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1.
World J Gastroenterol ; 27(25): 3863-3876, 2021 Jul 07.
Artigo em Inglês | MEDLINE | ID: mdl-34321850

RESUMO

BACKGROUND: The association between PPARGC1A rs8192678 and nonalcoholic fatty liver disease (NAFLD) requires further confirmation. In addition, it is still unknown whether PPARGC1A rs8192678 is associated with hepatic histological features in NAFLD in the Chinese population. AIM: To investigate the interaction between PPARGC1A rs8192678 and nonalcoholic steatohepatitis (NASH), and whether this polymorphism is associated with hepatic histological features. METHODS: Fifty-nine patients with liver biopsy-proven NAFLD and 93 healthy controls were recruited to a cohort representing the Chinese Han population. The SAF (steatosis, activity, and fibrosis) scoring system was used for hepatic histopathological evaluation. The polymorphisms of PPARGC1A rs8192678 and patatin-like phospholipase domain-containing protein 3 (PNPLA3) rs738409 were genotyped. The intrahepatic mRNA expression of PPARGC1A was evaluated by real-time polymerase chain reaction. RESULTS: Thirty-seven patients with NAFLD had NASH, of which 12 were nonobese. The PPARGC1A rs8192678 risk A allele (carrying GA and AA genotypes) had the lowest P value in the dominant model; the odds ratio (OR) for NAFLD was 2.321 [95% confidence interval (CI): 1.121-4.806]. After adjusting for age, sex, and the PNPLA3 rs738409 risk G allele, the PPARGC1A rs8192678 A allele was a risk factor for NAFLD (OR 2.202, 95%CI: 1.030-4.705, P = 0.042). The genetic analysis showed that patients with NAFLD, moderate-to-severe steatosis (S2-3), and Activity 2-4 (A ≥ 2) were more likely to carry A in PPARGC1A rs8192678 (OR 5.000, 95%CI: 1.343-18.620, P = 0.012; and OR 4.071, 95%CI: 1.076-15.402, P = 0.031). The multivariate logistic regression analysis showed that PPARGC1A rs8192678 risk A allele was also independently associated with S2-3, A ≥ 2, and NASH (OR 6.190, 95%CI: 1.508-25.410, P = 0.011; OR 4.506, 95%CI 1.070-18.978, P = 0.040; and OR 6.337, 95%CI: 1.135-35.392, P = 0.035, respectively) after adjusting for age, sex, body mass index, and PNPLA3 rs738409 risk G allele. The results also showed that this polymorphism was associated with nonobese NASH (OR 22.000, 95%CI: 1.540-314.292, P = 0.021). The intrahepatic expression of PPARGC1A mRNA was significantly lower in the group of patients who carried the risk A allele (P = 0.014). CONCLUSION: The PPARGC1A rs8192678 risk A allele is associated with NAFLD, and with S2-3, A ≥ 2 and NASH in NAFLD patients, independent of PNPLA3 rs738409, and may be associated with nonobese NASH.


Assuntos
Hepatopatia Gordurosa não Alcoólica , Predisposição Genética para Doença , Humanos , Lipase/genética , Fígado/metabolismo , Proteínas de Membrana/genética , Hepatopatia Gordurosa não Alcoólica/genética , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética , Polimorfismo de Nucleotídeo Único
2.
Ann Hepatol ; 24: 100316, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33515803

RESUMO

INTRODUCTION AND OBJECTIVES: Chronic hepatitis B virus (HBV) infection exerts an impact on lipid metabolism, but its interaction with dysmetabolism-based non-alcoholic fatty liver disease (NAFLD) remains uncertain. The purpose of the study was to investigate the effects of HBV infection on lipid metabolism, hepatic steatosis and related impairments of NAFLD patients. METHODS: Biopsy-proven Chinese NAFLD patients with (NAFLD-HBV group, n = 21) or without chronic HBV infection (NAFLD group, n = 41) were enrolled in the case-control study. Their serum lipidomics was subjected to individual investigation by ultra-performance liquid chromatography-tandem mass spectrometry. Steatosis, activity, and fibrosis (SAF) scoring revealed the NAFLD-specific pathological characteristics. RESULTS: Chronic HBV infection was associated with global alteration of serum lipidomics in NAFLD patients. Upregulation of phosphatidylcholine (PCs), choline plasmalogen (PC-Os) and downregulation of free fatty acids (FFAs), lysophosphatidylcholine (LPCs) dominated the HBV-related lipidomic characteristics. Compared to those of NAFLD group, the levels of serum hepatoxic lipids (FFA16:0, FFA16: 1, FFA18:1, FFA18:2) were significantly lowered in the NAFLD-HBV group. These low-level FFAs demonstrated correlation to statistical improvements in aspartate aminotransferase activity (FFA16:0, r = 0.33; FFA16:1, r = 0.37; FFA18:1, r = 0.32; FFA18:2, r = 0.42), hepatocyte steatosis (FFA16: 1, r = 0.39; FFA18:1, r = 0.39; FFA18:2, r = 0.32), and ballooning (FFA16:0, r = 0.30; FFA16:1, r = 0.45; FFA18:1, r = 0.36; FFA18:2, r = 0.30) (all P < 0.05). CONCLUSION: Chronic HBV infection may impact on the serum lipidomics and steatosis-related pathological characteristics of NAFLD.

