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Thermal fluctuations in two-dimensional (2D) isotropy systems at non-zero finite temperatures can destroy the long-range (LR) magnetic order due to the mechanisms addressed in the Mermin-Wanger theory. However, the magnetic anisotropy related to spin-orbit coupling (SOC) may stabilize magnetic order in 2D systems. Very recently, 2D FexGeTe2 (3 ≤ x ≤ 7) with a high Curie temperature (TC) has not only undergone significant developments in terms of synthetic methods and the control of ferromagnetism (FM), but is also being actively explored for applications in various devices. In this review, we introduce six experimental methods, ten ferromagnetic modulation strategies, and four spintronic devices for 2D FexGeTe2 materials. In summary, we outline the challenges and potential research directions in this field.
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Polymer-assisted deposition (PAD) has been widely used in the preparation of high-quality oxides and sulfides for basic research and applications. Specifically, diverse PAD-prepared magnetic material thin films such as ZnO, Ga2O3, SrRuO3, LaCoO3, LaMnO3, Y3Fe5O12, MoS2, MoSe2, and ReS2 thin films have been grown, in which thickness-dependent, strain-modulated, doping-mediated, and/or morphology-dependent room-temperature ferromagnetism (RTFM) have been explored. Inspired by the discovery of intrinsic low-temperature FM in two-dimensional (2D) systems prepared using mechanical exfoliation, the search for more convenient methods to prepare 2D ferromagnetic materials with high-temperature FM has seen explosive growth, but with little success. Fortunately, the very recent synthesis of 2D NiO by PAD has shed light on this challenge. Based on these abovementioned developments, the difficulties of PAD when preparing a-few-nanometer single-crystalline materials and the opportunities in PAD for novel materials such as chiral magnetic soliton material Cr1/3NbS2 are discussed.
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Substâncias Explosivas , Imãs , Temperatura Baixa , Polímeros , Fenômenos MagnéticosRESUMO
OBJECTIVE: The study aimed to evaluate the effects of phosphorus (P) deficiency in diets on growth performance, hepatic lipid metabolism, and antioxidant capacity in Yellow River Carp Cyprinus carpio haematopterus. METHODS: In this study, 72 healthy experimental fish (initial weight = 12.0 ± 0.1 g [mean ± SE]) were randomly selected and distributed to two groups, with three replicates in each group. The groups were fed either a P-sufficient diet or a P-deficient diet for 8 weeks. RESULT: The P-deficient feed significantly decreased the specific growth rate, feed efficiency, and condition factor of Yellow River Carp. Fish that were fed the P-deficient feed demonstrated higher contents of triglyceride, total cholesterol (T-CHO), and low-density lipoprotein cholesterol in the plasma and a higher T-CHO content in the liver compared to the P-sufficient diet group. In addition, the P-deficient diet significantly reduced the catalase activity level, decreased the glutathione content, and increased the malondialdehyde content in the liver and in the plasma. Furthermore, P deficiency in the diet significantly downregulated the messenger RNA expression of nuclear erythroid 2-related factor 2 and peroxisome proliferator-activated receptor α, whereas it upregulated the messenger RNA expression of tumor necrosis factor α and fatty acid synthase in the liver. CONCLUSION: Dietary P deficiency reduced fish growth performance, induced fat deposition and oxidative stress, and impaired liver health.
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Carpas , Fósforo na Dieta , Animais , Antioxidantes/metabolismo , Fósforo na Dieta/metabolismo , Metabolismo dos Lipídeos , Fósforo , Dieta/veterinária , Fígado/metabolismo , Colesterol , Ração Animal/análise , Suplementos NutricionaisRESUMO
Proanthocyanidins have been shown to inhibit the signaling pathways related to oxidative stress and inflammation, also improved cell membrane integrity. The effect of peanut skin proanthocyanidins (PSPc) on CD remains unknown. In this paper, the effect and mechanism of PSPc on glial protein-induced Caco-2 cytotoxicity were studied. The results showed that PSPc may inhibit oxidative stress in DPG-induced CD model in vitro by regulating SIRT1/NRF2 pathway. By regulating SIRT1 and IκB signaling pathways, inhibit the phosphorylation of NF-κB and the deacetylation of NF-κB, inhibit inflammatory response, reduce release of inflammatory cytokines (IL-1ß, IL-6, TNF-α), the cell survival rate was and the expression of TGM2 were improved, avoiding the damage of cell monolayer model. This experiment proved the prominent effect of PSPc on CD intervention. Studying the mechanism of PSPc in the treatment of CD injury will contribute to explore new therapies for CD which will be of great significance to supplement or replace gluten-free diets.
