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2.
Chin Med J (Engl) ; 2021 Oct 04.
Artigo em Inglês | MEDLINE | ID: mdl-34608069

RESUMO

ABSTRACT: Cell death occurs in various tissues and organs in the body. It is a physiological or pathological process that has different effects. It is of great significance in maintaining the morphological function of cells and clearing abnormal cells. Pyroptosis, apoptosis, and necrosis are all modes of cell death that have been studied extensively by many experts and scholars, including studies on their effects on the liver, kidney, the heart, other organs, and even the whole body. The heart, as the most important organ of the body, should be a particular focus. This review summarizes the mechanisms underlying the various cell death modes and the relationship between the various mechanisms and heart diseases. The current research status for heart therapy is discussed from the perspective of pathogenesis.

3.
Artigo em Inglês | MEDLINE | ID: mdl-34631198

RESUMO

Recently, "Object to Human" transmission route of SARS-CoV-2 with cold chain food as the medium has been confirmed by the frequent occurrence of Covid-19 infected patients who are practitioners of global cold chain logistics. The effective disinfection for cold chain food is the key to cut off this transmission route. However, there are great challenges to achieve the goal, due to the extremely massive commodities involved in global cold chain logistics of food, and the need to conduct disinfection at the temperature below freezing point. To solve this problem, in this study, a system of multi-stage barriers for virus transmission is established by making targeted disinfection strategies for five key steps throughout the whole life cycle of cold chain food (i.e. cold chain processing, refrigerated warehouse storage, refrigerated transportation and distribution, refrigerated retail, post-consumption). Moreover, the comparison of various disinfection methods which can be applied in the system is made to clarify the green disinfection. Conclusively, the cumulative disinfection for cold chain food provided by this system will play an important role on the normalized epidemic prevention and control.

4.
Mol Plant Pathol ; 2021 Oct 10.
Artigo em Inglês | MEDLINE | ID: mdl-34628700

RESUMO

The fungal pathogen Setosphaeria turcica causes leaf blight on maize, which leads to considerable crop losses. However, how S. turcica establishes sustained systemic infection is largely unknown. Here, we report several novel factors contributing to S. turcica pathogenicity, identified using a genomic and transcriptional screen at different stages of S. turcica appressorium development. We identified two cytoskeleton regulators, SLM1 and SLM2, that are crucial for hypha and appressorium development. The SLM1 and SLM2 transcripts accumulated during germling stage but their levels were notably reduced at the appressorium stage. Deletion of SLM2 dramatically affected cell morphology, penetration ability, and pathogenicity. We also identified three different types of S. turcica glycosyl hydrolases that are critical for plant cell wall degradation. Their transcripts accumulated during the appressorium infection stage induced by cellophane and maize leaf. Most importantly, we characterized a novel and specific S. turcica effector, appressorium-coupled effector 1 (StACE1), whose expression is coupled to appressorium formation in S. turcica. This protein is required for maize infection and induces cell death on expression in Nicotiana benthamiana. These observations suggest that the phytopathogen S. turcica is primed in advance with multiple strategies for maize infection, which are coupled to appressorium formation at the early infection stages.