3.
Biomed Res Int ; 2020: 8869674, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33294458

RESUMO

Single-nucleotide polymorphisms (SNPs) of apolipoprotein C3 (APOC3) play important role in lipid metabolism, and dyslipidemia underlies nonalcoholic fatty liver disease (NAFLD). But the correlation of serum lipidomics, APOC3 SNPs, and NAFLD remains limited understood. Enrolling thirty-four biopsy-proven NAFLD patients from Tianjin, Shanghai, Fujian, we investigated their APOC3 genotype and serum lipid profile by DNA sequencing and ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS), respectively. Scoring of hepatocyte steatosis, ballooning, lobular inflammation, and liver fibrosis was then performed to reveal the role of lipidomics-affecting APOC3 SNPs in NAFLD-specific pathological alterations. Here, we reported that APOC3 SNPs (rs4225, rs4520, rs5128, rs2070666, and rs2070667) intimately correlated to serum lipidomics in NAFLD patients. A allele instead of G allele at rs2070667, which dominated the SNPs underlying lipidomic alteration, exhibited downregulatory effect on triacylglycerols (TGs: TG 54 : 7, TG 54 : 8, and TG 56 : 9) containing polyunsaturated fatty acid (PUFA). Moreover, subjects with low-level PUFA-containing TGs were predisposed to high-grade lobular inflammation (TG 54 : 7, rho = -0.454 and P = 0.007; TG 54 : 8, rho = -0.411 and P =0.016; TG 56 : 9, rho = -0.481 and P = 0.004). The significant correlation of APOC3 rs2070667 and inflammation grading [G/G vs. G/A+A/A: 0.00 (0.00 and 1.00) vs. 1.50 (0.75 and 2.00), P = 0.022] further confirmed its pathological action on the basis of lipidomics-impacting activity. These findings suggest an inhibitory effect of A allele at APOC3 rs2070667 on serum levels of PUFA-containing TGs, which are associated with high-grade lobular inflammation in NAFLD patients.


Assuntos
Apolipoproteína C-III/genética , Predisposição Genética para Doença , Inflamação/sangue , Fígado/patologia , Hepatopatia Gordurosa não Alcoólica/sangue , Hepatopatia Gordurosa não Alcoólica/genética , Polimorfismo de Nucleotídeo Único/genética , Triglicerídeos/sangue , Adulto , Regulação para Baixo/genética , Feminino , Estudos de Associação Genética , Humanos , Inflamação/patologia , Lipidômica , Masculino
4.
Life Sci ; 243: 117255, 2020 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-31923418

RESUMO

BACKGROUND: The occurrence in drug resistance of chronic myeloid leukemia (CML) was accompanied by autophagy activation. Abnormal circular RNAs (circRNAs) participated in this progression. This study attempted to investigate the potential role of circ_0009910 in imatinib resistance of CML cells. METHODS: The expression of circ_0009910 and miR-34a-5p was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The characterization of circ_0009910 was investigated using oligo (dT)18 primers, Actinomycin D and RNase R. Cell viability (IC50 value) and apoptosis were assessed by Cell Counting Kit-8 (CCK8) assay and flow cytometry assay, respectively. The relative protein expression was quantified by western blot. The relationship among miR-34a-5p, circ_0009910 and ULK1 was predicted by online bioinformatics tool, and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP). RESULTS: The expression of circ_0009910 was up-regulated in the serum of imatinib-resistance CML patients and K562/R cells, and associated with unfavorable clinicopathologic features. Circ_0009910 in K562 and K562/R cells was mainly localized in the cytoplasm. Circ_0009910 knockdown inhibited cell proliferation and autophagy, but induced apoptosis in K562/R cells. Circ_0009910 targeted miR-34a-5p to regulate ULK1. MiR-34a-5p depression rescued the effects of circ_0009910 knockdown on apoptosis and autophagy in K562/R cells. CONCLUSION: Circ_0009910 accelerated imatinib-resistance in CML cells by modulating ULK1-induced autophagy via targeting miR-34a-5p, providing a potential target in imatinib resistance of CML.


Assuntos
Antineoplásicos/uso terapêutico , Proteína Homóloga à Proteína-1 Relacionada à Autofagia/fisiologia , Autofagia/fisiologia , Mesilato de Imatinib/uso terapêutico , Peptídeos e Proteínas de Sinalização Intracelular/fisiologia , Leucemia Mielogênica Crônica BCR-ABL Positiva/tratamento farmacológico , MicroRNAs/genética , Resistencia a Medicamentos Antineoplásicos , Humanos , Células K562 , Leucemia Mielogênica Crônica BCR-ABL Positiva/genética , Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia
5.
Hepatology ; 72(2): 454-469, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-31782176

