Publications by authors named "Michelle Fleming"

Background: Advancing health equity requires more contextualised evidence.

Objectives: To synthesise published evidence using an existing framework on the origins of health disparities and determine care-related outcome disparities for residents of long-term care, comparing minoritised populations to the context-specific dominant population.

Design: Systematic review.

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Adequate antioxidant supply is essential for maintaining metabolic homeostasis and reducing oxidative stress during detoxification. The emerging evidence suggests that certain classes of phytonutrients can help support the detoxification process by stimulating the liver to produce detoxification enzymes or acting as antioxidants that neutralize the harmful effects of free radicals. This study was designed to examine the effects of a guided 28-day metabolic detoxification program in healthy adults.

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The COVID-19 pandemic has negatively impacted the lives and well-being of long-term care home residents. This mixed-method study examined the health equity implications of the COVID-19 lockdown and visitation strategies in long-term care homes in Ontario. We recruited long-term care home residents, their family members and designated caregivers, as well as healthcare workers from 235 homes in Ontario, Canada.

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Purpose: Dry mouth is a highly prevalent and significant symptom in patients with advanced progressive diseases. It is a poorly understood area of research, and currently, there is no standardised outcome measure or assessment tool for dry mouth.

Methods: To assess responses to self-reported dry mouth questions, the impact of dry mouth, methods used to reduce symptoms and relevance of the questionnaire.

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Maternal and fetal sources of thyroid hormone are important for the development of many organ systems. Thyroid hormone deficiency causes variable intellectual disability and hearing impairment in mouse and man, but the basis for this variation is not clear. To explore this variation, we studied two thyroid hormone-deficient mouse mutants with mutations in pituitary-specific transcription factors, POU1F1 and PROP1, that render them unable to produce thyroid stimulating hormone.

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Purpose: Dry mouth (xerostomia) is one of the commonest symptoms in cancer patients and can adversely affect quality of life. The aim of this review was to determine the effectiveness of pharmacological and non-pharmacological interventions in treating xerostomia in adult advanced cancer patients.

Methods: The literature search was performed in February 2014 using databases including EMBASE, MEDLINE, CINAHL, BNI and Cochrane library.

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The hush puppy mouse mutant has been shown previously to have skull and outer, middle, and inner ear defects, and an increase in hearing threshold. The fibroblast growth factor receptor 1 (Fgfr1) gene is located in the region of chromosome 8 containing the mutation. Sequencing of the gene in hush puppy heterozygotes revealed a missense mutation in the kinase domain of the protein (W691R).

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Emx2 is a homeodomain protein that plays a critical role in inner ear development. Homozygous null mice die at birth with a range of defects in the CNS, renal system and skeleton. The cochlea is shorter than normal with about 60% fewer auditory hair cells.

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Genetic cases of congenital pituitary hormone deficiency are common and many are caused by transcription factor defects. Mouse models with orthologous mutations are invaluable for uncovering the molecular mechanisms that lead to problems in organ development and typical patient characteristics. We are using mutant mice defective in the transcription factors PROP1 and POU1F1 for gene expression profiling to identify target genes for these critical transcription factors and candidates for cases of pituitary hormone deficiency of unknown aetiology.

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The novel neurological mutant Cincinatti arose by genomic duplication of exon 5 in the glycine receptor gene Glra1. The mutant transcript results in premature protein truncation. A direct repeat of the pentamer GGGGC is present adjacent to the breakpoints and may have mediated the duplication event by a replication slippage mechanism.

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Primary mesenchyme cells in sea urchin embryos emerge from the epithelium of the blastula wall and move into the blastocoel in a process referred to as ingression. Ingressing cells are bottle-shaped with their basal end protruding into the blastocoel and their apical end narrowed into a thin strand. Soon after becoming bottle-shaped, the ingressing cells move into the blastocoel and form the primary mesenchyme which ultimately assembles the skeleton of the larva.

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