Agent swarms: cooperation and coordination under stringent communications constraint

Here we consider the communications tactics appropriate for a group of agents that need to ``swarm'' together in a highly adversarial environment. Specifically, whilst they need to exchange information with each other about their location and their plans; at the same time they also need to keep such communications to an absolute minimum. This might be due to a need for stealth, or otherwise be relevant to situations where communications are significantly restricted. Complicating this process is that we assume each agent has (a) no means of passively locating others, (b) it must rely on being updated by reception of appropriate messages; and if no such update messages arrive, (c) then their own beliefs about other agents will gradually become out of date and increasingly inaccurate. Here we use a geometry-free multi-agent model that is capable of allowing for message-based information transfer between agents with different intrinsic connectivities, as would be present in a spatial arrangement of agents. We present agent-centric performance metrics that require only minimal assumptions, and show how simulated outcome distributions, risks, and connectivities depend on the ratio of information gain to loss. We also show that checking for too-long round-trip-times can be an effective minimal-information filter for determining which agents to no longer target with messages.Comment: 11 pager, 7 figure

Use of a novel dataset to explore spatial and social variations in car type, size, usage and emissions

© 2015 The Authors. The 'MOT' vehicle inspection test record dataset recently released by the UK Department for Transport (DfT) provides the ability to estimate annual mileage figures for every individual light duty vehicle greater than 3 years old within Great Britain. Vehicle age, engine size and fuel type are also provided in the dataset and these allow further estimates to be made of fuel consumption, energy use, and per vehicle emissions of both air pollutants and greenhouse gases. The use of this data permits the adoption of a new vehicle-centred approach to assessing emissions and energy use in comparison to previous road-flow and national fuel consumption based approaches. The dataset also allows a spatial attribution of each vehicle to a postcode area, through the reported location of relevant vehicle testing stations. Consequently, this new vehicle data can be linked with socio-demographic data in order to determine the potential characteristics of vehicle owners.This paper provides a broad overview of the types of analyses that are made possible by these data, with a particular focus on distance driven and pollutant emissions. The intention is to demonstrate the very broad potential for this data, and to highlight where more focused analysis could be useful. The findings from the work have important implications for understanding the distributional impacts of transport related policies and targeting messaging and interventions for the reduction of car use

Techniques for the inference of mileage rates from MOT data

Mathematical and computational techniques are developed for the processing and analysis of annual MOT (roadworthiness) test data that the UK Department for Transport has placed in the public domain. Firstly, techniques are given that clean erroneous records and a linking procedure is provided that permits the inference of an individual vehicle's mileage between consecutive tests. Methods are then developed that analyse aggregate mileage totals, as a function of vehicle age, class and geography. The inference of aggregate mileage rates as a function of time is then considered

Primary ciliary dyskinesia with normal ultrastructure:three-dimensional tomography detects absence of DNAH11

In primary ciliary dyskinesia (PCD), motile ciliary dysfunction arises from ciliary defects usually confirmed by transmission electron microscopy (TEM). In 30% of patients, such as those with DNAH11 mutations, apparently normal ultrastructure makes diagnosis difficult. Genetic analysis supports diagnosis, but may not identify definitive causal variants. Electron tomography, an extension of TEM, produces three-dimensional ultrastructural ciliary models with superior resolution to TEM. Our hypothesis is that tomography using existing patient samples will enable visualisation of DNAH11-associated ultrastructural defects. Dual axis tomograms from araldite-embedded nasal cilia were collected in 13 PCD patients with normal ultrastructure (DNAH11 n=7, HYDIN n=2, CCDC65 n=3 and DRC1 n=1) and six healthy controls, then analysed using IMOD and Chimera software. DNAH11 protein is localised to the proximal ciliary region. Within this region, electron tomography indicated a deficiency of >25% of proximal outer dynein arm volume in all patients with DNAH11 mutations (n=7) compared to other patients with PCD and normal ultrastructure (n=6) and healthy controls (n=6). DNAH11 mutations cause a shared abnormality in ciliary ultrastructure previously undetectable by TEM. Advantageously, electron tomography can be used on existing diagnostic samples and establishes a structural abnormality where ultrastructural studies were previously normal

