The purpose of this dissertation is to explore whether rehabilitation counselor/consumer racial similarity is related to rehabilitation services provided and employment outcomes achieved. This research contributes additional information to the research base on how to educate and train practicing vocational rehabilitation counselors to support culturally and linguistically diverse (CLD) consumers more effectively. Information regarding racial dyads may help to articulate whether CLD counselors are more effective with CLD consumers. Utilizing the RSA-911 data file submitted by California for fiscal year 2006 as well as 189 Multicultural Counseling Inventory (MCI) surveys collected on practicing vocational rehabilitation counselors, ANOVA, MANOVA, ANCOVA and chi-square analysis were used to measure relationships among counselor and consumer dyads that were either similar or dissimilar in ethnicity and case service variables and outcome variables. Additional analysis focused on the influence of high versus low cultural competency of rehabilitation counselors and the same consumer case service and outcome variables. Study results revealed statistically significant differences on MCI total scores between counselor ethnic groups, with Hispanic counselors demonstrating the highest mean scores overall on the MCI. In addition, significant differences existed between counselor ethnic groups on MCI total scores, as well as all four subscale scores. Chi-square was used to investigate the effect of counselor ethnicity and cultural competency scores on the case service variables of job search, rehabilitation technology, maintenance and college training, as well as outcome variables of competitive employment. MANOVA and ANCOVA were used for the continuous outcome variables of cost of services, wages at closure and weekly earnings at closure. Significant chi-square results were found for some of the service and outcome variables for both the matched counselor/consumer dyads and the counselor competency score groups. More significant findings existed in the ANCOVA analysis for cultural competency scores than for matched ethnicity groups. Implications of the findings and suggestions for future research are discussed. / text

What various roles exist in corporate toxicity? In what environment does toxicity thrive? Do toxic leaders exhibit certain characteristics? Questions such as these can be discovered using this classroom tool! / This case study provides a real-world example of corporate toxicity to illustrate the toxic triangle model and show how situations like this one come to pass (Padilla, 2013). The primary focus will be on WorldCom/MCI and the events leading to the world famous accounting scandal that came to light in 2003. This case briefly examines the three major triangle elements, (1) the role of the leader, (2) the enabling efforts of colluding and conforming followers, and (3) the conducive nature of the specific organizational context, all in correlation with the eventual destruction of the organization. Identifying these elements provides an opportunity for students to analyze an actual account of corporate toxicity through critical thinking and discussion. The questions provided are intended to stimulate a discussion focused on the: (1) events leading to the demise of the organization, (2) characteristics of the primary leader and followers, (3) role the environment played in escalating the situation, and (4) the influences of social pressures.

I verbala minnestester brukar friska individer komma ihåg flera ord från början och från slutet av ordlistan (primacy- och recency-effekt) än från mitten av den. Detta fenomen kallas för seriepositionseffekt. Recency-effekten anses bero på arbetsminnet, medan episodiska minnet ansvarar för primacy-effekten. Svårigheter med episodiska minnet är ofta det första symtomet vid begynnande Alzheimers sjukdom. Femtiosju testprotokoll av Rey AVLT varav en tredjedel kom från patienter med Alzheimers sjukdom, en tredjedel från personer med diagnosen lindrig kognitiv störning och en tredjedel från friska kontrollpersoner, undersöktes med flera poängsättningsmetoder baserade på seriepositionseffekten, för att se om någon metod skapade tydligare skillnader mellan diagnosgrupperna än den sedvanliga poängsättningen. Resultatet av alternativa poängsättningsmetoder skilde sig överlag mindre än förväntat från den sedvanliga poängsättningen. Enbart primacy gav tydligt sämre resultat, medan metoder som ger poäng för alla ord förutom recency gav i vissa fall något bättre resultat än den sedvanliga poängsättningen.

