Teaching for conceptual change in security awareness education: A case study in higher education

In educational psychology, conceptual change is a process that revises a student's understanding of a topic in response to new information. Conceptual change pedagogy is particularly effective for security awareness education because instructors must deliver concepts to people who primarily just use computer networks and information systems rather than display expertise in the underlying technology.published_or_final_versio

Teaching for conceptual change in security awareness

The study focused on the teaching for conceptual change in security awareness, where the security awareness training is putting efforts into designing the curriculum for security awareness programs, to make trainees adhere to safe computing practices. The conceptual change is a process that revises the student's understanding of a topic in response to new information. These conceptual change belongs to constructivist pedagogies, and is effective in teaching and learning relatively advanced and complex scientific concepts. The security training often involves advanced terms and concepts, as the Secure Sockets Layer (SSL) and data encryption. The computer and network security demonstrations as anomalous data for training course can be used by the instructors. The study demonstrates the pedagogical model involved in the conceptual change as revealing students preconceptions, discussion and evaluation of preconceptions and creation of conceptual conflict with these preconceptions.published_or_final_versio

Hamming weights and Betti numbers of Stanley-Reisner rings associated to matroids

To each linear code over a finite field we associate the matroid of its parity check matrix. We show to what extent one can determine the generalized Hamming weights of the code (or defined for a matroid in general) from various sets of Betti numbers of Stanley-Reisner rings of simplicial complexes associated to the matroid

Synthesis, antitubercular activity and mechanism of resistance of highly effective thiacetazone analogues

Defining the pharmacological target(s) of currently used drugs and developing new analogues with greater potency are both important aspects of the search for agents that are effective against drug-sensitive and drug-resistant Mycobacterium tuberculosis. Thiacetazone (TAC) is an anti-tubercular drug that was formerly used in conjunction with isoniazid, but removed from the antitubercular chemotherapeutic arsenal due to toxic side effects. However, several recent studies have linked the mechanisms of action of TAC to mycolic acid metabolism and TAC-derived analogues have shown increased potency against M. tuberculosis. To obtain new insights into the molecular mechanisms of TAC resistance, we isolated and analyzed 10 mutants of M. tuberculosis that were highly resistant to TAC. One strain was found to be mutated in the methyltransferase MmaA4 at Gly101, consistent with its lack of oxygenated mycolic acids. All remaining strains harbored missense mutations in either HadA (at Cys61) or HadC (at Val85, Lys157 or Thr123), which are components of the bhydroxyacyl-ACP dehydratase complex that participates in the mycolic acid elongation step. Separately, a library of 31 new TAC analogues was synthesized and evaluated against M. tuberculosis. Two of these compounds, 15 and 16, exhibited minimal inhibitory concentrations 10-fold lower than the parental molecule, and inhibited mycolic acid biosynthesis in a dose-dependent manner. Moreover, overexpression of HadAB HadBC or HadABC in M. tuberculosis led to high level resistance to these compounds, demonstrating that their mode of action is similar to that of TAC. In summary, this study uncovered new mutations associated with TAC resistance and also demonstrated that simple structural optimization of the TAC scaffold was possible and may lead to a new generation of TAC-derived drug candidates for the potential treatment of tuberculosis as mycolic acid inhibitors

The Accumulation of Organic Carbon in Mineral Soils by Afforestation of Abandoned Farmland

The afforestation of abandoned farmland significantly influences soil organic carbon (OC). However, the dynamics between OC inputs after afforestation and the original OC are not well understood. To learn more about soil OC dynamics after afforestation of farmland, we measured the soil OC content in paired forest and farmland plots in Shaanxi Province, China. The forest plots had been established on farmland 18, 24, 48, 100, and 200 yr previously. The natural 13C abundance of soil organic matter was also analyzed to distinguish between crop- and forest-derived C in the afforested soils. We observed a nonlinear accumulation of total OC in the 0–80 cm depth of the mineral soil across time. Total soil OC accumulated more rapidly under forest stands aged 18 to 48 yr than under forest stands aged 100 or 200 yrs. The rate of OC accumulation was also greater in the 0–10 cm depth than in the 10–80 cm depth. Forest-derived OC in afforested soils also accumulated nonlinearly across time, with the greatest increase in the 0–20 cm depth. Forest-derived OC in afforest soils accounted for 52–86% of the total OC in the 0–10 cm depth, 36–61% of the total OC in the 10–20 cm depth, and 11–50% of the total OC in the 20–80 cm depth. Crop-derived OC concentrations in the 0–20 cm depth decreased slightly after afforestation, but there was no change in crop-derived OC concentrations in the 20–80 cm depth. The results of our study support the claim that afforestation of farmland can sequester atmospheric CO2 by increasing soil OC stocks. Changes in the OC stocks of mineral soils after afforestation appear to be influenced mainly by the input of forest-derived C rather than by the loss of original OC

