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Affected by global warming, the permafrost in Northeast China (NEC) has been continuously degrading in recent years. Many researchers have focused on the spatial and temporal distribution characteristics of permafrost in NEC, however, few studies have delved into the field scale. In this study, based on the Optimal Parameters-based Geographical Detector (OPGD) model and Receiver Operating Characteristic (ROC) test, the spatial stratified heterogeneity of permafrost distribution and the indicating performance of environmental variables on permafrost in NEC at the field scale were analyzed. Permafrost spatial distribution data were obtained from the Engineering Geological Investigation Reports (EGIR) of six highways located in NEC and a total of 19 environmental variables related to heat transfer, vegetation, soil, topography, moisture, and ecology were selected. The H-factors (variables with the highest contribution in factor detector results and interaction detector results): slope position (γ), surface frost number (SFN), elevation (DEM), topographic diversity (TD), and annual snow cover days (ASCD) were found to be the major contributors to the distribution of permafrost at the field scale. Among them, γ has the highest contribution and is a special explanatory variable for permafrost. In most cases, interaction can improve the impact of variables, especially the interaction between H-factors. The risk of permafrost decreases with the increase of TD, RN, and SBD, and increases with the increase of SFN. The performance of SFN to indicate permafrost distribution was found to be the best among all variables (AUC = 0.7063). There is spatial heterogeneity in the distribution of permafrost on highways in different spatial locations. This study summarized the numerical and spatial location between permafrost and different environmental variables at the field scale, and many results were found to be informative for environmental studies and engineering construction in NEC.
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Hielos Perennes , Suelo , Geografía , Análisis Espacial , ChinaRESUMEN
To study the residue and dietary risk of propiconazole in Panax notoginseng and the effects on physiological and bioche-mical properties of P. notoginseng, we conducted foliar spraying of propiconazole on P. notoginseng in pot experiments. The physiolo-gical and biochemical properties studied included leaf damage, osmoregulatory substance content, antioxidant enzyme system, non-enzymatic system, and saponin content in the main root. The results showed that at the same application concentration, the residual amount of propiconazole in each part of P. notoginseng increased with the increase in the times of application and decreased with the extension of harvest interval. After one-time application of propiconazole according to the recommended dose(132 g·hm~(-2)) for P. ginseng, the half-life was 11.37-13.67 days. After 1-2 times of application in P. notoginseng, propiconazole had a low risk of dietary intake and safety threat to the population. The propiconazole treatment at the recommended concentration and above significantly increased the malondialdehyde(MDA) content, relative conductivity, and osmoregulatory substances and caused the accumulation of reactive oxygen species in P. notoginseng leaves. The propiconazole treatment at half(66 g·hm~(-2)) of the recommended dose for P. ginseng significantly increased the activities of superoxide dismutase(SOD), peroxidase(POD), and catalase(CAT) in P. notoginseng leaves. The propiconazole treatment at 132 g·hm~(-2) above inhibited the activities of glutathione reductase(GR) and glutathione S-transferase(GST), thereby reducing glutathione(GSH) content. Proconazole treatment changed the proportion of 5 main saponins in the main root of P. notoginseng. The treatment with 66 g·hm~(-2) propiconazole promoted the accumulation of saponins, while that with 132 g·hm~(-2) and above propiconazole significantly inhibited the accumulation of saponins. In summary, using propiconazole at 132 g·hm~(-2) to prevent and treat P. notoginseng diseases will cause stress on P. notoginseng, while propiconazole treatment at 66 g·hm~(-2) will not cause stress on P. notoginseng but promote the accumulation of saponins. The effect of propiconazole on P. notoginseng diseases remains to be studied.
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Panax notoginseng , Panax , Saponinas , Panax notoginseng/química , Antioxidantes/farmacología , Saponinas/farmacología , Glutatión , Medición de RiesgoRESUMEN
Fourier single-pixel imaging (FSI) allows an image to be reconstructed by acquiring the Fourier spectrum of the image using a single-pixel detector. Fast FSI is typically achieved by acquiring a truncated Fourier spectrum, that is, only low-frequency Fourier coefficients are acquired, with the high-frequency coefficients discarded. However, the truncation of the Fourier spectrum leads to undesirable ringing artifacts in the resulting image. Ringing artifacts produce false edges in the image and reduce the image contrast, resulting in image quality degeneration. The artifact is particularly severe in dynamic FSI, where the sampling ratio is generally ultra-low. We propose an effective and fast deringing algorithm to achieve ringing-free fast FSI. The algorithm eliminates ringing artifacts through 2D sub-pixel shifting and preserves image details through image fusion. Both static and dynamic imaging results demonstrate that the proposed method can reconstruct ringing-free images from under-sampled data in FSI. The deringing algorithm not only provides FSI with the capability of fast high-quality single-pixel imaging but also might prove its applicability in other areas, such as Fourier-based data compression algorithms.