5.
Artigo em Inglês | MEDLINE | ID: mdl-34609929

RESUMO

Background: Genome-wide association studies (GWASs) have identified many genetic variants that are risk factors for numerous immune-mediated diseases. In particular, different immune-mediated diseases have been found to share the same susceptibility loci. Therefore, exploring the overlap between atopic dermatitis (AD) and other immune-mediated diseases in more detail may help identify additional common susceptibility loci shared by the common immune-mediated diseases. The latest evidence suggests that the 11q23.3 locus is a susceptibility locus shared between multiple immune-mediated diseases. Objective: This study investigated whether 11q23.3 locus single nucleotide polymorphisms (SNPs) are also associated with AD in the Han Chinese population. Methods: In total, 16 SNPs at 11q23.3 were genotyped using TaqMan genotyping assays in 1012 AD cases and 1362 controls. Among these SNPs, we selected rs638893 with association values of p < 5 × 10-2 for AD for further replication in the independent replication samples (1288 cases and 1380 controls) using the Sequenom MassARRAY system. The combined analyses were performed in two stages using a meta-analytical method. Results: We identified that a common variant at 11q23.3 (rs638893, p = 1.58 × 10-3, OR = 1.22) was significantly associated with AD. The genotype-based association analysis revealed that the recessive model provided the best fit for rs638893. Conclusion: Our study identified a novel variant on chromosome 11q23.3 that confers susceptibility to AD, thereby advancing our understanding of the genetic basis of AD.

6.
Molecules ; 26(20)2021 Oct 11.
Artigo em Inglês | MEDLINE | ID: mdl-34684716

RESUMO

Lipid deposition in the kidney can cause serious damage to the kidney, and there is an obvious epithelial-mesenchymal transition (EMT) and fibrosis in the late stage. To investigate the interventional effects and mechanisms of phenolic compounds from Mori Cortex on the EMT and fibrosis induced by sodium oleate-induced lipid deposition in renal tubular epithelial cells (NRK-52e cells), and the role played by CD36 in the adjustment process, NRK-52e cells induced by 200 µmol/L sodium oleate were given 10 µmoL/L moracin-P-2″-O-ß-d-glucopyranoside (Y-1), moracin-P-3'-O-ß-d-glucopyranoside (Y-2), moracin-P-3'-O-α-l-arabinopyranoside (Y-3), and moracin-P-3'-O-[ß-glucopyranoside-(1→2)arabinopyranoside] (Y-4), and Oil Red O staining was used to detect lipid deposition. A Western blot was used to detect lipid deposition-related protein CD36, inflammation-related protein (p-NF-κB-P65, NF-κB-P65, IL-1ß), oxidative stress-related protein (NOX1, Nrf2, Keap1), EMT-related proteins (CD31, α-SMA), and fibrosis-related proteins (TGF-ß, ZEB1, Snail1). A qRT-PCR test detected inflammation, EMT, and fibrosis-related gene mRNA levels. The TNF-α levels were detected by ELISA, and the colorimetric method was used to detects SOD and MDA levels. The ROS was measured by flow cytometry. A high-content imaging analysis system was applied to observe EMT and fibrosis-related proteins. At the same time, the experiment silenced CD36 and compared the difference between before and after drug treatment, then used molecular docking technology to predict the potential binding site of the active compounds with CD36. The research results show that sodium oleate can induce lipid deposition, inflammation, oxidative stress, and fibrosis in NRK-52e cells. Y-1 and Y-2 could significantly ameliorate the damage caused by sodium oleate, and Y-2 had a better ameliorating effect, while there was no significant change in Y-3 or Y-4. The amelioration effect of Y-1 and Y-2 disappeared after silencing CD36. Molecular docking technology showed that the Y-1 and Y-2 had hydrogen bonds to CD36 and that, compared with Y-1, Y-2 requires less binding energy. In summary, moracin-P-2″-O-ß-d-glucopyranoside and moracin-P-3'-O-ß-d-glucopyranoside from Mori Cortex ameliorated lipid deposition, EMT, and fibrosis induced by sodium oleate in NRK-52e cells through CD36.

7.
Microvasc Res ; 139: 104265, 2021 Oct 16.
Artigo em Inglês | MEDLINE | ID: mdl-34662588

RESUMO

The investigation aimed to evaluate the effects of Mcc950, an inhibitor of the NLRP3 inflammasome, on diabetic retinopathy (DR) mice. The general physiological condition of each group of mice was recorded. Retinal blood vessels were stained for observation of the density of blood vessels, and retinas were used for further morphological examination and fluorescent staining after the intravitreal injection of Mcc950. Mcc950 partially reversed hyperglycemia-induced vascular damage and had reduced histological changes compared to DR mice. IL-1ß production in mice retinas in the diabetic model (DM) group increased, but pretreatment with Mcc950 significantly reversed these changes. Additionally, Mcc950 engineered reduced FITC dextran extravasation and vascular leakage. Therefore, it played an apparent protective role in DR and could be a new treatment strategy for DR.

