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Search Results: 1 - 10 of 224782 matches for " R. Loch Macdonald "
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Acute Microvascular Changes after Subarachnoid Hemorrhage and Transient Global Cerebral Ischemia
Michael K. Tso,R. Loch Macdonald
Stroke Research and Treatment , 2013, DOI: 10.1155/2013/425281
Abstract:
Early Brain Injury: A Common Mechanism in Subarachnoid Hemorrhage and Global Cerebral Ischemia
Mohammed Sabri,Elliot Lass,R. Loch Macdonald
Stroke Research and Treatment , 2013, DOI: 10.1155/2013/394036
Abstract:
Acute Microvascular Changes after Subarachnoid Hemorrhage and Transient Global Cerebral Ischemia
Michael K. Tso,R. Loch Macdonald
Stroke Research and Treatment , 2013, DOI: 10.1155/2013/425281
Abstract: Subarachnoid hemorrhage and transient global cerebral ischemia result in similar pathophysiological changes in the cerebral microcirculation. These changes include microvascular constriction, increased leukocyte-endothelial interactions, blood brain barrier disruption, and microthrombus formation. This paper will look at various animal and preclinical studies that investigate these various microvascular changes, perhaps providing insight in how these microvessels can be a therapeutic target in both subarachnoid hemorrhage and transient global cerebral ischemia. 1. Introduction Subarachnoid hemorrhage (SAH) is a type of hemorrhagic stroke, most commonly caused by a ruptured intracranial aneurysm. At the time of aneurysm rupture, blood pours into the subarachnoid space, and the intracranial pressure (ICP) inside the rigid calvarium increases sharply, causing a corresponding decrease in cerebral blood flow (CBF). The patient’s clinical presentation on arrival to the hospital can depend on the degree and duration of this initial global cerebral ischemia. Patients with aneurysmal SAH may develop angiographic vasospasm and delayed cerebral ischemia (DCI) with onset 3–12 days after the initial rupture [1]. DCI may or may not be accompanied by large artery vasospasm as seen with vascular imaging [2]. A multicenter randomized clinical trial has not shown improvement in neurologic outcome despite ameliorating the delayed large artery vasospasm [3]. Whether this is due to efficacy of rescue therapy in the placebo groups or drug toxicity abrogating beneficial effects in the clazosentan groups has not been resolved. Nevertheless, as a result of these results, research in SAH has also investigated early brain injury and acute microvascular changes [4]. Nimodipine, an L-type calcium channel antagonist, is the only pharmacologic agent that has been shown to consistently improve neurologic outcomes in clinical trials of patients with SAH [5]. Similarly, cardiac arrest (CA) results in global cerebral ischemia that is transient in clinically relevant cases, since if cardiac function is not restored, the situation is of pathological interest only. Other causes of transient global cerebral ischemia (tGCI) include asphyxia, shock, and complex cardiac surgery [6]. The clinical presentation depends on the duration of cardiac arrest and time to initiating cardiopulmonary resuscitation. After global cerebral ischemia from SAH or tGCI, a cascade of molecular events occurs, resulting in variable degrees of brain injury and cerebrovascular changes. Global cerebral ischemia in
Early Brain Injury: A Common Mechanism in Subarachnoid Hemorrhage and Global Cerebral Ischemia
Mohammed Sabri,Elliot Lass,R. Loch Macdonald
Stroke Research and Treatment , 2013, DOI: 10.1155/2013/394036
Abstract: Early brain injury (EBI) has become an area of extreme interest in the recent years and seems to be a common denominator in the pathophysiology of global transient ischemia and subarachnoid hemorrhage (SAH). In this paper, we highlight the importance of cerebral hypoperfusion and other mechanisms that occur in tandem in both pathologies and underline their possible roles in triggering brain injury after hemorrhagic or ischemic strokes. 1. Introduction Aneurysmal subarachnoid hemorrhage (SAH) is associated with significant morbidity and mortality, accounting for up to ~5% of all stroke cases [1, 2]. The mortality from SAH is estimated at 40–45% by 30 days after hemorrhagic onset and up to 15% mortality before hospital admission [3]. After years of research and extensive pathophysiological investigations of SAH, much is known in animal models about pathways that are activated after SAH and that may contribute to brain injury. However, few have proven to be effective therapeutic targets in humans [4, 5]. SAH has been suggested in multiple reports to be complex, multisystem, and multifaceted pathogenesis that likely has multiple ongoing processes activated contributing to its final pathogenesis and highly morbid manifestations [4–8]. There are some common effects, however, such as vasoconstriction of both large and small cerebral arteries. As a result, it is difficult to research one pathway, one protein, and one target for potential therapeutic benefits. There has been a shift in research to understand how all the manifestations connect, interact, and further contribute to this pathology. Many strides have been made to understand the common secondary complications that occur after SAH, especially focusing on complications that occur early on, often known as early brain injury (EBI) [9, 10]. Some of the complications that EBI encompasses are delayed neuronal injury/death (DND), oxidative stress and inflammatory destruction of the parenchyma, and ischemic deficits leading to cortical spreading depression (CSD). These complications have been theorized to play a major role in the pathogenesis and may contribute significantly to poor morbidity and outcome after SAH. Individual studies on several secondary complications have shed light on shared mechanisms and pathways that may be activated after or during or even before the hemorrhage, which may explain a number of these secondary manifestations. Research has also shifted from considering primary angiographic vasospasm as a major contributor to poor outcome to other secondary mechanisms that may also occur
