Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 241
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Artigo em Inglês | MEDLINE | ID: mdl-31820097

RESUMO

It has been brought to our attention that in our article, explanations about cable bacteria are not rigorous. We apologize for these and note the specific reporting issues and errors below, with their corrections.

2.
Ther Adv Respir Dis ; 13: 1753466619888124, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31722614

RESUMO

BACKGROUND: Sepsis and septic shock are common in noninvasive ventilation (NIV) patients. However, studies on the association between sepsis and NIV failure are lacking. METHODS: A prospective multi-center observational study was performed in 16 Chinese intensive care units (ICUs). Patients who used NIV due to hypoxemic respiratory failure were enrolled. Sepsis and septic shock were diagnosed according to the guideline of sepsis-3. RESULTS: A total of 519 patients were enrolled. Sepsis developed in 365 patients (70%) and septic shock developed in 79 patients (15%). However, 75 patients (14%) had no sepsis. NIV failure was 23%, 38%, and 61% in patients, with no sepsis, sepsis, and septic shock, respectively. Multivariate analysis found that sepsis [odds ratio (OR) = 1.95, 95% confidence interval (CI): 1.06-3.61] and septic shock (OR = 2.47, 95% CI: 1.12-5.45) were independently associated with NIV failure. In sepsis and septic shock population, the NIV failure was 13%, 31%, 37%, 53%, and 67% in patients with sequential organ failure assessment (SOFA) scores of ⩽2, 3-4, 5-6, 7-8, and ⩾9, respectively. Patients with nonpulmonary induced sepsis had similar NIV failure rate compared with those with pulmonary induced sepsis, but had higher proportion of septic shock (37% versus 10%, p ⩽ 0.01) and lower ICU mortality (10% versus 22%, p ⩽ 0.01). CONCLUSIONS: Sepsis was associated with NIV failure in patients with hypoxemic respiratory failure, and the association was stronger in septic shock patients. NIV failure increased with the increase of organ dysfunction caused by sepsis. The reviews of this paper are available via the supplemental material section.

3.
Exp Ther Med ; 18(6): 4820-4828, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31772647

RESUMO

Dexmedetomidine (DEX) is widely used in perioperative settings for analgesia and sedation; however, little is known about its effects on the hypoxia-induced progression of tumor cells. In the present study, the effects of DEX on hypoxia-induced growth and metastasis of lung cancer cells and colorectal cancer cells was examined. A549 cells and HCT116 cells were treated with normoxia, hypoxia, co-treatment of hypoxia and DEX, and atipamezole (an α2 adrenoceptor antagonist) for 4 h. The proliferation rate of cells was determined by MTT assays. Cell metastatic potential was evaluated by Transwell assays. Survivin and hypoxia inducible factor (HIF)-1α were detected by western blotting. Matrix metalloproteinase (MMP)-2 and MMP-9 were measured using reverse transcription-quantitative PCR. It was demonstrated that hypoxia treatment promoted the proliferation and may promote the metastasis of the two cancer cell lines. DEX substantially contributed to the survival and aggressiveness of the two cancer cell lines following hypoxia. Furthermore, DEX upregulated the expression of survivin, MMP-2, MMP-9 and HIF-1α in the two cancer cell lines in response to hypoxia. Finally, the effects of DEX on the hypoxia-induced growth and metastatic potential of cancer cells were reversed by atipamezole. Collectively, DEX enhances the hypoxia-induced progression of lung cancer cells and colorectal cancer cells by regulating HIF-1α signaling, which may be associated with the α2 adrenoceptor pathway.

