Planning under uncertainty for safe robot exploration using Gaussian process prediction.

The exploration of new environments is a crucial challenge for mobile robots. This task becomes even more complex with the added requirement of ensuring safety. Here, safety refers to the robot staying in regions where the values of certain environmental conditions (such as terrain steepness or radiation levels) are within a predefined threshold.

Short-range multispectral imaging is an inexpensive, fast, and accurate approach to estimate biodiversity in a temperate calcareous grassland.

Image sensing technologies are rapidly increasing the cost-effectiveness of biodiversity monitoring efforts. Species differences in the reflectance of electromagnetic radiation can be used as a surrogate estimate plant biodiversity using multispectral image data. However, these efforts are often hampered by logistical difficulties in broad-scale implementation.

Author Correction: Epigenetic patterns associated with an ascidian invasion: a comparison of closely related clades in their native and introduced ranges.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Epigenetic patterns associated with an ascidian invasion: a comparison of closely related clades in their native and introduced ranges.

Environmentally induced epigenetic modifications have been proposed as one mechanism underlying rapid adaptive evolution of invasive species. Didemnum vexillum is an invasive colonial ascidian that has established in many coastal waters worldwide. Phylogenetic analyses have revealed that D.

Poor sleep quality is associated with obesity and depression in farmers.

Background: Farmers' work schedules can result in inconsistent sleep patterns which negatively impact health.

Purpose: To explore the relationships between sleep, obesity, and depression in working, older farmers and their spouses. Covariates included body mass index (BMI), age, and gender.

Effects of temperature and salinity stress on DNA methylation in a highly invasive marine invertebrate, the colonial ascidian .

Environmentally induced epigenetic changes may contribute to phenotypic plasticity, increase adaptive potential in changing environments, and play a key role in the establishment and spread of invasive species in new habitats. In this study, we used methylation-sensitive amplified polymorphism (MSAP) to assess environmentally induced DNA methylation changes in a globally invasive clonal ascidian, . We tested the effect of increasing temperature (19, 25 and 27 °C) and decreasing salinity (34, 32, 30, 28 and 26 practical salinity units (PSU)) on global DNA methylation, growth and survival rates.

Paenibacillus larvae Phage Tripp Genome Has 378-Base-Pair Terminal Repeats.

Paenibacillus larvae bacteriophage Tripp was isolated from an American foulbrood diseased honey bee hive in North Carolina, USA. The 54,439-bp genome is 48.3% G+C, encodes 92 proteins, no tRNAs, and has 378-bp direct terminal repeats.

Biological and artificial cognition: what can we learn about mechanisms by modelling physical cognition problems using artificial intelligence planning techniques?

Do we fully understand the structure of the problems we present to our subjects in experiments on animal cognition, and the information required to solve them? While we currently have a good understanding of the behavioural and neurobiological mechanisms underlying associative learning processes, we understand much less about the mechanisms underlying more complex forms of cognition in animals. In this study, we present a proposal for a new way of thinking about animal cognition experiments. We describe a process in which a physical cognition task domain can be decomposed into its component parts, and models constructed to represent both the causal events of the domain and the information available to the agent.

Age-related retinal degeneration (arrd2) in a novel mouse model due to a nonsense mutation in the Mdm1 gene.

We observed that a naturally occurring mouse strain developed age-related retinal degeneration (arrd2). These mice had normal fundi, electroretinograms (ERGs) and retinal histology at 6 months of age; vessel attenuation, RPE atrophy and pigmentary abnormalities at 14 months, which progressed to complete loss of photoreceptors and extinguished ERG by 22 months. Genetic analysis revealed that the retinal degeneration in arrd2 segregates in an autosomal recessive manner and the disease gene localizes to mouse chromosome 10.

Iris phenotypes and pigment dispersion caused by genes influencing pigmentation.

Spontaneous mutations altering mouse coat colors have been a classic resource for discovery of numerous molecular pathways. Although often overlooked, the mouse iris is also densely pigmented and easily observed, thus representing a similarly powerful opportunity for studying pigment cell biology. Here, we present an analysis of iris phenotypes among 16 mouse strains with mutations influencing melanosomes.

Allelic variance between GRM6 mutants, Grm6nob3 and Grm6nob4 results in differences in retinal ganglion cell visual responses.

An electroretinogram (ERG) screen identified a mouse with a normal a-wave but lacking a b-wave, and as such it was designated no b-wave3 (nob3). The nob3 phenotype mapped to chromosome 11 in a region containing the metabotropic glutamate receptor 6 gene (Grm6). Sequence analyses of cDNA identified a splicing error in Grm6, introducing an insertion and an early stop codon into the mRNA of affected mice (designated Grm6(nob3)).

Progressive morphological and functional defects in retinas from alpha1 integrin-null mice.

Purpose: The role of integrin/cell matrix interactions between the RPE and the basement membrane in retinal maintenance and function is not well characterized. In this study the functional importance of alpha1beta1 integrin for retinal pigment epithelial cell homeostasis and retinal health was assessed by comparing alpha1 integrin knockout mice with strain- and age-matched wild-type mice.

Methods: Immunolocalization and Western blot analysis of retinas and ARPE19 cells were performed to examine the expression of alpha1beta1 integrin in the RPE.

AAV-mediated gene therapy for retinal degeneration in the rd10 mouse containing a recessive PDEbeta mutation.

Purpose: To test AAV-mediated gene therapy in the rd10 mouse, a natural model of recessive RP caused by mutation of the beta-subunit of rod photoreceptor cGMP phosphodiesterase.