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Doença Celíaca , Proantocianidinas , Humanos , Proantocianidinas/farmacologia , Gliadina , NF-kappa B/metabolismo , Células CACO-2 , Arachis , Sirtuína 1 , InflamaçãoRESUMO
LncRNA RHPN1-AS1 (RHPN1-AS1) has been confirmed to promote tumor progression in multiple cancers and is upregulated in prostate cancer (PCa), but whether it has an effect on PCa progression remains unclear. In this study, we found that PCa patients with high RHPN1-AS1 expression had a shorter survival time, and RHPN1-AS1 was significantly upregulated in PCa tissues and cells. Based on informatics analysis we predicted that miR-7-5p binds to 3'UTR of RHPN1-AS1 and epidermal growth factor receptor (EGFR) and verified it by luciferase reporter gene assay. Subsequently, we transfected PCa cells with RHPN1-AS1 overexpression vector (RHPN1-AS1), knockdown plasmids (sh-RHPN1-AS1) and/or miR-7-5p mimics or inhibitor and/or overexpression vector (EGFR) or small interfering RNA of EGFR (si-EGFR) or its control, and found that overexpression of RHPN1-AS1 inhibited miR-7-5p expression and promoted EGFR expression, silencing RHPN1-AS1 inhibited proliferation and invasion, and induced G2/M arrest, apoptosis and autophagy in PCa cells. 3MA (an inhibitor of autophagy)-mediated autophagy inhibition attenuated RHPN1-AS1 inhibition-induced apoptosis. Overexpression miR-7-5p or silencing EGFR promoted LC3-I to LC3-II conversion, enhanced autophagy activity, induced cleaved-caspase-3 expression and apoptosis in PCa cells. Furthermore, overexpression of RHPN1-AS1 promoted phosphorylation of phosphatidylinositol 3-kinase (PI3K), AKT and mTOR, inhibited LC3-I to LC3-II conversion and reduced apoptosis in PCa cells, while GSK2126458 (an inhibitor of PI3K) reversed the effect of RHPN1-AS1 on PCa cells. In summary, RHPN1-AS1 acted as a ceRNA of miR-7-5p to upregulate EGFR expression, silencing RHPN1-AS1 suppressed PCa tumor progression by inducing autophagy and apoptosis in PCa cells through the miR-7-5p/EGFR/PI3K/AKT/mTOR pathway.
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MicroRNAs , Neoplasias da Próstata , RNA Longo não Codificante , Masculino , Humanos , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Apoptose/genética , Fosfatidilinositol 3-Quinase/metabolismo , Fosfatidilinositol 3-Quinase/farmacologia , Proliferação de Células/genética , Linhagem Celular Tumoral , Pontos de Checagem da Fase G2 do Ciclo Celular , MicroRNAs/genética , MicroRNAs/metabolismo , Serina-Treonina Quinases TOR/genética , Serina-Treonina Quinases TOR/metabolismo , Transdução de Sinais/genética , Neoplasias da Próstata/genética , Neoplasias da Próstata/patologia , Autofagia/genética , Receptores ErbB/genética , Receptores ErbB/metabolismoRESUMO
Protecting our environment while maintaining economic growth, requires a delicate balance among interlinked sustainable development policies. In this paper, we examine China's economic industries, including a high-resolution of the country's electricity sector during 2020-2030, using a multi-objective optimization model based on Input-Output analysis. This model, investigates the synergy and trade-offs of sustainable development goals in maximizing employment and GDP while minimizing energy and water consumption, CO2 emissions, and five major pollutants to advance a sustainable industrial structure adjustment pathway for China. Our results reveal that there exists both synergies and trade-offs among multiple objectives, e.g., synergy among goals of minimizing air pollutant emissions and trade-offs between minimizing energy consumption and maximizing employment. Through the planned industrial restructuring period (2020-2030), the GDP, employment, carbon emission, and energy consumption will increase respectively by, 96.1%, 7.2%, 16.8%, 16.8%, and 6.3%, while pollutant emissions would decrease. Moreover, our research indicates that energy and water conservation should be prioritized in industrial structure adjustment strategies and policies. Our model demonstrates how the synergies and trade-offs among multiple policy targets can empower policy-makers, especially in developing nations, to make more informed and optimized industrial structure adjustment policies for sustainable development.
