Šio darbo tikslas – įvertinti pacientų, patyrusių nugaros smegenų pažeidimą, savarankiško veiklos vertinimo reikšmę ergoterapijos taikymui ankstyvuoju reabilitacijos laikotarpiu. Tyrimo uždaviniai: įvertinti pacientų, patyrusių nugaros smegenų pažeidimą, funkcinę būklę ir veiklos sutrikimus, taikant tradicinius vertinimo metodus; įvertinti pacientų, patyrusių nugaros smegenų pažeidimą, veiklos sutrikimus, taikant savarankiško veiklos vertinimo metodus; bei nustatyti tradicinio ir savarankiško veiklos vertinimo metodų ryšį, vertinant pacientų, patyrusių nugaros smegenų pažeidimą, veiklos sutrikimus, priklausomai nuo pažeidimo pobūdžio bei amžiaus. Tyrimas buvo atliktas VšĮ VUL Santariškių klinikų, Reabilitacijos, Fizinės ir Sporto Medicinos Centro I – ame ir II – ame stacionariniuose skyriuose 2007 02 – 2008 04 mėn. Tyrime dalyvavo 29 pacientai, patyrę nugaros smegenų pažeidimą. Iš jų, 25 (86,2%) buvo vyrai ir 4 (13,8%) moterys, amžiaus vidurkis 35,03 (SD ± 14,2) metai. 16 (55,2%) pacientų atvyko su kaklinės nugaros smegenų dalies pažeidimu, 11 (37,9%) pacientų buvo pažeista krūtininė nugaros smegenų dalis, 2 (6,9%) pacientai atvyko su juosmeninės nugaros smegenų dalies pažeidimu. 13 (81,3%) pacientų, patyrusių kaklinės nugaros smegenų dalies pažeidimą, 5 (45,5%) pacientų, patyrusių krūtininės nugaros smegenų dalies pažeidimą, buvo nustatytas ASIA – A tipo pažeidimo laipsnis, juosmeninės nugaros smegenų dalies pažeidimą atyrusiems pacientams buvo nustatytas buvo ASIA –... [toliau žr. visą tekstą] / The aim of this study – to evaluate influence of self assessment for occupational therapy in early rehabilitation period, of patients with spinal cord injury. Goals of this study: to evaluate functional outcomes and occupational performance issues, using traditional assessment methods; to evaluate occupational performance issues, of patients with spinal cord injury, using client – centred methods; to determine the relation between traditional and client – centred assessment methods, dependantly on spinal cord injury level and patients` age. The research took place at a Vilnius University hospital Santariškių klinikos, Centre of Rehabilitation, Physical and Sports Medicine inpatient departmens in 2007 02 – 2008 04. The research contingent consisted of 29 patients with spinal cord injury: 25 (86,2%) were men and 4 (13,8%) women, average of age 35,03 (SD ± 14,2) years. According to the level of spinal cord injury, 16 (55,2%) patients suffered from cervical spinal cord injury, 11 (37,9%) patients suffered from thoracic spinal cord injury and 2 (6,9%) patients had lumbar spinal cord injury. For 13 (81,3%) patients with cervical spinal cord injury was identified complete (American Spinal Injury Association (ASIA-A)) injury, for 5 (45,5%) patients with thoracic spinal cord injury was identified complete (ASIA – A) injury and both patients with lumbar spinal cord injury were identified to have incomplete (ASIA – C) injury. The data were obtained from medical history records and... [to full text]