RESUMO

BACKGROUND AND AIMS: Hepatic macrophages can be activated by many factors such as gut-derived bacterial components and factors released from damaged hepatocytes. Macrophage polarization toward a proinflammatory phenotype (M1) represents an important event in the disease progression of nonalcoholic fatty liver disease (NAFLD). However, the underlying molecular mechanisms remain incompletely understood. Exosomes have been identified as important mediators for cell-cell communication by transferring various biological components such as microRNAs (miRs), proteins, and lipids. The role of exosomes in crosstalk between hepatocytes and macrophages in disease progression of NAFLD is yet to be explored. APPROACH AND RESULTS: In the present study, we reported that lipotoxic injury-induced release of hepatocyte exosomes enriched with miR-192-5p played a critical role in the activation of M1 macrophages and hepatic inflammation. Serum miR-192-5p levels in patients with NAFLD positively correlated with hepatic inflammatory activity score and disease progression. Similarly, the serum miR-192-5p level and the number of M1 macrophages, as well as the expression levels of the hepatic proinflammatory mediators, were correlated with disease progression in high-fat high-cholesterol diet-fed rat models. Lipotoxic hepatocytes released more miR-192-5p-enriched exosomes than controls, which induced M1 macrophage (cluster of differentiation 11b-positive [CD11b+ ]/CD86+ ) activation and increase of inducible nitric oxide synthase, interleukin 6, and tumor necrosis factor alpha expression. Furthermore, hepatocyte-derived exosomal miR-192-5p inhibited the protein expression of the rapamycin-insensitive companion of mammalian target of rapamycin (Rictor), which further inhibited the phosphorylation levels of Akt and forkhead box transcription factor O1 (FoxO1) and resulted in activation of FoxO1 and subsequent induction of the inflammatory response. CONCLUSIONS: Hepatocyte-derived exosomal miR-192-5p plays a critical role in the activation of proinflammatory macrophages and disease progression of NAFLD through modulating Rictor/Akt/FoxO1 signaling. Serum exosomal miR-192-5p represents a potential noninvasive biomarker and therapeutic target for nonalcoholic steatohepatitis.


Assuntos
Exossomos/metabolismo , Fatores de Transcrição Forkhead/fisiologia , Hepatócitos/metabolismo , Ativação de Macrófagos/fisiologia , MicroRNAs/fisiologia , Hepatopatia Gordurosa não Alcoólica/etiologia , Proteínas Proto-Oncogênicas c-akt/fisiologia , Proteína Companheira de mTOR Insensível à Rapamicina/fisiologia , Transdução de Sinais/fisiologia , Animais , Masculino , MicroRNAs/biossíntese , Ratos , Ratos Sprague-Dawley
6.
Medicine (Baltimore) ; 98(37): e17098, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31517837

RESUMO

Lung cancer has become the leading cause of cancer-related deaths around the world. In addition to genetic risk factors and smoking, the metabolic risk factors remain to be elusive.To evaluate the associations between obesity, nonalcoholic fatty liver disease (NAFLD) and pulmonary adenocarcinoma in patients with lung cancer.Consecutive operation-proven lung cancer patients with assessment of metabolic disorders and liver ultrasound in 2009 and 2013 were retrospectively enrolled. T-test and multivariate logistic regression were applied to evaluate the contribution of individual factors to lung adenocarcinoma, as well as the synergistic effects between these factors.Among 3664 lung cancer patients with ultrasound examination, 2844 cases were enrolled for further analysis. Of them, 1053 (37.0%) were females, 1242 (43.7%) were cigarette smokers, 1658 (58.3%) were diagnosed as lung adenocarcinoma, 744 (26.2%) had obesity, and 614 (21.6%) had NAFLD. Proportion of female gender, nonsmoker, obesity, NAFLD, and serum lipid levels in patients with adenocarcinoma were significantly higher than those in other subtypes of lung cancer, and in 2013 than in 2009 (all P < .01). NAFLD and obesity were shown as independent factors and positively associated with pulmonary adenocarcinoma, along with female gender and nonsmoking, higher serum levels of cholesterol. NAFLD and other contributing factors exhibited no synergistic effects on adenocarcinoma.Obesity and NAFLD might increase the risk for pulmonary adenocarcinoma, especially in nonsmoking females, and underscore the need for further study into carcinogenic mechanisms and preventive interventions.


Assuntos
Adenocarcinoma/etiologia , Neoplasias Pulmonares/classificação , Hepatopatia Gordurosa não Alcoólica/complicações , Obesidade/complicações , Adenocarcinoma/epidemiologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , China/epidemiologia , Feminino , Humanos , Modelos Logísticos , Neoplasias Pulmonares/epidemiologia , Neoplasias Pulmonares/cirurgia , Masculino , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Obesidade/epidemiologia , Estudos Retrospectivos , Fatores de Risco
7.
Mikrochim Acta ; 186(1): 28, 2018 12 18.
Artigo em Inglês | MEDLINE | ID: mdl-30564953

