Language transmission in the family in Wales: an example of innovative language planning.

This paper examines the achievements to date of Twf (“Growth”) — a project initiated as part of language planning efforts in Wales to encourage families to bring up their children to be bilingual. Evidence is presented of the ways in which the project has succeeded in raising awareness of the advantages of bilingualism amongst parents, prospective parents and the public at large by working strategically with health professionals and Early Years organizations, and by developing a range of highly innovative promotional materials. Given the central importance of the family as a site of intergenerational language transmission, the achievements of this project are likely to be of interest to those concerned with language planning in other minority communities in many other parts of the world. The lessons for language planning both in Wales and in other settings are discussed.

Intergenerational transmission of social anxiety: the role of social referencing processes in infancy

Responses to an unfamiliar adult were examined in infants of mothers with social phobia (N = 79) and infants of nonanxious comparison mothers (N = 77) at 10 and 14 months in a social referencing paradigm. On each occasion, a female stranger first interacted with the mother and then approached and interacted with the infant. Over time, infants of mothers with social phobia showed increasing avoidance of the stranger, particularly when they were behaviorally inhibited. In boys, maternal social phobia was associated with increasing fearful responses. Infant avoidance was predicted by expressed maternal anxiety and low levels of encouragement to interact with the stranger. The findings are discussed in relation to theories concerning the intergenerational transmission of social anxiety.

Transmission of social anxiety from mother to infant: an experimental study using a social referencing paradigm

In this experiment we investigated the impact of indirect expressions of maternal social anxiety on infant interactions with a stranger. A social referencing paradigm was used in which infants first observed their mothers interacting with a stranger and then interacted with the stranger themselves. Mothers made no direct communicative gestures to the infant concerning the stranger throughout the procedure. There were two experimental conditions experienced by all mother-infant pairs (N = 24; 12 boys)-non-anxious and socially anxious-and there were two male strangers. Infants were between 12 and 14 months (M = 12.8, SD =.76). Order of condition and stranger presentation were counterbalanced. Before testing, mothers, none of whom were significantly socially anxious, were trained to behave in a non-anxious and a socially anxious manner on the basis of clinical and empirical descriptions of social phobia. The results showed that, compared to their responses following their mothers interacting normally with a stranger, following a socially anxious mother-stranger interaction, infants were significantly more fearful and avoidant with the stranger. Infant-stranger avoidance was further modified by infant temperament; high fear infants were more avoidant in the socially anxious condition than low-fear infants. We discuss these findings in light of the possible mechanisms underpinning infant affective and behavioral responsiveness. (c) 2005 Elsevier Ltd. All rights reserved

Impact of transmission errors in enhanced relay-enabled distributed coordination function

This paper analyzes the performance of Enhanced relay-enabled Distributed Coordination Function (ErDCF) for wireless ad hoc networks under transmission errors. The idea of ErDCF is to use high data rate nodes to work as relays for the low data rate nodes. ErDCF achieves higher throughput and reduces energy consumption compared to IEEE 802.11 Distributed Coordination Function (DCF) in an ideal channel environment. However, there is a possibility that this expected gain may decrease in the presence of transmission errors. In this work, we modify the saturation throughput model of ErDCF to accurately reflect the impact of transmission errors under different rate combinations. It turns out that the throughput gain of ErDCF can still be maintained under reasonable link quality and distance.

Analysis of enhanced relay-enabled distributed coordination function under transmission errors

This paper analyzes the performance of enhanced relay-enabled distributed coordination function (ErDCF) for wireless ad hoc networks under transmission errors. The idea of ErDCF is to use high data rate nodes to work as relays for the low data rate nodes. ErDCF achieves higher throughput and reduces energy consumption compared to IEEE 802.11 distributed coordination function (DCF) in an ideal channel environment. However, there is a possibility that this expected gain may decrease in the presence of transmission errors. In this work, we modify the saturation throughput model of ErDCF to accurately reflect the impact of transmission errors under different rate combinations. It turns out that the throughput gain of ErDCF can still be maintained under reasonable link quality and distance.

On the design of opportunistic cooperative transmission strategies with partial CSI information

The aim of this paper is to study the impact of channel state information on the design of cooperative transmission protocols. This is motivated by the fact that the performance gain achieved by cooperative diversity comes at the price of the extra bandwidth resource consumption. Several opportunistic relaying strategies are developed to fully utilize the different types of a priori channel information. The information-theoretic measures such as outage probability and diversity-multiplexing tradeoff are developed for the proposed protocols. The analytical and numerical results demonstrate that the use of such a priori information increases the spectral efficiency of cooperative diversity, especially at low signal-to-noise ratio.

