In JoVE (2)

Other Publications (25)

Articles by David F. Cechetto in JoVE

Other articles by David F. Cechetto on PubMed

Propofol Anesthesia Compared to Awake Reduces Infarct Size in Rats

Anesthesiology. May, 2002  |  Pubmed ID: 11981160

Propofol has not been studied directly in animals subject to cerebral ischemia in the conscious state. Strokes are usually induced in animals while they are anesthetized, making it difficult to eliminate anesthetic interactions as a complicating factor. Therefore, to compare the neuroprotective effects of propofol to the unanesthetized state, experiments were performed using a model that induces a stroke in the conscious rat.

Propofol Neuroprotection in Cerebral Ischemia and Its Effects on Low-molecular-weight Antioxidants and Skilled Motor Tasks

Anesthesiology. May, 2004  |  Pubmed ID: 15114212

Propofol is neuroprotective when administered immediately after stroke. The therapeutic window, duration of administration, and antioxidant mechanisms of propofol in neuroprotection are not known. The effects of propofol after stroke were examined in the conscious animal. The authors have previously shown that light propofol anesthesia (25 mg x kg(-1) x h(-1)) for a period of 4 h, even if delayed 1 h after the onset of ischemia, decreases infarct volume 3 days after the stroke.

Human Cardiovascular and Gustatory Brainstem Sites Observed by Functional Magnetic Resonance Imaging

The Journal of Comparative Neurology. Apr, 2004  |  Pubmed ID: 15022263

The reflex control and relay to higher brain sites of visceral sensory information within the central nervous system is mediated via discrete sites in the brainstem. Anatomical characterization of these sites in humans has been limited due to the invasive nature of such research. The present study employed 4 Tesla functional magnetic resonance imaging (fMRI) to characterize brainstem sites involved in autonomic control in the human. Eight subjects performed tasks that activate the general visceral (the isometric hand-grip, maximal inspiration, Valsalva maneuver) or special visceral sensory systems (sucrose administration to the tongue). Activation of the nucleus of the solitary tract and parabrachial nucleus was consistently observed with all general visceral tasks. Periaqueductal gray area activation was observed during the maximal inspiration and Valsalva maneuver conditions and raphe activation was present in response to isometric hand-grip and maximal inspiration tasks. The activation in the nucleus of the solitary tract was consistently more rostral in the medulla during sucrose administration than during performance of the other experimental tasks. This finding is consistent with what has been previously demonstrated in animals. This is the first study to image the human brainstem with respect to visceral control and demonstrates the feasibility of using high-resolution fMRI to study the functional organization of the human brainstem.

Interaction Between a Rat Model of Cerebral Ischemia and Beta-amyloid Toxicity: II. Effects of Triflusal

Stroke; a Journal of Cerebral Circulation. Aug, 2005  |  Pubmed ID: 16040593

Clinical data suggest that Alzheimer disease (AD) and stroke together potentiate cognitive impairment. Our rat model demonstrates that this interaction may be mediated through inflammatory cells and pathways. Thus, anti-inflammatory agents such as Triflusal, a nonsteroidal anti-inflammatory agent (NSAID), may provide neuroprotection for susceptible neurons in AD and cerebral ischemia.

Relating Drug-induced Changes in Carotid Artery Mechanics to Cardiovagal and Sympathetic Baroreflex Control

Canadian Journal of Physiology and Pharmacology. May, 2005  |  Pubmed ID: 15897926

