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1
Clark, Andrew. "Tissue Nanotransfection Strategies for the Treatment of Diabetic Neuropathy and Volumetric Muscle Loss." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu158956655881658.
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Srinivasan, Sangeetha. "Diabetic peripheral neuropathy and retinal tissue thickness." Thesis, Queensland University of Technology, 2014. https://eprints.qut.edu.au/73847/1/Sangeetha_Srinivasan_Thesis.pdf.
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Using retinal imaging, the nature and extent of compromise of retinal structural integrity has been characterized in individuals suffering from diabetic peripheral neuropathy. These findings extend our understanding of the pathological processes involved in diabetic neuropathy and offer novel ophthalmic approaches to the diagnosis and monitoring of this debilitating condition.
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Perazzolo, Monica <1989>. "Sensorimotor integration processing in Diabetic Retinopathy and Diabetic Peripheral Neuropathy." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2018. http://amsdottorato.unibo.it/8482/1/perazzolo_monica_tesi.pdf.
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This study evaluated the direct link between visual perception and related motor output responses during an optic flow stimulation which induced a perception of forward movement, and during a driving task using a simulator. The experiments focussed on the evaluation of two different complications of diabetes, diabetic retinopathy and diabetic peripheral neuropathy (DPN), in order to evaluate the different contributions of both central and peripheral nervous factors in affecting the sensorimotor integration process in diabetes.
Study I. The aim was to assess how optic flow processing contributes to the control of posture and whether it requires the predominant activation of cortical networks involved in motion perception or the intervention of subcortical loops.
People with retinopathy and people who had undergone laser treatment showed a higher postural instability compared to control subjects. Differing retinal functionality produced different postural strategies. Based on these findings, postural control seems to be a process dependent on perceptual analysis via feed-forward cortical circuits.
Study II. The aim was to assess whether diabetes was associated with alterations of visual gaze behaviour and/or neuromuscular impairment that might adversely affect driving performance.
The potential for impaired driving performance with diabetes seems to be represented by diminished eye-steering coordination. While proprioception function seems to indicate the potential for improvement, a slower production of strength in the plantar flexor muscles seems not to influence accelerator pedal control during a driving simulation task in people with diabetes (with and without diabetic peripheral neuropathy).
These results confirm the role of visual perception and eye movements in guiding human movements during dailylife activities. In particular, we demonstrated the detrimental effects of diabetes and the different contribution of diabetic retinopathy and diabetic peripheral neuropathy in affecting both central and peripheral components of the sensorimotor integration process.
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Young, Matthew John. "Peripheral neuropathy and its effects on the diabetic foot." Thesis, University of Newcastle Upon Tyne, 1993. http://hdl.handle.net/10443/197.
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This thesis describes a number of studies which explore the hypothesis that endoneurial hypoxia is a major component of the pathogenetic mechanisms of diabetic peripheral neuropathy, and that peripheral neuropathy leads to structural changes in the diabetic foot. Microvascular blood flow and rheology were studied in three age and sex matched groups; diabetic patients with and without neuropathy, and non-diabetic control subjects. Peroneal nerve motor conduction velocity was significantly associated with transcutaneous oxygen tension, r=0.6.p<0.001. No significant differences in rheological parameters were found between non-neuropathic diabetic patients and controls, but significant adverse changes were found in rheological parameters, prostacyclin levels and fibrinolysis, in diabetic patients with neuropathy, in the absence of other complications. Peroneal nerve motor conduction velocity was measured in 10 non-diabetic and 6 diabetic patients before and after unilateral femoro-popliteal bypass surgery to assess the effect of improving tissue blood flow on nerve function. The contralateral leg served as a control. Restoring tissue oxygenation was associated with significant improvements in peroneal conduction velocity in both non-diabetic and diabetic patients, which may suggest new therapeutic strategies for peripheral neuropathy in man. The effects of diabetic neuropathy on the foot were examined by a radiographic survey of the prevalence of bone and soft tissue changes in the feet of diabetic patients and normal controls. This demonstrated that medial arterial calcification is significantly associated with peripheral neuropathy, making the use of ankle pressure indices unreliable in neuropathic patients. It also found an higher than previously recognised prevalence of traumatic and Charcot fractures amongst neuropathic diabetic patients. Further work demonstrated that Charcot patients have a global neurological impairment when compared to matched neuropathic patients without Charcot changes, and significantly reduced bone mineralisation, a possible predisposing factor for the fractures which often initiate the destructive phase of a Charcot joint. Finally, a new treatment for acute Charcot neuroarthropathy, intravenous Pamidronate, was evaluated, and proved effective in reducing the increased bone turnover, swelling and discomfort associated with the Charcot process.
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Walker, David. "Peripheral nerve pathology in diabetic neuropathy : human and animal studies." Thesis, University of Manchester, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488246.
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This thesis presents data from detailed light and electronmicroscopic studies in nerve from subjects with impaired glucose tolerance and diabetic patients with varying degrees of diabetic neuropathy. In addition, nerve pathology is characterised in patients with diabetic amyotrophy and two animal models; the streptozotocin-diabetic rat and the streptozotocinlalloxan-diabetic dog. Impaired glucose tolerance subjects demonstrate no abnormalities of the myelinated fibres whereas patients without clinical or neurophysiological evidence of neuropathy demonstrate myelinated fibre demyelination without axonal degeneration which progresses to myelinated fibre loss in patients with mild and severe neuropathy. Unmyelinated fibres exhibit pathological changes in subjects with impaired glucose tolerance in the form of early degeneration which progresses to a degree of regeneration and degeneration in patients without clinical manifestations of neuropathy and continued regeneration despite a high degree of degeneration in patients with established neuropathy. Endoneurial capillary morphology has been quantified and demonstrates an initial decrease in luminal area in both subjects with impaired glucose tolerance and diabetic patients without neuropathy followed by an increase in luminal area in patients with mild and severe forms of neuropathy. Endothelial cell hyperplasia and capillary basement membrane thickening are present prior to the development of diabetes in impaired glucose tolerance subjects and demonstrate an increase in diabetic patients progressing with the severity of neuropathy. Young Type 1 diabetic patients demonstrate myelinated fibre demyelination without axonal degeneration. Neither unmyelinated fibre degeneration or regeneration is demonstrated in these patients but a degree of unmyelinated fibre axonal atrophy is present. Endoneurial capillary morphology has been assessed in young Type 1 diabetic patients and a decrease in luminal area along with endothelial cell hyperplasia and basement membrane thickening have been characterised. Patients with painful diabetic amyotrophy are characterised by a reduction in proximal nerve conduction velocity. The underlying pathology consists of myelinated fibre degeneration and a reduction in axon calibre, which may constitute a preferential reduction in larger fibres, and unmyelinated fibre degeneration and regeneration. These changes may form a pathological basis for the painful symptoms experienced by these patients. Morphometric studies on peripheral nerve from animal models have demonstrated limited abnormalities in nerve fibres and endoneurial capillaries In the streptozotocin-diabetic rat. The streptozotocinialloxan diabetic dog demonstrates few abnormalities in peripheral nerve consisting mainly of an increase in basement membrane thickening of the endoneurial capillaries. In summary, this thesis has provided detailed morphometric quantification of both myelinated and unmyelinated fibre pathology in impaired glucose tolerance subjects, diabetic patients and animal models of diabetic neuropathy, demonstrating important abnormalities that occur prior to diabetes and in early diabetic neuropathy. In addition, proximal nerve pathology has been characterised in patients with diabetic amyotrophy. Endoneurial capillary pathology has been quantified and provides further evidence of the role of microangiopathy in the pathogenesis of diabetic neuropathy.
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Dines, Kevin C. "Essential fatty acid dysmetabolism and models of diabetic peripheral neuropathy." Thesis, University of Aberdeen, 1994. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU541429.
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Untreated streptozotocin-induced diabetes results in highly significant and reproducible alterations to peripheral nerve function. Thus, motor and sensor nerve conduction velocities (NCV) were decreased by approximately 21% and 14%, respectively whilst parameters of resistance to hypoxic conduction failure (RHCF) were increased by approximately 50%. NCV deficits were established after one month of untreated diabetes whilst increased RHCF continued to develop over at least two months of untreated diabetes. Dietary treatment of diabetic rats with evening primrose oil (EPO), thus overcoming the inhibition of -6 desaturase was able to prevent decreases in motor and sensor NCV whilst partially preventing the development of increased RHCF. Sciatic endoneurial capillary density was also increased. The effects of EPO were seen to be dependent on cyclo-oxygenase mediated metabolism and this, combined with the lack of effects with sunflower oil suggested gamma-linolenic acid (GLA) to be the active component in EPO. Thus, reversal and preventive treatment of diabetic rats with purified GLA, as well as iloprost (a prostacyclin (PGI2) analogue), had very similar effects to EPO. Therefore, it is likely that increased vasodilator PGI2 production underlies the mechanism of action. However, these highly beneficial effects of GLA (-6 essential fatty acid (EFA)) treatment were in contrast to the poor effects of the -3 EFAs found in fish oil. Furthermore, these -3 EFAs attenuated the actions of GLA. Both observations are linked to a possible attenuation of PGI2 synthesis and increased vasoconstrictor thromboxane (Tx) production. Several different GLA containing oils were found to be significantly less effective than EPO in the reversal of diabetic nerve conduction abnormalities.
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Pabbidi, Reddy M. "Role of transient receptor potential channels in diabetic peripheral neuropathy /." Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1456284721&sid=5&Fmt=2&clientId=1509&RQT=309&VName=PQD.
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Abbiati, F. "ROLE OF LIVER X RECEPTOR ACTIVATION ON DIABETIC PERIPHERAL NEUROPATHY." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/232581.
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Diabetic peripheral neuropathy (DPN) is associate with damages and abnormalities in myelin sheath. Similar changes have been observed in the peripheral nerves of streptozotocin (STZ)-treated rats, a model of type 1 diabetes. It is well known that diabetes blunt levels of neuroprotective molecules such as neuroactive steroids and we observed that the pathology induces a different lipid pattern in myelin due to an altered balance between saturated and unsaturated fatty acids, reduces cholesterol levels in myelin sheath and modifies expression of several important genes involved in lipid metabolism such as sterol regulatory element binding protein 1c (SREBP-1c).
Liver X Receptor (LXR) is a ligand-activated nuclear receptor that controls cholesterol and lipid metabolism directly regulating the expression of several genes involved in these pathways. In fact LXR family regulates adrenal steroidogenesis via their ability to control cholesterol homeostasis. Here we show that also in sciatic nerve of rat both LRXα and β isoforms are expressed and that these receptors are functional. We observed that activation of LXRs in rat, using a synthetic ligand, is able to increase most of the enzymes involved in steroidogenesis rising neurosteroids levels and triggering protective effect of the sciatic nerve against DPN ameliorating physiological and functional tests.