Alzheimer’s disease is a debilitating, progressive neurodegenerative disorder in the elderly, characterized by severe loss of memory and higher cognitive functions. In the hundred years since its discovery, Alzheimer’s disease (AD) has traversed from the status of a ‘rare neurological oddity’ to one of the greatest challenges faced by healthcare and medicine in this millennium. A reported 44 million people currently suffer from AD but only 1 in 4 people have been diagnosed. Although AD has been an area of intense research for almost 50 years now, most studies have focused on the end stage disease. Years of study on the pathological cause underlying AD; have conclusively shown that the accumulation of the sticky peptide, Aβ, is one of the major triggers of AD pathogenesis. However, after the initial Aβ trigger, multiple processes contribute to disease progression, so that by the time a patient is diagnosed on the basis of overt behavioral phenotypes, it is difficult to understand and differentiate between the causative mechanisms and the consequential effects of the disease. It is, perhaps, because of this, that we are still struggling to find therapies for AD which will stop or at the very least slow the course of the disease. In the 2015 report on AD, issued by the Alzheimer’s association, much emphasis has been placed on the early diagnosis of AD and the revision of the diagnostic criteria for AD. According to the new guidelines proposed in 2011, AD has been divided into three stages where the first stage occurs before the appearance of overt behavioral symptoms such as memory loss, whereas by the 1984 guidelines, cognitive disabilities must have already occurred for diagnoses of AD. This proposed preclinical stage of AD has been defined, reflecting the current belief that AD pathogenesis begins almost 20 years before the occurrence of behavioral dysfunction. However, no diagnostic criteria are currently available to establish this stage. Hence, there is a need to understand the early pathogenic mechanisms of AD, which will yield early therapeutic targets as well as early diagnostic markers of AD. One of the earliest documented events in AD pathogenesis is synaptic dysfunction, which is later manifested as loss of dendritic spines. Deficits in long term potentiation (LTP) has been demonstrated in Aβ exposed hippocampal slices as well as in mouse models of AD, much before the appearance of pathological hallmarks such as plaques and tangles as well as overt behavioral phenotypes. While these and other studies indicate clearly that elevated levels of soluble Aβ peptide leads to impairment of synaptic function, the underlying molecular mechanisms are yet to be elucidated. One of the purported mediators of Aβ induced dysfunction is oxidative stress. The Aβ peptide, especially the Aβ42, is a self aggregating peptide with a propensity to form peptidyl radicals. Interaction of the peptidyl radicals with biomolecules leads to the generation of more free radical species via cascading chain reactions. Additionally, Aβ peptide has also been demonstrated to have synaptotoxic effects via its effect on NMDA receptors and calcium influx leading to deregulated reactive oxygen species (ROS) production as well as excitotoxicity. Hence, with a view to understanding Aβ mediated early synaptic dysfunction in AD, we studied early signaling changes in the synaptosomes derived from the cortex of APP/PS1 mice model of AD at various ages. The APP/PS1 model contains a mouse/human chimeric APP gene bearing the KM670/671NL Swedish mutation and the human PS1 gene with an exon 9 deletion. These mice exhibit behavioral deficits from 7 months of age while plaque deposition and gliosis become apparent by 9 months of age. We chose to study both pre-symptomatic ages (1 and 3 months old) as well as post symptomatic (9 months old) mice. Post nuclear supernatant (PNS) as well as synaptosomes were isolated from the cortex of APP/PS1 and age matched control mice. We assayed the levels of reactive oxygen species (ROS) in the PNS and the synaptosomes of post symptomatic 9 months old APP/PS1 mice and age matched controls. In contrast to reports of enhanced oxidative stress markers in the brains of AD patients, we did not find any increase in the levels of ROS in the PNS of post symptomatic APP/PS1 mice compared to age matched controls. However, synaptosomes from the cortex of these animals exhibited a significant increase in ROS levels in APP/PS1 mice compared to controls. We further found that there was significant increase in the ROS levels in synaptosomes, but not PNS, of very young asymptomatic 1 and 3 months old APP/PS1 mice. This is a first demonstration of synapse specific increase in oxidative stress in AD mice, as young as 1 month of age, indicating that disease specific mechanisms operate at the synapse much before the appearance of any overt cellular or behavioral symptoms. The increase in synaptic ROS levels correlated with a small but significant increase in the levels of Aβ42 in the brains of APP/PS1 mice compared to controls. We also found a concurrent change in the redox status of the cytoskeletal protein, actin, at the synapse. As early as 1 month of age, there was a significant decrease in the protein level of reduced actin indicating that there is an increase in the level of oxidized actin at the synapse. This loss of reduced actin was specific to the fibrillar pool of actin while no significant change was observed in the redox status of the monomeric globular pool of actin. Oxidation of actin has been demonstrated to lead to its depolymerization. Concurrently, we found a significant loss of fibrillar actin in the synaptosomes of APP/PS1 mice. Actin is the major cytoskeletal protein at the synapse. Changes in the globular to fibrillar actin ratio at the synapse at early pre-symptomatic ages in APP/PS1 mice will likely lead to structural and consequent functional changes at the synapse. This could potentially be one of the triggers of synaptic dysfunction in AD. Furthermore, changes in the Akt-mTOR signaling pathway was also observed in the synaptosomes of 1 month old APP/PS1 mice, which is sustained at 9 months. There was a significant loss of the mTOR-pS6K-4EBP1 axis in the synaptosomes, but not PNS, of APP/PS1 mice. We found that loss of Akt signaling, as evinced by loss of Akt phosphorylation, Akt kinase activity as well as loss of phosphorylation of downstream effector GSK3β, potentially underlies the loss of mTOR signaling. Further, the loss of Akt signaling is mediated by synapse specific redox modification of Akt and consequent interaction with the protein phosphatase PP2a. Loss of the Akt-mTOR signaling at the synapse is indicative of deficits in local protein translation. Loss of this essential synaptic function, which plays critical roles in synapse maintenance as well as synaptic plasticity during learning and memory, at an early age, will have long ranging impact on synaptic function such as long term potentiation (LTP) in APP/PS1 mice. Our study is the first demonstration of oxidative stress and consequent signaling changes which occur specifically at the synapse of very young 1 month old APP/PS1 mice. These changes occur much before the appearance of overt phenotype such as plaque deposition and behavioral dysfunction but sustain till the appearance of classical pathological hallmarks. Hence, the study demonstrates that disease progression starts much before previously thought and provides us a critical time window during which therapeutic strategies designed to delay or stop these changes might change the course of AD.