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Poluentes Atmosféricos , Poluentes Ambientais , Carbono/análise , Dióxido de Carbono/análise , China , Desenvolvimento Econômico , IndústriasRESUMO
As the world's largest inland shipping channel, the Yangtze River Economic Belt (YREB) is strategic to China's sustainable development where policymakers are increasingly emphasizing not only this region's economic development but also its CO2 emission reduction targets. To achieve emission targets in the YREB region, it is essential to identify the driving forces of its CO2 emissions. However, existing studies are not very refined and only examine the overall effects of drivers on CO2 emission changes, while neglecting the sub-regional and sectoral level effects across China. More refined research, therefore, will provide better-targeted policies for emission reduction relevant to regional levels such as the YREB region. Towards this end, this paper integrates the methods of structural decomposition analysis and attribution analysis to demonstrate the driving forces, at both sub-regional and sectoral levels, for YREB's emission changes from 2002 to 2012. Our results reveal the following: (1) Jiangsu Province has always been the main regional source of increasing CO2 emissions in the YREB, accounting for more than 20% of total CO2 emission growth. (2) The Electricity and Heat Production and Supply sector is responsible for most of the increases in CO2 emissions, both in 2002-2007 (609.8 Mt, 54.8%) and 2007-2012 (287.6 Mt, 34%). (3) During the period of 2007-2012, changes in per capita final demand were the primary driving force for the increases in CO2 emissions, while changes in CO2 emission intensity were the largest driving force for decreasing CO2 emissions, respectively accounting for 179.9% and -119.4% of total emission changes in the YREB region. (4) Moreover, the effect of emission intensity mainly exists in the Electricity and Heat Production and Supply sector in the Jiangsu and Zhejiang provinces, accounting for respectively, 10% and 10.4% of the total effects across all economic sectors. Considering the diverse impacts of driving forces in different sub-regions and economic sectors, policymakers should apply more refined measures to utilize varying driving forces in different sub-regions and economic sectors towards sustainable development.
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Dióxido de Carbono , Rios , Dióxido de Carbono/análise , China , Desenvolvimento Econômico , Fatores SocioeconômicosRESUMO
Dibutyltin (DBT) is the degradation products of TBT, which is generally considered higher toxicity than TBT in the immune system. In order to learn more about the mechanisms of immune-toxic of DBT, we exposed zebrafish (Danio rerio) to 0, 1, 10 and 100 ng/L DBT for 8 weeks. At the end of the experiment, we determined the immune parameters and immune-related genes. The results showed that with an increase in TBT dose, lysozyme activities and IgM, C3, C4 content in intestine, skin and spleen were all significantly inhibited by the DBT exposure. Fish exposed to 10 ng/L and 100 ng/L showed significantly lower lysozyme activities and IgM, C3, C4 content than those of the control group. Zebrafish exposed to 10 ng/L and 100 ng/L DBT, the mRNA transcript levels of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), interferon γ2 (INFγ2), nuclear factor-κB p65 (NF-kB p65), inhibitor protein-κBα (IκBα), IκB kinases ß (IKKß), Janus family of protein tyrosine kinases (JAKs) and the signal transducers and activators of transcription proteins (STATs) all increased with the DBT levels in the intestine and spleen. Those parameters showed significantly higher values in 10 ng/L and 100 ng/L than those of fish in the control group. However, no significant difference was found in IκB kinases α (IKKα) and IκB kinase γ (IKKγ) mRNA levels in the intestine and spleen. These data imply that DBT might be via suppression on IKKß/IkBa/NF-kBp65 and JAK/STAT signaling pathways to regulate the immunity of zebrafish.