8.
J Virol ; : JVI0150021, 2021 Oct 06.
Artigo em Inglês | MEDLINE | ID: mdl-34613824

RESUMO

African swine fever (ASF), a devastating infectious disease in swine, severely threatens the global pig farming industry. Disease control has been hampered by the unavailability of vaccines. Here, we report that deletion of the QP509L and QP383R genes (ASFV-ΔQP509L/QP383R) from the highly virulent ASFV CN/GS/2018 strain results in complete viral attenuation in swine. Animals inoculated with ASFV-ΔQP509L/QP383R at a 104 50% hemadsorbing dose (HAD50) remained clinically normal during the 17-day observational period. All ASFV-ΔQP509L/QP383R-infected animals had low viremia titers and developed a low-level p30-specific antibody response. However, ASFV-ΔQP509L/QP383R did not induce protection against challenge with the virulent parental ASFV CN/GS/2018 isolate. RNA-sequencing analysis revealed that innate immune-related genes (Ifnb, Traf2, Cxcl10, Isg15, Rantes, and Mx1) were significantly lower in ASFV-ΔQP509L/QP383R-infected than in ASFV-infected porcine alveolar macrophages. In addition, ASFV-ΔQP509L/QP383R-infected pigs had low levels of IFN-ß based on ELISA. These data suggest that deletion of ASFV QP509L/383R reduces virulence but does not induce protection against lethal ASFV challenge. Importance African swine fever (ASF) is endemic to several parts of the word, with outbreaks of the disease devastating the swine farming industry; currently, no commercially available vaccine exists. Here, we report that deletion of the previously uncharacterized QP509L and QP383R viral genes completely attenuates virulence in the ASFV CN/GS/2018 isolate. However, ASFV-ΔQP509L/QP383R-infected animals were not protected from developing an ASF infection after challenge with the virulent parental virus. ASFV-ΔQP509L/QP383R induced lower levels of innate immune-related genes and IFN-ß than the parental virus. Our results increase our knowledge on developing an effective and live ASF attenuated vaccine.

9.
Small ; : e2103433, 2021 Sep 23.
Artigo em Inglês | MEDLINE | ID: mdl-34558176

RESUMO

Great efforts have been devoted to searching for efficient catalytic systems to produce ultra-high density single-walled carbon nanotube (SWNT) arrays, which lay the foundation for future electronic devices. However, one major obstacle for realizing high-density surface-aligned SWNT arrays is the poor stability of metal nanoparticles in chemical vapor deposition catalytic processes. Recently, Trojan catalyst has been reported to yield unprecedented high-density SWNT arrays with 130 SWNTs per µm on the a-plane (11-20) of the sapphire substrate. Herein, a concept of catalyst confinement effect is put forward to revealing the secret of remarkable growth efficiency of SWNT arrays by Trojan catalyst. Combined experimental and theoretical studies indicate that confinement of catalyst nanoparticles on discrete a-plane strips plays a key role in stabilizing the small nanoparticles. The highly dispersive and active states of catalysts are maintained, which promote the growth of super-dense SWNT arrays. By rationally designing the substrate reconstruction process, large areas of dense SWNT arrays (130 SWNTs per µm) covering the entire substrate are obtained. This approach may provide novel ideas for the synthesis of various high-density 1D nanomaterials.