Beside the effect on steroidogenesis, LXR is able to induce many genes involved in fatty acid biosynthesis. In particular we demonstrated that, in diabetic settings, LXR activation increases SREBP-1c function, restores myelin lipid species, strongly alterated by pathology, and recovers P0 expression levels to normal. Again, these LXR-modulated improvements are associated with restored myelin structure in sciatic nerve and enhanced performance in functional tests such as thermal nociceptive threshold and nerve conduction velocity. Moreover these lesson learned from the protective effects of LXR activation on DPN prompted us to focus our research on the possible cross talk between neurosteroids and lipogenesis.
We investigate if neuroactive steroids, in particular DHP and 3α-diol, may exert their protective effects by modulating the myelin lipid profile. Here, we observed that DHP and 3α-diol act on the lipogenic gene expression profile in the sciatic nerve of diabetic rats, restoring alterations in myelin sheath with an amelioration of the diabetic phenotype.
Ultimately these results suggest that LXR activation may represent a new pharmacological avenue to exert neuroprotective effects on diabetic peripheral neuropathy.
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Gregory, Joshua A. "Peripheral nerve function and structure in experimental models of diabetic neuropathy." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3335026.
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Thesis (Ph. D.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed December 5, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 197-225).
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Kellogg, Aaron. "Effect of Cyclooxygenase (COX)-2 Activation on Diabetic Neuropathy." University of Toledo Health Science Campus / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=mco1211909697.
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Jamali, Reza. "Peripheral Hypoglycaemic Neuropathy in Type 1 Diabetic Rats : Morphologic and Metabolic Studies." Doctoral thesis, Linköping : Univ, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7978.
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Henderson, Adrienne Dora. "Gait Alterations and Plantar Pressure in Diabetic Peripheral Neuropathy: A Preliminary Study." BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/6984.
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Background: Despite a lack of consensus on its utility, clinicians have traditionally relied on plantar pressure (PP) to predict ulcer risk and prescribe interventions in individuals with diabetic peripheral neuropathy (DPN). Joint kinematics and kinetics have the potential to contribute to DPN assessment and treatment, however previous studies have not accounted for walking speed nor integrated a full-body analysis with a detailed foot model. Purpose: To assess PP and gait alterations in DPN by controlling walking speed and incorporating a multisegment foot model into a full-body gait analysis. We hypothesize that hip and ankle kinetics will be altered consistent with distal muscle weakness. Methods: Ten subjects with DPN (height: 178.79 ± 8.55 cm, weight: 108.78 ± 16.67 kg, age: 61.5 ± 13.53 years), and 10 healthy matched controls (height: 180 ± 6.37 cm, weight: 92.87 ± 14.5 kg, age: 59.4 ± 7.5 years) participated in this cross-sectional study. Fifty-six reflective markers were attached to each subject according to a full-body model, including a multisegment foot. Subjects walked at a controlled speed (1 m/s) while plantar pressure, kinematic and kinetic data were collected. Functional data analysis was used to compare kinematic and kinetic data between groups, while independent t-tests and a Benjamini-Hochburg procedure was used to compare plantar pressure and joint work metrics. Results: Individuals with DPN presented with a delayed transition from hip extension to hip flexion moment and a decrease in peak hip flexion moment. There were no major changes found at the knee. There was an increase in peak dorsiflexion angle and delayed power generation in both the ankle and midtarsal joints. DPN subjects also showed a decreased midtarsal positive work. The only significant PP metric found was a decrease in peak PP under the lateral toes. Conclusion: Findings demonstrated that individuals with DPN use a hip compensation mechanism to overcome distal muscle weakness. Ankle and midfoot alterations are consistent with muscle weakness, requiring proximal compensations. Joint mechanics were more informative than PP measurements and may provide additional insight into DPN assessment and treatment.
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Maekawa, Tatsuya. "Studies on mechanisms of peripheral and central neuropathy in Spontaneously Diabetic Torii (SDT) fatty rats." Kyoto University, 2019. http://hdl.handle.net/2433/242679.
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Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(農学)<br>甲第21802号<br>農博第2315号<br>新制||農||1065(附属図書館)<br>学位論文||H31||N5174(農学部図書室)<br>京都大学大学院農学研究科応用生物科学専攻<br>(主査)教授 久米 新一, 教授 松井 徹, 教授 廣岡 博之<br>学位規則第4条第1項該当
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Janahi, Noor. "The role of pro-inflammatoy cytokines and autoimmune antibodies in diabetic peripheral neuropathy." Thesis, Queen Margaret University, 2014. https://eresearch.qmu.ac.uk/handle/20.500.12289/7430.
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Introduction – The pathogenetic vision of diabetes mellitus has changed in the last few years, with inflammatory and autoimmunity pathways playing roles in the development and progression of diabetic complications. This study was conducted to investigate whether inflammation and/or autoimmunity are associated with the pathogenesis of human diabetic peripheral neuropathy. Methods – A cross-sectional analysis was initially conducted to explore the population of patients with diabetes mellitus in the Kingdom of Bahrain. The demographics of patients diagnosed with diabetes mellitus in the Royal Medical Services-Bahrain Defence Force Hospital were randomly collected from 500 record cards. Case-control analysis included three groups: 30 patients with diabetic peripheral neuropathy, 30 patients with diabetes mellitus without neuropathy, and 30 healthy controls. Blood analysis was conducted to compare the levels of pro-inflammatory markers and autoimmune markers between the three groups. Secondary analysis investigated the correlations between the level of markers and sample demographics and neurological manifestations. Due to the limited time and financial resources available, this research was considered as a pilot/exploratory study encouraging further investigations to take place in the near future. Results – From the 500 sample initially selected, 48% were male (n=242) and 52% (n= 258) were female. The mean age was 55 ± 14 years and the mean BMI was 35 ± 9 kg/m². Type I DM was present in 8% (n=38) only as opposed to 92% (n=462) who had type II DM. From the sample randomly selected, 76% of the patients had other medical complications, the commonest being peripheral neuropathy; 26% (n=186) followed by vascular insufficiency; 20% (n=141). Case control analysis demonstrated very highly significant differences between the three groups in the levels of IL-6, IL-8 and IL-1β (p<0.001), highly significant differences in the levels of TNF-α, IFN-ɤ (p<0.01), and a significant difference in the levels of CRP (p<0.05). Highly significant differences between the percentages of positive and negative autoimmune antibodies (ANA) between the three groups were observed. The odds of positive values of ANAs in the neuropathy group were 50 times higher when compared to control groups. Secondary analysis detected a number of significant relationships between the levels of pro-inflammatory markers and sample demographics. Highly significant correlations were found to be associated with neurological characteristics in the neuropathy group at the levels of CRP, IL-8, and IL-1β. Conclusion – The present study demonstrated that human peripheral diabetic neuropathy is associated with increased biochemical markers of inflammation and autoimmunity. Furthermore, painful neuropathy may be associated with further increase in inflammation. These results indicate that inflammation and autoimmunity may be important contributors in the development of peripheral neuropathy in diabetes mellitus. The new pathogenic factors may lead to the consideration of new management plans involving new therapeutic approaches and disease markers.
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Moaven-Shahidi, Ayda. "Assessment of retinal structure and visual function in association with diabetic peripheral neuropathy." Thesis, Queensland University of Technology, 2011. https://eprints.qut.edu.au/46227/1/Ayda_Moaven-Shahidi_Thesis.pdf.
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Diabetes is an increasingly prevalent disease worldwide. Providing early management of the complications can prevent morbidity and mortality in this population. Peripheral neuropathy, a significant complication of diabetes, is the major cause of foot ulceration and amputation in diabetes. Delay in attending to complication of the disease contributes to significant medical expenses for diabetic patients and the community.
Early structural changes to the neural components of the retina have been demonstrated to occur prior to the clinically visible retinal vasculature complication of diabetic retinopathy. Additionally visual functionloss has been shown to exist before the ophthalmoscopic manifestations of vasculature damage. The purpose of this thesis was to evaluate the relationship between diabetic peripheral neuropathy and both retinal structure and visual function. The key question was whether diabetic peripheral neuropathy is the potential underlying factor responsible for retinal anatomical change and visual functional loss in people with diabetes.
This study was conducted on a cohort with type 2 diabetes. Retinal nerve fibre layer thickness was assessed by means of Optical Coherence Tomography (OCT). Visual function was assessed using two different methods; Standard Automated Perimetry (SAP) and flicker perimetry were performed within the central 30 degrees of fixation. The level of diabetic peripheral neuropathy (DPN) was assessed using two techniques - Quantitative Sensory Testing and Neuropathy Disability Score (NDS). These techniques are known to be capable of detecting DPN at very early stages. NDS has also been shown as a gold standard for detecting 'risk of foot ulceration'.
Findings reported in this thesis showed that RNFL thickness, particularly in the inferior quadrant, has a significant association with severity of DPN when the condition has been assessed using NDS. More specifically it was observed that inferior RNFL thickness has the ability to differentiate individuals who are at higher risk of foot ulceration from those who are at lower risk, indicating that RNFL thickness can predict late-staged DPN. Investigating the association between RNFL and QST did not show any meaningful interaction, which indicates that RNFL thickness for this cohort was not as predictive of neuropathy status as NDS. In both of these studies, control participants did not have different results from the type 2 cohort who did not DPN suggesting that RNFL thickness is not a marker for diagnosing DPN at early stages. The latter finding also indicated that diabetes per se, is unlikely to affect the RNFL thickness.
Visual function as measured by SAP and flicker perimetry was found to be associated with severity of peripheral neuropathy as measured by NDS. These findings were also capable of differentiating individuals at higher risk of foot ulceration; however, visual function also proved not to be a maker for early diagnosis of DPN. It was found that neither SAP, nor flicker sensitivity have meaningful associations with DPN when neuropathy status was measured using QST.
Importantly diabetic retinopathy did not explain any of the findings in these experiments. The work described here is valuable as no other research to date has investigated the association between diabetic peripheral neuropathy and either retinal structure or visual function.
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Leonard, Maureen Barbara. "Peripheral nerve changes in experimental diabetes and the effects of an aldose reductase inhibitor." Thesis, University of Aberdeen, 1986. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU367566.