The purpose of this thesis was to examine coronary heart disease (CHD) risk factors and secondary complications in individuals with spinal cord injury (SCI). In particular, this thesis was organized around the central theme of adiposity, which is a prevalent complication following SCI. Study 1 focused on understanding the relationships between activities of daily living (ADL) and CHD risk factors including central adiposity, lipoproteins, and triglycerides. Using generalized linear models, while controlling for pertinent covariates such as sex, age, and leisure time physical activity (LTPA), it was found that Mobility ADL (wheeling and transferring) were negatively associated with total and LDL-cholesterol. Study 2 examined whether individuals who considered themselves to be overweight subsequently had less favourable subjective well-being, and were more likely to report specific secondary complications than individuals who did not consider themselves to be overweight. Logistic regression analysis and partial correlations controlling for pertinent covariates such as sex, age, and injury severity, revealed that individuals who considered themselves to be overweight reported greater pain, depression, overuse injuries, and fatigue, and less satisfaction with life than individuals who did not consider themselves to be overweight. In summary, the findings suggest that a) participation in specific types of ADL (i.e. Mobility ADL) are associated with a lower CHD risk and should be further explored and that b) elevated perceived adiposity is associated with specific secondary complications and lower subjective well-being. Overall thesis findings support the overwhelming evidence of the benefits of daily physical activity and maintaining a healthy bodyweight in the SCI population. / Thesis (Master, Kinesiology & Health Studies) -- Queen's University, 2009-05-28 11:40:32.574

Acquiring knowledge of the morphological, molecular, and functional changes that occur to neurons following axotomy is a key step for a comprehensive understanding of the nervous system and how it reacts to injury. Propriospinal commissural interneurons (PCIs or CINs) are a class of neuron with axons that project through the ventral commissure to the contralateral spinal cord. My goal was to examine the morphological, molecular, and functional changes that occur to adult feline PCIs following a proximal axotomy. We first determined whether proximally axotomized PCIs develop de novo axons from their dendrites. C3 PCIs were proximally axotomized and several weeks later we stained PCIs and prepared the tissue for histological evaluation. Two primary classes of axotomized PCI were identified: those with a very short axon (called permanently axotomized) and those with an axon that projected across the injury site. Permanently axotomized PCIs had processes with morphological features typical of axons that emerged from their distal dendrites. These axonal processes of the distal dendrites also had GAP-43 (an axonal marker) and lacked MAP2a/b (a dendritic marker). We concluded that permanently axotomized PCIs develop de novo axons from distal dendrites. We then determined whether the axons that crossed the lesion site were representative of spontaneous functional regeneration. First, we showed that PCI axons regenerate through an environment that is typically highly inhibitory to regenerating axons. Second, we established that the regenerated axons conduct action potentials. Finally, we found that regenerated PCI axons form functional synaptic connections with neurons in the contralateral spinal cord. Collectively, these data indicated that spinal interneurons are capable of spontaneous functional regeneration through an injured spinal cord. PCI growth cones are complex and unlike growth cones previously described in the literature. The final study of the thesis examines the morphologies of PCI growth cones within spinal cord injury sites. We found that PCI growth cones have a wide range of morphologies that is independent of their location within the lesion site. Taken together, these data indicate that PCIs have a remarkable capacity for axonal elongation and contribute to remodelling of spinal circuitry following spinal injury. / Thesis (Ph.D, Physiology) -- Queen's University, 2009-12-07 11:21:47.036

Spinal cord injuries result in permanent loss of motor function, leaving those affected with long term physical and financial burdens. Strategies for spinal cord injury repair must overcome unique challenges due to scar tissue that seals off the injury site, preventing regeneration. Tissue engineering can address these challenges with scaffolds that serve as cell- and drug-delivery tools, replacing damaged tissue while simultaneously addressing the inhibitory environment on a biochemical level. To advance this approach, the choice of cells, biomaterial matrix, and drug delivery system must be investigated and evaluated. This research seeks to evaluate (1) the behaviour of murine induced pluripotent stem cells in previously characterized 3D fibrin matrices; (2) the 3D fibrin matrix as a platform to support the differentiation of human induced pluripotent stem cells; and (3) the ability of an affinity-based drug delivery system to control the release of emerging spinal cord injury therapeutic, heat shock protein 70 from fibrin scaffolds. / Graduate / 0541 / amy.lynn.montgomery@gmail.com