4.
3 Biotech ; 9(11): 386, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31656724

RESUMO

Brain-derived neurotrophic factor (BDNF) and microRNAs (miRNAs) play a significant role in the pathogenesis of acute ischemic stroke (AIS). The present study investigates the elevated expression of BDNF and miR-124 in AIS patients. In the present study, serum samples from AIS patients and healthy controls were collected to determine the regulatory role and mechanism of operation of BDNF and to determine the regulatory miRNAs involved in AIS. Using bioinformatics analysis, we identified putative and regulatory miR-124. The effect of miR-124 on BDNF expression was examined in human neuronal cell lines. Moreover, the function of miR-124 in regulating BDNF was analyzed by assessing the serum level of BDNF in both AIS patients and healthy controls. The results indicate that the BDNF level of AIS patients is very low compared with that of controls. In contrast, real-time polymerase chain reaction (RT-PCR) data revealed a very high serum level of miR-124 in AIS patients relative to healthy individuals. The associations of the National Institutes of Health (NIH) stroke scale (NIHSS) score with BDNF and BDNF-related miR-124 serum levels were calculated using Pearson's/Spearman's correlation coefficient. The findings revealed a negative correlation between NIHSS score and BDNF level, whereas a positive correlation was observed between NIHSS score and miR-124. In addition, the relationship between serum BDNF and miR-124 was negative in AIS patients. In conclusion, this study provides strong evidence that serum BDNF and the BDNF-regulatory miR-124 may serve as molecular markers for AIS.

5.
Artigo em Inglês | MEDLINE | ID: mdl-31659438

RESUMO

In this paper, a graphene/Fe2O3 (G/Fe2O3) modified anode was prepared through a simple one-step hydrothermal reduction method to improve the performance of microbial fuel cell (MFC). The power density of MFC with the G/Fe2O3 anode was 334 ± 4 mW/m2, which was 1.72 times and 2.59 times that of MFC with a graphene anode and an unmodified anode, respectively. Scanning electron microscopy and iron reduction rate experiment showed that G/Fe2O3 materials had good biocompatibility. Furthermore, microbial community analysis results indicated that the predominant populations on the anode biofilm belonged to Enterobacteriaceae, and the abundance of Desulfovibrio increased in the presence of the Fe2O3. Thus, the combination of graphene and Fe2O3 provided high electrical conductivity to facilitate extracellular electron transfer (EET) and improved biocompatibility to promote the cable bacteria formation and enhance electron transport efficiency over long distances. Therefore, G/Fe2O3 is an effective anode material for enhancing the performance of MFCs.

6.
Nucleic Acids Res ; 47(20): 10529-10542, 2019 Nov 18.
Artigo em Inglês | MEDLINE | ID: mdl-31584090

RESUMO

Conventional chemotherapy remains the primary treatment option for triple-negative breast cancer (TNBC). However, the current chemotherapeutic drugs have limited effects on TNBC, and often lead to serious side effects as well as drug resistance. Thus, more effective therapeutic options are sorely needed. As c-MYC oncogene is highly expressed during TNBC pathogenesis, inhibiting c-MYC expression would be an alternative anti-TNBC strategy. In this study, we designed and synthesized a serial of quinoxaline analogs that target c-MYC promoter G-quadruplex (G4), which is believed to be a repressor of c-MYC transcription. Among them, a difluoro-substituted quinoxaline QN-1 was identified as the most promising G4-stabilizing ligand with high selectivity to c-MYC G4 over other G4s, which is distinguished from many other reported ligands. Intracellular studies indicated that QN-1 induced cell cycle arrest and apoptosis, repressed metastasis and inhibited TNBC cell growth, primarily due to the downregulation of c-MYC transcription by a G4-dependent mechanism. Notably, inhibition by QN-1 was significantly greater for c-MYC than other G4-driven genes. Cancer cells with c-MYC overexpression were more sensitive to QN-1, relative to normal cells. Furthermore, QN-1 effectively suppressed tumor growth in a TNBC mouse model. Accordingly, this work provides an alternative strategy for treating TNBC.

