In response to increasing attention to the issues of teacher quality, quantity, and the mandate for highly qualified teachers, alternative approaches to teacher certification have become widespread. Alternative certification allows individuals who typically posses an undergraduate degree in a field other than education to participate in shortened training and/or on- the- job learning experiences that lead to full certification. The number of alternatively certified teachers in urban hard to staff schools is growing. There are many debates as to the effectiveness of alternative certification. At the core of the arguments are issues surrounding teacher pedagogy, classroom management, and knowledge of the teaching and learning experience in general. This study sought to determine public school principals' perceptions of alternatively certified teachers. The study asked principals to compare alternatively certified teachers to those teachers who have participated in a traditional university based teacher education program. Both groups of teachers had one to three years of experience in the classroom. Survey research was used to compare the effectiveness of alternatively certified teachers to traditionally certified teachers based upon principals' perceptions. There were five survey domains, including (1) content knowledge, (2) classroom management, (3) instructional planning, (4) human relations skills, and (5) professionalism. Results of this study indicated that principals perceived that alternatively certified teachers were perceived as slightly less effective than traditionally certified teachers. Teachers trained in the traditional teacher education programs were viewed as more effective with regard to content knowledge, classroom management, instructional planning, and professionalism.

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In many parts of the country principal candidates are being licensed through alternative pathways. Some view this movement as a plausible solution to the shortage of principals and inadequacy of principal preparation programs (Hess, 2003; Southern Regional Education Board, 2006; Thomas B. Fordham Institute, 2003). Others are insulted and threatened by the prospect of a person from a non-traditional background leading a school (Fenwick & Pierce, 2001). The debate as to whether or not these candidates possess the prerequisite skills and knowledge to effectively lead a school continues. But, will superintendents, as gatekeepers to school districts, afford these individuals the opportunity to prove their worth as principals? In this study, superintendents’ attitudes toward alternative licensure of school principals; past behaviors related to hiring alternatively licensed school personnel; attitudes toward specific alternatively licensed personnel; perceptions of the conditions in their school districts; anticipated concerns about hiring alternatively licensed principals; and the presence or absence of a clearly articulated induction program for new principals are used as predictors of superintendents' willingness to recommend hiring alternatively licensed principals to their school boards. The composite model of attitude-behavior consistency and data from a qualitative study of 18 superintendents were the bases for the development of a theory. To test the theory, an on-line questionnaire, using Likert and Thurstone scaled items, was administered to 1200 randomly selected superintendents who were members of the American Association of School Administrators (AASA) in 2005. Multiple regression analysis was used for the analysis of the quantitative data. Five of the 19 predictor variables were significant predictors of superintendents’ willingness to recommend hiring alternatively licensed principals. The strongest relationship existed between superintendents’ willingness to recommend hiring alternatively licensed principals and their perceptions of the instructional leadership ability of alternatively licensed principals. Other significant predictors were superintendents’ past experiences hiring alternatively licensed principals, perceptions of the community acceptance of alternatively licensed principals, general attitude toward alternative licensure, and willingness to hire under the given definition. Superintendents displayed a low neutral (more unfavorable) score on the Thurstone scale, which means they view the employment of alternatively licensed principals slightly unfavorably. / Ph. D.

Wound repair is a complex series of events that begins immediately after wounding, and can continue for a number of months to years. Various physiological and mechanical factors may impair the healing response, resulting in a chronic wound, characterised by a sustained inflammatory response. One of the main cells involved in both the inflammatory phase and proliferation phase of wound healing is the macrophage. There are thought to be different activation states which allow the macrophage to be involved in the two different phases of wound healing, namely the classically activated macrophage and the alternatively activated macrophage. Changes in the number of classically activated/alternatively activated macrophages in the wound is likely to have an effect on wound healing. Therefore a more thorough understanding of macrophage activation states during wound healing would broaden the understanding of the role of this cell in this process. The overall aim of this project was to investigate whether diabetic bone marrow progenitor cells or macrophages respond to activation stimuli differently in comparison to wild type cells. The hypothesis of this thesis is that diabetic macrophages will not respond to appropriate stimuli and thus alternative and classical macrophages will not behave 'appropriately', resulting in impaired healing. The results of this thesis indicate that impaired wound healing in the diabetic environment may be due to both the diabetic wound environment itself and intrinsic differences in diabetic macrophages. This work indicates that signals from the wound environment activates and influences macrophages, as these cells do not express activation markers until they enter the wound environment. However, the culture system devised in this study indicates that even before activation with signals they would receive in the wound environment, diabetic cells are more pro-inflammatory and have impaired migration. In addition, these macrophages respond differently to activation supporting the hypothesis that the macrophages are intrinsically different and that diabetic cells do not behave 'appropriately' which could contribute to impaired wound healing.