The notion of staging in the neurodegenerative disorders is modulated by the constant and progressive loss of several aspects of brain structural integrity, circuitry, and neuronal processes. These destructive processes eventually remove individuals' abilities to perform at sufficient and necessary functional capacity at several levels of disease severity. The classification of (a) patients on the basis of diagnosis, risk prognosis, and intervention outcome, forms the basis of clinical staging, and (b) laboratory animals on the basis of animal model of brain disorder, extent of insult, and dysfunctional expression, provides the components for the clinical staging and preclinical staging, respectively, expressing associated epidemiological, biological, and genetic characteristics. The major focus of clinical staging in the present account stems from the fundamental notions of Braak staging as they describe the course and eventual prognosis for Alzheimer's disease, Lewy Body dementia, and Parkinson's disease. Mild cognitive impairment, which expresses the decline in episodic and semantic memory performance below the age-adjusted normal range without marked loss of global cognition or activities of daily living, and the applications of longitudinal magnetic resonance imaging, major instruments for the monitoring of either disease progression in dementia, present important challenges for staging concepts. Although Braak notions present the essential basis for further developments, current staging conceptualizations seem inadequate to comply with the massive influx of information dealing with neurodegenerative processes in brain, advanced both under clinical realities, and discoveries in the laboratory setting. The contributions of various biomarkers of disease progression, e.g., amyloid precursor protein, and neurotransmitter system imbalances, e.g., dopamine receptor supersensitivity and interactive propensities, await their incorporation into the existing staging models thereby underlining the ongoing, dynamic feature of the staging of brain disorders.

No description available.

