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<p>  </p> <p>The rapid growth of the English Language Learner (ELL) population in Indiana has raised challenges for English language arts (ELA) instruction. This research adopts collective case studies and mixed-methods studies to explore the quality and quantity of ELA instruction (time allocation to literacy components and group configuration) for ELLs in Indiana elementary classrooms. Study one aims to further the understanding of the quality and quantity of ELL literacy instruction in Indiana first-grade classrooms through a collective case study. Then, a sequential mixed methods study is designed to examine the effect of professional development on ELL literacy instruction in second-grade classrooms (Study 2). To gain a deeper understanding of how Indiana schools have been coping with the COVID pandemic, another sequential mixed-methods study is designed to explore how the pandemic has impacted the quality and quantity of literacy instruction compared with the pre-pandemic era in K-5 classrooms (Study 3). These serial inquiries hold important implications for literacy educators with ELL students on how best to structure and plan for their English language arts (ELA) instruction. Also, they will inform schools on how to select professional development that yields significant transformations in teachers’ literacy practices, as well as how to better address ELL needs during the pandemic.</p>

Combinatorial Group Testing (CGT) is a process of identifying faulty interactions (“errors”) within a particular set of items. Error Locating Arrays (ELAs) are combinatorial designs that can be built from Covering Arrays (CAs) to not only cover all errors in a system (each involving up to a certain number of items), but to locate and identify the errors as well. In this thesis, we survey known results for CGT, as well as CAs, ELAs, and some other types of related arrays. More importantly, we give several new results. First, we give a new algorithm that can be used to test a system in which each component (factor) has two options (values), and at most two errors are present. We show that, for systems with at most two errors, our algorithm improves upon a related algorithm by Mart´ınez et al. in terms of both robustness and efficiency. Second, we give the first adaptive CGT algorithm that can identify, among a given set of k items, all faulty interactions involving up to three items. We then compare it, performance-wise, to current-best nonadaptive method that can identify faulty interactions involving up to three items. We also give the first adaptive ELA-building algorithm that can identify all faulty interactions involving up to three items when safe values are known. Both of our new algorithms are generalizations of ones previously given by Mart´ınez et al. for identifying all faulty interactions involving up to two items.

Cerca de 20 % dos casos familiares de esclerose lateral amiotrófica (ELAf) são causados por mutações na enzima Cu,Zn-superóxido dismutase (SOD1). Inicialmente se supôs que as enzimas mutantes teriam a atividade SOD comprometida, entretanto isto não foi comprovado. Atualmente, considera-se que as enzimas mutantes adquiram propriedades tóxicas. Quais seriam estas propriedades e como levariam à degeneração do neurônio motor são questões ainda não respondidas. Neste trabalho, comparamos neuroblastomas humanos transfectados com SOD1 G93A associada à ELAf (SH-SY5YG93A), e SOD1 selvagem (SH-SY5YWT) com células parentais (SH-SY5Y) em relação ao crescimento, viabilidade, produção basal de oxidantes, atividades SOD e peroxidásica e modificações estruturais da SOD. As células transfectadas apresentaram aumento na taxa de crescimento e na produção basal de oxidantes. As células SH-SY5YWT e SH-SY5YG93A mantiveram a expressão de SOD1 e atividade consistente com o aumento esperado de duas vezes, em estágios iniciais de cultura. A atividade peroxidásica do homogenato da célula SH-SY5YG93A foi maior. Após quatro semanas, a linhagem SH-SY5YG93A manteve a expressão de SOD1, mas as atividades dismutásica e peroxidásica diminuíram. A expressão de SOD1 aumentou a proporção de formas alteradas de SOD1, como enzima reduzida, multímeros formados por ponte dissulfeto e formas insolúveis em detergente, particularmente na linhagem SH-SY5YG93A. Entre estas formas insolúveis, identificamos um dímero covalente de SOD. Estas formas alteradas provavelmente são responsáveis pela ativação do proteassomo e estresse do retículo endoplasmático, verificados nas células transfectadas. Concluindo, a superexpressão da SOD1 foi suficiente para elevar as formas imaturas e oligomerizadas de SOD1 e a oxidação basal, e a mutação G93A ressaltou estes processos. / Some familial ALS (fALS) are caused by mutations in the Cu,Zn-superoxide dismutase enzyme (SOD1). It was thought that the mutated enzymes would have impaired SOD activity, but this has not been corroborated so far. Presently, it is more accepted that the mutated enzymes acquire a new toxic function. What this new toxic function is and how it relates to the degeneration of motor neurons remains debatable. Here, we compared human neuroblastoma cells transfected with fALS mutant G93A (SH-SY5YG93A) or wild-type SOD1 (SH-SY5YWT) with parent cells (SH-SY5Y) in regard to growth, viability, basal oxidant production, SOD and peroxidase activities, and SOD forms. Transfected cells presented increased growth rate and basal oxidant production. SH-SY5YWT and SH-SY5YG93A cells in early culture stage showed SOD expression and activity consistent with the expected two-fold increase; SH-SY5YWT homogenates showed increased peroxidase activity. After four weeks, SH-SY5YG93A maintained SOD1 expression levels but peroxidase and dismutase activities were lower. SOD1 expression increased the levels of altered SOD1 forms such as the reduced enzyme, disulfide multimers and detergent-insoluble forms, particularly in SH-SY5YG93A cells. Among the insoluble forms a covalent SOD dimer was identified. These altered SOD forms are probably responsible for proteasome activation and endoplasmatic reticulum stress response verified in transfected cells. In conclusion, SOD1 over-expression was sufficient to increase intracellular immature and oligomerized SOD1 forms and basal oxidation and the G93A mutation enhanced these processes.

