Reciprocal Change Research Articles

Significado clínico de los cambios recíprocos del segmento ST en pacientes con IAMCEST: estudio de imagen con resonancia magnética cardiaca

Introduction and objectivesWe sought to determine the association of reciprocal change in the ST-segment with myocardial injury assessed by cardiac magnetic resonance (CMR) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). MethodsWe performed CMR imaging in 244 patients who underwent primary PCI for their first STEMI; CMR was performed a median 3 days after primary PCI. The first electrocardiogram was analyzed, and patients were stratified according to the presence of reciprocal change. The primary outcome was infarct size measured by CMR. Secondary outcomes were area at risk and myocardial salvage index. ResultsPatients with reciprocal change (n=133, 54.5%) had a lower incidence of anterior infarction (27.8% vs 71.2%, P < .001) and shorter symptom onset to balloon time (221.5±169.8 vs 289.7±337.3min, P=.042). Using a multiple linear regression model, we found that patients with reciprocal change had a larger area at risk (P=.002) and a greater myocardial salvage index (P=.04) than patients without reciprocal change. Consequently, myocardial infarct size was not significantly different between the 2 groups (P=.14). The rate of major adverse cardiovascular events, including all-cause death, myocardial infarction, and repeat coronary revascularization, was similar between the 2 groups after 2 years of follow-up (P=.92). ConclusionsReciprocal ST-segment change was associated with larger extent of ischemic myocardium at risk and more myocardial salvage but not with final infarct size or adverse clinical outcomes in STEMI patients undergoing primary PCI.Full English text available from: www.revespcardiol.org/en

Postoperative Change of Thoracic Kyphosis after Corrective Surgery for Adult Spinal Deformity.

Introduction Correction of lumbar lordosis is the primary goal of surgical treatment of adult spinal deformity. However, only limited research has evaluated the effects of this correction on the adaptive curvature of the thoracic spine. The purpose of this study is to evaluate the change in thoracic curvature after corrective surgery to restore lumbar lordosis in patients with adult spinal deformity. Methods We completed a retrospective analysis of the radiological data of 65 patients, ≥50 years old, who underwent corrective surgery of lumbar spine lordosis from any level below T8 to the ilium. Patients with insufficient correction, defined by a pelvic incidence minus lumbar lordosis angle (PI-LL) > 10°, were excluded, with the data of 43 patients included in the analysis. The following radiological measures of spinal alignment were measured at three time points, preoperatively, on the first day of standing postoperatively and at 2 years post-surgery: sagittal vertical axis (SVA), lumbar lordosis (LL), thoracic kyphosis (TK), pelvic tilt (PT), and PI-LL. Results Postoperative change in TK was correlated to preoperative TK and age. The increase in TK was larger for patients <75 years of age, increasing from 23.1° to 38.0° after surgery and to 46.7° at 2-years postoperatively. In contrast, for patients >75 years, TK remained largely unchanged at 37.8° just after surgery but increased substantively to 50.1° at the 2-year follow-up. The postoperative change in TK immediately after surgery was determined using equation “predict change in TK = −0.21 × age − 0.6 × preoperative TK + 41.8” by multiple regression analysis. Conclusions Reciprocal change in TK after lumbar spine correction is correlated to preoperative TK and age.

Oxidative damage mediated iNOS and UCP-2 upregulation in rat brain after sub-acute cyanide exposure: dose and time-dependent effects

Cyanide-induced chemical hypoxia is responsible for pronounced oxidative damage in the central nervous system. The disruption of mitochondrial oxidative metabolism has been associated with upregulation of uncoupling proteins (UCPs). The present study addresses the dose- and time-dependent effect of sub-acute cyanide exposure on various non-enzymatic and enzymatic oxidative stress markers and their correlation with inducible-nitric oxide synthase (iNOS) and uncoupling protein-2 (UCP-2) expression. Animals received (oral) triple distilled water (vehicle control), 0.25 LD50 potassium cyanide (KCN) or 0.50 LD50 KCN daily for 21 d. Animals were sacrificed on 7, 14 and 21 d post-exposure to measure serum cyanide and nitrite, and brain malondialdehyde (MDA), reduced glutathione (GSH), glutathione disulfide (GSSG), cytochrome c oxidase (CCO), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and catalase (CA) levels, together with iNOS and UCP-2 expression, and DNA damage. The study revealed that a dose- and time-dependent increase in cyanide concentration was accompanied by corresponding CCO inhibition and elevated MDA levels. Decrease in GSH levels was not followed by reciprocal change in GSSG levels. Diminution of SOD, GPx, GR and CA activity was congruent with elevated nitrite levels and upregulation of iNOS and UCP-2 expression, without any DNA damage. It was concluded that long-term cyanide exposure caused oxidative stress, accompanied by upregulation of iNOS. The upregulation of UCP-2 further sensitized the cells to cyanide and accentuated the oxidative stress, which was independent of DNA damage.

