Conditional Cash Transfers in Guatemala

Innerhalb weniger Jahre haben sich die erst ab 1997 in Pilotprojekten in Mexiko und Brasilien angewandten Conditional Cash Transfers (CCT) zum vorrangigen Instrument ländlicher Armutsbekämpfung in lateinamerika entwickelt. Die Modalität der CCT besteht darin, fix definierte Summen monatlich an ländliche Haushalte zu transferieren, wenn diese bestimmte Investitionen in das sogenannte „Humankapital“ ihrer Kinder tätigen. Damit sollen zwei Ziele erreicht werden: einerseits armen oder extrem armen Haushalten ein minimales Konsumniveau zu ermöglichen; und andererseits durch die Schaffung des „Humankapitals“ der Generationsverlagerung der Armut entgegenzuwirken. Konkret sind Gesundheitsuntersuchungen (Impfungen, Gewichtskontrolle) und Schulbesuch der unter 15 jährigen Kinder vorgesehen. Während manche Autoren in den CCT einen paradigmatischen Wandel in der Entwicklungspolitik, vor allem seitens der Internationalen Finanzinstitutionen (Weltbank und Interamerikanische Entwicklungsbank), orten – nach ihnen wird ein neoliberales Modell, das sich durch eine Vertiefung der an sich schon hohen Ungleichheit kennzeichnet, durch ein weniger ungleiches ersetzt -, betrachten andere die CCT nicht mehr als die zweite Generation der sozial fokussierten Transferleistungen im Rahmen der für die marginalisierten Bevölkerungsgruppen schmerzhaften Strukturanpassungsmaßnahmen. Die Dissertation untersucht die konkrete Anwendung der CCT in Guatemala sowie ihren Anwendungskontext und sucht dabei an Hand zweier Fragen zu klären, was sie für die wichtigste Zielgruppe der CCT, die kleinbäuerlichen Familien (campesinos und campesinas), ihre gesellschaftliche Rolle und Identität sowie die sozialen Beziehungen im ländlichen Raum (real und potentiell) bedeuten: 1) Welche Auswirkungen haben CCT auf die human und social capabilities der campesinos und campesinas in Guatemala? Und 2) Wie hat sich der Vollzug des Menschenrechts auf angemessene Ernährung für die campesinos und campesinas seit der Implementierung der CCT in Guatemala entwickelt

Magnetic flux flow and superconductor stabilization Quarterly report, 1 Jan. - 31 Mar. 1968

Magnetic flux flow and stability of superconducting niobium titanium strip

Experimental simulation of large, high field, superconducting magnet operation First quarterly report, Mar. 1 - May 31, 1965

Magnetic coil testing and experiment preparations for magnet facility in simulation of large high field superconducting magnet operatio

Magnetic flux flow and superconductor stabilization Quarterly report, Apr. 1 - Jun. 30, 1967

Magnetic flux flow and superconductor stabilizatio

Placental DAPK1 and autophagy marker LC3B-II are dysregulated by TNF-α in a gestational age-dependent manner

Autophagy, a cell-survival process responsible for degradation of protein aggregates and damaged organelles, is increasingly recognized as another mechanism essential for human placentation. A substantial body of experiments suggests inflammation and oxidative stress as the underlying stimuli for altered placental autophagy, giving rise to placenta dysfunction and pregnancy pathologies. Here, the hypothesis is tested whether or not pro-inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-{alpha} are able to influence the expression profile of autophagy genes in human first-trimester villous placenta. Autophagy-focused qPCR arrays identified substantial downregulation of death-associated protein kinase 1 (DAPK1) in first-trimester placental explants in response to IL-6 and TNF-{alpha}, respectively. Immunohistochemistry of placental explants detected considerable DAPK1 staining in placental macrophages, villous cytotrophoblasts and less intense in the syncytiotrophoblast. Both immunohistochemistry and Western blot showed decreased DAPK1 protein in TNF-{alpha}-treated placental explants compared to control. On cellular level, DAPK1 expression decreased in SGHPL-4 trophoblasts in response to TNF-{alpha}. Observed changes in the expression profile of autophagy-related genes were reflected by significantly decreased lipidation of autophagy marker microtubule-associated protein light chain 3 beta (LC3B-II) in first trimester placental explants in response to TNF-{alpha}. Analysis of TNF-{alpha}-treated term placental explants showed decreased DAPK1 protein, whereas in contrast to first-trimester LC3B expression and lipidation increased. Immunohistochemistry of placental tissues from early-onset preeclampsia (PE) showed less DAPK1 staining, when compared to controls. Accordingly, DAPK1 mRNA and protein were decreased in primary trophoblasts isolated from early-onset PE, while LC3B-I and -II were increased. Results from this study suggest that DAPK1, a regulator of apoptosis, autophagy and programmed necrosis, decreases in human placenta in response to elevated maternal TNF-{alpha}, irrespective of gestational age. In contrast, TNF-{alpha} differentially regulates levels of autophagy marker LC3B in human placenta over gestation

