897 resultados para Hair.
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"November 1964."
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"March 1969."
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Top Row: Laura Anderson, Sherry Armstrong, Sarah Arnoldi, Rosalie Arzadon, Leslie Bair, Angela Baker, Kristy Barker, Elizabeth Barrios, Tamara J. Becker, Kristen Bekker, Kathryn Birkmeier, Lucinda Brach, Stacy Brege, Pamela K. Burke, Nicole Bushey
Row 2: Nancy Byington, Heidi Campbell, Jason Patton, Jodi Kaplan, Dawn Buhl, Colleen Carolan, Elizabeth Conklin, Krisanne Kircos, Margie Tucker, Jennifer Sanders, Angela Vitale, Kathleen S. Kemp, Tom Atkinson, Tanya M. Cerbins, Tamra Chute
Row 3: Kirsten A. Covell, Michelle Currie, Kristina Davis, Albert Deogracias, Deana Diokno, Elizabeth Donovan, Kathryn Drobitch, Andrea Dunbar, Carol Dunlap, Kelley Dutcheshen
Row 4: Shannon Fitzpatrick, Tracy Fouchey, Carol Gerstner, Holly Gray, Jacqueline Hair, Lisa Hart, Kristen Hawley, Joanna Hesford, Nicole Hill, Denise Hines, Matthew Hoffmann, Christa Holland
Row 5: Debra Horvath, Lisa Hottmann, Paul Howell, Susan Isley, Violet H. Barkauskas, Elisabeth Pennington, Rhetaugh G. Dumas, Janice Lindberg, Beverly Jones, Susie Jahan, Denielle Jordan, Kellie Kennon, Hanah Kiernan
Row 6: Sally A. Klyn, Ellen Kraft, Sheri Kurashige, Nancy Kushman, Jeannine Marie LaDouceur, Opal Lesse, Heather Joy Lirette, Dana Lloyd, Eileen Mac Innis, Sara MacKeigan, Marilyn Martin, Stephanie Martino, Lynette May, Amy Marie Mazur, Tracy McIntyre, Amy Marie McManur
Row 7: Lynne Michalski, Jennie Mille, Jennifer Moran, Marvella M. Muzik, Tara Nichols, Teri Nies, Maria Nistal, Lori Olivet, Constance Paglis, Andrea Pelham-Reichel, Michelle Perkins, Barbara persensky, Julianne Plaza, Sonia Prichard, Sarah Prush
Row 8: Michael Ranieri, Shanda Richards, Carleen Roberts, Marie Antoinette Robinson, Kelly A. Saran, Deborah Saunders, Christine Sawicki, Donna Schaldenbrand, Noelle Schellig, Marci Simon, Colleen Sirhal, Kathryn Smay, Susan Snyr, Diane Sobecki, Wendy Stevens, Carolyn A. Storck
Row 9: Maria Tandoc, Linda Tate, Nicole Theodore, William Troy, Diana Underwood, Maria Villegas, Jennifer Vite, Marianne Weir, Kelly Whitman, Angela Willbrandt, Wendy Winkler, Yvette Wright, Jill Yatcho, Catherine Zawacki, Theresa Zeiler
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"To the husband of the woman with the frizzled hair": p. [34]-35. "France complaining of the lewdness of her maidens": p. [36]-37.
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Levelling with Elisha.- Playing even for Obadiah.- By a hair.- The last chance.- Sanguinary Jeremiah.- Eliphaz, late Fairfax- The redemption handicap.- A morning workout.- Egyptian corn.- The modern judgment of Solomon.
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1896]--no. 9. Wild garlic. [By L.D. Dewey, 1897] Rev. ed.,
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Thesis (Master's)--University of Washington, 2016-06
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The relationships between MC1R gene variants and red hair, skin reflectance, degree of freckling and nevus count were investigated in 2331 adolescent twins, their sibs and parents in 645 twin families. Penetrance of each MC1R variant allele was consistent with an allelic model where effects were multiplicative for red hair but additive for skin reflectance. Of nine MC1R variant alleles assayed, four common alleles were strongly associated with red hair and fair skin (Asp84Glu, Arg151Cys, Arg160Trp and Asp294His), with a further three alleles having low penetrance (Val60Leu, Val92Met and Arg163Gln). These variants were separately combined for the purposes of this analysis and designated as strong 'R' (OR=63.3; 95% CI 31.9-139.6) and weak 'r ' (OR=5.1; 95% CI 2.5-11.3) red hair alleles. Red-haired individuals are predominantly seen in the R/R and R/r groups with 67.1 and 10.8%, respectively. To assess the interaction of the brown eye color gene OCA2 on the phenotypic effects of variant MC1R alleles we included eye color as a covariate, and also genotyped two OCA2 SNPs (Arg305Trp and Arg419Gln), which were confirmed as modifying eye color. MC1R genotype effects on constitutive skin color, freckling and mole count were modified by eye color, but not genotype for these two OCA2 SNPs. This is probably due to the association of these OCA2 SNPs with brown/green not blue eye color. Amongst individuals with a R/R genotype (but not R/r), those who also had brown eyes had a mole count twice that of those with blue eyes. This suggests that other OCA2 polymorphisms influence mole count and remain to be described.