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BACKGROUND: Glioblastomas are lethal brain tumors under the current combinatorial therapeutic strategy that includes surgery, chemo- and radio-therapies. Extensive changes in the tumor microenvironment is a key reason for resistance to chemo- or radio-therapy and frequent tumor recurrences. Understanding the tumor-nontumor cell interaction in TME is critical for developing new therapy. Glioblastomas are known to recruit normal cells in their environs to sustain growth and encroachment into other regions. Neural progenitor cells (NPCs) have been noted to migrate towards the site of glioblastomas, however, the detailed mechanisms underlying glioblastoma-mediated NPCs' alteration remain unkown. METHODS: We collected EVs in the culture medium of three classic glioblastoma cell lines, U87 and A172 (male cell lines), and LN229 (female cell line). U87, A172, and LN229 were co-cultured with their corresponding EVs, respectively. Mouse NPCs (mNPCs) were co-cultured with glioblastoma-derived EVs. The proliferation and migration of tumor cells and mNPCs after EVs treatment were examined. Proteomic analysis and western blotting were utilized to identify the underlying mechanisms of glioblastoma-derived EVs-induced alterations in mNPCs. RESULTS: We first show that glioblastoma cell lines U87-, A172-, and LN229-derived EVs were essential for glioblastoma cell prolifeartion and migration. We then demonstrated that glioblastoma-derived EVs dramatically promoted NPC proliferation and migration. Mechanistic studies identify that glioblastoma-derived EVs achieve their functions via activating PI3K-Akt-mTOR pathway in mNPCs. Inhibiting PI3K-Akt pathway reversed the elevated prolfieration and migration of glioblastoma-derived EVs-treated mNPCs. CONCLUSION: Our findings demonstrate that EVs play a key role in intercellular communication in tumor microenvironment. Inhibition of the tumorgenic EVs-mediated PI3K-Akt-mTOR pathway activation might be a novel strategy to shed light on glioblastoma therapy. Video Abstract.
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Vesículas Extracelulares , Glioblastoma , Células-Madre Neurales , Animales , Línea Celular Tumoral , Proliferación Celular , Vesículas Extracelulares/metabolismo , Femenino , Glioblastoma/patología , Masculino , Ratones , Recurrencia Local de Neoplasia/metabolismo , Células-Madre Neurales/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Proteómica , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal , Microambiente TumoralRESUMEN
The high background value of cadmium (Cd) in the Panax notoginseng planting soil is the main reason for the Cd content in P. notoginseng exceeding the limit standards. The main goal of this study was to reveal the mechanism by which potassium (K) reduces Cd accumulation in P. notoginseng from the perspective of the influences of soil microbial communities on soil pH, total organic matter (TOM) and cation exchange capacity (CEC). Pot experiments were conducted to study the effects of different types and amounts of applied K on the Cd content in P. notoginseng, and on the soil pH, TOM, CEC, and bioavailable Cd (bio-Cd) content in soil. Field experiments were conducted to study the effects of K2SO4 fertilizer on the microbial community, and its correlations with the soil pH, TOM and CEC were analyzed. A moderate application of K2SO4 (0.6 gâ kg-1) was found to be the most optimal treatment for the reduction of Cd in the pot experiments. The field experiments proved that K fertilizer (K2SO4) alleviated the decreases in pH, TOM and CEC, and reduced the content of bio-Cd in the soil. The application of K fertilizer inhibited the growth of Acidobacteria, but the abundances of Mortierellomycota, Proteobacteria and Bacteroidetes were promoted. The relative abundances of Acidobacteria and Proteobacteria in the soil bacteria exhibited significant negative and positive correlations with pH and CEC, respectively. In contrast, the relative abundance of Mortierellomycota was found to be positively correlated with the pH, TOM and CEC. The bio-Cd content was also found to be positively correlated with the relative abundance of Acidobacteriia but negatively correlated with the relative abundances of Proteobacteria and Mortierellomycota. The application of K fertilizer inhibited the abundance of Acidobacteria, which alleviated the acidification of the soil pH and CEC, and promoted increase in the abundances of Mortierellomycota, Proteobacteria and Bacteroidetes, which ultimately increased the soil TOM and CEC. Soil microorganisms were found to mitigated decreases in the soil pH, TOM, and CEC and reduced the bio-Cd content in the soil, which significantly reduced the accumulation of Cd in P. notoginseng.