Estrogen‐related Receptor α Overexpression Drives a Metabolic and Gene Expression Program Mimicking Aerobic Exercise in Skeletal Muscle

Aerobic exercise is considered one of the most effective interventions to prevent obesity and type 2 diabetes (T2D). Exercise increases skeletal muscle insulin sensitivity by stimulating mitochondrial respiration and fatty acid oxidation through coordinated regulation of metabolic genes. Transcriptional pathways that regulate exercise‐induced metabolic gene programs present an attractive class of therapeutic targets to combat obesity and related metabolic diseases. We and others have shown that the Estrogen‐related Receptor α (ERRα) nuclear receptor regulates mitochondrial biogenesis, respiration and fatty acid oxidation and is required for metabolic reprogramming in response to exercise training. The objective of these studies is to determine whether ERRα over‐expression is sufficient to mediate exercise‐induced adaptations in muscle. We generated a conditional ERRα transgenic mouse line that expresses the Flag‐tagged human ERRα in skeletal muscle‐specific manner when crossed with Mck‐Cre recombinase mice (ERRαMOE). We examined gene expression (trancript and protein) and characterized the metabolic phentoype of the ERRαMOE mice. ERRαMOE mice exhibited a reddening of the superficial gastrocnemius and quadriceps, characteristic of oxidative muscles, accompanied by a reciprocal change in myosin heavy chain (MHC) IIb (−35%) and IIa (+80%) expression. Mitochondrial content was higher in skeletal muscle and heart, but not in non‐muscle tissues, based on mtDNA quantitation and citrate synthase protein expression. Consistently, basal (+32%) and maximal (+70%) O2 consumption rates were increased in FDB fibers isolated from ERRα‐MOE compared to WT. Signaling through the AMP‐activated kinase (AMPK) pathway, which mediates exercise‐dependent metabolic reprogramming, was unchanged in the basal state; however, maximal activation by AICAR was enhanced in ERRα‐overexpressing myotubes. We assessed systemic glucose homeostasis in adult chow fed mice. Although fasting glucose (6 hr) was slightly lower in ERRαMOE, no significant difference in glucose tolerance was observed. However, the results of insulin tolerance tests showed that ERRαMOE mice were more insulin sensitive than WT. In future studies we will investigate whether ERRα activation in skeletal muscle protects against high fat diet‐induced insulin resistance. Based on the results from these studies, ERRα over‐expression mimics the effects of exercise on skeletal muscle mitochondrial respiratory capacity and improves whole body insulin sensitivity.Support or Funding InformationSupported by Diabetes and Metabolic Research Institute (DMRI) and Shared Resource Pilot Awards from the City of Hope and NIH U24DK097748This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Clinical Significance of Reciprocal ST-segment Changes in Patients With STEMI: A Cardiac Magnetic Resonance Imaging Study

Introduction and objectivesWe sought to determine the association of reciprocal change in the ST-segment with myocardial injury assessed by cardiac magnetic resonance (CMR) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). MethodsWe performed CMR imaging in 244 patients who underwent primary PCI for their first STEMI; CMR was performed a median 3 days after primary PCI. The first electrocardiogram was analyzed, and patients were stratified according to the presence of reciprocal change. The primary outcome was infarct size measured by CMR. Secondary outcomes were area at risk and myocardial salvage index. ResultsPatients with reciprocal change (n=133, 54.5%) had a lower incidence of anterior infarction (27.8% vs 71.2%, P < .001) and shorter symptom onset to balloon time (221.5±169.8 vs 289.7±337.3min, P=.042). Using a multiple linear regression model, we found that patients with reciprocal change had a larger area at risk (P=.002) and a greater myocardial salvage index (P=.04) than patients without reciprocal change. Consequently, myocardial infarct size was not significantly different between the 2 groups (P=.14). The rate of major adverse cardiovascular events, including all-cause death, myocardial infarction, and repeat coronary revascularization, was similar between the 2 groups after 2 years of follow-up (P=.92). ConclusionsReciprocal ST-segment change was associated with larger extent of ischemic myocardium at risk and more myocardial salvage but not with final infarct size or adverse clinical outcomes in STEMI patients undergoing primary PCI.

