Margaret Keenan Harrais: A Biography In Four Voices

Thesis (Ph.D.) University of Alaska Fairbanks, 2011Narrative strategies available to biography are explored through the life of Margaret Keenan Harrais---teacher, educational administrator, judge, and activist. Biography is a particular endeavor requiring flexible inquiry and creative presentation. Margaret is viewed through multiple lenses that explore personhood, encourage readers' introspection, and imply the importance of the individual in history. The four voices indicated in the title of this dissertation are editorial, analytical, sparsely Romantic, and expository. This biography aims to complicate readers' notions of what it means to be a person in relation to other people by focusing closely on selected episodes in Margaret's career; analyzing their historical, social, and literary import; and finally broadening the perspective to include the entirety of Margaret's life. The roles of the biographer and the reader are examined throughout in an attempt to explore the interconnections between biography and autobiography. Margaret's life is presented within the contexts of other women teachers in rural areas, as well as other men and women who wrote about territorial Alaska for a non-Alaskan audience. At heart this biography seeks to experiment with the narrative possibilities available to biographers, and to explore the ways in which the effects of these narratives allow for the contribution to general scholarship on the basis of particular experiences

The impact of California\u27s service delivery system on developmentally disabled youth emancipating from the child welfare system

The purpose of this study was to examine public child welfare and regional center workers\u27 perceptions of the experiences that developmentally disabled youth have as they emancipate from child welfare services into the adult developmental service sector. Data was collected by interviewing workers from Inland Regional Center and San Bernardino County\u27s Child Welfare Department. The sample of this study included nine case managers and social workers who presented nine cases. Qualitative Interviews were designed and conducted with workers from both agencies utilizing the same basic interview guide

Endogenous transforming growth factor β1 suppresses inflammation and promotes survival in adult CNS

Transforming growth factor β1 (TGFβ1) is a pleiotropic cytokine with potent neurotrophic and immunosuppressive properties that is upregulated after injury, but also expressed in the normal nervous system. In the current study, we examined the regulation of TGFβ1 and the effects of TGFβ1 deletion on cellular response in the uninjured adult brain and in the injured and regenerating facial motor nucleus. To avoid lethal autoimmune inflammation within 3 weeks after birth in TGFβ1-deficient mice, this study was performed on a T- and B-cell-deficient RAG2-/- background. Compared with wild-type siblings, homozygous deletion of TGFβ1 resulted in an extensive inflammatory response in otherwise uninjured brain parenchyma. Astrocytes increased in GFAP and CD44 immunoreactivity; microglia showed proliferative activity, expression of phagocytosis-associated markers [αXβ2, B7.2, and MHC1 (major histocompatibility complex type 1)], and reduced branching. Ultrastructural analysis revealed focal blockade of axonal transport, perinodal damming of axonal organelles, focal demyelination, and myelin debris in granule-rich, phagocytic microglia. After facial axotomy, absence of TGFβ1 led to a fourfold increase in neuronal cell death (52 vs 13%), decreased central axonal sprouting, and significant delay in functional recovery. It also interfered with the microglial response, resulting in a diminished expression of early activation markers [ICAM1 (intercellular adhesion molecule 1), α6β1, and αMβ2] and reduced proliferation. In line with axonal and glial findings in the otherwise uninjured CNS, absence of endogenous TGFβ1 also caused an ∼10% reduction in the number of normal motoneurons, pointing to an ongoing and potent trophic role of this anti-inflammatory cytokine in the normal as well as in the injured brain. Copyright © 2007 Society for Neuroscience

Effects of Copper Exchange Levels on Complexation of Ammonia in Cu (II)-exchanged X Zeolite

Copper (II)-exchanged faujasite-X zeolites at various loadings of copper per unit cell of zeolites were prepared and then exposed to ammonia. The copper ammine complexes of the various copper levels per unit cell were characterized and analyzed by a combination of diffuse reflectance, X-ray powder diffraction, FT-infrared spectroscopy, electron paramagnetic resonance and nuclear magnetic resonance spectroscopic methods. At low copper exchange levels (<5 copper atoms per unit cell), the major complex is [Cu(Ozeo)2(NH3)2]2+ and it is strongly bound to the zeolite framework walls at single four ring sites (site III). Above five copper atoms per unit cell, the major complex becomes [Cu(NH3)4]2+ and it is least interacting with the zeolite framework walls. The [Cu(NH3)4]2+ complex which was formed at higher copper levels per unit cell was most favoured by the presence of maximal amount of ammonia.Keywords: Cation Exchange, Catalysis, Copper, Complexation, Copper AmminesAttached PDF and Supplementary Fil

Decrease in excitatory neurons, astrocytes and proliferating progenitors in the cerebral cortex of mice lacking exon 3 from the Fgf2 gene

<p>Abstract</p> <p>Background</p> <p>The <it>Fgf2 </it>gene is expressed in the brain neuroepithelium during embryonic development and in astroglial cells throughout life. Previous knockout studies suggested that FGF2 plays a role in the proliferation of neural progenitors in the embryonic cerebral cortex. These studies exclusively used knockout alleles lacking the <it>Fgf2 </it>exon 1. However, the description of putative alternative exons located downstream from the canonical exon 1 raised the possibility that alternatively spliced transcripts may compensate for the lack of the canonical exon 1 in the <it>Fgf2 </it>-/- mice.</p> <p>Results</p> <p>We generated and characterized a new line of Fgf2 knockout mice lacking the expression of exon 3, which is conserved in all <it>Fgf2 </it>transcripts and contains essential heparin and receptor binding interfaces. The expression of <it>Fgf2 </it>exon 3 was prevented by inserting a transcriptional STOP cassette in the <it>Fgf2 </it>genomic locus. These mice demonstrate a phenotype in the adult neocortex characterized by decreased density and number of cortical excitatory neurons and astrocytes, which is virtually identical to that of the <it>Fgf2 </it>-/- mice lacking exon 1. In addition, we also show that the <it>Fgf2 </it>exon 3 knockout mice have decreased proliferation of precursors in the adult cerebral cortex, which had not been previously investigated in the other mutant lines.</p> <p>Conclusion</p> <p>The results demonstrate that the phenotype of two completely different <it>Fgf2 </it>KO mouse lines, lacking exon 1 or exon 3, is remarkably similar. The combined results from these KO models clearly indicate that FGF2 plays a role in cortical cell genesis during embryonic development as well as in adulthood. Thus, FGF2 may be required for the maintenance of the pool of adult cortical progenitor cells.</p

