On Robust Cross-View Consistency in Self-Supervised Monocular Depth Estimation

Remarkable progress has been made in self-supervised monocular depth estimation (SS-MDE) by exploring cross-view consistency, e.g., photometric consistency and 3D point cloud consistency. However, they are very vulnerable to illumination variance, occlusions, texture-less regions, as well as moving objects, making them not robust enough to deal with various scenes. To address this challenge, we study two kinds of robust cross-view consistency in this paper. Firstly, the spatial offset field between adjacent frames is obtained by reconstructing the reference frame from its neighbors via deformable alignment, which is used to align the temporal depth features via a Depth Feature Alignment (DFA) loss. Secondly, the 3D point clouds of each reference frame and its nearby frames are calculated and transformed into voxel space, where the point density in each voxel is calculated and aligned via a Voxel Density Alignment (VDA) loss. In this way, we exploit the temporal coherence in both depth feature space and 3D voxel space for SS-MDE, shifting the "point-to-point" alignment paradigm to the "region-to-region" one. Compared with the photometric consistency loss as well as the rigid point cloud alignment loss, the proposed DFA and VDA losses are more robust owing to the strong representation power of deep features as well as the high tolerance of voxel density to the aforementioned challenges. Experimental results on several outdoor benchmarks show that our method outperforms current state-of-the-art techniques. Extensive ablation study and analysis validate the effectiveness of the proposed losses, especially in challenging scenes. The code and models are available at https://github.com/sunnyHelen/RCVC-depth

Revealing of the Activation Pathway and Cathode Electrolyte Interphase Evolution of Li-Rich 0.5Li2MnO3·0.5LiNi0.3Co0.3Mn0.4O2 Cathode by in Situ Electrochemical Quartz Crystal Microbalance.

The first-cycle behavior of layered Li-rich oxides, including Li2MnO3 activation and cathode electrolyte interphase (CEI) formation, significantly influences their electrochemical performance. However, the Li2MnO3 activation pathway and the CEI formation process are still controversial. Here, the first-cycle properties of xLi2MnO3·(1- x) LiNi0.3Co0.3Mn0.4O2 ( x = 0, 0.5, 1) cathode materials were studied with an in situ electrochemical quartz crystal microbalance (EQCM). The results demonstrate that a synergistic effect between the layered Li2MnO3 and LiNi0.3Co0.3Mn0.4O2 structures can significantly affect the activation pathway of Li1.2Ni0.12Co0.12Mn0.56O2, leading to an extra-high capacity. It is demonstrated that Li2MnO3 activation in Li-rich materials is dominated by electrochemical decomposition (oxygen redox), which is different from the activation process of pure Li2MnO3 governed by chemical decomposition (Li2O evolution). CEI evolution is closely related to Li+ extraction/insertion. The valence state variation of the metal ions (Ni, Co, Mn) in Li-rich materials can promote CEI formation. This study is of significance for understanding and designing Li-rich cathode-based batteries

Insights into the toxicities of UV-328, UV-329, UV-P in HepG2 cells and their roles in AHR-mediated pathway

The widespread high concentrations of benzotriazole ultraviolet stabilizers (BUVSs) in many biotic and abiotic samples have raised urgent concerns of their adverse effects on environmental and human health. In this study, we investigated the toxicity of three typical BUVSs (UV-328, UV-329, UV-P) with HepG2 cells in vitro. Results indicated that the three BUVSs showed weak cytotoxicity in HepG2 cells at concentrations lower than 50 μM. Transcriptional analysis indicated that the toxic effects of the three chemicals followed the order of UV-P > UV-329 > UV-328. UV-P and UV-329 may act as potential environmental diabetogens by significantly enriching several diabetic related items in both GO and KEGG analysis. Moreover, UV-P and UV-329 significantly upregulated the expression of AHR target genes (CYP1A1, CYP1A2, UGT1A1, etc.), and increased the ethoxyresorufin-O-deethylase (EROD) activity and exhibited agonistic activity toward AHR in the XRE-mediated luciferase reporter gene assay. Molecular docking assay also indicated that UV-329 and UV-P had higher binding affinities to AHR-LBD than UV-328. In brief, our findings indicated that UV-P and UV-329 were potential agonist of AHR ligand, and may exert more toxicity than UV-328 in inducing liver toxicity