Olfactory function plays an important role in health and well-being. Deficits have been associated with a greater risk of cognitive decline, dementia, and death, indicating that olfactory ability may be an early marker of cognitive impairment and indicator of brain integrity. In the progression of cognitive impairment related to dementia, intraindividual variability in cognition may precede cognitive decline as an early risk factor, indicating that individuals with more variability in their cognitive performance may have an increased risk of cognitive impairment. Despite a significant amount of literature examining the relationship between olfaction and cognitive decline, to the best of our knowledge, no study has yet examined whether olfaction is associated with the earlier marker of cognitive decline, intraindividual variability in cognition. Project 1. In data drawn from the Rush Memory and Aging Project (N=1501), multistate models were used to estimate the association of olfactory identification with transition patterns through cognitive states including non-impaired cognitive functioning, clinically diagnosed mild cognitive impairment and dementia, and death. Additionally, multinomial regression models were fit to estimate life expectancies for overall and cognitively unimpaired years of life, relative to olfactory identification scores. This dissertation aims to contribute to the current body of literature suggesting potential for the use of olfactory identification as a clinically administered marker for the early detection of cognitive decline and risk of dementia. Project 2. In data collected by our lab (N=65), multilevel models were used to examine whether olfactory identification scores were associated with the magnitude and rate of change of intraindividual variability (IIV) in cognitive functioning. This dissertation aims to address whether olfactory identification is associated with IIV in cognition using self-administered mobile cognitive testing in a 14-day micro-longitudinal study. / Graduate

The aim of the thesis is to focus on issues of school and class climate in elementary school. The paper deals with comparing class climate in elementary schools based on the size of the city, where a given elementary school is located. The theoretical section defines the basic terms - the environment, atmosphere and climate. It also states climate typology and climate actors. It further focuses on accessing surveys and methods of measuring climate. At first, the practical part defines the used MCI method, then processes the research objectives and hypotheses. Subsequently it describes the results of the survey that took place in the sixth grade of elementary school. In the final part the set hypothesis are verified.

Introdução: Perda de memória é um dos sintomas mais comuns em pacientes nos estágios iniciais da doença de Alzheimer; esses déficits são um reflexo do envolvimento da formação do hipocampo. O BDNF tem sido relacionado com a plasticidade do hipocampo. Neste sentido, as combinações de biomarcadores, como, por exemplo, a volumetria do hipocampo, pode apresentar um maior valor preditivo para diferenciar doença de Alzheimer do envelhecimento normal em pacientes com comprometimento cognitivo leve. Objetivo: A presente tese de doutorado teve como objetivo avaliar os níveis séricos do BDNF e o volume do hipocampo em pacientes com demência devido à doença de Alzheimer, Comprometimento Cognitivo Leve (CCL) e idosos saudáveis. Métodos: Para realização do estudo foram selecionados 10 idosos saudáveis, 10 CCL e 13 pacientes com demência devido à doença de Alzheimer pelos critérios NIA-AA. Todos participantes foram submetidos a uma avaliação cognitiva. Para as análises do BDNF, foi utilizado método de ELISA e para as análises de volumetria do hipocampo as imagens foram obtidas por meio de equipamento de ressonância de 1.5T e os volumes obtidos por meio do programa NeuroQuant®. Resultados: Idosos saudáveis apresentaram níveis séricos mais elevados de BDNF do que os CCL e pacientes com demência. O grupo de pacientes com demência apresentou menor volume total do hipocampo do que os idosos saudáveis e os CCL. Não houve correlação significativa do BDNF sérico com volume do hipocampo. Conclusão: Considerando nossos resultados em conjunto (baixos níveis de BDNF nos grupos CCL e demência devido à DA e menor volume do hipocampo na demência devido à AD), podemos supor que a diminuição dos níveis de BDNF ocorre antes da lesão neuronal expressa pela redução do hipocampo. / Introduction: Memory impairment is the most common symptom in patients in the early stages of Alzheimer's disease; this deficit is a reflection of the involvement of the hippocampal formation. BDNF has been linked to the hippocampal plasticity. Combinations of biomarkers, such as the hippocampal volumetry may have higher predictive value for differentiating Alzheimer's disease from normal aging in patients with mild cognitive impairment. Objective: The objective of present thesis was to evaluate serum levels of BDNF and hippocampal volume in patients with Mild Cognitive Impairment (MCI) and dementia due to Alzheimer's disease, and healthy elderly participants. Method: Ten healthy elderly subjects, 10 MCI and 13 patients with dementia due to Alzheimer's Disease (NIA-AA criteria) were selected for the study. All participants were assessed cognitively. The ELISA method was used for BDNF analysis, and the analysis of hippocampal volumetric images were acquired with 1.5T magnetic resonance equipment and volumes obtained with NeuroQuant® program. Results: Healthy elderly had higher BDNF serum levels than MCI and dementia due to AD patients. The group of dementia patients had lower total hippocampal volume than MCI and healthy elderly participants. No significant correlation between serum BDNF and hippocampal volume was observed. Conclusion: Taking our results together (lower BDNF levels in MCI and dementia due to AD and smaller hippocampal volume in dementia due to AD) we can hypothesize that the decrease of BDNF may start before the establishment of neuronal injury expressed by the hippocampal reduction.