RESUMO

An aptamer-based fluorometric assay is described for the determination of bisphenol A (BPA). The aptamer against BPA is first attached to the surface of the red AuNPs, and this prevents the AuNPs from salt-induced formation of a blue-colored aggregate. Hence, the blue fluorescence of added nitrogen-doped carbon dots (NCDots) is quenched via an inner filter effect (IFE) caused by the red AuNPs. After addition of BPA, the BPA/aptamer complex is formed, and the AuNPs are no longer stabilized agains aggregation. This weakens the IFE and results in the recovery of the fluorescence of the NCDots which is measured best at excitation/emission wavelengths of 300/420 nm. The recovered fluorescence increases linearly in the 10 to 250 nM and 250 to 900 nM BPA concentration ranges, and the detection limit is 3.3 nM. The method was successfully applied to the determination of BPA in spiked environmental tap water samples. Graphical abstract Schematic presentation of a fluorometric aptamer based assay for bisphenol A (BPA). It is based on the inner filter effect of gold nanoparticles (AuNPs) on the fluorescence of nitrogen-doped carbon dots (NCDots).

8.
World J Clin Cases ; 6(10): 355-364, 2018 Sep 26.
Artigo em Inglês | MEDLINE | ID: mdl-30283798

RESUMO

AIM: To investigate the effect of PNPLA3 polymorphisms on serum lipidomics and pathological characteristics in nonalcoholic fatty liver disease (NAFLD). METHODS: Thirty-four biopsy-proven NAFLD patients from Northern, Central, and Southern China were subjected to stratification by genotyping their single nucleotide polymorphisms (SNPs) in PNPLA3. Ultra performance liquid chromatographytandem mass spectrometry was then employed to characterize the effects of PNPLA3 SNPs on serum lipidomics. In succession, correlation analysis revealed the association of PNPLA3-related lipid profile and hepatic pathological characteristics on a basis of steatosis, activity, and fibrosis assessment. The variant-based scoring of hepatocyte steatosis, ballooning, lobular inflammation, and liver fibrosis was finally performed so as to uncover the actions of lipidomics-affecting PNPLA3 SNPs in NAFLD-specific pathological alterations. RESULTS: PNPLA3 SNPs (rs139051, rs738408, rs738409, rs 2072906, rs2294918, rs2294919, and rs4823173) demonstrated extensive association with the serum lipidomics, especially phospholipid metabolites [lysophosphatidylcholine (LPC), lysophosphatidylcholine plasmalogen (LPCO), lysophosphatdylethanolamine (LPE), phosphatidylcholine (PC), choline plasmalogen (PCO), phosphatidylethanolamine (PE), ethanolamine plasmalogen (PEO)], of NAFLD patients. PNPLA3 rs139051 (A/A genotype) and rs2294918 (G/G genotype) dominated the up-regulatory effect on phospholipids of LPCs (LPC 17:0, LPC 18:0, LPC 20:0, LPC 20:1, LPC 20:2) and LPCOs (LPC O-16:1, LPC O-18:1). Moreover, subjects with high-level LPCs/LPCOs were predisposed to low-grade lobular inflammation of NAFLD (rho: -0.407 to -0.585, P < 0.05-0.001). The significant correlation of PNPLA3 rs139051 and inflammation grading [A/A vs A/G + G/G: 0.50 (0.00, 1.75) vs 1.50 (1.00, 2.00), P < 0.05] further demonstrated its pathological role based on the modulation of phospholipid metabolite profile. CONCLUSION: The A/A genotype at PNPLA3 rs139051 exerts an up-regulatory effect on serum phospholipids of LPCs and LPCOs, which are associated with low-grade lobular inflammation of NAFLD.

9.
Mikrochim Acta ; 185(10): 463, 2018 09 17.
Artigo em Inglês | MEDLINE | ID: mdl-30225568

RESUMO

An electrochemiluminescence (ECL) based assay is described for the determination of the endocrine disruptor bisphenol A (BPA). The method is based on the use of carboxylated graphitic carbon nitride (C-g-C3N4) carrying an immobilized aptamer against BPA. In the presence of BPA, the ECL signal decreases due to ECL energy transfer from excited-state C-g-C3N4 to the BPA oxidation product. Under the optimal conditions, ECL intensity increases linearly in the 0.1 pM to 1 nM BPA concentration range. The detection limit is as low as 30 fM. The assay has excellent sensitivity, outstanding stability and high selectivity. It was applied to the determination of BPA in spiked water samples. Graphical abstract Aptamer modified carboxylated graphitic carbon nitride was synthesized and applied in an electrochemiluminescence-based aptasensor for bisphenol A.


