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1
Schneiders, Anthony G., e n/a. "The influence of a back-support harness on the three dimensional kinematics and electromyography of the trunk in sheep shearers : implications for injury prevention". University of Otago. School of Physiotherapy, 2005. http://adt.otago.ac.nz./public/adt-NZDU20060803.160831.
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The occupation of sheep-shearing is classified as heavy to very-heavy physical work requiring a high level of energy expenditure while performing a repetitive task in a predominantly sustained trunk flexion posture. The task is further complicated by unpredictable animal behaviour. Shearing is considered to carry a high risk of injury particularly to the lumbar spine and epidemiological studies have demonstrated that the prevalence of low back pain (LBP) in shearers is high relative to other occupations. The emergence of a commercial shearing-aid (Warrie Back-Aid TM) that is purported to decrease loading on the spine, reduce injury rate and alleviate symptoms of spinal origin has been welcomed by many sectors of the wool-harvesting industry. However, the precise biomechanical influence of the Warrie Back-Aid TM (WBA) on the sheep-shearing task has not been quantified.
The purpose of this study was to investigate the effect of the WBA on three-dimensional kinematics and electromyography of the trunk for 12 experienced shearers during the occupational task of sheep-shearing.
Sheep-shearing is a highly patterned process comprised of specific interlinked phases. Nine distinct phases of the shearing-task where the harness was worn during the removal of the sheep�s fleece were investigated. The study used an opto-electronic motion analysis system and rigid body dynamic modelling. The shearer�s trunk and pelvis were considered as a series of three coupled rigid segments; pelvis, lumbar, and thorax with four passive retro-reflective markers defining each segment. The kinematic variables of angular displacement, velocity and acceleration at the thoraco-lumbar and lumbo-pelvic joint centres were calculated for each shearer while shearing with and without the WBA. An eight channel sEMG telemetry system was used to simultaneous record activity in four pairs of trunk muscles. Temporal analysis of the sEMG signal gave information on the duration and relative intensity of trunk muscle activity.
The results demonstrated that the task of sheep-shearing required endurance-based muscle activity and the adoption of quasi-static posturing combined with complex asymmetrical trunk motion for extensive periods of the task time. There was considerable variability in the trunk motion of individual shearers despite the pattern-taught and repeatable nature of the shearing task. The introduction of the WBA had no effect on the time taken to shear or trunk kinematics however it resulted in reductions in muscular activity of the trunk extensors. When the complete shearing task was analysed there was a statistically significant reduction in mean intensity of muscle activity for the left multifidus (p = 0.010), right multifidus (p = 0.001), right iliocostalis (p = 0.004) and right longissimus (p = 0.002) when the WBA was used. A reduction in muscular activity of the trunk extensors during the sheep-shearing task may result in a decrease in spinal loading, energy expenditure and muscular fatigue.
The clinical recommendation based on the biomechanical results of this and other studies is that the WBA should be incorporated into the practice of sheep-shearing to assist in the reduction of inherent risks associated with the shearing task. Prospective studies into the effect of the harness on LBP are required to endorse this recommendation.
2
Cole, Elaine. "Characterising factors predictive of infection in severely injured patients". Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/7975.
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Infection after trauma complicates the patients clinical course. Infection leads to longer critical care and hospital stays, has been associated with increased mortality rates and places considerable cost pressures on health economies. The predictors of infection after severe injury are not known, and the effects on outcomes other than mortality are under-reported. The overall objective of this research was to characterise factors predictive of infection in severely injured patients admitted to critical care. A prospective cohort study of 271 patients investigated admission factors predictive of the development of infection. A second study of 280 patients evaluated post-injury immune cell changes and the association with infection. Thirdly the relationship between early coagulopathy and infections was investigated in 158 patients. Finally a study of 385 patients examined the use of Tranexamic Acid (TXA) and its association with infection and other outcomes. Infection was a significant burden for severely injured patients. Admission hypoperfusion was the only early characteristic associated with the development of infection, and a dose dependent relationship was observed between severity of shock and increased percentage of infection (p<0.01). Lymphopenia prolonged to day four post injury was strongly predictive infection (OR 0.10, CI 0.02-0.48, p<0.01). At 24 hours, the anticoagulant Protein C was lower in those with infection (Infection: 70.2 iu/dL vs. No infection: 83.3 iu/dL p=0.02), and increased fibrinolysis was also associated with infectious complications (Infection: 6156 μg/L vs. No infection: 3324 μg/L p=0.03). There was a trend to a beneficial relationship between TXA and infection, and it was independently associated with reduced organ failure (OR 0.27, CI: 0.10 – 0.73, p=0.01) and mortality (OR 0.16 CI 0.03 - 0.86, p=0.03). In severely injured patients, admission shock, prolonged lymphopenia and early coagulation dysfunction post severe injury were independent predictors of infection. Timely modulation of these responses after trauma may help to reduce the burden of infection.
3
Franklin, Paula. "First aid when and where you need it, development of first aid self-care, patient education for web and mobile devices /". Online version of thesis, 2008. http://hdl.handle.net/1850/7903.
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4
Didier, Elizabeth. "Being Prepared for Show Livestock Injuries and Illnesses". College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2005. http://hdl.handle.net/10150/144742.
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5 pp.Arizona youth livestock quality assurance and food safety: Trainers reference. Arizona youth livestock quality assurance and food safety: Youth manual. Feeding management for show lambs. Feeding management for show steers. Swine nutrition for show animals.
Illness or injury to a show animal may be preventable by following a few guidelines. Providing a clean and safe environment and properly feeding, watering, and vaccinating animals will help to reduce the risks of experiencing illnesses and injuries. Owners should also learn how to identify signs of health problems, such as sudden changes in behavior or appearance, and prepare a first aid kit for use in the event of an emergency. Also, being familiar with emergency treatment guidelines will help owners protect themselves, prevent further injury to the animal, and properly administer care to the animal if appropriate.
5
Шкатула, Юрій Васильович, Юрий Васильевич Шкатула e Yurii Vasylovych Shkatula. "Urgent medical aid to children with polyorganic and polysystemic injuries at the prehospital stage". Thesis, Видавництво СумДУ, 2012. http://essuir.sumdu.edu.ua/handle/123456789/27525.
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6
Harish, Varun. "A Comprehensive Review of the Assessment of and Early Intervention for Burn Injuries in New South Wales, Australia with Recommendations for Clinical Practice". Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20428.
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Burn injuries are heterogeneous and dynamic problems. Accurate assessment and early intervention through calculation of the extent of the burn injury, implementation of cooling (first aid), and providing appropriate treatment of the wound, can limit progression of the burn injury and achieve wound healing. The aim of this clinically-based research was to validate the efficacy of the components of assessment and early intervention for burn injuries within New South Wales, Australia, and make recommendations for future burn care. The first study examined the accuracy of burn size estimation in a large series of adult burn injured patients that required retrieval and transfer to a specialised Burns Unit. Accuracy was found to be poor, and overestimation occurred at an alarming rate, indicating that current methods of burn size assessment are ineffective and should be challenged. The effect of cooling (first aid) as an early intervention was examined in a large series of both minor outpatient-based burns and severe burn injuries. Significant benefits were seen in a reduction in wound depth, body surface area burned, healing times, and decreased skin grafting requirements. These human cohort studies are the first to clinically corroborate landmark experimental animal studies. Practices of treating the acute burn wound were assessed by way of two clinical studies. Results indicated that multiple treatments are efficacious for the acute burn wound, and that perhaps the optimal treatment is prompt referral to the specialised Burns Unit where expertise in wound care and the use of bioengineered skin substitutes exists. This thesis has reviewed multiple phases of the assessment of and early intervention for burn injuries in New South Wales, Australia, and has provided a clinically-oriented evidence base for early burn care which was previously limited. Implications for clinical practice include novel methods to achieve definitive burn size calculation as well as further education of health care providers in hospital settings, global dissemination of first aid recommendations, and development of burn care models or pathways that involve early (within 12 hours) retrieval or transfer of partial thickness burn injuries to specialised Burn Units to facilitate burn wound treatment.
7
Kiroff, George Kosta. "Oesophageal mucosal injury by acid and bile salt /". Title page, table of contents and summary only, 1986. http://web4.library.adelaide.edu.au/theses/09MS/09msk59.pdf.
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Thesis (M.S.)--University of Adelaide, Dept. of Surgery, 1989.The experimental work described was performed in the Department of Surgery of the University of Adelaide during 1982-1983. Typescript (photocopy). Includes bibliographical references (leaves 191-211).
8
Reyes, Leila. "Involvement of inflammatory oxidants in cardiac ischaemia/reperfusion injury". Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/19667.