1936: Abilene Christian College Bible Lectures - Full Text

Delivered in the auditorium of Abilene Christian College, Abilene, Texas, February 193

Risk factors for situs defects and congenital heart disease in primary ciliary dyskinesia

Primary ciliary dyskinesia (PCD) is associated with abnormal organ positioning (situs) and congenital heart disease (CHD). This study investigated genotype–phenotype associations in PCD to facilitate risk predictions for cardiac and laterality defects. This retrospective cohort study of 389 UK patients with PCD found 51% had abnormal situs and 25% had CHD and/or laterality defects other than situs inversus totalis. Patients with biallelic mutations in a subset of nine PCD genes had normal situs. Patients with consanguineous parents had higher odds of situs abnormalities than patients with non-consanguineous parents. Patients with abnormal situs had higher odds of CHD and/or laterality defects

Clinical utility of NGS diagnosis and disease stratification in a multiethnic primary ciliary dyskinesia cohort

Background Primary ciliary dyskinesia (PCD), a genetically heterogeneous condition enriched in some consanguineous populations, results from recessive mutations affecting cilia biogenesis and motility. Currently, diagnosis requires multiple expert tests.Methods The diagnostic utility of multigene panel next-generation sequencing (NGS) was evaluated in 161 unrelated families from multiple population ancestries.Results Most (82%) families had affected individuals with biallelic or hemizygous (75%) or single (7%) pathogenic causal alleles in known PCD genes. Loss-of-function alleles dominate (73% frameshift, stop-gain, splice site), most (58%) being homozygous, even in non-consanguineous families. Although 57% (88) of the total 155 diagnostic disease variants were novel, recurrent mutations and mutated genes were detected. These differed markedly between white European (52% of families carry DNAH5 or DNAH11 mutations), Arab (42% of families carry CCDC39 or CCDC40 mutations) and South Asian (single LRRC6 or CCDC103 mutations carried in 36% of families) patients, revealing a striking genetic stratification according to population of origin in PCD. Genetics facilitated successful diagnosis of 81% of families with normal or inconclusive ultrastructure and 67% missing prior ultrastructure results.Conclusions This study shows the added value of high-throughput targeted NGS in expediting PCD diagnosis. Therefore, there is potential significant patient benefit in wider and/or earlier implementation of genetic screening

X-linked primary ciliary dyskinesia due to mutations in the cytoplasmic axonemal dynein assembly factor PIH1D3

By moving essential body fluids and molecules, motile cilia and flagella govern respiratory mucociliary clearance, laterality determination and the transport of gametes and cerebrospinal fluid. Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder frequently caused by non-assembly of dynein arm motors into cilia and flagella axonemes. Before their import into cilia and flagella, multi-subunit axonemal dynein arms are thought to be stabilized and pre-assembled in the cytoplasm through a DNAAF2–DNAAF4–HSP90 complex akin to the HSP90 co-chaperone R2TP complex. Here, we demonstrate that large genomic deletions as well as point mutations involving PIH1D3 are responsible for an X-linked form of PCD causing disruption of early axonemal dynein assembly. We propose that PIH1D3, a protein that emerges as a new player of the cytoplasmic pre-assembly pathway, is part of a complementary conserved R2TP-like HSP90 co-chaperone complex, the loss of which affects assembly of a subset of inner arm dyneins

Exposure to the Environmental Endocrine Disruptor TCDD and Human Reproductive Dysfunction: Translating Lessons from Murine Models

Humans and other animals are exposed to a wide array of man-made toxicants, many of which act as endocrine disruptors that exhibit differential effects across the lifespan. In humans, while the impact of adult exposure is known for some compounds, the potential consequences of developmental exposure to endocrine disrupting chemicals (EDCs) is more difficult to ascertain. Animal studies have revealed that exposure to EDCs prior to puberty can lead to adult reproductive disease and dysfunction. Specifically, in adult female mice with an early life exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), we demonstrated a transgenerational occurrence of several reproductive diseases that have been linked to endometriosis in women. Herein, we review the evidence for TCDD-associated development of adult reproductive disease as well as known epigenetic alterations associated with TCDD and/or endometriosis. We will also introduce new "Organ-on-Chip" models which, combined with our established murine model, are expected to further enhance our ability to examine alterations in gene-environment interactions that lead to heritable disease