No abstract

AKI is a devastating condition with high morbidity and mortality. The pathologic features of AKI are characterized by tubular injury, inflammation, and vascular impairment. Whether fibroblasts in the renal interstitium have a role in the pathogenesis of AKI is unknown. In this study, we investigated the role of fibroblast-specific -catenin signaling in dictating the outcome of AKI, using conditional knockout mice in which-catenin was specifically ablated in fibroblasts (Gli1--cat-/-). After ischemia-reperfusion injury (IRI), Gli1--cat-/- mice had lower serum creatinine levels and less morphologic injury than Gli1--cat+/+ littermate controls. Moreover, we detected fewer apoptotic cells, as well as decreased cytochrome C release; reduced expression of Bax, FasL, and p53; and increased phosphorylation of Akt, in the Gli1--cat-/- kidneys. Gli1--cat-/- kidneys also exhibited upregulated expression of proliferating cell nuclear antigen and Ki-67, which are markers of cell proliferation. Furthermore, Gli1--cat-/- kidneys displayed suppressed NF-κB signaling and cytokine expression and reduced infiltration of inflammatory cells. Notably, loss of -catenin in fibroblasts induced renal expression of hepatocyte growth factor (HGF) and augmented the tyrosine phosphorylation of c-met receptor after IRI., treatment with Wnt ligands or ectopic expression of active -catenin inhibited HGF mRNA and protein expression and repressed HGF promoter activity. Collectively, these results suggest that fibroblast-specific-catenin signaling can control tubular injury and repair in AKI by modulating HGF expression. Our studies uncover a previously unrecognized role for interstitial fibroblasts in the pathogenesis of AKI.

MicroRNAs (miRNAs) are non-coding RNAs that regulate the expression of target mRNAs. Altered expression of specific miRNAs in several tumor types has been reported. However, the expression levels of miR-31 in gastric cancers are unclear. The objective of the present study was to compare the expression profile of miR-31 between gastric cancer tissues and non-tumor tissues. Real-time quantitative reverse transcription-polymerase chain reaction technology was used to detect the levels of miR-31 expression. The expression levels of miR-31 in gastric cancer tissues were significantly lower than those in non-tumor tissues. This new information may help to clarify the molecular mechanisms involved in gastric carcinogenesis and to indicate that miR-31 may be a novel diagnostic biomarker of gastric cancer.

No abstract

No abstract

Real-world lighting often consists of multiple illuminants with different spectra. Separating and manipulating these illuminants in post-process is a challenging problem that requires either significant manual input or calibrated scene geometry and lighting. In this work, we leverage a flash/noflash image pair to analyze and edit scene illuminants based on their spectral differences. We derive a novel physicsbased relationship between color variations in the observed flash/no-flash intensities and the spectra and surface shading corresponding to individual scene illuminants. Our technique uses this constraint to automatically separate an image into constituent images lit by each illuminant. This separation can be used to support applications like white balancing, lighting editing, and RGB photometric stereo, where we demonstrate results that outperform state-of-theart techniques on a wide range of images. We introduce a novel reflectance-invariant property ofLambertian scenes that relates illuminant spectra to observed pixel intensities.2. We propose an algorithm to separate an image into its constituent illuminants, and present an analysis of the robustness and limitations of this technique.3. We leverage these separated images to enable a wide variety of applications including white balancing, light editing, camera response editing and photometric stereo.Assumptions. The techniques proposed in this paper assume that the imaged scene is Lambertian and that scene

No abstract

Diabetic nephropathy (DN), characterized by the chronic loss of kidney function during diabetes, is a long‐term kidney disease that affects millions of populations. However, the etiology of DN remains unclear. DN cell model was established by treating HK‐2 cells with high glucose (HG) in vitro. Expression of metastasis‐associated lung adenocarcinoma transcript‐1 (MALAT1), miR‐30c, nucleotide binding and oligomerization domain‐like receptor protein 3 (NLRP3), caspase‐1, IL‐1β, and IL‐18 in treated HK‐2 cells were tested by quantitative polymerase chain reaction. HK‐2 cell pyroptosis was assessed using flow cytometry analysis. Lactate dehydrogenase (LDH) activity was examined with a LDH assay kit. Correlation among MALAT1, miR‐30c, and NLRP3 was examined via dual‐luciferase reporter assay. Here, we revealed that MALAT1 was upregulated, but miR‐30c was downregulated in HG‐treated HK‐2 cells, leading to upregulation of NLRP3 expression and cell pyroptosis. Knockdown of MALAT1 or overexpression of miR‐30c protected HK‐2 cells from HG‐induced pyroptosis. Meanwhile, we found that MALAT1 promoted NLRP3 expression by sponging miR‐30c through dual‐luciferase reporter assay. Moreover, the co‐transfection of sh‐MALAT1 and miR‐30c inhibitor could reverse the protective effects of the sh‐MALAT1 on the HG‐induced pyroptosis. These results confirmed that MALAT1 regulated HK‐2 cell pyroptosis by inhibiting miR‐30c targeting for NLRP3, contributing to a better understanding of DN pathogenesis and help to find out the effective treatment for DN.