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The object of this study was to investigate the effects of an aldose reductase inhibitor, sorbinil (Pfizer inc), in relation to some of the biochemical, structural and functional changes associated with diabetic nerves. An animal model, the streptozotocin-induced diabetic rat was used and the following studies were performed: Motor nerve conduction velocity (MNCV) was measured in the tibial nerve over a 6 month period. A group of rats were examined at the onset of the experiment (OC) to provide a baseline for comparison to all other groups. Age matched control (AMC) animals showed a 13% increase in MNCV during the first 3 months of the experiment with little increase thereafter. The diabetic animals (DC) did not significantly differ over the experimental period from the OC animals and were thus slower conducting than the corresponding AMC group. Administration of sorbinil (25 mg/Kg) to rats from the onset of diabetes had no effect on MNCV by 3 months but had normalised values by 6 months. Nerve glucose, sorbitol, fructose and myo-inositol levels were examined by GLC. Sorbinil had no effect on nerve glucose values but prevented the 10-fold increase in nerve sorbitol values observed with the DC animals. Sorbinil partially normalised nerve fructose values after 3 months of treatment and fully normalised them after 6 months. Myo-inositol (MI) levels showed a 45% reduction by 3 months of diabetes but were normal after 6 months. Sorbinil showed a tendency to restore the reduced MI values by 3 months. Morphometric profiles were examined in the tibial nerve. Axon areas demonstrated a 14% reduction at both 3 and 6 months of diabetes while myelin areas were increased by 13 and 22% respectively. Sorbinil treatment allowed normal axon growth and normalised myelin areas. MNCV was examined in the tibial and gastrocnemius nerves. As above, diabetes prevented the normal MNCV maturation in the tibial nerve. Sorbinil administration (25 mg/Kg) to rats initially diabetic for 2 months, was ineffective in restoring MNCV in the tibial nerve though a partial recovery was observed after 4 months of treatment. MNCV in the gastrocnemius nerve of the DC animals continued to fall as the experiment progressed, reaching a 33% reduction below the OC animals by 3 months. A spontaneous recovery was observed thereafter. Sorbinil partially normalised MNCV in the gastrocnemius nerve after 1 month. These changes exactly paralleled the changes in nerve MI levels. Sorbinil reversed the already elevated nerve sorbitol levels after 1 month of treatment though nerve fructose levels were only partially normalised after 4 months. A morphometric evaluation of the triceps surae nerve (containing fibres to gastrocnemius and soleus muscles) after 4 months of the experiment demonstrated an 18% increase of myelin area in the DC animals. Axon areas were unaffected by diabetes. Sorbinil treatment for 2 months partially normalised myelin areas. Sorbinil administration at doses of 7.5, 12.5 and 25 mg/Kg to rats that had been diabetic for 2 months did not normalise MNCV in the tibial nerve. However, 12.5 and 25 mg/Kg produced a significant improvement in MNCV of the gastrocnemius nerve after 1 month of treatment. 7.5 mg/Kg had no effect in this nerve. All doses of sorbinil produced a trend towards reversing the already elevated nerve sorbitol levels, though 25 mg/Kg was effective after 1 month of treatment whereas 12.5 mg/Kg required 2 months. 7.5 mg/Kg did not fully normalise nerve sorbitol levels. Nerve fructose values remained elevated, though treatment with 25 mg/Kg of sorbinil produced a reduction towards normal values. All 3 doses partially normalised MI levels. For all DC groups, sciatic nerve water content was significantly elevated after a 1 month experimental period. Sorbinil treatment, either given from the induction of diabetes or given after rats were initially diabetic for 2 months, had only a small effect on water content and values remained elevated compared with the controls.
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Song, Zhentao, and 宋震濤. "Effects of Schwann cell-specific over-expression of aldose reductase on diabetic and galactosemic neuropathy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31240951.
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Eriksson, Malin Elisabeth Viktoria. "Sleep in patients with painful diabetic peripheral neuropathy : impact of pain, glucose and pharmacological intervention." Thesis, University of Surrey, 2010. http://epubs.surrey.ac.uk/804058/.
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Matthews, Laura Clare. "Chronic pain associated with diabetic peripheral neuropathy : impact on quality of life and cognitive function." Thesis, University of Surrey, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.543918.
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Siddiqui, Hafeez Ur Rehman. "Automated peripheral sensory neuropathy assessment of diabetic patients using optical imaging and binary processing techniques." Thesis, London South Bank University, 2016. http://researchopen.lsbu.ac.uk/1768/.
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A large proportion of individuals who live with type2 diabetes suffer from plantar sensory neuropathy (PSN). Regular testing and assessment for the condition is required to avoid ulceration or other damage to patients’ feet. Currently accepted practice involves a trained podiatrist testing patients’ feet manually with a hand-held nylon monofilament probe. The procedure is time consuming and labour intensive, requires training, is susceptible to error and is difficult to repeat. This thesis presents the first investigation into a novel automated approach to automatically identify the pressure points on a given patient’s foot for the examination of sensory neuropathy via optical image processing via RGB and HSV colour space incorporating plantar anthropometry. The developed system effectively automates the traditional Semmes–Weinstein monofilament examination (SWME). Further work presented demonstrates the development and demonstration of a generic automated lesion detection algorithms to recognise and avoid probe application on a plantar surface. A combination of local binary pattern and support vector machine methods in layered combination are used to avoid probe application where lesion and chosen pressure points overlap. The trained lesion detection and avoidance method was 100% effective on the lesions used.
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Narayanaswamy, Hema Malini. "An exploratory study to investigate potential sensory biomarkers of chemotherapy-induced and diabetic peripheral neuropathy." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9508.
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Aims: Identification of neurophysiological or skin innervation biomarkers which can be used to assess and monitor progression of diabetic sensory polyneuropathy (DPN) and chemotherapy-induced neuropathy (CIPN). Sensitive and robust measures are needed to detect changes in the relatively short duration of clinical trials aimed to modify progression of neuropathy. Methods: 40 patients with DPN were studied longitudinally over 1 year, and 33 patients with CIPN in a cross-sectional study. Clinical assessments, questionnaires, quantitative sensory testing, histamine-induced skin flare, nerve conduction studies and contact heat evoked potentials were measured. Repeat skin biopsies were performed at a 6 month interval to quantify intra- (IENF) and sub-epidermal (SENF) nerve fibres immunoreactive for PGP 9.5 (pan-neuronal marker), TRPV1 (heat and capsaicin receptor) and GAP-43 (marker of regenerating fibres) in the DPN group, and at baseline in the CIPN group. Results: There was no change in symptoms and sensory tests in the DPN group. However, there was a significant reduction in IENF and SENF for both PGP 9.5 and TRPV1 fibres in the second DPN skin biopsy (n = 29 had repeat biopsy). GAP- 43 fibres were present in the dermis and remained unchanged. Patients in the CIPN group had less painful neuropathy, but similar abnormalities on examination and sensory tests. Despite this, a preserved number of IENF and SENF were seen in the CIPN group, with abnormal morphology. This has not been reported previously. Conclusion: PGP 9.5 and TRPV1-immunoreactive nerve fibres in sequential skin biopsies provide objective markers of progression of neuropathy, while the preserved GAP 43-immunoreactive fibres may detect enhanced regeneration. Novel findings in the CIPN group suggest prevention of degeneration and restoration of function should be the treatment strategy, rather than enhancing regeneration.
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Dehghani, Cirous. "Longitudinal assessment of corneal subbasal nerve morphology as a potential measure of diabetic peripheral neuropathy." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/84833/1/Cirous_Dehghani_Thesis.pdf.
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This thesis represents a significant step forward in developing a validated measure for diabetic peripheral neuropathy – a debilitating and prevalent complication of diabetes. The candidate investigated corneal nerve structure in healthy people as well as in type 1 diabetic individuals in a 4-year longitudinal study. The outcomes of stability of the corneal small nerve fibre in healthy people and evidence of significant decline in diabetic individuals with peripheral neuropathy over time provide justification for the ongoing efforts to establish corneal nerve structure as an objective and appropriate adjunct to conventional measures of peripheral neuropathy.
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du, Plessis Ronél. "Effect of an exercise training programme on muscular strength, ankle mobility, balance and gait patterns in patients with diabetic peripheral neuropathy in the lower legs." University of the Western Cape, 2021. http://hdl.handle.net/11394/8049.
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>Magister Scientiae - MSc<br>Background: Patients who suffer from diabetic peripheral neuropathy in the leg experience a greater risk of developing gait deviations due to a decrease in strength of the lower extremities, especially the tibialis anterior and triceps surea muscle groups. Aim: The aim of the study was to determine the effect of an exercise training programme on blood pressure, fasting blood glucose, muscle strength, range of motion, balance and gait pattern deviations in patients with diabetic neuropathies. Methods: A total of fourteen participants, who had been diagnosed with diabetic peripheral neuropathy or nocturnal allodynia in either one or both extremities, were asked to participate in this study. Participants were purposively selected from two private Podiatry practices based on their signs and symptoms of diabetic neuropathy, age, gender and doctor’s clearance to participate in any form of physical activity. Dependent variables included isometric strength of the muscles surrounding the hip, knee and ankle, the range of motion of the ankle in plantarflexion and dorsiflexion using goniometry, an assessment of balance using the stork stand test, and a gait pattern analysis, using the modified Tinetti Gait pattern Assessment Scale. Study design: The study was a single-blinded, pre-test and post-test experimental study design using a quantitative approach. Intervention: The researcher (a registered biokineticist) developed a scientifically-based exercise intervention programme to specifically target the entire kinetic chain, and to reduce fall risks, improve quality of life and to assist in developing a standard protocol for patients with DPN. The intervention programme consisted of a combination of ankle, hip and knee rehabilitation, including gait pattern specific rehabilitation. The intervention took place 2-3 times a week for 45 minutes per session and was divided in four categories: Range of motion exercises, strengthening exercises, balance and proprioception and gait pattern training exercises. Results: The Mann-Whitney and Wilcoxon Sign Rank Tests were used to evaluate the differences in dependent variables from pre- to post-intervention. The level of significance was set at p<0.05. An increase in range of motion only in the left ankle dorsiflexion were observed and an increase in balance time for the left leg were observed in the intervention group after a 10-week follow up assessment. Clinical significance was observed in the intervention group, post-intervention, with a decrease in systolic (-9.09%) and diastolic blood pressure (-13.89%) and a decrease in blood glucose levels (-17.89%), however, an increase in these variables was observed in the control group post-intervention. An increase in plantarflexion, 8% (left) and 8% (right) and dorsiflexion 5.26% (left) and an 11.11% (right) increase in range of motion for both left and right ankles, and balance time for both legs, 200% (left) and 159% (right) was observed in the intervention group post-intervention. Although the muscular strength variables showed a mix of an increase and decrease in strength post-intervention in the intervention group, however a clinically significant decreased amount was observed in the control group post-intervention for the majority of muscular strength variables. Conclusions: Although not many findings of this study are statistically significant, clinical significance were observed with most of the variables of this study. The findings of this study can assist future researchers in the development of exercise interventions for patients who suffers from DPN.
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Hosein, Riad. "An investigation of in-shoe plantar pressures and shear stresses with particular reference to diabetic peripheral neuropathy." Thesis, King's College London (University of London), 1996. https://kclpure.kcl.ac.uk/portal/en/theses/an-investigation-of-inshoe-plantar-pressures-and-shear-stresses-with-particular-reference-to-diabetic-peripheral-neuropathy(b0ebff48-2d9e-4fb7-8730-4ae42704ad0b).html.
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Eid, Stéphanie A. "Neuropathic injury : new insights on NADPH oxidases in diabetic neuropathy." Electronic Thesis or Diss., Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB130.
