Quantifying the effect of maize tassel on canopy reflectance is essential for creating a tasseling progress monitoring index, aiding precision agriculture monitoring, and understanding vegetation canopy radiative transfer. Traditional field measurements often struggle to detect the subtle reflectance differences caused by tassels due to complex environmental factors and challenges in controlling variables. The three-dimensional (3D) radiative transfer model offers a reliable method to study this relationship by accurately simulating interactions between solar radiation and canopy structure. This study used the LESS (large-scale remote sensing data and image simulation framework) model to analyze the impact of maize tassels on visible and near-infrared reflectance in heterogeneous 3D scenes by modifying the structural and optical properties of canopy components. We also examined the anisotropic characteristics of tassel effects on canopy reflectance and explored the mechanisms behind these effects based on the quantified contributions of the optical properties of canopy components. The results showed that (1) the effect of tassels under different planting densities mainly manifests in the near-infrared band of the canopy spectrum, with a variation magnitude of ±0.04. In contrast, the impact of tassels on different leaf area index (LAI) shows a smaller response difference, with a magnitude of ±0.01. As tassels change from green to gray during growth, their effect on reducing canopy reflectance increases. (2) The effect of maize tassel on canopy reflectance varied with spectral bands and showed an obvious directional effect. In the red band at the same sun position, the difference in tassel effect caused by the observed zenith angle on canopy reflectance reaches 200%, while in the near-infrared band, the difference is as high as 400%. The hotspot effect of the canopy has a significant weakening effect on the shadow effect of the tassel. (3) The non-transmittance optical properties of maize tassels reduce canopy reflectance, while their high reflectance increases it. Thus, the dual effects of tassels create a game in canopy reflectance, with the final outcome mainly depending on the sensitivity of the canopy spectrum to transmittance. This study demonstrates the potential of using 3D radiative transfer models to quantify the effects of crop fine structure on canopy reflectance and provides some insights for optimizing crop structure and implementing precision agriculture management (such as selective breeding of crop optimal plant type).
Background/Aims: The present study investigated whether the transient receptor potential melastatin 4 (TRPM4) channel plays a role in high salt diet (HSD)-induced endothelial injuries. Methods: Western blotting and immunofluorescence were used to examine TRPM4 expression in the mesenteric endothelium of Dahl salt-sensitive (SS) rats fed a HSD. The MTT, TUNEL, and transwell assays were used to evaluate the cell viability, cell apoptosis, and cell migration, respectively, of human umbilical vein endothelial cells (HUVECs). Enzyme-linked immunosorbent assays were used to determine the concentrations of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), and E-selectin. Carboxy-H2DCFDA, a membrane-permeable reactive oxygen species (ROS)-sensitive fluorescent probe, was used to detect intracellular ROS levels. Results: TRPM4 was mainly expressed near the plasma membrane of mesenteric artery endothelial cells, and its expression level increased in SS hypertensive rats fed a HSD. Its protein expression was significantly upregulated upon treatment with exogenous hydrogen peroxide (H2O2) and aldosterone in cultured HUVECs. Cell viability decreased upon treatment with both agents in a concentration-dependent manner, which could be partially reversed by 9-phenanthrol, a specific TRPM4 inhibitor. Exogenous H2O2 induced apoptosis, enhanced cell migration, and increased the release of adhesion molecules, including ICAM-1, VCAM-1, and E-selectin, all of which were significantly attenuated upon treatment with 9-phenanthrol. Aldosterone and H2O2 induced the accumulation of intracellular ROS, which was significantly inhibited by 9-phenanthrol, suggesting that oxidative stress is one of the mechanisms underlying aldosterone-induced endothelial injury. Conclusions: Given the fact that oxidative stress and high levels of circulating aldosterone are present in hypertensive patients, we suggest that the upregulation of TRPM4 in the vascular endothelium may be involved in endothelial injuries caused by these stimuli.
Invasiveness is one of the key features of aggressive prostate cancer; however, our understanding of the precise mechanisms effecting invasion remains limited. The ceramide hydrolyzing enzyme acid ceramidase (AC), overexpressed in most prostate tumors, causes an aggressive and invasive phenotype through downstream effectors that have not yet been well characterized. Here, we demonstrate that AC, through generation of sphingosine-1-phosphate (S1P), promotes Ets1 nuclear expression and binding to the promoter region of matrix-degrading protease cathepsin B. Through confocal microscopy and flow cytometry, we found that AC overexpression promotes pericellular localization of cathepsin B and its translocation to the outer leaflet of the cell membrane. AC overexpressing cells have an increased abundance of cathepsin B-enriched invasive structures and enhanced ability to invade through a collagen matrix, but not in the presence of an inhibitor of cathepsin B. In human prostate tissues, AC and cathepsin B overexpression were strongly associated and may relate to poor outcome. These results demonstrate a novel pathway by which AC, through S1P, promotes an invasive phenotype in prostate cancer by causing overexpression and secretion of cathepsin B through activation and nuclear expression of Ets1. As prostate cancer prognosis is dramatically worse when invasion has occurred, this study provides critical insight into the progression toward lethal prostate cancer.