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Compostos Orgânicos de Estanho/toxicidade , Transdução de Sinais/efeitos dos fármacos , Peixe-Zebra/metabolismo , Animais , Quinase I-kappa B/genética , Quinase I-kappa B/metabolismo , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Interleucina-6/genética , Interleucina-6/metabolismo , Interleucina-8/genética , Interleucina-8/metabolismo , Mucosa Intestinal/metabolismo , Intestinos/efeitos dos fármacos , Intestinos/imunologia , Janus Quinase 2/genética , Janus Quinase 2/metabolismo , Inibidor de NF-kappaB alfa/genética , Inibidor de NF-kappaB alfa/metabolismo , Fator de Transcrição STAT3/genética , Fator de Transcrição STAT3/metabolismo , Pele/efeitos dos fármacos , Pele/imunologia , Pele/metabolismo , Baço/efeitos dos fármacos , Baço/imunologia , Baço/metabolismo , Fator de Transcrição RelA/genética , Fator de Transcrição RelA/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo , Peixe-Zebra/imunologiaRESUMO
Tributyltin (TBT) is a toxic compound released into aquatic ecosystems through antifouling paints. This study was designed to examine the effects of TBT on antioxidant ability and immune responses of zebrafish (Danio rerio). Three hundred sixty healthy zebrafish were randomly grouped into four groups and exposed to different doses of TBT (0, 1, 10 and 100ngL-1). At the end of 8 weeks, the fish were sampled, and antioxidant capability, immune parameters and immune-related genes were assessed. The results showed that with an increase in TBT dose, the concentration of malonaldehyde in the liver was significantly increased (p<0.05), whereas the activities of total superoxide dismutase, catalase and glutathione peroxidase were significantly decreased (p<0.05) compared to the control. The activity and expression of lysozyme and the content of immunoglobulin M were significantly decreased compared to those of the fish exposed to 0ngL-1 TBT (p<0.05). However, the expression of the HSP70, HSP90, tumor necrosis factor-α(TNF-α), interleukins (IL-1ß, IL-6), and nuclear factor-kappa B p65 (NF-κ B p65) genes were all enhanced with an increase in TBT dose. The results indicated that TBT induced oxidative stress and had immunotoxic effects on zebrafish.
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Desinfetantes/toxicidade , Imunidade/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Compostos de Trialquitina/toxicidade , Poluentes Químicos da Água/toxicidade , Peixe-Zebra , Animais , Antioxidantes/metabolismo , Catalase/metabolismo , Citocinas/metabolismo , Glutationa Peroxidase/metabolismo , Proteínas de Choque Térmico/metabolismo , Fígado/efeitos dos fármacos , Fígado/metabolismo , Malondialdeído/metabolismo , Muramidase/metabolismo , Distribuição Aleatória , Superóxido Dismutase/metabolismo , Compostos de Trialquitina/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Peixe-Zebra/imunologia , Peixe-Zebra/metabolismoRESUMO
microRNAs (miRNAs) act as a major regulator of acquired chemo-resistance in various types of cancer therapeutics. This study investigated the contribution of miRNAs in influencing multiple drug resistance in esophageal squamous cell carcinoma (ESCC). The sensitivity of four ESCC cell lines (EC109, EC9706, TE-1 and KYSE-150) to 5-fluorouracil (5-FU) and oxaliplatin (OX) was determined by MTT assay. A 5-FU and OX-resistant subline, EC9706R, was established by continuous exposure to stepwise increasing concentration of 5-FU and OX. Microarray technology was used to compare the differential expression of miRNAs between resistant cells and parental cells. Chemo-sensitivity assay was performed to evaluate drug response in EC9706R cells transfected with miRNA mimic or inhibitor. The direct targets of miRNA were identified by employing pathway analysis and then confirmed with luciferase assay. Sixty ESCC tissue samples and their paired adjacent normal tissues were collected to validate the expression of identified miRNA. Mouse models were further utilized to investigate the function of miRNA on acquired chemo-resistance. MicroRNA panel results indicated that a total of 12 miRNAs were differentially expressed and miR-141-3p was highly over expressed in resistant cells. Inhibition of miR-141-3p reversed acquired chemo-resistance in EC9706R cells by stimulating apoptosis. The expression of miR-141-3p was significantly increased in ESCC tissue samples compared to their matched distant normal tissues. In addition, the elevated miR-141-3p expression was found to be associated with ESCC differentiation status and TNM stage. Moreover, Phosphatase and tensin homolog (PTEN) was identified as direct target of miR-141-3p. Western blot exhibited altered protein levels of PTEN, Akt, and PI3k with miR-141-3p inhibitor. An inverse correlation between PTEN expression and miR-141-3p expression was also observed in tissue samples. EC9706R xenograft mouse model became sensitized to 5-FU and OX treatment following miR-141-3p inhibitor transfection in vivo. Our study demonstrated that miR-141-3p contributed to an acquired chemo-resistance through PTEN modulation both in vitro and in vivo.