The key to understanding any system, including physiologic and pathologic systems, is to obtain a truly comprehensive view of the system. The purpose of this dissertation was to develop foundational analytical and modeling tools, which would enable such a comprehensive view to be obtained of any physiological or pathological system by combining experimental, clinical, and theoretical viewpoints. Specifically, we focus on the development of analytical and modeling techniques capable of predicting and prioritizing the mechanisms, emergent dynamics, and underlying principles necessary in order to obtain a comprehensive system understanding. Since physiologic systems are inherently complex systems, our approach was to translate the philosophy of complex systems into a set of applied and quantitative methods, which focused on the relationships within the system that result in the system's emergent properties and behavior. The result was a set of developed techniques, referred to as relational modeling and analysis that utilize relationships as either a placeholder or bridging structure from which unknown aspects of the system can be effectively explored. These techniques were subsequently tested via the construction and analysis of models of five very different systems: synaptic neurotransmitter spillover, secondary spinal cord injury, physiological and pathological axonal transport, and amyotrophic lateral sclerosis and to analyze neurophysiological data of in vivo cat spinal motoneurons. Our relationship-based methodologies provide an equivalent means by which the different perspectives can be compared, contrasted, and aggregated into a truly comprehensive viewpoint that can drive research forward.

Disorders of the autonomic nervous system constitute serious complications of spinal cord injury (SCI) and their treatment is usually highly prioritised by spinal patients. Among these, autonomic dysreflexia and impaired thermoregulation are potentially life threatening conditions and require effective management. Olfactory ensheathing cells (OECs), progenitor cells and polymeric scaffolds have been tested in animal models of SCI and some of them have been considered for clinical trials. However, evaluation of the effect of such interventions on autonomic functions has received only rudimentary attention and would require a more thorough experimental assessment before the methods are utilised in human patients. This thesis tested two potential therapeutic strategies for autonomic dysreflexia and examined disorders of thermoregulatory functions in a rat model of spinal cord transection. Magnitude and duration of autonomic dysreflexia were evaluated with radio telemetry in spinalised animals treated with (i) implants of OECs and olfactory neurosphere-derived cells seeded in poly(lactic co glycolic) porous scaffolds or with (ii) transplants of OECs alone. (iii) Effects of SCI and of OECs on the morphology of sympathetic preganglionic neurons (SPNs; which are involved in pathogenesis of autonomic dysreflexia) stained for NADPH diaphorase were examined. (iv) Doppler ultrasonography and infrared thermography were used to assess responses of tail blood flow and surface temperature to cold. Transplants of OECs alone, but not in combination with olfactory neurosphere-derived cells and polymeric scaffolds, resulted in significantly shortened episodes of autonomic dysreflexia. This may be attributed to the alterations to the morphology of SPNs adjacent to the lesion: a transient increase in the morphometric features of the SPNs was evoked by spinal cord transection and this was further altered by transplantation of OECs. The thesis also showed that local responses of tail blood flow and temperature to cold were not abolished by complete SCI suggesting that temperature homeostasis could still be maintained in response to cold. It is hypothesised that OECs facilitate improved recovery from autonomic dysreflexia through alteration of the morphology of SPNs. Furthermore, it is suggested that the role of the tail in heat conservation can be regulated by mechanisms that are independent of the descendent neural control from supraspinal centres.

Biochemical assays and radioabsorptiometry evaluated the relationship of mineral and bone metabolism to the systemic response to neurotrauma or orthopaedic trauma of adult males. Forty-one adult males (29.4±9.3 years) participated of which 37 had a primary diagnosis of traumatic spinal cord injury (SCI) and four were vertebral fracture controls. Biochemical abnormalities found included hyperphosphataemia, in association with low or low normal serum levels of 1,25-dihydroxyvitmain D (1,25(OH)₂D) and of parathyroid hormone (PTH), whilst patients remained normocalcaemic. These disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone were strongly associated with the interval since injury and the severity of injury, but none of these relationships was correlated with the level of the injury, the sensory status of a patient or the presence of spine fracture. The disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone found in this study are a mirror image of the data of patients with the heritable disorders autosomal dominant hyperphosphataemic rickets (ADHR), which results from an inactivating mutation of the gene encoding fibroblast growth factor 23 (FGF23) and autosomal recessive hypophosphataemic rickets (ARHR), which is caused by a mutation of the gene encoding dentin matrix protein-1 (DMP-1). It is potentially important that the hormone/proteolytic enzyme/extra-cellular matrix protein cascade associated with these disorders is counter-regulated by 1,25(OH)₂D, acting either directly or indirectly. The present results suggest that the serum levels of 1,25(OH)₂D of the neurotrauma patients chosen for study may have been inappropriately high with respect to the “physiological and metabolic set” of serum levels of phosphate and ionised calcium in the period corresponding to the uncoupling of the resorption and formation of bone, at least in males, prompting further investigation. The findings are consistent with a new “physiological set,” possibly involving an abnormality in the synthesis or processing of the endocrine fibroblast growth factors or other circulating phosphatonins, which may act as an additional level of regulation of the renal–bone axis, rather than renal failure. Strongly supporting this was the dynamic pattern of the biochemistry and radiological data of these neurotrauma patients and also, preliminary evidence of disturbances in circulating levels of other systemic modulators of mineral and bone metabolism. The relationships that were observed potentially may be explained by the diversity of the physiological activities of the endocrine fibroblast growth factors and the modes of actions of secreted FGF23 in bone. The findings provide an understanding of why bone loss occurs and may form the target for safe and cost effective interventions. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1345019 / Thesis (Ph.D.) - University of Adelaide, School of Medicine, Discipline of Orthopaedics and Trauma, 2008