T1 Slope Minus Cervical Lordosis (TS-CL), the Cervical Answer to PI-LL, Defines Cervical Sagittal Deformity in Patients Undergoing Thoracolumbar Osteotomy.

Cervical kyphosis and C2-C7 plumb line (CPL) are established descriptors of cervical sagittal deformity (CSD). Reciprocal changes in these parameters have been demonstrated in thoracolumbar deformity correction. The purpose of this study was to investigate the development of CSD, using T1 slope minus cervical lordosis (TS-CL) to define CSD and to correlate TS-CL and a novel global sagittal parameter, cervical-thoracic pelvic angle (CTPA), with CPL. A multicenter, retrospective analysis of patients with thoracolumbar deformity undergoing three-column osteotomy was performed. Preoperative and postoperative cervical parameters were investigated. Linear regression for postoperative values resulted in a CPL of 4 cm corresponding to a TS-CL threshold of 17°. Patients were classified based on postoperative TS-CL into uncompensated (TS-CL > 17°) or compensated cohorts (TS-CL < 17°); the two were compared using an unpaired t test. Logistic regression modeling was used to determine predictors of postoperative CSD. A total of 223 patients with thoracolumbar deformity (mean age, 57.56 years) were identified. CTPA correlated with CPL (preoperative r = .85, postoperative r = .69). TS-CL correlated with CTPA (preoperative r = .52, postoperative r = .37) and CPL (preoperative r = .52; postoperative r = .37). CSD had greater preoperative CPL (P < .001) and CTPA (P < .001). The compensated cohort had a decrease in TS-CL (from 10.2 to 8.0) with sagittal vertical axis (SVA) correction, whereas the uncompensated had an increase in TS-CL (from 22.3 to 26.8) with all P < .001. Reciprocal change was demonstrated in the compensated group given that CL decreased with SVA correction (r = .39), but there was no such correlation in the uncompensated. Positive predictors of postoperative CSD included baseline TS-CL > 17° (P = .007), longer fusion (P = .033), and baseline CTPA (P = .029). TS-CL and CTPA correlated significantly with established sagittal balance measures. Whereas reciprocal change in cervical and thoracolumbar alignment was demonstrated in the compensated cohort, the uncompensated population had progression of their cervical deformities after three-column osteotomy. The balance between TS-CL mirrors the relationship between pelvic incidence minus lumbar lordosis in defining deformities of their respective spinal regions.

Abstract 4192: Targeting SHP-1/p-Lyn signaling shows therapeutic potential in diffuse large B-cell lymphoma

