Recent advances in the field of audiology have indicated that there has been a growing concern regarding the potential damage to the hearing mechanism induced by recreational noise exposure from personal music devices (PMD). Regular PMD use may have a long-term damaging effect on the outer- and inner hair cells of the cochlea which may result in a progressive hearing loss. As PMDs have advanced to a stage where the memory of the devices are able to contain hours of listening content, the environments where these devices are being used are rapidly expanding. Many young adults tend to use their PMDs whilst exercising. Exercise in itself induces physiological and metabolic changes such as increased blood flow and oxygen levels within the structures of the cochlea. The purpose of this study was to determine the differential impact and short-term effects of simultaneous cardiovascular workout and personal music device (PMD) use on the otoacoustic emissions of young adults. Seven female and five male subjects completed three testing conditions: (i) one hour exposure to PMD use in isolation, (ii) one hour exposure to cardiovascular workout in isolation, and (iii) one hour simultaneous exposure to PMD use and cardiovascular workout. Distortion product otoacoustic emissions (DPOAEs) were conducted prior to, as well as directly following each testing condition, as primary indicator of cochlear responses emitted through a preset stimulus frequency sequence measuring the 2f₁ - f₂ (75 – 70 dB SPL) and constructing a plot of DPOAE levels as a function of frequency. While each of the testing conditions on its own did not result in statistically significant changes of the DPOAE response, a highly significant different profile in the DPOAE response level increase/decrease for the higher frequencies (6-8 kHz) was obtained when comparing the different sessions to each other. Where exposure to cardiovascular workout showed a clear trend of an increased DPOAE response level between the pre-exposure and post-exposure testing from 2 kHz to 8 kHz with a maximum increase at 6 kHz, both the music only condition and the combined condition where the cardiovascular workout was combined with music resulted in a significant different profile. During combined exposure a clear trend of decreased DPOAE response amplitudes between the pre-exposure and post-exposure testing were seen for the higher frequencies. These findings may support the notion of a clear effect of cardiovascular workout on the otoacoustic emissions at higher test frequencies, measured by DPOAEs when performed with and without music exposure. / Dissertation (MLOG)--University of Pretoria, 2014. / tm2015 / Speech-Language Pathology and Audiology / MLOG / Unrestricted

Body depilation is a relatively new area of research inquiry. Although women in many industrialized cultures have engaged in body depilation for some time, this behavior has been documented only recently in men. While originally thought to be the practice of just a small percentage of men, recent studies suggest that more men engage in body depilation than had been previously hypothesized (Boroughs & Thompson, 2002; Boroughs, Cafri, & Thompson, 2005; Martins, Tiggemann, & Churchett, 2008; Tiggemann, Martins, & Churchett, 2008). Nevertheless, this area of research is understudied and the relationship between body depilation and men's overall body image is poorly understood. Since much of the documented evidence of men's body depilation is either descriptive anecdotes via media accounts (see Gomes, 2001; Smith, 2000; Stuever, 2000; Stein, 1999; Schuler, 2000) or scientific investigations of the behavior that were undertaken to provide descriptive data about body depilation by men (see Boroughs & Thompson, 2002; Boroughs, et al., 2005; Martins, et al., 2008; Porche, 2007; Tiggemann, et al., 2008), now the time has come to further the understanding of this behavior in men. The purpose of these studies was to increase both the breadth and depth of our understanding of body depilation in men and its correlates with general body image concerns. A central aim of the first study was to test Social Comparison Theory (Festinger, 1954) as a workable theoretical paradigm to explain the genesis and maintenance of body depilation. The second study investigated women's attitudes towards men's body hair and men's body depilation. Research questions that have provided the foundation for the design of this study include: a) is there a relationship between men's drive for muscularity, frequency of weekly exercise, and influence by others (via social comparison) that is related to their body depilation behaviors, b) do sexual minority men differ from heterosexual men with regard to depilation behaviors, c) what are women's attitudes toward men's body hair and body depilation by men, and d) how might the attitudes of sexual minority women differ from heterosexual women on the topic of men's body hair and body depilation by men?