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(1) Background: Flavonoids are the primary medicinal ingredient of Saussurea involucrate, which have significant antioxidant capacity. Optimizing the extraction of Saussurea involucrate flavonoids (SIFs) and exploring the ability to block melanin deposition caused by reactive oxygen can greatly promote the development of S. involucrate whitening products. (2) Methods: Ultrasonic extraction process was optimized using the Box-Behnken design (BBD) and response surface methodology (RSM). Then, the effect of SIFs on antioxidant activity and anti-deposition of melanin, and genes related to the melanin synthesis are studied. (3) Results: The optimal extraction procedures are as follows: the extraction time, ethanol content, and solvent ratio (v/w) are 64 min, 54%, and 54:1, respectively. The reducing activity and scavenging rates of 2,2-diphenyl-1-picrylhydrazyl (DPPH), superoxide anion, hydroxyl radical, and ABTS+ were promoted as more S. involucrate flavonoid extract was added. The SIFs extract induced a decrease in the melanin synthesis by inhibiting the human melanoma A375 cell tyrosinase activity. SIFs also depress expression of melanin synthesis related genes. (4) Conclusions: the highest SIFs content was obtained by using 54% ethanol and 54:1 solvent ratio (v/w) for 64 min. The extract of SIFs exhibited good ability of antioxidant and anti-deposition of melanin in human melanocytes.
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Flavonoides , Melaninas/metabolismo , Melanocitos/metabolismo , Saussurea/química , Ondas Ultrasónicas , Línea Celular Tumoral , Flavonoides/química , Flavonoides/aislamiento & purificación , Flavonoides/farmacología , Humanos , Melanocitos/citologíaRESUMEN
Angiogenesis is the process by which new vessels form from existing vascular networks. Human umbilical vein endothelial cells (HUVECs) may contribute to the study of vascular repair and angiogenesis. The chemokine CXCL12 regulates multiple cell functions, including angiogenesis, mainly through its receptor CXCR4. In contrast to CXCL12/CXCR4, few studies have described roles for CXCR7 in vascular biology, and the downstream mechanism of CXCR7 in angiogenesis remains unclear. The results of the present study showed that CXCL12 dose-dependently enhanced angiogenesis in chorioallantoic membranes (CAMs) and HUVECs. The specific activation of CXCR7 with TC14012 (a CXCR7 agonist) resulted in the significant induction of tube formation in HUVECs and in vivo. Further evidence suggested that CXCL12 induced directional polarization and migration in the HUVECs, which is necessary for tube formation. Moreover, CXCR7 translocalization was observed during the polarization of HUVECs in stripe assays. Finally, treatment with TC14012 also significantly increased PI3K/Akt phosphorylation, and tube formation was blocked by treating HUVECs with an Akt inhibitor. Overall, this study indicated that CXCL12-stimulated CXCR7 acts as a functional receptor to activate Akt for angiogenesis in HUVECs and that CXCR7 may be a potential target molecule for endothelial regeneration and repair after vascular injury.
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Quimiocina CXCL12/metabolismo , Células Endoteliales de la Vena Umbilical Humana/metabolismo , Neovascularización Fisiológica , Receptores CXCR/metabolismo , Animales , Células Cultivadas , Embrión de Pollo , Humanos , Fosfatidilinositol 3-Quinasas/metabolismo , Unión Proteica , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de SeñalRESUMEN
The application of combination antiretroviral therapy has greatly reduced the death rate from AIDS. However, up to 50% of patients on combination antiretroviral therapy develop HIV-associated neurocognitive disorders (HAND), which is associated with residual neuroinflammation and oxidative injury in the brain. Neural stem cells (NSCs) and progenitors play a vital role in repairing neuronal injuries. Therefore, we hypothesize that combination antiretroviral therapy may adversely affect NSCs/progenitors, contributing to the increasing prevalence of HAND. Here, we show that combined medication of three antiretroviral drugs tenofovir disoproxil fumarate (TDF), emtricitabine (FTC), and raltegravir (RAL) affects NSC homeostasis and progenitor proliferation in the mouse dentate gyrus (DG). Our results also show that TDF/FTC/RAL treatment prohibits proliferation and induces apoptosis of cultured mouse neural progenitor cells (NPCs), resulting in a reduction in the viability of NPCs. Moreover, we find that TDF, among the three drugs used in this combination antiretroviral treatment, accounts for most of the effects on neural progenitors. Together, our results offer a mechanistic explanation for the prevalence of HAND in AIDS patients treated with combination antiretroviral therapy.