7.
Respirology ; 2019 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-31610614

RESUMO

BACKGROUND AND OBJECTIVE: Isolated blockade of IL-25, IL-33 and thymic stromal lymphopoietin (TSLP) has been shown to reduce airways inflammation and hyperresponsiveness in murine asthma model. The hypothesis that combined blockade of all three cytokines can accomplish this more effectively has never been addressed. METHODS: We studied a murine asthma model employing sensitization and challenge with ovalbumin (OVA) or saline control. To discern the effects of IL-33 blockade, we compared outcomes in strain identical, wild-type and IL-33 receptor (St2 -/- ) gene-deleted mice. We then examined, in the St2 -/- animals, the effects of additional, single or combined blockade of IL-25 and TSLP with blocking antibodies. Outcomes included airways reactivity, inflammatory cellular infiltration, epithelial cell metaplasia, deposition of fibrosis-related proteins, local Th2-type cytokine expression and total and specific serum IgE concentrations measured by ELISA and quantitative immunohistochemistry. RESULTS: St2 -/- gene deletion significantly reduced airways reactivity, inflammatory cellular infiltration, lung tissue expression of Th2 cytokines and fibrosis related proteins and serum total IgE in response to OVA sensitization and challenge. Additional administration of anti-IL-25 and anti-TSLP blocking antibodies to the St2 -/- mice further significantly reduced inflammation, Th2 cytokine expression, airways fibrosis and IgE production, while anti-TSLP alone reduced eosinophil infiltration and local IL-4 expression. The airways inflammatory cellular infiltrate and lung tissue expression of Th2 cytokine, but not fibrosis-related proteins were also reduced in the presence of isotype identical, control antibodies. CONCLUSION: Combined blockade of these three cytokines may better ameliorate airways pathological changes in this murine asthma model, with implications for human asthma.

8.
Virol J ; 16(1): 123, 2019 Oct 29.
Artigo em Inglês | MEDLINE | ID: mdl-31665045

RESUMO

BACKGROUND: Human papillomavirus (HPV) is one of the most common sexually transmitted viruses. Data about HPV infection in Guizhou is limited. METHODS: 56,768 cervical samples were collected and genotyped for 15 main high risk and 6 main low risk HPV types. RESULTS: 16.95% (9623/56768) of samples were HPV positive; 90.70% (8728/9623) of HPV positive women were infected by high risk HPV. High risk and high risk mix infection (1458; 70.85%) was the most common mix HPV infection type. The highest HPV detection rate was found in age group 41-45 years old (detection rate = 17.89%) (χ2 = 204.77; P < 0.001); the highest within-group HPV infection rates were found in the ≤20 (25.62%) and ≥ 61 (24.67%) years old age groups, the lowest within-group HPV infection rate was found in the 31-35 years old age group (15.02%). The highest mix infection proportions were found in the ≥61 (36.06%) and ≤ 20 (33.63%) years old age groups (χ2 = 111.21; P < 0.001), the lowest mix infection proportion was found in the 41-45 (17.42%) years old age group. The highest high risk infection proportions were found in the 26-30 (92.98%), ≥61 (92.68%), and 36-40 (92.16%) years old age groups (χ2 = 31.72; P < 0.001), the lowest high risk infection proportion was found in the ≤20 (84.96%) years old age group. HPV infection rates varied with seasons in Guizhou. CONCLUSIONS: Characteristics of HPV distribution in Guizhou were identified. There were significant differences in HPV distribution among age groups, prevention strategies should be adjusted according to the characteristics.

9.
J Food Prot ; 82(10): 1650-1654, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31524538

RESUMO

Bongkrekic acid (BKA) is a tricarboxylic fatty acid that inhibits adenine nucleotide translocase as a kind of mitochondrial toxins. BKA is produced by the bacterium Burkholderia gladioli pathovar cocovenenans. An investigation was performed to determine the source of possible BKA poisoning of a family in H City, Guangdong Province, People's Republic of China, who consumed a commercially produced rice noodle product that was not fermented or noticeably spoiled. Clinical and food samples were tested. BKA concentration was detected by liquid chromatography-tandem mass spectrometry. We isolated and identified the suspicious strains from the rice noodles and performed toxicity determination through an animal experiment. BKA detected in the cases and the dead dog was 2.15 to about 343 µg/kg. The cases and dead dog shared a unique history of food exposure. The BKA in the factory's food samples was 150 and 160 µg/kg. All mice given the BKA extract by gavage died within 24 h. In conclusion, the food poisoning was caused by the high BKA concentration of expired (4 days over the 24-h shelf life) wet rice noodle products, with corn and wheat starch contaminated by B. gladioli cocovenenans. Different from traditional BKA poisoning caused by fermented and spoiled corn or coconut products, there was no noticeable spoilage because of the nonfermentation process and overused sodium dehydroacetate. The risk of BKA in wet rice noodle products and application of antiseptics, such as sodium dehydroacetate, in such food should be quantitatively evaluated to prevent the recurrence of similar events.