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Resistencia a Medicamentos Antineoplásicos , Neoplasias Esofágicas/metabolismo , Fluoruracila/farmacologia , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , MicroRNAs/biossíntese , Proteínas de Neoplasias/biossíntese , Compostos Organoplatínicos/farmacologia , PTEN Fosfo-Hidrolase/biossíntese , RNA Neoplásico/biossíntese , Animais , Neoplasias Esofágicas/tratamento farmacológico , Neoplasias Esofágicas/genética , Neoplasias Esofágicas/patologia , Feminino , Humanos , Masculino , Camundongos , MicroRNAs/genética , Proteínas de Neoplasias/genética , Oxaliplatina , PTEN Fosfo-Hidrolase/genética , RNA Neoplásico/genética , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
In the present study, the interleukin-6 gene (IL-6) cDNA in blunt snout bream (Megalobrama amblycephala) was identified and its expression profiles under ammonia stress and bacterial challenge were investigated. The IL-6 sequence consisted of 1045 bp, including a 696 bp ORF which translated into a 232 amino acid (AA) protein. The protein contained a putative signal peptide of 24 AA in length. IL-6 expression analysis showed that the it is differentially expressed in various tissues under normal conditions and the highest IL-6 level was observed in the intestine tissue, followed by the liver, and then in the gills. Under ammonia stress, the IL-6 mRNA level both in spleens and intestine increased significantly (P < 0.05), with the maximum levels attained at 6 h, 12 h (72, 10-fold, respectively). Thereafter, they all significantly decreased (P < 0.01) and returned to the basal value within 48 h. Whereas, in livers it slightly decreased at 3 h firstly (0.5-fold), and then significantly (P < 0.05) increased with the maximum level attained 12 h (3-fold). Further expression analysis showed that the mRNA level of IL-6 in spleens, intestine and livers of blunt snout bream all increased significantly (P < 0.05), with maximum values attained at 6 h, 3 h, 6 h (10, 6, 18-fold, respectively) after Aeromonas hydrophila (A. hydrophila) injection, and then decreased to the basal value within 24 h which suggested that IL-6 was involved in the immune response to A. hydrophila. The cloning and expression analysis of the IL-6 provide theoretical basis to further study the mechanism of anti-adverseness and expression characteristics under stress conditions in blunt snout bream.
