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1
Foroud, Afra, and University of Lethbridge Faculty of Arts and Science. "Moving from stroke to development : a deconstruction of skilled reaching in humans." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Neuroscience, c2008, 2008. http://hdl.handle.net/10133/1307.
Full textAbstract:
The purpose of this thesis is to describe the organization of the movements of skilled
reaching. Our knowledge of reaching behaviour has been limited to an understanding of
specific actions. Results from this thesis describe how reaching is the product of
interactions of various parameters that assemble in an integrative way in ontogeny, yet
can become dismantled on one level, or generally, throughout multiple levels of what
constitutes the behaviour after stroke in adults. These findings demonstrate that skilled
reaching constitutes motor parameters that may not be visible in a healthy adult, but that
function through development, and by inhibitory systems in adults, to create a smooth
and finely articulated action. An examination of the movement patterns of reaching
within the full context of the behaviour can be applied to therapeutic strategies for motor
disorders and, most importantly, deepen our understanding of the relations between
reaching and cognition.xiii, 254 leaves : ill. (some col.) ; 29 cm
2
Man, Lai-mei, and 文麗媚. "An exploratory study for the health seeking pattern of stroke survivors on alternative medicine." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31978617.
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Nicolakakis, Nektaria. "Investigation and treatment of ABeta- and TGF-Beta1- related cerebrovascular dysfunction in Alzheimer's Disease." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66738.
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ABSTRACT Alzheimer's disease (AD) is characterized by neurodegeneration, memory loss and premature cerebral circulatory deficits marked by a vascular structural pathology thought to involve elevated levels of amyloid-beta (Aβ) and transforming growth factor-beta 1 (TGF-β1). We sought to investigate the role of Aβ and TGF-β1 in promoting cerebrovascular dysfunction as well as disturbances in glial, neuronal and cognitive function using transgenic mice overexpressing either (APP, TGF mice) or both (APP/TGF mice) peptides. We attempted to remedy arterial and hemodynamic deficits using a pharmacological approach with free radical scavengers and the peroxisome proliferator-activated receptor γ (PPARγ) agonist pioglitazone, compounds known to correct peripheral vascular dysfunction. In addition, we evaluated treatment outcome on glial, neuronal and cognitive AD markers. We found that cerebrovascular dysfunction in APP mice was mediated by a pro-oxidant pathway activated by soluble Aβ, and that it was completely remedied with antioxidant treatment and pioglitazone, even at an advanced age. In contrast, cerebrovascular impairments of TGF mice were insensitive to antioxidants, related to alterations in signaling molecules within the vessel wall, accompanied by vascular fibrosis and responsive only to pioglitazone. APP mice also featured AD-like glial, neuronal and memory deficits, and contrary to an antioxidant, pioglitazone completely reversed most of these in aged animals, although earlier treatment may be warranted to restore memory. In contrast, TGF mice experiencing chronic cerebrovascular insufficiency lacked neuronal and cognitive impairments. This suggested that, alone or at insufficient levels, hemodynamic deregulation does not necessarily lead to memory loss, but constitutes an aggravating factor in the presence of underlying pathology. In APP/TGF mice, the vascular phenotype was predominantly TGF-like, featuringLa maladie d'Alzheimer (MA) est caractérisée par la mort neuronale, la perte de la mémoire, une dysfonction cérébrovasculaire et pathologie structurelle des vaisseaux cérébraux, que l'on croit associées aux niveaux élevés d'amyloïde-bêta (Aβ) et du «transforming growth factor-beta 1» (TGF-β1). Nous avons évalué le rôle de ces deux protéines dans la pathologie cérébrovasculaire associée à la MA, ainsi qu'aux changements gliaux, neuronaux et cognitifs, en se servant de souris transgéniques qui sur-expriment l'une ou les deux (modèles APP, TGF et APP/TGF) de ces protéines. Nous avons tenté d'améliorer les déficits artériels et hémodynamiques, ainsi que marqueurs gliaux, neuronaux et cognitifs, avec des antioxydants et un agoniste des récepteurs PPARγ, la pioglitazone, composés efficaces contre les troubles vasculaires périphériques. Chez les souris APP, les problèmes cérébrovasculaires ont été attribués au stress oxydatif engendré par l'Aβ soluble, et étaient complètement normalisés par les antioxydants et la pioglitazone, en dépit de l'âge avancé des souris. Seule la pioglitazone a été efficace chez les souris TGF, dont les dysfonctions cérébrovasculaires étaient accompagnées par une fibrose, et plutôt reliées à des changements dans les molécules vasomotrices de la paroi vasculaire. Les souris APP exhibaient des déficits gliaux, neuronaux et cognitifs, dont la plupart ont été complètement normalisés par la pioglitazone, quoiqu'un traitement précoce soit peut-être requis pour restaurer la mémoire. En revanche, malgré une insuffisance cérébrovasculaire chronique, les indices neuronaux et mnémoniques des souris TGF étaient intacts. Ceci suggère qu'un trouble hémodynamique seul ou au seuil observé dans le modèle TGF, en l'absence d'une pathologie sous-jacente, ne suffit pas à perturber la mémoire, et constitue donc un facteur aggravant dans la MA. Le$
4
Gu, Yong, and 顧勇. "Targeting caveolin-1 as a therapeutic approach to prevent blood-brain barrier breakdown in ischemic stroke : from mechanism to isoflavones treatment." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/197561.
Full textAbstract:
Our group previously reported that caveolin-1 (cav-1) was down-regulated by nitric oxide (NO) during cerebral ischemia and reperfusion (I/R). However, the role of cav-1 in regulating blood-brain barrier (BBB) permeability is unclear yet. This study aims to address whether the loss of cav-1 induced by NO production affects BBB permeability. Data showed that the expression of cav-1 in isolated cortical microvessels was down-regulated in ischemia-reperfused rat brains subjected to middle cerebral artery occlusion (MCAO). Treatment of NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, reserved cav-1 expression, inhibited matrix metalloproteinases (MMPs) activity and reduced the BBB permeability. Moreover, cav-1 knockdown remarkably increased MMPs activity in the culture medium of brain microvascular endothelial cells. Cav-1 deficiency mice displayed higher MMPs activity and BBB permeability than that of the wild-type mice. Interestingly, the effects of L-NAME on MMPs activity and BBB permeability were partly reversed in cav-1 deficiency mice. These results suggest that cav-1 plays important roles in regulating MMPs activity and BBB permeability in cerebral I/R injury.
After completing the mechanism study, I investigated the potential drug candidate that targets cav-1 for protecting BBB and neuronal damage during cerebral I/R. Results showed that calycosin, an isoflavones from Astragali Radix, up-regulated the expression of cav-1 and inhibited MMPs activity, and decreased the BBB permeability in the MCAO ischemia-reperfused rat brains. I further investigated the neuroprotective effects of isoflavones of Astragali Radix, with in vitro oxygen glucose deprivation (OGD) model and in vivo cerebral ischemia-reperfusion models. In addition to calycosin and formononetin, two major isoflavones in Astragali Radix, daidzein was also included because it is a metabolite of formononetin after absorption. Results showed that all three isoflavones decreased infarction volume and neurological scores in MCAO rats and dose-dependently attenuated neuronal death induced by L-glutamate treatment and oxygen-glucose deprivation plus reoxygenation (OGD/RO). The neuroprotective effects were inhibited by estrogen receptors (ER) antagonist ICI 182,780. Interestingly, combine treatment of isoflavones displayed synergistic effects in both OGD/RO and L-glutamate induced neuronal injury models, as well as in MCAO cerebral ischemia-reperfusion rat brains. Mechanistically, estrogen receptor antagonist partly reduced the synergism in these models. PI3K/Akt activation was synergistically induced by treatment of those isoflavones simultaneously.
In summary, cav-1 could be a potential therapeutic target for protecting the BBB in the treatment of cerebral I/R injury. Major findings in this thesis include: 1) Cav-1 plays an important role in maintaining BBB integrity through inhibition of MMPs activity. NO induced MMPs activities and BBB leakage are partially mediated by the down-regulation of cav-1 during cerebral I/R injury. 2) Calycosin treatment reserved cav-1 expression and reduced BBB permeability. 3) Isoflavones synergistically protected neurons against I/R-induced neuronal insults both in vitro and in vivo. The works provide a valuable step towards the clarification of the physiological and pathophysiological functions of cav-1, and a new clue for developing isoflavones as agents targeting cav-1 for the prevention or treatment of ischemic stroke.published_or_final_version
Chinese Medicine
Doctoral
Doctor of Philosophy
5
Silasi, Gergely, and University of Lethbridge Faculty of Arts and Science. "Novel treatments for inducing cortical plasticity and functional restitution following motor cortex stroke." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2005, 2005. http://hdl.handle.net/10133/278.
Full textAbstract:
Stroke remains a leading cause of disability in the western world, with symptoms ranging in severity from mild congnitive or motor impairments, to severe impairments in both cognitive and motor domains. Despite ongoing research aimed at helping stroke patients the disease cannot be prevented or cured, therefore a large body of research has been aimed at identifying effective rehabilitative strategies. Based on our understanding of normal brain function, and the meachanisms mediating the limited spontaneous recovery that is observed following injury, factors that promote brain plasticity are likely to be effective treatments for stroke symptoms. The current thesis investigated three novel treatments (COX-2 inhibitor drug, vitamin supplement diet, and social experience) in a rat model of focal ischemia in the motor cortex. All three treatments have been previously shown to alter plasticity in the normal brain, however the current experiments show that the treatments have differential effects following stroke. The COX-2 inhibitors provided limited improvement in functional performance, whereas the vitamin supplement treatment had no effect. Social experience on the other hand was found to block the usually observed spontaneous improvements following the stroke. These results suggest that factors that alter dendritic plasticity may in fact serve as effective stroke treatments depending on the site and the mechanisms whereby the plastic changes are induced.ix, 149 leaves : ill. ; 29 cm.
6
Gharbawie, Omar A., and University of Lethbridge Faculty of Arts and Science. "Modeling middle cerebral artery stroke in rats : an examination of the skilled reaching impairments." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2006, 2006. http://hdl.handle.net/10133/388.
Full textAbstract:
Middle cerebral artery (MCA) stroke can produce chronic incapacitating motor
impairments. Understanding the neural basis of the motor syndromes is complicated by
the diversity of neural structures damaged but the problem can be addressed in laboratory
rats by inducing selective infarcts. Nevertheless, the motor syndromes that ensue from
stroke in rats remain poorly understood and undermine its potential as a model for
clinical stroke. The objective of the present thesis was to document the skilled reaching
impairments from neocortical and subcortical MCA infarcts in rats. In addition, the
integrity of the motor system components spared by the infarct was assessed
neurophysiologically and neuroanatomically. Characteristic reaching impairments
emerged from each infarct but there were also some overlapping features that might be
explained by neural dysfunction extending beyond the boundaries of the infarct. The
present studies showed that the laboratory rat is an ideal animal model for studying
stroke, which should be of interest to both clinical and research scientists studying stroke.xiii, 345 leaves : ill. ; 29 cm. + 1 CD-ROM
7
Qi, Chuanjie, and 亓传洁. "Effects of notoginsenoside R1 against glutamate neurotoxicity in vitro and on mice brain following ischemic stroke in vivo." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206464.
Full textAbstract:
Ischemic stroke is a leading cause of disability and death around the world. Higher concentration of glutamate following ischemic stroke is a factor leading to cell death, including neural stem cell death. Up to now no effective treatments of ischemic stroke are available. Notoginsenoside R1 (Noto R1) is the main component of Panax notoginseng, which is a traditional Chinese medicine for the treatment of cardiovascular disease. Its protective effects on the neural cell were noted recently. The main purpose of this experimental study was to investigate the mechanism of Noto R1 against glutamate neurotoxicity on primary cultured mouse cortical neural stem cells in vitro, and its effects on ischemic stroke on mice brain in vivo.