Simvastatin Re-Couples Dysfunctional Endothelial Nitric Oxide Synthase in Experimental Subarachnoid Hemorrhage
Mohammed Sabri,Jinglu Ai,Philip A. Marsden,R. Loch Macdonald
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0017062
Abstract: Reduced endothelial nitric oxide synthase (eNOS) function has been linked to secondary complications of subarachnoid hemorrhage (SAH). We previously found that there is increased eNOS function after SAH but that it is uncoupled, leading to secondary complications such as vasospasm, microthromboembolism and neuronal apoptosis. Here we test the hypothesis that recoupling eNOS with simvastatin can prevent these complications. SAH was created in mice that were treated with vehicle or simvastatin starting 2 weeks before or 30 minutes after SAH. SAH increased phosphorylated eNOS which was prevented by pre- or post-treatment with simvastatin. Simvastatin pre-treatment also prevented the increase in eNOS monomer formation that was associated with SAH, decreased superoxide anion radical production and increased NO. These changes were associated with decreased vasospasm, microthromboemboli and neuronal injury. The data suggest that simvastatin re-couples eNOS after SAH, leading to decreased secondary complications such as vasospasm, microthromboemboli and neuronal injury.
Brain Injury after Transient Global Cerebral Ischemia and Subarachnoid Hemorrhage
Fatima A. Sehba,Ryszard M. Pluta,R. Loch Macdonald
Stroke Research and Treatment , 2013, DOI: 10.1155/2013/827154
Abstract:
Neurological and neurobehavioral assessment of experimental subarachnoid hemorrhage
Hyojin Jeon, Jinglu Ai, Mohamed Sabri, Asma Tariq, Xueyuan Shang, Gang Chen, R Loch Macdonald
BMC Neuroscience , 2009, DOI: 10.1186/1471-2202-10-103
Abstract: Mortality and morbidity from aneurysmal subarachnoid hemorrhage (SAH) have decreased with improvements in surgery, pharmacological treatment and intensive care. The overall outcome, however, remains relatively poor [1,2]. Management of SAH includes early obliteration of the ruptured aneurysm to prevent rebleeding, prevention of secondary brain injury from such things as decreased cerebral perfusion and prevention and treatment of delayed neurological deterioration secondary to cerebral vasospasm. The case fatality rate is approximately 50% and 30% of survivors remain dependent on others, mainly due to the persistent cognitive impairment rather than focal neurological deficits [3].Although the mechanisms underlying the cognitive deficits have not been well studied, they have nevertheless been attributed to ischemic brain injury occurring either during the initial hemorrhage or as a consequence of macro- and microvascular dysfunction and delayed ischemic neurological deterioration (Figure 1) [1]. Other mechanisms, including delayed neuronal death and cortical spreading depression have been suggested [4,5]. These processes may lead to large-artery territory infarction, smaller cortical laminar infarcts or possibly other types of selective neuronal death or perhaps even dysfunction in the absence of detectable death [6].Much work on SAH has focused on cerebral vasospasm. This is based on the assumption that severe vasospasm can reduce cerebral blood flow, cause brain ischemia and infarction and contribute to poor outcome [7]. For such studies, an acceptable dependent variable would be angiographic arterial diameter. This might not detect treatment toxicity, however. Considering the fact that the other proposed mechanisms do not necessarily cause focal cerebral infarctions, how to assess outcome is a problem. Clinically, neurobehavioral testing could be used and generally is done 3 to 6 months post-SAH.Animal studies have often relied on histological assessment of neuron
Red blood cell transfusion in patients with subarachnoid hemorrhage: a multidisciplinary North American survey
Andreas H Kramer, Michael N Diringer, Jose I Suarez, Andrew M Naidech, Loch R Macdonald, Peter D Le Roux
Critical Care , 2011, DOI: 10.1186/cc9977