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Le diabète, un problème majeur de santé publique, est associé à un certain nombre de facteurs de risque métaboliques qui contribuent à la progression de maladies micro- et macrovasculaires. Les mécanismes qui contribuent à l'apparition et au développement de ces complications sont encore mal déterminés. La neuropathie diabétique (DN) est la complication la plus fréquente du diabète dans le monde, touchant jusqu'à 50% de tous les patients diabétiques. La neuropathie périphérique diabétique (DPN), le type le plus courant de neuropathie diabétique est associé à des changements histologiques et des lésions fonctionnelles affectant les nerfs périphériques. La myélinisation des axones est un processus complexe réalisé par les cellules de Schwann (CS) dans le système nerveux périphérique (SNP). Pourtant, il faut noter que le mécanisme conduisant à la démyélinisation du nerf dans le diabète n'est pas bien caractérisé. Les gènes de myéline périphérique MPZ et PMP22 sont strictement régulés dans les CSs. Une simple fluctuation d'expression ou de changement des taux d'ARN de la PMP22 ou de la MPZ impacte profondément le développement et la préservation des fibres nerveuses et de leurs gaines de myéline. L'importance du glucose dans la pathogenèse du DPN a été récemment décrite. Cependant, les voies cellulaires et moléculaires impliquées sont encore inconnues. Les données obtenues lors de mes travaux de thèse montrent que la voie oxysterol/LXR, décrite pour son implication dans le processus de myélinisation, est altérée dans le diabète. Cependant, son implication dans la neuropathie périphérique induite par le diabète doit encore être élucidée. En plus, notre équipe, avait décrit, entre autres, le rôle de la voie mTORC1 dans la progression des complications diabétiques, mais le mécanisme exact de l'activation de mTORC1 n'est pas encore complètement élucidé. Dans ce travail, nous supposons que la voie LXR est dérégulée entrainant un stress oxydatif générant des ROS, suite à l'altération des niveaux et des activités de NADPH oxidases sélectionnés, Nox1 et Nox4, contribuant ainsi à l'apparition et la progression de DPN. Le stress oxydatif résultant conduit à l'altération de la signalisation des voies mTOR culminant dans l'altération de l'expression des gènes de la myéline et de la lésion des cellules de Schwann. D'un point de vue fondamental, ce travail permet l'identification de nouveaux mécanismes moléculaires impliqués dans le DPN et, sous l'angle clinique, il permettra le développement de stratégies thérapeutiques complémentaires efficaces pour inverser ou ralentir la progression du DPN<br>Diabetes, a major public health problem, is associated with a number of metabolic risk factors that contribute to a high rate of micro- and macrovascular events. The mechanisms that contribute to the onset and development of these complications are poorly defined. Diabetic neuropathy (DN) is the most common complication of diabetes worldwide, affecting up to 50% of all diabetic patients. Diabetic Peripheral Neuropathy (DPN), the most common type of diabetic neuropathy is associated with structural changes and functional injuries affecting the peripheral nerves. The myelination of axons is a complex process carried out by Schwann cells (SCs) in the peripheral nervous system (PNS). However, the mechanism leading to nerve demyelination in diabetes is not well characterized. Peripheral myelin genes MPZ and PMP22 expression is tightly regulated in SCs. A slight change in PMP22 or MPZ expression has a deep impact on the development and preservation of nerve fibers and their myelin sheaths. The importance of glucose in the pathogenesis of DPN has been described. However, the cellular and molecular pathways involved in DPN are still unknown. The data obtained during my PhD show that the oxysterol/LXR pathway, involved in the myelination process, is deregulated in diabetes. The alteration of the LXR pathway was paralleled by an increase in the levels and expressions of the NADPH oxidases Nox1 and Nox4 leading to an increase in ROS production. In parallel, our group and others have also described the role of mTORC1 pathway in the progression of diabetic complications. Yet, the exact mechanism of mTORC1 activation is not yet fully described. We hypothesize that oxidative stress generating ROS, secondary to alteration in the levels and activities of selected NADPH oxidases is altered through an LXR dependent pathway, and contribute to the onset and progression of DPN. The resulting oxidative stress leads to the alteration in the signaling of the mTOR pathways culminating in alteration of the expression of myelin genes, and Schwann cells injury. From a fundamental perspective, this project will allow the identification of novel molecular mechanisms involved in DPN and from the clinical angle it will allow the development of effective therapeutic strategies to reverse or slow the progression of DPN
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Meana-Esteban, Alejandro. "Diabetic peripheral neuropathy : primary pathologies and the role of physical activity as a treatment intervention : a preliminary study." Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/25767/.
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Diabetic peripheral neuropathy (DN) is the most common complication in diabetes mellitus affecting up to 50% of this population. Foot ulceration in DN is a major health problem, often leading to lower-limb amputations and increased mortality rates. A combination of gait and microcirculatory alterations increases the risk of foot ulcerations in DN subjects. DN is also linked to an increased risk of cardiovascular diseases and poor quality of life (QOL). Physical activity (PA) plays an important role in the prevention and treatment of diabetes mellitus. Thus, PA has been associated with positive changes in glucose control, obesity and blood pressure. However, almost all the studies investigating PA interventions in subjects with diabetes mellitus have been carried out in individuals without neuropathic complications, whereas the effect of PA programmes in DN subjects is still unknown. In addition to that, the vast majority of studies have investigated the association between PA and health problems commonly linked to type 2 diabetes whereas the relationship between PA and additional problems associated with DN (i.e. risk of foot ulceration, sensory neuropathy or QOL) have received minimal attention. Therefore, the principal aim of this study was twofold: 1) to quantify differences between DN and healthy individuals in the primary pathologies that may co-exist in DN, with special attention to gait and microcirculation due to their association with foot problems; and 2) to evaluate the overall effect of a PA intervention, based on strengthening and foot mobility exercises, in modifying the primary pathologies linked to DN. Prior to the main study, a number of reliability studies were carried out to determine the reliability of some the methods used in the main part of the study. Preliminary studies Three reliability studies were carried in the present investigation. One study investigated the reliability (within- between-day) of near infrared spectroscopy to quantify muscular blood flow and oxygen consumption in the lower limb using a venous occlusion method (microcirculation). The other two studies investigated the reliability (within-day) of two different approaches to calculate the time differences between electromyography data and mechanical output (force) (electromechanical delay) during different conditions. Substantial reliability (ICC>0.6) or higher was found in all the three studies. Electromechanical delay values for the distal leg muscles were significantly higher in DN subjects compared to healthy individuals. Main study The main study was composed of two parts. Part 1 (cross-sectional study) investigated group differences between subjects with DN (N=53) and healthy individuals (N=25) whereas part 2 (intervention study) investigated group differences over time between two groups of subjects with DN; one participating in a 16 week PA programme (N=21) and the other as controls (N=20). Both studies followed the same experimental protocol and investigated the same domains (general health, gait, microcirculation and QOL). IV Cross-sectional study This study confirmed that DN is a complex condition that affects all the domains measured in the present investigation. Thus, the DN group showed significant differences (p<0.05) in: 1) traditional cardiovascular risk factors (blood pressure); 2) gait (spatial-temporal characteristics, forefoot foot pressures and muscular activity patterns); 3) microcirculation (blood flow and oxygen consumption in response to exercise stress); and 4) QOL compared to the healthy group. Interestingly, the present investigation showed that EMG alterations in DN may be associated with changes in plantar foot pressures and consequently with higher risk of foot complications. Furthermore, results from the present study showed for the first time impairments in exercise-induced microcirculatory responses in subjects with DN compared to healthy individuals. These alterations in the microcirculation were observed both in the muscular vasodilatory capacity as well as in the ability of the muscle to consume oxygen. Intervention study This study demonstrated for the first time that 16 weeks of a PA programme based on strengthening and foot mobility exercises can influence a number of aspects of health that are altered in DN subjects. The most remarkable finding was that the exercise programme improved sensory neuropathy (p=0.027) whilst 16 weeks of strength training did not produce significant changes in strength levels (p>0.115 at least) in the DN subjects. In addition to this results from the present investigation showed that a well controlled strengthening training program does have beneficial effects (p<0.05) on the microcirculation, obesity, blood pressure as well as on mental health QOL. On the other hand, the exercise program did not seem to have a substantial effect on any aspect of gait and HbA1c. Importantly, no adverse effects related to the intervention were reported in any of the volunteers who participated in the physical activity program. Conclusions The present study demonstrated that DN is a condition that affects different aspects of health, of which some are modifiable by a well controlled PA programme (i.e. QOL, blood pressure and weight loss). Furthermore, the intervention seemed to trigger positive adaptations in the microcirculation, in particular in the ability of the muscle to recover from a stress condition (exercise stress). However, the most striking finding was that the intervention improved sensory neuropathy in individuals with DN. Surprisingly, changes in sensory neuropathy did not coincide with changes in muscular strength. This suggests that the lack of muscular adaptation to a PA programme may be caused by intrinsic changes in the muscle and not necessarily to lack of efferent muscle stimulation. In summary, results from the present investigation highlighted 1) the importance of PA as a therapeutic tool in subjects with DN to modify outcome measures associated with type 2 diabetes as well as sensory neuropathy; 2) the need to investigate the effect of PA on DN subjects to challenge the assumption that similar adaptations may occur in DN compared to individuals with type 2 diabetes and no neuropathic complications.
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Tam, Joseph. "Effect of Islet Neogenesis Associated Protein (INGAP) peptide on axonal regrowth in the peripheral sensory nervous system and its therapeutic implications for diabetic peripheral neuropathy." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103186.
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The majority of individuals with .long-term diabetes become afflicted with diabetic peripheral neuropathy (DPN), an often painful and debilitating secondary complication of the disease. Symptomatic treatments, which do not address the underlying nerve damage in diabetes, are currently the only therapeutic options for DPN, aside from rigorous control of blood glucose, which only occasionally reduces the incidence and severity of DPN. Given the progressive nature of disorder, and the failure of the classical neurotrophins in clinical trials for DPN, it is important to develop new therapeutics that can counteract the nerve damage in diabetes.<br>Pancreas-derived peptides that stimulate islet regeneration have gained increasing interest for use in DPN, in part due to the unique similarities that exist between pancreatic and neural tissues. We studied the effects of one such peptide, the Islet Neogenesis Associated Protein (INGAP) peptide, on axonal regrowth in the peripheral nervous system (PNS) in adult C57BLJ6 mice. Using dorsal root ganglia (DRG) explant cultures as in vitro model of axotomy, we found that INGAP peptide enhances axonal regrowth in a time- and concentration-dependent manner that involves cyclic AMP-dependent activation of protein kinase A (PKA) and stimulation of phosphatidylinositol-3 kinase (PI3K). The neuritogenic effects of INGAP peptide were reduced by blocking antibodies against a number of growth factors that are secreted by Schwann cells including nerve growth factor (NGF), insulin-like growth factor-I (IGF-I) and transforming growth factor-beta (TGF-(3), suggesting an indirect action of INGAP peptide on outgrowth from DRG neurons, achieved via a primary action on Schwann cells.<br>To further assess the potential usefulness of INGAP peptide in DPN, we used streptozotocin-induced type 1 diabetic mice and found that after two weeks of INGAP peptide administration, begun twelve weeks after the STZ treatment, sensory dysfunction (reduced sensitivity to heat stimulation) was corrected without inducing the hyperalgesia associated with direct administration of NGF. These effects were accompanied by increases in the levels of a number of structural proteins and transcription factors associated with nerve growth. Significantly, the beneficial effects of INGAP peptide on the PNS in vivo occurred independently of its normalizing effects on hyperglycemia. Finally, we found that INGAP peptide enhanced the mitochondrial inner transmembrane potential (DeltaPsim), and that the mitochondrial effects were largely mediated by PKA.<br>Taken together, these studies demonstrate that INGAP peptide enhances sensory axonal regrowth independently of islet neogenesis and the consequent secretion of insulin, and that it may be of benefit in the treatment of peripheral neuropathy associated with diabetes and possibly other clinical conditions.