Biochemical assays and radioabsorptiometry evaluated the relationship of mineral and bone metabolism to the systemic response to neurotrauma or orthopaedic trauma of adult males. Forty-one adult males (29.4±9.3 years) participated of which 37 had a primary diagnosis of traumatic spinal cord injury (SCI) and four were vertebral fracture controls. Biochemical abnormalities found included hyperphosphataemia, in association with low or low normal serum levels of 1,25-dihydroxyvitmain D (1,25(OH)₂D) and of parathyroid hormone (PTH), whilst patients remained normocalcaemic. These disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone were strongly associated with the interval since injury and the severity of injury, but none of these relationships was correlated with the level of the injury, the sensory status of a patient or the presence of spine fracture. The disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone found in this study are a mirror image of the data of patients with the heritable disorders autosomal dominant hyperphosphataemic rickets (ADHR), which results from an inactivating mutation of the gene encoding fibroblast growth factor 23 (FGF23) and autosomal recessive hypophosphataemic rickets (ARHR), which is caused by a mutation of the gene encoding dentin matrix protein-1 (DMP-1). It is potentially important that the hormone/proteolytic enzyme/extra-cellular matrix protein cascade associated with these disorders is counter-regulated by 1,25(OH)₂D, acting either directly or indirectly. The present results suggest that the serum levels of 1,25(OH)₂D of the neurotrauma patients chosen for study may have been inappropriately high with respect to the “physiological and metabolic set” of serum levels of phosphate and ionised calcium in the period corresponding to the uncoupling of the resorption and formation of bone, at least in males, prompting further investigation. The findings are consistent with a new “physiological set,” possibly involving an abnormality in the synthesis or processing of the endocrine fibroblast growth factors or other circulating phosphatonins, which may act as an additional level of regulation of the renal–bone axis, rather than renal failure. Strongly supporting this was the dynamic pattern of the biochemistry and radiological data of these neurotrauma patients and also, preliminary evidence of disturbances in circulating levels of other systemic modulators of mineral and bone metabolism. The relationships that were observed potentially may be explained by the diversity of the physiological activities of the endocrine fibroblast growth factors and the modes of actions of secreted FGF23 in bone. The findings provide an understanding of why bone loss occurs and may form the target for safe and cost effective interventions. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1345019 / Thesis (Ph.D.) - University of Adelaide, School of Medicine, Discipline of Orthopaedics and Trauma, 2008