10.
Mol Med Rep ; 20(4): 3840-3848, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31485654

RESUMO

Myocardial infarction (MI) is a leading cause of mortality in adults worldwide. Over the last two decades, gene therapy has been a hot topic in cardiology, and there has been a focus on cell cycle inhibitors and their protective effects on the myocardium post­MI. In our previous study, the haploinsufficiency of p27kip1 (p27) was demonstrated to improve cardiac function in mice post­MI by promoting angiogenesis and myocardium protection through the secretion of growth factors. Autophagy is an adaptive response of cells to environmental changes, such as nutrient deprivation, ischemia and hypoxia. The appropriate regulation of autophagy may improve myocardial function by preventing apoptosis of cardiomyocytes. In this study, we used immunoassays, transmission electron microscopy and cardiac ultrasound to confirm that p27 haploinsufficiency prevents myocardial apoptosis by restoring autophagy protein 5­mediated autophagy flux in the early stages of MI. The present study provides a novel method for studying MI or ischemic heart disease therapy.

11.
Biochem Biophys Res Commun ; 518(3): 451-458, 2019 Oct 20.
Artigo em Inglês | MEDLINE | ID: mdl-31472958

RESUMO

Parkinson's disease (PD) is the second most common neurodegenerative disorder, characterized by dopaminergic neuron loss, inflammation and oxidative stress injury in the substantia nigra pars compacta (SNpc). Tripartite motif 10 (TRIM10) belongs to the TRIM family of proteins and has been implicated to play a role in in PD, although supporting evidence has yet to be established. 1-methyl-4-phenylpyridinium (MPP+), the metabolite of MPTP (Mitochondrial parkinsonian neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine), is often used to generate a cellular model of PD. In this study, we found that MPP + inhibited cell proliferation and induced TRIM10 expression. Knockdown of TRIM10 alleviated cell apoptosis and ROS generation induced by MPP+. Further, MPP + decreased the expression of dual specificity phosphatase 6 (DUSP6) and this effect was reversed by TRIM10 knockdown. Moreover, DUSP6 alleviated cell apoptosis and ROS generation induced by TRIM10. Of note, TRIM10 suppressed DUSP6 by promoting DUSP6 ubiquitination. In conclusion, silencing of TRIM10 reduced cell apoptosis and ROS levels in a cellular model of PD, suggesting a potential role of TRIM10 in PD treatment.

12.
Leg Med (Tokyo) ; 41: 101622, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31518860

RESUMO

Bongkrekic acid (BA) poisoning can be caused by eating spoiled or fermented foods contaminated with pseudomonas cocovenenans. Although some in vitro studies have been reported on the use of purified BA to interfere with cell metabolism, few clinical or pathological data of BA poisoning on human due to food-borne factors are available for forensic appraisal. For the first time, we retrospectively report five cases of food-borne poisoning caused by eating rice noodles, a popular traditional food in Guangdong, China, and three of the victims died. All five victims were hospitalized with gastrointestinal symptoms such as nausea, vomiting and diarrhea and were treated with admission diagnosis of liver failure and acute kidney damage. Certain concentrations of BA were detected in the victims' peripheral blood serums at the hospitalization (ranging from 70-345 µg/L) and the suspected poisonous foods (0-810 ng/g) with LC-MS/MS technique. The results of forensic pathological examination showed that all three deceased had severe liver and kidney damage, accompanied by multiple organ congestion and edema, which were consistent with clinical diagnosis. Combined with the clinical records, we found that the difference in blood glucose between the deceased and survivors of the five victims may be an indication of the severity of the disease. In addition, we compared BA poisoning with other diseases that can cause acute liver function damage in terms of pathological characteristics and clinical manifestations, which has important reference significance for the diagnosis and forensic appraisal of this food-borne poisoning.