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Khan, Yosef M. "Examination of a cross sectional association between intake levels of the antioxidant vitamins E, C and B6 and diabetic peripheral neuropathy." The Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1407159781.
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TAIANA, MICHELA MARIA. "Schwann cells mediate the impairment of neurite growth by increased VEGF secretion in DRG neurons exposed to hyperglycemia." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29858.
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Diabetic polyneuropathy (DPN) causes axonal injury and Schwann cells (SCs) might are crucial in this process. We investigated the direct interaction between SCs and dorsal root ganglion (DRG) neurons under hyperglycaemic condition and the effects of Schwann cell-conditioned media on neurite outgrowth of DRG neurons. We observed that high glucose impaired axonal growth in neuron-Schwann cells co-culture and in neuron monoculture exposed to the medium obtained from Schwann cells cultured in high glucose. We found that VEGF concentrations were significantly higher in Schwann cells-media under the high glucose condition than in those under control condition. The reduced neurite outgrowth observed in hyperglycaemic co-culture was inhibited by VEGF neutralizing antibody. Our results suggest that an increase of VEGF secretion by SCs under the diabetic condition would cause a defect of axonal regeneration, resulting in the development of diabetic neuropathy.
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Handsaker, Joseph Charles. "Why are patients with diabetic peripheral neuropathy more likely to fall? : an examination of the underpinning biomechanical mechanisms of locomotion and the influence of intervention." Thesis, Manchester Metropolitan University, 2014. http://e-space.mmu.ac.uk/578167/.
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The research for this thesis examined the effects of diabetic peripheral neuropathy (DPN) on biomechanical factors related to the risk of falling during locomotor tasks, and the effects of a 16-week multi-factorial intervention on the identified impairments. The speed of ankle and knee strength generation, and muscular activations were measured during stair ascent and descent; and minimum toe clearance, stepping accuracy, and visual gaze parameters were measured during level ground walking. Patients with DPN, diabetes patients with no neuropathy and non-diabetic controls were measured before and after a 16-week intervention consisting of high-load resistance exercises and a visual gaze training task. Patients with DPN displayed slower ankle and knee strength generation during stair ascent and descent than healthy controls (p<0.05). Post-intervention, strength was generated faster at the ankle and knee during both tasks (p<0.05), which is expected to improve stability during the weight acceptance phase. During level ground walking, patients with DPN displayed a higher minimum toe clearance (p<0.05), which is expected to reduce the risk of tripping on smaller, less observable hazards; but displayed a decreased stepping accuracy (p<0.05), which may reduce the ability to avoid tripping hazards. Stepping accuracy was improved as a result of the intervention (p<0.05), which may originate from improvements in visual gaze strategy and motor control, contributing to reduce the risk of tripping in patients with DPN. Biomechanical impairments during locomotion were observed in patients with DPN; however, the intervention improved these aspects and may reduce the risk of falling in this population.
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Glasser, Samuel. "Sensory re-weighting for balance control and the effects of ankle foot orthoses and stance width : a comparison of people with diabetic peripheral neuropathy and healthy participants." Thesis, University of Plymouth, 2017. http://hdl.handle.net/10026.1/10238.
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Background: Diabetic peripheral neuropathy (DPN) is diagnosed clinically as a loss of sensation in the feet and affects over 2 million people in the UK. One of the functional effects of DPN is a decrease in standing stability giving rise to a risk of falls. In an attempt to stabilise in the mediolateral direction, people with DPN frequently walk with a wider base of support and stand with a larger stance width. This is often seen in the elderly and is not always beneficial for stability contributing to falls risk. Standing balance requires the integration of sensory information from somatosensory, vestibular and visual systems. Alterations in distal sensory input may result in a re-weighting of the effectiveness of remaining sensations in mediating a stabilising postural response; termed sensory re-weighting. Alterations in posture such as adopting a wider stance width and wearing Ankle Foot Orthoses (AFOs) may also affect sensory input as well as altering the mechanics of the ankle and hip joints. The impact of distal sensory loss on the sensory control of balance in people with DPN compared to the healthy population is unknown. Moreover, it is not known whether standing balance or the sensory control of balance is affected by the adoption of an increased stance width and wearing (AFOs) that restrict mediolateral ankle motion. A better understanding of the mechanisms underlying balance dysfunction in diabetic peripheral neuropathy and how it might be manipulated could inform the development of future interventions to improve balance. Aim: To explore the effects of ankle foot orthoses and stance width on standing balance and the sensory control of mediolateral balance in people with DPN and healthy controls. Objectives: To assess how mediolateral postural stability and the sensory control of balance is affected by (a) AFO use and alterations in stance width in healthy participants (study 1) (b) acute distal sensory loss in healthy participants (study 2) (c) chronic sensory loss in people with DPN and how this in turn is modulated by AFO use and alterations in stance width (study 3). Methods: Postural stability and the response to selective muscle vibration that stimulates muscle spindle afferents was measured by 3D motion analysis. Study 1 investigated the effects of stance width and AFOs on postural sway and the response to selective hip proprioception stimulation induced by vibration of the hip abductors in healthy participants. Study 2 investigated the effect of an acute reduction of somatosensory information induced by cooling in healthy participants on the response to ankle evertor and hip abductor vibration. This provided a model of the acute effects of sensory loss. Study 3 compared healthy people with people with chronic DPN. It investigated the impact on stance stability and whether there was a change in the postural response (gain) to ankle evertor and hip abductor vibration. It further explored the effect of altering the stance width and wearing an AFO on stability and the postural response to hip abductor vibration. Results: Study 1: In healthy controls postural sway was significantly reduced when wearing an ankle foot orthoses and when standing at wider stance widths. Whilst this was also seen during balance perturbation, trunk motion increased at larger stance widths. This could be the result of the AFO restricting ankle motion and affecting the interpretation of the hip vibratory input by the postural control system. Study 2: Experimental reduction in distal sensation by cooling resulted in a reduction in postural responses to ankle evertor muscle vibration. Conversely postural responses at the level of the hip, to proximal (hip) muscle vibration, significantly increased. Study 3: Baseline sway velocity was higher in people with DPN compared to healthy controls. Postural strategies were modified in the DPN group, with increased motion at more proximal segments of the shoulder and head. In both groups, AFO and stance width significantly reduced baseline sway velocity, and the size of postural responses (translations) to hip abductor muscle vibration. Conclusion: Alterations in stance width and the use of AFOs can affect postural sway and the response to selective proprioceptive stimulation. Whilst acute reductions in distal sensory loss are associated with sensory re-weighting of distal and proximal proprioceptive information this is not seen in people with chronic DPN, possibly resulting from long term adaptive changes in the multi-sensory control of balance. Novel differences were found in postural strategies between healthy and DPN groups. The increase in head and trunk motion in people with DPN may have a negative impact on visual acuity and therefore a risk factor for falls. In people with diabetic peripheral neuropathy AFOs and increased stance width led to a reduction in postural response size and postural sway. The effect of AFO on sway velocity was more pronounced in those with DPN at smaller stance widths. Clinically this suggests that an AFO could be used in those with diabetic peripheral neuropathy to slow down the velocity of sway and increase stability.
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Evangelista, Afrânio Ferreira. "Avaliação do efeito do transplante de células-tronco mesenquimais derivadas de medula óssea em modelo murino de neuropatia periférica diabética." Centro de Pesquisas Gonçalo Moniz, 2014. https://www.arca.fiocruz.br/handle/icict/9646.
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Previous issue date: 2014<br>Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil<br>O diabetes é uma doença de alta prevalência que, frequentemente, induz o comprometimento do sistema nervoso periférico. Na neuropatia diabética periférica, os sintomas mais encontrados são os sensitivos, no qual a dor neuropática, condição crônica caracterizada por alodinia e hiperalgesia, é a mais debilitante. Esta, prejudica a qualidade de vida do paciente, sendo muitas vezes não responsiva aos métodos farmacológicos convencionais de tratamento. Diante desse panorama, o desenvolvimento de novas abordagens terapêuticas que possuam ação efetiva neste tipo de dor é de grande relevância. O uso da terapia celular no tratamento de lesões do sistema nervoso tem demonstrado resultados promissores e o potencial terapêutico de células-tronco na neuropatia experimental tem sido proposto. Neste estudo, avaliou-se o efeito de células-tronco mesenquimais derivadas da medula óssea (CMsMO) na neuropatia diabética periférica estabelecida em modelo experimental de diabetes induzido por estreptozotocina (ETZ). Quatro semanas após a indução do modelo por ETZ (80 mg/kg; ip; 3 dias consecutivos), os animais receberam uma administração endovenosa de CMsMO (1 x 106) ou veículo. O tratamento com gabapentina (30 mg/kg; v.o. a cada 12 horas durante seis dias consecutivos) foi usado como padrão ouro. Os limiares nociceptivos térmico e mecânico foram avaliados durante todo o período experimental (90 dias), pelos métodos de hargreaves e von Frey. A avaliação da função motora foi realizada pelo teste de rota-rod. Em diferentes tempos e para todos os grupos experimentais, foram realizadas coletas de segmentos da medula espinal (L4-L5) para dosagem de citocinas por ELISA e segmentos do nervo isquiático foram também coletados para avaliação de alterações morfológicas por microscopia óptica e eletrônica de transmissão. Os dados comportamentais demonstraram que o tratamento com CMsMO reduziu a mecanoalodinia e a hipoalgesia térmica, levando os limiares nociceptivos de animais neuropáticos a níveis similares aos de animais não neuropáticos. Do mesmo modo, a administração de CMsMO normalizou a função motora dos animais neuropáticos. Dados de microscopia mostraram que animais neuropáticos apresentaram atrofia axonal, redução do número de fibras mielínicas e aparente redução do numero de fibras amielínicas no nervo isquiático. Animais neuropáticos tratados com CMsMO tiveram menor ocorrência de atrofia axonal e não apresentaram redução do numero de fibras mielínicas ou amielínicas, em relação aos neuropáticos tratados com salina. Além disso, animais neuropáticos tratados com CMsMO apresentaram menores níveis espinais de IL-1β e TNF-α, e maiores de IL-10 e TGF-β, em relação aos animais neuropáticos não tratados. Esse conjunto de resultados indica que CMsMO produzem efeito antinociceptivo duradouro na neuropatia diabética, seguido de modificações no padrão fisiopatológico da doença, o que aponta a terapia celular como uma interessante alternativa para o controle da neuropatia diabética periférica dolorosa.<br>Diabetes is a highly prevalent disease which frequently compromises the peripheral nervous system. In peripheral diabetic neuropathy, the most frequent symptoms are sensitive, in which the neuropathic pain, chronic condition characterized by allodynia and hyperalgesia, is the most debilitating. Neuropathic pain affects the quality of patients’ lives, and is often not responsive to pharmacological conventional treatment methods. Against this background, the development of new therapeutic approaches that have an effective action in this type of pain is of great importance. The use of cell therapy in the treatment of lesions in the nervous system has shown promising results and the therapeutic potential of stem cells in experimental neuropathy has been proposed. In this study, we evaluated the effect of mesenchymal stem cells derived from bone marrow (CMsMO) in peripheral diabetic neuropathy established in experimental model of streptozotocin (STZ) induced diabetes in mice. Four weeks after the induction of the model by administration of STZ (80 mg/kg, ip; 3 days) the animals received an CMsMO by intravenous administration (1x106) or vehicle. The treatment with gabapentin (30 mg/kg, orally every 12 hours for six days) was used as the gold standard. The thermal and mechanical nociceptive thresholds were assessed throughout the entire experimental period (90 days), using Hargreaves and von Frey methods, respectively. Motor function evaluation of was conducted using the rotarod test. At different times, were analyzes conducted in spinal cord segments (L4-L5) to determine cytokines profile by ELISA. Sciatic nerve segments were also collected for evaluation of morphological changes by optical and electron transmission microscopy. According to the behavioral data, the CMsMO treatment reduced the mecanoalodinia and the thermal hypoalgesia, leading nociceptive thresholds of neuropathic animals to levels similar to those of non-neuropathic animals. Similarly, CMsMO administration normalized motor function of neuropathic animals. Microscopy data demonstrated that neuropathic animals had axonal atrophy and an apparent decrease of the number of myelinated fibers as well a reduction in the number of unmyelinated fibers in the sciatic nerve, but neuropathic animals treated with CMsMO had a lower incidence of axonal atrophy, showed no decrease in the number of myelinated fibers and no apparent decrease in the amount of unmyelinated fibers in relation to neuropathics treated with saline. Furthermore, neuropathic animals treated with CMsMO presented lower levels of spinal IL-1β and higher levels of TNF-α, and IL-10 and TGF-β compared to neuropathic animals that received saline. These data indicate that CMsMO produces a lasting analgesic effect in diabetic neuropathy, followed by changes in the pathophysiological disease pattern, which indicates cell therapy as an interesting alternative for the control of painful peripheral diabetic neuropathy.
