Using student self-assessment to steer feedback

BACKGROUND Students might better engage with feedback if they are responsible for steering the feedback process. However, this requires them to first accurately assess the quality of their work. AIMS To determine whether providing students with a structured self-assessment method prior to submission influences their confidence with this process. DESCRIPTION OF INTERVENTION Students were asked to complete a brief self-assessment of one of their laboratory reports, which markers then used to guide their feedback to each student. DESIGN AND METHODS Participants were undergraduate students undertaking a second-year pharmacology unit in semester 2, 2018 (n=117/265 enrolled). Students were invited to complete an anonymous survey asking them about their perceptions of self-assessment. RESULTS 55% of respondents indicated that they found feedback useful following self-assessment. Of these respondents, 54% indicated that being able to first specify areas of difficulty was the reason why. However, 34% of all respondents indicated that they still lacked confidence in accurately evaluating their work. CONCLUSIONS Students’ lack of confidence in their ability to self-evaluate suggests that perhaps they are not given sufficient opportunity to practice this skill. Although our current model could be extended into any setting, the value of self-evaluation first needs to be understood by students in order to promote their full engagement with this process

Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension.

Recent studies have emphasized the role of perivascular inflammation in cardiovascular disease. We studied mechanisms of perivascular leukocyte infiltration in angiotensin II (Ang II)-induced hypertension and their links to vascular dysfunction. Chronic Ang II infusion in mice increased immune cell content of T cells (255 ± 130 to 1664 ± 349 cells/mg; P \u3c 0.01), M1 and M2 macrophages, and dendritic cells in perivascular adipose tissue. In particular, the content of T lymphocytes bearing CC chemokine receptor (CCR) 1, CCR3, and CCR5 receptors for RANTES chemokine was increased by Ang II (CCR1, 15.6 ± 1.5% vs. 31 ± 5%; P \u3c 0.01). Hypertension was associated with an increase in perivascular adipose tissue expression of the chemokine RANTES (relative quantification, 1.2 ± 0.2 vs. 3.5 ± 1.1; P \u3c 0.05), which induced T-cell chemotaxis and vascular accumulation of T cells expressing the chemokine receptors CCR1, CCR3, and CCR5. Mechanistically, RANTES(-/-) knockout protected against vascular leukocyte, and in particular T lymphocyte infiltration (26 ± 5% in wild type Ang II vs. 15 ± 4% in RANTES(-/-)), which was associated with protection from endothelial dysfunction induced by Ang II. This effect was linked with diminished infiltration of IFN-γ-producing CD8(+) and double-negative CD3(+)CD4(-)CD8(-) T cells in perivascular space and reduced vascular oxidative stress while FoxP3(+) T-regulatory cells were unaltered. IFN-γ ex vivo caused significant endothelial dysfunction, which was reduced by superoxide anion scavenging. In a human cohort, a significant inverse correlation was observed between circulating RANTES levels as a biomarker and vascular function measured as flow-mediated dilatation (R = -0.3, P \u3c 0.01) or endothelial injury marker von Willebrand factor (R = +0.3; P \u3c 0.01). Thus, chemokine RANTES is important in the regulation of vascular dysfunction through modulation of perivascular inflammation.-Mikolajczyk, T. P., Nosalski, R., Szczepaniak, P., Budzyn, K., Osmenda, G., Skiba, D., Sagan, A., Wu, J., Vinh, A., Marvar, P. J., Guzik, B., Podolec, J., Drummond, G., Lob, H. E., Harrison, D. G., Guzik, T. J. Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension

Assessment literacy: Exploring institutional, teacher and student perspectives

BACKGROUND Assessment literacy is students’ understanding of the purpose and process of assessment, the ability to judge/evaluate their response to assessments, identify strengths/weaknesses and strategies to improve their work. Engaging students with activities that foster assessment literacy enhances learning potential and ensures development/demonstration of attributes necessary for work and lifelong learning. AIMS Explore to what extent we provide students opportunities to develop assessment literacy. DESIGN AND METHODS We gathered institutional, staff and student data from final-year units in five courses. By developing a tool based on Monash’s Assessment Framework1, we mapped all assessments to identify the extent to which literacies are developed. Through staff interviews we investigated strategies adopted to develop assessment literacy, and surveyed students to explore their perspectives on assessment literacy. RESULTS Our tool effectively mapped assessment types, highlighting range, gaps and areas for improvement. Staff interviews revealed that strategies applied were course-specific, with vocational courses employing more career-focused assessments. Overall, final-year students demonstrated attributes associated with assessment literacy, critical for developing evaluative judgement. CONCLUSIONS Our systematic approach to mapping assessment literacy could potentially be applied to any course in order to ensure that assessments are fit for purpose. 1Monash Assessment Vision: http://www.intranet.monash/learningandteaching/learningandteachingquality/assessment-visio

Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension

Recent studies have emphasized the role of perivascular inflammation in cardiovascular disease. We studied mechanisms of perivascular leukocyte infiltration in angiotensin II (Ang II)-induced hypertension and their links to vascular dysfunction. Chronic Ang II infusion in mice increased immune cell content of T cells (255 ± 130 to 1664 ± 349 cells/mg; P < 0.01), M1 and M2 macrophages, and dendritic cells in perivascular adipose tissue. In particular, the content of T lymphocytes bearing CC chemokine receptor (CCR) 1, CCR3, and CCR5 receptors for RANTES chemokine was increased by Ang II (CCR1, 15.6 ± 1.5% vs. 31 ± 5%; P < 0.01). Hypertension was associated with an increase in perivascular adipose tissue expression of the chemokine RANTES (relative quantification, 1.2 ± 0.2 vs. 3.5 ± 1.1; P < 0.05), which induced T-cell chemotaxis and vascular accumulation of T cells expressing the chemokine receptors CCR1, CCR3, and CCR5. Mechanistically, RANTES−/− knockout protected against vascular leukocyte, and in particular T lymphocyte infiltration (26 ± 5% in wild type Ang II vs. 15 ± 4% in RANTES−/−), which was associated with protection from endothelial dysfunction induced by Ang II. This effect was linked with diminished infiltration of IFN-γ-producing CD8+ and double-negative CD3+CD4−CD8− T cells in perivascular space and reduced vascular oxidative stress while FoxP3+ T-regulatory cells were unaltered. IFN-γ ex vivo caused significant endothelial dysfunction, which was reduced by superoxide anion scavenging. In a human cohort, a significant inverse correlation was observed between circulating RANTES levels as a biomarker and vascular function measured as flow-mediated dilatation (R = −0.3, P < 0.01) or endothelial injury marker von Willebrand factor (R = +0.3; P < 0.01). Thus, chemokine RANTES is important in the regulation of vascular dysfunction through modulation of perivascular inflammation.—Mikolajczyk, T. P., Nosalski, R., Szczepaniak, P., Budzyn, K., Osmenda, G., Skiba, D., Sagan, A., Wu, J., Vinh, A., Marvar, P. J., Guzik, B., Podolec, J., Drummond, G., Lob, H. E., Harrison, D. G., Guzik, T. J. Role of chemokine RANTES in the regulation of perivascular inflammation, T-cell accumulation, and vascular dysfunction in hypertension

Kaliningrad Oblast and relations with Poland (crucial aspects)

Celem niniejszej pracy licencjackiej będzie zapoznanie czytelnika z historią kaliningradzkich ziemi, przedstawienie okoliczności przyłączenia Obwodu do Federacji Rosyjskiej oraz zaprezentowanie późniejszych relacji z sąsiadującą Polską, przy uwzględnieniu zmieniających się uwarunkowań politycznych. Obecnie historia regionu kaliningradzkiego jest znana jedynie lokalnej społeczności przygranicznych województw. Tymczasem Obwód Kaliningradzki wciąż odgrywa znaczącą rolę w kształtowaniu polityki europejskiej, w tym polskiej. Zatem istotną kwestią podjętą w tejże pracy dyplomowej będzie odpowiedź na pytanie: Jaka jest rola regionu kaliningradzkiego w rozwoju przygranicznych województw oraz jak wyglądała wzajemna kooperacja polsko-kaliningradzka w okresie 1945-2017?Prezentowane w niniejszej pracy licencjackiej informacje autorka opracowała na podstawie szczegółowej analizy dokumentów, międzypaństwowych umów, traktatów, artykułów naukowych oraz komunikatów z badań. Poszczególne osobiście sporządzone tabele oraz wykresy zostały oparte na podstawie obserwacji dokonanych przez rzetelne ośrodki specjalizujące się w sporządzaniu statystyk: Komendę Główną Straży Granicznej, jej warmińsko-mazurski oddział oraz Ośrodek Studiów Wschodnich.The purpose of this Bachelor's Thesis is to familiarize the reader with: the Kaliningrad region history, the circumstances of the Kaliningrad Oblast annexation to the Russian Federation and subsequent relations with Poland, including the changing political conditions. Currently the history of the Kaliningrad region is known only to the local society of border voivodships. Meanwhile, the Kaliningrad Oblast still plays a significant role in shaping European policy, also the Polish one. Therefore, the crucial point in this Thesis will be the answer to the questions: What is the role of the Kaliningrad region in the development of border voivodships of Poland and how was the Polish-Kaliningrad cooperation structured between 1945-2017? Presented information has been elaborated on the basis of a detailed analysis of documents, international agreements, treaties, scientific articles and research reports. Furthermore, the authoress presented own tables and graphs, based on observations made by reliable centers specializing in statistics: Border Guard Headquarters, its Warmińsko-Mazurskie’s Branch and Center of Eastern Studies

