Lehren und Lernen aus Sicht von Schülerinnen und Schülern im Politik-Unterricht der Gymnasialen Oberstufe. Ein Beitrag zur lernerorientierten, fachdidaktischen und qualitativen Unterrichtsforschung.

In dieser Untersuchung, die in unmittelbarer Nähe zum Unterrichts- und Lerngeschehen eines Grundkurses der Oberstufe durchgeführt wurde, werden die individuellen Lernprozesse der SchülerInnen zum Gegenstand gemacht und neue Erkenntnisse über das Lernen im Politikunterricht und den damit verbundenen Wahrnehmungsmuster erlangt. Lernen ist ein höchst individueller Vorgang. Aus diesem Grund müssen Untersuchungen, die das Lernverhalten der SchülerInnen zum Gegenstand haben, möglichst nahe am Lern- und Unterrichtsgeschehen platziert sein und die Schüler selbst so oft und so direkt wie möglich zu Wort kommen lassen. Dies hat Auswirkung auf die Wahl der Erhebungsinstrumente der vorliegenden Studie und bedingt deren vorwiegend qualitative Ausrichtung. Lernen ist darüber hinaus auch ein höchst komplexer Vorgang, was die Erweiterung einer rein fachdidaktischen Fragestellung und ihre Verknüpfung mit einer allgemeindidaktischen Fragestellung sinnvoll macht. Diese Zusammenhänge werden im ersten Teil der Arbeit in Gestalt der Aufarbeitung der entsprechenden allgemein- und fachdidaktischen Diskussion und der nötigen lernpsychologischen Grundlegung entwickelt. Im Zentrum des zweiten Teils steht die empirische Studie selbst. In dritten Teil der Studie werden die gewonnenen Erkenntnisse auf ihre politikdidaktischen und unterrichtspraktischen Konsequenzen hinterfragt. Vorschläge zu einem „verbesserten“ Politikunterricht schließen sich an. Dem Führen eines Lerntagebuchs kommt in der Untersuchung eine besondere Bedeutung zu. Das Lerntagebuch bietet eine Schnittstelle als didaktisches Mittel und als Erhebungsinstrument. Als didaktisches Mittel kann es zu Dokumentation und Evaluation des Unterrichts- und Lerngeschehens verwendet werden. Hier hat es vor allem auch eine Bedeutung für Lehrer zur Evaluation des eigenen Unterrichts und kann in der Hand des Schülers neben der Evaluation des eigenen Lernprozesses auch ein Medium oder eine Methode zur Veränderung des Lern-verhaltens sein. Als Datenquelle dient es der Rekonstruktion des Lernverhaltens, und kann im Sinn eines Diagnoseinstrumentes zu Aussagen über den Grad der Entwicklung von Lernkompetenz her-angezogen werden. Als Erhebungsinstrument verfügt das LB über folgende Besonderhei-ten: es wird ausschließlich von den betroffenen Subjekten selbst und direkt erstellt, es befindet sich in zeitlicher Nähe zum Unterrichtsgeschehen, es hat das Unterrichtsgeschehen selbst und das Lernen zum Gegenstand, es lässt durch die relativ offene Form freie Äußerungen zu, und kann zugleich auch für die Dauer der Untersuchung einen prozessualen Aspekt erfassen. Ergebnisse der Lerntagebucheinsatzes: Die Wirksamkeit des Lerntagebuchs als methodisches Mittel zur Veränderung des Lern-verhaltens und zur Steigerung der Lernkompetenz ist in hohem Maße mit der Struktur des Unterrichts und den damit verbundenen Lernarrangements verknüpft. Das Lerntagebuch ist keine für sich unabhängige, beliebig einzusetzende Methode, sondern komplementär zum Unterrichtsarrangement zu betrachten und in dieser Komplementarität genau an diesen anzupassen . Die Wirksamkeit des Lerntagebuch setzt die Veränderung des traditionellen unterrichtlichen Settings im Sinne von mehr offenem und selbstbestimmten Lernen voraus. In der Studie konnte gezeigt werden, dass das Führen des Lerntagebuchs zu einer Veränderung des Lernverhaltens geführt hat: Die Schüler setzten sich durch das Lerntagebuchführen bedingt intensiver mit den Unterrichtsinhalten auseinander, benutzen das Lerntagebuch als Lerngrundlage für die Klausur und zur Rekapitulation der Unterrichtsinhalte. Erfolgreich war das Lerntagebuch als Evaluationsgrundlage des Unterricht, wobei die Aussagen der Schüler aussagekräftiger wurden, wenn sie die Zusicherung hatten, dass die Eintragungen nicht von der Lehrerin gelesen würden. Erfolgreich war das Lerntagebuch auch in seiner diagnostischen Funktion. Es gestattet der Forscherin hilfreiche Erkenntnisse zum Lernen und vor allem zu eventuellen Lernpro-blemen bei Schülern. Lernerprofile: Zur Beschreibung des Lernverhalten der Schülerinnen und Schüler werden Lernerprofile an-gelegt, die in Form von Einzelfallanalysen die Daten sämtlicher Instrumente in einer Trian-gulation vereinen und zu Profilen innerhalb der Lernergruppe bündeln. Die so ausgewählten Fälle stellen im Gesamtspektrum der Lerngruppe deutlich zu unterscheidende Extremfälle dar, auf deren Grundlage Lernertypen zur Konturierung eines Spektrums konstruiert werden kön-nen, innerhalb dessen die gesamte Lernergruppe eingeordnet werden kann. Die Konstruktion von Lernertypen ist Systematisierung und Typisierung von möglichen individuellen Lernerpersönlichkeiten in einer Lerngruppe mit dem Anspruch von exemplarischer Repräsentativität. Dabei stellt der spezielle Zugang zum Lernen die Grundlage dar