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Tippana, Mangapathiraju. "Development of a novel tissue targeted nerve growth factor: Fibronectin chimeric protein as a potential therapeutic for peripheral nerve regeneration." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/120280/1/Mangapathiraju_Tippana_Thesis.pdf.
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This project sought to develop a novel regenerative fusion protein that directly targets nerve-tissue through the addition of a specific nerve-tissue binding domain. Combining select domains of the extracellular matrix protein fibronectin with nerve growth factor, a singular potent regenerative stimulant was developed. To better deliver the candidate therapeutic to nerve-tissue, a native tissue binding domain was added. This approach represents a novel approach to meet the challenges facing regenerative medicine, making use of growth factor: extracellular matrix interactions and tissue localisation to repair, regenerate and restore tissue function.
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Sacco, Isabel de Camargo Neves. "Influência da neuropatia diabética no comportamento de respostas biomecânicas e sensoriais no andar em esteira rolante." Universidade de São Paulo, 2001. http://www.teses.usp.br/teses/disponiveis/39/39132/tde-15032016-102229/.
Full textAbstract:
A investigação de parâmetros biomecânicos no movimento humano tem trazido importantes discussões sobre a função do sistema músculo-esquelético e o controle deste movimento. O andar humano é um dos comportamentos motores mais investigados pela biomecânica e seus aspectos mecânicos contribuem de forma a caracterizar, identificar e intervir em situações patológicas. A investigação de parâmetros dinâmicos, cinemáticos e eletromiográficos na marcha patológica pode beneficiar de forma significativa a compreensão dos mecanismos de controle do andar e as alterações compensatórias geradas, assim como contribuir nas intervenções terapêuticas e preventivas em sujeitos portadores de alguma doença que acometa o sistema músculo-esquelético. No presente estudo, buscou-se descrever e interpretar, sob a perspectiva da biomecânica, o andar em cadência auto-selecionada de sujeitos diabéticos neuropatas em esteira rolante, considerando os parâmetros dinâmicos, temporais, espaciais e eletromiográficos durante a fase de apoio. Investigou-se também aspectos sensoriais plantares e motores a fim de caracterizar os sujeitos neuropatas e controles estudados. Valores da sensibilidade somatossensorial e limiares de tolerância à dor nos sujeitos diabéticos neuropatas apresentaram significativamente maiores em relação ao grupo de sujeitos controle estudado, valores considerados fora do padrão de normalidade esperado. A cadência autoselecionada e a velocidade obtida na esteira rolante foram significativamente menores durante o andar dos neuropatas em relação aos sujeitos controle. Os tempos de apoio simples, duplo, comprimento da passada e do passo durante a marcha nos sujeitos diabéticos neuropatas apresentaram-se significativamente maiores em relação ao grupo controle. Foram observados menores picos de força vertical nos sujeitos neuropatas e menores deflexões da força vertical, conseqüências secundárias da estratégia de redução da velocidade do andar em neuropatas que buscam um padrão mais conservativo e estável do seu andar. As respostas eletromiográficas dos músculos da perna e coxa apresentaram-se com menores magnitudes e com picos de ativação atrasados em relação ao padrão normal de recrutamento, especialmente o m. tibial anterior bilateralmente nos neuropatas. Interpreta-se tal fato como uma provável alteração no mecanismo de controle central e/ou periférico da marcha em sujeitos diabéticos neuropatas decorrente dos déficits sensoriais periféricos e motores conseqüentes da doença investigada. O mecanismo de redução de choques na marcha apresentou-se de forma ineficiente em função das respostas atrasadas eletromiográficas tanto de m. vasto lateral, quanto de m. tibial anterior. Conclui-se que a neuropatia diabética periférica acomete não só respostas somatossensoriais e motoras periféricas mas também mecanismos intrínsecos de controle modificando a eficiência do tornozelo em seu papel na marcha, comprometendo desta forma alguns dos principais requisitos para o andar que são a progressão e o equilíbrio<br>Biomechanical investigation of the human movement has been bringing important discussions about the musculoskeletal system functions and the control of movement. The human walking is one of the most studied motor behaviors and its mechanical aspects contribute to characterize, identify, and intervene in pathological conditions. Dynamic, kinematic, and electromyographic analyses of pathological gait can significantly help the comprehension of the control mechanism of gait and its compensatory alterations. These analyses can also contribute to therapeutic and preventive interventions in patients whose walking behavior is altered due to some disease that accomplish the neuromotor system. In the present study, we described and interpreted self-cadence walking in a treadmill of neuropathic diabetic subjects under biomechanical considerations, such as dynamic, temporal, spatial, and electromyographic analysis during stance phase. We also studied sensorial and motor aspects in order to characterize the neuropathic and control subjects. The somatossensorial responses and pain tolerance threshold in the neuropathic subjects were significantly higher and considered away from the normal patterns. The self-cadence and the treadmill velocity were significantly lower in neuropathic gait. Single and double stance time, stride and step length were significantly higher during neuropathic gait. The neuropathic subjects showed lower vertical force peaks and lower deflections of vertical force and those findings were secondary consequences of the conservative strategy of lowering the gait velocity adopted by the neuropathic in order to reach a more stable locomotor pattern. The electromyographic responses of the thigh and leg muscles in neuropathic subjects showed lower magnitudes and were delayed comparing to the normal recruitment pattern, specially the anterior tibialis muscle right and left. These findings lead us to conclude that probably central and/or peripheral control mechanisms of the gait of neuropathic diabetic patients are altered due to somatossensorial and motor deficits. The mechanism of load reduction during walking was considered inefficient because of the activation delay of the lateral vastus and anterior tibialis muscles. We conclude that the peripheral diabetic neuropathy damages not only somatossensorial and motor sources but also intrinsic mechanisms of motor control leading to alterations in the ankle efficiency in gait. This resulting distal inefficiency compromises some of the principal requirements to gait, which are progression and balance
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Singh, Dhruvaraj Kailashnath. "Clinical studies in diabetic vasculopathy to assess interactions between blood, bone and kidney." Thesis, University of Hertfordshire, 2010. http://hdl.handle.net/2299/4186.
Full textAbstract:
Diabetic vasculopathy (DV) is the most important consequence of chronic hyperglycemia in patients with diabetes mellitus (DM). This thesis explores the interaction of blood, bone and kidney in the pathogenesis of DV by i) reviewing the current understanding of pathogenesis of macrovascular and microvascular diseases in DM to identify gaps in literature and generate hypotheses relating to various facets of DV ii) undertaking a series of prospective studies to examine these hypotheses iii) analysing the findings and integrating any new information obtained from the clinical studies into the current knowledge base and iv) generating hypotheses upon which future work might be based. The literature search was carried out with the aim of understanding current concepts of pathogenesis of DV and its potential modulators. The original reviews resulting from this process are presented in chapters 2 to 4. A series of pilot studies reported in chapters 7 to 11, were then carried out to interrogate hypotheses originating from this process. The first study was carried out in healthy individuals to define the biological variation of potential modulators of DV, namely erythropoietin (EPO), parathyroid hormone, 25 hydroxyvitamin D and 1, 25-dihydroxyvitamin D to facilitate the design and interpretation of subsequent studies. It revealed a wide biological variation of these modulators in the healthy population thus,emphasizing the need to have a control group in the subsequent study population. To examine whether tubulointerstitial dysfunction occurs before the onset of microalbuminuria, a measurement of the above mentioned parameters was carried out along with markers of tubulointerstitial injury in patients with type 1 and type 2 DM without microalbuminuria and in non-diabetic controls. It was found that tubulointerstitial dysfunction with low levels of EPO and 1, 25-dihydroxyvitamin D and higher excretion of tubular injury markers, occurs before the onset of microalbuminuria. Subsequently, diabetic and nondiabetic chronic kidney disease (CKD) patients with EPO deficiency anaemia were examined to study the effects of EPO therapy on the excretion of tubular injury markers. However, in these patient groups, we were unable to demonstrate an effect of EPO therapy on the markers of tubular injury in spite of a beneficial haematological response. To examine whether vascular calcification (VC) and bone mineral density (BMD) were linked in patients with diabetes mellitus and to explore their relationship to modulators of DV, an assessment of VC and BMD was undertaken in patients with type 2 DM with different degrees of proteinuria and normoalbuminuria. VC was assessed by CT scan and BMD by a DEXA scan. Modulators of DV were measured including serum Osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-b-ligand (RANKL). The findings were i) a high prevalence of VC and osteopenia in normoalbuminuric type 2 DM patients with normal serum creatinine ii) a weak inverse relationship between VC and osteopenia iii) proteinuric patients had worse VC but not osteopenia iv) weak relationships between OPG levels and both VC and osteopenia, masked by age in multivariate analysis. The final study examined the relationship between modulators of DV, including OPG and RANKL, and the degree of CKD. It was found that abnormalities of OPG and RANKL occur before the onset of microalbuminuria and progress with deterioration of renal function. Compared to nondiabetics, DM patients have higher OPG levels in the predialysis phase and lower levels in haemodialysis phase, a phenomenon that might indicate endothelial exhaustion in dialysis patients with DM. The derangements associated with DV seem to occur earlier than previously thought. Further work is required to untangle these complexities and to define the contribution of factors such as the adverse blood milieu, the vasculature, abnormal bone and mineral metabolism, and early tubulointerstitial damage. The findings from the studies reported here may help in the formulation of new hypotheses, which might contribute to future work in this area.