Differential Gene Expression during Larval Metamorphic Development in the Pearl Oyster, Pinctada fucata, Based on Transcriptome Analysis

P. fucata experiences a series of transformations in appearance, from swimming larvae to sessile juveniles, during which significant changes in gene expression likely occur. Thus, P. fucata could be an ideal model in which to study the molecular mechanisms of larval metamorphosis during development in invertebrates. To study the molecular driving force behind metamorphic development in larvae of P. fucata, transcriptomes of five larval stages (trochophore, D-shape, umbonal, eyespots, and spats) were sequenced using an Illumina HiSeq™ 2000 system and assembled and characterized with the transcripts of six tissues. As a result, a total of 174,126 unique transcripts were assembled and 60,999 were annotated. The number of unigenes varied among the five larval stages. Expression profiles were distinctly different between trochophore, D-shape, umbonal, eyespots, and spats larvae. As a result, 29 expression trends were sorted, of which eight were significant. Among others, 80 development-related, differentially expressed unigenes (DEGs) were identified, of which the majority were homeobox-containing genes. Most DEGs occurred among trochophore, D-shaped, and UES (umbonal, eyespots, and spats) larvae as verified by qPCR. Principal component analysis (PCA) also revealed significant differences in expression among trochophore, D-shaped, and UES larvae with ten transcripts identified but no matching annotations

Differential Gene Expression during Larval Metamorphic Development in the Pearl Oyster, Pinctada fucata, Based on Transcriptome Analysis

P. fucata experiences a series of transformations in appearance, from swimming larvae to sessile juveniles, during which significant changes in gene expression likely occur. Thus, P. fucata could be an ideal model in which to study the molecular mechanisms of larval metamorphosis during development in invertebrates. To study the molecular driving force behind metamorphic development in larvae of P. fucata, transcriptomes of five larval stages (trochophore, D-shape, umbonal, eyespots, and spats) were sequenced using an Illumina HiSeq™ 2000 system and assembled and characterized with the transcripts of six tissues. As a result, a total of 174,126 unique transcripts were assembled and 60,999 were annotated. The number of unigenes varied among the five larval stages. Expression profiles were distinctly different between trochophore, D-shape, umbonal, eyespots, and spats larvae. As a result, 29 expression trends were sorted, of which eight were significant. Among others, 80 development-related, differentially expressed unigenes (DEGs) were identified, of which the majority were homeobox-containing genes. Most DEGs occurred among trochophore, D-shaped, and UES (umbonal, eyespots, and spats) larvae as verified by qPCR. Principal component analysis (PCA) also revealed significant differences in expression among trochophore, D-shaped, and UES larvae with ten transcripts identified but no matching annotations

SCF/c-KIT Signaling Increased Mucin2 Production by Maintaining Atoh1 Expression in Mucinous Colorectal Adenocarcinoma

