Affording inclusive dyslexia-friendly online text reading

To date, guidelines for designing inclusive dyslexia-friendly online learning environments, which take into consideration both learners with and without dyslexia, are still scarce. As web text is one of the extensively used elements in online learning, this study aims to derive practical guidelines on this aspect by exploring the experience of learners with dyslexia and learners without dyslexia when using different online reading affordances. The study employed a within-subjects qualitative study and key patterns that emerged from the data collected via observations and interviews were interpreted based on two important aspects of learning experience, which were perceived learning and engagement. The study reveals that (1) the direct application of Printed Text on the web should be carefully considered, (2) existing web accessibility guidelines (limit to guidelines examined in this study) are appropriate and (3) the use of a Screen Reader for online reading should not be made compulsory and be available as an option instead. The comparison between the experience of learners with and without dyslexia in this study has yielded insights into affordances that are perceived positively by both groups of learners. As learners with dyslexia form a significant minority of the online learning population, the inclusive dyslexia-friendly guidelines derived from this study would better inform the future implementation of online reading affordances that acknowledge differences and similarities between online learners

Increase of ATP-sensitive potassium (KATP) channels in the heart of type-1 diabetic rats

<p>Abstract</p> <p>Background</p> <p>An impairment of cardiovascular function in streptozotocin (STZ)-diabetic rats has been mentioned within 5 days-to-3 months of induction. ATP-sensitive potassium (K_ATP) channels are expressed on cardiac sarcolemmal membranes. It is highly responsive to metabolic fluctuations and can have effects on cardiac contractility. The present study attempted to clarify the changes of cardiac K_ATPchannels in diabetic disorders.</p> <p>Methods</p> <p>Streptozotocin-induced diabetic rats and neonatal rat cardiomyocytes treated with a high concentration of glucose (a D-glucose concentration of 30 mM was used and cells were cultured for 24 hr) were used to examine the effect of hyperglycemia on cardiac function and the expression of K_ATPchannels. K_ATPchannels expression was found to be linked to cardiac tonic dysfunction, and we evaluated the expression levels of K_ATPchannels by Western blot and Northern blot analysis.</p> <p>Results</p> <p>The result shows diazoxide produced a marked reduction of heart rate in control group. Furthermore, the methods of Northern blotting and Western blotting were employed to identify the gene expression of K_ATPchannel. Two subunits of cardiac K_ATPchannel (SUR2A and kir 6.2) were purchased as indicators and showed significantly decreased in both diabetic rats and high glucose treated rat cardiac myocytes. Correction of hyperglycemia by insulin or phlorizin restored the gene expression of cardiac K_ATPin these diabetic rats.</p> <p>Conclusions</p> <p>Both mRNA and protein expression of cardiac K_ATPchannels are decreased in diabetic rats induced by STZ for 8 weeks. This phenomenon leads to result in desensitization of some K_ATPchannel drugs.</p

Minimum Joint Depth for Moment Frames with High-Strength Materials

This paper reports results from four large-scale interior beam column connections without transverse beams or slabs tested under reversed cyclic displacements. The specimens, which included the first of interior beam-column connections constructed with Grade 100 (690) reinforcement with bar deformations similar to those available in U.S. practice, had Grade 60 or 100 (420 or 690) bars, 4 or 10 ksi (28 or 69 MPa) concrete, and varied column depthto-beam bar diameter ratios. The specimens all exhibited strengths greater than the nominal strength, retained at least 80% of their strength to drift ratios exceeding 5%, and exceeded ACI 374 acceptance criteria at a 3% drift ratio for components of special moment frames, demonstrating that well-detailed joints constructed with high-strength materials behave satisfactorily. The data add evidence that joints constructed with high-strength concrete exhibit less bond decay, and recommendations are made for accounting for this effect in design. Results from the specimen constructed with normal-strength materials, considered in the context of prior tests, suggest a need to increase the minimum joint depth for special moment frames. Considerable improvement in behavior associated with reduced bond damage within the joint is obtained from a 20% increase in the minimum column depth-to-beam bar diameter ratio required in ACI 318-19