10.
Front Cardiovasc Med ; 8: 700424, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34490369

RESUMO

Background: The patient-tailored SyncAV algorithm shortens the QRS duration (QRSd) beyond what conventional biventricular (BiV) pacing can. However, evidence of the ability of SyncAV to improve the cardiac resynchronization therapy (CRT) response is lacking. The aim of this study was to evaluate the impact of CRT enhanced by SyncAV on echocardiographic and clinical responses. Methods and Results: Consecutive heart failure (HF) patients from three centers treated with a quadripolar CRT system (Abbott) were enrolled. The total of 122 patients were divided into BiV+SyncAV (n = 68) and BiV groups (n = 54) according to whether they underwent CRT with or without SyncAV. Electrocardiographic, echocardiographic, and clinical data were assessed at baseline and during follow-up. Echocardiographic response to CRT was defined as a ≥15% decrease in left ventricular end-systolic volume (LVESV), and clinical response was defined as a NYHA class reduction of ≥1. At the 6-month follow-up, the baseline QRSd and LVESV decreased more significantly in the BiV+SyncAV than in the BiV group (QRSd -36.25 ± 16.33 vs. -22.72 ± 18.75 ms, P < 0.001; LVESV -54.19 ± 38.87 vs. -25.37 ± 36.48 ml, P < 0.001). Compared to the BiV group, more patients in the BiV+SyncAV group were classified as echocardiographic (82.35 vs. 64.81%; P = 0.036) and clinical responders (83.82 vs. 66.67%; P = 0.033). During follow-up, no deaths due to HF deterioration or severe procedure related complications occurred. Conclusion: Compared to BiV pacing, BiV combined with SyncAV leads to a more significant reduction in QRSd and improves LV remodeling and long-term outcomes in HF patients treated with CRT.

11.
Am J Med Sci ; 2021 Sep 22.
Artigo em Inglês | MEDLINE | ID: mdl-34562416

RESUMO

Methotrexate (MTX) is an effective medication in the treatment of rheumatoid arthritis (RA), other rheumatic diseases and various solid tumors. However, its side effects, including gastrointestinal discomfort, oral ulcers, and especially bone marrow suppression, could be fatal and require special attention, particularly in patients with renal failure. We present two hemodialysis patients with RA who presented with a complication of severe pancytopenia after treatment with MTX. After receiving various supportive and blood purification treatments, both patients recovered. We reviewed twenty-four pancytopenia patients on dialysis associated with methotrexate. Among these patients, high morbidity and mortality were observed, indicating that MTX should be used cautiously in the absence of alternatives in such a population. Compared with the patients who recovered, the deceased patients showed a lower level of leukocytes. Which dialysis method might be the best choice is unclear. The mode of renal replacement therapy can be chosen according to the actual situation.

12.
J Biol Chem ; 297(5): 101190, 2021 Sep 10.
Artigo em Inglês | MEDLINE | ID: mdl-34517008

RESUMO

African swine fever virus (ASFV) is a large DNA virus that is highly contagious and pathogenic in domestic pigs with a mortality rate up to 100%. However, how ASFV suppresses JAK-STAT1 signaling to evade the immune response remains unclear. In this study, we found that the ASFV-encoded protein MGF-505-7R inhibited proinflammatory IFN-γ-mediated JAK-STAT1 signaling. Mechanistically, MGF-505-7R was found to interact with JAK1 and JAK2 and mediate their degradation. Further study indicated that MGF-505-7R promoted degradation of JAK1 and JAK2 by upregulating the E3 ubiquitin ligase RNF125 expression and inhibiting expression of Hes5, respectively. Consistently, MGF-505-7R-deficient ASFV induced high levels of IRF1 expression and displayed compromised replication both in primary porcine alveolar macrophages and pigs compared with wild-type ASFV. Furthermore, MGF-505-7R deficiency attenuated the virulence of the ASFV and pathogenesis of ASF in pigs. These findings suggest that the JAK-STAT1 axis mediates the innate immune response to the ASFV and that MGF-505-7R plays a critical role in the virulence of the ASFV and pathogenesis of ASF by antagonizing this axis. Thus, we conclude that deletion of MGF-505-7R may serve as a strategy to develop attenuated vaccines against the ASFV.

