Publications by authors named "Helena Morrison"

Middle cerebral artery occlusion (MCAO) is the gold-standard method for preclinical modeling of ischemic stroke in rodents. However, successful occlusion is not guaranteed by even the most skilled surgical hands. Errors primarily occur when the filament is not placed at the correct depth and include instances of either no infarction or vessel perforation, which can cause death.

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This paper presents a refined, user-friendly protocol for using boron-dipyrromethene (BODIPY) to assess and quantify foam cells and lipid droplet-accumulating microglia (LDAM) in mouse brain tissue. The protocol aims to enhance existing methodologies by offering precise and efficient evaluation of foam cells and LDAM burden in various neuropathological conditions linked to lipid metabolism and neuroinflammation. A notable challenge in analyzing tissue from mouse models of these neurodegenerative disorders is the interference caused by the autofluorescent molecule lipofuscin.

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Unlabelled: Idiopathic pulmonary fibrosis (IPF) is a restrictive chronic lung disease that results in scarring of the tissue due to an unknown cause. Dyspnea is experienced by 90 % of patients and is correlated with reduced quality of life and survival times. Breathing techniques can improve perceived dyspnea, however, are not readily taught outside of inpatient hospital settings and pulmonary rehabilitation programs, the latter being accessed by only 3 % of patients with chronic lung disease.

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Background: The health and well-being of children in foster care are of high concern. A resource with which to disrupt maladaptation and promote healing are positive relationships among children and caregivers within the foster home. The research question was: Can an online intervention improve family hardiness and sibling relationships within foster care families?

Objectives: To: (1) establish feasibility and acceptability of an online behavioral intervention within the foster family, (2) explore the effects of the intervention on relational quality outcomes, and (3) decompose the mechanisms driving improved family hardiness through mediation analysis.

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Ischemic stroke remains a leading cause of mortality and long-term disability worldwide, necessitating efforts to identify biomarkers for diagnosis, prognosis, and treatment monitoring. The present study aimed to identify novel plasma biomarkers of neurodegeneration and inflammation in a mouse model of stroke induced by distal middle cerebral artery occlusion. Using targeted lipidomic and global untargeted metabolomic profiling of plasma collected from aged male mice 24 h after stroke and weekly thereafter for 7 weeks, we discovered distinct acute and chronic signatures.

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Article Synopsis
  • Stroke is a major global health issue, particularly during recovery, and this study explores the chronic phase of healing beyond immediate interventions.
  • Researchers used various methods like MRI and plasma NFL measurement in male and female mice to track brain injury evolution and found ongoing issues like edema and tissue remodeling up to 30 days post-stroke.
  • The study highlights the role of chronic inflammation and blood-brain barrier dysfunction in long-term neurodegeneration, emphasizing the need for innovative treatment strategies for stroke recovery.
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Pituitary Adenylate Cyclase Activating Polypeptide (PACAP) is a pleiotropic peptide known to promote many beneficial processes following neural damage and cell death after stroke. Despite PACAP's known neurotrophic and anti-inflammatory properties, it has not realized its translational potential due to a poor pharmacokinetic profile (non-linear PK/PD), and limited Blood-Brain Barrier Penetration (BBB) permeability. We have previously shown that glycosylation of PACAP increases stability and enhances BBB penetration.

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Background: Little is known about hybrid PhD nursing students' experiences.

Method: The purpose of this study was to describe and analyze the experiences of PhD nursing students in a hybrid program using a convergent mixed methods design. Recent nursing PhD alumni ( = 18), and current PhD students ( = 4) were recruited at a research-intensive university in the southwestern United States.

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Following ischemic stroke, the degradation of myelin and other cellular membranes surpasses the lipid-processing capabilities of resident microglia and infiltrating macrophages. This imbalance leads to foam cell formation in the infarct and areas of secondary neurodegeneration, instigating sustained inflammation and furthering neurological damage. Given that mitochondria are the primary sites of fatty acid metabolism, augmenting mitochondrial biogenesis (MB) may enhance lipid processing, curtailing foam cell formation and post-stroke chronic inflammation.

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It is well established that decreased brain blood flow, increased reactive oxygen species production (ROS), and pro-inflammatory mechanisms accelerate neurodegenerative disease progressions, including vascular cognitive impairment and dementia (VCID). Previous studies in our laboratory have shown that our novel glycosylated Angiotensin-(1-7) Mas receptor agonist PNA5 reverses cognitive deficits, decreases ROS production, and inhibits inflammatory cytokine production in our preclinical mouse model of VCID that is induced by chronic heart failure (VCID-HF). In the present study, the effects of VCID-HF and treatment with PNA5 on microglia activation, blood-brain-barrier (BBB) integrity, and neurovascular coupling were assessed in our mouse model of VCID-HF.

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A considerable complication for stroke survivors is the subsequent development of cognitive decline or dementia. In this study, the relationship between the inflammation-centered comorbidity burden on post-stroke cognitive function among community-dwelling stroke survivors capable of independent living was examined. Data for this secondary analysis were collected from stroke survivors (n = 97) participating in a randomized clinical trial.