13.
Front Neurosci ; 13: 903, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31551677

RESUMO

Background: The differentiation of large vessel occlusion caused by intracranial atherosclerotic stenosis (ICAS) or intracranial embolism significantly impacts the course of treatment (i.e., intravenous thrombolysis versus mechanical thrombectomy) for acute cerebral infarction. Currently, there is no objective evidence to indicate ICAS-related middle cerebral artery M1 segment occlusion before treatment. In cases of ICAS, it is often observed that the infarct core caused by ICAS-related M1 segment middle cerebral artery occlusion (MCAO) is located in deeper parts of the brain (basal ganglia or semiovoid region). Objective: To evaluate whether the location of the infarct core, identified using diffusion-weighted imaging (DWI), can be used to differentiate ICAS from intracranial embolism. Methods: Thirty-one consecutive patients diagnosed with acute cerebral infarction caused by middle cerebral artery M1 segment occlusion were retrospectively included based on angiographic findings to distinguish ICAS from embolic occlusion. Patients were divided into two groups based on the location of the infarct core on DWI: in the deep part of the brain (basal ganglia or semiovoid region) or more superficially (i.e., cortex). Results: In 16 patients, the infarct core was mainly in the deep part of the brain on DWI [14 of 16 patients in the ICAS group and only 2 in the non-ICAS group (93.3 vs. 6.7%, respectively; P < 0.001)]. The diagnostic sensitivity of DWI for ICAS was 93.3%, with a specificity of 87.5%, a Positive predictive value (PPV) of 87.5%, and an Negative predictive value (NPV) of 93.3%, the accuracy was 88.5%. Conclusion: Intracranial atherosclerotic disease-related acute MCAO can be predicted using DWI.

14.
Front Neurol ; 10: 893, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31481925

RESUMO

Histone deacetylase inhibitors (HDACi) are a promising therapeutic intervention for stroke. The involvement of the anti-inflammatory effects of HDACi in their neuroprotection has been reported, but the underlying mechanisms are still uncertain. Given the post-stroke inflammation is a time-dependent process, starting with acute and intense inflammation, and followed by a prolonged and mild one, we proposed whether target the early inflammatory response could achieve the neuroprotection of HDACi? To test this hypothesis, a single dose of suberoylanilide hydroxamic acid (SAHA) (50 mg/kg), a pan HDACi, was intraperitoneally (i.p.) injected immediately or 12 h after ischemia onset in a transient middle cerebral artery occlusion (tMCAO) mouse model. Compared with delayed injection, immediate SAHA treatment provided more protection, evidenced by smaller infarction volume, and a better outcome. This protection was accompanied by suppression of pro-inflammatory cytokines and reduction of activated microglia in the early stage of post-stroke inflammation. Moreover, SAHA treatment suppressed M1 cytokine expression (IL-6, TNF-α, and iNOS) while promoted the transcription of M2 cytokines (Arg-1 and IL-10) in LPS-challenged mouse microglia, and enhanced CD206 (M2 marker) but decreased CD86 (M1 markers) levels in microglia isolated from the ipsilateral hemisphere of MCAO mice. Collectively, our data suggested that the protection of SAHA on ischemic brain injury was closely associated with its inhibition on the early inflammatory response, and this inhibition was related to its reducing microglia activation and priming the activated microglia toward a more protective phenotype.