Methods: One eye of a cohort of rd10 mice kept in a dark environment was subretinally injected at postnatal day (P) 14 with 1 microL AAV5-smCBA-PDEbeta. The contralateral eye was not injected.

Dense nuclear cataract caused by the gammaB-crystallin S11R point mutation.

Purpose: To identify the causative gene mutation for a new dominant cataract in mice and to investigate the molecular basis for how the mutated gene leads to a dense nuclear cataract.

Methods: Genomewide linkage analysis and DNA sequencing were used to determine the gene mutation. Histology, immunohistochemistry, and Western blotting were used to characterize lens phenotypes.

Genetic background modifies inner ear and eye phenotypes of jag1 heterozygous mice.

Mice heterozygous for missense mutations of the Notch ligand Jagged1 (Jag1) exhibit head-shaking behavior indicative of an inner ear vestibular defect. In contrast, mice heterozygous for a targeted deletion of the Jag1 gene (Jag1del1) do not demonstrate obvious head-shaking behavior. To determine whether the differences in inner ear phenotypes were due to the types of Jag1 mutations or to differences in genetic background, we crossed Jag1del1 heterozygous mice onto the same genetic background as the missense mutants.

Restoration of cone vision in a mouse model of achromatopsia.

Loss of cone function in the central retina is a pivotal event in the development of severe vision impairment for many prevalent blinding diseases. Complete achromatopsia is a genetic defect resulting in cone vision loss in 1 in 30,000 individuals. Using adeno-associated virus (AAV) gene therapy, we show that it is possible to target cones and rescue both the cone-mediated electroretinogram response and visual acuity in the Gnat2 ( cpfl3 ) mouse model of achromatopsia.

Two mouse retinal degenerations caused by missense mutations in the beta-subunit of rod cGMP phosphodiesterase gene.

We report the chromosomal localization, mutant gene identification, ophthalmic appearance, histology, and functional analysis of two new hereditary mouse models of retinal degeneration not having the Pde6brd1("r", "rd", or "rodless") mutation. One strain harbors an autosomal recessive mutation that maps to mouse chromosome 5. Sequence analysis showed that the retinal degeneration is caused by a missense point mutation in exon 13 of the beta-subunit of the rod cGMP phosphodiesterase (beta-PDE) gene (Pde6b).

Tool from ancient pharmacopoeia prevents vision loss.

Purpose: Bear bile has been used in Asia for over 3,000 years to treat visual disorders, yet its therapeutic potential remains unexplored in Western vision research. The purpose of this study was to test whether treatment of mice undergoing retinal degeneration with tauroursodeoxycholic acid (TUDCA), a primary constituent of bear bile, alters the course of degeneration.

Methods: Two retinal degeneration models were tested: the rd10 mouse, which has a point mutation in the gene encoding the beta subunit of rod phosphodiesterase, and light induced retinal damage (LIRD).

Premature truncation of a novel protein, RD3, exhibiting subnuclear localization is associated with retinal degeneration.

The rd3 mouse is one of the oldest identified models of early-onset retinal degeneration. Using the positional candidate approach, we have identified a C-->T substitution in a novel gene, Rd3, that encodes an evolutionarily conserved protein of 195 amino acids. The rd3 mutation results in a predicted stop codon after residue 106.

Cone photoreceptor function loss-3, a novel mouse model of achromatopsia due to a mutation in Gnat2.

Purpose: To report a novel mouse model of achromatopsia with a cpfl3 mutation found in the ALS/LtJ strain.

Methods: The effects of a cpfl3 mutation were documented using fundus photography, electroretinography (ERG), and histopathology. Genetic analysis was performed using linkage studies and PCR gene identification.

In-frame deletion in a novel centrosomal/ciliary protein CEP290/NPHP6 perturbs its interaction with RPGR and results in early-onset retinal degeneration in the rd16 mouse.

Centrosome- and cilia-associated proteins play crucial roles in establishing polarity and regulating intracellular transport in post-mitotic cells. Using genetic mapping and positional candidate strategy, we have identified an in-frame deletion in a novel centrosomal protein CEP290 (also called NPHP6), leading to early-onset retinal degeneration in a newly identified mouse mutant, rd16. We demonstrate that CEP290 localizes primarily to centrosomes of dividing cells and to the connecting cilium of retinal photoreceptors.

The nob2 mouse, a null mutation in Cacna1f: anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses.

Glutamate release from photoreceptor terminals is controlled by voltage-dependent calcium channels (VDCCs). In humans, mutations in the Cacna1f gene, encoding the alpha1F subunit of VDCCs, underlie the incomplete form of X-linked congenital stationary night blindness (CSNB2). These mutations impair synaptic transmission from rod and cone photoreceptors to bipolar cells.

Early transposable element insertion in intron 9 of the Hsf4 gene results in autosomal recessive cataracts in lop11 and ldis1 mice.

Lens opacity 11 (lop11) is an autosomal recessive mouse cataract mutation that arose spontaneously in the RIIIS/J strain. At 3 weeks of age mice exhibit total cataracts with vacuoles. The lop11 locus was mapped to mouse chromosome 8.

Deficiency of SHP-1 protein-tyrosine phosphatase in "viable motheaten" mice results in retinal degeneration.

Purpose: Viable motheaten mutant mice (abbreviated allele symbol me(v)) are deficient in Src-homology 2-domain phosphatase (SHP)-1, a critical negative regulator of signal transduction in hematopoietic cells. These mice exhibit immune dysfunction, hyperproliferation of myeloid cells, and regenerative anemia. This study focused on the role of SHP-1 in retinal homeostasis.