162eb79).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607117.
Council of Science Editors:
Alam U. Vitamin D and diabetic neuropathy. [Doctoral Dissertation]. University of Manchester; 2013. Available from: https://www.research.manchester.ac.uk/portal/en/theses/vitamin-d-and-diabetic-neuropathy(325ec59d-7fdd-40c3-a9d1-2db32162eb79).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607117
University of Sydney
15.
Nathani, Dev.
Clinical phenotyping and neuropathological correlates of neuromuscular disease
.
Degree: University of Sydney
URL: http://hdl.handle.net/2123/21886
► Peripheral neuropathies have a significant population prevalence which is likely to increase in the future. They can impose a significant burden on the quality of…
(more)
▼ Peripheral neuropathies have a significant population prevalence which is likely to increase in the future. They can impose a significant burden on the quality of life. The use of nerve biopsy is an important diagnostic tool in the assessment of patients with neuropathies. Newer techniques have emerged; reducing the reliance on nerve biopsies to assist with diagnosis. Nonetheless, the information obtained from histopathology may still help to distinguish clinical phenotypes which in turn can potentially modify the clinical management of patients. However, no clear guidelines currently exist to assist clinicians considering nerve biopsies for their patients. During this Master’s project, a comprehensive database was created based on the analysis of clinical and pathological information derived from the medical records of patients who were referred for nerve biopsy. This neuromuscular database was analysed to study the diagnostic utility of nerve biopsies in the clinical workup of selected types of neuropathies. Patients with suspected vasculitic neuropathy were studied to determine the clinical parameters that influenced the presence of neuropathological findings supportive of a diagnosis of vasculitic neuropathy. Stepwise clinical progression, the presence of both sensory and motor features, and asymmetric or multifocal presentation best differentiated systemic and non-systemic vasculitic neuropathy from other conditions. Additionally, parameters that best differentiated systemic vasculitic neuropathy from other conditions included the presence of selected autoantibodies and elevated inflammatory markers. Nerve conduction studies (NCS) in patients with pathologically confirmed vasculitic neuropathy frequently demonstrated a pure axonal neuropathy with sensorimotor abnormalities. In contrast, a diagnostic exclusion of vasculitis was highest in patients with normal NCS, patients with upper limb dominant symptoms, and in patients with cerebrospinal fluid (CSF) pleocytosis or CSF protein above 110mg/dL. Nerve biopsies in patients with symptoms that were purely sensory or chronic and symmetric as well as patients with dominant demyelinating features on NCS were unlikely to demonstrate evidence of vasculitis. Patients with suspected paraproteinaemic neuropathy were studied to determine the clinical parameters that influenced the presence of neuropathological findings supportive of a diagnosis of paraproteinaemic neuropathy. The presence of an IgM paraprotein and absence of an IgG paraprotein best differentiated biopsy findings consistent with paraproteinaemic neuropathy from other diagnoses. Patients with an eventual clinical diagnosis of paraproteinaemic neuropathy were studied separately and it was determined that regardless of whether the nerve biopsy report suggested a diagnosis of paraproteinaemic neuropathy, there was no difference in the prevalence of changes to the management plan or to clinical outcomes. Overall, this thesis has established that in a cohort of patients referred for nerve biopsy, several clinical…
Subjects/Keywords: nerve biopsy;
vasculitic neuropathy;
paraproteinaemic neuropathy;
peripheral neuropathy
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APA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Nathani, D. (n.d.). Clinical phenotyping and neuropathological correlates of neuromuscular disease
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/21886
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Nathani, Dev. “Clinical phenotyping and neuropathological correlates of neuromuscular disease
.” Thesis, University of Sydney. Accessed March 09, 2021.
http://hdl.handle.net/2123/21886.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Nathani, Dev. “Clinical phenotyping and neuropathological correlates of neuromuscular disease
.” Web. 09 Mar 2021.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Vancouver:
Nathani D. Clinical phenotyping and neuropathological correlates of neuromuscular disease
. [Internet] [Thesis]. University of Sydney; [cited 2021 Mar 09].
Available from: http://hdl.handle.net/2123/21886.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
Council of Science Editors:
Nathani D. Clinical phenotyping and neuropathological correlates of neuromuscular disease
. [Thesis]. University of Sydney; Available from: http://hdl.handle.net/2123/21886
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
University of Utah
16.
Campbell, David Douglas.
Health effects among refrigeration repair workers exposed to fluorocarbons.
Degree: MS;, Family & Preventive Medicine;, 1983, University of Utah
URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/643/rec/569
► Refrigeration repair workers may be intermittently exposed to fluorocarbons and their thermal decomposition products. An index case of peripheral neuropathy (distal axonopathy) in a commercial…
(more)
▼ Refrigeration repair workers may be intermittently exposed to fluorocarbons and their thermal decomposition products. An index case of peripheral neuropathy (distal axonopathy) in a commercial refrigeration repairman prompted an epidemiologic investigation of the health of refrigeration repair works. No additional cases of peripheral neuropathy were identified among the 27 refrigeration repair workers studied. A reference group of 14 non-refrigeration repair workers was also studied. No differences were noted between groups for the ulnar (motor and sensory), median (motor and sensory), peroneal, sural, or tribial nerve conduction velocities. Refrigeration repair workers reported palpitation and light-headiness significantly more often than did workers in the reference group. No clinical neurologic or electroneurophysiolocig abnormalities were detected among eight refrigeration repair workers followed for a three-year period during continuous employment.
Subjects/Keywords: Neuropathy; Refigeration; Physiology
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APA (6th Edition):
Campbell, D. D. (1983). Health effects among refrigeration repair workers exposed to fluorocarbons. (Masters Thesis). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/643/rec/569
Chicago Manual of Style (16th Edition):
Campbell, David Douglas. “Health effects among refrigeration repair workers exposed to fluorocarbons.” 1983. Masters Thesis, University of Utah. Accessed March 09, 2021.
http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/643/rec/569.
MLA Handbook (7th Edition):
Campbell, David Douglas. “Health effects among refrigeration repair workers exposed to fluorocarbons.” 1983. Web. 09 Mar 2021.
Vancouver:
Campbell DD. Health effects among refrigeration repair workers exposed to fluorocarbons. [Internet] [Masters thesis]. University of Utah; 1983. [cited 2021 Mar 09].
Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/643/rec/569.
Council of Science Editors:
Campbell DD. Health effects among refrigeration repair workers exposed to fluorocarbons. [Masters Thesis]. University of Utah; 1983. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/643/rec/569
17.
Santosh Kumar.
Investigation into cellular and molecular mechanisms
underlying diabetic cardiomyopathy: role of oxidative and nitrative
stress therapeutic potential of multiple antioxidants.
Degree: 2009, University of Pune
URL: http://shodhganga.inflibnet.ac.in/handle/10603/2606
► Cardiovascular complications characterized by cardiac dysfunction are a leading cause of morbidity and mortality associated with diabetes. There are ample evidences that excess generation of…
(more)
▼ Cardiovascular complications characterized by
cardiac dysfunction are a leading cause of morbidity and mortality
associated with diabetes. There are ample evidences that excess
generation of reactive oxygen species (ROS) and reactive nitrogen
species (RNS), largely due to hyperglycemia, causes oxidative and
nitrosative stress, which further exacerbates the development and
progression of diabetic cardiomyopathy. Overproduction and/or
insufficient removal of these free radicals result in cardiac
dysfunction, damage to cellular proteins, membrane lipids and
nucleic acids. Despite overwhelming evidence on the damaging
consequences of oxidative and nitrosative stress and its role in
experimental diabetes, large scale clinical trials with classic
antioxidants failed to demonstrate any benefit for diabetic
patients with cardiovascular complications. As our understanding of
the mechanisms of free radical generation evolves, it is becoming
clear that rather than merely scavenging reactive radicals, a more
comprehensive approach aimed at preventing the generation of these
reactive species as well as scavenging may prove more beneficial.