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Oxidative stress is a major feature of cardiac ischaemia/reperfusion (I/R) injury, with strong evidence implicating infiltrating leukocytes, in particular neutrophils, as a major source of oxidants in the infarcted myocardium. Activated leukocytes release the peroxidase enzyme, myeloperoxidase (MPO), which can produce the oxidants hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN). Chapter 3 examines the differential cellular effect of (patho)-physiological levels of HOCl and HOCN in cardiomyocytes. Both HOCl and HOSCN induced cellular damage characteristic of cardiac I/R injury and highlighted two very different cellular responses in cardiomyocytes. Chapter 4 explored the therapeutic effect of selenium supplements, specifically, the dietary supplement selenomethionine (SeMet) as a form of antioxidant therapy in the in vitro cardiomyocyte model exposed to HOCl and HOSCN or hypoxia/re-oxygenation (H/R). SeMet prevented a range of cellular damage mediated by HOCl, with the protection mainly attributed to the direct scavenging ability of SeMet. In contrast, SeMet was not able to protect against the HOSCN or H/R injury induced damage. Studies were extended in Chapter 5 to examine SeMet’s ability to modulate the cellular damage observed in an experimental in vivo model of cardiac I/R injury. SeMet (2 mg kg-1) for 8 weeks resulted in the elevation of tissue selenium levels and reduced apoptosis mediated by acute I/R injury, but not the accompanying cardiac dysfunction, adverse remodelling or impaired cardiac function during late stage I/R injury. Overall, this Thesis contributed to knowledge regarding the role of HOCl and HOSCN in cardiac I/R injury, with the results suggesting that both oxidants may contribute to oxidative stress and the associated downstream cellular damage. Furthermore, this work shows that SeMet could be beneficial as secondary treatment for cardiac I/R injury and be used in conjunction with current treatment methods.
9
LEHMAN, JUSTIN EUGENE. "THE PERCEIVED CONFIDENCE OF RURAL, NORTHWEST OHIO HIGH SCHOOL COACHES IN THEIR ABILITY TO HANDLE VARIOUS INJURIES AND ILLNESSES INVOLVING STUDENT ATHLETES". University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1154980798.
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10
Armstrong, Bridget Sarah. "Head and neck position sense in whiplash patients and healthy individuals and the effect of the "chin tuck" action this thesis is submitted to the Auckland University of Technology for the degree of Master of Health Science, February 2003". Full thesis. Abstract, 2003. http://puka2.aut.ac.nz/ait/theses/ArmstrongB.pdf.
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11
Kitamura, Jiro. "Chronic Lung Injury by Constitutive Expression of Activation-Induced Cytidine Deaminase Leads to Focal Mucous Cell Metaplasia and Cancer". Kyoto University, 2015. http://hdl.handle.net/2433/200440.
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12
Crack, Peter, Moses Zhang, Maria Morganti-Kossmann, Andrew Morris, Jonathan Wojciak, Jonathan Fleming, Ila Karve et al. "Anti-lysophosphatidic acid antibodies improve traumatic brain injury outcomes". BioMed Central, 2014. http://hdl.handle.net/10150/610194.
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BACKGROUND:Lysophosphatidic acid (LPA) is a bioactive phospholipid with a potentially causative role in neurotrauma. Blocking LPA signaling with the LPA-directed monoclonal antibody B3/Lpathomab is neuroprotective in the mouse spinal cord following injury.FINDINGS:Here we investigated the use of this agent in treatment of secondary brain damage consequent to traumatic brain injury (TBI). LPA was elevated in cerebrospinal fluid (CSF) of patients with TBI compared to controls. LPA levels were also elevated in a mouse controlled cortical impact (CCI) model of TBI and B3 significantly reduced lesion volume by both histological and MRI assessments. Diminished tissue damage coincided with lower brain IL-6 levels and improvement in functional outcomes.CONCLUSIONS:This study presents a novel therapeutic approach for the treatment of TBI by blocking extracellular LPA signaling to minimize secondary brain damage and neurological dysfunction.
13
Saunders, Royal Duane. "Arachidonic acid and lipid metabolism following spinal cord injury /". The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487260859496213.
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14
CRACCO, Laura. "Fatty acid-binding proteins as markers of brain injury". Doctoral thesis, Università degli Studi di Verona, 2009. http://hdl.handle.net/11562/337348.
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Le Fatty Acid-Binding Proteins (FABPS) sono proteine
intracellulari in grado di legare gli acidi grassi a
catena lunga con elevata affinità, regolandone il
trasporto all’interno delle cellule. Nell’uomo sono
state finora identificate 9 diverse isoforme, ciascuna
con un diverso profilo di espressione a livello di
tessuti. La proteina heart-type FABP (H-FABP) da anni è
considerata uno tra i più sensibili ed efficienti
marcatori di danno cerebrale e al miocardio, ma la sua
elevata espressione in differenti tessuti non la rende
un marker specifico di un particolare disordine.
Un’altra isoforma espressa nel cervello, chiamata BFABP
(brain-type FABP), potrebbe invece rappresentare
un marcatore specifico di danno cerebrale, essendo la
sua espressione limitata al tessuto nervoso.
Questo lavoro ha avuto come scopo la generazione di
anticorpi in grado di riconoscere la proteina B-FABP in
modo specifico e selettivo.
Il progetto si è articolato in due fasi. Nella prima
parte del lavoro la proteina ricombinante B-FABP è
stata espressa in E. coli e purificata mediante due
successive cromatografie. Essa è stata quindi inoculata
in conigli New Zealand e in topi BalbC, ottenendo dopo
diverso tempo 2 antisieri e 8 diverse cellule ibridoma.
Gli anticorpi presenti nel siero e nel surnatante delle
cellule ibridoma in coltura hanno evidenziato diversi
gradi di affinità nei confronti delle due isoforme, BFABP
e H-FABP; solamente una cellula ibridoma è stata
in grado di produrre un anticorpo specifico e selettivo
per la B-FABP ma purtroppo i successivi passaggi di
subclonaggio della cellula hanno evidenziato una
progressiva diminuzione dell’attività anticorpale, non
permettendo l’utilizzo di questo reagente per
l’individuazione della proteina stessa in campioni
biologici.
Nella seconda parte del lavoro si è quindi cercato di
analizzare e superare le problematiche riscontrate
nella prima fase mediante un nuovo approccio che, con
l’ausilio di software specifici, ha mirato
all’identificazione di due regioni potenzialmente
antigeniche della proteina stessa. Due peptidi
sintetici, di sequenza identica alle regioni
identificate, sono stati inoculati in conigli New
Zealand con l’ottenimento di due anticorpi policlonali,
pAb 2979/2980 e pAb 2981/2982. Questi anticorpi si sono
rivelati specifici e selettivi verso l’isoforma B-FABP
e non hanno evidenziato reazioni di cross-reazione
verso H-FABP.
Si può quindi affermare come l’approccio sperimentale
utilizzato abbia contribuito al raggiungimento
dell’obiettivo, la produzione di un anticorpo specifico
per B-FABP umana. Questo risultato suggerisce possibili
scenari nell’utilizzo futuro degli anticorpi, in
tecniche ELISA e western blot, per valutare se la
proteina B-FABP possa essere considerata un marcatore
ideale, specifico di danno neuronale, in disordini a
diversa eziologia (ischemica, infettiva o
degenerativa).Fatty acid–binding proteins (FABPs) are abundant intracellular proteins that bind long-chain fatty acids with high affinity. 9 different FABPs, with tissuespecific distribution, have been identified so far. The primary role of all the FABP family members is regulation of fatty acid uptake and intracellular transport. Heart-type FABP (H-FABP) is considered one of the most sensible and efficient markers of heart and brain damage, but to date the cross-reactivity limits its specific use. Brain-type FABP (B-FABP) might be considered as a good marker of brain damage, being expressed only in the nervous tissue. The aim of this work was to generate a diagnostic reagent specific for human B-FABP, not cross-reacting with H-FABP. The work has been articulated in two parts: in the first one, recombinant protein B-FABP was expressed in E. coli cells and purified by two subsequent chromatographies. The protein was then utilized as immunogen in New Zealand rabbits and BalbC mice, obtaining two antisera and 8 different hybridoma cells. The antibodies in the rabbit serum and in culture supernatant of hybridoma cells displayed different degrees of affinity for B-FABP and H-FABP; only one hybridoma cell was able to produce antibodies specific and selective for brain-type FABP, but the antibody low-titer level and the activity decrease after subsequent subcloning steps affected its application on B-FABP detection in biological fluids. To overcome the limits encountered in the first part of work, a computer-assisted approach on B-FABP was employed in order to identify the potentially most antigenic regions of the protein. Two synthetic peptides were produced with the selected sequences and inoculated in rabbits. Two polyclonal antibodies were obtained, pAb 2979/2980 and pAb 2981/2982. They showed specific and selective reactivity for human B-FABP, without crossreactions with H-FABP. Taken together, our experimental approach was effective for the generation of specific α-B-FABP antibodies; these results suggest the antibodies obtained could be utilized in ELISA and immunoblot analyses in order to value B-FABP as marker of neurological disorders with ischemic, infective and degenerative etiology.