Previous evidence indicates that sensitivity of the baroreflex cardiovagal and sympathetic arms is dissociated. In addition, pharmacologic assessment of baroreflex sensitivity (BRS) has revealed that cardiovagal, but not sympathetic, BRS is greater when blood pressure is increasing versus falling. The origin of this hysteresis is unknown. In this study, carotid artery distensibility and absolute distension (diameter) were assessed to test the hypothesis that vessel mechanics in barosensitive regions affect the BRS of cardiovagal, but not sympathetic, outflow. R-R interval (i.e. time between successive R waves), finger arterial blood pressure, muscle sympathetic nerve activity, and carotid artery dimensions (B-mode imaging) were measured during sequential infusions of sodium nitroprusside (SNP) and phenylephrine (PHE). Systolic and diastolic common carotid artery diameters and pulse pressure were recorded to calculate distensibility of this vessel under each drug condition. Cardiovagal BRS was greater when blood pressure was increasing versus decreasing (p < 0.01). Sympathetic BRS was not affected by direction of pressure change. Distensibility did not differ between SNP and PHE injections. However, compared with SNP, infusion of PHE resulted in larger absolute systolic and diastolic carotid diameters (p < 0.001). Therefore, cardiovagal reflex hysteresis was related to drug-induced changes in common carotid artery diameter but not distensibility. The lack of sympathetic hysteresis in this model suggests a relative insensitivity of this baroreflex component to carotid artery dimensions and provides a possible mechanism for the dissociation between cardiovagal and sympathetic BRS.

Interaction Between a Rat Model of Cerebral Ischemia and Beta-amyloid Toxicity: Inflammatory Responses

Stroke; a Journal of Cerebral Circulation. Jan, 2005  |  Pubmed ID: 15591213

Clinical data suggest that Alzheimer disease (AD) and stroke together potentiate cognitive impairment. Inflammatory mechanisms are involved in AD pathology and stroke and may be the mediator between AD and stroke toxicity.

Effects of Pyrrolidine Dithiocarbamate on Beta-amyloid (25-35)-induced Inflammatory Responses and Memory Deficits in the Rat

Neurobiology of Disease. Jul, 2006  |  Pubmed ID: 16624564

It has been well established that neuroinflammation is involved in Alzheimer disease (AD) pathogenesis. Accumulation and aggregation of beta-amyloid (Abeta) peptide in the brains of patients with AD result in activation of glial cells which, in turn, initiates neuroinflammatory responses that involve reactive oxygen intermediates and release of inflammatory cytokines. In this study, bilateral intracerebroventricular (i.c.v.) injections of Abeta (25-35) in the rat resulted in impairment in learning and spatial memory and increased immunoreactive staining of AD-related neuropathological markers (Abeta, APP) and inflammatory mediators (OX-6, COX-2) in CA1 and dentate gyrus regions of the hippocampus. Pyrrolidine dithiocarbamate (PDTC) given intraperitoneally 30 min before Abeta injection and daily for 7 days postsurgery significantly prevented Abeta-induced neuropathological and neuroinflammatory responses, as well as the learning and spatial memory deficits. The potential of PDTC for reducing cognitive and neuropathological deficits may provide preliminary evidence for a new approach of AD treatment.

Progressive Increase in Infarct Size, Neuroinflammation, and Cognitive Deficits in the Presence of High Levels of Amyloid

Stroke; a Journal of Cerebral Circulation. Dec, 2007  |  Pubmed ID: 17962591

In the elderly, cerebral ischemia (CI) occurs in the presence of high levels of amyloid. Neuroinflammation plays a critical role in the pathophysiology of Alzheimer's disease and CI. This study examined infarct size, neuroinflammation, and cognitive deficits over time in rat models of Alzheimer's disease and CI.

Sex Differences in Forebrain and Cardiovagal Responses at the Onset of Isometric Handgrip Exercise: a Retrospective FMRI Study

Journal of Applied Physiology (Bethesda, Md. : 1985). Oct, 2007  |  Pubmed ID: 17615282

