Publications by authors named "Remington L"

Competence in healthcare is a recognized expectation by consumers. In 2018 following an extensive review and consensus-building process, burn nursing practice competencies were published. Clinical nurse leaders were called upon to use these published competencies in practice as a basis for the requisite knowledge and skills needed in the care of the burn-injured individual.

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Purpose Of Review: This review examines the epidemiology, diagnosis, prognosis, treatment and prevention of community-acquired pneumonia (CAP) in adults.

Recent Findings: CAP is a significant cause of morbidity and mortality. Streptococcus pneumoniae is the most common CAP pathogen; however, microbial cause varies by geographic location and host factors.

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We have characterized the cellular response to demyelination/remyelination in the central nervous system using the toxin cuprizone, which causes reproducible demyelination in the corpus callosum. Microglia were distinguished from macrophages by relative CD45 expression (CD45(dim)) using flow cytometry. Their expansion occurred rapidly and substantially outnumbered infiltrating macrophages and T cells throughout the course of cuprizone treatment.

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The unambiguous identification of oligodendrocytes in tissue sections, especially in myelinated tracts, is often difficult. Most of the antibodies used to identify oligodendrocytes label the myelin sheath as well. Originally described as an inhibitor of axonal outgrowth, Nogo-A is known to be strongly expressed in mature oligodendrocytes in vivo.

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Multiple sclerosis is an inflammatory disease of the central nervous system that leads to loss of myelin and oligodendrocytes and damage to axons. We show that daily administration (days 8 to 24) of murine ciliary neurotrophic factor (CNTF), a neurotrophic factor that has been described as a survival and differentiation factor for neurons and oligodendrocytes, significantly ameliorates the clinical course of a mouse model of multiple sclerosis. In the acute phase of experimental autoimmune encephalomyelitis induced by myelin oligodendrocyte glycoprotein peptide 35-55, treatment with CNTF did not change the peripheral immune response but did reduce the number of perivascular infiltrates and T cells and the level of diffuse microglial activation in spinal cord.

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Regulation of inflammatory responses is critical to progression of organ-specific autoimmune disease. Although many candidate cell types have been identified, immunoregulatory activity has rarely been directly assayed and never from the CNS. We have analyzed the regulatory capability of Gr-1high neutrophils isolated from the CNS of mice with experimental autoimmune encephalomyelitis.

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Background: Automated perimeters (in general) are similar; however, caution may be exercised when visual field results from two different instruments are compared. The purpose of this study was to compare threshold measurements in the central field between the Synemed (Optifield 1) Glaucoma Test and the Humphrey 30-2 test in a young patient population.

Methods: One hundred twenty subjects were tested.

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Background: The automated perimeter is becoming the instrument of choice in the analysis of the visual field. There are a number of different perimeters in use and it can be difficult to compare results from different instruments. The purpose of this study was to compare visual field threshold measurements determined by the Humphrey Field Analyzer and the Dicon TKS 4000.

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Background: The effects of miotic drugs on visual field sensitivity have been well documented, but few studies have reported the effects of active pupillary dilation on visual field sensitivity. Since visual field testing is sometimes performed when a patient is undergoing pupillary dilation for fundus examination, the effects of active pupillary dilation is of concern to today's optometrist.

Methods: The effects of active pupillary dilation on automated static threshold perimetry were studied in 23 normal subjects using the Humphrey Field Analyzer and the 30-2, StatPac, and FastPac programs.

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Squamous cell carcinoma of the skin (SCC) can progress by stages: sun-damaged epidermis, with individual disordered keratinocytes; actinic keratosis (AK), spontaneously regressing keratinized patches having aberrant cell differentiation and proliferation; carcinoma in situ; SCC and metastasis. To understand how sunlight acts as a carcinogen, we determined the stage at which sunlight mutates the p53 tumour-suppressor gene and identified a function for p53 in skin. The p53 mutations induced by ultraviolet radiation and found in > 90% of human SCCs were present in AKs.

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The therapeutic responsiveness of genetically defined tumors expressing or devoid of the p53 tumor suppressor gene was compared in immunocompromised mice. Tumors expressing the p53 gene contained a high proportion of apoptotic cells and typically regressed after treatment with gamma radiation or adriamycin. In contrast, p53-deficient tumors treated with the same regimens continued to enlarge and contained few apoptotic cells.

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Homozygosity for a mutation in the Rb tumor suppressor gene causes mid-gestation embryonic lethality in the mouse. Using a two-step targeting protocol, we have constructed Rb homozygous mutant mouse embryonic stem cells and used them to create chimeric animals partially composed of Rb-deficient cells. Analysis of these chimeras demonstrates widespread contribution of the mutant cells to adult tissues, including the retina and mature erythrocytes.

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To determine the contribution of p53 loss to tumor progression, we have induced abnormal proliferation in the brain choroid plexus epithelium of transgenic mice using a SV40 T antigen fragment that perturbs pRB family function but does not affect p53 function. Tumors induced by this mutant develop slowly compared with those induced by wild-type T antigen. Suppressed tumor growth is directly attributable to p53 function, since rapid tumor development occurs when the T antigen fragment is expressed in p53-null mice.

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The tumour suppressor genes Rb and p53 are mutated in several types of human cancer, and many tumour types carry mutations in both genes. To study how these genes normally function, we and others have created mouse strains with Rb and p53 mutations. Here we describe the phenotypic effects of combined germline mutations in these two tumour suppressor genes.

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Background: The p53 tumor suppressor gene is mutated in a large percentage of human malignancies, including tumors of the colon, breast, lung and brain. Individuals who inherit one mutant allele of p53 are susceptible to a wide range of tumor types. The gene encodes a transcriptional regulator that may function in the cellular response to DNA damage.

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Androgen ablation induces programmed death of androgen-dependent prostatic glandular cells, resulting in fragmentation of their genomic DNA and the cells themselves into apoptotic bodies. Twenty percent of prostatic glandular cells undergo programmed death per day between day 2 and 5 after castration. During this same period, < 1% of prostatic glandular cells enter the S phase of the cell cycle, documenting that > 95% of these die in G0.

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Healthcare trends and statistics indicate the growing number of managed care contracts will continue. For patient accounts managers, this means more challenges in managing and administering different kinds of contracts. Communication, management, and feedback will become essential tools for ensuring successful administration of managed care contracts.

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The reservoir of Mycobacterium avium complex (MAC) during human infection is the mononuclear phagocyte. In these studies, the ability of certain macrophage-active cytokines to affect MAC growth in human alveolar macrophages was evaluated. Neither recombinant interferon-gamma (2 x 10(2) to 10(3) U/well of 5 x 10(5) cells) nor recombinant macrophage colony-stimulating factor (20 to 50 ng/well), when tested alone, exhibited a consistent ability to induce macrophage targets to inhibit the growth of a clinical strain of MAC serovar 4.

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