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Language engineering - a champion for European culture
Language is key to culture. It is a direct cultural medium as well as a means of recording and providing access to non-lingual elements of culture. Language is also fundamental to a sense of cultural identity. For this reason, it is vital, in a changing Europe, that we preserve the multi-lingual character of our society in order to move successfully towards closer co-operation at a political, economic, and social level.
Language engineering is the application of knowledge of language to the development of computer software which can recognise, understand, interpret, and generate human language in all its forms.
The paper provides a high level view of the ‘state of the art’ in language engineering and indicates ways in which it will have a profound impact on our culture in the future. It shows how advances in language engineering are an important aid in maintaining cultural diversity in a multi-lingual European society, while enabling the development of social cohesion across cultural and national divides. It addresses issues raised by the prospect of the Multi-lingual Information Society, including education, human communication with technology and information management, as well as aspects of digital cities such as tele-presence in digital libraries, virtual art galleries and electronic museums. The paper raises the issue of language as a factor in cultural domination, showing the contribution that language engineering can make towards countering it.
The paper also raises a number of controversial issues concerning the likely benefits arising from the ways in which language is likely to influence the culture of Europe
The effect of a drug use prevention curriculum on a measure of self-esteem
Longitudinal studies have indicated that drug use prevention curricula are effective in increasing students\u27 knowledge of the harmful effects of drugs, improving their social skills, and developing healthier interpersonal relationships. The purpose of this quasi-experimental study was to evaluate the effect of a drug use prevention curriculum on students\u27 self-esteem over a short time span. Sixty-seven students were pretested with a measure of self-esteem after being divided into a target and a control group. Five lessons were taught to the target group over a period of five weeks. All students were then posttested and the results were analyzed using a repeated measures t statistic. The findings indicated that the drug use prevention curriculum had a significant and positive effect on the target group\u27s measure of self-esteem. The control group showed no significant change from pretest to posttest on their measure of self-esteem. These findings indicate that a consistent use of a drug use prevention curriculum can provide short term benefits as well as long term benefits for students and their school systems
Magnetic flux flow and superconductor stabilization Quarterly report, 1 Jan. - 31 Mar. 1968
Magnetic flux flow and stability of superconducting niobium titanium strip
Occupational Therapy Students’ Test/Re-Test Reliability of the Readiness for Interprofessional Education Learning Scale and Interdisciplinary Education Perception Scale
The purpose of this study was to establish the test/re-test reliability of two interprofessional education (IPE) instruments, the Readiness for Interprofessional Learning Scale (RIPLS) and the Interdisciplinary Education Perception Scale (IEPS) among occupational therapy (OT) graduate students. The intent was to compare results based on previous IPE experience and year in the program. The RIPLS and IEPS were distributed to 111 OT students at one university. Both instruments were distributed a second time 10-14 days later. Cronbach’s alpha, weighted Kappas, intraclass correlation coefficients (ICC), standard error of measurement, and minimal detectable change were calculated for each instrument. Assessments occurred for all subjects, between students with and without previous IPE experience, and first and second-year students in the program. Overall and between group composite score reliability for the RIPLS and IEPS were fair to excellent (ICC≥0.72). RIPLS subscale ICC’s were variable per previous IPE experience and year in program, ranging from fair-excellent (ICC=0.45-0.93). IEPS subscale ICC’s were excellent for second-year students (ICC≥0.79), and fair-excellent for students with or without previous experience and first-year students (ICC=0.50-0.84). There were no differences for the RIPLS within or between sessions or groups. First-year students had significantly higher scores compared to second-year students within sessions for the IEPS composite score, Competency and Autonomy subscale, and Perception of Actual Cooperation subscale (p≤0.035). Both instruments have acceptable test-re-test reliability; however, previous IPE experience and year in program should be accounted for when distributing the instruments and interpreting the results
Day Ahead Electric Load Forecast: A Comprehensive LSTM-EMD Methodology and Several Diverse Case Studies