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Cyprinidae/genética , Doenças dos Peixes/imunologia , Proteínas de Peixes/genética , Regulação da Expressão Gênica/imunologia , Infecções por Bactérias Gram-Negativas/veterinária , Interleucina-6/genética , Aeromonas hydrophila/fisiologia , Sequência de Aminoácidos , Amônia/toxicidade , Animais , Sequência de Bases , Clonagem Molecular , Cyprinidae/classificação , DNA Complementar/genética , DNA Complementar/metabolismo , Proteínas de Peixes/química , Proteínas de Peixes/metabolismo , Perfilação da Expressão Gênica , Infecções por Bactérias Gram-Negativas/imunologia , Interleucina-6/química , Interleucina-6/metabolismo , Filogenia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Alinhamento de Sequência/veterinária , Poluentes Químicos da Água/toxicidadeRESUMO
OBJECTIVE: Secondary malignancy is a major life-threatening complication facing patients afflicted with acquired immunodeficiency syndrome (AIDS). This study aimed to retrospectively review clinical features and treatment course of five patients with AIDS-associated non-Hodgkin lymphoma (A-NHL) in Jilin Tumor Hospital. METHODS: Five A-NHL patients were retrospectively and consecutively hospitalized at our oncological unit between January 2012 and June 2014. All patients received pre-emptive highly active antiretroviral therapy (HAART) and chemotherapy, and were subsequently followed up at the outpatient clinic. All five patients were male, aged 27-53 years, and afflicted with A-NHL involving upper jaw, right inguinal region, right-side gingiva, mediastinum, or right-side neck. Histology showed diffuse large B-cell lymphoma (n = 3) or plasmablastic lymphoma (n = 2). RESULTS: Two patients achieved complete remission after HAART and chemotherapy, whereas other three patients required a second-line treatment, with two achieving stable disease and one dying within a follow-up period of 0.5-2 years. CONCLUSION: The findings of the present study showed that A-NHL is a disease often diagnosed in the middle-to-late stages, with diverse clinical manifestations and short overall survival. In the cases reviewed in this study, HAART in combination with standard dose or high-dose chemotherapy, HAART and molecular targeted chemotherapy was administered, and these treatments proved to be effective for improving the prognosis of these patients. Moreover, the CD4+ cell count was important for determining the prognosis of patients.
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BACKGROUND: Cyclooxygenase (COX) is a rate-limiting enzyme in prostaglandins synthesis which exists in two isoforms, COX-1 and COX-2. Over-expression of COX-2 was considered to increase the proliferation and enhance the invasiveness of breast cancer cells. It was suggested that genetic variations in COX-2 could influence its expression. Herein, the present study was aimed to investigate the associations between two mostly studied functional polymorphisms (-765 G > C and 8473 C > T) in COX-2 and breast cancer risk in Chinese Han women. METHODS: In the hospital-based case-control study, 465 breast cancer patients and 799 cancer-free controls were genotyped for the COX-2 -765 G > C and 8473 C > T polymorphisms using TaqMan assay. We estimated odds ratios (ORs) and 95% confidence intervals (95% CIs) using the logistic regression. RESULTS: Compared with the wild genotype of -765 G > C, we found a statistically significant increased risk of breast cancer associated with the variant genotypes [GC/CC vs. GG: OR = 1.56, 95% CI = 1.11-2.21]. In the stratified analysis, the increased risk was more predominant among the subgroups of younger subjects (OR = 1.61, 95% CI = 1.00-2.61). Furthermore, the variant genotypes were associated with large tumor size (OR = 3.01, 95% CI = 1.47-6.12). No significant association was observed for the 8473 C > T polymorphism. CONCLUSIONS: Our results suggest that the functional -765 G > C polymorphism in the promoter of COX-2 may influence the susceptibility and progression of breast cancer in the Chinese Han population.
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BACKGROUND: Published data on the association between AURKA polymorphisms and breast cancer (BC) risk are inconclusive. This meta-analysis was performed to derive a more precise estimation on the relationship between AURKA polymorphisms (rs2273535 and rs1047972) and BC risk. METHODS: PubMed, Web of Knowledge and Embase were searched for relevant studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to estimate the strength of associations. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were performed for allele contrast genetic model, homozygous genetic model, heterozygote genetic model, dominant model, and recessive model, respectively. RESULTS: A total of 13 studies (16,349 BC patients and 20,872 case-free controls) were involved in this meta-analysis. Meta-analysis showed that there was significant association between rs2273535 and BC risk in three genetic models in the overall population (A vs. T: OR = 1.08, 95% CI = 1.01-1.15, P = 0.02; AA vs. TT: OR = 1.36, 95% CI = 1.06-1.73, P < 0.00001; AA vs. TT + TA: OR = 1.15, 95% CI = 1.01-1.31, P = 0.04). In the subgroup analysis by ethnicity, the effects remained in Asians (allele contrast genetic model: OR = 1.12, 95% CI = 1.00-1.26, P = 0.04 and homozygote comparison: OR = 1.22, 95% CI = 1.06-1.41, P = 0.007). However, no genetic models reached statistical association in Cauasians. Rs1047972 polymorphism was associated with BC risk in the overall population based on homozygote comparison (AA vs. GG: OR = 0.81, 95% CI = 0.66-0.99, P = 0.04). When stratified by ethnicity, rs1047972 polymorphism had a decreased association with BC risk in Caucasians based on allele contrast genetic model, homozygote comparison, the dominant model and the recessive model. However, there was no association in any genetic model in Asians. CONCLUSIONS: This meta-analysis suggests that AURKA rs2273535 polymorphism has an increased risk with BC, especially in Asians. However, rs1047972 polymorphism has a decreased BC risk in Caucasians. Further large scale multicenter epidemiological studies are warranted to confirm this finding.