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Hammadi, Shumoos T. H. "Novel medical imaging technologies for processing epithelium and endothelium layers in corneal confocal images. Developing automated segmentation and quantification algorithms for processing sub-basal epithelium nerves and endothelial cells for early diagnosis of diabetic neuropathy in corneal confocal microscope images." Thesis, University of Bradford, 2018. http://hdl.handle.net/10454/16924.
Full textAbstract:
Diabetic Peripheral Neuropathy (DPN) is one of the most common types of diabetes that can affect the cornea. An accurate analysis of the corneal epithelium nerve structures and the corneal endothelial cell can assist early diagnosis of this disease and other corneal diseases, which can lead to visual impairment and then to blindness. In this thesis, fully-automated segmentation and quantification algorithms for processing and analysing sub-basal epithelium nerves and endothelial cells are proposed for early diagnosis of diabetic neuropathy in Corneal Confocal Microscopy (CCM) images. Firstly, a fully automatic nerve segmentation system for corneal confocal microscope images is proposed. The performance of the proposed system is evaluated against manually traced images with an execution time of the prototype is 13 seconds. Secondly, an automatic corneal nerve registration system is proposed. The main aim of this system is to produce a new informative corneal image that contains structural and functional information. Thirdly, an automated real-time system, termed the Corneal Endothelium Analysis System (CEAS) is developed and applied for the segmentation of endothelial cells in images of human cornea obtained by In Vivo CCM. The performance of the proposed CEAS system was tested against manually traced images with an execution time of only 6 seconds per image. Finally, the results obtained from all the proposed approaches have been evaluated and validated by an expert advisory board from two institutes, they are the Division of Medicine, Weill Cornell Medicine-Qatar, Doha, Qatar and the Manchester Royal Eye Hospital, Centre for Endocrinology and Diabetes, UK.
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Al-Fahdawi, Shumoos, Rami S. R. Qahwaji, Alaa S. Al-Waisy, and Stanley S. Ipson. "An automatic corneal subbasal nerve registration system using FFT and phase correlation techniques for an accurate DPN diagnosis." 2015. http://hdl.handle.net/10454/16601.
Full textAbstract:
yes<br>Confocal microscopy is employed as a fast and non-invasive way to capture a sequence of images from different layers and membranes of the cornea. The captured images are used to extract useful and helpful clinical information for early diagnosis of corneal diseases such as, Diabetic Peripheral Neuropathy (DPN). In this paper, an automatic corneal subbasal nerve registration system is proposed. The main aim of the proposed system is to produce a new informative corneal image that contains structural and functional information. In addition a colour coded corneal image map is produced by overlaying a sequence of Cornea Confocal Microscopy (CCM) images that differ in their displacement, illumination, scaling, and rotation to each other. An automatic image registration method is proposed based on combining the advantages of Fast Fourier Transform (FFT) and phase correlation techniques. The proposed registration algorithm searches for the best common features between a number of sequenced CCM images in the frequency domain to produce the formative image map. In this generated image map, each colour represents the severity level of a specific clinical feature that can be used to give ophthalmologists a clear and precise representation of the extracted clinical features from each nerve in the image map. Moreover, successful implementation of the proposed system and the availability of the required datasets opens the door for other interesting ideas; for instance, it can be used to give ophthalmologists a summarized and objective description about a diabetic patient’s health status using a sequence of CCM images that have been captured from different imaging devices and/or at different times
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Ruas, José João Marques da Rocha Moreira. "Thalamic volumetric abnormalities in diabetic "peripheral" neuropathy." Master's thesis, 2019. https://hdl.handle.net/10216/120581.
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Ruas, José João Marques da Rocha Moreira. "Thalamic volumetric abnormalities in diabetic "peripheral" neuropathy." Dissertação, 2019. https://hdl.handle.net/10216/120581.
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SHEN, YU-TING, and 沈郁婷. "The Relationship Between Diabetic Peripheral Neuropathy and Sleep Problems." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/86192705115998029598.
Full textAbstract:
碩士<br>國防醫學院<br>公共衛生學研究所<br>104<br>Background: Diabetes mellitus (DM) is an increasing global health problem due to rapid economic development, aging populations, and Westernized lifestyle. The prevalence of diabetes mellitus in Taiwan has increased 2.2 fold, from 13.1% to 28.5% in the past 10 years. Diabetic peripheral neuropathy (DPN) is the most common complications of long-standing diabetes and is a risk factor for foot ulceration and lower extremity amputation. Sleep is of critical concern for DPN because sleep impairment and its comorbidities may influence type 2 diabetes progression.
Objectives:A cross-sectional study was conducted to assess the association the risk factors for between sleep disturbance and DPN among patients with DM. And impacts of sleep problems such as sleep quality, sleep duration, insomnia and hypersomnia in patients with DPN.
Methods: Diabetes patients were recruited from the Diabetes Shared Care Network of the Chang-Bing Show-Chwan Memorial Hospital outpatient departments. DPN was diagnosed using nerve conduction velocity, and sleep quality was measured by the self-administered questionnaires. Odds ratios (OR’s) and 95%comfidence intervals(CIs) derived from evaluate the relationship sleep disturbance with DPN.
Results: A total of 191 diabetic patients with peripheral neuropathy(n=65) and non peripheral neuropathy(n=126) were recruited.The associations between diabetic peripheral neuropathy and daytime sleepiness, sleep quality and insomnia were not statistically significant.After stratified by sex was the results showed that male subjects with diabetic peripheral neuropathy have a higher risk of insomnia( OR=3.40,95% CI:1.02-11.27)and daytime sleepiness( OR=3.14,95% CI:1.10-8.92).
Conclusion:The association between diabetic peripheral neuropathy and daytime sleepiness and insomnia were significant in men. Further studies are needed to explore the gender difference disturbance in the association between sleep disturbance and DPN.
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Guzman, Ruben J. (Ruben Jacobo). "Effect of whole-body vibration on painful diabetic peripheral neuropathy." Thesis, 2012. http://hdl.handle.net/1957/30035.
Full textAbstract:
Introduction. Painful diabetic peripheral neuropathy (DPN) is a common
complication of diabetes that interferes with daily living and causes severe
pain. Pharmacotherapy is the accepted treatment strategy, however, this
strategy is associated with high cost, minimal reductions in pain, and adverse
side effects. Thus, a critical need exists to develop alternative treatment
strategies. Purpose. To determine if a 12-week whole-body vibration (WBV)
intervention reduces pain in adults with DPN. Methods. Twenty-one adults
with physician confirmed painful DPN volunteered to take part in a 26-week
time series design study. Pain was assessed with the Brief Pain Inventory
Short Form [BPI-sf] and a 0-10 numeric rating scale [NRS]. The BPI-sf
contains two indices that respectively measure how pain interferes with daily
living and severity. The intervention began after a 12-week control period. At
week 13, participants were asked to stand on a WBV machine 3 d/week for 4,
3-min bouts at 30-50 Hz with 1-min rest intervals between bouts. Pain levels
were reported using the NRS before and after each bout. Results. Comparing
post- to pre-intervention, BPI-sf pain interference scores decreased from
5.61±1.40 to 2.39±1.82 (p≤0.001). BPI-sf pain severity scores decreased
from 5.1±0.64 to 3.1±1.87 (p≤0.01). Analyses of the NRS scores indicate
that pain decreased each week following WBV and that between weeks, pain
continued to decrease. Conclusion. These findings demonstrate that whole-body
vibration was effective at reducing pain in a sample of adults with painful
DPN.<br>Graduation date: 2012
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"Microphysiological model with multiple fiber types for modeling diabetic peripheral neuropathy." Tulane University, 2018.
Find full textAbstract:
acase@tulane.edu<br>Microphysiological models, or “organ-on-a-chip” models are developing at a rapid rate due to their potential to decrease time and cost of preclinical trials in the pharmaceutical industry. This study proposes a physiological improvement to the current in vitro dual hydrogel microengineered model for the study of the peripheral nerve tissue, and an investigation of diabetic neuropathy to test the efficacy of the improved model. The model consists of hydrogel constructs with a growth restrictive polyethylene glycol diacrylate (PEG) boundary and a gelatin methacrylate (GelMA) growth permissive gel that allows for 3D neurite outgrowth from implanted embryonic rat dorsal root ganglion (DRG). The current model only contains nerve fibers developmentally dependent on nerve growth factor (NGF), which are small typically unmyelinated nociceptive nerve fibers. The other peripheral nerve fiber types, including proprioceptors and mechanoreceptors dependent on brain derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) have not been studied previously in this model. The objective of this study is to develop an in vitro model of diabetic peripheral neuropathy with multiple fiber types to quantify the effects of glucose neurotoxicity on specific fiber type degeneration and conduction. Histology and immunohistochemistry analysis demonstrated the presence of multiple axonal phenotypes and increased percentage myelination in BDNF and NT-3 added (MGF) constructs, and electrophysiological testing of the tissue resulted in a shift of compound action potential (CAP) distribution in MGF samples. Acute diabetic neuropathy testing did not result in large variations in histology or immunohistochemistry but did demonstrate degradation of CAP amplitudes of electrophysiological recordings. A complete physiologically relevant acute model of diabetic neuropathy with multiple fiber types remains elusive to this point, and more work is necessary to fully understand the effects of the disease on this 3D in vitro microphysiological model.<br>1<br>Keith Watza
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Hsieh, Pei-ling, and 謝佩伶. "Effects of Treadmill Exercise on Peripheral Neuropathy in Type 1 Diabetic Rats." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/09626514521980826626.
Full textAbstract:
碩士<br>國立成功大學<br>物理治療研究所<br>97<br>Background and Purpose: Diabetic patients suffer from many complications, and one of them is diabetic peripheral neuropathy (DPN). As heat shock protein 72 (HSP72) has the
neuroprotective function and can be induced from normal rats with exercise training. We hypothesize that exercise may induce HSP72 overexpression in peripheral nerves and
reduce the symptoms of DPN in streptozotocin-induced diabetic rats. Methods: Adult male Wistar rats were randomly assigned to one of the following groups: normal sedentary group, normal exercise group, and diabetic rats with/without exercise training groups.
