Self-assessment resource for EAL pre-service and in-service teachers and EAL K-16 educators in the MENA region

The purpose of this session is to describe and share sample items of a contextually relevant resource developed specifically for English as an Additional Language (EAL) student-teachers and EAL teachers in the Middle East and North Africa (MENA). Fifteen EAL and teacher/education academics created, reviewed and piloted the 300 multiple-choice-item resource. The resource supports teachers\u27 lifelong learning and measures their progress in applying strategies, methods, and theories in EAL teaching/learning in the five TESOL International domains: language foundations, culture, instruction, assessment and professionalism (2010). The resource supports EAL outcomes-based curricula and reinforces independent learning and self-assessment to improve EAL professional content knowledge, professional pedagogical skills and professional disposition. If used effectively, the self-assessment resource can be a powerful learning tool. This resource allows EAL student teachers and EAL teachers to engage in self assessing i..

Influence of oxygen on vascular tone during acute hypoxia

It is well acknowledged that molecular oxygen (O2) constricts vascular tissue under physiological conditions. In hypoxia, the decrease in partial pressure of O2 (pO2) within the tissue may be due to either a reduction in O2 supply or an increased O2 demand. The pulmonary circulation responds to a decrease in O2 by inducing vasoconstriction, whereas the systemic circulation induces vasorelaxation. Systemic vasorelaxation in hypoxia occurs by one of two presumed mechanisms, direct, in which smooth muscle cells can no longer sustain adequate contraction, or indirect, in which vasodilatory molecules are produced. Since the early 1990’s, several laboratories worldwide hypothesised that the vasodilatory molecules released under hypoxic conditions originated from the red blood cell (RBC). Several mechanisms have been proposed to date, including nitrite (NO2-) reduction by haemoglobin (Hb) to nitric oxide (NO), S-nitrosation of Hb to S-nitrosohaemoglobin (HbSNO) and adenosine triphosphate (ATP) binding to P2Y receptors on the vascular endothelium. Although there has been extensive research within this field, a clear mechanism by which vasorelaxation occurs is yet to be fully elucidated. Therefore, the aims of this thesis were to determine the vasodilatory specie(s) released from RBCs and the mechanism by which vasorelaxation occurs. Myography experiments were conducted using dissected rabbit thoracic aortae. Rings were equilibrated at various O2 concentrations, directly influencing tissue pO2. Bolus administration of oxygenated RBCs, isolated Hb or Krebs-Henseleit (KH) buffer to pre-constricted hypoxic rings induced a transient relaxation which was immediately followed by a post-constriction of equivalent magnitude. Interestingly, oxygenated KH buffer alone could induce relaxation of aortic rings in a similar manner to RBCs and Hb, demonstrating that O2 itself relaxes hypoxic vascular tissue. In addition, the extent of vasorelaxation was inversely related to the tissue pO2. Oxygenated KH buffer alone induced vasorelaxation in hypoxic pre-constricted rings pre-incubated with NOS inhibitor, L-NMMA, indicating an endothelium-independent mechanism. Subsequent experiments investigated the role of soluble guanylate cyclase (sGC) in the context of these findings. A number of studies have shown that sGC does not bind O2. However, the results present herein demonstrate that O2 can stimulate an enhanced activity of soluble guanylate cyclase (sGC), increasing the production of cyclic guanosine monophosphate (cGMP). Importantly, this could occur in the absence of NO but was found to be dependent upon the presence of haem. In order to compare O2-induced vasorelaxation in a vessel with an alternative function, the left anterior descending (LAD) artery was dissected from porcine hearts. Hypoxic pre-constricted LAD rings relaxed 20% more to a bolus of oxygenated RBCs or KH buffer compared to rabbit aortic rings and this was not due to an increased expression of sGC within the smooth muscle. Further experiments aimed to show whether vessel size had an effect upon the magnitude of O2-induced vasorelaxation in hypoxia. O2 induced a greater vasorelaxation in rings of smaller inner diameter. In conclusion, the results within this thesis show a direct relaxant effect of O2 that is mediated via the sGC-cGMP pathway and suggest a role for O2 in response of vascular smooth muscle in acute hypoxia

Measurements in two bases are sufficient for certifying high-dimensional entanglement

High-dimensional encoding of quantum information provides a promising method of transcending current limitations in quantum communication. One of the central challenges in the pursuit of such an approach is the certification of high-dimensional entanglement. In particular, it is desirable to do so without resorting to inefficient full state tomography. Here, we show how carefully constructed measurements in two bases (one of which is not orthonormal) can be used to faithfully and efficiently certify bipartite high-dimensional states and their entanglement for any physical platform. To showcase the practicality of this approach under realistic conditions, we put it to the test for photons entangled in their orbital angular momentum. In our experimental setup, we are able to verify 9-dimensional entanglement for a pair of photons on a 11-dimensional subspace each, at present the highest amount certified without any assumptions on the state.Comment: 11+14 pages, 2+7 figure

Oxygen mediates vascular smooth muscle relaxation in hypoxia.

The activation of soluble guanylate cyclase (sGC) by nitric oxide (NO) and other ligands has been extensively investigated for many years. In the present study we considered the effect of molecular oxygen (O2) on sGC both as a direct ligand and its affect on other ligands by measuring cyclic guanosine monophosphate (cGMP) production, as an index of activity, as well as investigating smooth muscle relaxation under hypoxic conditions. Our isolated enzyme studies confirm the function of sGC is impaired under hypoxic conditions and produces cGMP in the presence of O2, importantly in the absence of NO. We also show that while O2 could partially affect the magnitude of sGC stimulation by NO when the latter was present in excess, activation by the NO independent, haem-dependent sGC stimulator 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1) was unaffected. Our in vitro investigation of smooth muscle relaxation confirmed that O2 alone in the form of a buffer bolus (equilibrated at 95% O2/5% CO2) had the ability to dilate vessels under hypoxic conditions and that this was dependent upon sGC and independent of eNOS. Our studies confirm that O2 can be a direct and important mediator of vasodilation through an increase in cGMP production. In the wider context, these observations are key to understanding the relative roles of O2 versus NO-induced sGC activation

Krebs buffer samples introduced to hypoxic aortic rings.

<p>Maximum relaxation was demonstrated with 95% oxygenated buffer samples compared with 0% O₂ samples (all n = 6, **p<0.01 cf. 0%).</p

NO liberation from NOC-9 under normoxic versus hypoxic conditions.

<p>Gas and liquid samples drawn up from reaction vessels incubated with varying concentrations of NOC-9, were injected into the NOA. The solutions were either equilibrated at 0 or 95% O₂/5% CO₂ prior to the addition of NOC-9. There was no difference in the total NO detected in either gas or liquid samples under (n = 3, p<0.05).</p

The effect of sGC inhibitor, ODQ, upon O₂-mediated relaxation.

<p>In the presence of ODQ (10 µmol/L) the relaxation response to 95% oxygenated buffer was almost completely inhibited (both n = 7, ***p<0.001 cf. control).</p