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There is an unmet clinical need for curative therapies to treat neurodegenerative disorders. Most mainstay treatments currently on the market only alleviate specific symptoms and do not reverse disease progression. The Pituitary adenylate cyclase-activating polypeptide (PACAP), an endogenous neuropeptide hormone, has been extensively studied as a potential regenerative therapeutic.

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The aim of this study was to test whether poststroke oral administration of a small molecule p75 neurotrophin receptor (p75) modulator (LM11A-31) can augment neuronal survival and improve recovery in a mouse model of stroke. Mice were administered LM11A-31 for up to 12 weeks, beginning 1 week after stroke. Metabolomic analysis revealed that after 2 weeks of daily treatment, mice that received LM11A-31 were distinct from vehicle-treated mice by principal component analysis and had higher levels of serotonin, acetylcholine, and dopamine in their ipsilateral hemisphere.

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Depression is prevalent among one-third to two-thirds of acute and chronic stroke survivors. Despite the availability of pharmacotherapies and/or psychotherapies, depression persists, even for 5-10 years after stroke, reflecting limited treatment responses and/or adherence to this conventional care. Mind-body interventions are commonly used among adults to ameliorate depressive symptoms.

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Parkinson's disease (PD) is a neurodegenerative disease caused by the death of dopaminergic neurons in the substantia nigra pars compacta (SNpc), characterized by motor dysfunction. While PD symptoms are well treated with L-DOPA, continuous use can cause L-DOPA-induced dyskinesia (LID). We have previously demonstrated that sub-anesthetic ketamine attenuated LID development in rodents, measured by abnormal involuntary movements (AIMs), and reduced the density of maladaptive striatal dendritic mushroom spines.

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Background: Ischemic stroke is an acquired brain injury with gender-dependent outcomes. A persistent obstacle in understanding the sex-specific neuroinflammatory contributions to ischemic brain injury is distinguishing between resident microglia and infiltrating macrophages-both phagocytes-and determining cell population-specific contributions to injury evolution and recovery processes. Our purpose was to identify microglial and macrophage populations regulated by ischemic stroke using morphology analysis and the presence of microglia transmembrane protein 119 (TMEM119).

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Background: Nursing doctoral education now includes an option with a growing national interest: the PhD-DNP dual degree. Although programs have existed for 10 years, little is known about experiences of dual PhD-DNP degree nursing students (DDNS) during doctoral education, including their perceptions of mentorship during coursework, comprehensive exams, and dissertation readiness.

Objective: To explore and describe the experiences of DDNS during hybrid dual doctoral education at one Southwestern university.

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Persistent inflammation has been identified as a contributor to aging-related neurodegenerative disorders such as Alzheimer's disease. Normal aging, in the absence of dementia, also results in gradual cognitive decline and is thought to arise, in part, because of a chronic pro-inflammatory state in the brain. Toxoplasma gondii is an obligate intracellular parasite that establishes a persistent, asymptomatic infection of the central nervous system (CNS) accompanied by a pro-inflammatory immune response in many of its hosts, including humans and rodents.

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Up to 50% of traumatic brain injury (TBI) survivors demonstrate persisting and late-onset anxiety disorders indicative of limbic system dysregulation, yet the pathophysiology underlying the symptoms is unclear. We hypothesize that the development of TBI-induced anxiety-like behavior in an experimental model of TBI is mediated by changes in glutamate neurotransmission within the amygdala. Adult, male Sprague-Dawley rats underwent midline fluid percussion injury or sham surgery.

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Identifying differential responses between sexes following traumatic brain injury (TBI) can elucidate the mechanisms behind disease pathology. Peripheral and central inflammation in the pathophysiology of TBI can increase sleep in male rodents, but this remains untested in females. We hypothesized that diffuse TBI would increase inflammation and sleep in males more so than in females.

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A functional neurovascular unit (NVU) is central to meeting the brain's dynamic metabolic needs. Poststroke damage to the NVU within the ipsilateral hemisphere ranges from cell dysfunction to complete cell loss. Thus, understanding poststroke cell-cell communication within the NVU is of critical importance.

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Chronic neurological impairments can manifest from repetitive traumatic brain injury (rTBI), particularly when subsequent injuries occur before the initial injury completely heals. Herein, we apply post-traumatic sleep as a physiological biomarker of vulnerability, hypothesizing that a second TBI during post-traumatic sleep worsens neurological and histological outcomes compared to one TBI or a second TBI after post-traumatic sleep subsides. Mice received sham or diffuse TBI by midline fluid percussion injury; brain-injured mice received one TBI or rTBIs at 3- or 9-h intervals.

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Microglia are brain phagocytes that participate in brain homeostasis and continuously survey their environment for dysfunction, injury, and disease. As the first responders, microglia have important functions to mitigate neuron and glia dysfunction, and in this process, they undergo a broad range of morphologic changes. Microglia morphologies can be categorized descriptively or, alternatively, can be quantified as a continuous variable for parameters such as cell ramification, complexity, and shape.

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Determining regions of altered brain physiology after diffuse brain injury is challenging. Microglia, brain immune cells with ramified and dynamically moving processes, constantly surveil the parenchyma for dysfunction which, when present, results in a changed morphology. Our purpose was to define the spatiotemporal changes in microglia morphology over 28 days following rat midline fluid percussion injury (mFPI) as a first step in exploiting microglia morphology to reflect altered brain physiology.

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