15.
Gynecol Obstet Invest ; 84(6): 599-605, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31336374

RESUMO

AIMS: Early evaluation of pelvic floor muscle (PFM) in postpartum women is important for the treatment of stress urinary incontinence (SUI). Digital vaginal palpation and electromyography (EMG) evaluation based on Glazer protocol are widely used for the assessment of PFM. However, the correlation among digital palpation, EMG, and morbidity of postpartum SUI is still unclear. This study aims to investigate the relationship between postpartum SUI and PFM examinations. METHODS: This hospital-based cross-sectional study included 1,380 parturients during September 2016 to January 2018. We collected the clinical characteristics, PFM strength, and EMG variables of parturients 6-8 weeks after birth. Then the correlation among the results of EMG, digital palpation, and the occurrence of SUI was analyzed. RESULTS: There is no significant difference in digital palpation scores of PFM strength between SUI and non-SUI parturients. The EMG values were closely related to SUI: the multivariate logistic regression revealed that the most reliable evaluation indicators of postpartum SUI were pelvic floor contractile amplitude of endurance contraction (B = 0.021, p = 0.019) and pretest resting baseline (B = 0.056, p = 0.019). Correlation analysis demonstrated that the contraction variables of EMG had a significant correlation with the digital palpation PFM strength in postpartum women (r = 0.467-0.545, p < 0.001). CONCLUSION: The EMG proved to be reliable in assessing the PFM function in postpartum women. The decreased PFM activity, according to EMG, was correlated with postpartum SUI. Although digital palpation scores were positively correlated with EMG results, no correlation was observed with SUI incidence.

16.
PeerJ ; 7: e6932, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31143547

RESUMO

China has been the largest vehicle market in the world since 2009. The stalemate between the rapid development of the vehicle industry and delayed vehicle emission control has become increasingly prominent. Vehicle emission has become a significant source of air pollution in China's cities. Understanding the current barriers in the vehicle industry is necessary for the development of effective and sustainable measures and policy to manage vehicle-induced air pollution. This review provides insight into the circumstances and causes of vehicle-induced air pollution and outlines recent progress in policy-makers' long-term strategies and regulations. The development of an integrated mechanism of social participation, technical revolution, and regulatory innovation in vehicles, fuel, and roads is suggested to break the stalemate between air pollution and the automobile boom in China; the implications of this review extend to other countries facing the similar atmospheric pollution problems.

17.
Electrophoresis ; 40(14): 1848-1854, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-31070245

RESUMO

Congenital heart disease is one of the largest class of birth defects. Eight subjects with ventricular septal defect (VSD, a kind of congenital heart disease) and 11 health children were enrolled in tandem mass tags label-based quantitative proteomic analysis to compare plasma proteins differentially abundance. A total of 66 proteins were significantly upregulated or downregulated in VSD patients compared with healthy children. These proteins were involved in pathways linked to platelet activation, fructose and mannose metabolism, complement and coagulation cascades, glycolysis/gluconeogenesis, regulation of actin cytoskeleton, and carbon metabolism. The amount of ten proteins changed significantly (p < 0.05) in newly recruited 30 VSD compared with 15 control children, which were validated by ELISA. The areas under the receiver operating characteristic curve values of fructose-bisphosphate aldolase B (ALDOB) and thymosin beta-4 (Tß4) were higher than those of other candidate proteins. ALDOB and Tß4 might be potential biomarkers applied for identifying VSD in the further works.

18.
Int J Endocrinol ; 2019: 1524905, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30936916

RESUMO

Zinc level in the body is finely regulated to maintain cellular function. Dysregulation of zinc metabolism may induce a variety of diseases, e.g., diabetes. Zinc participates in insulin synthesis, storage, and secretion by functioning as a "cellular second messenger" in the insulin signaling pathway and glucose homeostasis. The highest zinc concentration is in the pancreas islets. Zinc accumulation in cell granules is manipulated by ZnT8, a zinc transporter expressed predominately in pancreatic α and ß cells. A common ZnT8 gene (SLC30A8) polymorphism increases the risk of type 2 diabetes mellitus (T2DM), and rare mutations may present protective effects. In type 1 diabetes mellitus (T1DM), autoantibodies show specificity for binding two variants of ZnT8 (R or W at amino acid 325) dictated by a polymorphism in SLC30A8. In this review, we summarize the structure, feature, functions, and polymorphisms of ZnT8 along with its association with diabetes and explore future study directions.