In general, cardiac regulation is dominated by the sympathetic and parasympathetic nervous systems in men and women, respectively. Our recent study had revealed sex differences in the forebrain network associated with sympathoexcitatory response to baroreceptor unloading. The present study further examined the sex differences in forebrain modulation of cardiovagal response at the onset of isometric exercise. Forebrain activity in healthy men (n = 8) and women (n = 9) was measured using functional magnetic resonance imaging during 5 and 35% maximal voluntary contraction handgrip exercise. Heart rate (HR), mean arterial pressure (MAP), and muscle sympathetic nerve activity (MSNA) were collected in a separate recording session. During the exercise, HR and MAP increased progressively, while MSNA was suppressed (P < 0.05). Relative to men, women demonstrated smaller HR (8 +/- 2 vs. 18 +/- 3 beats/min) and MAP (3 +/- 2 vs. 11 +/- 2 mmHg) responses to the 35% maximal voluntary contraction trials (P < 0.05). Although a similar forebrain network was activated in both groups, the smaller cardiovascular response in women was reflected in a weaker insular cortex activation. Nevertheless, men did not show a stronger deactivation at the ventral medial prefrontal cortex, which has been associated with modulating cardiovagal activity. In contrast, the smaller cardiovascular response in women related to their stronger suppression of the dorsal anterior cingulate cortex activity, which has been associated with sympathetic control of the heart. Our findings revealed sex differences in both the physiological and forebrain responses to isometric exercise.

Effects of Triflusal and Aspirin in a Rat Model of Cerebral Ischemia

Stroke; a Journal of Cerebral Circulation. Feb, 2007  |  Pubmed ID: 17194886

Neuroinflammation plays a critical role in the pathogenesis of cerebral ischemia. Triflusal, a selective cyclooxygenase-2, and its active metabolite 3-hydroxy-4-trifluoromethylbenzoic acid may inhibit apoptosis and inflammation after cerebral ischemia. An in vivo model of cerebral ischemia was used to investigate the effects of triflusal and aspirin treatment on infarct volume, and inflammation after cerebral ischemia in the rat.

Vascular Risk Factors and Alzheimer's Disease

Expert Review of Neurotherapeutics. May, 2008  |  Pubmed ID: 18457531

Vascular cognitive impairment risk factors include stroke, hypertension, diabetes and atherosclerosis. In the elderly, vascular risk factors occur in the presence of high levels of amyloid in the aging brain. Stroke alters the clinical expression of a given load of Alzheimer's disease (AD) pathology. Experimentally, large vessel infarcts or small striatal infarcts are larger in the presence of amyloid. Patients with minor cerebral infarcts and moderate AD lesions will develop the clinical manifestations of dementia. Moreover, there is also an association between other vascular risk factors and the clinical expression of cognitive decline and dementia. The risk of AD is increased in subjects with adult-onset diabetes mellitus, hypertension, atherosclerotic disease and atrial fibrillation. Experimentally, small striatal infarcts in the presence of high levels of amyloid in the brain exhibit a progression in infarct size over time with enhanced degree of cognitive impairment, AD-type pathology and neuroinflammation compared with striatal infarcts or high amyloid levels alone.

Functional Neuroanatomy of Autonomic Regulation

NeuroImage. Sep, 2009  |  Pubmed ID: 19446637

Considerable effort has been put into animal studies establishing the sites in the brain that are responsible for control of the autonomic nervous system. These studies relied on an electrophysiological or neurochemical response to the activation of peripheral autonomic receptors or chemical or electrical stimulation of central sites. A large number of excellent reviews summarize the results of these studies. More recently, functional imaging has been used to not only confirm the electrophysiological and anatomical studies in animals, but has allowed a more complete understanding of how the brain responds as a whole for effecting autonomic control. The earliest studies to examine forebrain control during functional imaging utilized tests that involved active participation of the subjects and included maximal inspiration, Valsalva manoeuvre, isometric handgrip and cold compress application. There were a few issues that arose from these studies. First, they involved areas of the brain that included active decision making, they were more prone to inducing movement artefact, and some of these tests could activate noxious regions in the brain in addition to autonomic sites. In fact, this dual modality activation represented a more severe complication for investigators determining nociceptive sites in the brain, since virtually all of their stimuli had concomitant autonomic responses. More recent investigations attempted to resolve these issues with more selective passive and active stimuli. In spite of the very different approaches taken to visceral activation in functional imaging studies, a consistent picture of the key areas involved in autonomic control has emerged.