Determination of quantitative expression levels of alternatively spliced isoforms provides an important approach to the understanding of the functional significance of each isoform. Real-time PCR using exon junction overlapping primers has been shown to allow specific detection of each isoform. However, this design often suffers from severe cross amplification of sequences with high homology at the exon junctions. We used human GFRα2b as a model to evaluate the specificity of primers substituted with locked nucleic acids (LNAs). We demonstrate here that single LNA substitutions at different positions of 3’ terminus could improve the discrimination of the primers against GFRα2a template, a highly homologous isoform. While LNA substitutions of GFRα2b primer at the residues possessing different sequences as GFRα2a has limited improvement in specificity, two consecutive LNA substitutions preceding the different sequences has dramatically improved the discrimination by greater than 100,000-fold compared to the non-substituted primer. Thus, LNA when substituted at certain residues can allow the discrimination of highly homologous sequences. / Singapore-MIT Alliance (SMA)

An estimated 45% of all deaths can be attributed to various chronic fibroproliferative diseases. Idiopathic pulmonary fibrosis (IPF) is the most common form of interstitial lung disease which is characterized by progressive decline in lung function. While the pathogenesis of IPF is not fully understood, alternatively activated macrophages (M2) have been implicated as a key contributor to the fibrotic process. The plasticity of macrophages in vivo challenges the ability to specifically target the M2 macrophage phenotype across species. Previous bioinformatic analysis from our lab identified Dectin-1/Clec7a as a unique marker of M2 macrophages in both human and murine model systems. The expression of the transmembrane receptor Dectin-1 has not been elucidated in the context of pulmonary fibrosis. To prevent the progression of fibrosis by targeting alternatively activated macrophages, we investigated the expression of Dectin-1 in IPF and an experimental model of fibrotic lung disease. Our data demonstrated that while protein expression of Dectin-1 was increased in archived lung tissues of patients with IPF, mRNA expression of this receptor was downregulated in the tissues of these IPF patients. Gene expression of Dectin-1 was shown to be increased in monocyte-derived macrophages, further suggesting a circulatory component contributing to lung fibrosis. As expected, we confirmed that Dectin-1 was highly expressed past the injury phase of the bleomycin-model of induced pulmonary fibrosis which aligns with the increased immune infiltrates at this time point. Preliminary work into the time dependency of the resolution phase of the bleomycin-induced model of lung fibrosis was shown. All in all, our data suggests that Dectin-1 may be a useful marker in characterizing and differentiating phenotypes of macrophages implicated in the fibrotic process. Future efforts aim to gain insight into the functional requirement of Dectin-1 in the alternative activation of profibrotic macrophages to identify novel therapeutic targets for fibrotic lung disease. / Thesis / Master of Science (MSc)

Resistin-like molecule alpha (RELMα) is a secreted protein implicated in murine models of allergen-induced asthma, bleomycin-induced pulmonary fibrosis, and helminth infection. Transient pulmonary overexpression of Oncostatin M by Adenovirus vector (AdOSM) induces lung inflammation biased toward Th2 cytokines, eosinophil and alternatively activated (AA/M2) macrophage accumulation. In AdOSM-treated C57Bl/6 and BALB/c mice, we observed RELMα mRNA and protein markedly induced. RELMα is recognized as a marker of AA/M2 macrophages, and we observed by chromogenic in situ hybridization that RELMα mRNA co-expresses with the macrophage marker CD68, and RELMα mRNA was also highly induced in columnar airway epithelial cells upon AdOSM treatment. Assessing IL-6 as a comparator gp130 cytokine, AdIL-6 induced RELMα at significantly lower levels, however maximal induction of RELMα by AdOSM in C57Bl/6 mice required IL-6, assessed in IL-6–/– mice. Maximal induction of RELMα by AdOSM also required IL-33 in C57Bl/6 mice but not in BALB/c mice, assessed in IL-33–/– mice. We investigated functions of RELMα in response to OSM, in RELMα–/– mice. Inflammatory cell infiltration and Th2-associated cytokine responses were not altered in RELMα–/– in comparison to wildtype mice. However, RELMα-deficiency resulted in less accumulation of CD206+ AA/M2 macrophages, IFNγ+ Th1 cells in the lung, reduced induction of extracellular matrix gene mRNAs for COL1A1, COL3A1, MMP13, TIMP1, and reduced parenchymal alpha smooth muscle actin. RELMα–/– mice also showed less airway epithelial hyperplasia, increased epithelial cell damage/death (assessed morphologically) and increased LDH and soluble CK18 in response to AdOSM. Our findings suggest that RELMα does not modulate Th2 cytokines, but does participate in matrix deposition, airway remodelling mechanisms, and protection from inflammation-induced damage due to OSM-overexpression in lungs of C57Bl/6 mice. / Dissertation / Master of Science (MSc)