High glucose (HG) generates reactive oxygen species (ROS) as a
result of glucose auto-oxidation. Since glucose oxidase catalyses
the oxidation of D-glucose in vitro, we exposed H9c2 cardiac
myoblast cells to high glucose (33 mM) and glucose oxidase (1.6
mU/ml) to generate ROS and/or RNS in vitro, and termed it G/GO.
Using this model, we tested the hypothesis that NAC, catalase and
GSH may exert a beneficial effect in preventing high-glucose
mediated cardiac cell apoptosis. Our invitro studies indicate that
NAC, catalase and GSH exerts a protective effect on G/GO-induced
apoptosis in H9C2 cardiac muscle cells via inhibition of ROS and
RNS generation and mitochondrial death pathways.
Abstract includes, Bibliography
p.108-147
Advisors/Committee Members: Sitasawad, Sandhya.
Subjects/Keywords: Biotechnology; Diabetes; Neuropathy; Retinopathy;
Cardiomyopathy; Insulin
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APA (6th Edition):
Kumar, S. (2009). Investigation into cellular and molecular mechanisms
underlying diabetic cardiomyopathy: role of oxidative and nitrative
stress therapeutic potential of multiple antioxidants. (Thesis). University of Pune. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/2606
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kumar, Santosh. “Investigation into cellular and molecular mechanisms
underlying diabetic cardiomyopathy: role of oxidative and nitrative
stress therapeutic potential of multiple antioxidants.” 2009. Thesis, University of Pune. Accessed March 09, 2021.
http://shodhganga.inflibnet.ac.in/handle/10603/2606.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kumar, Santosh. “Investigation into cellular and molecular mechanisms
underlying diabetic cardiomyopathy: role of oxidative and nitrative
stress therapeutic potential of multiple antioxidants.” 2009. Web. 09 Mar 2021.
Vancouver:
Kumar S. Investigation into cellular and molecular mechanisms
underlying diabetic cardiomyopathy: role of oxidative and nitrative
stress therapeutic potential of multiple antioxidants. [Internet] [Thesis]. University of Pune; 2009. [cited 2021 Mar 09].
Available from: http://shodhganga.inflibnet.ac.in/handle/10603/2606.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kumar S. Investigation into cellular and molecular mechanisms
underlying diabetic cardiomyopathy: role of oxidative and nitrative
stress therapeutic potential of multiple antioxidants. [Thesis]. University of Pune; 2009. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/2606
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Illinois – Chicago
18.
Berth, Sarah.
Mechanisms of Fast Axonal Transport Impairment by the HIV Glycoprotein gp120.
Degree: 2015, University of Illinois – Chicago
URL: http://hdl.handle.net/10027/19571
► Distal sensory polyneuropathy (DSP) is a prevalent neurological complication directly caused by human immunodeficiency virus (HIV). DSP is characterized by progressive dying-back degeneration of long…
(more)
▼ Distal sensory polyneuropathy (DSP) is a prevalent neurological complication directly caused by human immunodeficiency virus (HIV). DSP is characterized by progressive dying-back degeneration of long sensory axons at the distal extremities, which originate from dorsal root ganglion (DRG) neurons. Gp120, a neurotoxic HIV glycoprotein that is overproduced and shed by infected macrophages, has been linked to DSP. However, the role that gp120 plays in promoting degeneration of DRG axons remains uncertain. For my dissertation, I hypothesized that gp120 exerts its neurotoxic effects inside DRG neurons. My research consisted of 2 specific aims. The first was to evaluate the mechanisms of internalization and intracellular location of gp120. Using immunocytochemical and pharmacological experiments, I defined the endosomal pathway for gp120 internalization. Additional experiments using compartmentalized microfluidic chambers revealed retrograde transport of gp120 from DRG axons to their cell bodies. Since dying-back neurodegeneration has been linked to impaired fast axonal transport (FAT), I hypothesized that intracellular gp120 inhibits FAT. My second aim was to identify intra-axonal signaling pathways underlying gp120-induced alterations in fast axonal transport. Gp120 was perfused in isolated squid axoplasm, revealing axon-specific effects of gp120 on fast axonal transport (FAT). Coperfusion of gp120 with inhibitors of certain regulatory kinases and phosphatases for FAT delineated the signaling pathways that gp120 activated to impair anterograde and retrograde FAT. These results were confirmed with biochemical assays and microtubule binding assays in a mammalian cell line. The unique reliance of neurons on FAT mechanisms suggests that gp120-induced activation of phosphotransferases in the axonal compartment might represent a critical pathogenic event in DSP.
Advisors/Committee Members: Brady, Scott (advisor), Rasenick, Mark (Committee Chair), Hope, Tom (committee member), Morfini, Gerardo (committee member), Tobacman, Larry (committee member).
Subjects/Keywords: gp120; axon transport; kinesin; HIV neuropathy
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APA (6th Edition):
Berth, S. (2015). Mechanisms of Fast Axonal Transport Impairment by the HIV Glycoprotein gp120. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/19571
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Berth, Sarah. “Mechanisms of Fast Axonal Transport Impairment by the HIV Glycoprotein gp120.” 2015. Thesis, University of Illinois – Chicago. Accessed March 09, 2021.
http://hdl.handle.net/10027/19571.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Berth, Sarah. “Mechanisms of Fast Axonal Transport Impairment by the HIV Glycoprotein gp120.” 2015. Web. 09 Mar 2021.
Vancouver:
Berth S. Mechanisms of Fast Axonal Transport Impairment by the HIV Glycoprotein gp120. [Internet] [Thesis]. University of Illinois – Chicago; 2015. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/10027/19571.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Berth S. Mechanisms of Fast Axonal Transport Impairment by the HIV Glycoprotein gp120. [Thesis]. University of Illinois – Chicago; 2015. Available from: http://hdl.handle.net/10027/19571
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Otago
19.
Gould, Camilla Alice.
Nutritional Optic Neuropathy in Papua New Guinean Prisoners
.
Degree: 2012, University of Otago
URL: http://hdl.handle.net/10523/2095
► Since 2000, ophthalmologists providing clinical services in Madang, Papua New Guinea, have become aware of local adult prisoners presenting with gradual vision loss. An informal…
(more)
▼ Since 2000, ophthalmologists providing clinical services in Madang, Papua New Guinea, have become aware of local adult prisoners presenting with gradual vision loss. An informal assessment conducted in Beon Jail in 2007 indicated that at least 40 local inmates had a significant level of visual impairment. This was most commonly associated with atrophy of the optic nerves, a result of optic
neuropathy (ON) and suspected to be caused by nutritional deficiency.
A more detailed assessment of the prison population including clinical characterization of the ON, comprehensive dietary analysis and assessment of toxic risk factors was necessary to help determine disease aetiology and appropriate treatment for prisoners. In May 2010, a collaborative project between the Fred Hollows Foundation and the University of Otago was made to further investigate the occurrence of ON previously documented in Beon Prison.
