Alphabetisierung - bloß berufliche Notwendigkeit oder mehr?

Anstrengungen zur Verringerung der unzureichend gegebenen Elementarbildung jener Bevölkerungsgruppe, auf die hierzulande die Bezeichnung „AnalphabetInnen“ zutrifft, werden derzeit – so wie Bildungsbemühungen generell – fast durchwegs unter dem Gesichtspunkt des gesellschaftlichen Tausch- bzw. Marktwerts argumentiert. Sie gelten als eine Investition in die „Ressource Mensch“ – auf einen darüber hinausgehenden humanitären oder politischen Wert wird nur selten Bezug genommen. Auch wenn die Bedeutung der Kulturtechniken im Rahmen der ökonomischen Verwertung menschlicher Arbeitskraft selbstverständlich nicht ignoriert werden kann, bedeutet die Befähigung der Menschen zur schriftlichen Kommunikation weit mehr als ihre Zurichtung zu verwertbarem Humankapital. Literalität ist ein grundsätzlicher Aspekt der „Menschwerdung“ des Menschen, sie erst ermöglicht dem einzelnen Individuum eine Teilhabe am kulturellen und gesellschaftlichen Leben, darüber hinaus und darauf aufbauend aber auch die fortschreitende Emanzipation des Menschengeschlechts insgesamt. Die Teilhabemöglichkeit an der menschlichen Gemeinschaft ist nicht bloß ein Vorteil unter vielen anderen, der auf der gleichen Ebene wie die Möglichkeit, seine Arbeitskraft lukrativ verkaufen zu können, angesiedelt ist. Es geht dabei um wesentlich mehr – in letzter Konsequenz um die Überwindung der die Gesellschaft in allen Aspekten bestimmenden Verwertungsprämisse. (DIPF/Orig.

Partial Liver Kinase B1 (LKB1) Deficiency Promotes Diastolic Dysfunction, De Novo Systolic Dysfunction, Apoptosis, and Mitochondrial Dysfunction with Dietary Metabolic Challenge

Background - Myocardial hypertrophy and dysfunction are key features of metabolic heart disease due to dietary excess. Metabolic heart disease manifests primarily as diastolic dysfunction but may progress to systolic dysfunction, although the mechanism is poorly understood. Liver kinase B1 (LKB1) is a key activator of AMP-activated protein kinase and possibly other signaling pathways that oppose myocardial hypertrophy and failure. We hypothesized that LKB1 is essential to the heart's ability to withstand the metabolic stress of dietary excess. Methods and Results - Mice heterozygous for cardiac LKB1 were fed a control diet or a high-fat, high-sucrose diet for 4 months. On the control diet, cardiac LKB1 hearts had normal structure and function. After 4 months of the high-fat, high-sucrose diet, there was left ventricular hypertrophy and diastolic dysfunction in wild-type mice. In cardiac LKB1 (versus wild-type) mice, high-fat, high-sucrose feeding caused more hypertrophy (619 versus 553 μm(2), P<0.05), the de novo appearance of systolic dysfunction (left ventricular ejection fraction; 41% versus 59%, P<0.01) with left ventricular dilation (3.6 versus 3.2 mm, P<0.05), and more severe diastolic dysfunction with progression to a restrictive filling pattern (E/A ratio; 5.5 versus 1.3, P=0.05). Myocardial dysfunction in hearts of cardiac LKB1 mice fed the high-fat, high-sucrose diet was associated with evidence of increased apoptosis and apoptotic signaling via caspase 3 and p53/PUMA (p53 upregulated modulator of apoptosis) and more severe mitochondrial dysfunction. Conclusions - Partial deficiency of cardiac LKB1 promotes the adverse effects of a high-fat, high-sucrose diet on the myocardium, leading to worsening of diastolic function and the de novo appearance of systolic dysfunction. LKB1 plays a key role in protecting the heart from the consequences of metabolic stress.Edward J. Miller, Timothy Calamaras, Aly Elezaby, Aaron Sverdlov, Fuzhong Qin, Ivan Luptak, Ke Wang, Xinxin Sun, Andrea Vijay, Dominique Croteau, Markus Bachschmid, Richard A. Cohen, Kenneth Walsh, Wilson S. Colucc

Comparative assessment of multiple COVID-19 serological technologies supports continued evaluation of point-of-care lateral flow assays in hospital and community healthcare settings