Uncovering mechanisms of transcriptional regulations by systematic mining of cis regulatory elements with gene expression profiles

<p>Abstract</p> <p>Background</p> <p>Contrary to the traditional biology approach, where the expression patterns of a handful of genes are studied at a time, microarray experiments enable biologists to study the expression patterns of many genes simultaneously from gene expression profile data and decipher the underlying hidden biological mechanism from the observed gene expression changes. While the statistical significance of the gene expression data can be deduced by various methods, the biological interpretation of the data presents a challenge.</p> <p>Results</p> <p>A method, called CisTransMine, is proposed to help infer the underlying biological mechanisms for the observed gene expression changes in microarray experiments. Specifically, this method will predict potential cis-regulatory elements in promoter regions which could regulate gene expression changes. This approach builds on the MotifADE method published in 2004 and extends it with two modifications: up-regulated genes and down-regulated genes are tested separately and in addition, tests have been implemented to identify combinations of transcription factors that work synergistically. The method has been applied to a genome wide expression dataset intended to study myogenesis in a mouse C2C12 cell differentiation model. The results shown here both confirm the prior biological knowledge and facilitate the discovery of new biological insights.</p> <p>Conclusion</p> <p>The results validate that the CisTransMine approach is a robust method to uncover the hidden transcriptional regulatory mechanisms that can facilitate the discovery of mechanisms of transcriptional regulation.</p

Differentiation of human multipotent dermal fibroblasts into islet-like cell clusters

<p>Abstract</p> <p>Background</p> <p>We have previously obtained a clonal population of cells from human foreskin that is able to differentiate into mesodermal, ectodermal and endodermal progenies. It is of great interest to know whether these cells could be further differentiated into functional insulin-producing cells.</p> <p>Results</p> <p>Sixty-one single-cell-derived dermal fibroblast clones were established from human foreskin by limiting dilution culture. Of these, two clones could be differentiated into neuron-, adipocyte- or hepatocyte-like cells under certain culture conditions. In addition, those two clones were able to differentiate into islet-like clusters under pancreatic induction. Insulin, glucagon and somatostatin were detectable at the mRNA and protein levels after induction. Moreover, the islet-like clusters could release insulin in response to glucose in vitro.</p> <p>Conclusions</p> <p>This is the first study to demonstrate that dermal fibroblasts can differentiate into insulin-producing cells without genetic manipulation. This may offer a safer cell source for future stem cell-based therapies.</p

Exogenous Glucose Administration Impairs Glucose Tolerance and Pancreatic Insulin Secretion during Acute Sepsis in Non-Diabetic Mice

Objectives:The development of hyperglycemia and the use of early parenteral feeding are associated with poor outcomes in critically ill patients. We therefore examined the impact of exogenous glucose administration on the integrated metabolic function of endotoxemic mice using our recently developed frequently sampled intravenous glucose tolerance test (FSIVGTT). We next extended our findings using a cecal ligation and puncture (CLP) sepsis model administered early parenteral glucose support.Methods:Male C57BL/6J mice, 8-12 weeks, were instrumented with chronic indwelling arterial and venous catheters. Endotoxemia was initiated with intra-arterial lipopolysaccharide (LPS; 1 mg/kg) in the presence of saline or glucose infusion (100 μL/hr), and an FSIVGTT was performed after five hours. In a second experiment, catheterized mice underwent CLP and the impact of early parenteral glucose administration on glucose homeostasis and mortality was assessed over 24 hrs.Measurements:And MAIN RESULTS: Administration of LPS alone did not impair metabolic function, whereas glucose administration alone induced an insulin sensitive state. In contrast, LPS and glucose combined caused marked glucose intolerance and insulin resistance and significantly impaired pancreatic insulin secretion. Similarly, CLP mice receiving parenteral glucose developed fulminant hyperglycemia within 18 hrs (all > 600 mg/dl) associated with increased systemic cytokine release and 40% mortality, whereas CLP alone (85 ± 2 mg/dL) or sham mice receiving parenteral glucose (113 ± 3 mg/dL) all survived and were not hyperglycemic. Despite profound hyperglycemia, plasma insulin in the CLP glucose-infused mice (3.7 ± 1.2 ng/ml) was not higher than sham glucose infused mice (2.1 ± 0.3 ng/ml).Conclusions:The combination of parenteral glucose support and the systemic inflammatory response in the acute phase of sepsis induces profound insulin resistance and impairs compensatory pancreatic insulin secretion, leading to the development of fulminant hyperglycemia. © 2013 Watanabe et al