All adult prisoners detained in Beon Prison (264 persons) were invited to participate in the study. Beon prison guards were also invited to participate on the basis of some shared environmental exposures with prisoners. Consenting participants were individually interviewed regarding demography, general and ocular health, diet and lifestyle. Participants underwent a vision and ocular examination as well as a physical examination performed by a team of trained health workers. A 24-hour dietary recall interview was performed on each participant and a venous blood sample was collected by venipuncture for the analysis of nutrients and other biomarkers. As an additional measure of dietary intake, samples (n=30) of prison rations were weighed and analysed for nutrient content. Finally, prison food samples were analysed for lead and cadmium content.
Consent was obtained for 158 prisoners and 17 prison guards. Due to a low female contingent in the prison, only data collected from males was analysed. ON was found to be present in the prisoner population. Of the prisoners examined (n=135), 14 had ‘definite’ or ‘likely’ ON and 30 had ‘possible’ ON. No guards had ‘definite’ or ‘likely’ ON. No cases of peripheral
neuropathy were found in participants.
The prisoner diet predominantly consisted of rice, canned corned beef, canned tuna, water-crackers, tea and water. The fruit and vegetable consumption of the prisoners was low - 66% reported to never or rarely consume fruit and vegetables whilst in prison. Nutrient intake data generated from the 24 –hour recall suggested that less than 25% of prisoners met the estimated average requirement (EAR) for vitamin A, folate, vitamin C, vitamin E, potassium and calcium. Biochemical assessment indicated that over half of the prisoners fell below the cut-offs values of deficiency for biochemical indicators of vitamin A, folate and vitamin C. An elevated plasma homocysteine concentration was also found in 79% of prisoners. Blood concentrations of α-tocopherol, thiamin, B12 and selenium predominantly fell within normal ranges (<5% below recommended cut-offs).
Both age and time…
Advisors/Committee Members: Venn, Bernard (advisor).
Subjects/Keywords: Optic Neuropathy;
Nutritional deficiency;
Folate deficiency
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CSE |
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APA (6th Edition):
Gould, C. A. (2012). Nutritional Optic Neuropathy in Papua New Guinean Prisoners
. (Masters Thesis). University of Otago. Retrieved from http://hdl.handle.net/10523/2095
Chicago Manual of Style (16th Edition):
Gould, Camilla Alice. “Nutritional Optic Neuropathy in Papua New Guinean Prisoners
.” 2012. Masters Thesis, University of Otago. Accessed March 09, 2021.
http://hdl.handle.net/10523/2095.
MLA Handbook (7th Edition):
Gould, Camilla Alice. “Nutritional Optic Neuropathy in Papua New Guinean Prisoners
.” 2012. Web. 09 Mar 2021.
Vancouver:
Gould CA. Nutritional Optic Neuropathy in Papua New Guinean Prisoners
. [Internet] [Masters thesis]. University of Otago; 2012. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/10523/2095.
Council of Science Editors:
Gould CA. Nutritional Optic Neuropathy in Papua New Guinean Prisoners
. [Masters Thesis]. University of Otago; 2012. Available from: http://hdl.handle.net/10523/2095
University of Miami
20.
Brazill, Jennifer M.
Modulating Chemotherapy-Induced Peripheral Neuropathy and Sensory Dysfunction in Drosophila.
Degree: PhD, Molecular and Cellular Pharmacology (Medicine), 2018, University of Miami
URL: https://scholarlyrepository.miami.edu/oa_dissertations/2149
► The number of individuals living beyond a cancer diagnosis continues to increase due to advances in cancer diagnosis and treatment. Unfortunately, most cancer therapies…
(more)
▼ The number of individuals living beyond a cancer diagnosis continues to increase due to advances in cancer diagnosis and treatment. Unfortunately, most cancer therapies are associated with a range of complications that can affect the course and completion of treatment as well as patient quality of life. Chemotherapy-induced peripheral
neuropathy (CIPN) is a serious side effect of many commonly used chemotherapeutic agents, including the microtubule-targeting agent paclitaxel. Sensory symptoms typically present in the distal extremities and include feelings of numbness, spontaneous pain, and abnormal or exaggerated sensitivity. Currently there are no neuroprotective or effective symptomatic treatments for CIPN. The in vivo mechanisms of CIPN are poorly understood, and the difficulty of identifying cellular drivers of sensory dysfunction in traditional preclinical models remains a challenge to therapeutic translation. In this dissertation, I optimized a model of paclitaxel-induced peripheral
neuropathy using Drosophila larvae that recapitulates aspects of chemotherapy-induced sensory dysfunction. I showed that paclitaxel disrupts the organization of microtubule associated MAP1B/Futsch and leads to aberrant stabilization of peripheral sensory dendrites, consistent with its microtubule-stabilizing activity. Importantly, this work supports emerging evidence implicating the terminal sensory endings as a specifically vulnerable site in CIPN. Using this model, I uncovered a critical role for Nmnat in maintaining the integrity and function of peripheral sensory neurons and revealed Nmnat’s therapeutic potential against diverse sensory symptoms of CIPN. These findings establish a simple, yet robust model for studying peripheral mechanisms of CIPN and provide an amenable platform for screening modulators of sensory dysfunction associated with chemotherapy.
Advisors/Committee Members: R. Grace Zhai, Fulvia Verde, Pedro Salas, Pantelis Tsoulfas, Yogesh Wairkar.
Subjects/Keywords: Nmnat; paclitaxel; chemotherapy; neuropathy; sensory; neuroprotection
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APA (6th Edition):
Brazill, J. M. (2018). Modulating Chemotherapy-Induced Peripheral Neuropathy and Sensory Dysfunction in Drosophila. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/2149
Chicago Manual of Style (16th Edition):
Brazill, Jennifer M. “Modulating Chemotherapy-Induced Peripheral Neuropathy and Sensory Dysfunction in Drosophila.” 2018. Doctoral Dissertation, University of Miami. Accessed March 09, 2021.
https://scholarlyrepository.miami.edu/oa_dissertations/2149.
MLA Handbook (7th Edition):
Brazill, Jennifer M. “Modulating Chemotherapy-Induced Peripheral Neuropathy and Sensory Dysfunction in Drosophila.” 2018. Web. 09 Mar 2021.
Vancouver:
Brazill JM. Modulating Chemotherapy-Induced Peripheral Neuropathy and Sensory Dysfunction in Drosophila. [Internet] [Doctoral dissertation]. University of Miami; 2018. [cited 2021 Mar 09].
Available from: https://scholarlyrepository.miami.edu/oa_dissertations/2149.
Council of Science Editors:
Brazill JM. Modulating Chemotherapy-Induced Peripheral Neuropathy and Sensory Dysfunction in Drosophila. [Doctoral Dissertation]. University of Miami; 2018. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/2149
Boston University
21.
Collins, Malie Kawila.
Neurogenesis in the enteric nervous system: uncovering neurogenic potential through inducible models.