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Complejo SIDA Demencia/inducido químicamente , Fármacos Anti-VIH/toxicidad , Emtricitabina/toxicidad , Células-Madre Neurales/efectos de los fármacos , Raltegravir Potásico/toxicidad , Tenofovir/toxicidad , Animales , Terapia Antirretroviral Altamente Activa/efectos adversos , Proliferación Celular/efectos de los fármacos , Ratones , Ratones Endogámicos C57BLRESUMEN
This data article contains three figures and three videos related to the research article entitled "Applications of Stripe Assay in the Study of CXCL12-mediated Neural Progenitor Cell Migration and Polarization" Zhang et al. (2015) [1], which uses stripe assay to study mouse neural progenitor cell (NPC) migration and polarization. The current article describes the neurosphere method used to culture NPCs. NPCs in neurospheres and monolayer were characterized using immunocytochemistry method with antibodies against two classic NPC markers: nestin and SOX2. The article also describes method to obtain sufficient protein lysates from NPCs in the stripe assay. When protein lysates were subjected to Rac1 affinity precipitation, Rac1-GTP was detected in the pull-down samples. In addition, the articles provides live cell imaging data to better understand CXCL12-mediated cellular migration and polarization.
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The polarization and migration of neural progenitor cells (NPCs) are critical for embryonic brain development and neurogenesis after brain injury. Although stromal-derived factor-1α (SDF-1α, CXCL12) and its receptor CXCR4 are well-known to mediate the migration of NPCs in the developing brain, the dynamic cellular processes and structure-related molecular events remain elusive. Transwell and microfluidic-based assays are classical assays to effectively study cellular migration. However, both of them have limitations in the analysis of a single cell. In this study, we modified the stripe assay and extended its applications in the study of NPC polarization and intracellular molecular events associated with CXCL12-mediated migration. In response to localized CXCL12, NPCs formed lamellipodia in the stripe assay. Furthermore, CXCR4 and Rac1 quickly re-distributed to the area of lamellipodia, indicating their roles in NPC polarization upon CXCL12 stimulation. Although the chemokine stripes in the assay provided concentration gradients that can be best used to study cellular polarization and migration through immunocytochemistry, they can also generate live imaging data with comparable quality. In conclusion, stripe assay is a visual, dynamic and economical tool to study cellular mobility and its related molecule mechanisms.
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Bioensayo/métodos , Movimiento Celular/efectos de los fármacos , Polaridad Celular/efectos de los fármacos , Quimiocina CXCL12/farmacología , Células-Madre Neurales/citología , Animales , Técnicas de Cultivo de Célula , Dimetilpolisiloxanos/química , Fluorescencia , Ratones , Células-Madre Neurales/efectos de los fármacos , Transporte de Proteínas/efectos de los fármacos , Receptores CXCR4/metabolismoRESUMEN
Alzheimer's disease (AD) is a prominent form of dementia, characterized by aggregation of the amyloid ß-peptide (Aß) plaques and neurofibrillary tangles, loss of synapses and neurons, and degeneration of cognitive functions. Currently, although a variety of medications can relieve some of the symptoms, there is no cure for AD. Recent breakthroughs in the stem cell field provide promising strategies for AD treatment. Stem cells including embryonic stem cells (ESCs), neural stem cells (NSCs), mesenchymal stem cells (MSCs), and induced pluripotent stem cells (iPSCs) are potentials for AD treatment. However, the limitation of cell sources, safety issues, and ethical issues restrict their applications in AD. Recently, the direct reprogramming of induced neural progenitor cells (iNPCs) has shed light on the treatment of AD. In this review, we will discuss the latest progress, challenges, and potential applications of direct reprogramming in AD treatment.