Le follicule pileux est un micro-organe spécifique des mammifères responsable de la formation des poils. Au cours de la vie postnatale, le follicule pileux subit des phases récurrentes de croissance (anagène), régression (catagène) et repos (télogène). Les mécanismes cellulaires et moléculaires qui régulent le cycle pilaire rappellent certains des évènements qui ont lieu durant la morphogénèse. Bien qu’il y ait eu des avancées significatives dans la connaissance de la biologie du follicule pileux ; les mécanismes qui régulent le passage de la phase anagène à la phase catagène restent mystérieux. Fgf5, un membre de la famille des facteurs de croissance des fibroblastes, a été identifié comme un régulateur clé de la transition anagène-catagène. Les souris qui ne produisent pas de protéine Fgf5 active présentent un phénotype angora (go/go) caractérisé par une phase anagène plus longue et de longs poils. Cependant, les follicules pileux n’ayant pas Fgf5, entrent quand même dans la phase catagène, ce qui suggère que d’autres mécanismes contribuent au control du cycle pilaire. Des précédents résultats obtenus dans notre laboratoire ont établis une relation très proche entre le déclenchement de la phase catagène et le diamètre du poil. En utilisant le follicule de vibrisse comme modèle, nous avons confirmé ces résultats en démontrant, par in hybridation in situ, que l’expression du gène Fgf5 s’active dans les cellules de la gaine épithéliale externe localisées dans la région supra-bulbaire, progressivement l’expression de Fgf5 s’étend jusqu’à l’extrémité inférieur de la gaine épithéliale externe et s’éteint quelques jours avant le début de la phase catagène, de nouveau dans les cellules de la gaine épithéliale externe localisées dans la partie supra-bulbaire. Nous avons également démontré que le nombre de couche cellulaires dans la région du cortex du poil, augmente progressivement au cours du temps jusqu’à atteindre exactement le même nombre de couche, quelques jours avant la fin de la phase de croissance, chez la souris sauvage et la souris Fgf5LacZ/LacZ. Ces résultats confirment notre hypothèse établissant que Fgf5 ne déclenche pas de façon direct la phase catagène. Ensuite, nous avons démontré pour la première fois que les cellules progénitrices du cortex peuvent se diviser symétriquement. Ces divisions symétriques très rares se traduisent, quelques jours après, en la formation d’une nouvelle couche cellulaire dans le cortex du poil. Ces résultats appuient notre hypothèse qu’une boucle de régulation complexe impliquant, la gaine épithéliale externe, la papille dermique (qui exprime Fgfr1, le récepteur de Fgf5), la matrice et la région supra-bulbaire ; est indispensable au control du cycle pilaire. Nous avons ensuite démontré par qRT-PCR et des marquages immunologiques que plusieurs canaux mécano-sensitifs sont exprimés de façon spécifique dans ces régions d’intérêts. De plus, plusieurs gènes importants pour la signalisation, sont également exprimés dans ces régions. Tout cela mis ensemble nos résultats soutiennent l’hypothèse provocatrice que la croissance progressive de la largeur du poil induit une pression mécanique qui entraine l’activation de canaux mécano-sensitifs, qui vont à leur tour activer des voies de signalisation pour finalement contrôler l’expression de Fgf5 dans la région supra-bulbaire et ainsi contrôler le cycle pilaire. / The hair follicle is a skin micro-organ specific to mammals and responsible for the formation of the hair. During postnatal life, the hair follicle undergoes recurrent phases of growth (anagen), regression (catagen) and rest (telogen) termed the hair cycle. The cellular and molecular mechanisms that regulate the hair cycle recapitulate some of the events occurring during morphogenesis. Despite significant advances in the understanding of biology of the hair follicle, the mechanisms regulating the switch from anagen to catagen remain mysterious. Fgf5, a member of the fibroblast growth factor family, has been proposed as a key regulator of the transition between anagen and catagen. Mice that do not produce active Fgf5 have an angora (go/go) phenotype characterized by an extended anagen phase and long hairs. Nevertheless, Fgf5 null hair follicles still enter catagen, suggesting that other mechanisms contribute to the control of the hair cycle. Previous work in the laboratory using Fgf5Lacz/LacZ null mice has unraveled a close connection between the onset of catagen and the diameter of the hair. Using the whisker follicle as a model system, we have confirmed these results and demonstrated by in situ hybridization that the expression of the Fgf5 gene is switched-on in the supra-bulbar region of the outer root sheath, progressively extends towards the lower extremity of the outer root sheath and is switched-off in the supra-bulbar region of the outer root sheath several days before the onset of catagen. We have also demonstrated that the number of cell layers in the hair cortex progressively increases with time to reach the exact same number a few days before the end of anagen in both wild-type and Fgf5 null follicles confirming our working hypothesis that Fgf5 does not directly trigger catagen. Next, we have demonstrated for the first time that the basal cortex-forming cells could divide symmetrically. These rare symmetrical divisions result in the formation of additional cell layers in the cortex. These results support our working hypothesis that a complex regulatory loop involving the outer sheath, the dermal papilla (that express Fgfr1, the Fgf5 receptor), the cortical matrix and the supra bulbar region is critical in controlling whisker growth. We have then demonstrated by q-RTPCR and immunostaining that several mechanosensitive channels are specifically expressed in the regions of interest. Moreover, several genes important for signaling are also expressed in these regions. Altogether, our results support the provocative hypothesis that the progressive increase in the width of the hair induces a mechanical pressure that leads to the activation of mechanosensitive channels, which in turn activate specific signaling pathways and ultimately result in the control of the expression of the Fgf5 gene in the supra-bulbar region of the outer root sheath and then in the control of the hair cycle.

