Publications by authors named "Maria E Frazer"

Objective: Currently available treatments for neuropathic pain are only modestly efficacious when assessed in randomized clinical trials and work for only some patients in the clinic. Induced-pain or gain-of-function phenotypes have been shown to predict response to analgesics (vs placebos) in patients with neuropathic pain. However, the predictive value of these phenotypes has never been studied in post-traumatic neuropathic pain.

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This cohort study evaluates whether the incorporation of a pain tolerability question augments the information gathered from a numeric rating scale.

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Persistent pain after lumbar surgery (failed back surgery syndrome [FBSS]) remains a leading indication for chronic analgesia. However, no analgesics have proven efficacious for this condition. Although trials have evaluated gabapentinoids for chronic low back pain, none of these trials focused solely on FBSS.

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Objectives: To determine whether patients with neurogenic claudication associated with lumbar spinal stenosis would prefer a treatment that makes it possible for them to walk farther or walk with less pain; to examine associations between this treatment preference and patient-reported and in-clinic treadmill testing measures of walking ability and walking-associated pain.

Methods: In this cross-sectional study, 269 patients with neurogenic claudication were asked to report their pain intensity when walking, complete the Swiss Spinal Stenosis Questionnaire, rank their outcome preferences for treatment, and undergo standardized treadmill testing, including measures of final pain rating and time to first pain of moderate intensity (Tfirst). Descriptive statistics were used to characterize patient preferences for treatment outcome.

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Study Design: Randomized, double-blind, placebo-controlled, single-dose crossover study.

Objective: To test the analgesic efficacy of oxymorphone hydrochloride (OH) and propoxyphene/acetaminophen (PA) for patients with neurogenic claudication associated with lumbar spinal stenosis.

Summary Of Background Data: Although opioids are often prescribed for neurogenic claudication, no randomized controlled studies support their efficacy for this condition.

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Objectives: To test the effects of pregabalin on the induction of neurogenic claudication.

Methods: This study was a randomized, double-blind, active placebo-controlled, 2-period, crossover trial. Twenty-nine subjects were randomized to receive pregabalin followed by active placebo (i.

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Amyloid-beta (A beta) has been identified as a key component in Alzheimer's disease (AD). Significant in vitro and human pathological data suggest that intraneuronal accumulation of A beta peptides plays an early role in the neurodegenerative cascade. We hypothesized that targeting an antibody-based therapeutic to specifically abrogate intracellular A beta accumulation could prevent or slow disease onset.

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Alzheimer's disease (AD) is a progressively debilitating brain disorder pathologically defined by extracellular amyloid plaques, intraneuronal neurofibrillary tangles, and synaptic disintegrity. AD has not been widely considered a disease of white matter, but more recent evidence suggests the existence of abnormalities in myelination patterns and myelin attrition in AD-afflicted human brains. Herein, we demonstrate that triple-transgenic AD (3xTg-AD) mice, which harbor the human amyloid precursor protein Swedish mutant transgene, presenilin knock-in mutation, and tau P301L mutant transgene, exhibit significant region-specific alterations in myelination patterns and in oligodendrocyte marker expression profiles at time points preceding the appearance of amyloid and tau pathology.

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Immunotherapeutics designed to dissolve existing amyloid plaques or to interrupt amyloid-β (Aβ) accumulation may be feasible for treatment and/or prevention of Alzheimer's disease (AD). "Shaping" the immune responses elicited against Aβ is requisite toward generating an efficacious and safe outcome; this can be achieved by minimizing the possibility of deleterious inflammatory reactions in the brain as observed in clinical testing of Aβ peptide/adjuvant-based modalities. Herpes simplex virus (HSV)-based amplicons can coexpress multiple antigens and/or immunomodulatory genes due to their large genetic size capacity, thereby facilitating antigen-specific immune response shaping.

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Immunotherapeutics designed to dissolve existing amyloid plaques or to interrupt amyloid-beta (Abeta) accumulation may be feasible for treatment and/or prevention of Alzheimer's disease (AD). "Shaping" the immune responses elicited against Abeta is requisite toward generating an efficacious and safe outcome; this can be achieved by minimizing the possibility of deleterious inflammatory reactions in the brain as observed in clinical testing of Abeta peptide/adjuvant-based modalities. Herpes simplex virus (HSV)-based amplicons can coexpress multiple antigens and/or immunomodulatory genes due to their large genetic size capacity, thereby facilitating antigen-specific immune response shaping.

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