There is a clear requirement for an accurate SARS-CoV-2 antibody test, both as a complement to existing diagnostic capabilities and for determining community seroprevalence. We therefore evaluated the performance of a variety of antibody testing technologies and their potential use as diagnostic tools. Highly specific in-house ELISAs were developed for the detection of anti-spike (S), -receptor binding domain (RBD) and -nucleocapsid (N) antibodies and used for the cross-comparison of ten commercial serological assays-a chemiluminescence-based platform, two ELISAs and seven colloidal gold lateral flow immunoassays (LFIAs)-on an identical panel of 110 SARS-CoV-2-positive samples and 50 pre-pandemic negatives. There was a wide variation in the performance of the different platforms, with specificity ranging from 82% to 100%, and overall sensitivity from 60.9% to 87.3%. However, the head-to-head comparison of multiple sero-diagnostic assays on identical sample sets revealed that performance is highly dependent on the time of sampling, with sensitivities of over 95% seen in several tests when assessing samples from more than 20 days post onset of symptoms. Furthermore, these analyses identified clear outlying samples that were negative in all tests, but were later shown to be from individuals with mildest disease presentation. Rigorous comparison of antibody testing platforms will inform the deployment of point-of-care technologies in healthcare settings and their use in the monitoring of SARS-CoV-2 infections

Albiglutide, a Long Lasting Glucagon-Like Peptide-1 Analog, Protects the Rat Heart against Ischemia/Reperfusion Injury: Evidence for Improving Cardiac Metabolic Efficiency

BACKGROUND: The cardioprotective effects of glucagon-like peptide-1 (GLP-1) and analogs have been previously reported. We tested the hypothesis that albiglutide, a novel long half-life analog of GLP-1, may protect the heart against I/R injury by increasing carbohydrate utilization and improving cardiac energetic efficiency. METHODS/PRINCIPAL FINDINGS: Sprague-Dawley rats were treated with albiglutide and subjected to 30 min myocardial ischemia followed by 24 h reperfusion. Left ventricle infarct size, hemodynamics, function and energetics were determined. In addition, cardiac glucose disposal, carbohydrate metabolism and metabolic gene expression were assessed. Albiglutide significantly reduced infarct size and concomitantly improved post-ischemic hemodynamics, cardiac function and energetic parameters. Albiglutide markedly increased both in vivo and ex vivo cardiac glucose uptake while reducing lactate efflux. Analysis of metabolic substrate utilization directly in the heart showed that albiglutide increased the relative carbohydrate versus fat oxidation which in part was due to an increase in both glucose and lactate oxidation. Metabolic gene expression analysis indicated upregulation of key glucose metabolism genes in the non-ischemic myocardium by albiglutide. CONCLUSION/SIGNIFICANCE: Albiglutide reduced myocardial infarct size and improved cardiac function and energetics following myocardial I/R injury. The observed benefits were associated with enhanced myocardial glucose uptake and a shift toward a more energetically favorable substrate metabolism by increasing both glucose and lactate oxidation. These findings suggest that albiglutide may have direct therapeutic potential for improving cardiac energetics and function

Determination of the number of wounded nucleons in Pb+Pb collisions at 158 A GeV/c

The charged particle multiplicity distributions measured by two experiments, WA97 and NA57, in Pb+Pb collisions at 158 A GeV/c have been analyzed in the framework of the wounded nucleon model (WNM). We obtain a good description of the data within the centrality range of our samples. This allows us to make use of the measured multiplicities to estimate the number of wounded nucleons of the collision

Glucose-Insulin Therapy, Plasma Substrate Levels and Cardiac Recovery After Cardiac Ischemic Events

INTRODUCTION: The potential usefulness of glucose-insulin therapy relies to a large extent on the premise that it prevents hyperglycemia and hyperlipidemia following cardiac ischemic events. METHODS: In this review we evaluate the literature concerning plasma glucose and free fatty acids levels during and following cardiac ischemic events. RESULTS: The data indicate that hyperlipidemia and hyperglycemia most likely occur during acute coronary ischemic syndromes in the conscious state (e.g. acute myocardial infarction) and less so during reperfusion following CABG reperfusion. This is in accordance with observations that glucose-insulin therapy during early reperfusion post CABG may actually cause hypolipidemia, because substantial hyperlipidemia does not appear to occur during that stage of cardiac surgery. DISCUSSION: Considering recent data indicating that hypolipidemia may be detrimental for cardiac function, we propose that free fatty acid levels during reperfusion post CABG with the adjunct glucose-insulin therapy need to be closely monitored. CONCLUSION: From a clinical point of view, a strategy directed at monitoring and thereafter maintaining plasma substrate levels in the normal range for both glucose (4-6 mM) and FFA (0.2-0.6 mM) as well as stimulation of glucose oxidation, promises to be the most optimal metabolic reperfusion treatment following cardiac ischemic episodes. Future (preclinical and subsequently clinical) investigations are required to investigate whether the combination of glucose-insulin therapy with concomitant lipid administration may be beneficial in the setting of reperfusion post CAB

