Einfach so integriert? : Integration Lernbehinderter nach dem Konzept Schwerpunktschule in Rheinland-Pfalz ; eine Fallstudie

Einfach so integriert? : Integration Lernbehinderter nach dem Konzept &quot;Schwerpunktschule&quot; in Rheinland-Pfalz ; eine Fallstudie <br /> Die Integration beeinträchtigter Schüler in die Sekundarstufe I der Regelschule wird in Rheinland-Pfalz seit dem Schuljahr 2001/2002 nach dem Modell der sog. Schwerpunktschulen betrieben. Die ethnografische Fallstudie einer integrierten Gesamtschule dokumentiert über einen Zeitraum von drei Jahren exemplarisch, welche Entwicklungen im Mikrosystem der Schule für die integrierten lernbehinderten Schüler aus der Sicht der unmittelbar Beteiligten wirksam werden. Generell kommt die Studie zu dem Schluss, dass das untersuchte Umsetzungsmodell einer Schwerpunkt-schule insofern erfolgreich ist, als die lernbehinderten Schüler überwiegend sozial integriert sind, eine angemessene Leistungsentwicklung vollziehen und auch in ihrem Selbstkonzept keine Auffälligkeiten aufweisen, die auf die Integrationssituation zurückgeführt werden könnten. Es zeigt sich auch, dass bei Lehrern die veränderte Unterrichts-situation professionelle Entwicklungs-prozesse in Gang setzen kann. Aus den Untersuchungsergebnissen werden im Anschluss Hinweise für die weitere landesweite Ausgestaltung der Schwerpunktschule abgeleitet.Einfach so integriert? : Integration Lernbehinderter nach dem Konzept &quot;Schwerpunktschule&quot; in Rheinland-Pfalz ; eine Fallstudie <br /> The mainstreaming of handicapped children in secondary schools in Rheinland-Pfalz (a federal state in Germany) has been organized according to a model called Schwerpunktschule since the year of 2001. In this ethnographical case study lasting over a period of three years at a comprehensive school developments which influence the micro system for the mainstreamed learning disabled pupils are documented from different perspectives. Generally speaking the results of the study indicate that the investigated example of Schwerpunktschule is successful for learning disabled pupils as far as social and emotional integration, academic achievement and self-concept are concerned. Moreover it is shown that the modified teaching situation can influence teachers’ professional development. Conclusions from the results of the study draw attention to hints and suggestions for helpful arrangements which can support

Allan Smith--A Personal History

A tribute to Allan Smit

Preferential utilization of NADPH as the endogenous electron donor for NAD(P)H:quinone oxidoreductase 1 (NQO1) in intact pulmonary arterial endothelial cells

The goal was to determine whether endogenous cytosolic NAD(P)H:quinone oxidoreductase 1 (NQO1) preferentially uses NADPH or NADH in intact pulmonary arterial endothelial cells in culture. The approach was to manipulate the redox status of the NADH/NAD+ and NADPH/NADP+ redox pairs in the cytosolic compartment using treatment conditions targeting glycolysis and the pentose phosphate pathway alone or with lactate, and to evaluate the impact on the intact cell NQO1 activity. Cells were treated with 2-deoxyglucose, iodoacetate, or epiandrosterone in the absence or presence of lactate, NQO1 activity was measured in intact cells using duroquinone as the electron acceptor, and pyridine nucleotide redox status was measured in total cell KOH extracts by high-performance liquid chromatography. 2-Deoxyglucose decreased NADH/NAD+ and NADPH/NADP+ ratios by 59 and 50%, respectively, and intact cell NQO1 activity by 74%; lactate restored NADH/NAD+, but not NADPH/NADP+ or NQO1 activity. Iodoacetate decreased NADH/NAD+ but had no detectable effect on NADPH/NADP+ or NQO1 activity. Epiandrosterone decreased NQO1 activity by 67%, and although epiandrosterone alone did not alter the NADPH/NADP+ or NADH/NAD+ ratio, when the NQO1 electron acceptor duroquinone was also present, NADPH/NADP+ decreased by 84% with no impact on NADH/NAD+. Duroquinone alone also decreased NADPH/NADP+ but not NADH/NAD+. The results suggest that NQO1 activity is more tightly coupled to the redox status of the NADPH/NADP+ than NADH/NAD+ redox pair, and that NADPH is the endogenous NQO1 electron donor. Parallel studies of pulmonary endothelial transplasma membrane electron transport (TPMET), another redox process that draws reducing equivalents from the cytosol, confirmed previous observations of a correlation with the NADH/NAD+ ratio