13.
PhytoKeys ; 175: 137-149, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34475796

RESUMO

PolygonatumkingianumCollett et Hemsl.var.grandifolium D.M. Liu & W.Z. Zeng (1981), which sprouts twice a year, once in spring and once in autumn, differs from Polygonatumkingianum in leaves, bracts, perianth and filaments. Morphological comparison and molecular phylogeny indicate that it is identical to the newly-published Polygonatumhunanense H.H. Liu & B.Z. Wang (2021). Hence, we propose that P.kingianumvar.grandifolium should be recognised as a new synonym of P.hunanense. In addition, phylogenetic analyses confirmed that P.hunanense is sister to Polygonatumsect.Polygonatum, rather than P.kingianum of Polygonatumsect.Verticillata.

14.
Zhongguo Fei Ai Za Zhi ; 24(8): 538-547, 2021 Aug 20.
Artigo em Chinês | MEDLINE | ID: mdl-34334155

RESUMO

BACKGROUND: Lung cancer is the malignant tumor with the highest incidence and mortality in China, among which non-small cell lung cancer (NSCLC) accounts for about 80%. Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) targeted therapy has been playing an important role in treatment of NSCLC. However, unavoidable therapeutic resistance significantly limits the clinical efficacy of EGFR-TKI. As a key member of the forkhead box protein family, FOXC1 is aberrantly expressed in NSCLC and involved in NSCLC progression. The aim of this work is to investigate the effect and potential mechanism of FOXC1 on gefitinib resistance in NSCLC. METHODS: Western blot was performed to assess the expression of FOXC1 protein in HCC827/GR cells. Immunohistochemistry (IHC) assays were performed in human NSCLC tissues with gefitinib resistance. HCC827/GR cells were transfected with shRNA specifically targeting FOXC1 mRNA and stable cell lines were established. The effects of FOXC1 on cell viability and apoptosis were analyzed using a new methyl thiazolyl tetrazolium assay (MTS assay) and flow cytometry. Self-renewal ability was determined by mammosphere-formation analysis. Quantitative real-time PCR (qRT-PCR) and Western blot were employed to detect the expression of SOX2, Nanog, OCT4 and CD133. Flow cytometry analysis were further used to detect the level of CD133. IHC assays were used to detect the levels of SOX2 and CD133 in NSCLC tissues with genfitiinb resistance. Correlations of the expressions of FOXC1, CD133 and SOX2 with each other in lung adenocarcinoma samples were analyzed based on The Cancer Genome Atlas (TCGA) database. RESULTS: The expression of FOXC1 is significantly increased in HCC827/GR cells compared with HCC827 cells (P<0.05). IHC results showed FOXC1 was highly expressed in NSCLC tissues with gefitinib resisitance. Knockdown of FOXC1 significantly increased the sensitivity of HCC827/GR cells to gefitinib. The cell viability was decreased and the apoptosis was promoted (P<0.05). Moreover, FOXC1 knockdown apparently inhibited the expression of SOX2 and CD133, and decreased the mammosphere-formation capacity in HCC827/GR cells. In NSCLC tissues with gefitinib resistance, the expressions of SOX2 and CD133 were significantly higher compared with gefitinib-sensitive tissues (P<0.01). Meanwhile, the expressions of FOXC1, CD133 and SOX2 with each other were positively correlated (P<0.05). CONCLUSIONS: FOXC1 could increase gefitinib resitance in NSCLC, by which mechanism is related to the regulation of cancer stem cell properties.