Salivary Acinar Cells from Aquaporin 5-deficient Mice Have Decreased Membrane Water Permeability and Altered Cell Volume Regulation

Aquaporins (AQPs) are channel proteins that regulate the movement of water through the plasma membrane of secretory and absorptive cells in response to osmotic gradients. In the salivary gland, AQP5 is the major aquaporin expressed on the apical membrane of acinar cells. Previous studies have shown that the volume of saliva secreted by AQP5-deficient mice is decreased, indicating a role for AQP5 in saliva secretion; however, the mechanism by which AQP5 regulates water transport in salivary acinar cells remains to be determined. Here we show that the decreased salivary flow rate and increased tonicity of the saliva secreted byAqp5 − /− mice in response to pilocarpine stimulation are not caused by changes in whole body fluid homeostasis, indicated by similar blood gas and electrolyte concentrations in urine and blood in wild-type and AQP5-deficient mice. In contrast, the water permeability in parotid and sublingual acinar cells isolated from Aqp5 − /− mice is decreased significantly. Water permeability decreased by 65% in parotid and 77% in sublingual acinar cells fromAqp5 − /−mice in response to hypertonicity-induced cell shrinkage and hypotonicity-induced cell swelling. These data show that AQP5 is the major pathway for regulating the water permeability in acinar cells, a critical property of the plasma membrane which determines the flow rate and ionic composition of secreted saliva

Enhancing Osteogenic Differentiation of Mouse Embryonic Stem Cells by Nanofibers

Controlled differentiation of embryonic stem cells (ESC) is necessary to their use as a cell source for tissue engineering or regeneration. To date, most studies have concentrated on chemical cues to direct ESC differentiation. However, during normal embryonic development, multiple factors beyond chemical cues play a role, including the extracellular matrix (ECM) in bone development. In this study, we use nanofibrous (NF) matrices to mimic the morphology of the ECM to examine the contribution of the ECM morphology to the differentiation of mouse ESC. After 12h of differentiation culture, mouse ESC form protrusions interacting with NF matrices, while they appear not to interact with flat films. Immunofluorescence staining after 26 days of differentiation culture indicates a greater degree of differentiation for mouse ESC on NF matrices compared to flat films. Polymerase chain reaction results, also, show greater degree of osteogenic differentiation on NF matrices compared to flat films when osteogenic supplements are added to the culture. Overall, these results demonstrate that NF morphology contributes to the controlled differentiation of mouse ESC.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/78135/1/ten.tea.2008.0227.pd

Glypican-1, phosphacan/receptor protein-tyrosine phosphatase-ζ/β and its ligand, tenascin-C, are expressed by neural stem cells and neural cells derived from embryonic stem cells

The heparan sulfate proteoglycan glypican-1, the chondroitin sulfate proteoglycan phosphacan/RPTP (receptor protein-tyrosine phosphatase)-ζ/β and the extracellular matrix protein tenascin-C were all found to be expressed by neural stem cells and by neural cells derived from them. Expression of proteoglycans and tenascin-C increased after retinoic acid induction of SSEA1-positive ES (embryonic stem) cells to nestin-positive neural stem cells, and after neural differentiation, proteoglycans and tenascin-C are expressed by both neurons and astrocytes, where they surround cell bodies and processes and in certain cases show distinctive expression patterns. With the exception of tenascin-C (whose expression may decrease somewhat), expression levels do not change noticeably during the following 2 weeks in culture. The significant expression, by neural stem cells and neurons and astrocytes derived from them, of two major heparan sulfate and chondroitin sulfate proteoglycans of nervous tissue and of tenascin-C, a high-affinity ligand of phosphacan/RPTP-ζ/β, indicates that an understanding of their specific functional roles in stem cell neurobiology will be important for the therapeutic application of this new technology in facilitating nervous tissue repair and regeneration

Efficient Gene Targeting by Homologous Recombination in Rat Embryonic Stem Cells

The rat is the preferred experimental animal in many biological studies. With the recent derivation of authentic rat embryonic stem (ES) cells it is now feasible to apply state-of-the art genetic engineering in this species using homologous recombination. To establish whether rat ES cells are amenable to in vivo recombination, we tested targeted disruption of the hypoxanthine phosphoribosyltransferase (hprt) locus in ES cells derived from both inbred and outbred strains of rats. Targeting vectors that replace exons 7 and 8 of the hprt gene with neomycinR/thymidine kinase selection cassettes were electroporated into male Fisher F344 and Sprague Dawley rat ES cells. Approximately 2% of the G418 resistant colonies also tolerated selection with 6-thioguanine, indicating inactivation of the hprt gene. PCR and Southern blot analysis confirmed correct site-specific targeting of the hprt locus in these clones. Embryoid body and monolayer differentiation of targeted cell lines established that they retained differentiation potential following targeting and selection. This report demonstrates that gene modification via homologous recombination in rat ES cells is efficient, and should facilitate implementation of targeted, genetic manipulation in the rat