In the in vitro part, primary culture of neural stem cells was prepared from 12.5-day-old C57BL/6N mice embryos cortex. Neural stem cells were confirmed by nestin-staining and differentiation study afterwards. Then neural stem cells were incubated with Noto R1 and glutamate for 24 hours. Cells were fixed for TUNEL staining and caspase-3 staining. Protein was collected for western blot for Bax, Bcl-2, phos-AKT, JNK/SAPK, and phospho-p38 MAPK. Results showed that glutamate has cytotoxicity in a dose-dependent manner on neural stem cells. Noto R1 showed remarkable neuro-protective effects on neural stem cells exposed to excessive glutamate by higher viability. Noto R1 significantly reduced caspase-3 expression and TUNEL-positive cells. Furthermore, Noto R1 increased the protein expression of Bcl-2 and phospho-AKT, and reduced Bax expression. Moreover apoptosis pathway study showed phospho-p38 expression was suppressed in the Noto R1 group.
In the in vivo part, Noto R1 was administrated systemically to mice of MCAo followed by reperfusion. Behavior score and viability rate were assessed before sacrifice. TTC staining was performed for evaluating infarct area, volume and edema. H&E staining was applied for histological examination. TUNEL staining, IHC staining of Nestin, AQP4 and GFAP were performed. In the first part of Noto R1 of 40 mg/kg or PBS was injected into venous at the onset of blood vessel occlusion for 2 hours, and then followed by 22 hours of reperfusion. Results were all negative. In the second part, Noto R1 was injected intra-peritoneum for 10 days prior to MCAo which lasted for 1 hour 50 minutes, then reperfusion was allowed for 22 hours. Results showed Noto R1 improved behavior score and viability rate. Meanwhile Noto R1 significantly reduced ischemic area, volume and edema percentage. Moreover TUNEL-positive cells in the affected cortex were significantly decreased. Nestin-positive cell in the striatum were significantly increased in the Noto R1 group, and immunoactivity of AQP4 and GFAP was apparently decrease with Noto R1 treatment.
In conclusion, this study showed that Noto R1 protected cultured neural stem cells against glutamate neurotoxicity in vitro via p38 MAPK pathway by inhibiting Bax protein expression and enhancing protein expression of Bcl-2 and phospho-AKT. Moreover, it also demonstrated significant preventive effects against ischemic stroke with mice model in vivo. In a word Noto R1 presents a highly potential candidate preventing ischemic stroke clinically in the future.published_or_final_version
Anatomy
Doctoral
Doctor of Philosophy
8
金珍妮. "中風後抑鬱症針灸治療臨床文獻研究." HKBU Institutional Repository, 2016. https://repository.hkbu.edu.hk/etd_oa/243.
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中風後抑鬱症（ Post-strok Depression, PSD ）的發生率，在中風後患者中佔有較大比例，嚴重影響患者的康復。國外研究結果顯示中風後抑鬱症的發病率為28%-56%而國內臨床相關文獻提示中風後抑鬱的患病率大致為20% - 50%。臨床中存在有許多繼發於中風的抑鬱患者，診療未受到關注的現狀。而一些接受治療的病人，也因長期口服抗抑鬱藥導致副作用愈發突出。與此同時，針灸治療抑鬱的臨床優勢已經得到國內外醫學界的重視與肯定。本文著重以近10 年來針灸治療中風後抑鬱症的文獻為主進行研究，總結關於該病因病機及有特色針灸療法的最新研究進展，歸納選穴處方的規律特點，進而在已有研究基礎上融人自己的見解，對於PSD 這種身心疾病的治療提出相關值得探討的問題與對今後研究的展望。新近的國內外研究提示，在針灸治療中風後抑鬱領域目前主要有毫針針刺和特種針法，並結合電針、配合藥物以及心理健康教育等方法，可以促進中風後患者抑鬱情緒的調整，且一定程度上也加強其他肢體功能以及神經功能的康復。同時針刺在治療的臨床研究方面也已取得較大進展，部分實驗已設立自身前後對照研究及其他藥物或針刺對照比較觀察，在診斷及評定療效標準時使用了量表及統計分析，增強了療效的可信度及可比性。一些課題也已進入實驗室研究，從神經遞質、神經內分泌方面探求針刺治療PSD 的機制，並取得一定的進展。本研究得出今後應該加強隨機大樣本對照的前瞻性設計實驗的結論，認為中風後抑鬱症的臨床分型、穴位配伍、針刺手法、刺激量大小以及療效評價等方面，均將成為針灸治療本病的繼續研究之探索方向。
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吳明真. "中風後痙攣性偏癱針灸取穴規律的計量文獻研究." HKBU Institutional Repository, 2012. http://repository.hkbu.edu.hk/etd_ra/1344.
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10
曾偉賢 and Wai-yin Tsang. "Analysis of data from a double-blind, placebo-controlled randomised clinical trial for the treatment of stroke." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1993. http://hub.hku.hk/bib/B31977509.
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Tsang, Wai-yin. "Analysis of data from a double-blind, placebo-controlled randomised clinical trial for the treatment of stroke." Hong Kong : University of Hong Kong, 1993. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13787007.
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Rulli, Nestor Ezequiel, and na. "Ross River Virus Infection: Disease Mechanisms and Potential Treatment." University of Canberra. School of Health Sciences, 2007. http://erl.canberra.edu.au./public/adt-AUC20080227.091948.
Full textAbstract:
Ross River virus (RRV) is a mosquito-borne alphavirus and the aetiological agent of
epidemic polyarthritis (EPA). Arthropod borne-Alphaviruses that are related to RRV,
such as Chikungunya virus, Sindbis virus and Barmah Forest virus, are usually
associated with epidemics of infectious arthritides in different parts of the world. In
humans, RRV-induced disease symptoms include fever, rash, myalgia and pain and
stiffness of the joints. Muscle and joint pain are the most debilitating symptoms in RRV
patients and the best treatment available is non-steroidal anti-inflammatory drugs
(NSAID). Previous studies in mice have demonstrated that RRV infection results in
inflammation of skeletal muscle and joints and that macrophages play a primary role in
disease.
The present study was carried out to further elucidate the underlying mechanisms
mediating RRV-induced muscle and joint pathology. Previous studies have reported
that encephalitic alphaviruses trigger apoptosis of brain cells in mice and that blocking
apoptosis reduces mortality rates. In the present study, the ability of RRV to induce
muscle apoptosis was investigated in vitro, using a murine myoblast cell line (C1C12),
and in vivo, using a mouse model of RRV disease. RRV-infected C1C12 myofibres
displayed an array of morphological and biochemical makers of apoptosis. Apoptosis
was also observed in the skeletal muscle of RRV-infected C57BL/6J mice. Blocking
apoptosis by general caspase inhibition resulted in milder disease symptoms, reduced
myofibre damage and decreased inflammation of muscle and joint tissues. The total
number of cell infiltrates as well as the number of macrophages infiltrating muscle was
significantly reduced by the treatment with a caspase inhibitor.
The effects of RRV infection on the skeletal system were also investigated. Primary
human osteoblast cells were infected with RRV and monitored for viral-induced
cytopathic effect. Osteoblasts supported rapid virus growth and, by 48 hours after
infection, succumbed to viral-induced necrosis. In addition, histological examination of
bone tissue from RRV-infected C57BL/6J mice showed clear evidence of bone
resorption. Tibias from infected mice showed an increased number of activated
osteoclasts, a reduction in bone density and thinning of cortical bone.
The expression of host factors involved in inflammatory responses and bone
remodelling was studied in RRV-infected myofibres and osteoblast cell cultures and in
the muscle and joint tissues from infected mice. RRV-infected muscle cells and tissue
showed elevated mRNA levels for the chemokines CCL-2, CCL3, CCL5 and CXCL1,
all of which are known to mediate the migration of monocytic cells. With the exception
of CXCL1, these chemokines were also found to be up-regulated in RRV-infected
osteoblast cultures and in joint tissues from infected mice. Muscle and joint tissue from
infected mice also showed elevated mRNA levels for type I and type II interferons,
TNF- and NOS2. In addition, joint tissues from infected animals contained high levels
of IL-6 and IL-1, two cytokines known to mediate bone remodelling.
Finally, the therapeutic potential of the drug bindarit was investigated using the mouse
model of RRV disease. Bindarit is a known inhibitor of CCL-2 and TNF- and has
been found to prevent protein denaturation. Treatment with bindarit resulted in mice
developing milder disease symptoms, reduced muscle damage and decreased
inflammation of muscle and joint tissues. In particular, bindarit significantly reduced
macrophage infiltration into skeletal muscle tissue.
This thesis has contributed to the understanding of RRV pathogenesis. It has identified
novel mechanisms of RRV-induced muscle and bone pathology and provided further
evidence that associate pro-inflammatory host factors to RRV disease. This work has
also demonstrated that bindarit should be considered as a candidate for treating RRV
disease in humans.
13
Petoumenos, Kathy Public Health & Community Medicine Faculty of Medicine UNSW. "Treatment experience and HIV disease progression: findings from the Australian HIV observational database." Awarded by:University of New South Wales. School of Public Health and Community Medicine, 2006. http://handle.unsw.edu.au/1959.4/24937.
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The Australian HIV Observational Database (AHOD) is a collaboration of hospitals, sexual health clinics and specialist general practices throughout Australia, established in April 1999. Core data variables collected include demographic data, immunological and virological markers, AIDS diagnosis, antiretroviral and prophylactic treatment and cause of death. The first electronic data transfer occurred in September 1999 followed by six monthly data transfers thereafter. All analyses included in this thesis are based on patients recruited to AHOD by March 2004. By March 2004, 2329 patients had been recruited to AHOD from 27 sites throughout Australia. Of these, 352 (15%) patients were recruited from non-metropolitan clinics. The majority of patients were male (94%), and infected with HIV through male homosexual contact (73%). Almost 90% of AHOD patients are antiretroviral treatment experience, and the majority of patients are receiving triple therapy as mandated by standard of care guidelines in Australia. Antiretroviral treatment use has changed in Australia reflecting changes in the availability of new treatment strategies and agents. The crude mortality rate was 1.58 per 100 person years, and of the 105 deaths, more than half died from HIV-unrelated deaths. The prevalence of HBV and HCV in AHOD was 4.8% and 10.9%, respectively. HIV disease progression in the era of highly active antiretroviral treatment (HAART) among AHOD patients is consistent with what has been reported in developed countries. Common factors associated with HIV disease progression were low CD4 cell count, high viral load and prior treatment with mono or double therapy at the time of commencing HAART. This was demonstrated in AHOD in terms of long-term CD4 cell response, the rate of changing combination antiretroviral therapy and factors predicting death. HBV and HCV coinfection is also relatively common in AHOD, similar to other developed country cohorts. Coinfection does not appear to be serious impediments to the treatment of HIV infected patients. However, HIV disease outcome following HAART does appear to be adversely affected by HIV/HCV coinfection but not in terms of HIV/HBV coinfection. Patients attending non-metropolitan sites were found to be similar to those attending metropolitan sites in terms of both immunological response and survival.
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Price, Brittani Rae. "PRECLINICAL TARGETING OF TREM2 FOR THE TREATMENT OF ALZHEIMER'S DISEASE-TYPE PATHOLOGY IN A TRANSGENIC MOUSE MODEL." UKnowledge, 2019. https://uknowledge.uky.edu/physiology_etds/43.
Full textAbstract:
Alzheimer's disease (AD) is defined as a progressive neurodegenerative disorder and is characterized by a devastating mental decline. There are three pathological hallmarks of the disease necessary for its diagnosis, these are extracellular amyloid plaques comprised of the beta-amyloid (Aβ) protein, intracellular neurofibrillary tangles comprised of hyperphosphorylated tau protein, and marked neuronal loss. Active immunization against Aβ1-42 or passive immunization with monoclonal anti-Aβ antibodies has been shown to reduce amyloid deposition and improve cognition in transgenic mouse models of AD, aged beagles, and nonhuman primates. Unfortunately, due to cerebrovascular adverse events, both active and passive immunization strategies targeting Aβ have failed in clinical trials. It is, therefore, necessary to identify novel amyloid-clearing therapeutics that do not induce cerebrovascular adverse events. We hypothesized that neuroinflammatory modulation could be a potential novel target.