Degree: MS, Medical Sciences, 2015, Boston University
URL: http://hdl.handle.net/2144/13963
► Great strides have been made with regard to neurogenesis in the enteric nervous system (ENS), rapidly following in the wake of recent revelations about the…
(more)
▼ Great strides have been made with regard to neurogenesis in the enteric nervous system (ENS), rapidly following in the wake of recent revelations about the neurogenic properties of the central nervous system (CNS). As the ENS is more exposed, highly complex, and vulnerable to a variety of developmental, acquired, and multisystemic disorders, there is a sense of urgency for studies to address the potential within the gut to restore neurons that are injured or lost. It is the intricacies of the ENS and yet unclear relationships between agonists and embryonic precursors that have made demonstrating the arrival of new neurons in mature gut difficult under steady-state conditions.
This thesis demonstrates that inducible models of a wide range of insults to the gut have yielded crucial information about ENS neurogenesis, while in vivo experimentation under steady-state conditions has proven inconsistent. Specifically, the signaling pathways of Ret and PTEN have revealed the existence of a ‘natural block’ that normally regulates neurogenesis and keeps proliferation well controlled. Furthermore, the overwhelming effects of serotonin agonism on neuron density in response to injury have uncovered an essential role of neuronal transdifferentiation by enteric glial cells that extends beyond what was once understood to be a largely homeostatic role. The influence of extrinsic innervation of the gut will also be explored, physiology of which is important for both the utility of gut microbiota and the role of Schwann cell progenitors in the development of the ENS.
Therefore, this thesis will outline ENS organization and function, as well as describe common pathologies that serve as the foundation upon which neurogenesis is investigated. Critical inducible models to which chemical and molecular agonists are applied will be examined in detail, as it is through these models that therapeutics and biomedical engineering can be optimized in order to correct the pathophysiology of enteric neuropathies that as of now are still treated with surgical intervention.
Subjects/Keywords: Medicine; Hirschprung's; Enteric; Gastroenterology; Glia; Neurogenesis; Neuropathy
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APA ·
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APA (6th Edition):
Collins, M. K. (2015). Neurogenesis in the enteric nervous system: uncovering neurogenic potential through inducible models. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/13963
Chicago Manual of Style (16th Edition):
Collins, Malie Kawila. “Neurogenesis in the enteric nervous system: uncovering neurogenic potential through inducible models.” 2015. Masters Thesis, Boston University. Accessed March 09, 2021.
http://hdl.handle.net/2144/13963.
MLA Handbook (7th Edition):
Collins, Malie Kawila. “Neurogenesis in the enteric nervous system: uncovering neurogenic potential through inducible models.” 2015. Web. 09 Mar 2021.
Vancouver:
Collins MK. Neurogenesis in the enteric nervous system: uncovering neurogenic potential through inducible models. [Internet] [Masters thesis]. Boston University; 2015. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/2144/13963.
Council of Science Editors:
Collins MK. Neurogenesis in the enteric nervous system: uncovering neurogenic potential through inducible models. [Masters Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/13963
Boston University
22.
Bullock, Daniel.
Evaluation of behavior in transgenic mouse models to understand human congenital pain conditions.
Degree: MS, Medical Sciences, 2018, Boston University
URL: http://hdl.handle.net/2144/31217
► BACKGROUND: Containing a brain for signal processing and decision making, and a peripheral component for sensation and response, the nervous system provides higher organisms a…
(more)
▼ BACKGROUND: Containing a brain for signal processing and decision making, and a peripheral component for sensation and response, the nervous system provides higher organisms a powerful method of interacting with their environment. The specific neurons involved in pain sensation are known as nociceptors and are the source of normal nociceptive pain signaling to prompt appropriate responses. Though acute hypersensitization can be advantageous by encouraging an organism to allow an injured area to heal, chronic pain conditions can be pathological and can markedly reduce quality of life. While a variety of genes have been associated with congenital pain conditions, two rare cases examined in this study have not had their mutated genes identified. Potassium voltage-gated channel subfamily H member 8, or KCNH8, is involved in regulating action potential production and propagation, and has not been linked with pain processing of any kind to date. Here, a male patient evaluated at Boston Children’s Hospital contains a novel single-base KCNH8 mutation and possesses an extremely low sensitivity to cold temperatures and mechanical pain, but a higher sensitivity to warmer temperatures. A separate protein, intersectin-2, or ITSN2, normally functions in clathrin-mediated endocytosis and exocytosis. A second patient at Boston Children’s Hospital expresses a previously-unseen point mutation in ITSN2 and experiences erythromelalgia, characterized by episodes of intense pain and red, swollen limbs during ambient warm temperatures. Through the use of Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9 genome editing, this study will produce these specific genetic mutations in mouse lines to explore their effects on mammalian behavior.
OBJECTIVES: This project employs two transgenic mouse models to study the behavioral phenotypes associated with rare potentially damaging mutations in KCNH8 and ITSN2 exhibited in the human patients. Through these experiments, a greater understanding of neural pain signaling and sensitivity changes can occur.
METHODS: The differences in temperature preference of KCNH8 and ITSN2 mutant mice compared to wild type mice lacking these mutations was studied using thermal plates under cold and warm conditions. Direct application of acetone and von Frey filaments to mouse paws was used to study cold and mechanical sensitivity. Further testing of stamina, anxiety, coordination, and strength were also evaluated.
RESULTS: A marked decrease in sensitivity to von Frey stimulation (p<0.01) and acetone administration (p<0.05) was observed in KCNH8 mutant mice. Thermal preference testing demonstrated a decreased preference for warmer temperatures as compared to wild type mice. In addition, anxiety levels were also observed to be slightly higher in these mutant KCNH8 mice (p<0.05). The mutant ITSN2 mice spent less time at cooler temperatures, though surprisingly they significantly preferred warmer conditions as compared to their wild type littermates. A full and partial reversal of these…
Advisors/Committee Members: Toth, Louis J. (advisor), Costigan, Michael (advisor).
Subjects/Keywords: Neurosciences; Allodynia; CRISPR; Erythromelalgia; Hyperalgesia; Mutation; Neuropathy
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APA ·
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MLA ·
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Manager
APA (6th Edition):
Bullock, D. (2018). Evaluation of behavior in transgenic mouse models to understand human congenital pain conditions. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/31217
Chicago Manual of Style (16th Edition):
Bullock, Daniel. “Evaluation of behavior in transgenic mouse models to understand human congenital pain conditions.” 2018. Masters Thesis, Boston University. Accessed March 09, 2021.
http://hdl.handle.net/2144/31217.
MLA Handbook (7th Edition):
Bullock, Daniel. “Evaluation of behavior in transgenic mouse models to understand human congenital pain conditions.” 2018. Web. 09 Mar 2021.
Vancouver:
Bullock D. Evaluation of behavior in transgenic mouse models to understand human congenital pain conditions. [Internet] [Masters thesis]. Boston University; 2018. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/2144/31217.
Council of Science Editors:
Bullock D. Evaluation of behavior in transgenic mouse models to understand human congenital pain conditions. [Masters Thesis]. Boston University; 2018. Available from: http://hdl.handle.net/2144/31217
University of Manitoba
23.
Schartner, Emily.
Mechanisms of Sirtuin-2 (SIRT2) enhancement of mitochondrial function and axon regeneration in control and diabetic adult sensory neurons.