Assuntos
Aptâmeros de Nucleotídeos/metabolismo , Compostos Benzidrílicos/análise , Grafite/química , Limite de Detecção , Medições Luminescentes , Nitrilas/química , Fenóis/análise , Calibragem , Ácidos Carboxílicos/química , Eletroquímica , Modelos Moleculares , Conformação Molecular
10.
World J Clin Cases ; 6(8): 167-175, 2018 Aug 16.
Artigo em Inglês | MEDLINE | ID: mdl-30148144

RESUMO

Non-alcoholic fatty liver disease (NAFLD) has now become the leading cause of chronic liver disease with its growing incidence worldwide. Patatin-like phospholipase domain-containing protein 3 (PNPLA3) rs738409 C > G reflects one of the critical genetic factors that confers high-risk to NAFLD. However, the role of PNPLA3 polymorphism in NAFLD treatment remains uncertain. Here, the present review reveals that NAFLD patients with G-allele at PNPLA3 rs738409 (PNPLA3 148M variant) are sensitive to therapies of lifestyle modification, dipeptidyl peptidase-4 inhibitors, and bariatric surgery. They exhibit much significant reduction of liver fat content, in concurrence with weigh loss and abolished insulin resistance, as compared to those of C-allele carriers. In contrast, patients bearing PNPLA3 rs738409 C-allele (PNPLA3 148I variant), instead of G-allele, demonstrate greater beneficial effects by omega-3 poly-unsaturated fatty acids and statin intervention. Improved adipose tissue-liver interaction and decrease in intrahepatic triglyceride efflux may contribute to the PNPLA3 rs738409 related diversities in therapeutic efficacy. Therefore, PNPLA3 rs738409 underlies the response to a variety of treatments, which warrants a personalized, precise medicine in NAFLD on the basis of genotype stratification.

11.
J Transl Med ; 15(1): 235, 2017 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-29141648

RESUMO

BACKGROUND: Gene polymorphisms at microRNA-binding sites (poly-miRTS) may affect gene transcription and expression through miRNA regulation, which is associated with cancer susceptibility, sensitivity to chemotherapy and prognosis. This study investigated the association between poly-miRTS of Ara-C/anthracycline metabolic pathways genes and the outcome of acute myeloid leukemia (AML) in Chinese patients after Ara-C-based chemotherapy. METHODS: A total of 17 poly-miRTS were selected from the SNPinfo Web Server and genotyped in 206 Chinese Han non-FAB-M3 AML patients using the SEQUENOM Mass-ARRAY system. RESULTS: Among these 17 poly-miRTS, five Ara-C metabolic gene single nucleotide polymorphisms (SNPs, NT5C2 rs10786736 and rs8139, SLC29A1 rs3734703, DCTD rs7278, and RRM1 rs1042919) were identified to significantly associate with complete AML remission and/or overall and relapse-free survival (OS and RFS, respectively), and four anthracycline-metabolic gene SNPs (ABCC1 rs3743527, rs212091, and rs212090 and CBR1 rs9024) were significantly associated with chemotherapy-related toxicities. Moreover, SLC29A1 rs3734703 was shown to associate with both chemotherapy response and survival (adjusted OR 2.561 in the overdominant model; adjusted HR 2.876 for OS and 2.357 for RFS in the dominant model). CONCLUSIONS: The data from the current study demonstrated that the poly-miRTS of Ara-C/anthracyclines metabolic genes predicted the sensitivity and side effects of AML to Ara-C-based chemotherapy and patient survival. Further study will confirm them as biomarkers for AML patients after Ara-C-based chemotherapy.


Assuntos
Antraciclinas/farmacocinética , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Citarabina/metabolismo , Inativação Metabólica/genética , Leucemia Mieloide Aguda , MicroRNAs , Polimorfismo de Nucleotídeo Único , Adolescente , Adulto , Idoso , Antraciclinas/administração & dosagem , Sítios de Ligação/genética , Biomarcadores Tumorais/genética , Citarabina/administração & dosagem , Feminino , Seguimentos , Predisposição Genética para Doença , Humanos , Leucemia Mieloide Aguda/diagnóstico , Leucemia Mieloide Aguda/tratamento farmacológico , Leucemia Mieloide Aguda/genética , Leucemia Mieloide Aguda/mortalidade , Masculino , Redes e Vias Metabólicas/genética , MicroRNAs/genética , MicroRNAs/metabolismo , Pessoa de Meia-Idade , Prognóstico , Indução de Remissão , Análise de Sobrevida , Resultado do Tratamento , Adulto Jovem
12.
Environ Sci Pollut Res Int ; 24(36): 27788-27798, 2017 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-28983739

RESUMO

NO can be removed at the same time with SO2 by aqueous Co(NH3)62+ solution. The reduction of Co(NH3)63+ to Co(NH3)62+ is catalyzed by activated carbon to regain the NO absorption ability of the scrubbing solution. Oxalic acid solution is explored to change the carbon surface to ameliorate its catalytic capability. The experimental results suggest that the best catalyst is prepared by impregnating the carbon sample in 0.7 mol l-1 oxalic acid solution for 24 h followed by being activated at 600 °C for 5 h under nitrogen atmosphere. After being treated with oxalic acid solution, the surface area and the acidity on the carbon surface increase. The experiments show that the carbon modified with oxalic acid can get a much higher NO removal efficiency than the original carbon.