The first method for DNA analysis in forensics was presented in 1985. Since then, the introduction of the polymerase chain reaction (PCR) has rendered possible the analysis of small amounts of DNA and automated sequencing and fragment analysis techniques have facilitated the analyses. In most cases short tandemly repeated regions (STRs) of nuclear DNA are analysed in forensic investigations, but all samples cannot be successfully analysed using this method. For samples containing minute amounts of DNA or degraded DNA, such as shed hairs, analysis of mitochondrial DNA (mtDNA) is generally more successful due to the presence of thousands of copies of mtDNA molecules per cell. In Sweden, ~40 % of all households have cats or dogs. With ~9 million humans shedding ~100 scalp hairs per day, and ~1.6 million cats and ~1 million dogs shedding hairs it is not surprising that shed hairs are one of the most common biological evidence found at crime scenes. However, the match probability for domestic dog mtDNA analysis has only been investigated in a few minor studies. Furthermore, although breed –sequence correlations of the noncoding mtDNA control region (CR) have been analysed in a few studies, showing limited correlations, no largescale studies have been performed previously. Thus, there have not been any comprehensive studies of forensic informativity of dog mtDNA. In the two papers presented in this thesis we have tried to lay a foundation for forensic use of analysis of domestic dog mtDNA. In the first paper, CR sequences were analysed and the exclusion capacity was investigated for a number of different populations. This is also the first comprehensive study of the correlation between mtDNA CR type and breed, type, and geographic origin of domestic dogs. Since the exclusion capacity for analysis of domestic dog CR sequences is relatively low, it was investigated in the second paper to what extent the discrimination power is improved by analysis of coding sequence. The exclusion capacity improved considerably when 3,000 base pairs of coding sequences where analysed in addition to CR sequences. This study will hopefully work as a basis for future development of analysis of dog mtDNA for forensic purposes. / QC 20101123

No description available.