Degree: Pharmacology and Therapeutics, 2016, University of Manitoba
URL: http://hdl.handle.net/1993/31829
► Rationale and hypothesis: Diabetic sensory neuropathy involves a distal dying-back of nerve fibers. Neuronal mitochondrial function is impaired in diabetes and Sirtuin 2 (SIRT2) is…
(more)
▼ Rationale and hypothesis: Diabetic sensory
neuropathy involves a distal dying-back of nerve fibers. Neuronal mitochondrial function is impaired in diabetes and Sirtuin 2 (SIRT2) is a sensor of redox state that regulates cellular bioenergetics. The role of SIRT2 in regulating the phenotype of adult sensory neurons derived from both control and diabetic rats or wild type and SIRT2 knockout (KO) mice was studied. It was hypothesized that sensory neurons under a hyperglycemic state would have a lowered NAD+/NADH ratio thus deactivating the SIRT2 pathway. It was further hypothesized that the down regulation of SIRT2 would diminish the activity of the AMP-activated protein kinase (AMPK) pathway resulting in mitochondrial dysfunction. This defect would contribute to distal dying-back of axons observed in diabetes.
Methodology: Type 1 diabetes was induced in rodents by streptozotocin (STZ). Adult sensory neurons derived from control or STZ-diabetic rats or control and SIRT2 knockout (KO) mice were cultured in defined media with varying doses of neurotrophic factors and D-glucose. Protein levels were determined by quantitative Western blotting and neurite outgrowth quantified by immunocytochemistry. Plasmid transfection was initiated for overexpression of SIRT2 constructs and Seahorse XF24 analyzer was utilized to measure mitochondrial function of cultured neurons.
Results: Overexpression of SIRT2 elevated total neurite outgrowth in cultures derived from control and STZ-diabetic rats. Cultures derived from SIRT2 KO mice exhibited diminished neurite outgrowth. The AMPK pathway was inhibited under high glucose treatment through activation of the polyol pathway. Pharmacological inhibition of the polyol pathway improved mitochondrial bioenergetics and neurite outgrowth in sensory neurons. Augmented expression of electron transport proteins and increased mitochondrial mass was associated with enhanced bioenergetic function.
Conclusion: SIRT2 is a key component driving mitochondrial function and axon regeneration through the activation of AMPK pathway. In diabetes this pathway is suppressed via elevated polyol pathway activity.
Advisors/Committee Members: Fernyhough, Paul (Pharmacology and Therapeutics, Physiology) (supervisor), Dolinksy, Vernon (Pharmacology and Therapeutics).
Subjects/Keywords: SIRT2; Mitochondria; Diabetic Neuropathy; Axon regeneration
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APA ·
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Manager
APA (6th Edition):
Schartner, E. (2016). Mechanisms of Sirtuin-2 (SIRT2) enhancement of mitochondrial function and axon regeneration in control and diabetic adult sensory neurons. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/31829
Chicago Manual of Style (16th Edition):
Schartner, Emily. “Mechanisms of Sirtuin-2 (SIRT2) enhancement of mitochondrial function and axon regeneration in control and diabetic adult sensory neurons.” 2016. Masters Thesis, University of Manitoba. Accessed March 09, 2021.
http://hdl.handle.net/1993/31829.
MLA Handbook (7th Edition):
Schartner, Emily. “Mechanisms of Sirtuin-2 (SIRT2) enhancement of mitochondrial function and axon regeneration in control and diabetic adult sensory neurons.” 2016. Web. 09 Mar 2021.
Vancouver:
Schartner E. Mechanisms of Sirtuin-2 (SIRT2) enhancement of mitochondrial function and axon regeneration in control and diabetic adult sensory neurons. [Internet] [Masters thesis]. University of Manitoba; 2016. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/1993/31829.
Council of Science Editors:
Schartner E. Mechanisms of Sirtuin-2 (SIRT2) enhancement of mitochondrial function and axon regeneration in control and diabetic adult sensory neurons. [Masters Thesis]. University of Manitoba; 2016. Available from: http://hdl.handle.net/1993/31829
University of Manitoba
24.
Aulston, Brent.
Secreted amyloid precursor protein alpha as a therapeutic for insulin signaling dysfunction in the nervous system.
Degree: Pharmacology and Therapeutics, 2018, University of Manitoba
URL: http://hdl.handle.net/1993/33269
► Background: The amyloid precursor protein (APP) cleavage product secreted amyloid precursor protein alpha (sAPPα) is a neurotrophic factor demonstrated to be protective to neurons. Despite…
(more)
▼ Background: The amyloid precursor protein (APP) cleavage product secreted amyloid precursor protein alpha (sAPPα) is a neurotrophic factor demonstrated to be protective to neurons. Despite evidence that sAPPα activates the insulin signaling ,the effects of sAPPα on diabetes-induced pathology are unknown.
Hypothesis: We hypothesized that sAPPα could inhibit neuronal dysfunction in an animal model of diabetes. This hypothesis was tested in 3 aims.
AIM 1: To determine if sAPPα could inhibit the development of Alzheimer’s-like pathology in diabetic brain tissue.
AIM 2: To examine if sAPPα could slow the development of diabetes-induced peripheral
neuropathy.
AIM 3: In our final aim, we examined the effects of sAPPα overexpressing neural stem cells (sAPPα-NSCs) engrafted into the hippocampi on Morris water maze (MWM) performance of healthy mice.
Results: Analysis of brain tissue from diabetic sAPPα mice revealed that sAPPα blocked the development of Alzheimer’s-like pathology in the form of aberrant tau phosphorylation. Additionally, sAPPα decreased diabetes-induced activation of the unfolded protein response (UPR), a sign that diabetic sAPPα mice maintained better overall brain health compared to diabetic controls.
We found that sAPPα slowed the development of diabetes-induced thermal hypoalgesia, an indicator of sensory
neuropathy, in our model. Cell culture experiments demonstrated that the neurotrophic effects of sAPPα in the PNS are associated with up-regulation of the neuroprotective transcription factor NFκB and increased expression of the mitochondrial antioxidant MnSOD.
In the final set of experiments, we found that hippocampal injections of sAPPα-NSCs altered Morris water maze (MWM) performance of healthy SAMR1 mice. Although future studies are required to determine the effects of sAPPα-NSCs on cognition, these preliminary results nevertheless warrant future studies investigating the therapeutic potential of sAPPα-NSCs.
Conclusion: In total, the results presented in this thesis demonstrate that sAPPα can inhibit pathology in the diabetic nervous system. Therefore, the data generated from these studies has provided a foundation for the development of sAPPα based therapeutics, potentially in the form of sAPPα-NSCs, as a treatment option for diabetes and AD.
Advisors/Committee Members: Glazner, Gordon (Pharmacology and Therapeutics) (supervisor), Albensi, Benedict (Pharmacology and Therapeutics) Hatch, Grant (Pharmacology and Therapeutics) Czubryt, Michael (Physiology and Pathophysiology) Prado, Marco (Western University) (examiningcommittee).
Subjects/Keywords: Diabetes; Alzheimer's disease; Neuropathy; Secreted APP alpha
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APA (6th Edition):
Aulston, B. (2018). Secreted amyloid precursor protein alpha as a therapeutic for insulin signaling dysfunction in the nervous system. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/33269
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Aulston, Brent. “Secreted amyloid precursor protein alpha as a therapeutic for insulin signaling dysfunction in the nervous system.” 2018. Thesis, University of Manitoba. Accessed March 09, 2021.
http://hdl.handle.net/1993/33269.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Aulston, Brent. “Secreted amyloid precursor protein alpha as a therapeutic for insulin signaling dysfunction in the nervous system.” 2018. Web. 09 Mar 2021.
