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• The spatial variation of sediment connectivity in small watershed was quantified by IC. • Significant spatial variation and autocorrelation were detected in IC in black soil region. • Topographic and anthropogenic factors were main determinants of sediment connectivity spatial variation. Connectivity has become an important indicator of the sediment transfer potential through sediment sources to catchment sinks. Connectivity plays a vital role in investigating the rate of soil erosion caused by runoff and sediment output across the watershed landscape. However, there have been few quantitative studies on the spatial variations in sediment connectivity in the black soil region of Northeast China. Seven classic watersheds in the northeast black soil region were selected to discover spatial variations in sediment connectivity and their influencing factors. The connectivity index (IC) was used to study the spatial variation of sediment connectivity, and the weight of IC was calculated using the vegetation cover management factor (C), which reflected the influence of human activities on the soil erosion process caused by cultivated land expansion and encroachment of forest grassland. The redundancy analysis method (RDA) was used to determine the main factors affecting the spatial variation of IC. The results showed that IC decreased from north (0.45) to south (0.12). The spatial variations of watersheds in sediment connectivity showed significant spatial heterogeneity. IC was correlated with topographic, climatic, and artificial management characteristics at 0.01 or 0.05 levels except soil structural index; RDA results showed that topography and human activities were the main factors affecting sediment connectivity. Topographic and climatic factors explained more sediment connectivity changes in the southern watersheds than in the northern watersheds, while the human activities factor explanation was the opposite of topographic factors. Human activities refer to changes in vegetation cover and soil structure and properties resulting from human logging and farming that affect sediment connectivity. [ABSTRACT FROM AUTHOR]

Acute kidney injury (AKI) is a destructive clinical condition induced by multiple insults including ischemic reperfusion, nephrotoxic drugs and sepsis. It is characterized by a sudden decline in renal function, in addition to excessive inflammation, oxidative stress and programmed cell death of renal tubular epithelial cells. RIPK1-mediated necroptosis plays an important role in AKI. In the present study, we evaluated the treatment effects of Compound-71 (Cpd-71), a novel RIPK1 inhibitor, by comparing with Necrostatin-1 (Nec-1), a classic RIPK1 inhibitor, which has several drawbacks like the narrow structure-activity relationship (SAR) profile, moderate potency and non-ideal pharmacokinetic properties, in vivo and in vitro. Our results showed that pretreatment of Cpd-71 attenuated cisplatin-induced renal injury, restored renal function and suppressed renal inflammation, oxidative stress and cell necroptosis. In addition, Cpd-71 inhibited renal damage while reducing the up-regulated serum creatinine (Cr) and blood urea nitrogen (BUN) levels in established AKI mice model. Consistently, we confirmed that Cpd-71 exhibited more effectively suppressive effect on cisplatin-induced renal tubular cell necroptosis than Nec-1, by physically binding to the allosteric type III ligand binding site of RIPK1, thereby reduced RIPK1 kinase activity, RIPK1/RIPK3 complex formation and phosphor-MLKL membrane translocation by molecular docking, Western blot, co-immunoprecipitation and cellular thermal shift assay (CETSA). Taken together, we currently showed that targeting RIPK1 with Cpd-71 may serve as a promising clinical candidate for AKI treatment. [ABSTRACT FROM AUTHOR]

Abundant regulatory genes and complex circuits involving non-coding RNAs (ncRNAs) monitor the formation and development of hepatic fibrosis (HF). Circular RNAs (circRNAs) are a class of RNAs generated from protein coding genes by back-splicing, playing crucial roles in various pathological processes, including HF. However, little is known about mechanisms of action of circRNAs, let alone in HF. In this study, we found circUbe2k enhanced in CCl4-induced HF mice and LX-2 cells stimulated with TGF-β1, regulating the development of HF. Restraining the expression of circUbe2k inhibited α-SMA and Col1α1 expression in CCl4-induced HF mice and in LX-2 cells stimulated with TGF-β1. Furthermore, inhibiting circUbe2k expression reduced hepatic stellate cells (HSCs) activation and proliferation in vivo and in vitro. Mechanistically, we demonstrated a direct interaction between circUbe2k and miR-149-5p, which results in the modulation of TGF-β2 expressions. Together, circUbe2k may act as a “catalyst” of HSCs activation and HF through the circUbe2k/miR-149-5p/TGF-β2 axis. Our results provide unprecedented evidence for a significant role for circUbe2k to serve as a potential biomarker for HF therapy. [ABSTRACT FROM AUTHOR]