The major purpose of this study was to evaluate the impact of a science course for prospective elementary teachers on their perceptions of the learning environment, attitudes towards science, and understandings of the nature of science. The sample consisted of 525 female students enrolled in 27 classes of A Process Approach to Science (SCED 401) at a large urban university in Southern California. Also comparisons were made between SCED 401 and the students' previous laboratory course with regard to the learning environment and attitudes. Perceptions of the learning environment were measured using scales from the Science Laboratory Environment Inventory (Open-Endedness and Material Environment) and the What Is Happening In this Class? (Student Cohesiveness, Instructor Support, Cooperation, Investigation). Attitudes towards science were assessed using the Enjoyment of Science Lessons scale from the Test of Science-Related Attitudes (TOSRA). Students completed the Nature of Scientific Knowledge Survey (NSKS) based on their entire science education experience-not just the one laboratory class which they had taken previously. Comparisons were then made with their understandings after having completed SCED 401. Finally, associations between the learning environment and the student outcomes of attitudes and understandings of the nature of science were explored. This study embraced the current trend in classroom learning environments research of combining quantitative and qualitative methods. Qualitative components included items from the open-ended questionnaire, Views of Nature of Science, interviews with students, and an analysis of concept maps. The qualitative findings expanded and complemented the quantitative results and, in several cases, supported the construct validity of scales assessing the learning environment and attitudes. / Another purpose of this study was to investigate the effects of using real research data for growth rates of four species of Antarctic seabirds (i.e., implementing an 'intervention') in six classes of SCED 401. The objective of the intervention was to increase the authenticity and quality of an experimental design project. In addition, the wildlife biologist who collected the data guided the students during the project. Although the intervention did not lead to an appreciable improvement in students' perceptions of the learning environment, differences between intervention and nonintervention classes were statistically significant for Enjoyment of Science Lessons from the TOSRA and for Creative from the NSKS (effect sues were 2.64 and 2.06 standard deviations, respectively). Results of this study indicated that during a factor analysis, the large majority of learning environment items belonged to their a priori scale (43 out of 46 items had factor loadings above 0.40) A valid instrument for use with prospective elementary teachers was produced by combining relevant scales from the Science . Laboratory Environment Inventory and the What Is Happening In this Class? A weaker factor structure was found for the Nature of Scientific Knowledge Survey. However, by moving close to half of the -faulty' items from the NSKS, the internal consistency reliability of scales improved considerably. This study also found large and statistically significant differences between students' previous laboratory class and SCED 401 for all six leaning environment scales. The largest difference was found for the level of Open-Endedness (effect size was 6.74 standard deviations). / A statistically significant difference also was found for Enjoyment of Science Lessons (effect size was 2.98 standard deviations). Differences were not as dramatic with regard to understandings of the nature of science, although differences for two scales (Creative and Unified) from the NSKS were positive and statistically significant. This study replicated past research by finding statistically significant positive correlations between all six learning environment scales and Enjoyment of Science Lessons. However, by far, Instructor Support had the largest independent association with enjoyment, using both the individual and class mean as the units of analysis. A positive link between a favorable leaning environment and the student outcome of understanding nature of science also was found. This research makes a distinctive contribution to the learning environments field because it is the first study to investigate laboratory classroom environments at the university level with prospective elementary teachers. The study is also the first to build a bridge between the classroom learning environment and the student outcome of understanding the nature of science. The study has implications for undergraduate laboratory course instructors, for science teacher educators who develop and instruct in elementary teacher preparation programs, and for future elementary teachers and the science learning of their future students.