Vancouver:
Aulston B. Secreted amyloid precursor protein alpha as a therapeutic for insulin signaling dysfunction in the nervous system. [Internet] [Thesis]. University of Manitoba; 2018. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/1993/33269.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Aulston B. Secreted amyloid precursor protein alpha as a therapeutic for insulin signaling dysfunction in the nervous system. [Thesis]. University of Manitoba; 2018. Available from: http://hdl.handle.net/1993/33269
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
25.
Anantharaman, Kamakshi Pradeep.
Quantitative image analysis of peripheral nerves in whiplash injury patients.
Degree: PhD, 2018, University of Sussex
URL: http://sro.sussex.ac.uk/id/eprint/74969/
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742127
► The research in this thesis has examined the use of texture and shape analysis to characterise Magnetic Resonance (MR) images of peripheral nerves in order…
(more)
▼ The research in this thesis has examined the use of texture and shape analysis to characterise Magnetic Resonance (MR) images of peripheral nerves in order to provide a potential quantitative tool for better diagnosis and treatments. Texture and shape can be considered as inherent properties of all surfaces and have the potential to provide sensitive information which cannot be quantitatively perceived by human vision. Texture analysis has been successfully used in image classification of aerial and satellite imagery and the diagnosis and prognosis of several types of cancer. However, to date, it has never been used in investigating peripheral nerve damage. In this thesis, we study the application of texture and shape analysis to the peripheral nerves in the upper extremities of patients suffering from Whiplash Associated Disorders (WAD). Specifically, quantitative texture analysis was performed on MR images of the carpal tunnel which contains the median nerve. The median nerve was studied to identify differences in textural patterns. Texture methods such as: first order features; co-occurrence matrices; run-length matrices and autocorrelation function were applied and their performance was assessed. Texture analysis was also performed to investigate nerve damage in the MR images of the brachial plexus, both in controls and patients. Further, spatial domain shape metrics were used to quantify and study the morphological differences of the median nerve in controls and patients. This highlighted that some significant differences exist between groups and thus could potentially be reliably used in combination with clinical scale metrics to identify possible nerve damage. As MR images contain noise, locating the median nerve accurately to perform image analysis is very important. Therefore, we further investigated the application of an enhanced correlation filtering method that could be trained on images of the median nerve and then applied to detect the median nerve in test images. The Optimal Trade-off Maximum Average Correlation Height (OT-MACH) filter includes the expected distortions in the target in the construction of the filter reference function. The OT-MACH filter was tuned in a bandpass to maximize the correlation peak and thereby successfully locate the position of the median nerve in the carpal tunnel. This study has successfully demonstrated that texture and shape analysis can be used to investigate possible peripheral nerve damage. Further research is required using larger datasets to establish a quantitative image analysis tool to support clinical decision making and thereby improve patient care and treatment outcome.
Subjects/Keywords: 620; RZ0399 Osteo-magnetics; neuropathy; etc.
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APA (6th Edition):
Anantharaman, K. P. (2018). Quantitative image analysis of peripheral nerves in whiplash injury patients. (Doctoral Dissertation). University of Sussex. Retrieved from http://sro.sussex.ac.uk/id/eprint/74969/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742127
Chicago Manual of Style (16th Edition):
Anantharaman, Kamakshi Pradeep. “Quantitative image analysis of peripheral nerves in whiplash injury patients.” 2018. Doctoral Dissertation, University of Sussex. Accessed March 09, 2021.
http://sro.sussex.ac.uk/id/eprint/74969/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742127.
MLA Handbook (7th Edition):
Anantharaman, Kamakshi Pradeep. “Quantitative image analysis of peripheral nerves in whiplash injury patients.” 2018. Web. 09 Mar 2021.
Vancouver:
Anantharaman KP. Quantitative image analysis of peripheral nerves in whiplash injury patients. [Internet] [Doctoral dissertation]. University of Sussex; 2018. [cited 2021 Mar 09].
Available from: http://sro.sussex.ac.uk/id/eprint/74969/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742127.
Council of Science Editors:
Anantharaman KP. Quantitative image analysis of peripheral nerves in whiplash injury patients. [Doctoral Dissertation]. University of Sussex; 2018. Available from: http://sro.sussex.ac.uk/id/eprint/74969/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742127
University of Manchester
26.
Fadavi, Hassan.
The mechanistic basis of vascular and neural dysfunction in patients with diabetes : the role of ethnic differences.
Degree: PhD, 2014, University of Manchester
URL: https://www.research.manchester.ac.uk/portal/en/theses/the-mechanistic-basis-of-vascular-and-neural-dysfunction-in-patients-with-diabetesthe-role-of-ethnic-differences(38b1ca0a-157e-406b-8c89-2f9a265fc1ab).html
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.677734
► Neuropathy is one of the main long term complications of diabetes affecting 30-50% of patients. It is the major contributing factor for foot ulceration with…
(more)
▼ Neuropathy is one of the main long term complications of diabetes affecting 30-50% of patients. It is the major contributing factor for foot ulceration with a life time risk which may be as high as 25%. Hence neuropathy leads to reduced pain and pressure perception, anatomic deformities and an impaired microcirculation. More specifically, unperceived minor trauma results in cutaneous injury which when combined with an inadequate pressure induced vasodilator response leads to tissue breakdown and ulceration. Once ulcers form, healing may be delayed or difficult to achieve, particularly if infection occurs in the deeper tissues and bone which can then lead to amputation. In the UK, South Asians (people originating from India, Pakistan and Bangladesh) have an excess mortality for coronary artery disease (CAD), stroke and end-stage renal disease when compared to white Europeans. However, it has been shown that South Asian people with type 2 diabetes in the UK are only one third as likely to have a foot ulcer compared with White European diabetic patients. This has been attributed to lower levels of peripheral neuropathy in Asians, but has not been systematically explored in detail. In the present study, both neurological and vascular deficits in a group of South Asian and European patients with type II diabetes have been assessed. The results demonstrate that: • South Asian diabetic patients have poorer glycaemic control, but paradoxically lower triglycerides. This finding may be relevant to the finding that they have a lower incidence of neuropathy, as triglycerides have been related to neuropathy and foot ulceration. • South Asians compared to Europeans have better small fibre function and a trend for better structure (Intra epidermal nerve fibre density and corneal nerve morphology) and large fibre function assessed with nerve conduction studies. • South Asians have higher foot skin oxygenation and hyperaemic blood flow response to heating. • South Asians have a thicker epidermis and a trend for a better capillary density. Therefore these alterations may protect South Asians from the development of foot ulceration.
Subjects/Keywords: 616.4; Diabetic neuropathy; foot ulcer; ethnicity
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APA (6th Edition):
Fadavi, H. (2014). The mechanistic basis of vascular and neural dysfunction in patients with diabetes : the role of ethnic differences. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/the-mechanistic-basis-of-vascular-and-neural-dysfunction-in-patients-with-diabetesthe-role-of-ethnic-differences(38b1ca0a-157e-406b-8c89-2f9a265fc1ab).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.677734
Chicago Manual of Style (16th Edition):
Fadavi, Hassan. “The mechanistic basis of vascular and neural dysfunction in patients with diabetes : the role of ethnic differences.” 2014. Doctoral Dissertation, University of Manchester. Accessed March 09, 2021.
https://www.research.manchester.ac.uk/portal/en/theses/the-mechanistic-basis-of-vascular-and-neural-dysfunction-in-patients-with-diabetesthe-role-of-ethnic-differences(38b1ca0a-157e-406b-8c89-2f9a265fc1ab).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.677734.
