Neural Potential Field for Obstacle-Aware Local Motion Planning

Model predictive control (MPC) may provide local motion planning for mobile robotic platforms. The challenging aspect is the analytic representation of collision cost for the case when both the obstacle map and robot footprint are arbitrary. We propose a Neural Potential Field: a neural network model that returns a differentiable collision cost based on robot pose, obstacle map, and robot footprint. The differentiability of our model allows its usage within the MPC solver. It is computationally hard to solve problems with a very high number of parameters. Therefore, our architecture includes neural image encoders, which transform obstacle maps and robot footprints into embeddings, which reduce problem dimensionality by two orders of magnitude. The reference data for network training are generated based on algorithmic calculation of a signed distance function. Comparative experiments showed that the proposed approach is comparable with existing local planners: it provides trajectories with outperforming smoothness, comparable path length, and safe distance from obstacles. Experiment on Husky UGV mobile robot showed that our approach allows real-time and safe local planning. The code for our approach is presented at https://github.com/cog-isa/NPField together with demo video

Verification of Photometric Parallaxes with Gaia DR2 Data

Results of comparison of Gaia DR2 parallaxes with data derived from a combined analysis of 2MASS (Two Micron All-Sky Survey), SDSS (Sloan Digital Sky Survey), GALEX (Galaxy Evolution Explorer), and UKIDSS (UKIRT Infrared Deep Sky Survey) surveys in four selected high-latitude $|b|>48^{\circ}$ sky areas are presented. It is shown that multicolor photometric data from large modern surveys can be used for parameterization of stars closer than 4400 pc and brighter than $g_{SDSS} = 19.^m6$, including estimation of parallax and interstellar extinction value. However, the stellar luminosity class should be properly determined.Comment: 11 pages, 5 figure

A 125 kDa RNase E/G-like protein is present in plastids and is essential for chloroplast development and autotrophic growth in Arabidopsis*

Endoribonuclease E (RNase E) is a regulator of global gene expression in Escherichia coli and is the best studied member of the RNase E/G ribonuclease family. Homologues are present in other bacteria but the roles of plant RNase E/G-like proteins are not known. Arabidopsis thaliana contains a single nuclear gene (At2g04270) encoding a product with the conserved catalytic domain of RNase E/G-like proteins. At2g04270 and the adjacent At2g04280 gene form converging transcription units with a ∼40 base overlap at their 3’ ends. Several translation products were predicted from the analyses of At2g04270 cDNAs. An antibody raised against a recombinant A. thaliana RNase E/G-like protein recognized a 125 kDa protein band in purified chloroplast preparations fractionated by SDS-PAGE. The 125 kDa RNase E/G-like protein was detected in cotyledons, rosette and cauline leaves. T-DNA insertions in exon 6 or intron 11 of At2g04270 result in loss of the 125 kDa band or truncation to a 110 kDa band. Loss of At2g04270 function resulted in the arrest of chloroplast development, loss of autotrophic growth, and reduced plastid ribosomal, psbA and rbcL RNA levels. Homozygous mutant plants were pale-green, contained smaller plastids with fewer thylakoids and shorter granal stacks than wild-type chloroplasts, and required sucrose at all growth stages following germination right up to flowering and setting seeds. Recombinant A. thaliana RNase E/G-like proteins rescued an E. coli RNase E mutant and cleaved an rbcL RNA substrate. Expression of At2g04270 was highly correlated with genes encoding plastid polyribonucleotide phosphorylase, S1 RNA-binding, and CRS1/YhbY domain proteins

Three-dimensional electron microscopy reveals the evolution of glomerular barrier injury

Open access articleGlomeruli are highly sophisticated filters and glomerular disease is the leading cause of kidney failure. Morphological change in glomerular podocytes and the underlying basement membrane are frequently observed in disease, irrespective of the underlying molecular etiology. Standard electron microscopy techniques have enabled the identification and classification of glomerular diseases based on two-dimensional information, however complex three-dimensional ultrastructural relationships between cells and their extracellular matrix cannot be easily resolved with this approach. We employed serial block face-scanning electron microscopy to investigate Alport syndrome, the commonest monogenic glomerular disease, and compared findings to other genetic mouse models of glomerular disease (Myo1e−/−, Ptpro−/−). These analyses revealed the evolution of basement membrane and cellular defects through the progression of glomerular injury. Specifically we identified sub-podocyte expansions of the basement membrane with both cellular and matrix gene defects and found a corresponding reduction in podocyte foot process number. Furthermore, we discovered novel podocyte protrusions invading into the glomerular basement membrane in disease and these occurred frequently in expanded regions of basement membrane. These findings provide new insights into mechanisms of glomerular barrier dysfunction and suggest that common cell-matrix-adhesion pathways are involved in the progression of disease regardless of the primary insult