Lung surfactant in subacute pulmonary disease

Pulmonary surfactant is a surface active material composed of both lipids and proteins that is produced by alveolar type II pneumocytes. Abnormalities of surfactant in the immature lung or in the acutely inflamed mature lung are well described. However, in a variety of subacute diseases of the mature lung, abnormalities of lung surfactant may also be of importance. These diseases include chronic obstructive pulmonary disease, asthma, cystic fibrosis, interstitial lung disease, pneumonia, and alveolar proteinosis. Understanding of the mechanisms that disturb the lung surfactant system may lead to novel rational therapies for these diseases

Sequential analysis of surfactant, lung function and inflammation in cystic fibrosis patients

BACKGROUND: In a cross-sectional analysis of cystic fibrosis (CF) patients with mild lung disease, reduced surfactant activity was correlated to increased neutrophilic airway inflammation, but not to lung function. So far, longitudinal measurements of surfactant function in CF patients are lacking and it remains unclear how these alterations relate to the progression of airway inflammation as well as decline in pulmonary function over time. METHODS: As part of the BEAT trial, a longitudinal study to assess the course of airway inflammation in CF, we studied lung function, surfactant function and endobronchial inflammation using bronchoalveolar lavage fluid from 20 CF patients with normal pulmonary function (median FEV(1 )94% of predicted) at three times over a three year period. RESULTS: There was a progressive loss of surfactant function, assessed as minimal surface tension. The decline in surfactant function was negatively correlated to an increase in neutrophilic inflammation and a decrease in lung function, assessed by FEV(1), MEF(75/25%VC), and MEF(25%VC). The concentrations of the surfactant specific proteins A, C and D did not change, whereas SP-B increased during this time period. CONCLUSION: Our findings suggest a link between loss of surfactant function driven by progressive airway inflammation and loss of small airway function in CF patients with limited lung disease

Surfactant Protein-A Suppresses Eosinophil-Mediated Killing of Mycoplasma pneumoniae in Allergic Lungs