Triflusal Reduces Cerebral Ischemia Induced Inflammation in a Combined Mouse Model of Alzheimer's Disease and Stroke

Brain Research. Dec, 2010  |  Pubmed ID: 20934412

Clinical data has shown that stroke exacerbates dementia in Alzheimer's disease (AD) patients. Previous work, combining rat models of AD and stroke have shown that neuroinflammation may be the common mediator between AD and stroke toxicity. This study examined the effects of triflusal (2-acetoxy-4-trifluoromethylbenzoic acid) in APP(23) transgenic mice receiving strokes. Six month-old APP(23) mice over-expressing mutant human amyloid precursor protein (APP) were used to model AD in this study. Unilateral injections of a potent vasoconstrictor, endothelin-1, into the striatum were used to mimic small lacunar infarcts. Immunohistochemical analysis was performed to examine AD-like pathology and inflammatory correlates of stroke and AD. APP(23) mice showed increases in AD-like pathology and inflammatory markers of AD in the cortex and hippocampus. Endothelin-induced ischemia triggered an inflammatory response along with increases in AD pathological markers in the region of the infarct. Triflusal reduced inflammation surrounding the endothelin-induced infarct only. At the dose used, anti-inflammatory treatment may be beneficial in reducing the AD and inflammatory correlates of stroke in a combined AD-stroke mouse model.

Oleic Acid Ameliorates Amyloidosis in Cellular and Mouse Models of Alzheimer's Disease

Brain Pathology (Zurich, Switzerland). May, 2011  |  Pubmed ID: 21040071

Several lines of evidence support protective as well as deleterious effects of oleic acid (OA) on Alzheimer's disease (AD) and other neurological disorders; however, the bases of these effects are unclear. Our investigation demonstrates that amyloid precursor protein (APP) 695 transfected Cos-7 cells supplemented with OA have reduced secreted amyloid-beta (Aβ) levels. An early-onset AD transgenic mouse model expressing the double-mutant form of human APP, Swedish (K670N/M671L) and Indiana (V717F), corroborated our in vitro findings when they were fed a high-protein, low-fat (18% reduction), cholesterol-free diet enriched with OA. These mice exhibited an increase in Aβ40/Aβ42 ratio, reduced levels of beta-site APP cleaving enzyme (BACE) and reduced presenilin levels along with reduced amyloid plaques in the brain. The decrease in BACE levels was accompanied by increased levels of a non-amyloidogenic soluble form of APP (sAPPα). Furthermore, the low-fat/+OA diet resulted in an augmentation of insulin-degrading enzyme and insulin-like growth factor-II. These results suggest that OA supplementation and cholesterol intake restriction in a mouse model of AD reduce AD-type neuropathology.

Cortical Circuitry Associated with Reflex Cardiovascular Control in Humans: Does the Cortical Autonomic Network "speak" or "listen" During Cardiovascular Arousal

Anatomical Record (Hoboken, N.J. : 2007). Sep, 2012  |  Pubmed ID: 22848047

Beginning with clinical evidence of fatal cardiac arrhythmias in response to severe stress, in epileptic patients, and following stroke, the role of the cerebral cortex in autonomic control of the cardiovascular system has gained both academic and clinical interest. Studies in anesthetized rodents have exposed the role of several forebrain regions involved in cardiovascular control. The introduction of functional neuroimaging techniques has enabled investigations into the conscious human brain to illuminate the temporal and spatial activation patterns of cortical regions that are involved with cardiovascular control through the autonomic nervous system. This symposia report emphasizes the research performed by the authors to understand the functional organization of the human forebrain in cardiovascular control during physical stressors of baroreceptor unloading and handgrip exercise. The studies have exposed important associations between activation patterns of the insula cortex, dorsal anterior cingulate, and the medial prefrontal cortex and cardiovascular adjustments to physical stressors. Furthermore, these studies provide functional anatomic evidence that sensory signals arising from baroreceptors and skeletal muscle are represented within the insula cortex and the medial prefrontal cortex, in addition to the sensory cortex. Thus, the cortical pathways subserving reflex cardiovascular control integrate viscerosensory inputs with outgoing traffic that modulates the autonomic nervous system.