Mucinous colorectal adenocarcinoma (MCA) patients often a show high risk of malignant potential and a poorer survival rate. Given that the pathological feature and oncobiological characteristics of MCA are correlated with its abundant extracellular mucin2 (MUC2), we paid interest toward investigating the key factor that promotes MUC2 production exposure to highly-activated stem cell factor (SCF)/c-KIT signaling, which we believed to contribute to MCA formation. Long-term azoxymethane and dextran sodium sulfate treatment successfully induced MCA only in wild-type (WT) mice at week 37 and 43, while all c-kit loss-of-function mutant mice (Wadsm/m) developed non-MCA. Significantly, MUC2 and its key transcriptional factor Atonal homologue 1 (Atoh1) were remarkably expressed in MCA mice compared with non-MCA mice. Atoh1 was significantly elevated in colorectal cancer (CRC) cells stimulated by exogenous SCF or overexpressing c-KIT in vitro, while decreased by the blockage of SCF/c-KIT signaling with Imatinib. Furthermore, the maintained Atoh1 protein level was due to the inactive glycogen synthase kinase 3β (p-GSK3β) by virtue of the activated SCF/c-KIT-Protein Kinase B (AKT) signaling. Similar results were obtained from the ONCOMINE database and CRC patients. In conclusion, we suggested that SCF/c-KIT signaling promoted MUC2 production and MCA tumorigenesis by maintaining Atoh1 expression. Therefore, targeting the related key molecules might be beneficial for treating MCA patients

Lipopolysaccharide induces the early enhancement of mice colonic mucosal paracellular permeability mainly mediated by mast cells

The alteration of intestinal mucosal barrier is considered to be the central pathophysiological process in response to gastrointestinal infections, and mucosal microstructural damage is a major factor for enhancing epithelial permeability in persistent bacterial infections. However, the mechanism involved in hyperpermeability in the early stage of acute bacterial infections is not fully understood. In the present study, fluorescein isothiocyanate-dextran across and transepithelial resistance measured in Ussing chambers were used to assess the intestinal paracellular permeability. Mast cell activation was evaluated by western blotting for the presence of tryptase released from mast cells. Serum levels of interleukin-6 were evaluated using enzymelinked immunosorbent assay. Our results indicated that mast cells played a pivotal role in colonic mucosal hyperpermeability in wild type mice treated with lipopolysaccharide (LPS) for 2 h. And the effect of LPS was mainly dependent on mast cell degranulation, while no change in permeability was observed in the mast celldeficient mice (Wads-/- ) after LPS administration. No obvious changes of the mucosal structure including histomorphological architecture and expression of intercellular junction proteins were obtained in either wild type or Wads-/- mice after LPS stimulation by hematoxylin and eosin staining, immunofluorescence staining and western blot analysis. Furthermore, the selfrenewal of intestinal epithelia, detected by using proliferation marker 5’-bromo-2’-deoxyuridine, was not involved in increased permeability. Collectively, activation of mast cells induced by LPS mediated intestinal hyperpermeability in the initial stage, and played a crucial role in barrier dysfunction rather than mucosal microstructural damage in acute enterogenous bacterial infection

Distribution of interstitial cells of Cajal in Meriones unguiculatus and alterations in the development of incomplete intestinal obstruction

The interstitial cells of Cajal (ICCs) act as pacemaker cells that are involved in gastrointestinal (GI) motility disorders, although the pathogenesis of these disorders is still unclear. The GI tract of Mongolian gerbils shares similar anatomical features with that of humans, but no investigation of ICCs has been reported in the GI tracts of this animal. In the present study, we first observed the distribution and morphological features of ICCs in the Mongolian gerbil GI tract. The ICCs were mainly distributed within the smooth muscle layers (ICC-IM), the myenteric plexus (ICC-MY), the deep muscular plexus in the small intestine (ICC-DMP) and the submucosal surface of the circular muscle layer in the colon (ICC-SM). The density of the ICC-IM gradually decreased from the stomach to the colon, whereas the density of the ICC-MY gradually increased. Second, we compared differences in the ICCs between the control and obstructed intestines, and no significant difference was observed in the number of ICCs after 7 days of obstruction. However, the numbers were reduced by approximately day 14 of obstruction. The pattern of immunoreactivity also partly differed from that of the control group, i.e., a scattered and interrupted network of ICCs was often observed. Western blotting revealed that p-Kit and SCF were significantly reduced in the dilated intestines by day 14. Our results indicate that the Mongolian gerbil may be a good animal model for studying changes in ICCs that may contribute to the pathogenesis of GI motility disorders