MLA Handbook (7th Edition):
Fadavi, Hassan. “The mechanistic basis of vascular and neural dysfunction in patients with diabetes : the role of ethnic differences.” 2014. Web. 09 Mar 2021.
Vancouver:
Fadavi H. The mechanistic basis of vascular and neural dysfunction in patients with diabetes : the role of ethnic differences. [Internet] [Doctoral dissertation]. University of Manchester; 2014. [cited 2021 Mar 09].
Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-mechanistic-basis-of-vascular-and-neural-dysfunction-in-patients-with-diabetesthe-role-of-ethnic-differences(38b1ca0a-157e-406b-8c89-2f9a265fc1ab).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.677734.
Council of Science Editors:
Fadavi H. The mechanistic basis of vascular and neural dysfunction in patients with diabetes : the role of ethnic differences. [Doctoral Dissertation]. University of Manchester; 2014. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-mechanistic-basis-of-vascular-and-neural-dysfunction-in-patients-with-diabetesthe-role-of-ethnic-differences(38b1ca0a-157e-406b-8c89-2f9a265fc1ab).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.677734
University of Manchester
27.
Petropoulos, Ioannis.
Corneal nerve pathology in diabetes.
Degree: PhD, 2013, University of Manchester
URL: https://www.research.manchester.ac.uk/portal/en/theses/corneal-nerve-pathology-in-diabetes(9912e560-1032-45cd-8f0a-0477d6605a98).html
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588113
► The accurate detection and quantification of human diabetic somatic polyneuropathy (DSPN) are important to define at risk patients, anticipate deterioration, and assess new therapies. Current…
(more)
▼ The accurate detection and quantification of human diabetic somatic polyneuropathy (DSPN) are important to define at risk patients, anticipate deterioration, and assess new therapies. Current methods lack sensitivity, require expert assessment and have major shortcomings when employed to define therapeutic efficacy. In recent years, in vivo corneal confocal microscopy (IVCCM) has shown potential as a surrogate endpoint for DSPN.This study aims to investigate fundamental aspects of IVCCM such as repeatability and optimal scanning methodology and establish changes in corneal nerve morphology in relation to the severity of DSPN and regeneration in response to normalisation of hyperglycaemia. Furthermore, it aims to provide a novel fully automated image analysis algorithm for the quantification of corneal nerve morphology and establish the diagnostic ability of CCM.IVCCM shows high repeatability which is enhanced with more experienced observers. Central corneal innervation is comparable to adjacent peripheral innervation in mild diabetic neuropathy but the central cornea may be more sensitive to change. Corneal nerve loss is symmetrical and progressive with increasing neuropathic severity and corneal nerves show significant regenerative capacity following rapid normalisation of glycaemic control after simultaneous pancreas and kidney transplantation. The novel image analysis algorithm strongly correlates with human expert annotation and therefore represents a rapid, objective and repeatable means of assessing corneal nerve morphology. Automated image quantification may replace human manual assessment with high diagnostic validity for DSPN.
Subjects/Keywords: 616.4; Diabetic Neuropathy; Corneal Confocal Microscopy; Diabetes
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APA (6th Edition):
Petropoulos, I. (2013). Corneal nerve pathology in diabetes. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/corneal-nerve-pathology-in-diabetes(9912e560-1032-45cd-8f0a-0477d6605a98).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588113
Chicago Manual of Style (16th Edition):
Petropoulos, Ioannis. “Corneal nerve pathology in diabetes.” 2013. Doctoral Dissertation, University of Manchester. Accessed March 09, 2021.
https://www.research.manchester.ac.uk/portal/en/theses/corneal-nerve-pathology-in-diabetes(9912e560-1032-45cd-8f0a-0477d6605a98).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588113.
MLA Handbook (7th Edition):
Petropoulos, Ioannis. “Corneal nerve pathology in diabetes.” 2013. Web. 09 Mar 2021.
Vancouver:
Petropoulos I. Corneal nerve pathology in diabetes. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2021 Mar 09].
Available from: https://www.research.manchester.ac.uk/portal/en/theses/corneal-nerve-pathology-in-diabetes(9912e560-1032-45cd-8f0a-0477d6605a98).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588113.
Council of Science Editors:
Petropoulos I. Corneal nerve pathology in diabetes. [Doctoral Dissertation]. University of Manchester; 2013. Available from: https://www.research.manchester.ac.uk/portal/en/theses/corneal-nerve-pathology-in-diabetes(9912e560-1032-45cd-8f0a-0477d6605a98).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588113
28.
Ferdousi, Maryam.
Assessment of corneal pathology using corneal confocal microscopy in peripheral neuropathies.
Degree: PhD, 2017, University of Manchester
URL: https://www.research.manchester.ac.uk/portal/en/theses/assessment-of-corneal-pathology-using-corneal-confocal-microscopy-in-peripheral-neuropathies(53cb63fb-b645-4389-9fed-f9a028eaea90).html
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756833
► The validity of corneal confocal microscopy (CCM) in assessing peripheral neuropathy has been studied extensively in several studies with a large cohort of subjects with…
(more)
▼ The validity of corneal confocal microscopy (CCM) in assessing peripheral neuropathy has been studied extensively in several studies with a large cohort of subjects with diabetes and in a handful of studies with small sample sizes in subjects with other systemic conditions. The non-invasive nature of this technique as well as its high reproducibility, moderate to high sensitivity and specificity, and ease of use make it an ideal biomarker for diagnosing onset, severity and progression of peripheral neuropathy. This thesis aims to further investigate the potential of CCM by evaluating abnormalities in the corneal sub-basal nerve plexus, Langerhans Cells (LCs) and epithelial cells in neuropathy related to diabetes and cancer. This thesis has established that evaluating the sub-basal nerve plexus in the centre and at the inferior whorl increases the diagnostic performance of CCM. In addition to diagnosing clinical and subclinical neuropathy in children and adults with diabetes CCM can also identify sub-clinical nerve damage in patients with upper gastrointestinal cancer and assess the effects of chemotherapy. CCM also identifies differences in small fibre pathology between diabetic patients with and without painful neuropathy. Although there was an increased prevalence and severity of dry eye and LCs' density, this was not related to an abnormality of corneal nerves in diabetic patients with no or mild neuropathy. Epithelial cell morphology was not associated with corneal nerve damage and did not alter in patients with Type 1 diabetes. In conclusion, CCM has been shown to be an ideal marker for quantifying early small fibre pathology and assessing peripheral neuropathies.
Subjects/Keywords: 617.7; Peripheral neuropathy; Corneal Confocal Microscopy
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APA (6th Edition):
Ferdousi, M. (2017). Assessment of corneal pathology using corneal confocal microscopy in peripheral neuropathies. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/assessment-of-corneal-pathology-using-corneal-confocal-microscopy-in-peripheral-neuropathies(53cb63fb-b645-4389-9fed-f9a028eaea90).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756833
Chicago Manual of Style (16th Edition):
Ferdousi, Maryam. “Assessment of corneal pathology using corneal confocal microscopy in peripheral neuropathies.” 2017. Doctoral Dissertation, University of Manchester. Accessed March 09, 2021.
https://www.research.manchester.ac.uk/portal/en/theses/assessment-of-corneal-pathology-using-corneal-confocal-microscopy-in-peripheral-neuropathies(53cb63fb-b645-4389-9fed-f9a028eaea90).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756833.