Visual aesthetics play a vital role in today’s Western society. We built up a society where physical appearance represents high values in our everyday life. Not only the way we consume things and engage with the internet have a connection to how we see and place ourselves in society but the way the system works and treats us. Under the word “system” I refer to the intertwined connection of patriarchy and capitalism. With this project, I explore this connection as well as how the system influences social norms, body aesthetics and acceptance. More specifically, I take shaving and myself as an example and examine the question of “Why do women shave?”. The representation of women in our current society shapes our idea and opinion on shaving therefore I work with questions such as: How are social norms created and how do they influence us? What are the ways to challenge and break these norms, if it is possible at all? How can our capacity for developing autonomy remain while being influenced by the system? My practice investigates these questions comprehensively and addresses the importance of discussions and the understanding of the roots of our behavior as well as how we as individuals contribute to the influence of society and the system.

Mit der Zucht von Haarschafen reagieren Schafhalter weltweit auf die veränderte Situation des internationalen Woll- und Textilmarktes. Schafwolle ist nach wie vor ein wertvoller nachwachsender Rohstoff für die Textilindustrie, sie wird vorwiegend als Feinwolle benötigt und kostengünstig in Australien und Südamerika produziert. In Europa rückte bereits in den fünfziger Jahren die Fleischproduktion über das Schaf immer mehr in den Mittelpunkt. Schafrassen mit hoher Mastleistung und sehr guter Schlachtkörperqualität bestimmten die züchterischen Aktivitäten der letzten Jahrzehnte. In Deutschland begann die Haltung von Haarschafrassen zunächst im Hobbybereich zur Vermeidung von Schurkosten. Diesen Punkt aufgreifend begann die gezielte Zucht einer speziellen Haarschafpopulation mit dem NOLANA-Projekt der Fachhochschule Osnabrück im Jahr 1995. In der ersten Phase der Arbeit wurden hierbei regionale Schafhalter im Arbeitsgebiet der Fachhochschule einbezogen. Im Jahr 1998 begann eine erweiterte Zusammenarbeit mit anderen wissenschaftlichen Einrichtungen, in die auch das vorliegende Projekt und das Lehr- und Versuchsgut Köllitsch der Sächsischen Landesanstalt für Landwirtschaft einbezogen worden sind.

The project Kera-Plast aims to re-loop humans and nature by questioning the current systems and ethics through materiality. Human hair, currently considered as waste, functions as the base for the material exploration fabricated through thermo-compression molding. The flexible, short and opaque keratin-fibers get glued together with heat, pressure and water, acting as a plasticizer during the compression molding process. The results are stiff and remind on plastic due to shine and translucency. Aesthetics and function of the resulting material are controlled and designed by traditional textile techniques as knitting, weaving and non-woven processes. The material samples display the potential of Kera-Plast in the categories of 3D surface structures, patterns, shapeability and the influence of light. The findings also provide information about the parameters for designing with keratin fibers through the thermo-compression process. It can be concluded that despite all ethical and cultural factors, Kera-Plast and its fabrication method has the potential to add a sustainable, functional and aesthetical value to the design field and our future material consumption.