15
Potts, Geoffrey. "Biomechanic analysis of 'heavy-load eccentric calf muscle' exercise used in the rehabilitation of achilles tendinosis a dissertation submitted in partial fulfilment for the degree of Master of Health Science, Auckland University of Technology, January 2005". Full thesis. Abstract, 2005. http://puka2.aut.ac.nz/ait/theses/PottsG.pdf.
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Sturrock, James Lee. "A Behavioral Modification Analysis of the Effects of Multimedia First Aid Training on Injuries in an Industrial Setting". Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc331593/.
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Past research has shown a correlation between first-aid training and the reduction of injuries. This connection has been noted in off-the-job situations in addition to industrial studies. This project is an extension of those past findings with three notable differences: total population training was studied, as the intervention instead of just saturation treatment; attention was given to the effect that the half-life of training had upon injury reduction; and three randomly chosen small groups we're studied to determine short range effects. The theoretical bases from which the study hypothesis was developed originated in the Behavioral Science and Psychology literature. Discussions are developed around the mental structuring of accidental potential situations in the case of a person trained in first-aid principles. Behavior Modification was one of the principles of change that offered a.safer environment through first-aid training. Group contagion provided the setting for development of a safer place to work because of socialization to a "safe attitude." The intervention, American National Red Cross Standard Multimedia First-Aid Course, provided some of the mental developments toward modification of behavior. These were the modeling and rehearsal features of the course. A connection between group deviance and accident "proneness" led to a proposal that avoidance behavior was the resultant of the training.
17
López, Serrano Clara. "Role of lysophosphatidic acid receptors in spinal cord injury physiopathology". Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/458682.
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La médula espinal, la cual constituye una parte vital para el sistema nervioso central (SNC), puede resultar dañada a pesar de estar muy bien protegida por la columna vertebral, dando lugar a importantes consecuencias. La lesión medular provoca una alteración de las redes neuronales que están involucradas en diversas funciones fisiológicas. De hecho, dado que los axones del SNC de mamíferos adultos no pueden regenerarse tras una lesión, y que las células dañadas no pueden ser reparadas, esta patología viene acompañada de una pérdida funcional irreversible para los pacientes afectados.
La fisiopatología de la lesión medular se compone de dos fases degenerativas. La fase primaria es consecuencia directa del trauma en la médula, la cual provoca muerte celular, daño axonal y pérdida de mielina. Esta primera fase es sucedida por una secundaria, en la cual se produce un proceso inflamatorio, crucial para el desarrollo de la enfermedad. Aunque la regeneración de los axones dañados y el reemplazo de las neuronas perdidas tras la lesión son objetivos importantes, minimizar el daño secundario a axones, neuronas, mielina y células gliales que sigue al trauma inicial es posiblemente más interesante desde un punto de vista terapéutico. En concreto, la respuesta inflamatoria de esta fase secundaria juega un papel muy importante en la lesión, siendo, por tanto, una buena diana para la búsqueda de una terapia efectiva.
Una de las moléculas involucradas en el proceso inflamatorio es el ácido lisofosfatídico (del inglés, LPA), el cual es un lípido bioactivo extracelular que juega un papel importante en diversas funciones fisiológicas. El LPA señaliza a través de seis receptores acoplados a proteína G (LPA1-6), los cuales se clasifican en dos familias: la familia del gen de diferenciación endotelial (del inglés, Edg), que comprende los receptores LPA1-3, y la familia de receptores que no pertenecen a la familia Edg, es decir, Non-Edg (LPA4-6). El LPA se sintetiza a partir de dos vías principales: (i) mediante la acción de la enzima autotaxina (ATX), la cual es la responsable de la síntesis de LPA en plasma, y (ii) mediante la acción de fosfolipasas de tipo de A2 (PLA2), las cuales se encargan de la síntesis en tejido.
El LPA juega un papel importante en la fase secundaria de la lesión medular, ya que sus niveles se ven aumentados en el parénquima medular tras el trauma, dando lugar a desmielinización y pérdida de la función locomotora. De hecho, la ausencia de los receptores LPA1 y LPA2 tras la lesión medular mejora la recuperación funcional de los animales y la preservación mielínica en la médula. En esta tesis, revelamos que la activación de los receptores LPA1 y LPA2 microgliales provoca la muerte de los oligodendrocitos. Además, mostramos que los efectos citotóxicos que se desencadenan tras la estimulación de dichos receptores son mediados por la secreción de purinas y la subsecuente activación del receptor P2X7 en oligodendrocitos. Por otro lado, también demostramos que, al contrario de los receptores LPA1 y LPA2, los receptores LPA4 y LPA5 no contribuyen a la fisiopatología de la lesión medular.
En el presente trabajo, también mostramos que la inhibición farmacológica de la ATX no tiene ningún efecto en la recuperación funcional ni el daño secundario tras la lesión medular, lo cual sugiere que la fuente principal de LPA en esta patología no es la síntesis en plasma. Además, demostramos que el bloqueo combinado de LPA1 y LPA2 no tiene efectos aditivos en la lesión medular.
En general, los resultados de esta tesis sugieren que la inhibición farmacológica del LPA1 y, preferiblemente el LPA2, abren una nueva ventana terapéutica para el tratamiento de la lesión medularThe spinal cord is an extremely vital part of the central nervous system (CNS) and, although it is well protected by the spinal column, it can be damaged, resulting in serious consequences. Spinal cord injury (SCI) leads to a disruption of the neuronal networks that are involved in many physiological functions. Since CNS axons of adult mammals do not regenerate following the lesion, and dead neurons and glial cells are not successfully replaced, this results in an irreversible functional loss in patients suffering from SCI. The pathophysiology of SCI involves two degenerative stages, known as primary and secondary injury. The first one results from the direct mechanical trauma to the spinal cord, directly causing cell death, damage to axons, and loss of myelin. This is followed by a secondary wave of tissue degeneration that can extend for several weeks, in which inflammation plays a crucial role. Although regeneration of damaged axons and replacement of lost neurons and glial cells are important goals for the restoration of the injured spinal cord, minimizing secondary damage to axons, neuronal cell bodies, myelin and glial cells that follows the initial trauma is likely to be more easily amenable to treatment. Since inflammation is a major contribution to secondary damage in SCI, targeting the detrimental actions of this physiological response could result in the development of novel approaches for the treatment of this pathology. Lysophosphatidic acid (LPA) is an extracellular bioactive lipid with many physiological functions. It signals through six known G-protein coupled receptors (LPA1-6), which are classified into two families: Endothelial differentiation family gene (Edg) LPA receptors (LPA1-3) and Non-Edg family gene LPA receptors (LPA4-6). LPA synthesis is carried out by two different pathways: (i) by the action of the enzyme named autotaxin (ATX), which is the main responsible in synthesis of this lipid in plasma, and (ii) by action of the phospholipase A2 (PLA2) family enzymes, which are the main route of LPA synthesis in tissues. LPA is a key trigger of secondary damage after SCI, since its increased levels in the spinal cord parenchyma following injury leads to demyelination. Indeed, the lack of LPA1 and LPA2 signalling after SCI enhances functional recovery and myelin sparing. In this thesis, we show that activation of microglial LPA1 and LPA2 leads to oligodendrocyte cell death. We reveal that the cytotoxic actions underlying by microglial cells stimulated with LPA are mediated by the release of purines and the subsequent activation of P2X7 in oligodendrocytes. We also show that, unlike LPA1 and LPA2, LPA4 and LPA5 receptors do not contribute to SCI physiopathology. In the present thesis, we also show that pharmacological inhibition of ATX does not have any effect in functional outcomes and secondary tissue damage after SCI, suggesting that this enzyme is unlikely to be involved in the production of LPA in the spinal cord parenchyma after injury. We also demonstrate that combinatory targeting of LPA1 and LPA2 does not results in additive effects in SCI. Overall, the results shown here suggest that pharmacological inhibition of LPA1, and preferably LPA2, may open a new therapeutic avenue for the treatment of SCI.
18
King, P. "Branched chain amino/keto acid supplementation following severe burn injury". Thesis, University of Salford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376875.
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James, Masheika. "Vitamin A and retinoic acid in neonatal hyperoxic lung injury /". Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/james.pdf.
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20
Esson, Ken. "A cost analysis of accidents and injuries in the open cut coalmining industry". Thesis, Federation University Australia, 1992. http://researchonline.federation.edu.au/vital/access/HandleResolver/1959.17/97254.
