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

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

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

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

Preparation and Characterization of Homogeneous YBCO Single Crystals with Doping Level near the SC-AFM Boundary

High-purity and homogeneous YBa2Cu3Oy single crystals with carrier doping level near the AFM-SC boundary have been obtained in the oxygen content range between y = 6.340 and 6.370. The crystals are ortho-II phase at room temperature and undergo the orthorhombic to tetragonal transition at about 140_Degree_C. They show sharp superconducting transitions, with Tc between 4 and 20 K. Tc changes by 0.8 K when the oxygen content y is changed by 0.001, and is also sensitive to annealing conditions near room temperature, due to the dependence of doping on oxygen ordering correlation lengths. Crystals with oxygen content y lower than 6.345 are non-superconducting.Comment: 6 page

Hole depletion and localization due to disorder in insulating PrBa2Cu3O7-d: a Compton scattering study

The (mostly) insulating behaviour of PrBa2Cu3O7-d is still unexplained and even more interesting since the occasional appearance of superconductivity in this material. Since YBa2Cu3O7-d is nominally iso-structural and always superconducting, we have measured the electron momentum density in these materials. We find that they differ in a striking way, the wavefunction coherence length in PrBa2Cu3O7-d being strongly suppressed. We conclude that Pr on Ba-site substitution disorder is responsible for the metal-insulator transition. Preliminary efforts at growth with a method to prevent disorder yield 90K superconducting PrBa2Cu3O7-d crystallites.Comment: 4 pages, 3 figures, revised version submitted to PR

Observation of out-of-phase bilayer plasmons in YBa_2Cu_3O_7-delta

The temperature dependence of the c-axis optical conductivity \sigma(\omega) of optimally and overdoped YBa_2Cu_3O_x (x=6.93 and 7) is reported in the far- (FIR) and mid-infrared (MIR) range. Below T_c we observe a transfer of spectral weight from the FIR not only to the condensate at \omega = 0, but also to a new peak in the MIR. This peak is naturally explained as a transverse out-of-phase bilayer plasmon by a model for \sigma(\omega) which takes the layered crystal structure into account. With decreasing doping the plasmon shifts to lower frequencies and can be identified with the surprising and so far not understood FIR feature reported in underdoped bilayer cuprates.Comment: 7 pages, 3 eps figures, Revtex, epsfi

Allan Smith--A Personal History

A tribute to Allan Smit

Experimental evidence for fast cluster formation of chain oxygen vacancies in YBa2Cu3O7-d being at the origin of the fishtail anomaly

We report on three different and complementary measurements, namely magnetisation measurements, positron annihilation spectroscopy and NMR measurements, which give evidence that the formation of oxygen vacancy clusters is on the origin of the fishtail anomaly in YBa2Cu3O7-d. While in the case of YBa2Cu3O7.0 the anomaly is intrinsically absent, it can be suppressed in the optimally doped state where vacancies are present. We therefore conclude that the single vacancies or point defects can not be responsible for this anomaly but that clusters of oxygen vacancies are on its origin.Comment: 10 pages, 4 figures, submitted to PR