Solar thermal water splitting (STWS) produces renewable hydrogen from water using concentrated sunlight. Because it utilizes energy from the entire solar spectrum to directly drive the redox reactions that split water, it can achieve high theoretical solar-to-hydrogen efficiencies. In two-step STWS, a metal oxide is first heated by concentrated sunlight to high temperatures to reduce it and produce O 2 . In the second step, the reduced material is exposed to H 2 O to reoxidize it to its original oxidation state and produce H 2 . Various aspects of this process are reviewed in this work, including the reduction and oxidation chemistries of the active redox materials, the effects of operating conditions, and the solar thermal reactors in which the STWS reactions occur, and a perspective is given on the future optimization of STWS.

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Sanitation access in urban areas of low-income countries is provided through unstandardized onsite technologies containing accumulated faecal sludge. The demand for infrastructure to manage faecal sludge is increasing, however, no reliable method exists to estimate total accumulated quantities and qualities (Q&Q) This proposed approach averages out complexities to estimate conditions at a centralized to semi-centralized scale required for management and treatment technology solutions, as opposed to previous approaches evaluating what happens in individual containments. Empirical data, demographic data, and questionnaires were used in Kampala, Uganda to estimate total faecal sludge accumulation in the city, resulting in 270 L/cap∙year for pit latrines and 280 L/cap∙year for septic tanks. Septic tank sludge was more dilute than pit latrine sludge, however, public toilet was not a distinguishing factor. Non-household sources of sludge represent a significant fraction of the total and have different characteristics than household-level sludge. Income level, water connection, black water only, solid waste, number of users, containment volume, emptying frequency, and truck size were predictors of sludge quality. Empirical relationships such as a COD:TS of 1.09 ± 0.56 could be used for more resource efficient sampling campaigns. Based on this approach, spatially available demographic, technical and environmental (SPA-DET) data and statistical relationships between parameters could be used to predict Q&Q of faecal sludge.

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Evidence is emerging that the ability of the placenta to supply nutrients to the developing fetus adapts according to fetal demand. To examine this adaptation further, we tested the hypothesis that placental maternofetal transport of calcium adapts according to fetal calcium requirements. We used a mouse model of fetal growth restriction, the placental-specific Igf2 knockout (P0) mouse, shown previously to transiently adapt placental System-A amino acid transporter activity relative to fetal growth. Fetal and placental weights in P0 mice were reduced when compared with WT at both embryonic day 17 (E17) and E19. Ionized calcium concentration [Ca 2+ ] was significantly lower in P0 fetal blood compared with both WT and maternal blood at E17 and E19, reflecting a reversal of the fetomaternal [Ca 2+ ] gradient. Fetal calcium content was reduced in P0 mice at E17 but not at E19. Unidirectional maternofetal calcium clearance ( Ca K mf ) was not different between WT and P0 at E17 but increased in P0 at E19. Expression of the intracellular calcium-binding protein calbindin-D 9K , previously shown to be rate-limiting for calcium transport, was increased in P0 relative to WT placentas between E17 and E19. These data show an increased placental transport of calcium from E17 to E19 in P0 compared to WT. We suggest that this is an adaptation in response to the reduced fetal calcium accumulation earlier in gestation and speculate that the ability of the placenta to adapt its supply capacity according to fetal demand may stretch across other essential nutrients.fetal growth restriction | calbindin | PMCA | pregnancy

WH, Makuc DM, Schatzkin AG. The low cholesterol-mortality association in a national cohort. J Clin Epidemiol 1992;6:595-601. . Established populations for epidemiologic studies of the elderly: study design and methodology. Aging: Clinical and Experimental Research 1993;5:27-37. 18 Radloff, IS. The CES-D scale: a self-report depression scale for research in

The role of parathyroid hormone-related protein (PTHrP) in fetal calcium homeostasis and placental calcium transport was examined in mice homozygous for the deletion of the PTHrP gene (PTHrP −/− null; NL) compared to PTHrP +/+ (wild-type; WT) and PTHrP +/− (heterozygous; HZ) littermates. Fetal blood ionized calcium was significantly reduced in NL fetuses compared to WT and HZ groups at 18 days of pregnancy (dp) with abolition of the fetomaternal calcium gradient. In situ placental perfusion of the umbilical circulation at 18 dp was used to measure unidirectional clearance of 45 Ca across the placenta in maternofetal ( Ca K mf ) and fetoplacental ( Ca K fp ) directions; Ca K fp was < 5% of Ca K mf for all genotypes. At 18 dp, Ca K mf across perfused placenta and intact placenta ( Ca K mf(intact) ) were similar and concordant with net calcium accretion rates in vivo.Ca K mf was significantly raised in NL fetuses compared to WT and HZ littermates. Calcium accretion was significantly elevated in NL fetuses by 19 dp. Placental calbindin-D 9K expression in NL fetuses was marginally enhanced (P < 0.07) but expression of TRPV6/ECaC2 and plasma membrane Ca 2+ -ATPase (PMCA) isoforms 1 and 4 were unaltered. We conclude that PTHrP is an important regulator of fetal calcium homeostasis with its predominant effect being on unidirectional maternofetal transfer, probably mediated by modifying placental calbindin-D 9K expression. In situ perfusion of mouse placenta is a robust methodology for allowing detailed dissection of placental transfer mechanisms in genetically modified mice.

The Ca(2+)- and phospholipid-binding protein Anx-A1 (annexin 1; lipocortin 1) has been described both as an inhibitor of phospholipase A(2) (PLA(2)) activity and as a mediator of glucocorticoid-regulated cell growth and eicosanoid generation. Here we show that, when compared with Anx-A1(+/+) cells, lung fibroblast cell lines derived from the Anx-A1(-/-) mouse exhibit an altered morphology characterized by a spindle-shaped appearance and an accumulation of intracellular organelles. Unlike their wild-type counterparts, Anx-A1(-/-) cells also overexpress cyclo-oxygenase 2 (COX 2), cytosolic PLA(2) and secretory PLA(2) and in response to fetal calf serum, exhibit an exaggerated release of eicosanoids, which is insensitive to dexamethasone (10(-8)- 10(-6) M) inhibition. Proliferation and serum-induced progression of Anx-A1(+/+) cells from G(0)/G(1) into S phase, and the associated expression of extracellular signal-regulated kinase 2 (ERK2), cyclin-dependent kinase 4 (cdk4) and COX 2, is strongly inhibited by dexamethasone, whereas Anx-A1(-/-) cells are refractory to the drug. Loss of the response to dexamethasone in Anx-A1(-/-) cells occurs against a background of no apparent change in glucocorticoid receptor expression or sensitivity to non-steroidal anti-inflammatory drugs. Taken together, these observations suggest strongly that Anx-A1 functions as an inhibitor of signal-transduction pathways that lead to cell proliferation and may help to explain how glucocorticoids regulate these processes.