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In this chapter we draw together the major themes of our five-year project and imagine in to the future. In chapter 1 we described social change as endemic in modern society and argued that 'education' is inextricably linked to economic and cultural change in the now firmly entrenched policies of governments and employers. This is a period of unprecedented opportunities for the education sector, but it also puts serious questions to the schools and teacher education sectors about their roles and functions. As, chapter 3 detailed, there are numerous state and national reports about the 'education' workforce, the changing nature of teacher engagement within the workplace and the potential impact on educational outcomes for children in schools. Not surprisingly, education systems require new and different capabilities from their teacher workforce and, in turn, teacher preparation programs. The BLM is both a precursor and an effect of these circumstances.

There is not a single education policy document these days that does not herald the arrival of fundamental social change as the mainstay for the reform of schooling and teacher education. The case that social change is endemic and that 'education' is inextricably linked to economic and cultural change and developments is now firmly entrenched in the policy milieu of governments and employers.

Intolerance -- Intolerance, Part II (stories from the field) -- Subterfuge -- Subterfuge, Part II (stories from the field) -- Intrusiveness -- Intrusiveness, Part II (stories from the field) -- Craftiness -- Craftiness, Part II (stories from the field) -- Favoritism -- Favoritism, Part II (stories from the field) -- Cruelty -- Cruelty, Part II (stories from the field) -- Subservience to authority -- Subservience to authority, Part II (stories from the field) -- Botched justice : poorly decided legal cases of the past.

BACKGROUND: Exposure to inhalational hazards during post-9/11 deployment to Southwest Asia and Afghanistan puts military personnel at risk for respiratory symptoms and disease. Pulmonary function and qualitative chest high resolution computed tomography (HRCT) are often normal in "deployers" with persistent respiratory symptoms. We explored the utility of quantitative HRCT imaging markers of large and small airways abnormalities, including airway wall thickness, emphysema, and air trapping, in symptomatic deployers with clinically-confirmed lung disease compared to controls. METHODS: Chest HRCT images from 45 healthy controls and 82 symptomatic deployers with asthma, distal lung disease or both were analyzed using Thirona Lung quantification software to calculate airway wall thickness (by Pi10), emphysema (by percentage of lung volume with attenuation < -950 Hounsfield units [LAA%-950]), and three parameters of air trapping (expiratory/inspiratory total lung volume and mean lung density ratios, and LAA%-856). SAS v.9.4 was used to compare demographic and clinical characteristics between deployers and controls using Chi-Square, Fisher Exact or t-tests. Linear regression was used to assess relationships between pulmonary function and quantitative imaging findings. RESULTS: Gender and smoking status were not statistically significantly different between groups, but deployers were significantly younger than controls (42 vs 58 years, p < 0.0001), had higher body mass index (31 vs 28 kg/m(2), p = 0.01), and had fewer total smoking pack-years (8 vs. 26, p = 0.007). Spirometric measures were not statistically significantly different between groups. Pi10 and LAA%-950 were significantly elevated in deployers compared to controls in unadjusted analyses, with the emphysema measure remaining significantly higher in deployers after adjustment for age, sex, smoking, BMI, and expiratory total lung volume. Air trapping parameters were more common in control images, likely due to differences in age and smoking between ...

AbstractPurpose/aimThe aim of this pilot study was to evaluate feasibility and gather initial data for a definitive study to test the clinical and microbiological effectiveness of a nursing facility (NF) customized oral hygiene protocol, intended to be delivered by dental hygienists and NF personnel.Materials and methodsA convenience sample of 8 Eastern Iowa NFs was recruited, and each NF was assigned to one of three intervention groups: (1) control (current oral hygiene practice), (2) educational program only, and (3) educational program plus 1% chlorhexidine varnish monthly application. Demographic information, systemic health data, patient centered data, oral health data, and microbiology samples were collected at baseline and after 6 months.ResultsRecruitment response rates were 21% for NFs and 23% for residents. A total of 81 residents were examined at baseline and of those, 49 were examined at 6 months (39.5% attrition). There were no statistically or clinically significant differences among the intervention groups at 6 months for any of the recorded clinical or microbiological outcomes.ConclusionsRecruitment and retention posed a significant challenge to this trial, even with a relatively short observation period. Results from this pilot study did not encourage further investigation of this customized oral hygiene protocol.

Abstract
Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by the deficiency of mitochondrial protein frataxin, which plays a crucial role in iron–sulphur cluster formation and ATP production. The cellular function of frataxin is not entirely known. Here, we demonstrate that frataxin controls ketone body metabolism through regulation of 3-Oxoacid CoA-Transferase 1 (OXCT1), a rate limiting enzyme catalyzing the conversion of ketone bodies to acetoacetyl-CoA that is then fed into the Krebs cycle. Biochemical studies show a physical interaction between frataxin and OXCT1 both in vivo and in vitro. Frataxin overexpression also increases OXCT1 protein levels in human skin fibroblasts while frataxin deficiency decreases OXCT1 in multiple cell types including cerebellum and skeletal muscle both acutely and chronically, suggesting that frataxin directly regulates OXCT1. This regulation is mediated by frataxin-dependent suppression of ubiquitin–proteasome system (UPS)-dependent OXCT1 degradation. Concomitantly, plasma ketone bodies are significantly elevated in frataxin deficient knock-in/knockout (KIKO) mice with no change in the levels of other enzymes involved in ketone body production. In addition, ketone bodies fail to be metabolized to acetyl-CoA accompanied by increased succinyl-CoA in vitro in frataxin deficient cells, suggesting that ketone body elevation is caused by frataxin-dependent reduction of OXCT1 leading to deficits in tissue utilization of ketone bodies. Considering the potential role of metabolic abnormalities and deficiency of ATP production in FRDA, our results suggest a new role for frataxin in ketone body metabolism and also suggest modulation of OXCT1 may be a potential therapeutic approach for FRDA.