Idiopathic pulmonary fibrosis (IPF) is a disease of unknown pathogenesis characterized by scarring of the lung and declining respiratory function. Originating from bone marrow, circulating monocytes can be recruited into the lung tissue and polarized toward the alternatively activated (M2) profibrotic macrophage phenotype. Recent literature has shown that cluster of differentiation 14 positive (CD14+) monocytes are more abundant in IPF patient blood and are associated with disease outcome and acute exacerbation. Additionally, a 52-gene risk profile from peripheral blood mononuclear cells for outcome prediction in IPF was recently published. Here, we began by characterizing macrophages in human IPF lung tissue. We then assembled a biobank and examined transcriptomic characteristics of blood-derived circulating monocytes from IPF patients. Various histological assessments were completed on a tissue microarray including lung biopsies from 24 IPF patients and 17 controls, to characterize M2 macrophage expression in human tissue. Whole blood samples were collected from 50 IPF patients and 12 control subjects. CD14+ monocytes were isolated and mRNA was extracted for bulk RNA sequencing. Data were analyzed for differential expression (DE), and Gene Set Enrichment Analysis (GSEA) was performed to examine enrichment of the previously published 52-gene risk profile in our dataset. We found that M2 macrophage expression was increased in IPF lung tissue compared to controls. CD14+ monocyte levels were significantly elevated in IPF patients in our cohort compared to control participants, and was negatively correlated with forced vital capacity (FVC). DE analysis comparing IPF and control monocytes yielded a 35-gene signature, with 16 up-regulated genes and 19 down-regulated genes. When comparing the signature related to long transplant-free survival from the published dataset to our data, GSEA demonstrated that this signature is enriched in donors from our dataset, supporting concurrence between the meanings of the two datasets. Overall, these results provide insight to identify targets to modulate monocyte/macrophage function in IPF and potentially affect progressive disease. / Thesis / Master of Science (MSc) / Idiopathic pulmonary fibrosis (IPF) is a disease of unknown cause that results in excessive scarring of the lungs and progressive impairment in lung function. We believe that white blood cells called monocytes and macrophages play a key role in the development and progression of this disease. Overall, it is thought that monocytes, which circulate in the blood, enter the lung tissue and become macrophages. These macrophages then lead to the formation of scar tissue, which is characteristic to IPF. In order to better understand how these cells contribute to IPF, we studied their properties in blood and lung biopsies from IPF patients. We found significant differences between monocytes/macrophages in IPF than those in healthy controls, that may help explain disease progression. We hope that these findings will provide insight into causes of the IPF, and potential avenues for therapeutic intervention.