Training started from day 3 after inducement until day 14, day 28 or day 56. The trained rats run on a treadmill 5 days/week, 30-60 min/day at 20-25m/min. We use von Frey
filaments and plantar test to evaluate the symptoms of DPN and compare the difference between each group. In addition, HSP72 expressions in peripheral nerves were determined
by western blot with monoclonal anti-HSP72 antibody. Results: There were significant improvements in tactile allodynia and thermal hyperalgesia in diabetic rats with exercise training. However, the effects on allodynia can not maintain for long term. HSP72 expressions in spinal cord, sciatic nerve and peripheral nerves were significantly greater in diabetic rats with exercise training than those without exercise. Conclusions: Exercise
training conferred significant improvements in the symptoms of DPN and that could be correlated with the overexpression of HSP72 in peripheral nerves
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Ross, Courtney. "The nutritional intake of persons with type 2 diabetes mellitus who have peripheral neuropathy, compared to those who do not have peripheral neuropathy." 2010. http://hdl.handle.net/1993/4231.
Full textAbstract:
Objectives: The incidence of type 2 diabetes mellitus (DM2) is on the rise worldwide. The primary objective was to determine the prevalence of nutrient inadequacy and excessiveness in persons with DM2 with and without diabetic peripheral neuropathy (DPN).
Study Design: A validated semi-quantitative food frequency questionnaire was used to determine the prevalence of inadequacy of nutrients with an estimated average requirement; the mean intake of nutrients with an adequate intake; and the proportion of persons not meeting the recommendations for the acceptable macronutrient distribution range (AMDR).
Results: Differences were observed in the prevalence of inadequacy of vitamin A and the proportion of persons not meeting the AMDR for total fat, linoleic acid and carbohydrate.
Conclusion: The aforementioned nutrients may have a significant role in the progression/development of DPN and should be studied in further detail. We recommend a balanced diet and use of a multi-vitamin for persons with DM2.
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Otel, Iulian. "Evaluation of corneal nerve morphology for detection and follow-up of diabetic peripheral neuropathy." Master's thesis, 2012. http://hdl.handle.net/10316/25113.
Full textAbstract:
A Diabetes Mellitus, principalmente a Diabetes tipo 2, é uma das doenças crónicas mais prevalentes, e mais desafiantes. A diabetes atinge uma grande parte da população mundial, com este número a aumentar consideravelmente nos últimos anos. Esta doença metabólica afeta substancialmente a qualidade da vida, resultando em complicações graves, que são as principais causas da morbidez e mortalidade.
Estão associadas à diabetes várias complicações crónicas. Uma das mais frequentes é a neuropatia diabética periférica (DPN) – a principal causa de incapacidade em diabéticos. Esta condição patológica inclui uma variedade de danos neurológicos periféricos, que são progressivos e que afetam principalmente os nervos sensitivos proximais e distais, bem como os nervos motores.
O diagnóstico e a classificação da neuropatia é geralmente baseada numa combinação de sintomas clínicos e sinais neuropáticos, e em estudos electrofisiológicos. Adicionalmente, são utilizados outros métodos, como os estudos de condução nervosa (NCS) e os testes sensitivos quantitativos (QST). Estes métodos conferem maior exatidão ao diagnóstico efetuado por exame clínico, sendo extremamente úteis na caraterização da expressão neuropática.
Estudos recentes mostraram que as anomalias dos nervos periféricos estão diretamente relacionadas com as alterações no plexo nervoso sub-basal corneano, sugerindo que a neuropatia periférica pode ser diagnosticada e avaliada através da análise morfométrica dos nervos da córnea. Esta abordagem tem recebido uma crescente atenção.
A microscopia confocal da córnea (CCM) é uma técnica frequentemente utilizada para adquirir in vivo imagens dos nervos da córnea. Esta técnica é não-invasiva e permite a obtenção de imagens da córnea em tempo real. A microscopia confocal representa um método ideal para investigação e avaliação clínica, produzindo imagens com alta qualidade e permitindo a visualização das camadas e das células da córnea com uma resolução elevada.
VI
Apresentamos Aqui um estudo piloto em que se avalia a deteção e classificação da neuropatia periférica através da análise morfométrica dos nervos da córnea. O estudo consiste numa avaliação pormenorizada dum pequeno grupo de 12 voluntários não-diabéticos e 8 doentes diabéticos tipo 2, classificados consoante a presença e o grau de severidade da neuropatia.
Os resultados que obtivemos são promissores e similares aos reportados em estudos anteriores. Os parâmetros Densidade de Fibras Nervosas (NFD), Comprimento de Fibras Nervosas (NFL), Largura de Fibras Nervosas (NFW) e Densidade de Branching de Nervos (NBD) apresentaram o melhor desempenho na avaliação da neuropatia diabética. Os valores de NFD, NFL e NBD são significativamente mais baixos (p <0.05) nos doentes diabéticos quando comparados com os controlos, e exibem correlações inversas com o grau de severidade da neuropatia. Os valores de NFW são significativamente superiores nos doentes diabéticos, variando com o grau de severidade da neuropatia. Os parâmetros NFD e NFL mostram diferenças estatisticamente significativas (p <0.05) entre os casos sem neuropatia e os doentes com neuropatia, mostrando também diferenças significativas (p <0.05) entre os grupos dos diabéticos (classificados consoante a severidade da neuropatia), diferenciando os grupos com grau ligeiro e moderado de neuropatia, do grupo de controlos não-diabéticos.
Concluímos que a CCM pode ser utilizada com êxito para complementar os resultados de avaliação da neuropatia periférica, obtidos através de exames clínicos e electrofisiológicos.
Palavras-Chave: diabetes, neuropatia diabética periférica, microscopia confocal da córnea, nervos da córnea, parâmetros morfométricos.
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Ferreira, Leonardo Miguel. "Thalamic volumetric differences between painful and non-painful diabetic peripheral neuropathy: do they really matter?" Master's thesis, 2018. https://hdl.handle.net/10216/112683.
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Ferreira, Leonardo Miguel. "Thalamic volumetric differences between painful and non-painful diabetic peripheral neuropathy: do they really matter?" Dissertação, 2018. https://hdl.handle.net/10216/112683.
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Nowakowski, Patricia E. "A meta-analysis of the diagnostic accuracy of the monofilament in detecting diabetic peripheral neuropathy." 2008. http://proquest.umi.com/pqdweb?did=1542148911&sid=5&Fmt=2&clientId=39334&RQT=309&VName=PQD.
Full textAbstract:
Thesis (Ph.D.)--State University of New York at Buffalo, 2008.<br>Title from PDF title page (viewed on Nov. 25, 2008) Available through UMI ProQuest Digital Dissertations. Thesis adviser: Donnelly, James P. Includes bibliographical references.
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Al-Modhefer, Zainab. "Evaluating non-invasive cytokine sampling to detect diabetic peripheral neuropathy : a proof-of-concept study." Thesis, 2021. http://hdl.handle.net/1959.7/uws:68013.
Full textAbstract:
Diabetic Peripheral Neuropathy (DPN) is the most common form of peripheral neuropathy worldwide. However, there are limited treatments for DPN, thus early diagnosis and prevention are essential. A large component of the pathophysiology of diabetes and DPN is based on the presence of inflammation that consequently leads to the complications associated with DPN. The focus of this proof-of-concept study is investigating the link between local inflammatory factors on the skin and comparing them to the circulating cytokines in the blood. This will provide insight into whether the same cytokines associated with DPN that have been previously identified in the blood – mainly Interleukin-6 (IL-6), Interluekin-1 (IL-1), Interleukin-8 (IL-8), Tumour Necrosis Factor Alpha (TNF-α), C-Reactive Protein (CRP) and Interkeukin-10 (IL-10) – are also present on the skin of people with diagnosed peripheral neuropathy. Twenty-five participants with diabetes were recruited to undergo both functional and objective assessments to determine DPN diagnosis and severity: the Michigan Neuropathy Screening Instrument (MNSI) in conjunction with Quantitative Sensory Testing (QST), and nerve conduction testing. Sebum from the foot and blood samples were collected from participants and analysed by an external lab. While there were no statistically significant results due to the small sample size, this pilot study provided some direction for future research with a larger sample size. Finding an association between local inflammatory factors on the skin and those circulating in the blood might provide an opportunity for the development of a localised, skin sebum test that is non-invasive, inexpensive, and accessible for a more reliable, measurable, and standardised diagnostic tool for DPN.
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Chin, Yen Fan, and 靳燕芬. "Development a model of the foot self-care behavior in patients with diabetic peripheral neuropathy." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/05280187706688845797.
Full textAbstract:
博士<br>長庚大學<br>臨床醫學研究所<br>101<br>Identification of the factors affecting the foot self-care behaviors of diabetic individuals can be helpful in designing foot-care promotion strategies for diabetic patients. However, such evidence-based data is rare. The purposes of this study were to explore the predictors of foot-care behaviors and to test the model fit of a proposed prediction model for diabetic foot-care behaviors.
A cross-sectional design was utilized. Two hundred and ninety-five patients with diabetic neuropathy were recruited from March 1, 2010, to May 31, 2011. Data were collected using the Smilkstein (1978) Family APGAR, the fear thermometer, and four questionnaires designed by the researcher (specifically, a diabetes foot self-care behavior scale, a diabetes foot self-care knowledge scale, a diabetes foot self-care self-efficacy scale, and a diabetic foot ulcer health belief scale). The multiple regression and structural equation model were used to analyze the data.
The results showed that the following factors were associated with better diabetic foot-care behavior: Higher foot-care self-efficacy, having had the foot examined by a clinician, having received advice on taking care of the foot, fewer foot-care barrier beliefs, having received foot care education, and lower limb amputation. The above six predictors explained 31.1% of the variance in foot-care behavior. Among them, the foot-care self-efficacy was the most powerful predictor, explaining 14.4% of the variance in foot-care behavior.
The proposed prediction model had a poor model fit. After modification, the fitting index were improved (root mean square error of approximation = .068, CMIN/DF = 2.379, comparative fit index = .897, normal fit index = .837, goodness-of-fit index = .908, and adjusted goodness-of-fit index = .873). According to the modified model, the foot-care self-efficacy indirectly influences foot-care behaviors by influencing the foot ulcer threat beliefs. Family support indirectly influences foot-care behaviors by influencing the “foot-care benefit beliefs minus barrier beliefs”. Foot-care knowledge indirectly influences foot-care behaviors by influencing the “foot-care benefit beliefs minus barrier beliefs” and foot ulcer threat beliefs.
In this study, foot-care self-efficacy was found to be the most powerful predictor of foot-care behavior in the regression model. We suggest that in order to promote patients’ foot-care behaviors, clinicians should promote patient foot-care self-efficacy by providing mental support to relieve patients’ negative emotions regarding foot care and by establishing patients’ successful experiences in foot self-care.