Emerging And Disruptive Technologies For Education: An Analysis Of Planning, Implementation, And Diffusion In Florida\u27s Eleven State University System Institutions

The purpose of the study was to understand and appreciate the methodologies and procedures used in determining the extent to which an information technology (IT) organization within the eleven member State University Systems (SUS) of Florida planned, implemented, and diffused emerging educational technologies. Key findings found how critical it was that flexibility be given during the planning stages and not rely on standardized models which may or may not be of use any longer. Research also found that the SUS institutions have to be prepared to organize and preserve the deluge of digital data if they intended to remain relevant as a tower of knowledge transmissions. The literature found that institutions of higher education needed to keep abreast of the new technologies, new pedagogies, and never before open-access concepts because authors found these ideas were converging and producing an unprecedented period of innovation in learning. Furthermore, the implications of perpetual connectivity to information, peers, and teachers garnered a great deal of attention among educational technologists. However, those implications had not been gauged, especially in Florida\u27s SUS institutions. A survey of those institutions regarding how technologies were planned for, implemented logically, and thoroughly diffused, along with lessons learned could potentially save resources and ensure Florida\u27s institutions continue to be on higher learning\u27s forefront

Forests and Carbon: A Synthesis of Science, Management, and Policy for Carbon Sequestration in Forests

The goal of this volume is to provide guidance for land managers and policymakers seeking to understand the complex science and policy of forest carbon as it relates to tangible problems of forest management and the more abstract problems of addressing drivers of deforestation and negotiating policy frameworks for reducing CO2 emissions from forests. It is the culmination of three graduate seminars at the Yale School of Forestry & Environmental Studies focused on carbon sequestration in forest ecosystems and their role in addressing climate change

Giving credit when credit is due : improvement initiatives in three diverse school districts to increase on-time graduation

One of the most important measures of success of a high school is its graduation rate. There are many factors that influence whether or not students graduate in the traditional four-year schedule. Student motivation and achievement certainly are primary reasons students may meet this expectation, but oftentimes there are other issues that contribute to the delay of on-time graduation. Sometimes these factors are actually beyond the control of the student. Frequent student mobility, socio-economic disadvantages, and behavioral issues are reasons that often impede on-time graduation for students. Students affected by these issues desperately need schools to be flexible and find options to keep them in school and on course to graduate with their cohort. Of the students who eventually drop out, one-third are behind in their coursework in the 9th grade (Alliance for Excellent Education, 2010)The purpose of this initiative was to examine the impact of student mobility, socio-economic distress, and chronic negative behavior on on-time graduation, as well, evaluate and develop programs and protocols that provide options to help students retain and regain credits needed to graduate with their cohort. This work studied students and personnel in three demographically different high schools in North Carolina: a large, urban school in Cary, NC drawing from an affluent area; a large school located near a military base in Fayetteville, NC; and a small, mountain school serving many students who are socio-economically disadvantaged in Murphy, NC.Data were gathered through the spring, summer, and fall semesters of 2015. The research practitioners investigated data drawn from a variety of credit recovery and retention options, including, a personalized registration program and several on-line programs, such as GradPoint, Study Island, and Edgenuity. One research practitioner also identified effective strategies to create a training program for school counselors to assist students in retaining and regaining credits toward graduation. This qualitative data gives voice to the students who often have no voice when it comes to making decisions when they fall behind their cohort, and provides counselors with the tools to assist these students. Qualitative data were gathered through a variety of research methods, including surveys, interviews, case studies, and focus groups. These methods were selected because of their ability to solicit the thoughts, feelings, and experiences of those participating in the improvement change (Creswell, 2012). The intent of this work was to increase options for students at risk of not graduating on time, thereby improving their chance of staying in school and graduating with their cohort

The effect of stress on the expression of the amyloid precursor protein in rat brain