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Following a study of back injuries in the Queensland Coal Industry, there arose several questions that needed further research. One of these was the cost of accident and injuries, and the impact of this cost would have on an organisation. The project's research involved a comprehensive study of literature pertaining to the cost of accidents and injuries. This included both insured and uninsured costs. The following four classifications of accidents were researched; first aid treatments; first aid doctor treatments; lost time injury cases; and equipment accident damage cases. A coal mine was selected for the pilot study and, data was collected on the four classifications over a complete year. This means a year that has no out standing accident cases or liablilities. The research was then considered to determine its support for the acceptance or rejection of the hypothesis whic postulates that the current methods used to analyse the cost of accidents or injuries in the coal mining industry are inadequate. As a result of the above condsiderations, a number of key points are put forward in support of the acceptance of the hypothesis. The research established costs both insured and uninsured for the four classifications under review. Then a calculation of a weighted ratio of uninsured costs was made. The paper concludes by making certain recommendations and supporting the need for further research into accident costing within the coal mining fraternity.Masters in Applied Science in Occupational Health and Safety
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Schizas, Nikos. "Neuroprotection in the Injured Spinal Cord : Novel Strategies using Immunomodulation, Stem cell Transplantation and Hyaluronic acid Hydrogel carriers". Doctoral thesis, Uppsala universitet, Ortopedi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-251477.
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The overall aim of this thesis was to establish strategies to minimize secondary damage to the injured spinal cord. Secondary damage that follows spinal cord injury (SCI) involves inflammatory and excitotoxic pathways. Regulation of these pathways using immunomodulatory and neuroprotective substances potentially protects the injured spinal cord from further damage. We also developed and studied resorbable biomaterials to be used as carriers for potential neuroprotectants to the injured spinal cord. We used transversal spinal cord slice cultures (SCSCs) derived from postnatal mice as a model. SCSCs were maintained on different biomaterials and were studied after treatment with immunomodulatory and/or neurotrophic factors. They were further excitotoxically injured and subsequently treated with interleukin-1 receptor antagonist (IL1RA) or by neural crest stem cell (NCSC)-transplantation. The results show that biocompatible and resorbable hydrogels based on hyaluronic acid (HA) preserved neurons in SCSCs to a much higher extent than a conventional collagen-based biomaterial or standard polyethylene terephthalate (PET) membrane inserts. Glial activation was limited in the cultures maintained on HA-based hydrogel. The anti-inflammatory factor IL1RA protected SCSCs from degenerative mechanisms that occur during in vitro incubation, and IL1RA also protected SCSCs from excitotoxic injury induced by N-Methyl-d-Aspartate (NMDA). IL1RA specifically protected neurons that resided in the ventral horn, while other neuronal populations such as dorsal horn neurons and Renshaw cells did not respond to treatment. Finally, transplantation of NCSCs onto excitotoxically injured SCSCs protected from neuronal loss, apoptosis and glial activation, while NCSCs remained undifferentiated. The results presented in this thesis indicate that carriers based on HA seem to be more suitable than conventional collagen-based biomaterials since they enhance neuronal survival per se. The observed neuroprotection is likely due to biomechanical properties of HA. IL1RA protects SCSCs from spontaneous degeneration and from NMDA-induced injury, suggesting that excitotoxic mechanisms can be modulated through anti-inflammatory pathways. Different neuronal populations are affected by IL1RA to various degrees, suggesting that a combination of different neuroprotectants should be used in treatment strategies after SCI. Finally, NCSCs seem to protect SCSCs from excitotoxic injury through paracrine actions, since they remain undifferentiated and do not migrate into the tissue during in vitro incubation. It seems that combinations of neuroprotectants and carrier substances should be considered rather than one single strategy when designing future treatments for SCI. Incorporation of neuroprotectants such as IL1RA combined with stem cells in injectable biocompatible carriers based on HA is the final goal of our group in the treatment of SCI.
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Salmon, Elizabeth. "DEVELOPMENT OF AN EEG BRAIN-MACHINE INTERFACE TO AID IN RECOVERY OF MOTOR FUNCTION AFTER NEUROLOGICAL INJURY". UKnowledge, 2013. http://uknowledge.uky.edu/cbme_etds/8.
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Impaired motor function following neurological injury may be overcome through therapies that induce neuroplastic changes in the brain. Therapeutic methods include repetitive exercises that promote use-dependent plasticity (UDP), the benefit of which may be increased by first administering peripheral nerve stimulation (PNS) to activate afferent fibers, resulting in increased cortical excitability. We speculate that PNS delivered only in response to attempted movement would induce timing-dependent plasticity (TDP), a mechanism essential to normal motor learning. Here we develop a brain-machine interface (BMI) to detect movement intent and effort in healthy volunteers (n=5) from their electroencephalogram (EEG). This could be used in the future to promote TDP by triggering PNS in response to a patient’s level of effort in a motor task. Linear classifiers were used to predict state (rest, sham, right, left) based on EEG variables in a handgrip task and to determine between three levels of force applied. Mean classification accuracy with out-of-sample data was 54% (23-73%) for tasks and 44% (21-65%) for force. There was a slight but significant correlation (p<0.001) between sample entropy and force exerted. The results indicate the feasibility of applying PNS in response to motor intent detected from the brain.
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McDevitt, Jane K. "N-METHYL-D-ASPARTIC ACID RECEPTOR SUBUNIT NR2A REPEAT". Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/216597.
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KinesiologyPh.D.
During a concussion, mechanical forces cause neuron cell strain that initiates dysfunction through the indiscriminate movement of ions through protein channels. Extracellular glutamate binds with cell membrane proteins (e.g. NR2A), which exacerbates the Ca2+ ion influx and prolongs neuron dysfunction. Genetic variation may be a factor in regulating glutamate binding and therefore cell recovery time. The NR2A subunit of NMDA contains a variable (GT)n nucleotide tandem repeat (VNTR) within GRIN2A promoter region. This VNTR has been shown to regulate transcription levels in a length dependent manner, where longer repeat decreases transcription of the NR2A subunit. The purpose of this study was to determine the association of the GRIN2A VNTR and recovery (days) as well as concussion severity scores within concussed athletes. The independent variable was VNTR (long allele vs. short allele). The primary dependent variable, recovery time, was defined as injury date to return to play (RTP) clearance date as determined by the physician. Participant RTP time was categorized as normal ( 20 days). Secondary dependent variables were assessed at the initial evaluation and included vestibular ocular score, Balance Error Scoring System (BESS) score, and Immediate Post Concussion and Cognitive Testing (ImPACT) module scores. All 51 participants were athletes, comprised of 38 males and 13 females with a mean age of 18.69 6.65. Participants were evaluated at a university concussion center. The standardized concussion evaluation consisted of cranial nerve, vestibular ocular tests, balance (Balance Error Scoring System), signs and symptoms (s/s), and neurocognitive (ImPACT) testing. Each participant was genotyped via saliva sample for the GRIN2A (GT)n repeat polymorphism (rs3219790). Data analysis consisted of descriptive and inferential statistics. Chi-squares were used to assess the association between VNTR (long allele versus short allele) and concussion recovery (prolonged versus normal). Regression analyses were used to estimate extent to which non-genetic factors and genotype contributed to concussion recovery group assignment. One-way ANOVAs were used to identify any significant differences in vestibular ocular, BESS, and ImPACT module scores between long and short alleles. Primary potential non-genetic contributing factors were age, race, sex, concussion history, dizziness at time of injury, history of migraines, and history of ADHD. The alpha level was set at p ≤ .05. There were no differences between demographic or health history within the VNTR or recovery groups. There was a significant association (x2 = 4.01, p = 0.045) between the VNTR group (dominant model: LL versus SS + LS) and recovery, where the chance of prolonged recovery was 4.3 times greater for carriers of the homozygous long allele. There were no differences in concussion severity scores between VNTR group and concussion severity scores. This was the first study to investigate the association of the (GT)n VNTR within GRIN2A. We established a DNA collection, estimation, and genotyping protocol of the (GT)n VNTR for 96 samples and demonstrated accuracy of this genotyping method. Clinically, athletes carrying the long allele genotype may be predisposed to prolonged recovery following a concussive injury.
Temple University--Theses
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Li, Ruifu. "A Novel Thiolated Hyaluronic acid Hydrogel for Spinal Cord Injury Repair". Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31410.