Adaptive alarm processor for fault diagnosis on power transmission networks

The authors describe a learning classifier system (LCS) which employs genetic algorithms (GA) for adaptive online diagnosis of power transmission network faults. The system monitors switchgear indications produced by a transmission network, reporting fault diagnoses on any patterns indicative of faulted components. The system evaluates the accuracy of diagnoses via a fault simulator developed by National Grid Co. and adapts to reflect the current network topology by use of genetic algorithms.

Precision of quasi-optical null-balanced bridge techniques for transmission and reflection coefficient measurements

The precision of quasioptical null-balanced bridge instruments for transmission and reflection coefficient measurements at millimeter and submillimeter wavelengths is analyzed. A Jones matrix analysis is used to describe the amount of power reaching the detector as a function of grid angle orientation, sample transmittance/reflectance and phase delay. An analysis is performed of the errors involved in determining the complex transmission and reflection coefficient after taking into account the quantization error in the grid angle and micrometer readings, the transmission or reflection coefficient of the sample, the noise equivalent power of the detector, the source power and the post-detection bandwidth. For a system fitted with a rotating grid with resolution of 0.017 rad and a micrometer quantization error of 1 μm, a 1 mW source, and a detector with a noise equivalent power 5×10−9 W Hz−1/2, the maximum errors at an amplitude transmission or reflection coefficient of 0.5 are below ±0.025.

Inhibition of synaptic transmission and G protein modulation by synthetic CaV2.2 Ca2+ channel peptides

Abstract: Modulation of presynaptic voltage-dependent Ca+ channels is a major means of controlling neurotransmitter release. The CaV 2.2 Ca2+ channel subunit contains several inhibitory interaction sites for Gβγ subunits, including the amino terminal (NT) and I–II loop. The NT and I–II loop have also been proposed to undergo a G protein-gated inhibitory interaction, whilst the NT itself has also been proposed to suppress CaV 2 channel activity. Here, we investigate the effects of an amino terminal (CaV 2.2[45–55]) ‘NT peptide’ and a I–II loop alpha interaction domain (CaV 2.2[377–393]) ‘AID peptide’ on synaptic transmission, Ca2+ channel activity and G protein modulation in superior cervical ganglion neurones (SCGNs). Presynaptic injection of NT or AID peptide into SCGN synapses inhibited synaptic transmission and also attenuated noradrenaline-induced G protein modulation. In isolated SCGNs, NT and AID peptides reduced whole-cell Ca2+ current amplitude, modified voltage dependence of Ca2+ channel activation and attenuated noradrenaline-induced G protein modulation. Co-application of NT and AID peptide negated inhibitory actions. Together, these data favour direct peptide interaction with presynaptic Ca2+ channels, with effects on current amplitude and gating representing likely mechanisms responsible for inhibition of synaptic transmission. Mutations to residues reported as determinants of Ca2+ channel function within the NT peptide negated inhibitory effects on synaptic transmission, Ca2+ current amplitude and gating and G protein modulation. A mutation within the proposed QXXER motif for G protein modulation did not abolish inhibitory effects of the AID peptide. This study suggests that the CaV 2.2 amino terminal and I–II loop contribute molecular determinants for Ca2+ channel function; the data favour a direct interaction of peptides with Ca2+ channels to inhibit synaptic transmission and attenuate G protein modulation. Non-technical summary: Nerve cells (neurones) in the body communicate with each other by releasing chemicals (neurotransmitters) which act on proteins called receptors. An important group of receptors (called G protein coupled receptors, GPCRs) regulate the release of neurotransmitters by an action on the ion channels that let calcium into the cell. Here, we show for the first time that small peptides based on specific regions of calcium ion channels involved in GPCR signalling can themselves inhibit nerve cell communication. We show that these peptides act directly on calcium channels to make them more difficult to open and thus reduce calcium influx into native neurones. These peptides also reduce GPCR-mediated signalling. This work is important in increasing our knowledge about modulation of the calcium ion channel protein; such knowledge may help in the development of drugs to prevent signalling in pathways such as those involved in pain perception.