Amyloid Burden, Neuroinflammation, and Links to Cognitive Decline After Ischemic Stroke

Stroke; a Journal of Cerebral Circulation. Sep, 2014  |  Pubmed ID: 25005439

Hemodynamic Effects of Combined Focal Cerebral Ischemia and Amyloid Protein Toxicity in a Rat Model: a Functional CT Study

PloS One. 2014  |  Pubmed ID: 24971942

Clinical evidence indicates that cerebral ischemia (CI) and a pathological factor of Alzheimer's disease, the β-amyloid (Aβ) protein, can increase the rate of cognitive impairment in the ageing population. Using the CT Perfusion (CTP) functional imaging, we sought to investigate the interaction between CI and the Aβ protein on cerebral hemodynamics.

Comorbid Aβ Toxicity and Stroke: Hippocampal Atrophy, Pathology, and Cognitive Deficit

Neurobiology of Aging. Jul, 2014  |  Pubmed ID: 24491422

Numerous clinical and epidemiological reports indicate that patients with history of vascular illness such as stroke are more likely to develop dementia as the clinical manifestation of Alzheimer's disease. However, there are little data regarding the pathologic mechanisms that link vascular risk factors to the factors associated with dementia onset. We provide evidence that suggests intriguing detrimental interactions between stroke and β-amyloid (Aβ) toxicity in the hippocampus. Stroke was induced by unilateral striatal injection of endothelin-1, the potent vasoconstrictor. Aβ toxicity was modeled by bilateral intracerebroventricular injections of the toxic fragment Aβ. Gross morphologic changes in comorbid Aβ and stroke rats were enlargement of the lateral ventricles with concomitant shrinkage of the hippocampus. The hippocampus displayed a series of synergistic biochemical alterations, including microgliosis, deposition of Aβ precursor protein fragments, and cellular degeneration. In addition, there was bilateral induction of connexin43, reduced neuronal survival, and impaired dendritic development of adult-born immature neurons in the dentate gyrus of these rats compared with either rats alone. Behaviorally, there was impairment in the hippocampal-based discriminative fear-conditioning to context task indicating learning and memory deficit. These results suggest an insight into the relationship between hippocampal atrophy, pathology, and functional impairment. Our work not only highlights the exacerbated pathology that emerges when Aβ toxicity and stroke occur comorbidly but also demonstrates that this comorbid rat model exhibits physiopathology that is highly characteristic of the human condition.

Cortical Control of the Autonomic Nervous System

Experimental Physiology. Feb, 2014  |  Pubmed ID: 24121283

What is the topic of this review? The pathways in the brain by which visceral information, in particular cardiopulmonary afferents, ascend to the cerebral cortex have been delineated in animal models. Studies using functional magnetic resonance imaging in humans have confirmed what was known from the animal studies and established the critical sites in the cerebral cortex of humans for autonomic control and the significance of these sites for cognitive emotional function. What advances does it highlight? Stimulation of cardiopulmonary afferents in humans has consistently resulted in activation in the insular cortex and the anterior cingulate cortex. It has been shown that individuals who are characterized as cardiovascular responders to mental stress have a different pattern of activity in the cortex related to the cardiac changes. A number of animal studies in the rat and cat have been particularly useful for determining the pathways and the sites in the forebrain and cortex that are responsible for autonomic control. For example, these experiments have demonstrated that there is a viscerotopically organized pathway, with the first site of termination in the nucleus of the solitary tract and with subsequent relays in the parabrachial nucleus and the ventroposterior parvocellular nucleus of the thalamus before final visceral afferent inputs in the insular cortex. Several neuroimaging studies in humans, using cardiopulmonary manipulations, have confirmed the importance of the insular cortex as a site of for visceral afferent inputs. The anterior cingulate cortex has also been implicated in cardiopulmonary control. Both the insular cortex and the infralimbic cortex have been shown to be involved in descending control of the cardiovascular system. Neuroimaging with functional magnetic resonance imaging has demonstrated that the cortical autonomic control pathways are different in individuals who are characterized as cardiovascular reactors to mental stress. There is evidence that this alteration in pathways in the cortex may be due to past experiences, including childhood trauma.