AbstractThe abnormal processing of the amyloid precursor protein (APP) is a pivotal event in the development of the unique pathology that defines Alzheimer's disease (AD). Stress, and the associated increase in corticosteroids, appear to accelerate brain ageing and may increase vulnerability to Alzheimer's disease via altered APP processing. In this study, rats were repeatedly exposed to an unavoidable stressor, an open elevated platform. Previous studies in this laboratory have shown that a single exposure produces a marked increase in plasma corticosterone levels but animals develop tolerance to this effect between 10 and 20 daily sessions. Twenty-four hours after stress, there was an increase in the ratio of the deglycosylated form of APP in the particulate fraction of the brain, which subsequently habituated after 20 days. The levels of soluble APP (APPs) tended to be lower in the stress groups compared to controls except for a significant increase in the hippocampus after 20 days of platform exposure. Since APPs is reported to have neurotrophic properties, this increased release may represent a neuroprotective response to repeated stress. It is possible that the ability to mount this response decreases with age thus increasing the vulnerability to stress-induced AD-related pathology

Comparative analyses of proteins from Haemophilus influenzae biofilm and planktonic populations using metabolic labeling and mass spectrometry

BACKGROUND: Non-typeable H. influenzae (NTHi) is a nasopharyngeal commensal that can become an opportunistic pathogen causing infections such as otitis media, pneumonia, and bronchitis. NTHi is known to form biofilms. Resistance of bacterial biofilms to clearance by host defense mechanisms and antibiotic treatments is well-established. In the current study, we used stable isotope labeling by amino acids in cell culture (SILAC) to compare the proteomic profiles of NTHi biofilm and planktonic organisms. Duplicate continuous-flow growth chambers containing defined media with either “light” (L) isoleucine or “heavy” (H) (13)C(6)-labeled isoleucine were used to grow planktonic (L) and biofilm (H) samples, respectively. Bacteria were removed from the chambers, mixed based on weight, and protein extracts were generated. Liquid chromatography-mass spectrometry (LC-MS) was performed on the tryptic peptides and 814 unique proteins were identified with 99% confidence. RESULTS: Comparisons of the NTHi biofilm to planktonic samples demonstrated that 127 proteins showed differential expression with p-values ≤0.05. Pathway analysis demonstrated that proteins involved in energy metabolism, protein synthesis, and purine, pyrimidine, nucleoside, and nucleotide processes showed a general trend of downregulation in the biofilm compared to planktonic organisms. Conversely, proteins involved in transcription, DNA metabolism, and fatty acid and phospholipid metabolism showed a general trend of upregulation under biofilm conditions. Selected reaction monitoring (SRM)-MS was used to validate a subset of these proteins; among these were aerobic respiration control protein ArcA, NAD nucleotidase and heme-binding protein A. CONCLUSIONS: The present proteomic study indicates that the NTHi biofilm exists in a semi-dormant state with decreased energy metabolism and protein synthesis yet is still capable of managing oxidative stress and in acquiring necessary cofactors important for biofilm survival. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12866-014-0329-9) contains supplementary material, which is available to authorized users

Francisella tularensis Schu S4 lipopolysaccharide core sugar and o-antigen mutants are attenuated in a mouse model of tularemia

The virulence factors mediating Francisella pathogenesis are being investigated, with an emphasis on understanding how the organism evades innate immunity mechanisms. Francisella tularensis produces a lipopolysaccharide (LPS) that is essentially inert and a polysaccharide capsule that helps the organism to evade detection by components of innate immunity. Using an F. tularensis Schu S4 mutant library, we identified strains that are disrupted for capsule and O-antigen production. These serum-sensitive strains lack both capsule production and O-antigen laddering. Analysis of the predicted protein sequences for the disrupted genes (FTT1236 and FTT1238c) revealed similarity to those for waa (rfa) biosynthetic genes in other bacteria. Mass spectrometry further revealed that these proteins are involved in LPS core sugar biosynthesis and the ligation of O antigen to the LPS core sugars. The 50% lethal dose (LD(50)) values of these strains are increased 100- to 1,000-fold for mice. Histopathology revealed that the immune response to the F. tularensis mutant strains was significantly different from that observed with wild-type-infected mice. The lung tissue from mutant-infected mice had widespread necrotic debris, but the spleens lacked necrosis and displayed neutrophilia. In contrast, the lungs of wild-type-infected mice had nominal necrosis, but the spleens had widespread necrosis. These data indicate that murine death caused by wild-type strains occurs by a mechanism different from that by which the mutant strains kill mice. Mice immunized with these mutant strains displayed >10-fold protective effects against virulent type A F. tularensis challenge