After the publication of the article, it has been brought to the authors' attention by an interested reader that we had made an error regarding the presentation of certain data in the manuscript. The error relates to the presentation of Figs. 1 and 2 in the paper: The control panels for Fig. 1C [labelled 'cyclopamine (µM)'] and Figs. 2B and C [labelled 'rhSSH (µg/ml)'] were derived from the same image. The control U251 cells, featured in Fig. 1 and Figs. 2B and C, were treated without cyclopamine and rhSHH. Therefore, the U251 cells treated without cyclopamine and rhSHH were considered as a control group compared with U251 cells that were separately treated with cyclopamine or rhSHH, and these were photographed randomly. A new Fig. 2 is provided, which contains the correct data for the control panels for Figs. 2B and C. The selection of the same image for the control panels in Figs. 1 and 2 do not affect the overall conclusions in the paper. We would like to thank the reader who pointed out this error, and to apologize for any inconvenience caused. [the original article was published in the Molecular Medicine Reports 12: 6702-6710, 2015; DOI: 10.3892/mmr.2015.4229].
Hypoxia in most solid tumors is a major challenge for photodynamic therapy (PDT), and the combination of hypoxia-activated chemotherapy and PDT is a promising approach for enhanced anticancer activity. Herein, we designed hypoxia-responsive polymeric nanoprodrug PNPs to co-deliver photosensitizer 5,10,5,20-tetrakis(4-aminophenyl)-porphine (TAPP) and chlorambucil (CB) to improve the overall therapeutic efficacy. Upon laser irradiation, the central TAPP converted oxygen to produce single oxygen (
Statins decrease heart disease risk, but their mechanisms are not completely understood. We examined the role of the TGF-β receptor III (TGFBR3) in the inhibition of cardiac fibrosis by simvastatin.Myocardial infarction (MI) was induced by ligation of the left anterior descending coronary artery in mice given simvastatin orally for 7 days. Cardiac fibrosis was measured by Masson staining and electron microscopy. Heart function was evaluated by echocardiography. Signalling through TGFBR3, ERK1/2, JNK and p38 pathways was measured using Western blotting. Collagen content and cell viability were measured in cultures of neonatal mouse cardiac fibroblasts (NMCFs). Interactions between TGFBR3 and the scaffolding protein, GAIP-interacting protein C-terminus (GIPC) were detected using co-immunoprecipitation (co-IP). In vivo, hearts were injected with lentivirus carrying shRNA for TGFBR3.Simvastatin prevented fibrosis following MI, improved heart ultrastructure and function, up-regulated TGFBR3 and decreased ERK1/2 and JNK phosphorylation. Simvastatin up-regulated TGFBR3 in NMCFs, whereas silencing TGFBR3 reversed inhibitory effects of simvastatin on cell proliferation and collagen production. Simvastatin inhibited ERK1/2 and JNK signalling while silencing TGFBR3 opposed this effect. Co-IP demonstrated TGFBR3 binding to GIPC. Overexpressing TGFBR3 inhibited ERK1/2 and JNK signalling which was abolished by knock-down of GIPC. In vivo, suppression of cardiac TGFBR3 abolished anti-fibrotic effects, improvement of cardiac function and changes in related proteins after simvastatin.TGFBR3 mediated the decreased cardiac fibrosis, collagen deposition and fibroblast activity, induced by simvastatin, following MI. These effects involved GIPC inhibition of the ERK1/2/JNK pathway.
Cardiac fibrosis is a common pathological cardiac remodeling in a variety of heart diseases, characterized by the activation of cardiac fibroblasts.Our previous study uncovered that promyelocytic leukemia protein (PML)-associated SUMO processes is a new regulator of cardiac hypertrophy and heart failure.The present study aimed to explore the role of PML in cardiac fibroblasts activation.Here we found that PML is significantly upregulated in cardiac fibrotic tissue and activated cardiac fibroblasts treated with transforming growth factor-β1 (TGF-β1).Gain-and loss-of-function experiments showed that PML impacted cardiac fibroblasts activation after TGF-β1 treatment.Further study demonstrated that p53 acts as the transcriptional regulator of PML, and participated in TGF-β1 induced the increase of PML expression and PML nuclear bodies (PML-NBs) formation.Knockdown or pharmacological inhibition of p53 produced inhibitory effects on the activation of cardiac fibroblasts.We further found that PML also may stabilize p53 through inhibiting its ubiquitin-mediated proteasomal degradation in cardiac fibroblasts.Collectively, this study suggests that PML crosstalk with p53 regulates cardiac fibroblasts activation, which provides a novel therapeutic strategy for cardiac fibrosis.
There are many gynecological diseases, among which breast cancer (BC), cervical cancer (CC), endometriosis (EMs), and polycystic ovary syndrome (PCOS) are common and difficult to cure. Stem cells (SCs) are a focus of regenerative medicine. They are commonly used to treat organ damage and difficult diseases because of their potential for self-renewal and multidirectional differentiation. SCs are also commonly used for difficult-to-treat gynecological diseases because of their strong directional differentiation ability with unlimited possibilities, their tendency to adhere to the diseased tissue site, and their use as carriers for drug delivery. SCs can produce exosomes in a paracrine manner. Exosomes can be produced in large quantities and have the advantage of easy storage. Their safety and efficacy are superior to those of SCs, which have considerable potential in gynecological treatment, such as inhibiting endometrial senescence, promoting vascular reconstruction, and improving anti-inflammatory and immune functions. In this paper, we review the mechanisms of the regenerative and anti-inflammatory capacity of SCs and exosomes in incurable gynecological diseases and the current progress in their application in genetic engineering to provide a foundation for further research.
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