15.
Mol Biol Rep ; 48(9): 6259-6267, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34392450

RESUMO

BACKGROUND: Crossostephium chinense is a traditional Chinese medicinal herb and it is often cultivated as an ornamental plant. Previous studies on this species mainly focused on its chemical composition and it was rarely represented in genetic studies, and thus genomic resources remain scarce. METHODS AND RESULTS: Both chloroplast and nuclear polymorphic microsatellites of C. chinense were screened from genome skimming data of two individuals. 64 and 63 cpSSR markers were identified from two chloroplast genomes of C. chinense. A total of 133 polymorphic nSSRs were developed. Ten nSSRs were randomly selected to test their transferability across 35 individuals from three populations of C. chinense, and 20 individuals each of Artemisia stolonifera and A. argyi. Cross-amplifications were successfully done for C. chinense and were partially amplified for both Artemisia species. The number of alleles varied from two to nine. The observed heterozygosity and expected heterozygosity per locus ranged from 0.000 to 0.286 and from 0.029 to 0.755, respectively. CONCLUSIONS: In this study, we developed polymorphic cpSSRs and nSSRs markers for C. chinense based on genome skimming sequencing. These genomic resources will be valuable for population genetics and conservation studies in C. chinense and Artemisia.

16.
Mol Brain ; 14(1): 124, 2021 08 12.
Artigo em Inglês | MEDLINE | ID: mdl-34384467

RESUMO

To understand the role of intracellular zinc ion (Zn2+) dysregulation in mediating age-related neurodegenerative changes, particularly neurotoxicity resulting from the generation of excessive neurotoxic amyloid-ß (Aß) peptides, this study aimed to investigate whether N, N, N', N'-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN), a Zn2+-specific chelator, could attenuate Aß25-35-induced neurotoxicity and the underlying electrophysiological mechanism. We used the 3-(4, 5-dimethyl-thiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay to measure the viability of hippocampal neurons and performed single-cell confocal imaging to detect the concentration of Zn2+ in these neurons. Furthermore, we used the whole-cell patch-clamp technique to detect the evoked repetitive action potential (APs), the voltage-gated sodium and potassium (K+) channels of primary hippocampal neurons. The analysis showed that TPEN attenuated Aß25-35-induced neuronal death, reversed the Aß25-35-induced increase in intracellular Zn2+ concentration and the frequency of APs, inhibited the increase in the maximum current density of voltage-activated sodium channel currents induced by Aß25-35, relieved the Aß25-35-induced decrease in the peak amplitude of transient outward K+ currents (IA) and outward-delayed rectifier K+ currents (IDR) at different membrane potentials, and suppressed the steady-state activation and inactivation curves of IA shifted toward the hyperpolarization direction caused by Aß25-35. These results suggest that Aß25-35-induced neuronal damage correlated with Zn2+ dysregulation mediated the electrophysiological changes in the voltage-gated sodium and K+ channels. Moreover, Zn2+-specific chelator-TPEN attenuated Aß25-35-induced neuronal damage by recovering the intracellular Zn2+ concentration.

17.
Adv Sci (Weinh) ; 8(19): e2100850, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34382370

RESUMO

Pathological angiogenesis is a crucial factor that causes atherosclerotic plaque rupture. Sinoporphyrin sodium-mediated sonodynamic therapy (DVDMS-SDT) induces regression of plaque neovascularization in humans without causing obvious side effects. However, a clinical noninvasive theranostic strategy for atherosclerotic plaque neovascularization is urgently needed. A nanoplatform designed for multimodality imaging-guided SDT in plaque angiogenesis theranostics, termed PFP-HMME@PLGA/MnFe2 O4 -ramucirumab nanoparticles (PHPMR NPs), is fabricated. It encapsulates manganese ferrite (MnFe2 O4 ), hematoporphyrin monomethyl ether (HMME), and perfluoropentane (PFP) stabilized by polylactic acid-glycolic acid (PLGA) shells and is conjugated to an anti-VEGFR-2 antibody. With excellent magnetic resonance imaging (MRI)/photoacoustic/ultrasound imaging ability, the distribution of PHPMR NPs in plaque can be observed in real time. Additionally, they actively accumulate in the mitochondria of rabbit aortic endothelial cells (RAECs), and the PHPMR NP-mediated SDT promotes mitochondrial-caspase apoptosis via the production of reactive oxygen species and inhibits the proliferation, migration, and tubulogenesis of RAECs. On day 3, PHPMR NP-mediated SDT induces apoptosis in neovessel endothelial cells and improves hypoxia in the rabbit advanced plaque. On day 28, PHPMR NP-mediated SDT reduces the density of neovessels, subsequently inhibiting intraplaque hemorrhage and inflammation and eventually stabilizing the plaque. Collectively, PHPMR NP-mediated SDT presents a safe and effective theranostic strategy for inhibiting plaque angiogenesis.