Planetary Fever: Climate Change and the Medical Profession

Climate change is a major challenge facing human societies in the 21st century. In the complexity of its causes and breadth of its consequences, it touches on virtually all dimensions of human existence and social organisation, one of these dimensions being human health. In consideration thereof, members of the medical profession have become engaged in climate activism and advocacy in various forms, from patient communication to direct action efforts. Despite the rise in prominence of these efforts, little attention has been given to this phenomenon within social scientific research on climate change. To address this lacuna, this thesis explores how climate change is constructed, engagement with the issue is given meaning, and the efficacy in the pursuit thereof is understood by medical professional climate activists and advocates. Drawing on in-depth interviews, this work analyses medical climate activism and advocacy through a Bourdieusian framework as a practice unfolding in particular social sites (fields), informed by sets of fundamental presuppositions (doxa), structured in its meaning by dispositions (habitus), and drawing on the operationalisation of particular resources in its pursuit (capital). This analysis shows medical climate activism and advocacy to rest on careful negotiations between—in some parts congruent and others incongruent—medical and radical ecological sensibilities and commitments. This thesis contributes to three distinct efforts. Empirically, it presents an in-depth account that illuminates and positions a contemporary practice of civic engagement on which to date little research exists. Theoretically, it advances the application of Bourdieu’s thinking tools to the sociological study of climate change in particular and negotiated practice at the intersection of different fields more broadly. Practically, it develops suggestions for the facilitation of this engagement by stressing the importance of the social determinants of health model, the congruence of climate concerns and medical practice, and the availability of supportive networks

Characterization of theThreshold for NAD(P)H:quinone Oxidoreductase Activity in Intact Sulforaphane-treated Pulmonary Arterial Endothelial Cells

Treatment of bovine pulmonary arterial endothelial cells in culture with the phase II enzyme inducer sulforaphane (5 μM, 24 h; sulf-treated) increased cell-lysate NAD(P)H:quinone oxidoreductase (NQO1) activity by 5.7 ± 0.6 (mean ± SEM)-fold, but intact-cell NQO1 activity by only 2.8 ± 0.1-fold compared to control cells. To evaluate the hypothesis that the threshold for sulforaphane-induced intact-cell NQO1 activity reflects a limitation in the capacity to supply NADPH at a sufficient rate to drive all the induced NQO1 to its maximum activity, total KOH-extractable pyridine nucleotides were measured in cells treated with duroquinone to stimulate maximal NQO1 activity. NQO1 activation increased NADP+ in control and sulf-treated cells, with the effect more pronounced in the sulf-treated cells, in which the NADPH was also decreased. Glucose-6-phosphate dehydrogenase (G-6-PDH) inhibition partially blocked NQO1 activity in control and sulf-treated cells, but G-6-PDH overexpression via transient transfection with the human cDNA alleviated neither the restriction on intact sulf-treated cell NQO1 activity nor the impact on the NADPH/NADP+ ratios. Intracellular ATP levels were not affected by NQO1 activation in control or sulf-treated cells. An increased dependence on extracellular glucose and a rightward shift in the Km for extracellular glucose were observed in NQO1-stimulated sulf-treated vs control cells. The data suggest that glucose transport in the sulf-treated cells may be insufficient to support the increased metabolic demand for pentose phosphate pathway-generated NADPH as an explanation for the NQO1 threshold

Persuasion, facilitation… contestation?