Molecular role of GATA binding protein 4 (GATA-4) in hyperglycemia-induced reduction of cardiac contractility

<p>Abstract</p> <p>Background</p> <p>Diabetic cardiomyopathy, a diabetes-specific complication, refers to a disorder that eventually leads to left ventricular hypertrophy in addition to diastolic and systolic dysfunction. In recent studies, hyperglycemia-induced reactive oxygen species (ROS) in cardiomyocytes have been linked to diabetic cardiomyopathy. GATA binding protein 4 (GATA-4) regulates the expression of many cardio-structural genes including cardiac troponin-I (cTnI).</p> <p>Methods</p> <p>Streptozotocin-induced diabetic rats and H9c2 embryonic rat cardiomyocytes treated with a high concentration of glucose (a D-glucose concentration of 30 mM was used and cells were cultured for 24 hr) were used to examine the effect of hyperglycemia on GATA-4 accumulation in the nucleus. cTnI expression was found to be linked to cardiac tonic dysfunction, and we evaluated the expression levels of cTnI and GATA-4 by Western blot analysis.</p> <p>Results</p> <p>Cardiac output was lowered in STZ-induced diabetic rats. In addition, higher expressions of cardiac troponin I (cTnI) and phosphorylated GATA-4 were identified in these rats by Western blotting. The changes were reversed by treatment with insulin or phlorizin after correction of the blood sugar level. In H9c2 cells, ROS production owing to the high glucose concentration increased the expression of cTnI and GATA-4 phosphorylation. However, hyperglycemia failed to increase the expression of cTnI when GATA-4 was silenced by small interfering RNA (siRNA) in H9c2 cells. Otherwise, activation of ERK is known to be a signal for phosphorylation of serine105 in GATA-4 to increase the DNA binding ability of this transcription factor. Moreover, GSK3β could directly interact with GATA-4 to cause GATA-4 to be exported from the nucleus. GATA-4 nuclear translocation and GSK3β ser9 phosphorylation were both elevated by a high glucose concentration in H9c2 cells. These changes were reversed by tiron (ROS scavenger), PD98059 (MEK/ERK inhibitor), or siRNA of GATA-4. Cell contractility measurement also indicated that the high glucose concentration decreased the contractility of H9c2 cells, and this was reduced by siRNA of GATA-4.</p> <p>Conclusions</p> <p>Hyperglycemia can cause systolic dysfunction and a higher expression of cTnI in cardiomyocytes through ROS, enhancing MEK/ERK-induced GATA-4 phosphorylation and accumulation in the cell nucleus.</p

Activation of β-Adrenoceptors by Dobutamine May Induce a Higher Expression of Peroxisome Proliferator-Activated Receptors δ (PPARδ) in Neonatal Rat Cardiomyocytes

Recent evidence showed the role of peroxisome proliferator-activated receptors (PPARs) in cardiac function. Cardiac contraction induced by various agents is critical in restoring the activity of peroxisome proliferator-activated receptors δ (PPARδ) in cardiac myopathy. Because dobutamine is an agent widely used to treat heart failure in emergency setting, this study is aimed to investigate the change of PPARδ in response to dobutamine. Neonatal rat cardiomyocytes were used to examine the effects of dobutamine on PPARδ expression levels and cardiac troponin I (cTnI) phosphorylation via Western blotting analysis. We show that treatment with dobutamine increased PPARδ expression and cTnI phosphorylation in a time- and dose-dependent manner in neonatal rat cardiomyocytes. These increases were blocked by the antagonist of β1-adrenoceptors. Also, the action of dobutamine was related to the increase of calcium ions and diminished by chelating intracellular calcium. Additionally, dobutamine-induced action was reduced by the inhibition of downstream messengers involved in this calcium-related pathway. Moreover, deletion of PPARδ using siRNA generated the reduction of cTnI phosphorylation in cardiomyocytes treated with dobutamine. Thus, we concluded that PPARδ is increased by dobutamine in cardiac cells