Surfactant protein-A (SP-A) has well-established functions in reducing bacterial and viral infections but its role in chronic lung diseases such as asthma is unclear. Mycoplasma pneumoniae (Mp) frequently colonizes the airways of chronic asthmatics and is thought to contribute to exacerbations of asthma. Our lab has previously reported that during Mp infection of non-allergic airways, SP-A aides in maintaining airway homeostasis by inhibiting an overzealous TNF-alpha mediated response and, in allergic mice, SP-A regulates eosinophilic infiltration and inflammation of the airway. In the current study, we used an in vivo model with wild type (WT) and SP-A−/− allergic mice challenged with the model antigen ovalbumin (Ova) that were concurrently infected with Mp (Ova+Mp) to test the hypothesis that SP-A ameliorates Mp-induced stimulation of eosinophils. Thus, SP-A could protect allergic airways from injury due to release of eosinophil inflammatory products. SP-A deficient mice exhibit significant increases in inflammatory cells, mucus production and lung damage during concurrent allergic airway disease and infection (Ova+Mp) as compared to the WT mice of the same treatment group. In contrast, SP-A deficient mice have significantly decreased Mp burden compared to WT mice. The eosinophil specific factor, eosinophil peroxidase (EPO), which has been implicated in pathogen killing and also in epithelial dysfunction due to oxidative damage of resident lung proteins, is enhanced in samples from allergic/infected SP-A−/− mice as compared to WT mice. In vitro experiments using purified eosinophils and human SP-A suggest that SP-A limits the release of EPO from Mp-stimulated eosinophils thereby reducing their killing capacity. These findings are the first to demonstrate that although SP-A interferes with eosinophil-mediated biologic clearance of Mp by mediating the interaction of Mp with eosinophils, SP-A simultaneously benefits the airway by limiting inflammation and damage

Catecholamine up-regulates MMP-7 expression by activating AP-1 and STAT3 in gastric cancer

<p>Abstract</p> <p>Background</p> <p>Stress, anxiety and depression can cause complex physiological and neuroendocrine changes, resulting in increased level of stress related hormone catecholamine, which may constitute a primary mechanism by which physiological factors impact gene expression in tumors. In the present study, we investigated the effects of catecholamine stimulation on MMP-7 expression in gastric cancer cells and elucidated the molecular mechanisms of the up-regulation of MMP-7 level by catecholamine through an adrenergic signaling pathway.</p> <p>Results</p> <p>Increased MMP-7 expression was identified at both mRNA and protein levels in the gastric cancer cells in response to isoproterenol stimulation. β2-AR antigonist effectively abrogated isoproterenol-induced MMP-7 expression. The activation of STAT3 and AP-1 was prominently induced by isoproterenol stimulation and AP-1 displayed a greater efficacy than STAT3 in isoproterenol-induced MMP-7 expression. Mutagenesis of three STAT3 binding sites in MMP-7 promoter failed to repress the transactivation of MMP-7 promoter and silencing STAT3 expression was not effective in preventing isoproterenol-induced MMP-7 expression. However, isoproterenol-induced MMP-7 promoter activities were completely disappeared when the AP-1 site was mutated. STAT3 and c-Jun could physically interact and bind to the AP-1 site, implicating that the interplay of both transcriptional factors on the AP-1 site is responsible for isoproterenol-stimulated MMP-7 expression in gastric cancer cells. The expression of MMP-7 in gastric cancer tissues was found to be at the site where β2-AR was overexpressed and the levels of MMP-7 and β2-AR were the highest in the metastatic locus of gastric cancer.</p> <p>Conclusions</p> <p>Up-regulation of MMP-7 expression through β2-AR-mediated signaling pathway is involved in invasion and metastasis of gastric cancer.</p