Understanding the genetic architecture of complex disorders is important for identifying disease mechanisms and potential molecular targets for therapeutic interventions. Genetic diseases are broadly classified as either Mendelian (monogenic) diseases or complex (polygenic) diseases. Common, polygenic disorders result from inheritance of multiple common variants with low penetrance. In contrast, monogenic, Mendelian disorders are caused by rare variants with high penetrance at a single genetic locus. However, an increasing number of studies support a role for rare variants of moderate effect size in complex diseases. As a result, genetic approaches previously utilized for discovering rare variants in Mendelian diseases, such as next generation sequencing, can now effectively be applied to complex diseases to define the contribution of both rare and common variants to the genetic burden of polygenic traits and diseases. Alopecia Areata (AA) is a complex autoimmune disease characterized by non-scarring hair loss that is due to a combination of both enviornmental and genetic factors. Our previous Genome-wide Association Study (GWAS) identified at least 14 genetic regions contributing to AA disease susceptibility. Although useful in identifying disease-associated loci and surrounding linkage disequilibrium (LD) blocks, GWAS is not sufficiently granular to 1) elucidate causal (association-driving) variants; and 2) discover rare risk variants. This level of resolution can only be achieved by deep sequencing followed by functional validation of variants. The goal of this thesis was to address these challenges in AA using two genetic approaches that have not been previously utilized in the context of this disease. In Chapter 2, I performed a hypothesis-driven analysis of common variants in a GWAS-associated locus using targeted genomic sequencing. In Chapter 3, I utilized whole exome sequencing (WES) in an unbiased approach to assess rare variant contribution in AA disease risk. To conduct these analyses simultaneously, we designed a whole exome sequencing (WES) chip that also included custom capture of 24 Mb of genomic regions covering the 14 genetic loci previously identified using GWAS. I applied these two sequencing approaches in a large AA patient cohort and identified potentially causal variants in several genes. To interrogate the consequences of these variants, I performed functional analyses to determine the effects of disease-causing variants on the target organ of AA attack, the hair follicle (HF). In Chapter 2, I report on the use of targeted genomic sequencing to interrogate the coding and non-coding regions surrounding a previously implicated GWAS locus. This approach provided fine mapping of coding and non-coding common variants in regions that may be contributing to disease risk. In this thesis, I focused on the effect of genetic perturbations on the end-organ HF, and consequentially prioritized my functional analysis using two criteria: 1) genes expressed in the (HF) and; 2) GWAS regions that were not previously implicated in other autoimmune diseases. One of the regions that satisfied these criteria harbored the Syntaxin 17 (STX17) gene, which encodes a SNARE protein involved in autophagy and mitochondrial fission. Targeted genomic sequencing of the STX17 region in 849 AA cases identified 35 non-coding and 0 coding variants in high LD with the GWAS SNP. Thirty-three variants were significantly enriched in cases compared to controls, and the remaining two were nominally significant. Thirty-two of the significantly associated AA variants were confirmed to be AA skin eQTLs that downregulated expression of STX17 in affected scalp skin of AA patients. Downstream analyses incorporated in silico and functional cell assays that uncovered a novel autophagy-independent role for STX17 in melanocyte biology. I discovered that a reduction of STX17 expression was associated with an accumulation of a melanocyte-specific antigen and increased immunogenicity, as seen by CD8+ T cell infiltrates in the skin of AA patients with low levels of STX17 expression. I used a targeted sequencing approach to successfully identify candidate causal variants driving the GWAS association at the STX17 locus, and propose a novel mechanism underlying STX17-dependent melanocyte perturbation and AA disease. In the second section of this thesis, we used the WES feature of the chip to assess the genetic contribution of rare variation in AA, in a genome-wide and unbiased manner. WES data and gene-level burden analyses of 18,653 genes in 849 AA patients was compared to 15,640 controls to identify rare variants associated with AA. Unexpectedly, this analysis identified one gene, encoding a hair-specific keratin, Keratin 82 (KRT82) that harbored significantly more rare damaging mutations in AA cases compared to controls (p=2.68E-06). Eleven rare damaging mutations were found in 51 AA patients in the heterozygous state (6.01%) compared to 2.58% controls. These variants resided in evolutionary conserved amino acid residues, and nine out of the eleven mutations were located in established disease-causing domains in keratin proteins. I determined that KRT82 expression was absent or largely reduced in AA hair follicles, including the bulb region, the site of AA immune attack. Moreover, AA patients with damaging variants and reduced KRT82 expression had increased perifollicular CD8+ T cell infiltrates in comparison to control HFs with intact KRT82 expression remaining. I proposed that damaging mutations in the coding regions of KRT82 resulted in loss of functional protein, thereby weakening the protective HF cuticle and predisposing the HF to immune attack. In summary, I used two genetic approaches (targeted genomic sequencing and WES) to identify common (Chapter 2) and rare variants (Chapter 3) with novel contributions to the complex genetic architecture of AA. I focused my functional studies on genes expressed in the target HF, with the goal of defining the role of unidentified, variant-mediated end-organ disruption in the predisposition of AA patient HFs to aberrant autoimmune attack. Up to now, most efforts in AA mechanistic studies have focused on the aberrant immune response. The work in my thesis uncovered novel roles for perturbations in the HF itself as a participating factor in AA disease risk.

No description available.