We share the results from a year-long randomized control trial study targeting a comprehensive approach to teach grade aligned ELA via an App for middle school students with significant disabilities. Participants will learn about the embedded evidence-based practices that led to significant outcomes.

This pilot study sought to develop and evaluate the use of a treatment package that included systematic and direct instruction on acquisition of literacy skills aligned with middle school English/Language Arts standards for students with moderate to severe disabilities, including autism. Participants included five teachers and 15 middle school students with moderate to severe disabilities who were primarily served in a self-contained setting. A one-group, nonrandomized, pre-posttest design was implemented to measure vocabulary, comprehen- sion of familiar text and unfamiliar text, poetry, research, and writing skills. Results indicated significant gains in vocabulary and comprehension of familiar text. Limitations, implications, and the need for future research are discussed.

Combinatorial Group Testing (CGT) is a process of identifying faulty interactions (“errors”) within a particular set of items. Error Locating Arrays (ELAs) are combinatorial designs that can be built from Covering Arrays (CAs) to not only cover all errors in a system (each involving up to a certain number of items), but to locate and identify the errors as well. In this thesis, we survey known results for CGT, as well as CAs, ELAs, and some other types of related arrays. More importantly, we give several new results. First, we give a new algorithm that can be used to test a system in which each component (factor) has two options (values), and at most two errors are present. We show that, for systems with at most two errors, our algorithm improves upon a related algorithm by Mart´ınez et al. in terms of both robustness and efficiency. Second, we give the first adaptive CGT algorithm that can identify, among a given set of k items, all faulty interactions involving up to three items. We then compare it, performance-wise, to current-best nonadaptive method that can identify faulty interactions involving up to three items. We also give the first adaptive ELA-building algorithm that can identify all faulty interactions involving up to three items when safe values are known. Both of our new algorithms are generalizations of ones previously given by Mart´ınez et al. for identifying all faulty interactions involving up to two items.