Alterations in the human lung proteome with lipopolysaccharide

<p>Abstract</p> <p>Background</p> <p>Recombinant human activated protein C (rhAPC) is associated with improved survival in high-risk patients with severe sepsis; however, the effects of both lipopolysaccharide (LPS) and rhAPC on the bronchoalveolar lavage fluid (BALF) proteome are unknown.</p> <p>Methods</p> <p>Using differential in gel electrophoresis (DIGE) we identified changes in the BALF proteome from 10 healthy volunteers given intrapulmonary LPS in one lobe and saline in another lobe. Subjects were randomized to pretreatment with saline or rhAPC.</p> <p>Results</p> <p>An average of 255 protein spots were detected in each proteome. We found 31 spots corresponding to 8 proteins that displayed abundance increased or decreased at least 2-fold after LPS. Proteins that decreased after LPS included surfactant protein A, immunoglobulin J chain, fibrinogen-γ, α₁-antitrypsin, immunoglobulin, and α₂-HS-glycoprotein. Haptoglobin increased after LPS-treatment. Treatment with rhAPC was associated with a larger relative decrease in immunoglobulin J chain, fibrinogen-γ, α₁-antitrypsin, and α₂-HS-glycoprotein.</p> <p>Conclusion</p> <p>Intrapulmonary LPS was associated with specific protein changes suggesting that the lung response to LPS is more than just a loss of integrity in the alveolar epithelial barrier; however, pretreatment with rhAPC resulted in minor changes in relative BALF protein abundance consistent with its lack of affect in ALI and milder forms of sepsis.</p

Antimicrobial proteins and polypeptides in pulmonary innate defence

Inspired air contains a myriad of potential pathogens, pollutants and inflammatory stimuli. In the normal lung, these pathogens are rarely problematic. This is because the epithelial lining fluid in the lung is rich in many innate immunity proteins and peptides that provide a powerful anti-microbial screen. These defensive proteins have anti-bacterial, anti- viral and in some cases, even anti-fungal properties. Their antimicrobial effects are as diverse as inhibition of biofilm formation and prevention of viral replication. The innate immunity proteins and peptides also play key immunomodulatory roles. They are involved in many key processes such as opsonisation facilitating phagocytosis of bacteria and viruses by macrophages and monocytes. They act as important mediators in inflammatory pathways and are capable of binding bacterial endotoxins and CPG motifs. They can also influence expression of adhesion molecules as well as acting as powerful anti-oxidants and anti-proteases. Exciting new antimicrobial and immunomodulatory functions are being elucidated for existing proteins that were previously thought to be of lesser importance. The potential therapeutic applications of these proteins and peptides in combating infection and preventing inflammation are the subject of ongoing research that holds much promise for the future

Paenibacillus infection with frequent viral coinfection contributes to postinfectious hydrocephalus in Ugandan infants

Postinfectious hydrocephalus (PIH), which often follows neonatal sepsis, is the most common cause of pediatric hydrocephalus worldwide, yet the microbial pathogens underlying this disease remain to be elucidated. Characterization of the microbial agents causing PIH would enable a shift from surgical palliation of cerebrospinal fluid (CSF) accumulation to prevention of the disease. Here, we examined blood and CSF samples collected from 100 consecutive infant cases of PIH and control cases comprising infants with non-postinfectious hydrocephalus in Uganda. Genomic sequencing of samples was undertaken to test for bacterial, fungal, and parasitic DNA; DNA and RNA sequencing was used to identify viruses; and bacterial culture recovery was used to identify potential causative organisms. We found that infection with the bacterium Paenibacillus, together with frequent cytomegalovirus (CMV) coinfection, was associated with PIH in our infant cohort. Assembly of the genome of a facultative anaerobic bacterial isolate recovered from cultures of CSF samples from PIH cases identified a strain of Paenibacillus thiaminolyticus. This strain, designated Mbale, was lethal when injected into mice in contrast to the benign reference Paenibacillus strain. These findings show that an unbiased pan-microbial approach enabled characterization of Paenibacillus in CSF samples from PIH cases, and point toward a pathway of more optimal treatment and prevention for PIH and other proximate neonatal infections