Unsupervised Monocular Depth Estimation for Night-time Images using Adversarial Domain Feature Adaptation

In this paper, we look into the problem of estimating per-pixel depth maps from unconstrained RGB monocular night-time images which is a difficult task that has not been addressed adequately in the literature. The state-of-the-art day-time depth estimation methods fail miserably when tested with night-time images due to a large domain shift between them. The usual photo metric losses used for training these networks may not work for night-time images due to the absence of uniform lighting which is commonly present in day-time images, making it a difficult problem to solve. We propose to solve this problem by posing it as a domain adaptation problem where a network trained with day-time images is adapted to work for night-time images. Specifically, an encoder is trained to generate features from night-time images that are indistinguishable from those obtained from day-time images by using a PatchGAN-based adversarial discriminative learning method. Unlike the existing methods that directly adapt depth prediction (network output), we propose to adapt feature maps obtained from the encoder network so that a pre-trained day-time depth decoder can be directly used for predicting depth from these adapted features. Hence, the resulting method is termed as "Adversarial Domain Feature Adaptation (ADFA)" and its efficacy is demonstrated through experimentation on the challenging Oxford night driving dataset. Also, The modular encoder-decoder architecture for the proposed ADFA method allows us to use the encoder module as a feature extractor which can be used in many other applications. One such application is demonstrated where the features obtained from our adapted encoder network are shown to outperform other state-of-the-art methods in a visual place recognition problem, thereby, further establishing the usefulness and effectiveness of the proposed approach.Comment: ECCV 202

The responses of evapotranspiration due to changes of LUCC under seawater intrusion in a coastal region

The paper provides a coherent pattern identification analysis of the impacts of coastal land use and land cover (LULC) on evapotranspiration (ET) under the impact of seawater intrusion. The study applied the Landsat satellite data to characterize the LULC at Laizhou Bay, Shandong Province, China. Then, the ET and heat fluxes were estimated using the surface energy balance algorithm for land model with two-time phase thermal infrared band images and regional surface parameters. This allowed for the eventual linkage of seawater intrusion to land use/cover changes (LUCC) and ET variations over time. The case study discussed in this paper carried out a coastal landscape dynamics assessment using multi-source and multi-sensor remote sensing technologies. The results are: (1) due to its distance from the sea, the vegetation index (modified soil-adjusted vegetation index, MSAVI) gradually increases with the gradual increase of land use grade (Uindex); (2) there are a variety of types of relational patterns between parameters (LST, G(n), MSAVI, and Uindex) and ET (positive, negative, and no relationship); and (3) seawater intrusion significantly affected the spatial pattern of LUCC, which evidently affected the spatial distribution of ET. The spatial distribution pattern and change characteristics of ET were formed by double driving forces of seawater intrusion and LUCC under the background effects of regional climate.The paper provides a coherent pattern identification analysis of the impacts of coastal land use and land cover (LULC) on evapotranspiration (ET) under the impact of seawater intrusion. The study applied the Landsat satellite data to characterize the LULC at Laizhou Bay, Shandong Province, China. Then, the ET and heat fluxes were estimated using the surface energy balance algorithm for land model with two-time phase thermal infrared band images and regional surface parameters. This allowed for the eventual linkage of seawater intrusion to land use/cover changes (LUCC) and ET variations over time. The case study discussed in this paper carried out a coastal landscape dynamics assessment using multi-source and multi-sensor remote sensing technologies. The results are: (1) due to its distance from the sea, the vegetation index (modified soil-adjusted vegetation index, MSAVI) gradually increases with the gradual increase of land use grade (Uindex); (2) there are a variety of types of relational patterns between parameters (LST, G(n), MSAVI, and Uindex) and ET (positive, negative, and no relationship); and (3) seawater intrusion significantly affected the spatial pattern of LUCC, which evidently affected the spatial distribution of ET. The spatial distribution pattern and change characteristics of ET were formed by double driving forces of seawater intrusion and LUCC under the background effects of regional climate