The causes and consequences of climate change are to varying degrees understood, produced and faced by various societies across the planet. The projected scope of its consequences and the underdetermination thereof causes much public contestation. Scholars of climate change communication express various positions towards the nature of the issue and the purpose of science communicative efforts. Through a literature review of research articles on climate change communication published between 2010 and 2018, I show that top-down approaches to communication based on psychological considerations are frequently argued to provide the necessary response to public uncertainty and disagreement on the issue. Linking these, and other, positions to epistemological and political considerations, I offer a liberal democratic critique of this conception of climate change communication as both ideologically and pragmatically questionable

Depleted Energy Charge and Increased Pulmonary Endothelial Permeability Induced by Mitochondrial Complex I inhibition are Mitigated by Coenzyme Q\u3csub\u3e1\u3c/sub\u3e in the Isolated Perfused Rat Lung

Mitochondrial dysfunction is associated with various forms of lung injury and disease that also involve alterations in pulmonary endothelial permeability, but the relationship, if any, between the two is not well understood. This question was addressed by perfusing isolated intact rat lung with a buffered physiological saline solution in the absence or presence of the mitochondrial complex I inhibitor rotenone (20 μM). Compared to control, rotenone depressed whole lung tissue ATP from 5.66±0.46 (SEM) to 2.34±0.15 µmol·g−1 dry lung, with concomitant increases in the ADP:ATP and AMP:ATP ratios. Rotenone also increased lung perfusate lactate (from 12.36±1.64 to 38.62±3.14 µmol·15 min−1 perfusion·g−1 dry lung) and the lactate:pyruvate ratio, but had no detectable impact on lung tissue GSH:GSSG redox status. The amphipathic quinone coenzyme Q1 (CoQ1; 50 μM) mitigated the impact of rotenone on the adenine nucleotide balance, wherein mitigation was blocked by NAD(P)H-quinone oxidoreductase 1 or mitochondrial complex III inhibitors. In separate studies, rotenone increased the pulmonary vascular endothelial filtration coefficient (Kf) from 0.043±0.010 to 0.156±0.037 ml·min−1·cm H2O−1·g−1 dry lung, and CoQ1 protected against the effect of rotenone on Kf. A second complex I inhibitor, piericidin A, qualitatively reproduced the impact of rotenone on Kf and the lactate:pyruvate ratio. Taken together, the observations imply that pulmonary endothelial barrier integrity depends on mitochondrial bioenergetics as reflected in lung tissue ATP levels and that compensatory activation of whole lung glycolysis cannot protect against pulmonary endothelial hyperpermeability in response to mitochondrial blockade. The study further suggests that low-molecular-weight amphipathic quinones may have therapeutic utility in protecting lung barrier function in mitochondrial insufficiency

Magnetic Dynamics in Underdoped YBa₂Cu₃O₇₋ₓ: Direct Observation of a Superconducting Gap

Polarized and unpolarized triple-axis neutron measurements were performed on an underdoped crystal of YBa2Cu3O7-x (x = 0.4 ± 0.02, Tc = 62.7 K). Our results indicate, contrary to earlier evidence, that the spin excitations in the superconducting state are essentially the same as those in the fully doped material except that the unusual 41 meV resonance is observed at 34.8 meV. The normal state spin excitations are characterized by a weakly energy-dependent continuum whose temperature dependence shows the clear signature of a superconducting gap at Tc. The enhancement at the resonance is accompanied by a suppression of magnetic fluctuations at both higher and lower energies

Reduced cortical thickness with increased lifetime burden of PTSD in OEF/OIF Veterans and the impact of comorbid TBI☆

Posttraumatic stress disorder (PTSD) and mild traumatic brain injury (mTBI) in military personnel is increasing dramatically following the OEF/OIF conflicts and is associated with alterations to brain structure. The present study examined the relationship between PTSD and cortical thickness, and its possible modification by mTBI, in a 104-subject OEF/OIF veteran cohort ranging in age from 20 to 62 years. For each participant, two T1-weighted scans were averaged to create high-resolution images for calculation of regional cortical thickness. PTSD symptoms were assessed using the Clinician Administered PTSD Scale (CAPS) and scores were derived based on the previous month's symptoms (“current”) and a Cumulative Lifetime Burden of PTSD (CLB-P) reflecting the integral of CAPS scores across the lifetime. Mild TBI was diagnosed using the Boston Assessment of TBI-Lifetime (BAT-L). Results demonstrated a clear negative relationship between current PTSD severity and thickness in both postcentral gyri and middle temporal gyri. This relationship was stronger and more extensive when considering lifetime burden (CLB-P), demonstrating the importance of looking at trauma in the context of an individual's lifetime, rather than only at their current symptoms. Finally, interactions with current PTSD only and comorbid current PTSD and mTBI were found in several regions, implying an additive effect of lifetime PTSD and mTBI on cortical thickness