Crystal Structure Defects in Titanium Nickelide after Abc Pressing at Lowered Temperature

The experimental results regarding the effect of warm (573 K) abc pressing with an increase in the specified true strain, e, up to 9.55, on the microstructure and crystal structure defects (dislocations, vacancies) of the Ti49.8Ni50.2 (at %) alloy are presented. It is shown that all samples (regardless of e) have a two-level microstructure. The grains-subgrains of the submicrocrystalline scale level are in the volumes of large grains. The average sizes of both large grains and subgrain grains decrease with increasing e to 9.55 (from 27 to 12 µm and from 0.36 to 0.13 µm, respectively). All samples had a two-phase state (rhombohedral R and monoclinic B19′ martensitic phases) at 295 K. The full-profile analysis of X-ray reflections of the B2 phase obtained at 393 K shows that the dislocation density increases from 1014 m−2 to 1015 m−2 after pressing with e = 1.84 and reaches 2·1015 m−2 when e increases to 9.55. It has been established by positron annihilation lifetime spectroscopy that dislocations are the main type of defects in initial samples and the only type of defects in samples after abc pressing. The lifetime of positrons trapped by dislocations is 166 ps, and the intensity of this component increases from 83% in the initial samples to 99.4% after pressing with e = 9.55. The initial samples contain a component with a positron lifetime of 192 ps (intensity 16.4%), which corresponds to the presence of monovacancies in the nickel sublattice of the B2 phase (concentration ≈10−5). This component is absent in the positron lifetime spectra in the samples after pressing. The results of the analysis of the Doppler broadening spectroscopy correlate with the data obtained by the positron annihilation lifetime spectroscopy

Commercial articulated collaborative in situ 3D bioprinter for skin wound healing

In situ bioprinting is one of the most clinically relevant techniques in the emerging bioprinting technology because it could be performed directly on the human body in the operating room and it does not require bioreactors for post-printing tissue maturation. However, commercial in situ bioprinters are still not available on the market. In this study, we demonstrated the benefit of the originally developed first commercial articulated collaborative in situ bioprinter for the treatment of full-thickness wounds in rat and porcine models. We used an articulated and collaborative robotic arm from company KUKA and developed original printhead and correspondence software enabling in situ bioprinting on curve and moving surfaces. The results of in vitro and in vivo experiments show that in situ bioprinting of bioink induces a strong hydrogel adhesion and enables printing on curved surfaces of wet tissues with a high level of fidelity. The in situ bioprinter was convenient to use in the operating room. Additional in vitro experiments (in vitro collagen contraction assay and in vitro 3D angiogenesis assay) and histological analyses demonstrated that in situ bioprinting improves the quality of wound healing in rat and porcine skin wounds. The absence of interference with the normal process of wound healing and even certain improvement in the dynamics of this process strongly suggests that in situ bioprinting could be used as a novel therapeutic modality in wound healing.publishersversionPeer reviewe

Exploring van der Waals materials with high anisotropy: geometrical and optical approaches

The emergence of van der Waals (vdW) materials resulted in the discovery of their giant optical, mechanical, and electronic anisotropic properties, immediately enabling countless novel phenomena and applications. Such success inspired an intensive search for the highest possible anisotropic properties among vdW materials. Furthermore, the identification of the most promising among the huge family of vdW materials is a challenging quest requiring innovative approaches. Here, we suggest an easy-to-use method for such a survey based on the crystallographic geometrical perspective of vdW materials followed by their optical characterization. Using our approach, we found As2S3 as a highly anisotropic vdW material. It demonstrates rare giant in-plane optical anisotropy, high refractive index and transparency in the visible range, overcoming the century-long record set by rutile. Given these benefits, As2S3 opens a pathway towards next-generation nanophotonics as demonstrated by an ultrathin true zero-order quarter-waveplate that combines classical and the Fabry-Perot optical phase accumulations. Hence, our approach provides an effective and easy-to-use method to find vdW materials with the utmost anisotropic properties.Comment: 11 pages, 5 figure