Abstract Background: Diffuse large B cell lymphoma (DLBCL) is one aggressive form of non-Hodgkin’s lymphoma. Genetic analyses revealed molecular heterogeneity of DLBCL tumors, classifying the cell-of-origin into two distinct molecular subtypes: germinal center B-cell (GCB) and activated B-cell (ABC). ABC-type DLBCL has a worse survival after upfront chemotherapy compared to GCB-type DLBCL, thus ABC-type DLBCL patients have an unmet medical need that warrants additional research efforts and new therapeutic options. In current study we explored the biological role and potential therapeutic implication of a protein phosphatase SHP-1 in DLBCL. Methods: DLBCL cell lines including ABC-like cell lines U2932, Ly-3 and GC-like cell lines DHL-6, Ly-7 and DB were used for in vitro studies. Cell viability was examined by MTT assay. Apoptotic effects were examined by flow cytometry and Western blot. Signal transduction pathways in cells were assessed by Western blot. In vivo therapeutic testing of SHP-1 agonists were performed in nude mice with DLBCL xenografts. Results: We first examined the protein expression of SHP-1 and its downstream p-STAT3 in a panel of DLBCL cell lines, and identified in general SHP-1/p-STAT3 expression was higher in ABC-like cells. Interestingly, the expressions of p-Lyn (Tyr396), p-BTK (Tyr223), key members of B-cell receptor (BCR) signaling pathway, were also higher in ABC-like cells. Knockdown or overexpression of SHP-1 protein expression revealed a reciprocal change of p-Lyn, suggesting SHP-1 negatively regulates phosphorylation of Lyn kinase. Immunoprecipitation experiments confirmed SHP-1 interact with Lyn in DLBCL cells. We previously developed direct SHP-1 agonists, namely SC-43 and SC-60, which could increase SHP-1 activities and induce apoptosis. Here we tested SC-43 and SC-60 in comparison to ibrutinib, a selective Bruton's tyrosine kinase (BTK) inhibitor. The SHP-1 agonists showed in general superior anti-proliferative and apoptotic effects, comparing to ibrutinib. Mechanistically, SHP-1 agonists enhanced SHP-1 activity, decreased BCR signaling p-Lyn and p-BTK, which led to apoptosis. In addition, SHP-1 agonists also down-regulated p-STAT3 as previously reported, which also contributes to anti-cancer effects. In vivo, SC-43 at doses of 10mg/kg/day and 30mg/kg/day orally showed comparable anti-tumor effects with ibrutinib at doses of 12.5 mg/kg/day and 25 mg/kg/day in mice bearing U2932 xenografts, respectively. Western blot confirmed SC-43 downregulation on p-Lyn and p-BTK in vivo. Conclusions: SHP-1 negatively regulates phosphorylation of Lyn, and targeting SHP-1/p-Lyn with direct SHP-1 agonists shows therapeutic potential in DLBCL. Citation Format: Chun-Yu Liu, Man-Hsin Hung, Ming-Hsien Tsai, Pei-Yi Chu, Tzu-Ting Huang, Chun-Teng Huang, Chung-Wai Shiau, Kuen-Feng Chen. Targeting SHP-1/p-Lyn signaling shows therapeutic potential in diffuse large B-cell lymphoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4192. doi:10.1158/1538-7445.AM2017-4192

Risk score to predict false-positive ST-segment elevation myocardial infarction in the emergency department: a retrospective analysis

BackgroundThe best treatment approach for ST-segment elevation myocardial infarction (STEMI) is prompt primary percutaneous coronary intervention (PCI). However, some patients show ST elevation on electrocardiography (ECG), but do not have myocardial infarction. We sought to identify the frequency of and to develop a prediction model for false-positive STEMI.MethodsThis study was conducted in the emergency departments (EDs) of two hospitals using the same critical pathway (CP) protocol to treat STEMI patients with primary PCI. The prediction model was developed in a derivation cohort and validated in internal and external validation cohorts.ResultsOf the CP-activated patients, those for whom ST elevation did not meet the ECG criteria were excluded. Among the patients with appropriate ECG patterns, the incidence of false-positive STEMI in the entire cohort was 16.3%. Independent predictors extracted from the derivation cohort for false-positive STEMI were age < 65 years (odds ratio [OR], 2.54; 95% confidence interval [CI], 1.35–4.89), no chest pain (OR, 12.04; 95% CI, 5.92–25.63), atypical chest pain (OR, 7.40; 95% CI, 3.27–17.14), no reciprocal change (OR, 4.80; 95% CI, 2.54–9.51), and concave-morphology ST elevation (OR, 14.54; 95% CI, 6.87–34.37). Based on the regression coefficients, we established a simplified risk score. In the internal and external validation cohorts, the areas under the receiver operating characteristic curves for our risk score were 0.839 (95% CI, 0.724–0.954) and 0.820 (95% CI, 0.727–0.913), respectively; the positive predictive values were 40.9% and 22.0%, respectively; and the negative predictive values were 94.9% and 96.7%, respectively.DiscussionOur prediction model would help them make rapid decisions with better rationale.ConclusionWe devised a model to predict false-positive STEMI. Larger-scale validation studies are needed to validate our model, and a prospective study to determine whether this model is effective in reducing improper primary PCI in actual clinical practice should be performed.

The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.