Phenolic Compounds Protect Cultured Hippocampal Neurons against Ethanol-Withdrawal Induced Oxidative Stress
Ethanol withdrawal is linked to elevated oxidative damage to neurons. Here we report our findings on the contribution of phenolic antioxidants (17β-estradiol, p-octyl-phenol and 2,6-di-tert-butyl-4-methylphenol) to counterbalance sudden ethanol withdrawal-initiated oxidative events in hippocampus-derived cultured HT-22 cells. We showed that ethanol withdrawal for 4 h after 24-h ethanol treatment provoked greater levels of oxidative damage than the preceding ethanol exposure. Phenolic antioxidant treatment either during ethanol exposure or ethanol withdrawal only, however, dose-dependently reversed cellular oxidative damage, as demonstrated by the significantly enhanced cell viability, reduced malondialdehyde production and protein carbonylation, compared to untreated cells. Interestingly, the antioxidant treatment schedule had no significant impact on the observed neuroprotection. In addition, the efficacy of the three phenolic compounds was practically equipotent in protecting HT-22 cells in spite of predictions based on an in silico study and a cell free assay of lipid peroxidation. This finding implies that free-radical scavenging may not be the sole factor responsible for the observed neuroprotection and warrants further studies to establish, whether the HT-22 line is indeed a suitable model for in vitro screening of antioxidants against EW-related neuronal damage
A Tale of Three Watersheds: Nonpoint Source Pollution and Conservation Practices across Iowa
Resource /Energy Economics and Policy, Q25,
Estrogens as neuroprotectants: Estrogenic actions in the context of cognitive aging and brain injury
There is ample empirical evidence to support the notion that the biological impacts of estrogen extend beyond the gonads to other bodily systems, including the brain and behavior. Converging preclinical findings have indicated a neuroprotective role for estrogen in a variety of experimental models of cognitive function and brain insult. However, the surprising null or even detrimental findings of several large clinical trials evaluating the ability of estrogen-containing hormone treatments to protect against age-related brain changes and insults, including cognitive aging and brain injury, led to hesitation by both clinicians and patients in the use of exogenous estrogenic treatments for nervous system outcomes. That estrogen-containing therapies are used by tens of millions of women for a variety of health-related applications across the lifespan has made identifying conditions under which benefits with estrogen treatment will be realized an important public health issue. Here we provide a summary of the biological actions of estrogen and estrogen-containing formulations in the context of aging, cognition, stroke, and traumatic brain injury. We have devoted special attention to highlighting the notion that estrogen appears to be a conditional neuroprotectant whose efficacy is modulated by several interacting factors. By developing criteria standards for desired beneficial peripheral and neuroprotective outcomes among unique patient populations, we can optimize estrogen treatments for attenuating the consequences of, and perhaps even preventing, cognitive aging and brain injury
Extracellular Vesicles Secreted in Response to Cytokine Exposure Increase Mitochondrial Oxygen Consumption in Recipient Cells
Extracellular vesicles (EVs) are small, membrane-bound nanoparticles released from most, if not all cells, and can carry functionally active cargo (proteins, nucleic acids) which can be taken up by neighboring cells and mediate physiologically relevant effects. In this capacity, EVs are being regarded as novel cell-to-cell communicators, which may play important roles in the progression of neurodegenerative diseases, like Alzheimer’s disease (AD). Aside from the canonical physical hallmarks of this disease [amyloid β (Aβ) plaques, neurofibrillary tangles, and widespread cell death], AD is characterized by chronic neuroinflammation and mitochondrial dysfunction. In the current study, we sought to better understand the role of tumor necrosis factor-alpha (TNF-α), known to be involved in inflammation, in mediating alterations in mitochondrial function and EV secretion. Using an immortalized hippocampal cell line, we observed significant reductions in several parameters of mitochondrial oxygen consumption after a 24-h exposure period to TNF-α. In addition, after TNF-α exposure we also observed significant upregulation of two microRNAs (miRNAs; miR-34a and miR-146a) associated with mitochondrial dysfunction in secreted EVs. Despite this, when naïve cells are exposed to EVs isolated from TNF-α treated cells, mitochondrial respiration, proton leak, and reactive oxygen species (ROS) production are all significantly increased. Collectively these data indicate that a potent proinflammatory cytokine, TNF-α, induces significant mitochondrial dysfunction in a neuronal cell type, in part via the secretion of EVs, which significantly alter mitochondrial activity in recipient cells
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