Triggering receptor expressed on myeloid cells-2 (TREM2) is a lipid and lipoprotein binding receptor expressed exclusively in the brain by microglia. Homozygous TREM2 loss of function mutations cause early-onset progressive presenile dementia while heterozygous, function-reducing point mutations triple the risk of sporadic, late-onset AD. Heterozygous TREM2 point mutations, which reduce either ligand binding or cell surface expression, are associated with a reduction in the number of microglia surrounding amyloid plaques, microglial inability to phagocytose compact Aβ deposits and form a barrier between plaques and neurons, an increase in the number of phospho- tau-positive dystrophic neurites and increased tau in the cerebrospinal fluid. Heterozygous mutations also double the rate of brain atrophy and decrease the age of AD onset by 3-6 years. Although human genetics supports the notion that loss of TREM2 function exacerbates neurodegeneration, it is unclear whether activation of TREM2 in a disease state is beneficial.
The work we present here characterizes a TREM2 agonizing antibody as a potential therapeutic for amyloid reduction. We found that its administration results in immune modulation, recruitment of microglia to the site of amyloid plaques, reduced amyloid deposition and improvement in spatial learning and novel object recognition memory in the 5xFAD model of AD. More specifically, we show that intracranial injection of TREM2 agonizing antibodies into the frontal cortex and hippocampus of 5xFAD mice leads to clearance of diffuse and compact amyloid. We also show that systemic injection of TREM2 agonizing antibodies weekly over a period of 14 weeks results in clearance of diffuse and compact amyloid as well as elevated plasma concentrations of Aβ1-40 and Aβ1-42. Furthermore, systemic administration of these antibodies led to immune modulation and enhanced cognitive performance on radial arm water maze and novel object recognition tests. Importantly, we show the TREM2 agonizing antibody does not induce the adverse cerebrovascular events known to accompany amyloid modifying therapies. Though systemic administration of both TREM2 agonizing and anti-Abantibodies does not further enhance amyloid clearance or cognitive performance, co-administration mitigates the adverse cerebrovascular events associated with anti-Aβ antibodies.
Collectively, these data indicate TREM2 activators may be an effective therapeutic target for the treatment of AD.
15
Rosell, Johan. "Long-term effects of adjuvant tamoxifen treatment on cardiovascular disease and cancer." Doctoral thesis, Linköpings universitet, Avdelningen för kliniska vetenskaper, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-112085.
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The aims of this thesis were to investigate the long-term effects of adjuvant tamoxifen treatment on breast cancer recurrence and mortality, cardiovascular disease, and the incidence of secondary cancer. Between 1982 and 1992, postmenopausal patients with early stage breast cancer were included in a randomized clinical study of 2 or 5 years of postoperative tamoxifen therapy. The trial was planned by the Swedish Breast Cancer Group, and it included 4610 patients. Follow-up on causes of death, hospitalizations and secondary cancers were obtained from national population-based registries. All-cause mortality, breast cancer-specific mortality and mortality from coronary heart disease were decreased in the 5-year group, but the incidence of endometrial cancer was increased (Paper I). The incidence and mortality of cerebrovascular diseases were increased during the active treatment phase, and reduced after the active treatment (Paper II). Similar results were seen for subgroups of cerebrovascular diseases such as stroke and ischemic stroke. In the 5-year group, the morbidity from coronary heart disease was reduced during treatment but not after treatment was stopped (Paper III). This was the case also for heart failure and for atrial fibrillation/flutter. For secondary cancers the lung cancer risk was reduced, as well as the lung cancer mortality (Paper IV). An increased risk was observed for endometrial cancer, but appeared to decrease over time. The risk of contralateral breast cancer was reduced, with most of the reduction after treatment was stopped. For distance recurrences the risk was reduced both during treatment and a few years after treatment was stopped. The breast cancer mortality was also reduced, especially during the post-treatment phase.
16
Luo, Dan, and 骆丹. "Anti-inflammatory mechanisms of compound C from gastrodia and uncaria decoction, a commonly used post-stroke decoction." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/211556.
Full textAbstract:
Ischemic stroke is a leading cause of death and long-term disability in the world. Although many pathological aspects of mechanisms are considered to be involved in the stroke, accumulating evidences implicated that inflammation accounts for its progression and complications. Tumor necrosis factor-alpha (TNF-α) and nitric oxide are considered as key mediators produced by cells like microglia in the pathogenesis of the disease. Therefore, the development of therapies targeting at the suppression of nitric oxide and TNF-α productions may ameliorate the severity of ischemic stroke.
Gastrodia and Uncaria Decoction (GUD) is a traditional herbal decoction that is commonly used in the therapy of post-ischemic stroke in China. Although it shows great efficacy in clinical treatment, few studies have been conducted to investigate the mechanisms of action of GUD. Furthermore, GUD contains a complex mixture of constituents and the effects of these compounds are unknown. In this study, individual herbs from GUD were extracted and the bioactive fractions were further separated using liquid-liquid partition, silica gel chromatography and high performance liquid chromatography (HPLC). The inhibitory effect of the extracts on lipopolysaccharide (LPS)-stimulated nitric oxide production in BV-2 microglial cells was utilized as the biological marker for the screening. After several rounds of purification, a purified bioactive compound was isolated. After spectroscopic analysis by nuclear magnetic resonance and gas chromatography-mass spectrometry, the compound was identified as genipin (1R,4aS,5,7aS-tetrahydro-1-hydroxy-7-(hydroxymethyl)-cyclopenta[c]pyran-4-carboxylic acid, methyl ester). Mechanisms of the suppressive action on signaling pathways were investigated in the LPS-activated BV-2 cells.
Our results demonstrated that genipin can dose-dependently inhibit LPS-stimulated nitric oxide overproduction. It can also suppress mRNA levels and protein expressions of inducible nitric oxide synthase (iNOS) and TNF-αupon LPS-induction. In addition, the phosphorylations of phosphoinositide-3 kinase (PI3K) and protein kinase B (Akt) were suppressed. In contrast, the phosphorylations of mitogen-activated protein kinases (MAPKs), nuclear translocation of nuclear factor-κB (NF-κB) p65 and degradation of inhibitory κB-α (IκB-α) were not affected by genipin. Finally, genipin protected murine Neuro-2a neuroblast against neurotoxicity stimulated by the conditioned media transferred from LPS-challenged BV-2 cells.
In conclusion, the anti-inflammatory effects of genipin are via the modulation of PI3K/Akt signaling pathway. Genipin and its synthetic analogues may have great potential for developing into new drugs in treating ischemic stroke. In addition, genipin can be used as the chemical marker to standardize the extract of Eucommia ulmoides Oliver as anti-inflammatory agents for treating inflammatory conditions associated with ischemic stroke.published_or_final_version
Paediatrics and Adolescent Medicine
Master
Master of Philosophy
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Kirkland, Scott, and University of Lethbridge Faculty of Arts and Science. "Modulation of recovery and compensation after stroke." Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2007, 2007. http://hdl.handle.net/10133/387.
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Stress has been shown to exacerbate cell death and cognitive deficits after ischemic
injury in rodents, however, little is known of the effects of stress on motor recovery. The
objective of this present thesis is to examine the effects of chronic stress on skilled motor
recovery after devascularization lesion in rats. It was found that pre-lesion stress induced
the most behavioural impairments, while post-lesion stress exacerbated infarct volume.
The effects of chronic multiple stress on skilled motor recovery after lesion was also
examined. Chronic multiple stress did not modulate skilled motor recovery nor did it
have any influence on infarct volume. Additionally, stress had effect on edema after
devascularization lesion. The present thesis suggests that the time of exposure to chronic
stress in respect to the ischemic lesion, in addition to the type of stress, will differentially
affect recovery and compensation in rats.xii, 122 leaves : ill. ; 29 cm.
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張桂鴻. "針灸治療中風痙攣性癱瘓的臨床研究." HKBU Institutional Repository, 2008. http://repository.hkbu.edu.hk/etd_ra/957.
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周榮富. "針灸治療缺血性中風後遺症的方法學評價." HKBU Institutional Repository, 2010. http://repository.hkbu.edu.hk/etd_ra/1126.
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Chen, Xi, and 陈曦. "Exploring molecular targets and active compounds from buyang huanwu decoction for promoting neurogenesis in post-ischemic stroke treatment." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193430.
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Katzenellenbogen, Judith Masha. "Use of data linkage to enhance burden of disease estimates in Western Australia : the example of stroke." University of Western Australia. School of Population Health, 2009. http://theses.library.uwa.edu.au/adt-WU2009.0117.
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[Truncated abstract] The Disability-Adjusted Life Year index, developed by the Global Burden of Disease Study, is used extensively to compare disease burden between locations and over time. While calculation of the fatal component of this measure, Years of Life Lost, is relatively straight-forward, the non-fatal component, Years Lived with Disability, is based on parameters that are challenging to estimate. This thesis pioneers the use of the Western Australian Data Linkage System to enhance epidemiological parameters underpinning Years Lived with Disability, providing, by way of illustration, a robust quantitative profile of burden of stroke in the state of Western Australia at the turn of the 21st century. The principal methodological objective was to utilise data linkage analytic methods for the specific requirements of burden of disease estimation. The principal stroke-related objectives were: 1. To estimate the parameters underpinning the non-fatal burden of stroke (Years Lived with Disability) in Western Australia in 2000. 2. To estimate the total burden of stroke (Disability-Adjusted Life Years) in Western Australia in 2000. 3. To investigate differentials in stroke burden between different sub-populations in Western Australia. 4. To calculate projections of stroke burden for Western Australia in 2016. Years Lived with Disability from stroke were calculated for Western Australia from nonfatal stroke incidence, expected duration and disability (severity) weights. Non-fatal incidence was estimated using linked hospital and death records of first-ever hospitalised stroke 28-day survivors in 2000. This was then adjusted for out-of-hospital cases determined from the population-based Perth Community Stroke Study. iv Analysis of mortality in hospitalised 28-day survivors using linked data revealed that the excess mortality in prevalent, rather than incident cases was the main disease-specific parameter required for modelling stroke duration using DisMod II specialised software. ... Access to data linkage and population-based stroke studies in Western Australia allowed more accurate estimation of non-fatal stroke burden, with previous reports most likely underestimating disability as a contributor to total burden. Although predominantly affecting the growing aged population, stroke also affects a sizable number under the age of 65 years, the age group where differentials in stroke burden are the greatest. The findings highlight the continued need for primary prevention efforts for all ages, targeting especially younger people in disadvantaged groups. The shift to greater disability burden in the future and the needs of disadvantaged groups must be considered when planning stroke services. The multiple studies undertaken for this thesis contribute to ongoing improvement of data quality and methodological refinements underpinning estimates of Years Lived with Disability, specifically for stroke, but applicable also to other diseases. Similar linked data approaches can be used in other Australian states in the future once infrastructure is developed, thereby improving estimates of disease burden for health policy and planning in the future.
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甘錫森. "針灸治療中風的機理研究 : 針灸對中風高血脂症的調節作用." HKBU Institutional Repository, 2008. http://repository.hkbu.edu.hk/etd_ra/959.
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狄荻. "针灸治疗中风后失语症的临床文献评估." HKBU Institutional Repository, 2015. https://repository.hkbu.edu.hk/etd_oa/138.
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中风后失语，现代医学称“急性交流障碍” ，它是急性脑血管病的常见症状之一，古代医籍中称失语为“喑痹” 、“风懿” 、“风喑” 、“风癔” 、“难言” 、“不语”等。〈素问－脉解〉云：“所谓入中为喑者’阳盛己衰，故为喑也。内夺而厥，则为喑痹。”《素问－刺禁论〉云：“……刺足少阴脉’重虚出血’为舌难以言。”《金匮要略·中风历节病脉证治〉：“邪入于腑，即不识人；邪入于脏’舌即难言’口吐涎”等。 言语障碍是脑血管疾病的常见症状，在卒中急性期，合并有失语的患者比例高达21%-38% ，据国内报道，脑血管疾病患者约25%伴有言语障碍。另外，卒中患者中除了明显失语之外，仍有60%患者在交流上存在问题。由于中风失语不仅给家庭、社会和国家带来沉重的经济负担，同时也给中风患者的身心带来了巨大伤害，故探索有效的中风失语治疗方案、提高其临床疗效、改善失语症患者的生存质量是当今亟待解决的问题。 本文对于中风后失语症的论述主要分为两大部分： 第一部分从中、西医角度认识中风后失语症。中风的病因是以正气不足、肝肾阴亏、肝阳上扰、肝风内动、血脉不通、风邪留而不去为致病之本，以风、火、痰、湿、气、血为致病之标。由此而并发的失语症主要是舌体瘫痪强直、记忆力下降健忘或认知障碍思维不清所导致，其病在心（脑），肝涉及脾、肾等脏腑。众多研究者进行了对于中风后失语症的各种治疗方法的多方面研究， 笔者收集了2010年1月至2014年12月的相失临床文献并进行了整理分析。 第二部分从针灸临床角度，对所收集到关于针灸治疗中风后失语的文献进行综合分析。运用计量学评价方法，从期刊分布、年份分布、诊断标准、随机对照、言法、脱落病例、样本量、治疗方法等多个方面， 对针灸治疗中风后失语症的研究状况做一个全面系统的分析及，并在此基础上对临床研究质量的总体水平作出评价，讨论中风后失语症的针灸临床规范研究方案，筛选有效的针灸处方，提高针灸临床科研的质量。 關键词：中风后失语症 针灸治疗
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胡鵬. "電針治療急性缺血性中風的作用機理探討." HKBU Institutional Repository, 2014. https://repository.hkbu.edu.hk/etd_oa/1.