Dendritic polyglycerol nanoparticles show charge dependent bio-distribution in early human placental explants and reduce hCG secretion

A thorough understanding of nanoparticle bio-distribution at the feto-maternal interface will be a prerequisite for their diagnostic or therapeutic application in women of childbearing age and for teratologic risk assessment. Therefore, the tissue interaction of biocompatible dendritic polyglycerol nanoparticles (dPG-NPs) with first- trimester human placental explants were analyzed and compared to less sophisticated trophoblast-cell based models. First-trimester human placental explants, BeWo cells and primary trophoblast cells from human term placenta were exposed to fluorescence labeled, ∼5 nm dPG-NPs, with differently charged surfaces, at concentrations of 1 µM and 10 nM, for 6 and 24 h. Accumulation of dPGs was visualized by fluorescence microscopy. To assess the impact of dPG-NP on trophoblast integrity and endocrine function, LDH, and hCG releases were measured. A dose- and charge- dependent accumulation of dPG-NPs was observed at the early placental barrier and in cell lines, with positive dPG-NP-surface causing deposits even in the mesenchymal core of the placental villi. No signs of plasma membrane damage could be detected. After 24 h we observed a significant reduction of hCG secretion in placental explants, without significant changes in trophoblast apoptosis, at low concentrations of charged dPG-NPs. In conclusion, dPG-NP’s surface charge substantially influences their bio-distribution at the feto- maternal interface, with positive charge facilitating trans-trophoblast passage, and in contrast to more artificial models, the first-trimester placental explant culture model reveals potentially hazardous influences of charged dPG-NPs on early placental physiology

Application Of Numerical Modelling For Conceptualizing Abstraction Rate Control In A Well Field Under Complex Boundary Conditions

This paper aims at presenting a concept for regulating water abstraction from a well field which ensures an efficient exploration of river filtrate while complying with defined minimum residence time of inflowing water. Being located on an island between a river and an attendant channel, the investigated well field consists of eight radial collector wells aligned parallel to the river flow direction. The water-level in the river is kept comparatively constant due to a downstream hydropower plant. In the channel, the water level is controlled by two weirs. Following a defined hydrograph with an amplitude of about one meter, the channel water level is on average four meters below the water level of the river. Therefore, the boundary conditions for the well field are subject to strong seasonal fluctuations. For legal reasons, water originating from the channel must remain in the underground for at least 60 days. To analyse on-site flow conditions, a three dimensional finite difference model was developed, calibrated and validated. The water balances of 23 observed steady state conditions with different abstractions from the wells and varying basic conditions were computed with the model. The computed inflow rates from the channel were analysed by comparing them with observed hydraulic heads and it was possible to show a high correlation with the ratio of certain hydraulic head gradients. A linear correlation (R² \u3e0.9) of the quantity and the flow time of inflowing water from the channel could be formulated by analysing the modelling results. By combining these findings, it was possible to develop a criterion for restricting the abstraction from each well according to a minimum water-flow time without the requirement of a parallel operated numerical model. The underlying parameters are computed from hydraulic head values enabling automatically real time control of a non-measurable value through measurable parameters

Downregulation of p53 drives autophagy during human trophoblast differentiation

The placental barrier is crucial for the supply of nutrients and oxygen to the developing fetus and is maintained by differentiation and fusion of mononucleated cytotrophoblasts into the syncytiotrophoblast, a process only partially understood. Here transcriptome and pathway analyses during differentiation and fusion of cultured trophoblasts yielded p53 signaling as negative upstream regulator and indicated an upregulation of autophagy-related genes. We further showed p53 mRNA and protein levels decreased during trophoblast differentiation. Reciprocally, autophagic flux increased and cytoplasmic LC3B-GFP puncta became more abundant, indicating enhanced autophagic activity. In line, in human first trimester placenta p53 protein mainly localized to the cytotrophoblast, while autophagy marker LC3B as well as late autophagic compartments were predominantly detectable in the syncytiotrophoblast. Importantly, ectopic overexpression of p53 reduced levels of LC3B-II, supporting a negative regulatory role on autophagy in differentiating trophoblasts. This was also shown in primary trophoblasts and human first trimester placental explants, where pharmacological stabilization of p53 decreased LC3B-II levels. In summary our data suggest that differentiation-dependent downregulation of p53 is a prerequisite for activating autophagy in the syncytiotrophoblast