Abstract: We performed a survey of North American academic neurointensivists, vascular neurosurgeons and multidisciplinary intensivists who regularly care for patients with SAH to determine hemoglobin (Hb) concentrations which commonly trigger a decision to initiate transfusion. We also assessed minimum and maximum acceptable Hb goals in the context of a clinical trial and how decision-making is influenced by advanced neurological monitoring, clinician characteristics and patient-specific factors.The survey was sent to 531 clinicians, of whom 282 (53%) responded. In a hypothetical patient with high-grade SAH (WFNS 4), the mean Hb concentration at which clinicians administered RBCs was 8.19 g/dL (95% CI, 8.07 to 8.30 g/dL). Transfusion practices were comparatively more restrictive in patients with low-grade SAH (mean Hb 7.85 g/dL (95% CI, 7.73 to 7.97 g/dL)) (P < 0.0001) and more liberal in patients with delayed cerebral ischemia (DCI) (mean Hb 8.58 g/dL (95% CI, 8.45 to 8.72 g/dL)) (P < 0.0001). In each setting, there was a broad range of opinions. The majority of respondents expressed a willingness to study a restrictive threshold of ≤8 g/dL (92%) and a liberal goal of ≥10 g/dl (75%); in both cases, the preferred transfusion thresholds were significantly higher for patients with DCI (P < 0.0001). Neurosurgeons expressed higher minimum Hb goals than intensivists, especially for patients with high-grade SAH (β = 0.46, P = 0.003), and were more likely to administer two rather than one unit of RBCs (56% vs. 19%; P < 0.0001). Institutional use of transfusion protocols was associated with more restrictive practices. More senior clinicians preferred higher Hb goals in the context of a clinical trial. Respondents were more likely to transfuse patients with brain tissue oxygen tension values <15 mmHg and lactate-to-pyruvate ratios >40.There is widespread variation in the use of RBC transfusions in SAH patients. Practices are heavily influenced by the specific dynamic clinical charact
An Integrated Approach to Address Endemic Fluorosis in Jharkhand, India  [PDF]
Luke H. MacDonald, Gopal Pathak, Burton Singer, Peter R. Jaffé
Journal of Water Resource and Protection (JWARP) , 2011, DOI: 10.4236/jwarp.2011.37056
Abstract: This paper presents the grounds for an integrated approach to address endemic fluorosis in Jharkhand, India, an approach that encompasses health monitoring, community-based water systems management, and locally synthesized hydroxyapatite, a sustainable water treatment technology. The results of this study, focusing on kinetics and sorption isotherms, demonstrate that an inexpensive, locally synthesized hydroxyapatite effectively removes fluoride from water and that the Dean Index, a measure of dental fluorosis, of school children provides a sensitive, rapid biometric to track the success of a fluoride water treatment intervention. Previous efforts to manage the fluoride problem in Jharkhand were unsuccessful, largely due to lack of accountability and inadequate community involvement. This paper explores how integrating the production of a locally synthesized hydroxyapatite with community health monitoring via the Dean Index fits into a management strategy with robust accountability mechanisms and community participation that, as historical examples suggest, is likely to succeed in Jharkhand.
Spuren von Traumatisierungen in narrativen Interviews Traces of Traumatizations in Narrative Interviews Rastros de traumatización en entrevistas narrativas
Ulrike Loch
Forum : Qualitative Social Research , 2008,
Abstract: Traumatische Kindheitserfahrungen k nnen zur Ausbildung von Dissoziation als Reparaturmechanismus und infolgedessen zu fragmentierten Erinnerungen führen. In narrativen Interviews zeigen sich diese Fragmentierungen als Spuren im Ausdrucksfeld der Sprache. In diesem Beitrag wird anhand von Fallbeispielen aufgezeigt, wie sich Dissoziationen als Folge von Traumatisierungen in der Vergangenheit wie auch in der Gegenwart sprachlich ausdrücken k nnen und welche unterstützenden M glichkeiten Interviewer/innen in Forschungssituationen haben. Denn erst das Erkennen von traumatisch bedingten Inkonsistenzen erm glicht das Verstehen von Lebensgeschichten traumatisierter Menschen jenseits von kollektiv wirksamen Tabuisierungen. Auf diese Weise vermeiden Forscher/innen die Reproduktion von gesellschaftlich relevanten Schweigegeboten bzw. Verleugnungsprozessen im wissenschaftlichen Kontext. URN: urn:nbn:de:0114-fqs0801544 Traumatic childhood experiences often lead to the development of dissociation as a defense mechanism, and subsequently to fragmented memories. In narrative interviews this fragmentation is traced in the expressive field of language. In this article a range of case studies are used to illustrate how dissociations, resulting from traumatic experiences in the past as well as the present, may express themselves and how we, as interviewers, can give support to the client in interview situations. Only by understanding the inconsistencies caused by these traumatic experiences, interviewees are able to tell their life histories beyond the collectively effective taboos. By becoming aware of these mechanisms, the researcher can steer clear of reproducing the socially relevant silencing effects, i.e. denial processes, within the context of social scientific research. URN: urn:nbn:de:0114-fqs0801544 Experiencias infantiles traumáticas a menudo conducen al desarrollo de la disociación como un mecanismo de defensa y, por consiguiente, a memorias fragmentadas. En las entrevistas narrativas esta fragmentación se localiza en los campos expresivos del lenguaje. En este artículo un conjunto de estudios de caso ilustran como las disociaciones, resultantes de experiencias traumáticas tanto del pasado como del presente, pueden expresarse y como nosotros, en tanto entrevistadores, podemos brindar apoyo a los clientes en las situaciones de entrevista. Solamente mediante la comprensión de las inconsistencias causadas por esas experiencias traumáticas, los entrevistados son capaces de decir sus historias de vida más allá de los tabúes colectivamente efectivos. Al ser concient
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