A quantitative brain map of experimental cerebral malaria pathology

The murine model of experimental cerebral malaria (ECM) has been utilised extensively in recent years to study the pathogenesis of human cerebral malaria (HCM). However, it has been proposed that the aetiologies of ECM and HCM are distinct, and, consequently, no useful mechanistic insights into the pathogenesis of HCM can be obtained from studying the ECM model. Therefore, in order to determine the similarities and differences in the pathology of ECM and HCM, we have performed the first spatial and quantitative histopathological assessment of the ECM syndrome. We demonstrate that the accumulation of parasitised red blood cells (pRBCs) in brain capillaries is a specific feature of ECM that is not observed during mild murine malaria infections. Critically, we show that individual pRBCs appear to occlude murine brain capillaries during ECM. As pRBC-mediated congestion of brain microvessels is a hallmark of HCM, this suggests that the impact of parasite accumulation on cerebral blood flow may ultimately be similar in mice and humans during ECM and HCM, respectively. Additionally, we demonstrate that cerebrovascular CD8+ T-cells appear to co-localise with accumulated pRBCs, an event that corresponds with development of widespread vascular leakage. As in HCM, we show that vascular leakage is not dependent on extensive vascular destruction. Instead, we show that vascular leakage is associated with alterations in transcellular and paracellular transport mechanisms. Finally, as in HCM, we observed axonal injury and demyelination in ECM adjacent to diverse vasculopathies. Collectively, our data therefore shows that, despite very different presentation, and apparently distinct mechanisms, of parasite accumulation, there appear to be a number of comparable features of cerebral pathology in mice and in humans during ECM and HCM, respectively. Thus, when used appropriately, the ECM model may be useful for studying specific pathological features of HCM

Pancreatic ductal adenocarcinoma cells employ integrin α6β4 to form hemidesmosomes and regulate cell proliferation

Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis due to its aggressive progression, late detection and lack of druggable driver mutations, which often combine to result in unsuitability for surgical intervention. Together with activating mutations of the small GTPase KRas, which are found in over 90% of PDAC tumours, a contributory factor for PDAC tumour progression is formation of a rigid extracellular matrix (ECM) and associated desmoplasia. This response leads to aberrant integrin signalling, and accelerated proliferation and invasion. To identify the integrin adhesion systems that operate in PDAC, we analysed a range of pancreatic ductal epithelial cell models using 2D, 3D and organoid culture systems. Proteomic analysis of isolated integrin receptor complexes from human pancreatic ductal epithelial (HPDE) cells predominantly identified integrin α6β4 and hemidesmosome components, rather than classical focal adhesion components. Electron microscopy, together with immunofluorescence, confirmed the formation of hemidesmosomes by HPDE cells, both in 2D and 3D culture systems. Similar results were obtained for the human PDAC cell line, SUIT-2. Analysis of HPDE cell secreted proteins and cell-derived matrices (CDM) demonstrated that HPDE cells secrete a range of laminin subunits and form a hemidesmosome-specific, laminin 332-enriched ECM. Expression of mutant KRas (G12V) did not affect hemidesmosome composition or formation by HPDE cells. Cell-ECM contacts formed by mouse and human PDAC organoids were also assessed by electron microscopy. Organoids generated from both the PDAC KPC mouse model and human patient-derived PDAC tissue displayed features of acinar-ductal cell polarity, and hemidesmosomes were visible proximal to prominent basement membranes. Furthermore, electron microscopy identified hemidesmosomes in normal human pancreas. Depletion of integrin β4 reduced cell proliferation in both SUIT-2 and HPDE cells, reduced the number of SUIT-2 cells in S-phase, and induced G1 cell cycle arrest, suggesting a requirement for α6β4-mediated adhesion for cell cycle progression and growth. Taken together, these data suggest that laminin-binding adhesion mechanisms in general, and hemidesmosome-mediated adhesion in particular, may be under-appreciated in the context of PDAC. Proteomic data are available via ProteomeXchange with the identifiers PXD027803, PXD027823 and PXD027827

Heimler Syndrome is Caused by Hypomorphic Mutations in the Peroxisome-Biogenesis Genes PEX1 and PEX6

Heimler syndrome (HS) is a rare recessive disorder characterized by sensorineural hearing loss (SNHL), amelogenesis imperfecta, nail abnormalities and occasional or late onset retinal pigmentation. We ascertained eight families with HS, and - using a whole exome sequencing approach - identified biallelic mutations in PEX1 or PEX6 in six of them. Loss of function mutations in both genes are known causes of a spectrum of autosomal recessive peroxisome biogenesis disorders (PBDs), including Zellweger syndrome. PBDs are characterized by leukodystrophy, hypotonia, SNHL, retinopathy, and skeletal, craniofacial, and liver abnormalities. We demonstrate that each HS family has at least one hypomorphic allele that results in extremely mild peroxisomal dysfunction. Although individuals with HS share some subtle clinical features found in PBDs, the overlap is minimal and the diagnosis was not suggested by routine blood and skin fibroblast analyses used to detect PBDs. In conclusion, our findings define Heimler syndrome as a mild PBD, expanding the pleiotropy of mutations in PEX1 and PEX6