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Spinal Cord Injury (SCI) often causes cell death, demyelination, axonal degeneration and cavitation, resulting in functional motor and sensory loss below the site of injury. In an attempt to overcome SCI, the regenerating neurons require a permissive environment to promote their ability to reconnect. We report a novel thiolated hyaluronic acid (HA) hydrogel scaffold that can be used to repair the injured spinal cord. More specifically, thiolated hyaluronic acid hydrogels with varying thiol concentrations were successfully synthesized. The amount of thiol groups was measured spectrophotometrically using Ellman’s test. HA gels with different crosslinking densities were synthesized and the water content of the hydrogels was determined. The thermal behavior of the HA gels were studied by DSC. The strength of the hydrogels with varying thiol group content was evaluated by a rheometer. In addition, in vitro enzymatic degradation was performed through submerge the hydrogels in 200U/ml of hyaluronidase solution and incubate at 37°C. According to the result of the present study, this novel hydrogel shows great potential to serve as a 3D cell-patterning scaffold which can be inserted into a hollow fiber channel that could be used to promote regeneration after the SCI.
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Euler, Mia von. "Experimental spinal cord injuries : a histopathological, neurological, and pharmacological study in the rat /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3461-4/.
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Timko, Tamara C. "Effects of first aid training on seeking adult assistance in response to simulated injuries by young children with disabilities /". The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487940308434287.
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Müller, Christian. "α-Lipoic Acid Attenuates Ischemia Reperfusion Injury of the Rat Liver". Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-2394.
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Weight, Simon C. "The role of nitric acid in renal warm ischaemia reperfusion injury". Thesis, University of Leicester, 1998. http://hdl.handle.net/2381/29558.
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The purpose of the work described in this thesis was twofold. Firstly, to determine what role nitric oxide (NO) played in renal warm ischaemia reperfusion injury and secondly, once the role was clarified, to assess if this injury could be ameliorated by the pharmacological manipulation of renal NO. The introduction to this thesis comprises two parts. Chapter 1 reviews the pathophysiology of renal ischaemia reperfusion and outlines some of the treatment modalities that have been used in response. Chapter 2 focuses on the physiology of NO and the pathophysiological role it plays in renal reperfusion injury and contrasts some apparent differences between the kidneys and other organs. The three main experimental Chapters are then presented. The first of these describes the development and verification of a NO assay for use with renal tissue homogenate. The next Chapter describes the development of a new model of renal warm ischaemia reperfusion injury in a rodent model which allows the collation of renal NO levels with comparative renal functional, pathological and pathophysiological data. The final experimental Chapter details both the effect of warm ischaemia reperfusion injury on renal NO generation and the subsequent effect of pharmacologically manipulating NO on the degree of renal injury sustained. In the final Chapter the experimental results are reviewed and possible avenues of further investigation are discussed.
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Neese, Steven L. "The neuroprotective effects of Z-bisdehydrodoisynolic acid following traumatic brain injury /". Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1342727221&sid=4&Fmt=2&clientId=1509&RQT=309&VName=PQD.
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James, Bryce. "(+/-)-Z-bisdehydrodoisynolic acid and specific enantiomers : effects on traumatic brain injury /". Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1459903541&sid=1&Fmt=2&clientId=1509&RQT=309&VName=PQD.
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Humphries, Duncan Charles. "Investigating the cerebral/pulmonary axis following traumatic brain injury in a preclinical model". Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/19511.
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Traumatic Brain Injury (TBI) accounts for 1,000,000 hospital admissions in the European Union every year and is the leading cause of death in individuals under 45 years of age in both Europe and the United States. This thesis examines the consequences to both the brain and lung following TBI using the lateral fluid percussion injury (FPI) in an in-vivo murine model. In the murine FPI model, alongside cerebral inflammation (associated with neuronal damage and the infiltration of inflammatory cells), there is significant neutrophil accumulation within the pulmonary interstitium 6 and 24 hours after TBI. This was associated with pulmonary haemorrhage and increased vascular permeability. In an attempt to reduce pulmonary injury, 17-DMAG, an HSP90 inhibitor, was applied but proved to be nonprotective. Since patients with TBI show increased susceptibility to bacterial infection, microaspiration and ventilator-induced lung injury, a double-hit model was established whereby mice first received the head injury and then received a lung injury. This demonstrated worse lung injury following intra-tracheal administration of hydrochloric acid after TBI. Depleting neutrophils with an anti-LY-6G depleting antibody improved outcome in this model, indicating increased susceptibility to damage was neutrophil dependent. To test whether neutrophil accumulation within the pulmonary interstitium was specifically related to brain injury, lung tissue following other distant organ injury such as renal ischemia-reperfusion injury (IRI) and renal transplantation were assessed. Significant pulmonary interstitial neutrophil accumulation was seen following both models and was associated with significant pulmonary haemorrhage. Inducing HSP70 activity with an HSP90 inhibitor was shown to be protective by reducing the degree of pulmonary haemorrhage in these models. In an attempt to identify the mechanisms behind neutrophil accumulation in TBI, renal IRI and renal transplantation, ICAM-1 (CD54), a marker of the reverse transmigration of neutrophils was investigated. No differences in ICAM-1 expression were seen following TBI, indicating that another mechanism must be responsible. This mechanism is the focus of on going work within the laboratory. Hypoxia is believed to contribute towards the development of secondary brain injury however little is known regarding its direct contribution. Working alongside chemists at the University of Edinburgh, a number of novel fluorescent hypoxia probes were designed and tested, but none proved to be able to detect hypoxia in-vitro. In conclusion, this thesis has demonstrated that following mild TBI, the lungs are “primed” with a massive interstitial neutrophil influx and that a subsequent micro aspiration of acid induces exaggerated lung injury. The mechanism by which this occurs is the focus of on-going investigation. Pulmonary sequestration of neutrophils is also a predominant feature of other distant organ injuries.
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Reveruzzi, Bianca. "The protective mechanisms of first aid training within a school-based program for early adolescents". Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/82759/1/Bianca_Reveruzzi_Thesis.pdf.
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This thesis was concerned with the protective mechanisms of first aid training in the context of peer support. Using a randomised control trial design the current program of research explores first aid training in the school setting and identifies the key components of effective school-based first aid training programs. In particular, examining whether first aid training and associated knowledge could be protective for early adolescents. This broader framing considered whether first aid impacted on increasing behaviour and attitudes towards helping an injured friend, and reducing personal risk taking and related injury.
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Stapleton, Sally C. "A preliminary investigation into the use of mobile phones as a memory aid for individuals with traumatic brain injury". Thesis, University of East Anglia, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396732.
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Yin, Terry. "Loss of acid sensing ion channel-1a and bicarbonate administration attenuate the severity of traumatic brain injury". Thesis, University of Iowa, 2013. https://ir.uiowa.edu/etd/2423.
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Traumatic brain injury (TBI) is a common cause of morbidity and mortality in people of all ages. Following the acute mechanical insult, TBI evolves over the ensuing minutes and days. Understanding the secondary factors that contribute to TBI might suggest therapeutic strategies to reduce the long-term consequences of brain trauma. To assess secondary factors that contribute to TBI, we studied a lateral fluid percussion injury (FPI) model in mice. Following FPI, the brain cortex became acidic, consistent with data from humans following brain trauma. Administering HCO3- after FPI prevented the acidosis and reduced the extent of neurodegeneration. Because acidosis can activate acid sensing ion channels (ASICs), we also studied ASIC1a-/- mice and found reduced neurodegeneration after FPI. Both HCO3- administration and loss of ASIC1a also reduced functional deficits caused by FPI. These results suggest that FPI induces cerebral acidosis that activates ASIC channels and contributes to secondary injury in TBI. They also suggest a therapeutic strategy to attenuate the adverse consequences of TBI.
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Santos, Nogueira Eva. "Spinal cord injury: Role of endothelial differentiation gene family lysophosphatidic acid receptors". Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/285416.
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El daño tisular secundario que se produce tras una lesión de la médula espinal contribuye de manera significativa a las pérdidas funcionales que se observan pacientes que padecen este tipo de afectación. Aunque la regeneración axonal y la sustitución de las neuronas dañadas tras el traumatismo medular son objetivos importantes para reparar estas lesiones, el desarrollo de estrategias experimentales que tengan como meta evitar el daño secundario sobre axones, neuronas, mielina y las células gliales, sea probablemente más factible de conseguir.
La respuesta inflamatoria que se produce después de la lesión contribuye de manera significativa al daño secundario. Actualmente se conocen varios mecanismos encargados de promover el reclutamiento de leucocitos de la circulación periférica al tejido medular lesionado, y la activación de las células gliales endógenas. Sin embargo, las moléculas que desencadenan y modulan estas respuestas no se conocen con detalle.
El ácido lisofosfatídico (LPA) es un potente mediador lipídico que activa y regula una gran variedad de respuestas celulares, tales como la homeostasis de calcio, la remodelación del citoesqueleto, la proliferación y supervivencia , la adhesión y migración, y la respuesta inflamatoria . El LPA ejerce todas estas funciones biológicas mediante la activación de 6 receptores acoplados a proteínas G, conocidos como LPARs (LPAR1-6).