Assuntos
Carbono/análise , Poluentes Ambientais/química , Recuperação e Remediação Ambiental/métodos , Óxido Nítrico/química , Ácido Oxálico/análise , Catálise , Carvão Vegetal/análise , Cobalto
13.
Sci Rep ; 7(1): 1529, 2017 05 08.
Artigo em Inglês | MEDLINE | ID: mdl-28484247

RESUMO

Non-alcoholic steatohepatitis (NASH) is an epidemic metabolic disease with limited therapeutic strategies. Cumulative data support the pivotal role of gut microbiota in NASH. Here, we investigated the hypothesis regarding whether fecal microbiota transplantation (FMT) is effective in attenuating high-fat diet (HFD)-induced steatohepatitis in mice. Mice were randomized into control, HFD and HFD + FMT groups. After an 8-week HFD, FMT treatment was initiated and carried out for 8 weeks. The gut microbiota structure, butyrate concentrations of the cecal content, liver pathology and intrahepatic lipid and cytokines were examined. Our results showed that after FMT, the gut microbiota disturbance was corrected in HFD-fed mice with elevated abundances of the beneficial bacteria Christensenellaceae and Lactobacillus. FMT also increased butyrate concentrations of the cecal content and the intestinal tight junction protein ZO-1, resulting in relief of endotoxima in HFD-fed mice. Steatohepatitis was alleviated after FMT, as indicated by a significant decrease in intrahepatic lipid accumulation (reduced Oli-red staining, decreased intrahepatic triglyceride and cholesterol), intrahepatic pro-inflammatory cytokines, and the NAS score. Accordingly, intrahepatic IFN-γ and IL-17 were decreased, but Foxp3, IL-4 and IL-22 were increased after FMT intervention. These data indicate that FMT attenuated HFD-induced steatohepatitis in mice via a beneficial effect on the gut microbiota.


Assuntos
Transplante de Microbiota Fecal , Microbioma Gastrointestinal , Hepatopatia Gordurosa não Alcoólica/microbiologia , Hepatopatia Gordurosa não Alcoólica/terapia , Tecido Adiposo/patologia , Animais , Peso Corporal , Ácido Butírico/metabolismo , Ceco/metabolismo , Dieta Hiperlipídica , Endotoxemia/patologia , Epididimo/patologia , Inflamação/sangue , Inflamação/patologia , Resistência à Insulina , Intestino Delgado/patologia , Fígado/imunologia , Fígado/lesões , Fígado/metabolismo , Fígado/patologia , Masculino , Camundongos Endogâmicos C57BL , Hepatopatia Gordurosa não Alcoólica/sangue , Obesidade/microbiologia , Obesidade/terapia , Junções Íntimas/metabolismo , Transaminases/sangue
14.
J Thorac Dis ; 9(3): 577-581, 2017 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-28449465

RESUMO

BACKGROUND: Currently the available techniques for the placement of nasoenteric feeding tube (NET), utilizing transnasal gastroscope are fast and tolerable, which is known as the most popular method. However, lots of hospitals don't have this endoscopic system. Bronchoscope, which is the basic respiratory endoscope, not only has the advantages of transnasal endoscopy, but also is popular in common hospitals. We used oxygen instillation as air supply plant of the bronchoscope, which broke its application limitation in digestive tract. The aim of this study is to evaluate the feasibility and availability of the method of placing NET with the bronchoscope in patients with esophagectomy. METHODS: From January 2013 to January 2016, a total of 48 patients with esophagectomy who underwent NET placement with the bronchoscope were included in our study. Information concerning age, gender, as well as background disease of the patients was collected. The success rate, procedure duration, and complications were recorded for each patient. RESULTS: The technique success rate reached 100%, procedure time ranged from 150 to 750 s, with an average time of 257 s. All patients tolerated well under local anesthesia, no complication of epistaxis or perforation occurred. CONCLUSIONS: The new technique of placing NET with the bronchoscope is fast, safe, effective, and well tolerated for patients with esophagectomy.

15.
World J Gastroenterol ; 23(46): 8140-8151, 2017 Dec 14.
Artigo em Inglês | MEDLINE | ID: mdl-29290651

RESUMO

AIM: To evaluate the levels of miR-192-5p in non-alcoholic fatty liver disease (NAFLD) models and demonstrate the role of miR-192-5p in lipid accumulation. METHODS: Thirty Sprague Dawley rats were randomly divided into three groups, which were given a standard diet, a high-fat diet (HFD), and an HFD with injection of liraglutide. At the end of 16 weeks, hepatic miR-192-5p and stearoyl-CoA desaturase 1 (SCD-1) levels were measured. MiR-192-5p mimic and inhibitor and SCD-1 siRNA were transfected into Huh7 cells exposed to palmitic acid (PA). Lipid accumulation was evaluated by oil red O staining and triglyceride assays. Direct interaction was validated by dual-luciferase reporter gene assays. RESULTS: The HFD rats showed a 0.46-fold decrease and a 3.5-fold increase in hepatic miR-192-5p and SCD-1 protein levels compared with controls, respectively, which could be reversed after disease remission by liraglutide injection (P < 0.01). The Huh7 cells exposed to PA also showed down-regulation and up-regulation of miR-192-5p and SCD-1 protein levels, respectively (P < 0.01). Transfection with miR-192-5p mimic and inhibitor in Huh7 cells induced dramatic repression and promotion of SCD-1 protein levels, respectively (P < 0.01). Luciferase activity was suppressed and enhanced by miR-192-5p mimic and inhibitor, respectively, in wild-type SCD-1 (P < 0.01) but not in mutant SCD-1. MiR-192-5p overexpression reduced lipid accumulation significantly in PA-treated Huh7 cells, and SCD-1 siRNA transfection abrogated the lipid deposition aggravated by miR-192-5p inhibitor (P < 0.01). CONCLUSION: This study demonstrates that miR-192-5p has a negative regulatory role in lipid synthesis, which is mediated through its direct regulation of SCD-1.