Increased Expression of Simple Ganglioside Species GM2 and GM3 Detected by MALDI Imaging Mass Spectrometry in a Combined Rat Model of Aβ Toxicity and Stroke

PloS One. 2015  |  Pubmed ID: 26086081

The aging brain is often characterized by the presence of multiple comorbidities resulting in synergistic damaging effects in the brain as demonstrated through the interaction of Alzheimer's disease (AD) and stroke. Gangliosides, a family of membrane lipids enriched in the central nervous system, may have a mechanistic role in mediating the brain's response to injury as their expression is altered in a number of disease and injury states. Matrix-Assisted Laser Desorption Ionization (MALDI) Imaging Mass Spectrometry (IMS) was used to study the expression of A-series ganglioside species GD1a, GM1, GM2, and GM3 to determine alteration of their expression profiles in the presence of beta-amyloid (Aβ) toxicity in addition to ischemic injury. To model a stroke, rats received a unilateral striatal injection of endothelin-1 (ET-1) (stroke alone group). To model Aβ toxicity, rats received intracerebralventricular (i.c.v.) injections of the toxic 25-35 fragment of the Aβ peptide (Aβ alone group). To model the combination of Aβ toxicity with stroke, rats received both the unilateral ET-1 injection and the bilateral icv injections of Aβ25-35 (combined Aβ/ET-1 group). By 3 d, a significant increase in the simple ganglioside species GM2 was observed in the ischemic brain region of rats who received a stroke (ET-1), with or without Aβ. By 21 d, GM2 levels only remained elevated in the combined Aβ/ET-1 group. GM3 levels however demonstrated a different pattern of expression. By 3 d GM3 was elevated in the ischemic brain region only in the combined Aβ/ET-1 group. By 21 d, GM3 was elevated in the ischemic brain region in both stroke alone and Aβ/ET-1 groups. Overall, results indicate that the accumulation of simple ganglioside species GM2 and GM3 may be indicative of a mechanism of interaction between AD and stroke.

Comorbid Rat Model of Ischemia and β-amyloid Toxicity: Striatal and Cortical Degeneration

Brain Pathology (Zurich, Switzerland). Jan, 2015  |  Pubmed ID: 24725245

Levels of cerebral amyloid, presumably β-amyloid (Abeta), toxicity and the incidence of cortical and subcortical ischemia increases with age. However, little is known about the severe pathological condition and dementia that occur as a result of the comorbid occurrence of this vascular risk factor and Abeta toxicity. Clinical studies have indicated that small ischemic lesions in the striatum are particularly important in generating dementia in combination with minor amyloid lesions. These cognitive deficits are highly likely to be caused by changes in the cortex. In this study, we examined the viability and morphological changes in microglial and neuronal cells, gap junction proteins (connexin43) and neuritic/axonal retraction (Fer Kinase) in the striatum and cerebral cortex using a comorbid rat model of striatal injections of endothelin-1 (ET1) and Abeta toxicity. The results demonstrated ventricular enlargement, striatal atrophy, substantial increases in β-amyloid, ramified microglia and increases in neuritic retraction in the combined models of stroke and Abeta toxicity. Changes in connexin43 occurred equally in both groups of Abeta-treated rats, with and without focal ischemia. Although previous behavioral tests demonstrated impairment in memory and learning, the visual discrimination radial maze task did not show significant difference, suggesting the cognitive impairment in these models is not related to damage to the dorsolateral striatum. These results suggest an insight into the relationship between cortical/striatal atrophy, pathology and functional impairment.