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現代醫學上中風可分為出血性中風和缺血性中風兩種。缺血性腦中風是指因腦血液供應障礙所引起的局限性腦組織的缺血性壞死或軟化。常見臨床類型包括動脈粥樣硬化性血栓性腦梗死、腦栓塞、腔隙性腦梗死。 中風病以其高發病率、高死亡率、高致殘率嚴重危害著人類健康，為社會和家庭帶來了沉重的負擔。因此，對該病的防治是重要的醫學和社會課題。針灸治療中風在我國有著悠久的歷史，以其簡單、便捷、靈驗在缺血性中風的治療中佔有一定的優勢，而且其療效已得到世界衛生組織的認同。為了更系統更全面地探討電針治療缺血性中風的作用機制，本文從以下幾個方面進行了研究。 一、背景資料 推本溯源，從我國第一部中醫學經典著作《黃帝内經》開始，到唐、宋、元、明、清等時期，對古代文獻中有關中風的病名和病因病機進行了探討。此外，本文還分別探討了目前中醫在中風病治療上的常用方法，特別是針灸臨床的常用方法。 二、電針作用機理的探討 電針對腦組織急性缺血性損傷的保護機理是歷年來的研究熱點。本文收集近10年電針治療急性缺血性中風作用機理的相關文獻，研究者多使用大鼠或小鼠局部腦缺血模型進行電針幹預，觀察電針幹預後動物模型腦部血流的變化，從神經細胞可塑性、細胞凋亡通道、腦缺血耐受、血管功能修復、炎症因子、血小板凝集、氧化應激等多角度闡述電針治療急性缺血性中風的起效機理。 二、結論 1.通過對古今文獻的研究，我們認為針剌治療缺血性中風具有科學的理論依據和良好的臨床療效。 2.通过電針作用機理相關文獻的探討，電針證實對急性缺血性中風具有治療作用，其作用機理與神經幹細胞或祖細胞的增殖、神經活性因子表達的上調、突觸的重塑、提高基因轉錄、調控内源性凋亡途徑、改善損傷内環境、開放側支循环、調節血管舒縮、促進血管網新生、減輕炎症損傷、抑制血小板活化、對抗氧化應激等方面有關。電針治療缺血性中風具有多方位、多靶點的特點，既可抑制腦缺血時的損傷因子，又可以激發機體自身的修復能力，共同達到針灸治療的目的。 希望通過此次文獻研究，為電針治療急性缺血性中風的起效機理提供參考，使本病的論治更加系統化、科學化，临床治療更加具有针对性。 關鍵字：電針、急性缺血性中風、腦卒中、作用機理
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Xie, Lixia. "Effects of salvianolic acid B against apoptosis and adhesion molecules expression in the vascular endothelial cells." HKBU Institutional Repository, 2009. http://repository.hkbu.edu.hk/etd_ra/1082.
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蕭偉雄. "頭針為主治療缺血性中風的臨床研究文獻評價." HKBU Institutional Repository, 2010. http://repository.hkbu.edu.hk/etd_ra/1129.
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Rendle, Jessica Amy Jane. "Epidemiology of lumpy jaw in captive macropods across Australia and Europe: An investigation of disease risk and treatment approaches." Thesis, Rendle, Jessica Amy Jane (2019) Epidemiology of lumpy jaw in captive macropods across Australia and Europe: An investigation of disease risk and treatment approaches. PhD thesis, Murdoch University, 2019. https://researchrepository.murdoch.edu.au/id/eprint/49721/.
Full textAbstract:
Lumpy jaw is a well-recognised cause of morbidity and mortality in captive macropods (Macropodidae) worldwide. The extent and causes of the disease are largely unknown, although multiple risk factors associated with a captive environment are thought to contribute to the development of clinical disease. Identification of risk factors associated with lumpy jaw would assist with the development of preventive management strategies, potentially reducing mortalities.
A cross-sectional study was undertaken from 2011 to 2015, to determine prevalence and risk factors for this disease through the distribution of a survey to 527 institutions across Australia and Europe; two regions where macropods are popular exhibits. Veterinary and husbandry records from the period 1st January 1995 up to and including 28th November 2016 (the last date when data were extracted from zoo records) were analysed in a retrospective cohort study, examining risk factors for developing disease and treatments used, over time. Computed tomography was used to examine disease occurrence in wild macropods using skulls from population management culls.
The prevalence of lumpy jaw was found to differ between the two regions (p < 0.0002). A review of 6178 records for 2759 macropods housed within eight zoos across the Australian and European regions, found incidence rates and risk of infection differed between geographic regions and individual institutions. Risk of developing lumpy jaw increased with age, particularly for macropods >10 years (Australia IRR 7.63, p < 0.001; Europe IRR 7.38, p < 0.001). Treatment approach varied and prognosis was typically poor with 62.5% mortality for Australian and European regions combined. Lumpy jaw was detected in all captive genera examined, but was absent from the wild populations studied.
Geographic region influenced the incidence of lumpy jaw, the risks associated with developing clinical disease, and preferred treatment approach. Despite advances in antibiotic therapy and surgical techniques, treatment of lumpy jaw is largely unrewarding for the individual and should be approached on an individual basis. This research provides new information about this refractory disease and makes practical recommendations to reduce disease risk. This information may assist institutions in providing optimal long-term health management for captive macropods; such efforts having a positive impact on both welfare and conservation, including but not limited to captive breeding and translocation programs.
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Rahman, Rosanna, and n/a. "Potential causes of the delayed neural damage observed post-stroke & the effects of epigallocatechin gallate administration." University of Otago. Department of Pharmacology & Toxicology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070508.122246.
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Stroke is the 3rd leading cause of death and the leading cause of major disability worldwide. Currently, there are no neuroprotective drugs approved for the acute treatment of ischaemic stroke. The vast majority of stroke therapeutics failed in clinical trials due to toxic side effects and/or a clinically irrelevant therapeutic window. This thesis is focused on exploiting the delayed neurodegeneration that occurs in the compromised penumbra, as these cells may be capable of being saved by therapeutic intervention in a clinically obtainable window. In order to investigate the ischaemic cascade and be able to draw conclusions that are applicable to humans, the international gold standard animal model for cerebral ischaemia, the filament insertion middle cerebral artery occlusion (MCAO) model, was established at the University of Otago. This model was validated under new laboratory conditions and employed adult male Sprague Dawley rats. After testing multiple occlusion lengths, it was concluded that a 2hr ischaemic period was sufficient to produce a consistent infarct of optimal size. It has been well documented that neuroinflammation contributes to much of the delayed progression of neural injury post-stroke. Therefore, the catechin (-)-epigallocatechin gallate (EGCG), which is an anti-inflammatory, anti-oxidant and free-radical scavenging agent was investigated in the MCAO model of stroke. 50mg/kg i.p. of EGCG or saline was administered immediately post-MCAO and animals were sacrificed at 72hr post-filament insertion. The results confirmed that treatment with EGCG was neuroprotective and non-toxic. However, EGCG also induced an over 50% increase in the risk of haemorrhagic conversions. The anti-platelet effects of EGCG and lack of toxicity suggests that the catechin may prove to be an efficacious prophylactic for stroke. The contrary findings for EGCG treatment led to the re-evaluation of the neuroinflammatory pathway for alternate mechanisms to target therapeutic interventions.
The temporal profile of the primary inducible enzymes nitric oxide synthase (NOS), cyclooxygenase (COX) and arginase (and their isoforms) were quantified 0, 3 and 7 days post-stroke. In both hemispheres, total NOS activity exhibited a significant and sustained up-regulation to 7 days post-occlusion. In the ipsilateral hemisphere at least half of the total increase was accounted for by inducible NOS (iNOS) expression. Arginase, which competes with NOS for L-arginine, demonstrated a delayed but significant increase in activity by day 7 in the infarcted hemisphere, thereby correlating well with the downward slope of NOS activity (illustrating the switch in the conversion pathway). COX activity was observably increased in the ipsilateral hemisphere, but the up-regulation did not reach significance by day 7. Alternately, the contralateral hemisphere displayed a significant decrease in activity by day 3. These results give conclusive evidence that the contralateral hemisphere is NOT an appropriate internal control and imply that NOS and COX inhibitors may prove to be efficacious for a much longer therapeutic window than current treatments. However, the delayed induction of COX activity may also indicate that this enzyme has a finite therapeutic window, as it may also stimulate remodelling of surviving neural networks. The prolonged up-regulation of inflammatory mediators implies that there may be an induction of an autoimmune component to the response. Therefore, the thymus (T) lymphocyte activation was quantified up to 14 days post-stroke. Cluster of differentiation (CD) 3⁺ T lymphocytes (equally contributed to by CD4⁺ and CD8⁺ T cells) exhibited a significant and sustained up-regulation in the infarcted region from day 3 up to at least day 14 post-ischaemia. Quantitative analysis of all cells present post-stroke determined that immune cells make up an average of 73% of all cells present in the 'peak' ischaemic areas. The CD4⁺ T helper cell response was delineated by double immunohistochemical labelling. Interferon-γ positively labelled with CD4⁺ T cells at days 3, 7 and 14 post-insult detailing a Th1-driven pro-inflammatory response. This evidence indicates that the autoimmune response is critical post-ischaemia and that it may be highly susceptible to modification by anti-inflammatory therapeutic intervention.
The primary downstream effect of the pro-inflammatory/immune cascade is apoptosis. The main organelle responsible for the 'go, no go' response to apoptotic factors is the mitochondria. In order to distinguish whether mitochondrial dysfunction was initiated shortly after ischaemia induction or if it was delayed, like the inflammatory/immune response, to a clinically relevant window, the temporal profile of mitochondrial complex inactivation was studied. It was found that mitochondrial membrane viability was impaired by day 3, followed by a significant decrease in respiratory complex activation and an increase in tissue injury by oxidative stress by 7 days post-ischaemia. These results indicate that targeting the early decrease in membrane viability or mitochondrial permeability transition pore opening combined with anti-apoptotic therapeutics, may attenuate the proceeding mitochondrial impairment in oxidative phosphorylation, reactive oxygen species generation and subsequent cell death cascades. The current investigations into the temporal profile and quantitative contributions of the inflammatory, immune and apoptotic mechanisms post-stroke highlight potential strategies for modulation by acute stroke therapeutics. Furthermore, the general knowledge amassed from these studies dictates the necessity of a new approach to therapeutic intervention. The acknowledgement of so many contributing systems suggests that in addition to a thrombolytic, a combination therapy involving multiple neuroprotectants should be employed to account for the multifaceted nature of the sequelae of ischaemic stroke.
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Mpofu, Tariro Ann-Maureen. "Comparison of the neuroprotective potential of theanine and minocycline." Thesis, Rhodes University, 2010. http://hdl.handle.net/10962/d1003253.