Assuntos
Lipogênese/genética , Fígado/patologia , MicroRNAs/metabolismo , Hepatopatia Gordurosa não Alcoólica/patologia , Estearoil-CoA Dessaturase/genética , Animais , Linhagem Celular Tumoral , Dieta Hiperlipídica/efeitos adversos , Modelos Animais de Doenças , Regulação para Baixo , Técnicas de Silenciamento de Genes , Humanos , Lipogênese/efeitos dos fármacos , Liraglutida/uso terapêutico , Masculino , MicroRNAs/genética , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/genética , Ácido Palmítico/farmacologia , RNA Interferente Pequeno/metabolismo , Ratos , Ratos Sprague-Dawley , Estearoil-CoA Dessaturase/metabolismo , Regulação para Cima
16.
J Dig Dis ; 17(11): 708-715, 2016 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-27628945

RESUMO

Nonalcoholic fatty liver disease (NAFLD) is a complicated disease affected by the interaction of environmental and genetic factors; however, the precise pathogenesis of the disease has not been fully determined. There is a need to better understand the pathogenesis of NAFLD and to identify non-invasive diagnostic modalities. Recent advances in systematic biology and epigenetics have improved our understanding of the genotype-phenotype relationships in NAFLD. MicroRNAs (miRNAs) are important regulators of a wide range of biological processes. MiRNAs are extremely stable and protect from RNAase-mediated degradation in body fluids, making them attractive candidate biomarkers for the early detection of the disease and the monitoring of disease progression. In this review, we summarized the current knowledge on miRNAs as potential biomarkers of NAFLD at different stages and for the prognosis of advanced diseases. Furthermore, we discussed the implications of miRNAs that functioning in lipid metabolism and hepatic steatosis as well as in hepatic inflammation and fibrosis with regard to the pathogenesis of NAFLD.


Assuntos
MicroRNAs/genética , Hepatopatia Gordurosa não Alcoólica/genética , Animais , Epigênese Genética/genética , Marcadores Genéticos/genética , Humanos , Fígado/patologia , Fígado/fisiopatologia , Hepatopatia Gordurosa não Alcoólica/patologia , Hepatopatia Gordurosa não Alcoólica/fisiopatologia , Prognóstico
17.
Exp Ther Med ; 12(3): 1345-1348, 2016 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-27602065

RESUMO

Primary liver cancer has a high incidence and high mortality rates, and currently the only viable option is surgery, although there are a number of difficulties related to this method. The aim of the present study was to investigate the potential advantages of the real-time contrast-enhanced ultrasonography (CEUS) for microwave ablation of primary liver cancer. One hundred patients with primary liver cancer were included in the study. The patients were divided into the ordinary ultrasonography and the CEUS groups. For the ordinary ultrasonography group, the ordinary ultrasonography-guided microwave ablation method was used, while microwave ablation under the guidance of CEUS was conducted for the CEUS group. The size of lesions and clearness of the tumor boundary prior to surgery in the two groups were compared. Additionally, postoperative complications and the survival rate were monitored. Lesion boundary areas measured by CEUS were significantly larger than those measured with ordinary ultrasonography. The incidence rate of postoperative pain, fever, intra-abdominal hemorrhage and infection and other complications in the ordinary ultrasonography group were significantly higher than that in the CEUS group. The tumor recurrence rate in the CEUS group was significantly lower than that in the ordinary ultrasonography group. Seventy-two percent of patients in the CEUS group showed no progress, compared to 48% of in the ordinary ultrasonography group. The progress-free survival rate in the CEUS group after 6 months was significantly higher than that in the ordinary ultrasonography group. Disease-free survival time in the CEUS group was considerably longer than the control group. In conclusion, the guidance of real-time CEUS on the primary liver cancer microwave ablation treatment can achieve good intra-operative results. It offers a real-time guidance effect, improves survival time and reduces the incidence of complications.