MLA Handbook (7th Edition):
Ferdousi, Maryam. “Assessment of corneal pathology using corneal confocal microscopy in peripheral neuropathies.” 2017. Web. 09 Mar 2021.
Vancouver:
Ferdousi M. Assessment of corneal pathology using corneal confocal microscopy in peripheral neuropathies. [Internet] [Doctoral dissertation]. University of Manchester; 2017. [cited 2021 Mar 09].
Available from: https://www.research.manchester.ac.uk/portal/en/theses/assessment-of-corneal-pathology-using-corneal-confocal-microscopy-in-peripheral-neuropathies(53cb63fb-b645-4389-9fed-f9a028eaea90).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756833.
Council of Science Editors:
Ferdousi M. Assessment of corneal pathology using corneal confocal microscopy in peripheral neuropathies. [Doctoral Dissertation]. University of Manchester; 2017. Available from: https://www.research.manchester.ac.uk/portal/en/theses/assessment-of-corneal-pathology-using-corneal-confocal-microscopy-in-peripheral-neuropathies(53cb63fb-b645-4389-9fed-f9a028eaea90).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.756833
University of Minnesota
29.
Kim, Amy.
Role of Schwann cell-derived Exosomes in Cisplatin-induced Hyperalgesia.
Degree: MS, Oral Biology, 2018, University of Minnesota
URL: http://hdl.handle.net/11299/206164
► Painful peripheral neuropathy is a common dose-limiting side effect associated with cisplatin treatment. Cisplatin is unable to cross the blood-brain barrier, and its neurotoxicity is…
(more)
▼ Painful peripheral neuropathy is a common dose-limiting side effect associated with cisplatin treatment. Cisplatin is unable to cross the blood-brain barrier, and its neurotoxicity is limited to the peripheral nervous system (PNS). In the PNS, Schwann cells are an essential component supporting dorsal root ganglion (DRG) neuron viability, and impairments in Schwann cell biology contribute to cisplatin-induced painful neuropathy. We explored the role of Schwann cell-derived exosomes in the development of cisplatin-induced hyperalgesia. Consistent with our previous reports, daily injection of cisplatin (1 mg/kg, i.p.) for 7 days produced mechanical hyperalgesia in C3H/HeN mice. To investigate the impact of exosome signaling in the development of cisplatin-induced hyperalgesia, exosomes isolated from the sciatic nerves of cisplatin-treated mice were injected intrathecally into naïve mice for 5 consecutive days (7 g of total protein/10 l, i.t.). Mechanical hyperalgesia was observed after the second injection of exosomes, mimicking the effect of cisplatin alone and supporting the involvement of integrated exosome signaling in hyperalgesia produced by cisplatin. Intrathecal administration of Schwann cell-derived exosomes activated microglia, and analysis of exosomal content indicated mediators of neuronal sensitization at the central level. Collectively, our results indicate that Schwann cells affected by cisplatin contribute to mechanical hyperalgesia and exosomes are an important signaling mediator for glia-neuronal communication.
Subjects/Keywords: Cisplatin; Exosomes; Hyperalgesia; Neuropathy; Pain; Schwann Cell
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APA (6th Edition):
Kim, A. (2018). Role of Schwann cell-derived Exosomes in Cisplatin-induced Hyperalgesia. (Masters Thesis). University of Minnesota. Retrieved from http://hdl.handle.net/11299/206164
Chicago Manual of Style (16th Edition):
Kim, Amy. “Role of Schwann cell-derived Exosomes in Cisplatin-induced Hyperalgesia.” 2018. Masters Thesis, University of Minnesota. Accessed March 09, 2021.
http://hdl.handle.net/11299/206164.
MLA Handbook (7th Edition):
Kim, Amy. “Role of Schwann cell-derived Exosomes in Cisplatin-induced Hyperalgesia.” 2018. Web. 09 Mar 2021.
Vancouver:
Kim A. Role of Schwann cell-derived Exosomes in Cisplatin-induced Hyperalgesia. [Internet] [Masters thesis]. University of Minnesota; 2018. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/11299/206164.
Council of Science Editors:
Kim A. Role of Schwann cell-derived Exosomes in Cisplatin-induced Hyperalgesia. [Masters Thesis]. University of Minnesota; 2018. Available from: http://hdl.handle.net/11299/206164
Loughborough University
30.
Sardar, Asif Mohammed.
Autonomic nervous function in experimentally diabetic rats : the effects of aldose reductase inhibition, dietary myo-inositol and thyroid hormone replacement.
Degree: PhD, 1992, Loughborough University
URL: http://hdl.handle.net/2134/26818
► Neuropathy, a common complication of human diabetes, is not prevented by current antidiabetic therapy. Several mechanisms, some reversible, have been proposed. Clinical assessment of drug…
(more)
▼ Neuropathy, a common complication of human diabetes, is not prevented by current antidiabetic therapy. Several mechanisms, some reversible, have been proposed. Clinical assessment of drug efficacy in this condition is difficult because of its slow and unpredictable development and its possible irreversibility, once established. A reliable animal model of diabetic neuropathy would be very useful. Changes such as reduced nerve conduction velocity are used as models but their relationship to neuropathy is uncertain. The main purpose of this study was to examine autonomic changes in the experimentally diabetic rat with the aim of identifying more appropriate models. The effects of three treatments which correct specific biochemical abnormalities which may underlie diabetic complications, were also studied.
Subjects/Keywords: 572; Diabetic neuropathy
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APA (6th Edition):
Sardar, A. M. (1992). Autonomic nervous function in experimentally diabetic rats : the effects of aldose reductase inhibition, dietary myo-inositol and thyroid hormone replacement. (Doctoral Dissertation). Loughborough University. Retrieved from http://hdl.handle.net/2134/26818
Chicago Manual of Style (16th Edition):
Sardar, Asif Mohammed. “Autonomic nervous function in experimentally diabetic rats : the effects of aldose reductase inhibition, dietary myo-inositol and thyroid hormone replacement.” 1992. Doctoral Dissertation, Loughborough University. Accessed March 09, 2021.
http://hdl.handle.net/2134/26818.
MLA Handbook (7th Edition):
Sardar, Asif Mohammed. “Autonomic nervous function in experimentally diabetic rats : the effects of aldose reductase inhibition, dietary myo-inositol and thyroid hormone replacement.” 1992. Web. 09 Mar 2021.
Vancouver:
Sardar AM. Autonomic nervous function in experimentally diabetic rats : the effects of aldose reductase inhibition, dietary myo-inositol and thyroid hormone replacement. [Internet] [Doctoral dissertation]. Loughborough University; 1992. [cited 2021 Mar 09].
Available from: http://hdl.handle.net/2134/26818.
Council of Science Editors:
Sardar AM. Autonomic nervous function in experimentally diabetic rats : the effects of aldose reductase inhibition, dietary myo-inositol and thyroid hormone replacement. [Doctoral Dissertation]. Loughborough University; 1992. Available from: http://hdl.handle.net/2134/26818
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Open Access Theses and Dissertations