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Stroke is one of the most common causes of disability and death worldwide. The most commonly experienced stroke in the clinical setting is focal ischaemia in which the middle cerebral artery (MCA) is occluded and leads to a complex series of various pathophysiological pathways that ultimately lead to neuronal cell death. Several studies have been conducted on various therapeutic agents in the search for a neuroprotective drug and various animal models have been used to carry out this research. While theanine, a component of green tea and minocycline, a tetracycline antibiotic, have been shown to possess some neuroprotective properties, the mechanisms by which these two agents carry out these effects still remains unclear. The objectives of this study were to investigate the mechanisms by which these drugs carry out these neuroprotective effects and their neuroprotective ability in a MCA occlusion model of focal ischaemia. Ischaemia leads to oxidative stress due to the imbalance of free radicals and the endogenous antioxidant defence system. An antioxidant assay using the stable 2, 2-diphenyl-1-picrylhydrazyl (DPPH●) radical was used to assess the antiradical properties of each drug. It was found that minocycline showed superior antioxidant activity in vitro when compared to theanine. Further studies on the drugs‟ ability to attenuate the Fenton reaction (in which iron catalyses the formation of reactive species) were elucidated using electrochemical analysis, UV/VIS studies, ferrozine and ferritin assays. It was found that minocycline, in contrast to theanine, was able to bind to iron ions and thus potentially prevent the participation of iron in metal catalysed radical reaction. The antioxidant activity of both drugs was further investigated by assessing their effect on cyanide-induced superoxide generation and quinolinic acid (QA)-induced lipid peroxidation (LP). Experimental evidence shows that both drugs had no significant effect on the generation of superoxide in vitro and that there was a significant decrease in LP for minocycline in vitro and theanine in vivo. The metal binding and antioxidant properties were postulated to be a possible mechanism through which these agents reduced lipid peroxidation. A study was conducted to determine the effects of the drugs on the biosynthesis of the neurotoxin, QA and it was found that minocycline increases the levels of holoenzyme activity of tryptophan-2, 3-dioxygenase (TDO) in vitro and that theanine reduces the levels of the same enzyme in vivo after treatment for 10 days. TDO is the enzyme that converts tryptophan to other products that enable enzymatic activity to change it to QA. Minocycline was thought to bring about this effect as it has been shown from preceding experimental studies that it is an effective reducing agent. Theanine on the other hand is hypothesised to bring about a reduction in holoenzyme activity by changing the binding of tryptophan to the enzyme or affecting the radicals that participate in the enzymatic degradation of tryptophan. A focal ischaemic model of stroke was induced by occluding the MCA. Histological examination of the hippocampus post -ischaemia shows a reduction in the size of the infarct after pre-treatment with minocycline only. A further study into the effects of the drugs on the generation of superoxide and on the levels of the endogenous glutathione after a stroke was carried out. Pre-treatment of the animals with either theanine or minocycline showed no significant effects on the generation of the radical species or of the endogenous antioxidant which ruled out these as a mechanism of neuroprotection of both drugs, post-ischaemia.The findings of this study provide novel information on the possible mechanisms by which both theanine and minocycline act to bring about neuroprotection. In particular in this study, pre-treatment with minocycline has shown promise in the focal ischaemic model of stroke.
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Hu, Guang. "Pharmacological characterization of angiogenesis effect of Astragali Radix." Thesis, University of Macau, 2012. http://umaclib3.umac.mo/record=b2586303.
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Mannan, Haider Rashid. "Development and use of a Monte Carlo-Markov cycle tree model for coronary heart disease incidence-mortality and health service usage with explicit recognition of coronary artery revascularization procedures (CARPs)." University of Western Australia. School of Population Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0101.
Full textAbstract:
[Truncated abstract] The main objective of this study was to develop and validate a demographic/epidemiologic Markov model for population modelling/forecasting of CARPs as well as CHD deaths and incidence in Western Australia using population, linked hospital morbidity and mortality data for WA over the period 1980 to 2000. A key feature of the model was the ability to count events as individuals moved from one state to another and an important aspect of model development and implementation was the method for estimation of model transition probabilities from available population data. The model was validated through comparison of model predictions with actual event numbers and through demonstration of its use in producing forecasts under standard extrapolation methods for transition probabilities as well as improving the forecasts by taking into account various possible changes to the management of CHD via surgical treatment changes. The final major objective was to demonstrate the use of model for performing sensitivity analysis of some scenarios. In particular, to explore the possible impact on future numbers of CARPs due to improvements in surgical procedures, particularly the introduction of drug eluting stents, and to explore the possible impact of change in trend of CHD incidence as might be caused by the obesity epidemic. ... When the effectiveness of PCI due to introduction of DES was increased by reducing Pr(CABG given PCI) and Pr(a repeat PCI), there was a small decline in the requirements for PCIs and the effect seemed to have a lag. Finally, in addition to these changes when other changes were incorporated which captured that a PCI was used more than a CABG due to a change in health policy after the introduction of DES, there was a small increase in the requirements for PCIs with a lag in the effect. Four incidence scenarios were developed for assessing the effect of change in secular trends of CHD incidence as might be caused by the obesity epidemic in such a way that they gradually represented an increasing effect of obesity epidemic (assuming that other risk factors changed favourably) on CHD incidence. The strategy adopted for developing the scenarios was that based on past trends the most dominant component of CHD incidence was first gradually altered and finally the remaining components were altered. iv The results showed that if the most dominant component of CHD incidence, eg, Pr(CHD - no history of CHD) levelled off and the trends in all other transition probabilities continued into future, then the projected numbers of CABGs and PCIs for 2001-2005 were insensitive to these changes. Even increasing this probability by as much as 20 percent did not alter the results much. These results implied that the short-term effect on projected numbers of CARPs caused by an increase in the most dominant component of CHD incidence, possibly due to an ?obesity epidemic, is small. In the final incidence scenario, two of the remaining CHD incidence components-Pr(CABG - no history of CHD) and Pr(CHD death - no CHD and no history of CHD) were projected to level off over 2001-2005 because these probabilities were declining over the baseline period of 1998-2000. The projected numbers of CABGs were more sensitive (compared to the previous scenarios) to these changes but PCIs were not.
32
常瀟月. "電針治療中風後抑鬱臨床文獻的方法學評價." HKBU Institutional Repository, 2014. https://repository.hkbu.edu.hk/etd_oa/5.
Full textAbstract:
一、背景 中風是臨床常見病多發病，病死率與致殘率均高，流行病學調查結果顯示，我國中風發病率為（109.17〜217)/10萬，中風發病6個月以後仍遺留程度不同的偏癱、麻木、言語蹇澀不利、口眼喎斜、癡呆、情感障礙等後遺症，患者生活品質嚴重降低，其後遺症之一情感障礙以中風後抑鬱症（post stroke depression，PSD)為主。隨著中風的發病率持續增高，中風後抑鬱症同樣呈上升趨勢，國內外研究顯示，中風發病後6個月至2年間PSD的發生率和嚴重程度最高，發病率為30%〜70%，高於其他肢體殘疾患者人群抑鬱發生率（15.1%〜22.5%)及普通人群抑鬱發生率(3%〜6%)。中風後抑鬱症能推遲神經功能缺損恢復，延長恢復時間並使勞動力喪失，降低患者的生活品質，加重患者的精神痛苦，而且使患者對康復方案的實施缺乏積極性和主動性，嚴重影響治療和健康，甚至還會導致患者死亡。近年來，隨著中風患者存活率的提高、神經康復的普及和神經心理學的發展，中風後抑鬱症也越來越引起人們的廣泛關注。中西醫治療中風後抑鬱症有著較好的療效，尤其是針灸治療中風後抑鬱症有著效果顯著、不良反應很少出現、明顯提高患者的生存率和生活品質等優勢。筆者將对近年電針治療中風後抑鬱症的临床文獻做一次評價和探討。 二、目的 通過對近五年針灸治療中風後抑鬱症的國內外臨床研究文獻進行全面檢索，通過對其48篇相關文章的方法學品質評價，對該治療方法進行分析總結，以使電針在治療中風後抑鬱症發揮更好的作用，從而為臨床醫療服務。 三、方法 採用中國生物醫學文獻光碟資料庫（CBM disc）、中國期刊全文資料庫（CNKI,期刊全文資料庫，學位論文資料庫）、中文科技期刊全文資料庫（VIP)，檢索近5年國內有關電針治療中風後抑鬱症的臨床研究文獻，用循證醫學的方法對所收集的符合標準的文獻進行系統評價和分析，並對其文獻品質以及目前電針治療中風後抑鬱症的臨床取穴規律、方法等進行總結，為臨床實踐提供更可靠的依據。 四、結果 在收集的電針治療中風後抑鬱症的文獻中，同時採用國家級的HAMD和CCMD-3有28篇文獻，占58.3%。有中醫診斷標準的文獻有12篇，占25.0%。共同使用HAMD和抑鬱自評量表（SDS)作為評價指標的文獻有14篇，占29.2%。文獻中治療中風後抑鬱症的十大常用穴位為百會、太沖、内關、印堂、神庭、合穀、足三裡、四神聰、神門、三陰交。 五、結論 我國近5年來電針治療中風後抑鬱症的文獻表明電針治療有效，但文獻中採用的隨機方法的品質及可信度較低，盲法幾乎未被應用。這些問題在一定程度上阻礙和減弱了電針治療中風後抑鬱症的推廣和普及。為了提高電針治療中風後抑鬱症的臨床水準，需要採用高品質的臨床研究設計，從而為臨床實踐提供更為可靠的依據。 六、關鍵字 電針 中風後 腦卒中 抑鬱症 臨床研究
33
Stewart, Katy J. E. "Speech and swallowing rehabilitation in the home: A comparison of two service delivery models for stroke survivors." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2014. https://ro.ecu.edu.au/theses/1579.
Full textAbstract:
Background and Aims
Speech and swallowing difficulties are common sequelae for people who have suffered a stroke. Recently, there has been an increase in early discharge, community rehabilitation and the use of therapy assistants to support health professionals in stroke rehabilitation. However, the impact of these factors on communication and swallowing outcomes remains under researched. This research explored Rehabilitation in the Home (RITH) Speech Pathology (SP) services for stroke survivors with dysarthria and dysphagia. More specifically, this research investigated whether traditional speech pathology interventions, supplemented with a home practice program are effective, as well as compare usual treatment to that provided by a therapy assistant. Additionally, the experiences of the key stakeholders were also examined.
Methods and Procedures
Stroke survivors and their carers were recruited from RITH services in Perth, Western Australia into this pilot comparative group study. Stroke survivors with a recent stroke diagnosis and associated dysarthria and/or oral stage dysphagia were randomly allocated to either: a) treatment as usual with a speech pathologist (TAU) or b) intensive treatment with a speech pathologist and a supervised therapy assistant (INT). Evidence-based dysarthria and dysphagia treatment program content was controlled for both groups and all participants were encouraged to complete independent home practice daily. The stroke survivors were assessed at three time points, at baseline, immediately post therapy and at two months post stroke with a range of speech, swallowing and psycho-social outcome measures. The perceptions, experiences and preferences of the stroke survivors and the carers were collected through questionnaires after therapy had ceased. The speech and swallowing outcome measures were analysed using a 2x2 mixed model ANOVA and the questionnaires were analysed using qualitative content analysis.
Results
Ten stroke survivors and their carers (n= 10) were recruited into TAU (n=5) or INT (n=5) intervention groups. The stroke survivors had an average time post onset of stroke of 39.6 days. Stroke survivors participated in regular and intensive levels of RITH SP and all completed some degree of home practice. Therapy was provided over a three week period and TAU participants received M= 470 mins (SD=85.22) and INT participants received M= 909 mins (SD=175.58) of professionally led therapy. Within groups analyses revealed a statistically significant treatment effect over time for scores on the Dysarthria Impact Profile, oral motor function, speech intelligibility, water swallow test and the chewed cookie test. There was no significant difference over time for speech rate. There were no statistically significant differences between the TAU and the INT groups on any of the measures. Carers and stroke survivors gave positive reports of RITH SP with both groups noting improvements in the stroke survivors’ speech and swallowing and commenting on the benefits of receiving rehabilitation in the home. Many stroke survivors valued and desired intensive speech pathology services; with the use of therapy assistants viewed positively by those in the INT group. Stroke survivors reported that they had difficulty practicing independently with most carers being involved with home-based speech pathology intervention.