Raised interleukin 31 transcription in a canine model of acute atopic dermatitis does not correlate with T cell infiltration

Interleukin 31 (IL-31) has been identified as an important cytokine in the pathophysiology of atopic dermatitis (AD) in both humans and dogs, and is a key mediator in the pruritus and TH2-weighted inflammation which characterizes this allergic condition.1 IL-31 is produced predominantly by activated T cells and memory T cells, preferentially TH2, and also by mast cells, eosinophils, basophils, macrophages and dendritic cells.1,2 However the origin of IL-31 in the skin is unclear: one study identified IL-31 transcription in infiltrating cells, presumed to be T cells, but another study associated IL-31 protein immunostaining with CD11b+ or CD11c+ cells in the skin, but not CD3+ T cells.3,4 IL-31 is thought to have diverse functions in the skin including regulation of keratinocyte differentiation and filaggrin expression, promoting interaction between keratinocytes and eosinophils, eosinophil chemotaxis, promoting nerve growth and stimulating secretion of proinflammatory cytokines, chemokines, and matrix metalloproteinase by keratinocytes and dendritic cells.5-11 In addition, IL-31 has been shown to directly activate sensory neurons in the skin, providing a critical link between cells of the immune and nervous systems in communicating the sensation of pruritus associated with allergic skin disease.12 Over the last 20 years, numerous studies have established the striking similarities between human (AD) and canine atopic dermatitis (cAD), leading to the proposition that cAD can be used as a relevant model for humans.13-15 Naturally occurring cAD is very common in dogs, and its epidemiology, clinical presentation, diagnosis and pathophysiology appear to closely parallel that of AD in human patients, with the exception that dogs very rarely develop allergic asthma and rhinitis.13-15 As in humans, the hallmarks of cAD are epidermal barrier defects and aberrant T helper type 2 (TH2)-weighted immune responses to environmental allergens.13-15 Likewise, 80% of affected dogs have classical cAD, with allergen-specific IgE, while 20% have cAD-like disease which is clinically indistinguishable but presents without detectable allergen-specific IgE.13 Concomitant food allergies, dysbiosis of the skin microbiome and secondary Staphylococcal infection are also common in dogs.13,16 The management and treatment of cAD is also similar human AD, with the addition of allergen-specific immunotherapy, Janus Kinase (JAK) inhibitors and anti-IL-31 therapeutic monoclonal antibody being in general use for cAD.13-15 The development and adoption of novel treatments for cAD, such as JAK inhibitors and anti-IL-31 monoclonals, is often accelerated by the reduced expense of clinical trials and lower regulatory requirements in veterinary medicine.13,15 Levels of IL-31 in the serum of atopic dogs has been found to correlate with the severity of clinical signs, and transcription of IL-31 mRNA has been shown to be increased in peripheral blood mononuclear cells from atopic dogs.17-19 Early studies failed to demonstrate IL-31 transcription in canine skin, however Olivry et al demonstrated increased IL-31 mRNA in lesional skin from an experimental canine model of acute house dust mite-induced AD. 20,21 A recent study of IL-31 transcription in canine skin demonstrated very low levels of IL-31 transcription in both healthy and atopic dogs using in-situ hybridization, but this study did not examine which cells in the skin were responsible or changes during inflammation.22The objectives of our studies were to identify transcription of IL-31 in normal and atopic canine skin, to examine how transcription is affected during allergic inflammation, and to examine whether transcription of IL-31 correlates with changes in eosinophils and CD3+ T cells in the skin of atopic dogs over the course of an acute inflammatory response. <br/