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Skin penetration of the tetrapeptide Ac-Ala-Ala-Pro-Val-NH2 was assessed. This peptide sequence fits the P-P-1 subsites of elastase and inhibits human neutrophil elastase competitively. Consequently this peptide may be therapeutically useful in a variety of inflammatory disorders, including psoriasis. in which elevated levels of human neutrophil elastase have been reported. Peptide penetration was assessed across whole human skin, whole skin with the stratum corneum removed by tape stripping and epidermis, which had been removed from the dermis by heat separation. The influence of 75% aqueous ethanol as a potential penetration enhancer of the tetrapeptide across epidermis was also assessed. The tetrapeptide did not penetrate whole human skin or epidermis, even under the influence of 75% aqueous ethanol. However, when the stratum corneum was removed tetrapeptide flux of 73.39 mug cm(-2) h(-1) was achieved. The study demonstrates that the stratum corneum is the main barrier to tetrapeptide skin penetration and must be overcome if therapeutically relevant amounts of tetrapeptide are to be delivered to the skin.
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Much of the hearing loss that occurs in old age is likely to be due to the long-term deterioration of the mitochondria in the different structures of the cochlea. The current review surveys some of the basic information on mitochondria and mitochondrial DNA, as a background to their possible involvement in presbyacusis. It is likely that oxygen radicals damage mitochondrial DNA and other components of the mitochondria, such as their proteins and lipids. This further compromises both oxidative phosphorylation and the repair processes in mitochondria, setting up a vicious cycle of degradation. Evidence is presented from inherited point mutations on the possibly most critical sites for mutations in mitochondrial DNA associated with hearing loss. It is suggested that random sorting and clonal expansion of mutations both maintain the integrity of the pool of mitochondrial DNA molecules and give rise to the apoptosis that leads to loss of vulnerable cells, and hence to deafness. It is moreover suggested that apoptosis of the vulnerable cells of the inner ear may to some extent be preventable, or at least delayed. Copyright (C) 2004 S. Karger AG, Basel.
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Several recent papers have tried to address the genetic determination of eye colour via microsatellite linkage, testing of pigmentation candidate gene polymorphisms and the genome wide analysis of SNP markers that are informative for ancestry. These studies show that the OCA2 gene on chromosome 15 is the major determinant of brown and/or blue eye colour but also indicate that other loci will be involved in the broad range of hues seen in this trait in Europeans.
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Despite the well-characterised role of sonic hedgehog (Shh) in promoting interfollicular basal cell proliferation and hair follicle downgrowth, the role of hedgehog signalling during epidermal stem cell fate remains largely uncharacterised. In order to determine whether the three vertebrate hedgehog molecules play a role in regulating epidermal renewal we overexpressed sonic (Shh), desert (Dhh) and Indian (Ihh) hedgehog in the basal cells of mouse skin under the control of the human keratin 14 promoter. We observed no overt epidermal morphogenesis phenotype in response to Ihh overexpression, however Dhh overexpression resulted in a range of embryonic and adult skin manifestations indistinguishable from Shh overexpression. Two distinct novel phenotypes were observed amongst Shh and Dhh transgenics, one exhibiting epidermal progenitor cell hyperplasia with the other displaying a complete loss of epidermal tissue renewal indicating deregulation of stem cell activity. These data suggest that correct temporal regulation of hedgehog activity is a key factor in ensuring epidermal stem cell maintenance. In addition, we observed Shh and Dhh transgenic skin from both phenotypes developed lesions reminiscent of human basal cell carcinoma (BCC), indicating that BCCs can be generated despite the loss of much of the proliferative (basal) compartment. These data suggest the intriguing possibility that BCC can arise outside the stem cell population. Thus the elucidation of Shh (and Dhh) target gene activation in the skin will likely identify those genes responsible for increasing the proliferative potential of epidermal basal cells and the mechanisms involved in regulating epidermal stem cell fate.
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alpha-Melanocyte-stimulating hormone (alpha-MSH) activates the melanocortin-1 receptor (MC1R) on melanocytes to promote a switch from red/yellow pheomelanin synthesis to darker eumelanins via positive coupling to adenylate cyclase. The human MC1R locus is highly polymorphic with the specific variants associated with red hair and fair skin (RHC phenotype) postulated to be loss-of-function receptors. We have examined the ability of MC1R variants to activate the cAMP pathway in stably transfected REK293 cells. The RHC associated variants, Arg151Cys, Arg160Trp and Asp294His, demonstrated agonist-mediated increases in cAMP and phosphorylation of cAMP-responsive element-binding protein (CREB). Whereas the Asp294His variant showed severely impaired functional responses, the Arg151Cys and Arg160Trp variants retained considerable signaling capacity. Melanoma cells homozygous for either the Arg151Cys variant or consensus sequence both elicited CREB phosphorylation in response to alpha-MSH in the presence of IBMX. The common RHC alleles, Arg151Cys, Arg160Trp and Asp294His, are neither complete loss-of-function receptors nor are they functionally equivalent. (c) 2005 Elsevier Inc. All rights reserved.
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Genetic analysis in animals has been used for many applications, such as kinship analysis, for determining the sire of an offspring when a female has been exposed to multiple males, determining parentage when an animal switches offspring with another dam, extended lineage reconstruction, estimating inbreeding, identification in breed registries, and speciation. It now also is being used increasingly to characterize animal materials in forensic cases. As such, it is important to operate under a set of minimum guidelines that assures that all service providers have a template to follow for quality practices. None have been delineated for animal genetic identity testing. Based on the model for human DNA forensic analyses, a basic discussion of the issues and guidelines is provided for animal testing to include analytical practices, data evaluation, nomenclature, allele designation, statistics, validation, proficiency testing, lineage markers, casework files, and reporting. These should provide a basis for professional societies and/or working groups to establish more formalized recommendations.