Estudios recientes ponen de manifiesto la implicación del LPA en el desarrollo de varias patologías, coma la arteriosclerosis, el cáncer y la fibrosis pulmonar, entre otros. Sin embargo, escasos estudios han evaluado hasta el momento si LPA está implicado en el transcurso de patologías que afectan sistema nervioso. Varias observaciones que proceden de cultivos celulares revelan que el LPA es capaz de activar las células microgliales y astrogliales, de inducir la muerte de neuronas, y promover la retracción axonal. Estudios realizados con animales de experimentación también muestran que el LPA está implicado en la etiología de la hidrocefalia fetal, y en el desarrollo de dolor neuropático tras la lesión del nervio ciático y tras isquemia cerebral. Sin embargo, se desconoce actualmente si el LPA participa de manera activa en la fisiopatología de la lesión medular.
Durante los últimos 3 años hemos obtenido datos experimentales que demuestran que los niveles de LPA aumentan rápidamente en la médula espinal lesionada. También tenemos evidencias convincentes que sugieren que el aumento de los niveles de LPA que se produce en el parénquima medular tras una lesión por contusión desempeña un papel clave en la activación de una respuesta inflamatoria y en el desarrollo del daño secundario, y consecuentemente, en la aparición de déficits funcionales.
En la presente tesis hemos elucidado qué receptores del LPA pertenecientes a la familia génica de diferenciación endotelial (LPA1-3) ejercen efectos nocivos en la lesión medular. Demostramos que los receptores LPA1 y LPA2 contribuyen a la generación del daño tisular tras la lesión medular y a la generación de déficits functionales, mientras que el receptor LPA3 ejerce efectos neutrales. Asimismo, describimos los mecanismos por los cuales los receptores LPA1 y LPA2 promueven daño neuronal y desmielinización. Dado que las principales compañías farmacéuticas están interesadas en el desarrollo de agonistas y antagonistas de los distintos receptores del LPA para el tratamiento de varias patologías de gran repercusión clínica, dicha estrategia tiene una gran posibilidad de traslación clínica.Secondary tissue damage that occurs after spinal cord injury (SCI) contributes significantly to permanent functional disabilities. Although regeneration of damaged axons and replacement of lost neurons are important goals to repair the injured spinal cord, the secondary damage to axons, neurons, myelin and glial cells that follows the initial trauma is likely to be more easily amenable to treatment. Therefore, preventing or minimizing such secondary damage after SCI is expected to substantially reduce functional deficits. The inflammatory response that occurs after SCI strongly contributes to secondary injury. A number of mechanisms underlie the recruitment of leukocytes from the peripheral circulation, and the activation of these cells and endogenous microglia and astrocytes within the injured spinal cord. However, the molecules that trigger these responses are not completely known. Lysophosphatidic acid (LPA) is a potent, biologically active lipid mediator that regulates many physiological functions such as of cellular Ca2+ homeostasis, cytoskeleton remodeling, proliferation and survival, adhesion and migration and inflammation. LPA exerts all these functions by signaling via 6 G-protein coupled receptors known as LPARs (LPA1-6). Recent studies highlight the involvement of LPA in the development of many human diseases, such as atherosclerosis, cancer and pulmonary fibrosis. However, few studies have assessed so far whether LPA contributes to nervous system pathologies. Several in vitro observations reveal that LPA activates astrocytes and microglial cells, causes neuronal cell death, and promotes axonal retraction. In vivo studies also show that LPA is involved in the etiology of fetal hydrocephalus, as well as the development of neuropathic pain after sciatic nerve injury and cerebral ischemia. However, whether LPA is involved in the pathophysiology of SCI is still unknown. We currently have novel unpublished data demonstrating that LPA levels rapidly increased in the contused spinal cord. We have also clear evidences indicating that administration of LPA into the uninjured spinal cords triggers glial cell activation and demyelination, and leads to motor impairments. Altogether, our preliminary results strongly suggest that the increased levels of LPA that occurs after SCI may play an important role in triggering secondary damage and functional impairments. The present thesis aimed at assessing which of endothelial differentiation gene family LPA receptors (LPA1-3) exert such harmful effects in SCI. We found that LPA1 and LPA2 contribute to tissue damage and functional impairments after SCI, whereas LPA3 has a neutral effect.. Moreover, we reveal the mechanisms underlying neuronal cell death and demyelination triggered by LPA1 and LPA2. Since major pharmaceutical companies are interested in the development of LPA receptor agonists and antagonists for the treatment of several human diseases, such treatments have a high likelihood of progressing rapidly to the clinic.
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Mallek, Jennifer de Toledo. "Hyaluronic acid-olfactory ensheathing cell compositions for spinal cord injury nerve regeneration". [Gainesville, Fla.] : University of Florida, 2006. http://purl.fcla.edu/fcla/etd/UFE0015880.
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Chaykovska, Lyubov [Verfasser]. "Role of 20-Hydroxyeikosatetraenoic acid in experimental acute kidney injury / Lyubov Chaykovska". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1025353870/34.
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Huebenthal, Jan. "Injury & Resistance: Centering HIV/AIDS Histories in Times of Queer Equality". W&M ScholarWorks, 2019. https://scholarworks.wm.edu/etd/1563898925.
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Using methods of critical queer genealogy and discourse analysis, Injury & Resistance historicizes the HIV/AIDS epidemic through four lenses—activism, criminalization, memory, and “post-AIDS” queer health—in national and transnational U.S. locales from 1987 to the present. Unlike in the 1980s, when white middle-class gay men were the most visible demographic of what was known as the “gay plague,” today’s American AIDS epidemic is becoming more and more racialized. And unlike 30 years ago, HIV today is a chronic condition that is effectively treatable with antiretroviral drug regimens. Concurrent with the medical survivability of HIV/AIDS, queer Americans have won legal rights to marry, serve openly in the military, and adopt and raise children. Meanwhile, however, for many the AIDS crisis has remained just that: a crisis. If current patterns persist, today one in two African American gay men will become HIV-positive within his lifetime—amidst a healthcare landscape in which racial, regional, and socioeconomic disparities abound. To date, little scholarly work has attended to how the epidemic’s American histories, having fueled an LGBT politics of individual “equality,” have in fact produced these stark simultaneities in which HIV is a chronic reality for some but has remained an emergency for others. Indebted to Michel Foucault, Injury & Resistance historicizes this evolution through a queer “history of the present” that explores the non-linear and asynchronous motions between and among AIDS past and HIV present. In the absence of a multitemporal critique, I argue, we risk ceding the urgency of HIV/AIDS to the past and preclude confronting what is an ongoing public health epidemic. Sources include oral histories from the ACT UP Oral History Project, memoirs of survival, activist photography, medical science statistics and publications, public health campaigns, newspaper records, and documentary film, as well as archival holdings from the Smithsonian National Archive Center, the Archiv der Sozialen Bewegungen (Archive of Social Movements) in Hamburg, Germany, the Special Collections at the James Branch Cabell Library at Virginia Commonwealth University (VCU), and the New York Public Library, among others. This diverse body of sources re-contextualizes national and transnational U.S. AIDS histories that anticipate an ongoing crisis with peculiar dualities: yesterday yet today, ghostly yet present, and acute yet chronic. Arranged loosely from past to present, the four chapters and epilogue present evidence, readings, theories, and speculations, listening for past and present echoes of HIV/AIDS histories that reverberate in experiential chasms between injury and resistance. Chapters present a critical genealogy of feminist activism in the New York chapter of the AIDS Coalition to Unleash Power (ACT UP) from 1987 to 1993, explore a 1987 West German court case against African American ex-soldier Linwood Boyette for alleged HIV transmission, trace Derridean hauntology and queer temporalities in two AIDS memoirs and the National AIDS Memorial Grove, place narratives of “post-AIDS” queer health in relation to neoliberal LGBT rights politics, and consider Uganda’s 2011 “Kill the Gays Bill” as a transcultural circulation of U.S. anti-queer affect and violence. Throughout, this dissertation insists that the ongoing HIV/AIDS crisis, with its rich histories of resistance and dissent, must again become cornerstones of contemporary queer culture and politics.
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Carter-Allison, Samantha Natalie. "Diagnosis threat and injury beliefs after mid traumatic brain injury". Thesis, King's College London (University of London), 2015. https://kclpure.kcl.ac.uk/portal/en/theses/diagnosis-threat-and-injury-beliefs-after-mid-traumatic-brain-injury(c6ba3d52-13d9-46ea-aeee-d34ed2e43943).html.
