Parental health and children’s cognitive and non-cognitive development: New evidence from the Longitudinal Survey of Australian Children

This paper examines the effects of parental health on cognitive and non-cognitive development in Australian children. The underlying nationally representative panel data and a child fixed effects estimator are used to deal with unobserved heterogeneity. We find that only father’s serious mental illness worsens selected cognitive and non-cognitive skills of children. Maternal poor health also deteriorates some cognitive and non-cognitive outcomes of children of lone mothers only. Our results demonstrate that either failing to account for parent-child fixed effects or using child non-cognitive skills reported by parents could over-estimate the harmful impact of poor parental health on child development

Educational effects of early or later secondary school tracking in Germany

This paper examines educational outcomes of pupils selected to secondary school types by different tracking regimes in a German state: Pupils are alternatively streamed after fourth grade or after sixth grade. Regression results indicate that, estimated on the mean, there are no negative effects of later tracking on educational outcomes in the middle of secondary school. Positive effects are observed for pupils with a less favorable family background. Quantile regressions reveal that the estimated effects of later tracking are positive for the lower quantiles but decrease monotonically over the conditional distribution of test scores

Entwicklung und Ungleichheit von Fähigkeiten : Anmerkungen aus ökonomischer Sicht

Nirgends sonst im ökonomischen Handeln fallen Kosten und Nutzen im Zeitablauf und aufgeteilt nach Investoren und Nutznießern so eklatant auseinander wie bei Bildungsinvestitionen. In dem vorliegenden Beitrag wird argumentiert, dass in der sozialen Realität die Bildungsungleichheit im Vorschulalter eine der wichtigsten Ursachen für die Ungleichheit von Fähigkeiten und Kompetenzen auch im Schulalter und im Erwerbsleben ist. Für benachteiligte Kinder scheint somit die Bildungsungleichheit vor dem Schulalter bei uns, ebenso wie in anderen Ländern mit hohen Bildungsausgaben und hoher Wirtschaftskraft ihren schicksalhaften Charakter noch keineswegs verloren zu haben. Um dies zu ändern, bleibt es eine vordringliche Aufgabe auch der Bildungspolitik, den Zugang zu einer angemessenen emotionalen Fürsorge von Anfang an weiter zu verbessern. Darüber hinaus ist es notwendig, den betroffenen Kindern bis ins Jugendalter altersgemäß und individuell zur Seite zu stehen

The Evolution of the School-Entry Age Effect in a School Tracking System

In Germany, students are streamed at age ten into an academic or non-academic track. We demonstrate that the randomly allocated disadvantage of being born just before as opposed to just after the cutoff date for school entry leads to substantially different schooling experiences. Relatively young students are initially only two-thirds as likely to be assigned to the academic track. The possibility to defer tracking to age 12 does not attenuate school-entry age’s effect on track attendance. Some mitigation of the effect occurs only at the second time when educational institutions facilitate track modification when students are about age 16.

J Biotech

Gene transfer is a basic requirement for optimizing bioactive natural substances produced by an increasing number of industrially used microorganisms. We have analyzed quantitatively horizontal gene transfer from Escherichia coli to Actinomycetes. The efficiencies of DNA transfer of four different systems were compared that consist of conjugative and mobilizable plasmids with a broad-host range. Three novel binary vector set-ups were constructed based on: (i) the IncQ group of mobilizable plasmids (RSF1010), (ii) IncQ-like pTF-FC2 and (iii) pSB102 that belongs to a new class of broad-host-range plasmids. The established system based on the IncPα group of conjugative plasmids served as the reference. For all plasmids constructed, we confirmed the functional integrity of the selected transfer machineries by intrageneric matings between E. coli strains. We demonstrate that the transfer systems introduced in this study are efficient in mediating gene transfer from E. coli to Actinomycetes and are possible alternatives for gene transfer into Actinomycetes for which the IncPα-based transfer system is not applicable. The use of plasmids that integrate into the recipients’ chromosomes compared to that of plasmids replicating autonomously is shown to allow the access to a wider range of hosts

Interaction of plasminogen activator inhibitor type-1 (PAI-1) with vitronectin - Characterization of different PAI-1 mutants

The serpin plasminogen activator inhibitor type 1 (PAI-1) plays an important role in physiological processes such as thrombolysis and fibrinolysis, as well as pathophysiological processes such as thrombosis, tumor invasion and metastasis. In addition to inhibiting serine proteases, mainly tissue-type (tPA) and urokinase-type (uPA) plasminogen activators, PAI-1 interacts with different components of the extracellular matrix, i.e. fibrin, heparin (Hep) and vitronectin (Vn). PAI-1 binding to Vn facilitates migration and invasion of tumor cells. The most important determinants of the Vn-binding site of PAI-1 appear to reside between amino acids 110-147, which includes alpha helix E (hE, amino acids 109-118). Ten different PAI-1 variants (mostly harboring modifications in hE) as well as wild-type PAI-1, the previously described PAI-1 Mutant Q123K, and another serpin, PAI-2, were recombinantly produced in Escherichia coli containing a His(6) tag and purified by affinity chromatography. As shown in microtiter plate-based binding assays, surface plasmon resonance and thrombin inhibition experiments, all of the newly generated mutants which retained inhibitory activity against uPA still bound to Vn. Mutant A 114-118, in which all amino-acids at positions 114-118 of PAI-1 were exchanged for alanine, displayed a reduced affinity to Vn as compared to wildtype PAI-1. Mutants lacking inhibitory activity towards uPA did not bind to Vn. Q123K, which inhibits uPA but does not bind to Vn, served as a control. In contrast to other active PAI-1 mutants, the inhibitory properties of A 114-118 towards thrombin as well as uPA were significantly reduced in the presence of Hep. Our results demonstrate that the wild-type sequence of die region around hE in PAI-1 is not a prerequisite for binding to Vn