Chd1 (Chromodomain Helicase DNA Binding Protein 1) is a conserved ATP-dependent chromatin remodeler that maintains the nucleosomal structure of chromatin, but the determinants of its specificity and its impact on gene expression are not well defined. To identify the determinants of Chd1 binding specificity in the yeast genome, we investigated Chd1 occupancy in mutants of several candidate factors. We found that several components of the PAF1 transcription elongation complex contribute to Chd1 recruitment to highly transcribed genes and identified Spt4 as a factor that appears to negatively modulate Chd1 binding to chromatin. We discovered that CHD1 loss alters H3K4me3 and H3K36me3 patterns throughout the yeast genome. Interestingly, the aberrant histone H3 methylation patterns were predominantly observed within 1 kb from the transcription start site, where both histone H3 methylation marks co-occur. A reciprocal change between the two marks was obvious in the absence of Chd1, suggesting a role for CHD1 in establishing or maintaining the boundaries of these largely mutually exclusive histone marks. Strikingly, intron-containing genes were most susceptible to CHD1 loss and exhibited a high degree of histone H3 methylation changes. Intron retention was significantly lower in the absence of CHD1, suggesting that CHD1 function as a chromatin remodeler could indirectly affect RNA splicing.

Celebrating Afropolitan Identities? Contemporary African World Literatures in English

AbstractAgainst the background of today’s debate on Afropolitanism, this article discusses three contemporary African novels as instances of world literatures, focusing on their creative modelling of open, non-Eurocentric worlds in motion. Taking existing research in the field of world literature into account, we argue that the affective and effective uniqueness of world literatures only comes to the fore when considering their distinct power to creatively make worlds. We suggest understanding world literatures in terms of their capacity to create open, polycentric worlds, which enmesh diverse places, multiple temporalities, situated practices and locally grounded experiences into open networks of reciprocal change. In theorizing world literatures as pluralized and multiple, we also try to overcome the privileging of western literature. The final section negotiates how these imaginative worlds interact, intersect and possibly collide with that world which is configured by labelling, marketing and canonizing a specific text as ‘world literature’.

急性心筋梗塞における reciprocal ST change の評価

急性心筋梗塞における reciprocal ST change の評価

Coexistence of Diffuse Panbronchiolitis and Asthma: Reciprocal Change Between Neutrophilic and Eosinophilic Inflammation

Coexistence of Diffuse Panbronchiolitis and Asthma: Reciprocal Change Between Neutrophilic and Eosinophilic Inflammation

MED28 Regulates Epithelial-Mesenchymal Transition Through NFκB in Human Breast Cancer Cells.

MED28, a mammalian Mediator subunit, was found highly expressed in several types of malignancy, including breast cancer. Recently, we have identified a role of MED28 in regulating both cell growth and migration in human breast cancer cells. In epithelium-derived solid tumor, migration and invasion are preceded by the progression of epithelial-mesenchymal transition (EMT) which calls for downregulation of epithelial markers as well as upregulation of mesenchymal markers, among other features. The objective of this study was to investigate a putative role of MED28 in the progression of EMT in human breast cancer cells. In fibroblast-like MDA-MB-231 cells, suppression of MED28 attenuated the mesenchymal morphology, concomitantly with a reduction of several mesenchymal biomarkers and Snail, a transcriptional repressor of E-cadherin. The suppression effect was also accompanied by downregulation of p-NFκB/p65. However, overexpression of MED28 exhibited in an opposite manner. In epithelial MCF7 cells, administration of Adriamycin®, an experimental EMT induction system, led to a mesenchyme-like appearance correlated with increased expression of MED28, p-p65, and Snail, and a reciprocal change of epithelial and mesenchymal markers. Furthermore, suppression of MED28 attenuated the experimental EMT effect and restored the original expression status of E-cadherin and MMP9 in MCF7 cells. Our data indicate that MED28 modulates the development of EMT through NFκB in human breast cancer cells, further reinforcing the significance of MED28 in the progression of breast cancer on top of its role in cell growth and migration. J. Cell. Physiol. 232: 1337-1345, 2017. © 2016 Wiley Periodicals, Inc.