Conclusions
Stroke survivors in an early phase of recovery were able to participate in RITH SP and benefitted from a speech pathology intervention program targeting dysarthria and dysphagia. Intensive speech pathology and therapy assistant intervention was as effective as usual care by a speech pathologist with improvements made by all stroke survivors across the majority of speech and swallowing measures. Stroke survivors were able to complete home practice and provided positive reports on the program, staff and setting. Home practice may be difficult for stroke survivors in the early stages post stroke, and may require support with its completion. Further investigation into the effectiveness and acceptability of home based therapy, the use of therapy assistants and the role of the carer as well as the ease and impact of home programs is required
34
Potter, Kathleen. "The effects of long-term homocysteine-lowering treatment with folic acid, vitamin B6 and Vitamin B12 on vascular structure and function in stroke." University of Western Australia. School of Medicine and Pharmacology, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0020.
Full textAbstract:
[Truncated abstract] An elevated total plasma homocysteine concentration (tHcy) is associated with an increased risk of myocardial infarction and ischemic stroke. Folic acid, vitamin B6 and B12 supplements significantly reduce tHcy even in people who are not overtly vitamin deficient. If homocysteine is a causal risk factor for atherothrombotic events, treatment with B-vitamins might prove a simple and cost-effective means to reduce cardiovascular risk. However, it remains unclear whether elevated tHcy causes atherosclerosis or is simply a risk marker. To prove that homocysteine is a modifiable risk factor for cardiovascular disease it is necessary to show that lowering tHcy reduces vascular risk. The aim of this study was to determine whether long-term homocysteine-lowering with B-vitamins would improve vascular structure and function in people with a history of stroke. This study was a cross-sectional sub-study of the Vitamins TO Prevent Stroke trial (VITATOPS), a multi-centre, randomised, double-blind, placebo-controlled clinical trial designed to test the efficacy and safety of B-vitamins (folic acid 2mg, vitamin B6 25mg and vitamin B12 0.5mg) in the prevention of vascular events in patients with a recent history of stroke or transient ischemic attack. 173 VITATOPS participants were recruited for the current study. Age, sex, stroke type, medications, cardiovascular risk factors and smoking history were recorded and blood pressure, height, weight, waist and hip girth were measured in all subjects at least two years after randomisation. ... After a mean treatment period of 3.9 ± 0.9 years, the subjects randomised to vitamin treatment had significantly lower tHcy than the subjects randomised to placebo (7.9mol/L, 95%CI 7.5, 8.4 versus 11.8mol/L, 95%CI 10.9, 12.8; p<0.001). There were no significant differences between groups in CIMT (0.84 ± 0.17mm vitamins versus 0.83 ± 0.18mm placebo; p=0.74) or FMD (median of 4.0%, IQR 0.9, 7.2, vitamins versus 3.0%, IQR 0.6, 6.6 placebo; p=0.48). Pooled estimates from the meta-analyses showed that B-vitamin treatment reduces CIMT by 0.10mm (95%CI 0.20, -0.01mm) and increases FMD by 1.4%, (95%CI 0.7, 2.2), although these estimates may have been influenced by positive publication bias. The improvement in FMD was significant in studies of less than eight weeks duration but not in studies with longer treatment periods. The association between tHcy and CIMT and FMD was eliminated by adjustment for renal function and long-term B-vitamin treatment did not alter the strong linear relationship between tHcy and cystatin C. Lowering tHcy did not alter arterial wall inflammation assessed by 18FDG-PET, although small subject numbers meant we were unable to exclude a minor treatment effect. Long-term homocysteine-lowering with B-vitamin treatment did not improve CIMT or FMD or reduce arterial wall inflammation in people with a history of stroke. The relationship between tHcy and these markers of vascular risk was eliminated by adjustment for renal function. Our data are consistent with the hypothesis that elevated tHcy is a risk marker for cardiovascular disease rather than a modifiable causal risk factor.
35
Nelson, Merlisa Claudia. "Ultrasound evaluation of the extracranial cerebrospinal venous system and carotid arteries in patients with multiple sclerosis." Thesis, Cape Peninsula University of Technology, 2013. http://hdl.handle.net/20.500.11838/1565.
Full textAbstract:
Thesis submitted in fulfilment of the requirements for the degree
Master of Technology: Radiography
in the Faculty of Health and Wellness Sciences
at the Cape Peninsula University of Technology
Supervisor: Ms. Ferial Isaacs
Co-supervisor: Prof. Susan J. Van Rensburg
Bellville
September 2013Multiple Sclerosis (MS) is characterised by demyelination within the central nervous system (CNS), which may result in neurological disabilities over time, causing considerable hardship to patients and their families, in addition to being costly to treat. Recent studies have linked MS to impaired cerebral blood flow, called chronic cerebrospinal venous insufficiency (CCSVI). Anecdotal evidence has suggested that surgical correction thereof results in improvement of symptoms experienced by MS patients. To my knowledge, no information is available in the literature on carotid artery disease in MS. The USA National MS Society has therefore called for more research to be done in this area. This cross-sectional observational sub-study will determine, by ultrasound (B-Mode, Colour and Pulsed-wave Doppler), the prevalence of chronic venous insufficiency (CCSVI) and carotid artery disease in the selected sample of MS patients within the region of the Western Cape, South Africa. Biochemical data; lifestyle factors such as physical activity and smoking; and nutritional status of MS patients were determined from the main study entitled: “The development of a comprehensive gene-based, pathology supported intervention program for improved quality of life in patients diagnosed with multiple sclerosis” (Division of Chemical Pathology, NHLS, Tygerberg Hospital, and University of Stellenbosch). Twenty-nine (29) patients were aged between 28-64years and they suffered from MS for 0.83-27years. A larger proximal and mid cross-sectional diameter (CSD) of the right IJV compared to the left (differences significant, P= 0.026 and P=0.023) was demonstrated. Increased intima media thickness (IMT) was present in 13.33% of the non-smoking MS group and 20% in the smoking MS group. IJV reflux was evident in 13.33% of the MS group. A significant reduction of cross-sectional diameters of the IJV’s was evident in smoking MS patients; suggesting that smoking is not only a risk factor for atherosclerotic disease but could also be related to narrowing of the major neck veins. This study also supports findings of other studies viz that there’s no significant correlation between extracranial venous abnormalities and MS. Early carotid artery disease was noted in smoking and non-smoking MS patients, however the findings were non-significant.
36
Yip, Man-tat (Albert). "Stroke prevention and hospital management." 2008. http://hdl.handle.net/2440/50515.
Full textAbstract:
Stroke is a preventable disease. Minor stroke and transient ischaemic attack (TIA) are important warning signs of the possibility of a major stroke. Worldwide, stroke is the third most common killer and the largest cause of disability. The incidence of stroke is predicted to increase with the predominance of unhealthy lifestyles and the aging population. The adoption of a healthy lifestyle can reduce many of the risk factors. This descriptive study was designed to explore patients’ understanding of modifiable risk factors of cerebrovascular disease. It investigated lifestyle changes actually made, as well as the factors affecting patients’ decisions about whether to make lifestyle changes. The two major factors considered were patients’ sources and level of knowledge and their attitudes and beliefs around making changes. A convenience sample of patients who had suffered a minor stroke or TIA was recruited through a major metropolitan hospital. Thirty-five subjects responded to a postal questionnaire. The mean age was 68 years and 37% of the subjects had sustained some disability as a result of the TIA or minor stroke. The results demonstrated that many subjects had a poor understanding of risk factors of stroke. While smoking was well recognised as a risk factor, subjects showed less awareness of other risk factors, such as excessive alcohol consumption and obesity. Subjects also reported significant confusion regarding diet. Sixty-six percent of subjects depended on doctors as their main source of health information. This may be problematic as the current shortages of General Practitioners has put pressure on doctors to keep appointment times short and reduce the time available for health education. The main barriers to lifestyle change, were lack of motivation, and inadequate, knowledge, guidance, and support and the inability to access good information. Although 83% of subjects suffered from hypertension, medication was the accepted method of control, few subjects realised the significance of lifestyle factors. Nine percent of subjects were only diagnosed with hypertension after their stroke or TIA and few monitor their own blood pressure, despite the wide availability of home monitoring devices. From the findings of this study it is concluded that health promotion and education are very important strategies in the prevention of stroke and it is recommended that this kind of education begins in childhood with tailored, age-specific programs delivered to the public over the lifespan. The role of health screening cannot be underestimated in the detection of risk factors such as hypertension and obesity. Early detection makes effective treatment possible and helps prevent the occurrence of strokes, thus reducing the cost to the community. Long-term health strategies such as improving health resource distribution and enhancing health education are needed where patients and their families participate together in comprehensive education programs. It is hoped that this may lead to a shared understanding, which may translate to patients being more supported, and therefore more able, to make the necessary lifestyle changes. Dysphagia is a common complication following stroke, which can result in significant morbidity and mortality. Multidisciplinary collaboration facilitates management strategies, decision-making and the efficiency of rehabilitation. Nurses are responsible for coordination of management and in particular for continuous monitoring, assessment of swallowing and nutritional state, maintaining safety and preventing complications. An understanding of the issues and strategies relating to management may provide valuable information to enhance the safety, cost-effectiveness and quality of care. A retrospective review of patients’ medical records was used to collect data. A sample of ninety-five adults who were admitted to an Australian public hospital between January 2003 and April 2006, with a diagnosis of dysphagic stroke were recruited. Statistical Package for Social Sciences (SPSS) was used to analyse the quantitative data, while content analysis was used to analyse the qualitative data. All subjects were assessed by a speech pathologist, the mean age was 75 years and 50.5% were male. Except for critically ill subjects, almost all were assessed within three days. Ninety-six percent of subjects had communication problems and 81% had upper limb motor impairment. During hospitalisation almost 60% of subjects had an improvement in their oral intake including 8% resuming their premorbid diet. Eighteen percent were on enteral tube feeding upon discharge, 4% deteriorated and 16% died. It appears that oral intake of most subjects was unsatisfactory. When recorded the mean body weight lost was 2.3kg. At least 22% had malnutrition or dehydration. Forty-five percent aspirated and 22% had respiratory infection. Almost half of the subjects (48%) were discharged to aged care facilities. Eighty percent had no documented follow-up scheduled for management of their dysphagia. Early identification of dysphagia, prudent supervising of appropriate oral intake and mouth care may help to maintain safe swallowing, preventing aspiration and chest infection. Regular checks of body weight, serum albumin level, oral intake and early enteral feeding are essential to guide nutritional support, minimise malnutrition and problematic medication administration. Encouraging oral intake and providing families with support could promote recovery of swallowing skills and help patients to regain the ability to eat independently. Providing helpful information on the care options available may allay patient and family anxiety. A qualified nurse practitioner could assess patients and ensure that a tailored care plan was designed to meet patients’ needs and this may improve the outcomes considerably.http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1320650
Thesis (D.Nurs.) - University of Adelaide, School of Population Health and Clinical Practice, 2008
37
Yip, Man-tat (Albert). "Stroke prevention and hospital management." Thesis, 2008. http://hdl.handle.net/2440/50515.
Full textAbstract:
Stroke is a preventable disease. Minor stroke and transient ischaemic attack (TIA) are
important warning signs of the possibility of a major stroke. Worldwide, stroke is the
third most common killer and the largest cause of disability. The incidence of stroke is
predicted to increase with the predominance of unhealthy lifestyles and the aging
population. The adoption of a healthy lifestyle can reduce many of the risk factors.
This descriptive study was designed to explore patients’ understanding of modifiable
risk factors of cerebrovascular disease. It investigated lifestyle changes actually made,
as well as the factors affecting patients’ decisions about whether to make lifestyle
changes. The two major factors considered were patients’ sources and level of
knowledge and their attitudes and beliefs around making changes.
A convenience sample of patients who had suffered a minor stroke or TIA was
recruited through a major metropolitan hospital. Thirty-five subjects responded to a
postal questionnaire. The mean age was 68 years and 37% of the subjects had
sustained some disability as a result of the TIA or minor stroke.
The results demonstrated that many subjects had a poor understanding of risk factors
of stroke. While smoking was well recognised as a risk factor, subjects showed less
awareness of other risk factors, such as excessive alcohol consumption and obesity.
Subjects also reported significant confusion regarding diet. Sixty-six percent of
subjects depended on doctors as their main source of health information. This may be
problematic as the current shortages of General Practitioners has put pressure on
doctors to keep appointment times short and reduce the time available for health
education.