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BACKGROUND: A meta-analysis was performed to estimate the association between HIF-1α polymorphism (C1772T) and breast cancer risk. MATERIAL AND METHODS: The relevant published literature was retrieved from PubMed, Web of Knowledge, and Embase. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the strength of the associations. RESULTS: Six case-control studies, including 2043 cases and 2146 controls were identified. Meta-analysis showed that there was no marked association between C1772T polymorphism and breast cancer risk in the overall population in the dominant model. The subgroup analysis showed an increased breast cancer risk in Asians based on homozygote comparison and the recessive model. There were no associations between C1772T polymorphism with clinicopathological parameters and habits. CONCLUSIONS: The present meta-analysis suggests that HIF-1α C1772T polymorphism is a risk factor for susceptibility to breast cancer in Asians.
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Neoplasias da Mama/genética , Estudos de Associação Genética , Predisposição Genética para Doença , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Polimorfismo de Nucleotídeo Único/genética , Estudos de Casos e Controles , Feminino , Frequência do Gene/genética , HumanosRESUMO
Matrine has been used in anti-inflammatory and anti-cancer therapies for a long time. However, the anti-metastatic effect and related mechanism(s) in colorectal cancer (CRC) are still unclear. In this study, we investigated whether the administration of matrine could inhibit the proliferation, motility, and invasion of human CRC cells via regulating p38 signaling pathway. Results showed that matrine inhibited migration and invasion of CRC cells in vitro and in vivo. Additionally, after being treated with matrine for 24 h, the expression levels of matrix metalloproteinase-2 (MMP-2) and MMP-9 as well as proteinase activity in CRC cells were reduced in a dose-dependent manner. Moreover, matrine reduced the phosphorylation level of p38 obviously. Combined treatment with p38 inhibitor (SB203580) and matrine resulted in a synergistic reduction of invasion as well as MMP-2/-9 expression in CRC cells. It was also found that matrine inhibited the proliferation and metastasis of CRC tumor in vivo. In conclusion, p38 signaling pathway may involve in matrine's inhibitory effects on migration and invasion of CRC cells by reducing the expression of MMP-2/-9, suggesting that matrine may be a potential therapeutic agent for CRC.
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Alcaloides/farmacologia , Proliferação de Células/efeitos dos fármacos , Neoplasias Colorretais/patologia , Invasividade Neoplásica/prevenção & controle , Quinolizinas/farmacologia , Transdução de Sinais/efeitos dos fármacos , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Animais , Linhagem Celular Tumoral , Neoplasias Colorretais/enzimologia , Humanos , Camundongos , Camundongos Endogâmicos BALB C , MatrinasRESUMO
Since single-layer graphene [...].
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In recent years, carbon nanotubes (CNTs) have gained tremendous attention due to their widespread application. Previous research indicated that carbon nanomaterials can affect the toxicity of some pollutants. In this study, we investigated the influence of multi-walled CNTs (MWCNTs) on the toxicity of ZnO nanoparticles (ZnONPs) in the intestine of common carp (Cyprinus carpio). After four-week exposure, histopathological observation and TUNEL assay showed concentration ratio-dependent intestinal lesions and apoptosis, with the most severe in the HSC-ZnONPs group (50 mg L-1 ZnONPs and 2.5 mg L-1 MWCNTs), less severe in the ZnONPs group (50 mg L-1 ZnONPs) and the least in the LSC-ZnONPs group (50 mg L-1 ZnONPs and 0.25 mg L-1 MWCNTs). Furthermore, ICP-OES indicated that intercellular zinc accumulation was significantly decreased by the presence of the MWCNTs, which suggested the varied contribution of ZnONPs to intestine injury in different groups. Moreover, 16 s rDNA sequencing revealed that ZnONPs alone and in combination with MWCNTs significantly altered the microbial community diversity and composition of the gut microbiota compared with controls. In addition, the predominant phylum, class, order, family, and genus were significantly different among these groups. In conclusion, the influence of MWCNTs on the toxicity of ZnONPs was related to the concentration and concentration ratio of the mixture.