18.
Oncol Lett ; 12(2): 951-955, 2016 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-27446375

RESUMO

The number of cases with hepatocellular carcinoma (HCC) are on the increase. The aim of the present study was to investigate the clinical effect and relevant mechanism of combined sorafenib and radiofrequency ablation (RFA) in the treatment of the early small HCC. A total of 120 cases of patients with small HCC that presented during the period of May 2007 to June 2010 were selected and divided into the surgery (n=60) and RF (n=60) groups according to the treatment method employed. The surgery group was treated with a laparotomy resection and the RF group was treated with combined sorafenib and RFA, and a comparative analysis was made between the two groups with regard to recurrence rates, adverse reactions, and survival rates. After treatment of 1 month, the radical effective rate of the surgery and RF groups was 100%. Contrast-enhanced ultrasound images of the patients in the RF group were taken. During the 5-year follow-up, the tumor recurrence rate in the surgery group was 18.3%, significantly lower than that in the RF group where the tumor recurrence rate was 38.3% (P<0.05). The occurrence rate of postoperative pain, fever, abdominal bleeding, infection, and other complications of patients in the surgery group was significantly higher than the complication occurrence rate (P<0.05) of the patients in the RF group. The average survival time of the patients in the surgery group was 51.2±1.5 months and the survival rates during the first, third and fifth year were 90.7, 71.5 and 56.7%, respectively. Additionally, the average survival time of the patients in the RF group was 64.6±2.4 months and the survival rates during the first, third and fifth year were 91.1, 72.8 and 57.5%, respectively. The difference between the two groups was not statistically significant. The tumor-free survival rates in the surgery group during the first, third and fifth year were 87.8, 44.3 and 33.2%, respectively, while the tumor-free survival rates in the RF group during the first, third and fifth year were 86.2, 48.3 and 34.6%, respectively, and the difference between the two groups was not statistically significant. In conclusion, the combined sorafenib and RFA method, and laparotomy resection method have their advantages in the treatment of early small HCC, and under specific medical conditions, the former can partially replace the latter and be used as a preferred treatment means in the treatment of early small HCC.

19.
J Diabetes Investig ; 7(2): 206-11, 2016 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-27042272

RESUMO

AIMS/INTRODUCTION: The present study aimed to explore the incidence of type 2 diabetes, and to develop a risk-scoring model for predicting diabetes among the adult health check-up population in East China. MATERIALS AND METHODS: Participants from the Shanghai Baosteel Cohort (age ≥20 years) without diabetes at baseline were recruited in a 6-year follow-up study. In order to explore risk factors for diabetes, this cohort was categorized into two groups: new diabetes and no diabetes. Three models were developed by Cox regression analysis. The model accuracy was assessed using the area under the receiver operating characteristic curve. RESULTS: A total of 6,542 individuals were included in the Shanghai Baosteel Cohort Study. Of them, 368 (5.6%) developed type 2 diabetes at the end of the follow-up period. Cox regression analysis found a close association between incident type 2 diabetes and several risk factors including non-alcoholic fatty liver diseases at baseline. The Shanghai Baosteel Score including advanced age (2 points), hypertriglyceridemia (2 points), obesity (2 points), non-alcoholic fatty liver diseases (2 points) and impaired fasting glucose (3 points) had a good diagnostic performance with estimated area under the receiver operating characteristic curve (0.724), sensitivity (57.9%) and specificity (72.2%) at a cut-off point of >3. CONCLUSIONS: A risk-scoring system including non-alcoholic fatty liver diseases can help identify individuals at a high risk of diabetes in the East Chinese population.


Assuntos
Diabetes Mellitus Tipo 2/diagnóstico , Hepatopatia Gordurosa não Alcoólica/complicações , Adulto , Glicemia , China , Estudos de Coortes , Diabetes Mellitus Tipo 2/epidemiologia , Feminino , Humanos , Hiperlipidemias/complicações , Masculino , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais , Análise de Regressão , Fatores de Risco
20.
Oncol Rep ; 35(6): 3371-86, 2016 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-27108960

RESUMO

Mutations in the epidermal growth factor receptor (EGFR) make lung adenocarcinoma cells sensitive to EGFR tyrosine kinase inhibitors (TKIs). Long-term cancer therapy may cause the occurrence of acquired resistance to EGFR TKIs. Long non-coding RNAs (lncRNAs) play important roles in tumor formation, tumor metastasis and the development of EGFR-TKI resistance in lung cancer. To gain insight into the molecular mechanisms of EGFR-TKI resistance, we generated an EGFR-TKI-resistant HCC827-8-1 cell line and analyzed expression patterns by lncRNA microarray and compared it with its parental HCC827 cell line. A total of 1,476 lncRNA transcripts and 1,026 mRNA transcripts were dysregulated in the HCC827­8-1 cells. The expression levels of 7 chosen lncRNAs were validated by real-time quantitative PCR. As indicated by functional analysis, several groups of lncRNAs may be involved in the bio-pathways associated with EGFR-TKI resistance through their cis- and/or trans­regulation of protein-coding genes. Thus, lncRNAs may be used as novel candidate biomarkers and potential targets in EGFR-TKI therapy in the future.


Assuntos
Adenocarcinoma/tratamento farmacológico , Receptores ErbB/antagonistas & inibidores , Neoplasias Pulmonares/tratamento farmacológico , Inibidores de Proteínas Quinases/uso terapêutico , RNA Longo não Codificante/análise , Adenocarcinoma/genética , Adenocarcinoma de Pulmão , Linhagem Celular Tumoral , Resistencia a Medicamentos Antineoplásicos , Fator de Transcrição E2F1/fisiologia , Humanos , Neoplasias Pulmonares/genética , MicroRNAs/análise , Análise de Sequência com Séries de Oligonucleotídeos , Reação em Cadeia da Polimerase em Tempo Real , Fatores Estimuladores Upstream/fisiologia
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