Tim-3 Negatively Regulates IL-12 Expression by Monocytes in HCV Infection

T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3) is a newly identified negative immunomodulator that is up-regulated on dysfunctional T cells during viral infections. The expression and function of Tim-3 on human innate immune responses during HCV infection, however, remains poorly characterized. In this study, we report that Tim-3 is constitutively expressed on human resting CD14+ monocyte/macrophages (M/MØ) and functions as a cap to block IL-12, a key pro-inflammatory cytokine linking innate and adaptive immune responses. Tim-3 expression is significantly reduced and IL-12 expression increased upon stimulation with Toll-like receptor 4 (TLR4) ligand - lipopolysaccharide (LPS) and TLR7/8 ligand - R848. Notably, Tim-3 is over-expressed on un-stimulated as well as TLR-stimulated M/MØ, which is inversely associated with the diminished IL-12 expression in chronically HCV-infected individuals when compared to healthy subjects. Up-regulation of Tim-3 and inhibition of IL-12 are also observed in M/MØ incubated with HCV-expressing hepatocytes, as well as in primary M/MØ or monocytic THP-1 cells incubated with HCV core protein, an effect that mimics the function of complement C1q and is reversible by blocking the HCV core/gC1qR interaction. Importantly, blockade of Tim-3 signaling significantly rescues HCV-mediated inhibition of IL-12, which is primarily expressed by Tim-3 negative M/MØ. Tim-3 blockade reduces HCV core-mediated expression of the negative immunoregulators PD-1 and SOCS-1 and increases STAT-1 phosphorylation. Conversely, blocking PD-1 or silencing SOCS-1 gene expression also decreases Tim-3 expression and enhances IL-12 secretion and STAT-1 phosphorylation. These findings suggest that Tim-3 plays a crucial role in negative regulation of innate immune responses, through crosstalk with PD-1 and SOCS-1 and limiting STAT-1 phosphorylation, and may be a novel target for immunotherapy to HCV infection

Growth of centimeter scale carbon wires using in-liquid AC arc discharge:

A novel observation of the formation of carbon wire in a carbon-based liquid solvent, using in liquid high voltage AC arc discharge is described. The authors describe the observed phenomenon, technical equipment needed to achieve the effect and preliminary qualitative results of obtained material. The wire consisted of well packed layers of carbon elements. The arc-discharge method is a simple, low cost method for the production of three dimensional carbon structures. A further research is needed to get a thorough understanding of the phenomenon

SHP-2 Promotes the Maturation of Oligodendrocyte Precursor Cells Through Akt and ERK1/2 Signaling In Vitro

Background: Oligodendrocyte precursor cells (OPCs) differentiate into oligodendrocytes (OLs), which are responsible for myelination. Myelin is essential for saltatory nerve conduction in the vertebrate nervous system. However, the molecular mechanisms of maturation and myelination by oligodendrocytes remain elusive. Methods and Findings: In the present study, we showed that maturation of oligodendrocytes was attenuated by sodium orthovanadate (a comprehensive inhibitor of tyrosine phosphatases) and PTPi IV (a specific inhibitor of SHP-2). It is also found that SHP-2 was persistently expressed during maturation process of OPCs. Down-regulation of endogenous SHP-2 led to impairment of oligodendrocytes maturation and this effect was triiodo-L-thyronine (T3) dependent. Furthermore, overexpression of SHP-2 was shown to promote maturation of oligodendrocytes. Finally, it has been identified that SHP-2 was involved in activation of Akt and extracellular-regulated kinases 1 and 2 (ERK1/2) induced by T3 in oligodendrocytes

Nucleosomes Correlate with In Vivo Progression Pattern of De Novo Methylation of p16 CpG Islands in Human Gastric Carcinogenesis

BACKGROUND: The exact relationship between nucleosome positioning and methylation of CpG islands in human pathogenesis is unknown. METHODOLOGY/PRINCIPAL FINDINGS: In the present study, we characterized the nucleosome position within the p16 CpG island and established a seeding methylation-specific PCR (sMSP) assay based on bisulfite modification to enrich the p16 alleles containing methylated-CpG at the methylation "seeding" sites within its intron-1 in gastric carcinogenesis. The sMSP-positive rate in primary gastric carcinoma (GC) samples (36/40) was significantly higher than that observed in gastritis (19/45) or normal samples (7/13) (P<0.01). Extensive clone sequencing of these sMSP products showed that the density of methylated-CpGs in p16 CpG islands increased gradually along with the severity of pathological changes in gastric tissues. In gastritis lesions the methylation was frequently observed in the region corresponding to the exon-1 coding-nucleosome and the 5'UTR-nucleosome; the methylation was further extended to the region corresponding to the promoter-nucleosome in GC samples. Only few methylated-CpG sites were randomly detected within p16 CpG islands in normal tissues. The significantly inversed relationship between the p16 exon-1 methylation and its transcription was observed in GC samples. An exact p16 promoter-specific 83 bp-MSP assay confirms the result of sMSP (33/55 vs. 1/6, P<0.01). In addition, p16 methylation in chronic gastritis lesions significantly correlated with H. pylori infection; however, such correlation was not observed in GC specimens. CONCLUSIONS/SIGNIFICANCE: It was determined that de novo methylation was initiated in the coding region of p16 exon-1 in gastritis, then progressed to its 5'UTR, and ultimately to the proximal promoter in GCs. Nucleosomes may function as the basic extension/progression unit of de novo methylation of p16 CpG islands in vivo