Assuntos
Carpas , Microbiota , Nanotubos de Carbono , Óxido de Zinco , Animais , Óxido de Zinco/toxicidade , Nanotubos de Carbono/toxicidade , Intestinos , ApoptoseRESUMO
BACKGROUND: Cancer-associated fibroblasts (CAFs) have been reported that can affect cancer cell proliferation, metastasis, ferroptosis, and immune escape. METTL3-mediated N6-methyladenine (m6A) modification is involved in the tumorigenesis of colorectal cancer (CRC). Herein, we investigated whether METTL3-dependent m6A in CAFs-derived exosomes (exo) affected CRC progression. METHODS: qRT-PCR and western blotting analyses detected levels of mRNAs and proteins. Cell proliferation and metastasis were evaluated using MTT, colony formation, transwell, and wound healing assays, respectively. Cell ferroptosis was assessed by detecting cell viability and the levels of Fe+, reactive oxygen species, and glutathione after erastin treatment. Exosomes were isolated from CAFs by ultracentrifugation. The m6A modification profile was determined by methylated RNA immunoprecipitation assay and the interaction between METTL3 and ACSL3 (acyl-CoA synthetase 3) was verified using dual-luciferase reporter assay. Animal models were established for in vivo analysis. RESULTS: CAFs promoted CRC cell proliferation and metastasis, and suppressed cell ferroptosis. METTL3 was enriched in CAFs and was packaged into exosomes. The m6A modification and METTL3 expression were increased in CRC samples. Knockdown of METTL3 in CAFs-exo suppressed CRC cell proliferation and metastasis, and induced cell ferroptosis. Mechanistically, METTL3 induced ACSL3 m6A modification and stabilized its expression. The anticancer effects mediated by METTL3-silenced CAFs-exo could be rescued by ACSL3 overexpression. Moreover, in vivo assay also showed that CAFs-exo with decreased METTL3 could hinder CRC growth and metastasis in mice models. CONCLUSION: CAFs promoted the proliferation and metastasis, and restrained the ferroptosis in CRC by exosomal METTL3-elicited ACSL3 m6A modification.
Assuntos
Fibroblastos Associados a Câncer , Proliferação de Células , Coenzima A Ligases , Neoplasias Colorretais , Exossomos , Ferroptose , Metiltransferases , Ferroptose/genética , Metiltransferases/metabolismo , Metiltransferases/genética , Exossomos/metabolismo , Exossomos/genética , Neoplasias Colorretais/genética , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/patologia , Humanos , Camundongos , Fibroblastos Associados a Câncer/metabolismo , Animais , Coenzima A Ligases/genética , Coenzima A Ligases/metabolismo , Metástase Neoplásica , Linhagem Celular Tumoral , Camundongos Nus , MasculinoRESUMO
Ara h1 was the highest content of peanut allergen protein, identified as a biomarker of peanut allergen. In this study, Ara h1 was covalently complexed with caffeic acid (CA) to research the effects of covalent conjugation on the antigenicity and protein structural properties of Ara h1. After the covalent complexing of Ara h1 and CA, the IgG-binding capacity of Ara h1 was reduced compared with that of control Ara h1. Moreover, the structure of Ara h1 changed from ordered to disordered, the number of intermolecular hydrogen bonds decreased, and some hydrophobic groups were exposed or hydrophobic peptides were released. The carboxyl group in CA reacted with the amino group in Ara h1. The digestibility of Ara h1-CA was increased. The antigenicity of Ara h1-CA was undetectable after 30 min of digestion in vitro. These findings can serve as a reference for further research on hypoallergenic peanut products.