Opposing roles of endothelial and smooth muscle phosphatidylinositol 3-kinase in vasoconstriction: effects of rho-kinase and hypertension. J Pharmacol Exp Ther 313: 1248–1253

ABSTRACT Phosphatidylinositol 3-kinase (PI3K) can activate endothelial nitric oxide synthase (eNOS), leading to production of the vasodilator NO. In contrast, vascular smooth muscle (VSM) PI3K may partially mediate vascular contraction, particularly during hypertension. We tested whether endothelial and VSM PI3K may have opposing functional roles in regulating vascular contraction. Secondly, we tested whether the procontractile protein rho-kinase can suppress endothelial PI3K/eNOS activity in intact arteries, thus contributing to vasoconstriction by G protein-coupled receptor (GPCR) agonists. We studied contractile responses to the GPCR agonist phenylephrine, and the receptor-independent vasoconstrictor KCl, in aortic rings from Sprague-Dawley rats. In endothelium-intact rings, the PI3K inhibitor wortmannin (0.1 M) markedly augmented responses to phenylephrine (P Ͻ 0.05) by ϳ50% but not to KCl. However, in endothelium-denuded or N G -nitro-L-arginine methyl ester (L-NAME) (100 M)-treated rings, wortmannin reduced responses to phenylephrine and KCl (P Ͻ 0.05). Furthermore, the rhokinase inhibitor Y-27632 (R-[ϩ]-trans-N-[4-pyridyl]-4-[1-aminoethyl]-cycloheaxanecarboxamide; 1 M) abolished responses to phenylephrine, and this effect was partially reversed by wortmannin or L-NAME. The ability of wortmannin to oppose the effect of rho-kinase inhibition on contractions to phenylephrine was L-NAME-sensitive. In aortas from angiotensin II-induced hypertensive rats, relaxation to acetylcholine (10 M) was impaired (P Ͻ 0.05), and vasoconstriction by phenylephrine was markedly enhanced and not further augmented by wortmannin. These data suggest that endothelial PI3K-induced NO production can modulate GPCR agonist-induced vascular contraction and that this effect is impaired in hypertension in association with endothelial dysfunction. In addition, endothelial rho-kinase may act to suppress PI3K activity and, hence, attenuate NO-mediated relaxation and augment GPCR-dependent contraction

Partial carotid ligation is a model of acutely induced disturbed flow, leading to rapid endothelial dysfunction and atherosclerosis

Atherosclerosis is closely associated with disturbed flow characterized by low and oscillatory shear stress, but studies directly linking disturbed flow to atherogenesis is lacking. The major reason for this has been a lack of an animal model in which disturbed flow can be acutely induced and cause atherosclerosis. Here, we characterize partial carotid ligation as a model of disturbed flow with characteristics of low and oscillatory wall shear stress. We also describe a method of isolating intimal RNA in sufficient quantity from mouse carotid arteries. Using this model and method, we found that partial ligation causes upregulation of proatherogenic genes, downregulation of antiatherogenic genes, endothelial dysfunction, and rapid atherosclerosis in 2 wk in a p47phox-dependent manner and advanced lesions by 4 wk. We found that partial ligation results in endothelial dysfunction, rapid atherosclerosis, and advanced lesion development in a physiologically relevant model of disturbed flow. It also allows for easy and rapid intimal RNA isolation. This novel model and method could be used for genome-wide studies to determine molecular mechanisms underlying flow-dependent regulation of vascular biology and diseases