Thioredoxin is a metabolic rheostat controlling regulatory B cells

Metabolic programming is important for B cell fate, but the bioenergetic requirement for regulatory B (B reg) cell differentiation and function is unknown. Here we show that B reg cell differentiation, unlike non-B reg cells, relies on mitochondrial electron transport and homeostatic levels of reactive oxygen species (ROS). Single-cell RNA sequencing analysis revealed that TXN, encoding the metabolic redox protein thioredoxin (Trx), is highly expressed by B reg cells, unlike Trx inhibitor TXNIP which was downregulated. Pharmacological inhibition or gene silencing of TXN resulted in mitochondrial membrane depolarization and increased ROS levels, selectively suppressing B reg cell differentiation and function while favoring pro-inflammatory B cell differentiation. Patients with systemic lupus erythematosus (SLE), characterized by B reg cell deficiencies, present with B cell mitochondrial membrane depolarization, elevated ROS and fewer Trx + B cells. Exogenous Trx stimulation restored B reg cells and mitochondrial membrane polarization in SLE B cells to healthy B cell levels, indicating Trx insufficiency underlies B reg cell impairment in patients with SLE. </p

The Cortical Signature of Alzheimer's Disease: Regionally Specific Cortical Thinning Relates to Symptom Severity in Very Mild to Mild AD Dementia and is Detectable in Asymptomatic Amyloid-Positive Individuals

Alzheimer's disease (AD) is associated with neurodegeneration in vulnerable limbic and heteromodal regions of the cerebral cortex, detectable in vivo using magnetic resonance imaging. It is not clear whether abnormalities of cortical anatomy in AD can be reliably measured across different subject samples, how closely they track symptoms, and whether they are detectable prior to symptoms. An exploratory map of cortical thinning in mild AD was used to define regions of interest that were applied in a hypothesis-driven fashion to other subject samples. Results demonstrate a reliably quantifiable in vivo signature of abnormal cortical anatomy in AD, which parallels known regional vulnerability to AD neuropathology. Thinning in vulnerable cortical regions relates to symptom severity even in the earliest stages of clinical symptoms. Furthermore, subtle thinning is present in asymptomatic older controls with brain amyloid binding as detected with amyloid imaging. The reliability and clinical validity of AD-related cortical thinning suggests potential utility as an imaging biomarker. This “disease signature” approach to cortical morphometry, in which disease effects are mapped across the cortical mantle and then used to define ROIs for hypothesis-driven analyses, may provide a powerful methodological framework for studies of neuropsychiatric diseases.Psycholog

The Cortical Signature of Alzheimer's Disease: Regionally Specific Cortical Thinning Relates to Symptom Severity in Very Mild to Mild AD Dementia and is Detectable in Asymptomatic Amyloid-Positive Individuals

Alzheimer's disease (AD) is associated with neurodegeneration in vulnerable limbic and heteromodal regions of the cerebral cortex, detectable in vivo using magnetic resonance imaging. It is not clear whether abnormalities of cortical anatomy in AD can be reliably measured across different subject samples, how closely they track symptoms, and whether they are detectable prior to symptoms. An exploratory map of cortical thinning in mild AD was used to define regions of interest that were applied in a hypothesis-driven fashion to other subject samples. Results demonstrate a reliably quantifiable in vivo signature of abnormal cortical anatomy in AD, which parallels known regional vulnerability to AD neuropathology. Thinning in vulnerable cortical regions relates to symptom severity even in the earliest stages of clinical symptoms. Furthermore, subtle thinning is present in asymptomatic older controls with brain amyloid binding as detected with amyloid imaging. The reliability and clinical validity of AD-related cortical thinning suggests potential utility as an imaging biomarker. This “disease signature” approach to cortical morphometry, in which disease effects are mapped across the cortical mantle and then used to define ROIs for hypothesis-driven analyses, may provide a powerful methodological framework for studies of neuropsychiatric diseases