Submitted by Jaqueline Silva (jtas29@gmail.com) on 2014-10-03T18:19:16Z No. of bitstreams: 2 Dissertação - Vânia Beatriz Lopes Moura - 2010.pdf: 929596 bytes, checksum: 432fcdfb3a382e721d28d0a4c6c4642d (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) / Approved for entry into archive by Jaqueline Silva (jtas29@gmail.com) on 2014-10-03T20:38:21Z (GMT) No. of bitstreams: 2 Dissertação - Vânia Beatriz Lopes Moura - 2010.pdf: 929596 bytes, checksum: 432fcdfb3a382e721d28d0a4c6c4642d (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) / Made available in DSpace on 2014-10-03T20:38:21Z (GMT). No. of bitstreams: 2 Dissertação - Vânia Beatriz Lopes Moura - 2010.pdf: 929596 bytes, checksum: 432fcdfb3a382e721d28d0a4c6c4642d (MD5) license_rdf: 23148 bytes, checksum: 9da0b6dfac957114c6a7714714b86306 (MD5) Previous issue date: 2010-04-30 / Conselho Nacional de Pesquisa e Desenvolvimento Científico e Tecnológico - CNPq / The role of arginase on experimental cysticercosis induced by Taenia crassiceps Murine infection by Taenia crassiceps cysticerci is used as an experimental model for human and animal cysticercosis. In this infection parasites can be found inside an inflammatory infiltrated enriched with macrophages. These macrophages can be divided in alternatively activated, that express high amount of the arginase enzyme and classically activated (CMø) that express high amount of induced nitric oxide sintase enzyme (iNOS). Arginase uses the substrate L-arginine to produce ornithine favoring the cellular proliferation and collagen synthesis. The iNOS uses the same substrate to synthesize nitric oxide (NO), which is a highly microbicide compound responsible for the cysticerci control. To observe if there is an association between macrophages expressing arginase and an increase of the susceptibility to T. crassiceps, BALB/c mice were infected IP with 10 cysticerci and followed up by 84 days. It was measured the number and stages of the cysticerci, profile of systemic cytokines, profile of the macrophages in inflamed tissue and collagen deposition over the peritoneum. Besides, infected mice were treated with arginase inhibitor or L-arginine and followed up by 56 days. The parasitic load was observed, which increased significantly after the 30th day. At the end of experimental period number of cysticerci was 1022 (±230). The serum interferon- (IFN-) of infected animals was higher than controls at the 28th day after infection and IL-4 at the 42th day. Macrophages were the major cells observed at the infected site, and the polimorphonuclear cells (PMN) picked at the 14th day after the infection, returning to the normal values at the 42th day. Cells carrying the marker CD301, present on AAMø, and high arginase activity increased in the early phase after infection. The presence of collagen in the peritoneum of infected animals decreased until 14th day after the infection, however, in the latest phases the collagen increases and become superior to the control. The treatment with the arginase inhibitor or L-arginine did not alter the profile of the infection; however the arginase inhibitor inhibited the deposition of collagen in the peritoneum. These results suggest that the enzyme arginase does not interfere with the control of the cysticerci during experimental infection with T. crassiceps cysticerci, but it is important for the formation of fibrosis in cysticercosis. / A infecção murina por cisticercos de Taenia crassiceps vem sendo utilizada como um modelo experimental para estudo da cisticercose humana e animal. Nesta infecção encontram-se parasitos presentes em um infiltrado inflamatório rico em macrófagos. Estes macrófagos podem ser divididos em alternativamente ativados (AAMØ), que expressam uma grande quantidade da enzima arginase ou classicamente ativados (CMØ,) que expressam uma grande quantidade da enzima óxido nítrico sintase induzida (iNOS). A arginase utiliza o substrato L-arginina para produção de ornitina, favorecendo a proliferação celular e a síntese de colágeno. A iNOS utiliza o mesmo substrato para síntese de óxido nítrico (NO) que é um gás microbicida responsável pelo controle dos cisticercos. Para observar se há uma associação entre a presença de macrófagos expressando arginase com aumento da susceptibilidade à infecção por T. crassiceps, camundongos BALB/c foram infectados IP com 10 cisticercos e acompanhados diariamente por 84 dias. Foi avaliado o número dos cisticercos, o perfil sistêmico de citocinas, o perfil dos macrófagos do infiltrado e a deposição de colágeno no peritônio ao longo da infecção. Adicionalmente, os camundongos infectados foram tratados com inibidor de arginase ou com L-arginina. A carga parasitária aumentou significativamente após o 30º dia, atingindo 1022 (±230) cisticercos no final do período experimental. O interferon γ (IFNγ) sérico dos animais infectados foi superior ao dos controles no 28o dia após a infecção e a IL-4 no 42o dia. Os macrófagos foram predominantes durante todo período experimental e os polimorfonucleares (PMN) apresentaram um pico no 14o dia após a infecção, retornando aos valores normais no 42o dia. Células portando o marcador CD301 presente em AAMø e com alta atividade da enzima arginase aumentaram nas duas primeiras semanas após a infecção mantendo-se alta por todo período experimental. A presença de colágeno no peritônio dos animais infectados diminuiu até 14o dia após a infecção, porém, nas fases mais tardias o colágeno aumentou tornando-se superior ao dos controles. O tratamento com o inibidor da arginase ou L-arginina não alterou o perfil da infecção, porém, o inibidor de arginase inibiu a deposição de colágeno no peritônio. Estes resultados sugerem que a enzima arginase não interfere no controle dos cisticercos durante a infecção experimental por cisticercos de T. crassiceps, mas ela é importante na formação de fibrose característica da cisticercose.

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