18.
Oncogene ; 40(39): 5854-5865, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34345015

RESUMO

Breast cancer is the most frequently diagnosed cancer among women worldwide. Though advances in diagnosis and treatment have prolonged overall survival (OS) for patients with breast cancer, metastasis remains the major obstacles to improved survival for breast cancer patients. The existence of breast cancer stem cells (BCSCs) is a major reason underlying cancer metastasis and recurrence. Therefore, understanding the molecular pathways sustaining BCSC properties and targeting BCSCs will ultimately improve breast cancer treatments. In this study, we found that activation of ß-Catenin directly regulated CCL2 expression at the transcriptional level, and in turn promoted macrophages infiltration and M2 polarization. Moreover, macrophages co-cultured with breast cancer cells showed a significant increase in CCL2 expression and promoted ß-Catenin-induced BCSCs properties, whereas depletion of CCL2 by adding neutralizing antibodies suppressed BSCSs properties. In addition, we found that ß-Catenin-mediated CCL2 secretion recruited macrophages into tumor microenvironment and promoted breast cancer growth and metastasis in vivo. Clinically, we observed a significant positive correlation between ß-Catenin, CCL2 and CD163 expression, and increased expression of ß-Catenin, CCL2 and CD163 predicted poor prognosis in breast cancer. Furthermore, pharmacological inhibition of CCR2 and ß-Catenin synergistically suppressed BCSC properties and breast cancer growth. Collectively, our findings suggested that ß-Catenin-mediated CCL2 secretion forms a paracrine feedback loop between breast cancer cells and macrophages, which in turn promotes BCSC properties and supports breast cancer growth and metastasis. Targeting ß-Catenin/CCL2 signaling might be an effective strategy for breast cancer therapy.

19.
Sci Total Environ ; 800: 149627, 2021 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-34426308

RESUMO

Excessive application of chemical fertilizers can lead to serious environmental problems. In this study, we explored the use of nanobubble water for irrigation of crop rice as a means of reducing fertilizer use. The effect of nanobubbles on plant growth and nutrient uptake was evaluated in the laboratory, while crop yield and the efficiency of fertilizer use were evaluated in a field study. The laboratory experiments indicated that nanobubbles significantly improve plant height and root length in rice seedlings. Nanobubble treatment stimulated synthesis of the growth hormone gibberellin and upregulated the plant nutrient absorption genes OsBT, PiT-1 and SKOR, resulting in increased nutrient uptake and utilization by the roots. The field experiments verified the laboratory observations, showing that nanobubble treatment significantly increases rice yield by almost 8% when using similar levels of fertilizer as controls. Moreover, the same yield as controls was achieved with approximately 25% less fertilizer. As well as their impact on growth hormones and nutrient absorption genes, nanobubbles, due to hydrophobic and surface charge properties, enhance the release and absorption of soil nutrients, thereby reducing fertilizer demand. Overall, this study highlights a new and sustainable water irrigation strategy for enhancing crop yield and reducing chemical fertilizer waste.


Assuntos
Oryza , Agricultura , Fertilizantes/análise , Hormônio do Crescimento , Nitrogênio/análise , Nutrientes , Oryza/genética , Solo
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