19.
Biotechnol Biofuels ; 12: 71, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30976321

RESUMO

Background: Microbial electrosynthesis (MES) is a biocathode-driven process, in which electroautotrophic microorganisms can directly uptake electrons or indirectly via H2 from the cathode as energy sources and CO2 as only carbon source to produce chemicals. Results: This study demonstrates that a hydrogen evolution reaction (HER) catalyst can enhance MES performance. An active HER electrocatalyst molybdenum carbide (Mo2C)-modified electrode was constructed for MES. The volumetric acetate production rate of MES with 12 mg cm-2 Mo2C was 0.19 ± 0.02 g L-1 day-1, which was 2.1 times higher than that of the control. The final acetate concentration reached 5.72 ± 0.6 g L-1 within 30 days, and coulombic efficiencies of 64 ± 0.7% were yielded. Furthermore, electrochemical study, scanning electron microscopy, and microbial community analyses suggested that Mo2C can accelerate the release of hydrogen, promote the formation of biofilms and regulate the mixed microbial flora. Conclusion: Coupling a HER catalyst to a cathode of MES system is a promising strategy for improving MES efficiency.

20.
Inflamm Res ; 68(4): 325-336, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30820607

RESUMO

OBJECTIVE AND DESIGN: Renal ischemia-reperfusion (IR)-induced acute kidney injury (AKI) remains a major challenge in clinic. The histone methyltransferases enhancer of zest homolog-2 (EZH2) is associated with the development of renal injury. However, the molecular mechanism has not been fully elucidated. MATERIALS: AKI in C57BL/6 mice was generated by renal IR. TREATMENTS: The 3-deazaneplanocin A (DZNeP), a selective EZH2 inhibitor, or vehicle was administrated in mice after IR. HK-2 cells were exposed to hypoxia-reoxygenation (H/R) stress. METHODS: Apoptosis was detected by TUNEL assay or flow cytometry. EZH2, caspase-3, p38, F4/80+ macrophages, and CD3+ T cells were examined by immunohistochemistry or Western blot. Tumor necrosis factor (TNF)-α, monocyte chemoattractant protein (MCP)-1, IL-6, and IL-18 were measured using RT-PCR. RESULTS: Mice treated with DZNeP exhibited less severe renal dysfunction and tubular injury following IR. EZH2 inhibition decreased apoptotic cells while reducing activation of caspase-3 in kidneys under IR condition. Moreover, EZH2 inhibition impaired the recruitment of CD3+ T cells and F4/80+ cells in kidneys with IR. Administration of DZNeP suppressed the production of TNF-α, MCP-1, IL-6, and IL-18 in IR-treated kidneys. Of note, EZH2 inhibition reduced p38 phosphorylation in kidneys after IR. In H/R-treated HK-2 cells, DZNeP treatment or EZH2 knockdown reduced apoptosis. EZH2 inhibition inactivated p38 resulting in reduction of active caspase-3 and proinflammatory molecules. By contrast, EZH2 overexpression induced p38 phosphorylation, caspase-3 activation, and production of proinflammatory molecules, which was reversed by SB203580. CONCLUSIONS: EZH2 plays a crucial role in IR-induced AKI via modulation of p38 signaling. Targeting EZH2/p38 signaling pathway may offer novel strategies to protect kidneys from acute kidney injury induced by ischemia-reperfusion.


Assuntos
Lesão Renal Aguda/metabolismo , Proteína Potenciadora do Homólogo 2 de Zeste/metabolismo , Traumatismo por Reperfusão/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Lesão Renal Aguda/etiologia , Lesão Renal Aguda/genética , Lesão Renal Aguda/patologia , Animais , Caspase 3/metabolismo , Linhagem Celular , Proteína Potenciadora do Homólogo 2 de Zeste/genética , Humanos , Rim/metabolismo , Rim/patologia , Masculino , Camundongos Endogâmicos C57BL , Traumatismo por Reperfusão/complicações , Traumatismo por Reperfusão/genética , Traumatismo por Reperfusão/patologia , Transdução de Sinais
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA