Long-term effects of synthetic versus analytic phonics teaching on the reading and spelling ability of 10 year old boys and girls

A comparison was made of 10-year-old boys and girls who had learnt to read by analytic or synthetic phonics methods as part of their early literacy programmes. The boys taught by the synthetic phonics method had better word reading than the girls in their classes, and their spelling and reading comprehension was as good. In contrast, with analytic phonics teaching, although the boys performed as well as the girls in word reading, they had inferior spelling and reading comprehension. Overall, the group taught by synthetic phonics had better word reading, spelling, and reading comprehension. There was no evidence that the synthetic phonics approach, which early on teaches children to blend letter sounds in order to read unfamiliar words, led to any impairment in the reading of irregular words

Orientable total domination in graphs

Given a directed graph $D$, a set $S \subseteq V(D)$ is a total dominating set of $D$ if each vertex in $D$ has an in-neighbor in $S$. The total domination number of $D$, denoted $\gamma_t(D)$, is the minimum cardinality among all total dominating sets of $D$. Given an undirected graph $G$, we study the maximum and minimum total domination numbers among all orientations of $G$. That is, we study the upper (or lower) orientable domination number of $G$, $\rm{DOM}_t(G)$ (or $\rm{dom}_t(G)$), which is the largest (or smallest) total domination number over all orientations of $G$. We characterize those graphs with $\rm{DOM}_t(G) =\rm{dom}_t(G)$ when the girth is at least $7$ as well as those graphs with $\rm{dom}_t(G) = |V(G)|-1$. We also consider how these parameters are effected by removing a vertex from $G$, give exact values of $\rm{DOM}_t(K_{m,n})$ and $\rm{dom}_t(K_{m,n})$ and bound these parameters when $G$ is a grid graph

Comparative Toxicity of Diphacinone to Northern Bobwhite (\u3ci\u3eColinus virginianus\u3c/i\u3e) and American Kestrels (\u3ci\u3eFalco sparverius\u3c/i\u3e)

The acute oral toxicity of the anticoagulant rodenticide diphacinone was found to be about 20 times greater to American kestrels (LD50=97 mg/kg) than to northern bobwhite (LD50=2,014 mg/kg). Several precise and sensitive clotting assays (prothrombin time, Russell’s Viper venom time, thrombin clotting time) were adapted for use in these species, and this combination of assays is recommended to detect effects of diphacinone and other rodenticides on coagulation. Oral administration of diphacinone over a range of doses (sublethal to the extrapolated LD15) prolonged prothrombin time and Russell’s Viper venom time within 24 to 48 hrs post-exposure. Prolongation of in vitro clotting time reflects impaired coagulation complex activity and was detected before or at the onset of overt signs of toxicity and lethality. These data will assist in the development of a pharmacodynamic model to assess and predict rodenticide toxicity to non-target avian species

Comparative Toxicity of Diphacinone to Northern Bobwhite (\u3ci\u3eColinus virginianus\u3c/i\u3e) and American Kestrels (\u3ci\u3eFalco sparverius\u3c/i\u3e)

The acute oral toxicity of the anticoagulant rodenticide diphacinone was found to be about 20 times greater to American kestrels (LD50=97 mg/kg) than to northern bobwhite (LD50=2,014 mg/kg). Several precise and sensitive clotting assays (prothrombin time, Russell’s Viper venom time, thrombin clotting time) were adapted for use in these species, and this combination of assays is recommended to detect effects of diphacinone and other rodenticides on coagulation. Oral administration of diphacinone over a range of doses (sublethal to the extrapolated LD15) prolonged prothrombin time and Russell’s Viper venom time within 24 to 48 hrs post-exposure. Prolongation of in vitro clotting time reflects impaired coagulation complex activity and was detected before or at the onset of overt signs of toxicity and lethality. These data will assist in the development of a pharmacodynamic model to assess and predict rodenticide toxicity to non-target avian species

The Effect of Comb Architecture on Complex Coacervation

Complex coacervation is a widely utilized technique for effecting phase separation, though predictive understanding of molecular-level details remains underdeveloped. Here, we couple coarse-grained Monte Carlo simulations with experimental efforts using a polypeptide-based model system to investigate how a comb-like architecture affects complex coacervation and coacervate stability. Specifically, the phase separation behavior of linear polycation-linear polyanion pairs was compared to that of comb polycation-linear polyanion and comb polycation-comb polyanion pairs. The comb architecture was found to mitigate cooperative interactions between oppositely charged polymers, as no discernible phase separation was observed for comb-comb pairs and complex coacervation of linear-linear pairs yielded stable coacervates at higher salt concentration than linear-comb pairs. This behavior was attributed to differences in counterion release by linear vs. comb polymers during polyeletrolyte complexation. Additionally, the comb polycation formed coacervates with both stereoregular poly(L-glutamate) and racemic poly(D,L-glutamate), whereas the linear polycation formed coacervates only with the racemic polyanion. In contrast, solid precipitates were obtained from mixtures of stereoregular poly(L-lysine) and poly(L-glutamate). Moreover, the formation of coacervates from cationic comb polymers incorporating up to ~90% pendant zwitterionic groups demonstrated the potential for inclusion of comonomers to modulate the hydrophilicity and/or other properties of a coacervate-forming polymer. These results provide the first detailed investigation into the role of polymer architecture on complex coacervation using a chemically and architecturally well-defined model system, and highlight the need for additional research on this topic

Cross-correlation Weak Lensing of SDSS Galaxy Clusters III: Mass-to-light Ratios

We present measurements of the excess mass-to-light ratio measured aroundMaxBCG galaxy clusters observed in the SDSS. This red sequence cluster sample includes objects from small groups with masses ranging from ~5x10^{12} to ~10^{15} M_{sun}/h. Using cross-correlation weak lensing, we measure the excess mass density profile above the universal mean \Delta \rho(r) = \rho(r) - \bar{\rho} for clusters in bins of richness and optical luminosity. We also measure the excess luminosity density \Delta l(r) = l(r) - \bar{l} measured in the z=0.25 i-band. For both mass and light, we de-project the profiles to produce 3D mass and light profiles over scales from 25 kpc/ to 22 Mpc/h. From these profiles we calculate the cumulative excess mass M(r) and excess light L(r) as a function of separation from the BCG. On small scales, where \rho(r) >> \bar{\rho}, the integrated mass-to-light profile may be interpreted as the cluster mass-to-light ratio. We find the M/L_{200}, the mass-to-light ratio within r_{200}, scales with cluster mass as a power law with index 0.33+/-0.02. On large scales, where \rho(r) ~ \bar{\rho}, the M/L approaches an asymptotic value independent of cluster richness. For small groups, the mean M/L_{200} is much smaller than the asymptotic value, while for large clusters it is consistent with the asymptotic value. This asymptotic value should be proportional to the mean mass-to-light ratio of the universe . We find /b^2_{ml} = 362+/-54 h (statistical). There is additional uncertainty in the overall calibration at the ~10% level. The parameter b_{ml} is primarily a function of the bias of the L <~ L_* galaxies used as light tracers, and should be of order unity. Multiplying by the luminosity density in the same bandpass we find \Omega_m/b^2_{ml} = 0.02+/-0.03, independent of the Hubble parameter.Comment: Third paper in a series; v2.0 incorporates ApJ referee's suggestion

Transient Hypoxia Alters Striatal Catecholamine Metabolism in Immature Brain: An In Vivo Microdialysis Study

Microdialysis probes were inserted bilaterally into the striatum of 7-day-old rat pups (n = 30) to examine extracellular fluid levels of dopamine, its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA). The dialysis samples were assayed by HPLC with electrochemical detection. Baseline levels, measured after a 2-h stabilization period, were as follows: dopamine, not detected; DOPAC, 617 ± 33 fmol/min; HVA, 974 ± 42 fmol/min; and 5-HIAA, 276 ± 15 fmol/min. After a 40-min baseline sampling period, 12 animals were exposed to 8% oxygen for 120 min. Hypoxia produced marked reductions in the striatal extracellular fluid levels of both dopamine metabolites ( p < 0.001 by analysis of variance) and a more gradual and less prominent reduction in 5-HIAA levels ( p < 0.02 by analysis of variance), compared with controls (n = 12) sampled in room air. In the first hour after hypoxia, DOPAC and HVA levels rose quickly, whereas 5-HIAA levels remained suppressed. The magnitude of depolarization-evoked release of dopamine (elicited by infusion of potassium or veratrine through the microdialysis probes for 20 min) was evaluated in control and hypoxic animals. Depolarization-evoked dopamine efflux was considerably higher in hypoxic pups than in controls: hypoxic (n = 7), 257 ± 32 fmol/min; control (n = 12), 75 ± 14 fmol/min ( p < 0.001 by analysis of variance). These data demonstrate that a brief exposure to moderate hypoxia markedly disrupts striatal catecholamine metabolism in the immature rodent brain.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66218/1/j.1471-4159.1990.tb01914.x.pd

Better reporting of interventions : template for intervention description and replication (TIDieR) checklist and guide

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