The main barriers to lifestyle change, were lack of motivation, and inadequate,
knowledge, guidance, and support and the inability to access good information.
Although 83% of subjects suffered from hypertension, medication was the accepted
method of control, few subjects realised the significance of lifestyle factors. Nine
percent of subjects were only diagnosed with hypertension after their stroke or TIA
and few monitor their own blood pressure, despite the wide availability of home
monitoring devices. From the findings of this study it is concluded that health promotion and education are very important strategies in the prevention of stroke and it is recommended that this
kind of education begins in childhood with tailored, age-specific programs delivered
to the public over the lifespan. The role of health screening cannot be underestimated
in the detection of risk factors such as hypertension and obesity. Early detection
makes effective treatment possible and helps prevent the occurrence of strokes, thus
reducing the cost to the community. Long-term health strategies such as improving
health resource distribution and enhancing health education are needed where patients
and their families participate together in comprehensive education programs. It is
hoped that this may lead to a shared understanding, which may translate to patients
being more supported, and therefore more able, to make the necessary lifestyle
changes.
Dysphagia is a common complication following stroke, which can result in significant
morbidity and mortality. Multidisciplinary collaboration facilitates management
strategies, decision-making and the efficiency of rehabilitation. Nurses are responsible
for coordination of management and in particular for continuous monitoring,
assessment of swallowing and nutritional state, maintaining safety and preventing
complications. An understanding of the issues and strategies relating to management
may provide valuable information to enhance the safety, cost-effectiveness and
quality of care.
A retrospective review of patients’ medical records was used to collect data. A sample
of ninety-five adults who were admitted to an Australian public hospital between
January 2003 and April 2006, with a diagnosis of dysphagic stroke were recruited.
Statistical Package for Social Sciences (SPSS) was used to analyse the quantitative
data, while content analysis was used to analyse the qualitative data.
All subjects were assessed by a speech pathologist, the mean age was 75 years and
50.5% were male. Except for critically ill subjects, almost all were assessed within
three days. Ninety-six percent of subjects had communication problems and 81% had
upper limb motor impairment. During hospitalisation almost 60% of subjects had an
improvement in their oral intake including 8% resuming their premorbid diet.
Eighteen percent were on enteral tube feeding upon discharge, 4% deteriorated and
16% died. It appears that oral intake of most subjects was unsatisfactory. When
recorded the mean body weight lost was 2.3kg. At least 22% had malnutrition or
dehydration. Forty-five percent aspirated and 22% had respiratory infection. Almost
half of the subjects (48%) were discharged to aged care facilities. Eighty percent had
no documented follow-up scheduled for management of their dysphagia.
Early identification of dysphagia, prudent supervising of appropriate oral intake and
mouth care may help to maintain safe swallowing, preventing aspiration and chest
infection. Regular checks of body weight, serum albumin level, oral intake and early
enteral feeding are essential to guide nutritional support, minimise malnutrition and
problematic medication administration. Encouraging oral intake and providing families with support could promote recovery of swallowing skills and help patients
to regain the ability to eat independently. Providing helpful information on the care
options available may allay patient and family anxiety. A qualified nurse practitioner
could assess patients and ensure that a tailored care plan was designed to meet
patients’ needs and this may improve the outcomes considerably.Thesis (D.Nurs.) - University of Adelaide, School of Population Health and Clinical Practice, 2008
38
Turner, Renée Jade. "Characterising the role of substance P in acute ischaemic stroke." 2007. http://hdl.handle.net/2440/56839.
Full textAbstract:
More than 15 million people worldwide will suffer a stroke each year two thirds will die or be left permanently disabled. Accordingly, stroke represents an enormous financial burden on the community, due to the cost of hospitalisation, treatment and rehabilitation of stroke patients. Despite the significance of this public health problem, a safe and widely applicable stroke therapeutic remains elusive. Cerebral oedema is widely recognised as a common and often fatal complication of stroke that is associated with worsened outcome. However, the exact mechanisms of oedema formation remain unclear, with current therapies largely ineffective in addressing the mechanisms of cerebral swelling, and also being associated with their own negative side-effect profile. This thesis characterises the role of neurogenic inflammation and the neuropeptide, substance P (SP), in mediating the development of blood brain barrier breakdown, cerebral oedema and resultant functional deficits following stroke, using a rodent model of reversible cerebral ischaemia. The findings of this thesis demonstrate that increased SP immunoreactivity, particularly of the penumbral tissue vasculature, is a feature of tissue perfusion following stroke, but not in non-reperfused infarcts. The central role for SP in the breakdown of the BBB following stroke and the associated deleterious effects of such breakdown was confirmed by studies using an NK₁ receptor antagonist. These antagonists conferred a profound attenuation of BBB breakdown, cerebral oedema formation, neuronal death and injury, and the associated development of functional deficits following reversible stroke. Similarly, depletion of all neuropeptides by capsaicin pre-treatment also reduced both histological abnormalities and functional deficits following stroke, confirming the central role of neuropeptides in the secondary injury process after stroke. The NK₁ receptor antagonist was able to be safely combined with the currently approved treatment for stroke, tPA, producing a synergistic effect of greater protection from the ischaemic insult. In particular, histological and functional outcome were markedly improved, as well as a reduction in the risk of intracerebral haemorrhage and death. Furthermore, the NK₁ receptor antagonist was effective even when administered up to 8 h following the onset of ischaemia, and in a variety of stroke severities. We conclude that SP plays a central role in the secondary injury that occurs following stroke, in particular, the genesis of BBB breakdown and cerebral oedema. Accordingly, combination therapy of tPA and an NK₁ receptor antagonist may offer a novel therapeutic strategy for the clinical management of ischaemic stroke of varying severity.http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1298280
Thesis (Ph.D.) -- The University of Adelaide, School of Medical Sciences, 2007
39
Turner, Renée Jade. "Characterising the role of substance P in acute ischaemic stroke." Thesis, 2007. http://hdl.handle.net/2440/56839.
Full textAbstract:
More than 15 million people worldwide will suffer a stroke each year two thirds will die or be left permanently disabled. Accordingly, stroke represents an enormous financial burden on the community, due to the cost of hospitalisation, treatment and rehabilitation of stroke patients. Despite the significance of this public health problem, a safe and widely applicable stroke therapeutic remains elusive. Cerebral oedema is widely recognised as a common and often fatal complication of stroke that is associated with worsened outcome. However, the exact mechanisms of oedema formation remain unclear, with current therapies largely ineffective in addressing the mechanisms of cerebral swelling, and also being associated with their own negative side-effect profile.
This thesis characterises the role of neurogenic inflammation and the neuropeptide, substance P (SP), in mediating the development of blood brain barrier breakdown, cerebral oedema and resultant functional deficits following stroke, using a rodent model of reversible cerebral ischaemia. The findings of this thesis demonstrate that increased SP immunoreactivity, particularly of the penumbral tissue vasculature, is a feature of tissue perfusion following stroke, but not in non-reperfused infarcts. The central role for SP in the breakdown of the BBB following stroke and the associated deleterious effects of such breakdown was confirmed by studies using an NK₁ receptor antagonist. These antagonists conferred a profound attenuation of BBB breakdown, cerebral oedema formation, neuronal death and injury, and the associated development of functional deficits following reversible stroke. Similarly, depletion of all neuropeptides by capsaicin pre-treatment also reduced both histological abnormalities and functional deficits following stroke, confirming the central role of neuropeptides in the secondary injury process after stroke.
The NK₁ receptor antagonist was able to be safely combined with the currently approved treatment for stroke, tPA, producing a synergistic effect of greater protection from the ischaemic insult. In particular, histological and functional outcome were markedly improved, as well as a reduction in the risk of intracerebral haemorrhage and death. Furthermore, the NK₁ receptor antagonist was effective even when administered up to 8 h following the onset of ischaemia, and in a variety of stroke severities.
We conclude that SP plays a central role in the secondary injury that occurs following stroke, in particular, the genesis of BBB breakdown and cerebral oedema. Accordingly, combination therapy of tPA and an NK₁ receptor antagonist may offer a novel therapeutic strategy for the clinical management of ischaemic stroke of varying severity.Thesis (Ph.D.) -- The University of Adelaide, School of Medical Sciences, 2007
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Liu, Junguang, University of Western Sydney, College of Health and Science, and Centre for Complementary Medicine. "Development of an evidence-based Chinese herbal medicine for the management of vascular dementia." 2008. http://handle.uws.edu.au:8081/1959.7/33046.
Full textAbstract:
Vascular dementia (VaD), the second most common cause of dementia, causes substantial distress to patients and represents a significant burden to their families and communities. Currently, there is no effective treatment to reverse the brain damage associated with VaD. In general the drugs available for the management of cognitive problems in VaD are expensive and outcomes are uncertain. It is, therefore, important to seek out alternative approaches, which may prove effective, cheaper and safer. Chinese herbal medicine (CHM) has been used for the treatment of dementia-like disorders for centuries. Data from many preclinical studies and some clinical studies have suggested the potential effectiveness of CHM for the treatment of VaD. Based on the literature review conducted as part of this thesis, however, most of the studies were published in Chinese literature and failed to demonstrate methodological rigour or to report sufficient methodological detail. Randomised controlled trials (RCTs) using scientific methods of diagnosis and outcome measures are urgently needed. Wei Nao Kang (WNK) is a three-herb formula developed by Xi Yuan Hospital, China Academy of Chinese Medical Sciences. Preclinical experiments of WNK have demonstrated significant improvement in learning and memory function in VaD animal models in rats and mice. Human case studies have also signalled the potential value of WNK in VaD. Although the results of these studies were encouraging, strong scientific evidence from a well-designed RCT is still required. A rigorous clinical trial methodology, including scientific diagnostic criteria and outcome measures, was designed and applied to the evaluation of WNK for VaD. The trial was successfully conducted over a two-year period. Cognitive functions, as evidenced by the ADAS-cog, were significantly improved in the study group taking WNK herbal medication compared with the placebo group. The ADAS-cog was simultaneously validated as a measure of cognitive function in VaD. Blinding was verified and no major adverse effects were found related to WNK treatment. However, neither group demonstrated long-lasting effect on a 16 weeks follow-up after completion of treatment. WNK demonstrated a significant effect on quality of life (measured by SF-36) and some effect on activities of daily living (measured by ADCS-ADL) in VaD patients. The SF-36 was validated as a measure of general health status and the ADCS-ADL as a measure of activities of daily living in patients with VaD. Both scales were proven sensitive to the presence of VaD, and provided useful supplementary outcome measures for VaD. A cerebral perfusion study was conducted to identify changes in cerebral blood flow and its relationship with clinical symptoms. The study showed that WNK had marked increases in blood flow in the inferior frontal and anterior temporal regions, both of which are closely related to cognitive function in human brains. This study has provided scientific evidence in support of the clinical effect of WNK on VaD. In addition, it validated several outcome measures in assessing improvements in cognitive functions, activities of daily living and quality of life in VaD patients. One of the highlights of this study is the application of SPECT scans as an outcome measure. This provided an excellent objective parameter for assessing the effects of WNK. To the best of our knowledge, SPECT scanning has never been used in VaD trials of herbal medicines.Doctor of Philosophy (PhD)
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"Diagnosis, microemboli detection and hemodynamic monitoring of intracranial atherosclerosis by transcranial Doppler in the ischemic stroke." Thesis, 2008. http://library.cuhk.edu.hk/record=b6074600.
Full textAbstract:
Early deterioration and long-term recurrence were common after stroke or transient ischemic attach (TIA), however, it is unclear whether they were correlated with active embolization and the consequent new cerebral infarct in acute phase. By employing TCD and diffusion weighted imaging (DWI), we studied the significance of the progression of MES and infarcts during acute phase on the clinical outcomes. We found that the disappearance of MES was correlated with better improvement on day 7 of recruitment; for the long-term outcome, occurrence of exacerbating infarct tended to predict recurrent stroke. Treatment aiming to reduce MES and prevent infarct exacerbation in acute phase may improve the prognosis after stroke.Finally, one study was performed to assess the changes of hemodynamic parameters after stenting of severe stenosis in the MCA. We aimed to investigate whether TCD can reflect the lumen changes after revascularization and detect hyperperfusion. The findings showed that the velocity of stented MCA in most patients normalized within 24 hours after procedure, but the role of TCD in detecting restenosis in long run needed to be verified; no one suffered from hyperperfusion during the period of our study. The long-term outcomes of patients with normalized velocity versus those with persistently high velocity needed to be further studied. Apart from the velocity changes, changes of the collateral flow after intervention may also be an important part of hemodynamic changes. (Abstract shortened by UMI.)