Strangeness enhancement at mid-rapidity in Pb-Pb collisions at 158 GeV/c

$K^{0}_{s}$, $\Lambda$, $\Xi$, $\Omega$ and negative particle yields and transverse mass spectra have been measured at central rapidity in Pb-Pb and p-Pb collisions at 158 $A$ GeV/$c$. The yields in Pb-Pb interactions % are presented as a function of the collision centrality and compared with those obtained from p-Pb collisions. Strangeness enhancement in Pb-Pb relative to p-Pb collisions increases with the strangeness content of the particle. Going from p-Pb to Pb-Pb, the strange particle yields increase faster than linearly with the number of participants $N_{part}$ up to $N_{part} \approx 100$, thereafter the increase becomes %linear with $N_{part}$. Yields are studied as a function of the number of nucleons participating in the collision $N_{part}$, which is estimated with the Glauber model. From p-Pb to Pb-Pb collisions the particle yields per participant increase substantially. The enhancement is more pronounced for multistrange particles, and exceeds an order of magnitude for the $\Omega$. For a number of participants, $N_{part}$, greater than $100$, however, all yields per participant appear to be constant

Results on cascade production in lead-lead interactions from the NA57 experiment

The NA57 experiment has been designed to study the production of strange and multi-strange particles in Pb-Pb and p-Be collisions at the CERN SPS. The predecessor experiment WA97 has measured an enhanced abundance of strange particles in Pb-Pb collisions relative to p-A reactions at 160 GeV/c per nucleon beam momentum. NA57 has extended the WA97 measurements to investigate the evolution of the strangeness enhancement pattern as a function of the beam energy and over a wider centrality range. In this paper, we report results on cascade production for about the 60% most central collisions at 160 GeV/c per nucleon

DAF-16/FoxO directly regulates an atypical AMP-activated protein kinase gamma isoform to mediate the effects of insulin/IGF-1 signaling on aging in Caenorhabditis elegans

The DAF-16/FoxO transcription factor controls growth, metabolism and aging in Caenorhabditis elegans. The large number of genes that it regulates has been an obstacle to understanding its function. However, recent analysis of transcript and chromatin profiling implies that DAF-16 regulates relatively few genes directly, and that many of these encode other regulatory proteins. We have investigated the regulation by DAF-16 of genes encoding the AMP-activated protein kinase (AMPK), which has ?, ? and ? subunits. C. elegans has 5 genes encoding putative AMP-binding regulatory ? subunits, aakg-1-5. aakg-4 and aakg-5 are closely related, atypical isoforms, with orthologs throughout the Chromadorea class of nematodes. We report that ?75% of total ? subunit mRNA encodes these 2 divergent isoforms, which lack consensus AMP-binding residues, suggesting AMP-independent kinase activity. DAF-16 directly activates expression of aakg-4, reduction of which suppresses longevity in daf-2 insulin/IGF-1 receptor mutants. This implies that an increase in the activity of AMPK containing the AAKG-4 ? subunit caused by direct activation by DAF-16 slows aging in daf-2 mutants. Knock down of aakg-4 expression caused a transient decrease in activation of expression in multiple DAF-16 target genes. This, taken together with previous evidence that AMPK promotes DAF-16 activity, implies the action of these two metabolic regulators in a positive feedback loop that accelerates the induction of DAF-16 target gene expression. The AMPK ? subunit, aakb-1, also proved to be up-regulated by DAF-16, but had no effect on lifespan. These findings reveal key features of the architecture of the gene-regulatory network centered on DAF-16, and raise the possibility that activation of AMP-independent AMPK in nutritionally replete daf-2 mutant adults slows aging in C. elegans. Evidence of activation of AMPK subunits in mammals suggests that such FoxO-AMPK interactions may be evolutionarily conserved