Combinatorial Group Testing (CGT) is a process of identifying faulty interactions (“errors”) within a particular set of items. Error Locating Arrays (ELAs) are combinatorial designs that can be built from Covering Arrays (CAs) to not only cover all errors in a system (each involving up to a certain number of items), but to locate and identify the errors as well. In this thesis, we survey known results for CGT, as well as CAs, ELAs, and some other types of related arrays. More importantly, we give several new results. First, we give a new algorithm that can be used to test a system in which each component (factor) has two options (values), and at most two errors are present. We show that, for systems with at most two errors, our algorithm improves upon a related algorithm by Mart´ınez et al. in terms of both robustness and efficiency. Second, we give the first adaptive CGT algorithm that can identify, among a given set of k items, all faulty interactions involving up to three items. We then compare it, performance-wise, to current-best nonadaptive method that can identify faulty interactions involving up to three items. We also give the first adaptive ELA-building algorithm that can identify all faulty interactions involving up to three items when safe values are known. Both of our new algorithms are generalizations of ones previously given by Mart´ınez et al. for identifying all faulty interactions involving up to two items.

Cerca de 20 % dos casos familiares de esclerose lateral amiotrófica (ELAf) são causados por mutações na enzima Cu,Zn-superóxido dismutase (SOD1). Inicialmente se supôs que as enzimas mutantes teriam a atividade SOD comprometida, entretanto isto não foi comprovado. Atualmente, considera-se que as enzimas mutantes adquiram propriedades tóxicas. Quais seriam estas propriedades e como levariam à degeneração do neurônio motor são questões ainda não respondidas. Neste trabalho, comparamos neuroblastomas humanos transfectados com SOD1 G93A associada à ELAf (SH-SY5YG93A), e SOD1 selvagem (SH-SY5YWT) com células parentais (SH-SY5Y) em relação ao crescimento, viabilidade, produção basal de oxidantes, atividades SOD e peroxidásica e modificações estruturais da SOD. As células transfectadas apresentaram aumento na taxa de crescimento e na produção basal de oxidantes. As células SH-SY5YWT e SH-SY5YG93A mantiveram a expressão de SOD1 e atividade consistente com o aumento esperado de duas vezes, em estágios iniciais de cultura. A atividade peroxidásica do homogenato da célula SH-SY5YG93A foi maior. Após quatro semanas, a linhagem SH-SY5YG93A manteve a expressão de SOD1, mas as atividades dismutásica e peroxidásica diminuíram. A expressão de SOD1 aumentou a proporção de formas alteradas de SOD1, como enzima reduzida, multímeros formados por ponte dissulfeto e formas insolúveis em detergente, particularmente na linhagem SH-SY5YG93A. Entre estas formas insolúveis, identificamos um dímero covalente de SOD. Estas formas alteradas provavelmente são responsáveis pela ativação do proteassomo e estresse do retículo endoplasmático, verificados nas células transfectadas. Concluindo, a superexpressão da SOD1 foi suficiente para elevar as formas imaturas e oligomerizadas de SOD1 e a oxidação basal, e a mutação G93A ressaltou estes processos. / Some familial ALS (fALS) are caused by mutations in the Cu,Zn-superoxide dismutase enzyme (SOD1). It was thought that the mutated enzymes would have impaired SOD activity, but this has not been corroborated so far. Presently, it is more accepted that the mutated enzymes acquire a new toxic function. What this new toxic function is and how it relates to the degeneration of motor neurons remains debatable. Here, we compared human neuroblastoma cells transfected with fALS mutant G93A (SH-SY5YG93A) or wild-type SOD1 (SH-SY5YWT) with parent cells (SH-SY5Y) in regard to growth, viability, basal oxidant production, SOD and peroxidase activities, and SOD forms. Transfected cells presented increased growth rate and basal oxidant production. SH-SY5YWT and SH-SY5YG93A cells in early culture stage showed SOD expression and activity consistent with the expected two-fold increase; SH-SY5YWT homogenates showed increased peroxidase activity. After four weeks, SH-SY5YG93A maintained SOD1 expression levels but peroxidase and dismutase activities were lower. SOD1 expression increased the levels of altered SOD1 forms such as the reduced enzyme, disulfide multimers and detergent-insoluble forms, particularly in SH-SY5YG93A cells. Among the insoluble forms a covalent SOD dimer was identified. These altered SOD forms are probably responsible for proteasome activation and endoplasmatic reticulum stress response verified in transfected cells. In conclusion, SOD1 over-expression was sufficient to increase intracellular immature and oligomerized SOD1 forms and basal oxidation and the G93A mutation enhanced these processes.