It was suggested that anti-platelet therapy can reduce the MES, but little was known about the efficacy of low molecular weight heparin (LMWH) although in theory LMWH can reduce the red fibrin-dependent thromboemboli. As a sub-analysis of Fraxiparine in Ischemic Stroke (FISS)-tris study, our study did not show advantages of LMWH in eliminating MES compared with aspirin.
Previous studies showed the accuracy of TCD in diagnosis of middle cerebral artery (MCA) stenosis was variable and the positive predictive value (PPV) was less than 50% in a recent report. One of the important reasons was that most criteria were based on the velocity-only method, ignoring other non-velocity information. Thus, we tried to establish new diagnostic criteria by means of designing an assessment form which integrated more characteristics apart from the velocity acceleration. A composite score for each MCA was calculated according to following parameters in the form: Velocity Scale (score 0-6 for peak systolic velocities<140 to ≥300cm/s), Hemodynamic Scale (score 0-5 for focal or diffuse velocity increase; score 0-6 for differences between bilateral MCA; score 17 for damping velocity), Spectrum Scale (score 0-2 for normal spectrum, turbulence and musical murmurs). Our results showed that compared with the previously reported criteria, the score calculated from the assessment form yielded much more balanced accuracy against magnetic resonance angiography (MRA) and digital subtraction angiography (DSA). However, the composition of the assessment form was only based on personal experience and need to be further modified. Multicenter studies with large sample size are also needed to confirm the advantages of this new method.
Second, we performed three studies to investigate the relationship between the progression of MES and the short or long-term outcome and the relationship between MES and different treatments.
Hao, Qing.
Adviser: Ka Sing Wong.
Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3419.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2008.
Includes bibliographical references (leaves 155-181).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
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Miller, Kristine Kay. "Therapeutic-yoga after stroke : effect on walking recovery." Thesis, 2013. http://hdl.handle.net/1805/3776.
Full textAbstract:
Indiana University-Purdue University Indianapolis (IUPUI)Stroke is a sudden and devastating medical condition. People who experience a stroke tend to have long-term physical limitations including impaired walking as part of the ongoing consequences of stroke. While a variety of rehabilitation interventions have demonstrated efficacy for improving walking after stroke, none of the interventions have emerged as superior, and prior to this study, therapeutic-yoga had not been tested as an intervention to improve walking recovery after stroke. METHODS: This study was a secondary data analysis of group therapeutic-yoga on walking recovery measures including walking speed, walking distance, and spatiotemporal step parameter symmetry. The walking recovery measures were collected as secondary outcomes in a sub-sample (n=12) in a pilot randomized controlled study (n=47) designed to test the efficacy of 8-weeks of group therapeutic-yoga on balance and fear of falling. Participants in the current study completed 12-weeks of group therapeutic yoga with outcome assessments at baseline, 8-weeks, and 12-weeks. The main analysis was repeated measures ANOVA to assess the main effect of time with additional analyses including effect sizes, percent of participants achieving change greater than or equal to minimal detectable change (MDC), and mean change score comparisons between baseline and 8-weeks, 8-weeks and 12-weeks, and baseline and 12-weeks. RESULTS: Twelve people with chronic stroke enrolled in the study with 9 completing the intervention and all 3 assessments. No significant main effect of time was found on any of the variables of interest. Walking distance demonstrated a trend toward significant change (p=0.064) and step length symmetry demonstrated significant change (p=0.05) between baseline and 12-weeks. Several spatiotemporal step parameter symmetry ratios demonstrated small to medium effect sizes with the majority (91%) being a negative effect. CONCLUSION: Twelve weeks of group therapeutic-yoga appears to be feasible in a population of people with chronic stroke. Walking distance and step parameter symmetry should be tested in a larger sample. An improved understanding of the impact, progression, and remediation of walking asymmetry is needed.
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Seabi, Mmakgomo Eunice. "Formulation of carbamazepine and sodium valproate fixed dose combination for management of epilepsy." Thesis, 2019. http://hdl.handle.net/10386/3084.
Full textAbstract:
Thesis ((M. Pharm. (Pharmaceutics)) -- University of Limpopo, 2019Epilepsy is the fourth most common neurological disorder after migraine, stroke and Alzheimer’s disease and it affects about fifty million people worldwide. Careful consideration should be taken when deciding to initiate treatment in epilepsy as it should consider the balance between the possibility of further seizures and their associated risks, including the possible risk of sudden expected death, inconvenience and the risks of taking regular medication for each individual. In the early 1980’s, the first-line treatment for epilepsy was polytherapy. This was due to findings that smaller doses of two drugs rather than larger doses of one drug can achieve synergistic effects or less drug toxicity. However, following more trials on the treatment of epilepsy, this was later changed to monotherapy as first-line treatment. Despite the change, patients remain uncontrolled on a single anti-epileptic drug, thus they are initiated on polytherapy, one such combination being carbamazepine in combination with sodium valproate. The use of these in combination has pharmacological threats such as compliance, the control of side effects and the achievement of synergistic effects. The development of a Fixed Dose Combination (FDC) has often been used to resolve pharmacological threats, and this study aims to develop a fixed dose combination tablet of carbamazepine and sodium valproate to resolve the pharmacological threats in epilepsy. Samples of carbamazepine and sodium valproate and a physical mixture (1:1 w/w) of both drugs and excipients were prepared for compatibility with thermal analysis and spectroscopy techniques. Data was analysed by comparing the DSC curves, FTIR spectra, XRPD peaks and TAM analysis of carbamazepine and sodium valproate alone and in their physical mixture (1:1 w/w) and with excipients. Both carbamazepine and sodium valproate were evaluated for flowability using angle of repose, tapped and bulk density, compressibility index and particle size distribution. To formulate the proposed FDC tablet of carbamazepine and sodium valproate, direct compression and wet granulation methods were employed. The tablets were then evaluated for official and non-official post formulation parameters (weight variation, crushing strength, friability, diameter and thickness, and disintegration) according to BP and USP standards. A standardised HPLC method was developed and validated for analytical procedures. Dissolution studies were conducted xiii according to USP methods to verify and quantify the release of the APIs from the FDC tablet. Carbamazepine and sodium valproate were tested for compatibility with excipients using DSC, FTIR, XRPD and TAM analysis. The overall results confirmed that carbamazepine and sodium valproate are compatible, with each other and the excipients used in the study. Powder flow of carbamazepine and sodium valproate was poor, hence they were subjected to granulation prior to compression to improve flowability. The specifications of the fixed-dose combination were developed in accordance with the FDA’s quality by design concept and WHO recommendations. The tablets were subjected to non-official and official pharmacopoeial tests, and passed all the tests. Dissolution studies according to a USP method were conducted to verify and quantify the release of the APIs in the fixed-dose combination. The initial dissolution rate (DRi) of carbamazepine and sodium valproate in the SLS dissolution medium was rapid as required for an immediate release formulation. The study aimed at developing a fixed dose combination of carbamazepine and sodium valproate to try to reduce the burden of taking more than one tablet for epilepsy. Based on the results obtained from preformulation studies to assay of the final product, the study was successful.
Chieta bursary and HWseta
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Coutinho, Michelle. "Art therapy with stroke patients in a group context." Thesis, 2012. http://hdl.handle.net/10210/5702.
Full textAbstract:
M.A."Stroke is one of the leading causes of death and disability in all races in South Africa" (Fritz & Penn, 1992, p 1). It has devastating effects, and may impact on every aspect of the person's functioning. Research shows that depression is common after stroke, becoming more of a problem with time, and having a greater effect on quality of life than the actual disability (Lezak, 1995). Despite such evidence psychologists have played a very limited role in the rehabilitation of this group. Those with communication problems especially have been excluded from research and therapy, which usually require competence with language to be successful. This study attempts to find an alternative method of research and therapy in order to include this group. Following the model of learned helplessness (Seligman, in, Bleiberg, 1986), it was proposed that the unavoidable, inescapable effects of stroke lead to feelings of helplessness, which are also impossible to escape, and the person soon looses the motivation to attempt to control the situation. This then leads to depression. A method of therapy which breaks this cycle, and allows for the person to experience how their actions do have an effect on their lives is needed. In addition to this, an alternative means of self expression for those with communication difficulties needs to be provided. Art therapy was found to address the problems presented by this group (Dailey, 1984). It has proved useful with other populations that have not been able to benefit from traditional psychotherapy. It becomes an alternative means of self expression for those whose communication ability is compromised. It is accessible to most people, as it only requires the ability to make marks on paper. A theme centred, art therapy approach was therefore chosen for the study. The aims of the study were; to create a therapeutic milieu which allowed for self expression, specifically the expression of emotions, which included all the participants; to investigate the effects of introducing an opportunity for self expression on self concept and group process; and to look at the themes which emerge from the art. The participants were members of a pre-existing support group for stroke survivors. A quasiexperimental design was used. The Draw a Person Test, was administered pre and post intervention. Additional information was gathered using the Beck's Depression Inventory and a demographic questionnaire. This study uses a qualitative method, which includes information regarding the researcher's experience, and is interpreted from the researcher's perspective. It was found that art therapy had a positive effect on self concept. It influenced group process, as participants who were previously marginalised became more central. Numerous themes emerged, some which were specific to individuals, but others that were of relevance to the group as a whole. It proved rewarding for the researcher, both as a therapist and in terms of her relationship with her father who is a stroke survivor with aphasia. Art therapy therefore seems to be a useful tool to be used with this group that has traditionally been excluded from therapy and research. It is suggested that further research would be useful, and suggestions regarding future research are discussed.
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Hill, Valerie A. "The relationship between touch sensation of the hand and occupational performance in individuals with chronic stroke." Thesis, 2014. http://hdl.handle.net/1805/4651.
Full textAbstract:
Indiana University-Purdue University Indianapolis (IUPUI)Stroke is the main cause of disability in the United States. Individuals with stroke commonly report sensory impairment affects their recovery. Motor recovery and sensory impairment are related and impact individuals’ ability to perform valued occupations. Despite the prevalence of sensation impairment after stroke, many occupational therapists fail to include sensation assessment and intervention in treatment planning. The exclusion of sensation in occupational therapy interventions during stroke rehabilitation may be due to the lack of literature supporting the association between sensation and occupational performance. The current study aimed to determine the relationship between touch sensation of the affected hand and occupational performance and satisfaction in individuals with chronic stroke. Using a cross-sectional study design, this study associated factors related to hand sensation and function in individuals with chronic stroke. Fifty individuals with chronic stroke participated in a one-time testing session in which assessments related to sensation, movement of the hand and engagement in daily activities were administered. Correlation analyses were utilized to determine relationships between touch sensation of the affected hand with individuals’ abilities to engage in valued daily activities, arm and hand disability, and manual abilities. The main finding of the study was that individuals with intact sensation reported greater ability to perform valued occupations and satisfaction with their performance, as compared with individuals with touch sensation impairment. For individuals with impaired touch sensation of the affected hand, impairment of touch sensation of the hand did not correlate with individuals’ performance or satisfaction with valued occupations, arm or hand movement, or manual abilities. Collectively, the results of this study reflect the complex interaction between touch sensation, occupational performance, motor functioning, and manual abilities of the affected hand for individuals’ who have experienced a stroke. This study informs therapists, rehabilitation scientists, and other healthcare professionals that client-centered, individualized approaches, including a wide array of clinical assessments and intervention, including assessment of occupational performance and sensation, remain important components in stroke rehabilitation.
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"In vivo and in vitro studies of the anti-oxidative, anti-inflammatory and anti-apoptotic effects of Gastrodiae Rhizoma water extract on ischemic stroke." 2013. http://library.cuhk.edu.hk/record=b5884430.
Full textAbstract:
Hung, Sze Man.Thesis (M.Phil.)--Chinese University of Hong Kong, 2013.
Includes bibliographical references (leaves 186-192).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts also in Chinese.