The role of astroglial proteins in the brains of rats under the influence of doxorubicin and Humilid

Doxorubicin causes toxic side effects which result in profound changes in various organs including the heart muscle, which leads to the development of cardiomyopathy, with further complications, as our earlier studies have shown. But there are complications in treatment by anthracycline chemotherapy. The reduction of toxicity of cytotoxic drugs without reduction of their antitumor action remains an important medical challenge. The S-100b and glial fibrillar acid protein (GFAP) are the key astroglial proteins which are widely used as biomarkers for neurotraumas and strokes. Thus the purpose of our work was to study the GFAP and S-100b levels under the experimental model of doxorubicin-induced cardiomyopathy and the effect of the cytostatic separately or combined with Humilid. The level of studied proteins was measured by ELISA using monospecific antibodies against GFAP and S-100b (Sigma, USA), secondary anti-IgG labeled with horseradish peroxidase (Sigma, USA) and GFAP and S-100b standards (Sigma, USA). The experiment was conducted on white Wistar male rats weighing 210 ±50 g, which were divided into 3 groups with 8 animals in each: 1 – control, rats received saline i/p, 2 – doxorubicin 1 mg/kg i/p once weekly during 4 weeks, 3 – doxorubicin by the same scheme plus 0.01% solution of Humilid during 4 weeks. Under impact of doxorubicin an increase of fibrillar GFAP content in the rats’ hippocampus was shown, which may have occurred as a result of the proliferation of astrocytes. An increase of concentration of S-100b to 20–26% compared with the control animals was also detected in the hippocampus, thalamus and the cerebral cortex of the studied animals. Concomitant administration of doxorubicin with Humilid partially prevented the increase in concentration of GFAP and S-100b in the rats’ hippocampus. The reciprocal change in the level of S-100b and GFAP in the peripheral nervous system of the heart tissue was defined with a high degree of correlation under impact of doxorubicin. Accordingly, we have proposed the hypothesis that the increase in of the filament GFAP in the hippocampus may occur due to the development of the ischemic state under the impact of doxorubicin-induced cardiomyopathy. Humilid with doxorubicin prevented changes in the researched astroglial proteins of the heart muscle and brain parts of rats.

Methodological Considerations for Development of Research Support Systems

The article introduces the development of research support systems (RSS) as a special form of information systems (IS) development. Building on experiences from a concrete case several crucial differences between RSS development and development of conventional business support systems (BSS) are identified. So, development for RSS means less of mission and more of continues collaboration, less of producing and more of reciprocal learning and social change. It also involves an expanded universe of discourse that requires support more from an IS researcher and less of a conventional IS-developer. Further, there are issues of ethics and funding that makes RSS development extra challenging. All this represents a shift in focus away from How to do things, toward, What things to do. The article is closed with some tentative guidelines for RSS development. Those include preparing, learning, working arena, anticipatory acting, prototyping and stepwise improvement and scrutiny.

MiR-29a differentially regulates cell survival in astrocytes from cornu ammonis 1 and dentate gyrus by targeting VDAC1

Neurons in the cornu ammonis 1 (CA1) region of the hippocampus are vulnerable to cerebral ischemia, while dentate gyrus (DG) neurons are more resistant. This effect is mediated by local astrocytes, and may reflect differences in subregional hippocampal expression of miR-29a. We investigated the role of miR-29a on survival of hippocampal astrocytes cultured selectively from CA1 and DG in response to glucose deprivation (GD). CA1 astrocytes exhibited more cell death and a greater decrease in miR-29a than DG astrocytes. A reciprocal change was observed in the mitochondrial voltage dependent cation channel-1 (VDAC1), a regulator of mitochondria and target of miR-29a. In CA1 astrocytes, increasing miR-29a decreased VDAC1 and improved cell survival, while knockdown of VDAC1 improved survival. Finally, the protective effect of miR-29a was eliminated by inhibition of miR-29a/VDAC1 binding. These findings suggest that the selective vulnerability of the CA1 to injury may be due in part to a limited miR-29a response in CA1 astrocytes, allowing a greater increase in VDAC1-mediated cellular dysfunction in CA1 astrocytes.