The Targeted Antioxidant, Catalase-SKL, Reduces Beta-amyloid Toxicity in the Rat Brain

Brain Pathology (Zurich, Switzerland). Feb, 2016  |  Pubmed ID: 26919450

Accumulation of beta-amyloid (Aβ) in the brain has been implicated as a major contributor to the cellular pathology and cognitive impairment observed in Alzheimer's disease. Beta-amyloid may exert its toxic effects by increasing reactive oxygen species and neuroinflammation in the brain. This study set out to investigate whether a genetically engineered derivative of the peroxisomal antioxidant enzyme catalase (CAT-SKL), is able to reduce the toxicity induced by intracerebroventricular injection of Aβ25-35 in the mature rat brain. Histopathological and immunohistochemical analyses were used to evaluate neuroinflammation, and neuronal loss. Spatial learning and reference memory was assessed using the Morris water maze. CAT-SKL treatment was able to reduce the pathology induced by Aβ25-35 toxicity by significantly decreasing microglia activation in the basal forebrain and thalamus, and reducing cholinergic loss in the basal forebrain. Aβ25-35 animals showed deficits in long-term reference memory in the Morris water maze, while Aβ25-35 animals treated with CAT-SKL did not demonstrate long-term memory impairments. This preclinical data provides support for the use of CAT-SKL in reducing neuroinflammation and long-term reference memory deficits induced by Aβ25-35. This article is protected by copyright. All rights reserved.

Assessing the Effects of Acute Amyloid β Oligomer Exposure in the Rat

International Journal of Molecular Sciences. Aug, 2016  |  Pubmed ID: 27563885

Alzheimer's disease (AD) is the most common form of dementia, yet there are no therapeutic treatments that can either cure or delay its onset. Currently, the pathogenesis of AD is still uncertain, especially with respect to how the disease develops from a normal healthy brain. Amyloid β oligomers (AβO) are highly neurotoxic proteins and are considered potential initiators to the pathogenesis of AD. Rat brains were exposed to AβO via bilateral intracerebroventricular injections. Rats were then euthanized at either 1, 3, 7 or 21-days post surgery. Rat behavioural testing was performed using the Morris water maze and open field tests. Post-mortem brain tissue was immunolabelled for Aβ, microglia, and cholinergic neurons. Rats exposed to AβO showed deficits in spatial learning and anxiety-like behaviour. Acute positive staining for Aβ was only observed in the corpus callosum surrounding the lateral ventricles. AβO exposed rat brains also showed a delayed increase in activated microglia within the corpus callosum and a decreased number of cholinergic neurons within the basal forebrain. Acute exposure to AβO resulted in mild learning and memory impairments with co-concomitant white matter pathology within the corpus callosum and cholinergic cell loss within the basal forebrain. Results suggest that acute exposure to AβO in the rat may be a useful tool in assessing the early phases for the pathogenesis of AD.

Correlates of Performance of Healthcare Workers in Emergency, Triage, Assessment and Treatment Plus Admission Care (ETAT+) Course in Rwanda: Context Matters

PloS One. 2016  |  Pubmed ID: 27030974

The Emergency, Triage, Assessment and Treatment plus Admission care (ETAT+) course, a comprehensive advanced pediatric life support course, was introduced in Rwanda in 2010 to facilitate the achievement of the fourth Millennium Development Goal. The impact of the course on improving healthcare workers (HCWs) knowledge and practical skills related to providing emergency care to severely ill newborns and children in Rwanda has not been studied.

Pediatric Emergency Care Capacity in a Low-resource Setting: An Assessment of District Hospitals in Rwanda

PloS One. 2017  |  Pubmed ID: 28257500

Health system strengthening is crucial to improving infant and child health outcomes in low-resource countries. While the knowledge related to improving newborn and child survival has advanced remarkably over the past few decades, many healthcare systems in such settings remain unable to effectively deliver pediatric advance life support management. With the introduction of the Emergency Triage, Assessment and Treatment plus Admission care (ETAT+)-a locally adapted pediatric advanced life support management program-in Rwandan district hospitals, we undertook this study to assess the extent to which these hospitals are prepared to provide this pediatric advanced life support management. The results of the study will shed light on the resources and support that are currently available to implement ETAT+, which aims to improve care for severely ill infants and children.

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