Noise is usually undesired yet inevitable in science and engineering. However, by introducing the engineered noise to the precise solution of Jones matrix elements, we break the fundamental limit of polarization multiplexing capacity of metasurfaces that roots from the dimension constraints of the Jones matrix. We experimentally demonstrate up to 11 independent holographic images using a single metasurface illuminated by visible light with different polarizations. To the best of our knowledge, it is the highest capacity reported for polarization multiplexing. Combining the position multiplexing scheme, the metasurface can generate 36 distinct images, forming a holographic keyboard pattern. This discovery implies a new paradigm for high-capacity optical display, information encryption, and data storage. [ABSTRACT FROM AUTHOR]

MLKL is a central mediator for necroptosis. Its knockout significantly relieves acute kidney injury (AKI). However, its upstream regulatory mechanism in AKI has not been fully elucidated. We recently reviewed how microRNAs (miRNAs), a type of well-studied epigenetic regulator, play critical roles in AKI. Here, we evaluated miRNAs that potentially target MLKL and evaluated their function in human tubular epithelial cells in response to toxic and ischemic insults. TargetScan analysis showed that miR-194-5P, miR-338-3P, miR-500a-3P, and miR-577 had MLKL binding sites. Although all 4 miRNAs are reduced in AKI, our data show that only hsa-miR-500a-3P was significantly suppressed in cisplatin-treated human tubular epithelial (HK2) cells. We further found that hsa-miR-500a-3P alleviated cisplatin-induced HK2 cell death, which was confirmed by transmission electron microscopy and flow cytometry. In addition, overexpression of hsa-miR-500a-3P decreased kidney injury molecule-1 mRNA and protein levels. Real-time PCR, ELISA, and immunofluorescence data show that hsa-miR-500a-3P protected against inflammatory response, evidenced by decreased monocyte chemotactic protein-1 and proinflammatory cytokines TNF-α and IL-8. Further, hsa-miR-500a-3P attenuated P65 NF-κB phosphorylation and promoter activity. Mechanistically, luciferase reporter assay showed that hsa-miR-500a-3P bound the 3′UTR of MLKL, thereby suppressing phosphorylation and membrane translocation of MLKL. In agreement with these findings, we identified that overexpression of hsa-miR-500a-3P attenuated cell injury and the inflammatory response in response to sodium azide treatment in an in vitro model. Results show that circulating exosomes from patients with AKI down-regulated miR-500a-3P, which suppressed cell injury and inflammation in HK2 cells. hsa-miR-500a-3P alleviated toxic and ischemic insults that were triggered by cell necroptosis and the inflammatory response in human HK2 cells by targeting MLKL. This may serve as a novel therapeutic target for treatment of AKI. [ABSTRACT FROM AUTHOR]

Themain goal of image fusion is to combine substantial information fromdifferent images of the same scene into a single image that is suitable for human andmachine perception or for further image-processing tasks. In this study, a simple and efficient image fusion approach based on the application of the histogram of infrared images is proposed. A fusion scheme to select adaptively weighted coefficients for preserving salient infrared targets fromthe infrared image and for obtainingmost spatial detailed information from the visible image is presented. Moving and static infrared targets in the fused image are labeled with different colors. This technique enhances perception of the image for the human visual system. In view of the modalities of infrared images, low resolution, and low signal-to-noise ratio, an anisotropic diffusion equation model is adopted to remove noise and to effectively preserve edge information before the fusion stage. By using the proposed method, relevant spatial information is preserved and infrared targets are clearly identified in the resulting fused images. [ABSTRACT FROM AUTHOR]