AMPKα1

With our increasingly aged and dysmetabolic population, the deleterious consequences of globally perturbed calcium metabolism become increasingly apparent.1 Net loss of bone mineral quantity and quality increases risk for osteoporotic fracture,2 whereas accumulating arterial calcium loads stiffen conduit arteries and impairs Windkessel physiology—the rubbery elasticity of conduit vessels that ensures smooth distal tissue perfusion throughout the cardiac cycle.3 Murine models were first used to identify that reciprocal change in skeletal versus vascular calcium accrual can occur in response to the dysmetabolic states of diabetes mellitus, uremia, and dyslipidemia4. However, the Multiethnic Study of Atherosclerosis (MESA) firmly established the general connection between accrual of metabolic syndrome parameters—impaired fasting glucose, hypertension, obesity, low high-density lipoprotein, hypertriglyceridemia, or frank type 2 diabetes mellitus (T2D)—and arterial calcium load in humans.5 Recent studies implementing high-resolution peripheral quantitative computed tomography have shown that older men and women with T2D exhibit greater cortical bone porosity—a feature that compromises bone strength and increases fracture risk.6,7 Patients with calcified peripheral arterial disease also exhibit deficiencies in trabecular bone structure on high-resolution peripheral quantitative computed tomography, further solidifying the relationship.8 Elegant human genetic studies by Mani et al9 highlighted that osteoporosis–atherosclerosis relationships are genetically determined in part by LRP6 signaling—with the cell-autonomous (osteoblast and vascular smooth muscle) contributions of …

Reflection for learning, learning for reflection: Developing Indigenous competencies in higher education

Reflection is an essential part of students’ critically reflective development within experiential-learning contexts; it is arguably even more important when working cross-culturally. This paper reports from a national, arts-based service-learning project in which students in creative arts, media and journalism, and pre-service teachers worked with Aboriginal people in urban and rural areas of Australia. The paper uses Ryan and Ryan’s (2010) 4Rs model of reflective thinking for reflective learning and assessment in higher education to ascertain the effectiveness of the project work toward engendering a reflective mindset. The paper discusses how students learned to engage in critical self-monitoring as they attended to their learning experiences, and it describes how they “wrote” their experiences and shaped their professional identities as they developed and refined the philosophy that related to their developing careers. Examples taken from the narratives of students, community partners and academic team members illustrate the principal finding, which is that through a process of guided reflection, students learned to reflect in three stages: a preliminary drawing out of existing attitudes and expectations; a midway focus on learning from and relating to past experiences; and a final focus on reciprocal learning, change and future practice. The three stages were apparent regardless of program duration. Thus, program phase rather than academic year level emerged as the most important consideration when designing the supports that promote and scaffold reflection.

Reflection for Learning, Learning for Reflection: Developing Indigenous Competencies in Higher Education.

Reflection is an essential part of students’ critically reflective development within experiential-learning contexts; it is arguably even more important when working cross-culturally. This paper reports from a national, arts-based service-learning project in which students in creative arts, media and journalism, and preservice teachers worked with Aboriginal people in urban and rural areas of Australia. The paper uses Ryan and Ryan’s (2010) 4Rs model of reflective thinking for reflective learning and assessment in higher education to ascertain the effectiveness of the project work toward engendering a reflective mindset. The paper discusses how students learned to engage in critical self-monitoring as they attended to their learning experiences, and it describes how they “wrote” their experiences and shaped their professional identities as they developed and refined the philosophy that related to their developing careers. Examples taken from the narratives of students, community partners and academic team members illustrate the principal finding, which is that through a process of guided reflection, students learned to reflect in three stages: a preliminary drawing out of existing attitudes and expectations; a midway focus on learning from and relating to past experiences; and a final focus on reciprocal learning, change and future practice. The three stages were apparent regardless of program duration. Thus, program phase rather than academic year level emerged as the most important consideration when designing the supports that promote and scaffold reflection. This journal article is available in Journal of University Teaching & Learning Practice: http://ro.uow.edu.au/jutlp/vol13/iss2/7 Reflection for learning, learning for reflection: Developing Indigenous competencies in higher education Dawn Bennett, Curtin University, dawn.bennett@curtin.edu.au Anne Power, Western Sydney University Chris Thomson, Curtin University Bonita Mason, Curtin University Brydie-Leigh Bartleet, Griffith University

Theory of relativity in quaternion spinors

It is shown that the theory of relativity, apart from the standard format and the comparatively new quaternion formulation, can also be presented in terms of quaternion spinors. Mathematically, the spinor format is fundamental while technically it is primitive since it links transformations of reference frames (including non-inertial frames) with an instant rotation of a unique vector “about itself.” Such a rotation in its turn can be regarded as a reciprocal change of scales of two orthogonal directions on a 2D plane, in general, a complex number valued one. This allows for considering any transformation of relative groups SO(3,ℂ) and SL(2,ℂ) and the localized Lorentz group as a deformations of the fractal (pregeometric) spin surface.