Biochemical assays and radioabsorptiometry evaluated the relationship of mineral and bone metabolism to the systemic response to neurotrauma or orthopaedic trauma of adult males. Forty-one adult males (29.4±9.3 years) participated of which 37 had a primary diagnosis of traumatic spinal cord injury (SCI) and four were vertebral fracture controls. Biochemical abnormalities found included hyperphosphataemia, in association with low or low normal serum levels of 1,25-dihydroxyvitmain D (1,25(OH)₂D) and of parathyroid hormone (PTH), whilst patients remained normocalcaemic. These disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone were strongly associated with the interval since injury and the severity of injury, but none of these relationships was correlated with the level of the injury, the sensory status of a patient or the presence of spine fracture. The disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone found in this study are a mirror image of the data of patients with the heritable disorders autosomal dominant hyperphosphataemic rickets (ADHR), which results from an inactivating mutation of the gene encoding fibroblast growth factor 23 (FGF23) and autosomal recessive hypophosphataemic rickets (ARHR), which is caused by a mutation of the gene encoding dentin matrix protein-1 (DMP-1). It is potentially important that the hormone/proteolytic enzyme/extra-cellular matrix protein cascade associated with these disorders is counter-regulated by 1,25(OH)₂D, acting either directly or indirectly. The present results suggest that the serum levels of 1,25(OH)₂D of the neurotrauma patients chosen for study may have been inappropriately high with respect to the “physiological and metabolic set” of serum levels of phosphate and ionised calcium in the period corresponding to the uncoupling of the resorption and formation of bone, at least in males, prompting further investigation. The findings are consistent with a new “physiological set,” possibly involving an abnormality in the synthesis or processing of the endocrine fibroblast growth factors or other circulating phosphatonins, which may act as an additional level of regulation of the renal–bone axis, rather than renal failure. Strongly supporting this was the dynamic pattern of the biochemistry and radiological data of these neurotrauma patients and also, preliminary evidence of disturbances in circulating levels of other systemic modulators of mineral and bone metabolism. The relationships that were observed potentially may be explained by the diversity of the physiological activities of the endocrine fibroblast growth factors and the modes of actions of secreted FGF23 in bone. The findings provide an understanding of why bone loss occurs and may form the target for safe and cost effective interventions. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1345019 / Thesis (Ph.D.) - University of Adelaide, School of Medicine, Discipline of Orthopaedics and Trauma, 2008

Biochemical assays and radioabsorptiometry evaluated the relationship of mineral and bone metabolism to the systemic response to neurotrauma or orthopaedic trauma of adult males. Forty-one adult males (29.4±9.3 years) participated of which 37 had a primary diagnosis of traumatic spinal cord injury (SCI) and four were vertebral fracture controls. Biochemical abnormalities found included hyperphosphataemia, in association with low or low normal serum levels of 1,25-dihydroxyvitmain D (1,25(OH)₂D) and of parathyroid hormone (PTH), whilst patients remained normocalcaemic. These disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone were strongly associated with the interval since injury and the severity of injury, but none of these relationships was correlated with the level of the injury, the sensory status of a patient or the presence of spine fracture. The disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone found in this study are a mirror image of the data of patients with the heritable disorders autosomal dominant hyperphosphataemic rickets (ADHR), which results from an inactivating mutation of the gene encoding fibroblast growth factor 23 (FGF23) and autosomal recessive hypophosphataemic rickets (ARHR), which is caused by a mutation of the gene encoding dentin matrix protein-1 (DMP-1). It is potentially important that the hormone/proteolytic enzyme/extra-cellular matrix protein cascade associated with these disorders is counter-regulated by 1,25(OH)₂D, acting either directly or indirectly. The present results suggest that the serum levels of 1,25(OH)₂D of the neurotrauma patients chosen for study may have been inappropriately high with respect to the “physiological and metabolic set” of serum levels of phosphate and ionised calcium in the period corresponding to the uncoupling of the resorption and formation of bone, at least in males, prompting further investigation. The findings are consistent with a new “physiological set,” possibly involving an abnormality in the synthesis or processing of the endocrine fibroblast growth factors or other circulating phosphatonins, which may act as an additional level of regulation of the renal–bone axis, rather than renal failure. Strongly supporting this was the dynamic pattern of the biochemistry and radiological data of these neurotrauma patients and also, preliminary evidence of disturbances in circulating levels of other systemic modulators of mineral and bone metabolism. The relationships that were observed potentially may be explained by the diversity of the physiological activities of the endocrine fibroblast growth factors and the modes of actions of secreted FGF23 in bone. The findings provide an understanding of why bone loss occurs and may form the target for safe and cost effective interventions. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1345019 / Thesis (Ph.D.) - University of Adelaide, School of Medicine, Discipline of Orthopaedics and Trauma, 2008