Intense endoplasmic reticulum stress (ERS) / IRE1α enhanced Oxaliplatin efficacy by decreased ABCC10 in colorectal cancer cells

Abstract Background Attenuated Oxaliplatin efficacy is a challenge in treating colorectal cancer (CRC) patients, contributory to the failure in chemotherapy and the risks in relapse and metastasis. However, the mechanism of Oxaliplatin de-efficacy during CRC treatment has not been completely elucidated. Methods Microarray screening, western blot and qPCR on clinic CRC samples were conducted to select the target gene ABCC10 transporter. The Cancer Genome Atlas data was analyzed to figure out the correlation between the clinical manifestation and ABCC10 expression. ABCC10 knock-down in CRC cells was conducted to identify its role in the Oxaliplatin resistance. Cell counting kit-8 assay was conducted to identify the CRC cell viability and Oxaliplatin IC50. Flow cytometry was conducted to detect the cell apoptosis exposed to Oxaliplatin. The intracellular Oxaliplatin accumulation was measured by ultra-high performance liquid chromatography coupled to tandem mass spectrometry. Results CRC patients with higher ABCC10 were prone to relapse and metastasis. Differential ABCC10 expression in multiple CRC cell lines revealed a strong positive correlation between ABCC10 expression level and decreased Oxaliplatin response. In ABCC10 knock-down CRC cells the Oxaliplatin sensitivity was evidently elevated due to an increase of intracellular Oxaliplatin accumulation resulted from the diminished drug efflux. To explore a strategy to block ABCC10 in CRC cells, we paid a special interest in the endoplasmic reticulum stress (ERS) / unfolded protein response (UPR) that plays a dual role in tumor development. We found that neither the inhibition of ERS nor the induction of mild ERS had anti-CRC effect. However, the CRC cell viability was profoundly decreased and the pro-apoptotic factor CHOP and apoptosis were increased by the induction of intense ERS. Significantly, the Oxaliplatin sensitivity of CRC cells was enhanced in response to the intense ERS, which was blocked by inhibiting IRE1α branch of UPR. Finally, we figured out that the intense ERS down-regulated ABCC10 expression via regulated IRE1-dependent decay activity. Conclusion Oxaliplatin was a substrate of ABCC10 efflux transporter. The intense ERS/IRE1α enhanced Oxaliplatin efficacy through down-regulating ABCC10 in addition to inducing CHOP. We suggested that introduction of intense ERS/UPR could be a promising strategy to restore chemo-sensitivity when used in combination with Oxaliplatin or other chemotherapeutic drugs pumped out by ABCC10

First Report on Development of Genome-Wide Microsatellite Markers for Stock (<i>Matthiola incana</i> L.)

Stock (Matthiola incana (L.) R. Br.) is a famous annual ornamental plant with important ornamental and economic value. The lack of DNA molecular markers has limited genetic analysis, genome evolution, and marker-assisted selective breeding studies of M. incana. Therefore, more DNA markers are needed to support the further elucidation of the biology and genetics of M. incana. In this study, a high-quality genome of M. incana was initially assembled and a set of effective SSR primers was developed at the whole-genome level using genome data. A total of 45,612 loci of SSRs were identified; the di-nucleotide motifs were the most abundant (77.35%). In total, 43,540 primer pairs were designed, of which 300 were randomly selected for PCR validation, and as the success rate for amplification. In addition, 22 polymorphic SSR markers were used to analyze the genetic diversity of 40 stock varieties. Clustering analysis showed that all varieties could be divided into two clusters with a genetic distance of 0.68, which were highly consistent with their flower shape (potted or cut type). Moreover, we have verified that these SSR markers are effective and transferable within the Brassicaceae family. In this study, potential SSR molecular markers were successfully developed for 40 M. incana varieties using whole genome analysis, providing an important genetic tool for theoretical and applied research on M. incana