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Background: Diagnosis threat is a form of stereotype threat, where individuals with a history of mild traumatic brain injury (mTBI) have shown performance decrements on cognitive tasks, owing to negative expectancies around cognitive ability elicited by cues in the environment. This study systematically reviews experimental studies to gauge the presence/absence of an effect of diagnosis threat on neuropsychological task performance in mTBI. It also investigates whether methodological variation and methodological quality contribute to variation in study findings. Method: A systematic search of four online databases (Medline, PyscINFO, SportDISCUS, PsycEXTRA) was conducted to identify diagnosis threat studies that employed an experimental paradigm. Neuropsychological test outcomes were extracted, along with information on inclusion criteria, mTBI diagnostic criteria, participant characteristics and study design. Methodological quality was assessed using modified Scottish Intercollegiate Guidelines Network (SIGN) criteria. Results: A total of nine studies were identified. Evidence for diagnosis threat was found, although there was considerable heterogeneity across study results. The most robust finding was the impact of diagnosis threat on the cognitive domain of attention/working memory. No clear associations between methodological variation, methodological quality and study outcome were noted. Conclusions: The review found evidence for diagnosis threat, although the strength of this effect may be smaller than previously thought. Although there was heterogeneity across elements of study design, there was no obvious relationship between these factors and outcome. However, the substantial variation makes comparison difficult. These issues are similar to findings in other examinations of stereotype threat. Further research is needed to replicate findings and add clarity to the impact of diagnosis threat on both objective and subjective measures, and to further investigate the role of possible moderating variables. A more formal meta-analysis in the area may also be helpful to clarify findings in the research field. Future studies should aim to create established operational definitions and outcomes to improve consistency and comparability between studies.
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Ferguson, Scott. "Smartphone technology : everyday prompts for those with prospective memory difficulties following brain injury". Thesis, University of Hertfordshire, 2013. http://hdl.handle.net/2299/19859.
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BACKGROUND: Prospective memory difficulties are one of the most common deficits following acquired brain injury. The application of smartphones as a compensatory aid to these difficulties has shown promising results. This study looked to investigate these benefits further. OBJECTIVE: The aims of this study were to investigate whether receipt of reminder prompts through ones smartphone improved completion of pre-planned tasks, in addition to whether it also had secondary implications for participant's wellbeing, confidence, independent functioning, and whether it had any impact on caregiver strain levels. METHOD: This study used an ABAB case series design with mild to moderate acquired brain injury. Task completion rates were monitored across four phases (prompts vs. no prompts). Quantitative questionnaires were administered pre, post and at three months follow up to assess coping with memory difficulties. A qualitative questionnaire explored the perceived impact of the smartphone reminders on everyday functioning, in addition to a 3 month follow up measure assessing attrition rates in smartphone use. RESULTS: Visual inspection analysis suggested greater task completion when reminders were provided. The quantitative questionnaires showed increased use of a Smartphone as reminder device post intervention and at follow up. A basic thematic analysis highlighted a perception that the smartphone system increased task completion, confidence in coping with memory demands, supported emotional wellbeing and reduced dependence on others. As a memory aid it was also less stigmatising and promoted dignity. The three month follow up questionnaire highlighted that all participants continued to use their smartphone as a memory aid. CONCLUSIONS: Use of a smartphone as a memory compensation aid may improve completion of pre-set tasks. Secondary benefits may include increased confidence in coping with memory demands, reduced dependence on others for help, and reduced anxiety or frustration around forgetting.
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Moldrich, Randal Xavier Joseph 1975. "Functional roles of group II metabotropic glutamate receptors in injury and epilepsy". Monash University, Dept. of Pharmacology, 2002. http://arrow.monash.edu.au/hdl/1959.1/7710.
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Badion, Yu. "Duration of prehospital assistance to victims with traumatic injuries in rural areas". Thesis, Sumy State University, 2016. http://essuir.sumdu.edu.ua/handle/123456789/45942.
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Emergency aid – one of the most important parts of a unified system of care to the population of our country.
We know that there is a direct correlation between the severity of traumatic injuries and timely arrival of medical personnel to the affected.
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McGeorge, Nicolette M. "The effect of training, aim pattern and target type on the ergonomics and efficiency of handheld scanners /". Online version of thesis, 2009. http://hdl.handle.net/1850/10643.
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Angus, Ruth. "In vivo and in vitro studies on docosahexaenoic acid in traumatic brain injury". Thesis, Queen Mary, University of London, 2017. http://qmro.qmul.ac.uk/xmlui/handle/123456789/30628.
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Traumatic brain injury (TBI) is a devastating disease causing disability and death, and currently there are no effective treatments available. Therefore, there is an utmost need to improve our understanding of the pathophysiology of TBI and to identify potential therapies that can provide neuroprotection after injury. The aims of this thesis were to develop an in vivo and in vitro model of TBI, in which to assess the potential neuroprotective effects of an omega-3 polyunsaturated fatty acid (PUFAs), docosahexaenoic acid (DHA). Method The controlled cortical impact (CCI) in vivo model of TBI was optimized and performed in mice. Both a behavioural (Morris water maze (MWM) for cognitive deficits) and histological endpoints (astrogliosis, lesion size and activated microglia) were used to assess severity and neuroprotective effects of DHA. An in vitro model of mechanical TBI was also set up and optimized. This model employed 3D astrocyte cultures obtained from GFP positive rat pups. The CCI impactor from the in vivo studies was used to damage the cultures, and at 24 hours, 5 days and 10 days the astrogliosis and cell number was measured. Results The optimization of the in vivo studies demonstrated that at impaction depth of 2.2 mm produced an injury that was significantly different to the sham injury, in MWM performance and increased astrogliosis. Interestingly, there was an increase in the amount of astrogliosis on the contralateral side of the brain. A second study performed using the 2.2 mm injury parameters was performed, where an injection of DHA was administered via the tail vein 30 min after injury. The DHA-treated group did not demonstrate any neuroprotection compared to the injury-only group. However, there was an increase in the amount of astrogliosis in the contralateral hippocampus of the DHA-treat group. In the fat-1 studies it was shown that older male mice performed worse in the MWM, that the fat-1 gene did not confer neuroprotection but did lead to increased astrogliosis. The in vitro study revealed that astrocytes in the lesioned gels demonstrated an increase in astrogliosis, there was also an increase in the number of cell in the cultures following the lesion. Conclusion In conclusion, the in vivo model of CCI replicated components of the human TBI including a behavioural deficit and pathophysiological changes. Omega-3 PUFAs failed to demonstrate functional neuroprotection in this model, but histologically, promoted an increase in reactive astrogliosis. The development of a novel in vitro model of focal injury in a 3D culture system, that elicits reactive astrogliosis, could be used to support further studies of the astrocytic responses to mechanical injury.
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Li, Guangbi. "Podocyte Dedifferentiation and Glomerular Injury Mediated by Lysosome Dysfunction: Role of Acid Ceramidase". VCU Scholars Compass, 2017. https://scholarscompass.vcu.edu/etd/5169.
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Cell differentiation and senescence in podocytes are attributed to normal autophagy and associated cellular activities. It is possible that derangement of autophagy under different pathological conditions activates or enhances podocyte dedifferentiation leading to glomerular injury and ultimate glomerular disease. To test this hypothesis, we first tested whether autophagic deficiency due to lysosome dysfunction enhances podocyte dedifferentiation and explored the molecular mechanisms by which this lysosome dysfunction trigger or enhance podocyte dedifferentiation. By Western blot and confocal analysis, lysosome inhibition using an inhibitor or siRNA of V-ATPase inhibitor was found to markedly decrease the epithelial markers (P-cadherin and ZO-1) and increase the mesenchymal markers (FSP-1 and α-SMA). This enhancement of podocyte dedifferentiation (formerly referred to as epithelial-mesenchymal transition, EMT) was accompanied by deficient autophagic flux, as demonstrated by marked increases in LC3B-II and p62/Sequestosome 1. However, inhibition of autophagosome formation using spautin-1 (SP-1) significantly attenuated both enhancement of podocyte dedifferentiation and deficiency of autophagic flux. To explore the mechanisms by which deficient autophagic flux enhances podocyte dedifferentiation, we tested the role of accumulated p62 as a signal hub in this process. Neither the nuclear factor erythroid 2-related factor 2 (Nrf2) nor nuclear factor kappa (NFκ)-light-chain-enhancer pathway regulating p62 function was found to contribute to enhanced dedifferentiation. However, inhibition of cyclin-dependent kinase 1 (CDK1) activity reduced the phosphorylation of p62 and enhanced podocyte dedifferentiation similar to lysosome dysfunction, which indicates that enhanced podocyte dedifferentiation due to lysosome dysfunction may be triggered by accumulation of p62 and associated reduction of p62 phosphorylation. Given the essential role of sphingolipid-ceramide metabolism and transient receptor potential-mucolipin-1 (TRPML1) channel activity in lysosome function, we next sought to test whether altered ceramide metabolism by acid ceramidase (AC) leads to deficient lysosome trafficking and fusion to autophagosome in podocytes and thereby results in autophagic deficiency and podocyte dedifferentiation. Inhibition of AC by a potent and selective inhibitor, carmofur markedly reduced lysosome trafficking and fusion to both autophagosomes and multivesicular bodies (MVBs). Concurrently, enhancement of podocyte AC activity or exposure of podocytes to sphingosine, a product of ceramide metabolism by AC, remarkably increased lysosome trafficking and fusion to autophagosomes and MVBs, indicating that AC activity is critical for lysosome function in podocytes. To further explore the mechanisms by which AC activity contributes to lysosome trafficking, we examined the effects of various sphingolipids related to ceramide metabolism on transient receptor potential-mucolipin-1 (TRPML1) channel, a Ca2+ channel essential for lysosome trafficking and function. It was found that sphingomyelin (SM), a precursor for ceramide production blocked TRPML1 channel activity induced by ML-SA1 (a specific TRPML1 agonist), while ceramide had no effects on TRPML1 channel activity induced by ML-SA1. Interestingly, sphingosine, an AC product of ceramide remarkably enhanced TRPML1 channel activity induced by ML-SA1. These results demonstrate that AC product of ceramide, sphingosine may enhance TRPML1 channel activity, but an upstream sphingolipid, SM may exert inhibitory action on lysosome TRPML1 channel activity. AC may be a key enzyme gating TRPML1 channels by production of sphingosine and changes in upstream substrate SM. These results from in vitro cell studies led us hypothesize that a deficient AC activity may induce podocyte injury through lysosome dysfunction, leading to glomerular damage and proteinuria. To test this hypothesis, we generated a mouse colony with podocyte-specific gene deletion of AC α subunit, namely, Asah1fl/fl/PodoCre mice. In these mice, severe proteinuria and albuminuria were shown compared to their littermates, but they were without global and even focal glomerular sclerosis. These mice also had hypoalbuminemia and edema, and under transmission electron microscopy (TEM) ultrastructural changes of podocytes from their glomeruli exhibited diffuse and flat foot process (podocyte effacement), vacuolation, and microvillus formation, which were not observed in their littermates. Treatment of corticosteroids and specific expression patterns of dystroglycans in glomeruli confirmed that albuminuria in these Asah1fl/fl/PodoCre mice may be resistant to corticosteroids. Together, these results from in vivo animal studies indicate that podocyte-specific gene deletion of AC α subunit may induce a corticosteroid-resistant minimal change disease (MCD). Based on all results from our in vitro and in vivo studies, we conclude that the normal lysosome function is essential for maintenance of autophagic flux and podocyte differentiation, which is regulated by a lysosomal AC-mediated signaling pathway through a TRPML1 channel gating mechanism. AC gene defect or deficiency of its activity induces podocyte injury, which is characterized by a corticosteroid-resistant MCD. These findings indicate an important pathological role of AC deficiency and associated lysosome dysfunction in podocytes injury and corticosteroid-resistant MCD, which may help develop novel therapeutic strategies for prevention or treatment of corticosteroid-resistant MCD.
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Fahy, Katherine Erin. "Thermal Burn Injury Induced Microvesicle Particle Release". Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright149383031006972.
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Wang, Hongrui. "Developing Novel Methods to Mitigate Freezing Injury in Grapevines". The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1564743163557437.
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Gouda, Mazen M. "Axon Initial Segment Integrity in Aging and Traumatic Brain Injury". VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5993.
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According to the Center for Disease Control’s (CDC) report to the Congress, there are 2.2 million emergency department visits; 80,000 hospitalizations; and 50,000 deaths each year due to traumatic brain injury. Adults 65 years and older account substantially for the majority of the hospitalization and deaths. Over 70% of the traumatic brain injuries of the older adults are classified as mild to moderate; however, even with these milder injuries, older adults present with a significantly higher morbidity and mortality compared to all other age groups (LeBlanc et al., 2006). With that in mind, it seems essential to develop a deeper understanding of the causes behind higher mortality and morbidity of traumatic brain injury in the elder population. It is well documented that increased age is accompanied by increased CNS inflammation. Recently, our laboratory showed that inflammation drives brain pathology. Specifically, we reported that the axon initial segment of cortical neurons was structurally and functionally compromised in an inflamed CNS environment. With this in mind, we proposed that age-related inflammation predisposes that brain to exacerbated pathologic consequence. To test this hypothesis, we administered a mild to moderate central fluid percussion brain injury in aged and young adult mice. Using immunocytochemical labeling against the axon initial segment protein ankyrinG combined with laser scanning confocal microscopy, we quantitatively compared axon initial segment number and length between age groups and within age groups with and without injury. Additionally, we also quantified global axonal pathology by immunolabeling for amyloid precursor protein (APP) positive swelling as an indicator of compromised axonal transport. We proposed that ankyrinG labeling will be both reduced in the aged injured mice compared against aged uninjured, young adult injured and young adult non-injured. We observed a significant increase in APP accumulations due to injury independent of aging, and due to aging independent of injury. No significant changes in the effect of injury between young and aged injured mice were observed. Although AIS length was not altered between age groups following injury, our results demonstrate that the elderly population presents with significantly shorter initial segments. The consequence of this shortening is not clear but may reflect compensatory changes in the brain to maintain homeostasis.
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Hawes, Carol V. "The impact of ozone on the physiology and growth of beech". Thesis, Lancaster University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267192.
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Sapiro, Jessica M., e Jessica M. Sapiro. "Molecular Mechanisms Associated with All-Trans-Retinoic Acid-Mediated Cytoprotection against Renal Cell Injury". Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/625452.
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Chemical-induced nephrotoxicity is a major cause of acute kidney injury. My dissertation reveals that all-trans-retinoic acid (ATRA) affords cytoprotection against renal cell injury. Pretreatment with ATRA (25 μM, 24 hr) affords selective cytoprotection against p-aminophenol (PAP), iodoacetamide (IDAM), and 2-(glutathion-S-yl)-hydroquinone-induced necrosis. In contrast, pretreatment of cells with ATRA provides no protection against cisplatin-induced apoptosis. Inhibition of protein synthesis blunts ATRA-mediated cytoprotection, suggesting that critical cell survival signaling pathways are activated prior to toxicant exposure. Oxidative stress is a major contributor to cellular damage. To investigate the mechanism(s) by which ATRA affords cytoprotection, we determined its effects on ROS generation using a DCFDA assay. ATRA did not alter PAP or MGHQ-induced ROS levels. Moreover, ATRA had no effect on GSH levels nor Nrf2 expression, suggesting that other cytoprotective mechanisms are engaged by ATRA. Elevated ROS disrupt endoplasmic reticulum protein folding guided by the molecular chaperone Grp78. During ATRA-mediated pretreatment, the ER stress proteins Grp78 and p-eIF2α were induced (2-fold) in a time-dependent manner (24 and 4 hr respectively). In addition to influencing organelle stress proteins in the ER, ATRA rapidly (15 min) induced levels of the cellular stress kinases p-ERK and p-AKT with maximum levels achieved at 30 min. Moreover, induction of these stress kinases was observed at concentrations of ATRA (10 and 25 μM) required for cytoprotection. Inhibition of p-ERK with PD98059 reduced the ability of ATRA to provide protection against PAP toxicity, implying a role for p-ERK and downstream target genes in the protective effects of ATRA. Gene ontology analysis of a microarray experiment of cells treated with ATRA revealed that ATRA rapidly (0.5, 1 hr) induced growth factors and genes involved in cell proliferation, with subsequent (4, 8, 12 hr) induction of genes involved in ribosome biogenesis, DNA replication and repair, and cell cycle regulation. Complementary data from a cell stress protein array and western blot analyses indicated that ATRA induced HIF1α 3-fold at 8 hr. Furthermore, the microarray data indicated the HIF1α target gene BHLHE40 (which encodes a basic-helix-loop-helix protein involved in cell differentiation) was increased 3-fold. As ATRA induced genes that were associated with cell proliferation, related assays were employed. ATRA had a small effect on cell cycle distribution demonstrated by an increase in the population of cells in the S and G2 phases between 8 and 24 hr. In addition, ATRA markedly increased total DNA content and cell number at 24 hr suggesting that mitogenic/proliferative effects contribute to ATRA cytoprotection. The present studies indicate that a signaling cascade of proteins downstream of p-ERK associated with mitogenesis work cooperatively to afford ATRA protection against renal cell injury. Understanding the mechanism of ATRA-mediated cytoprotection will provide insights into the development of novel therapeutic strategies for renal pathological conditions.