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1.
Water Res ; 216: 118258, 2022 Jun 01.
Artículo en Inglés | MEDLINE | ID: mdl-35320769

RESUMEN

This work analyzed, for the first time, the bioenergetics of PAOs and GAOs in full-scale wastewater treatment plants (WWTPs) for the uptake of different carbon sources. Fifteen samples were collected from five full-scale WWTPs. Predominance of different PAOs, i.e., Ca. Accumulibacter (0.00-0.49%), Tetrasphaera (0.37-3.94%), Microlunatus phosphovorus (0.01-0.18%), etc., and GAOs, i.e., Ca. Competibacter (0.08-5.39%), Defluviicoccus (0.05-5.34%), Micropruina (0.17-1.87%), etc., were shown by 16S rRNA gene amplicon sequencing. Despite the distinct PAO/GAO community compositions in different samples, proton motive force (PMF) was found as the key driving force (up to 90.1%) for the uptake of volatile fatty acids (VFAs, acetate and propionate) and amino acids (glutamate and aspartate) by both GAOs and PAOs at the community level, contrasting the previous understanding that Defluviicoccus have a low demand of PMF for acetate uptake. For the uptake of acetate or propionate, PAOs rarely activated F1, F0- ATPase (< 11.7%) or fumarate reductase (< 5.3%) for PMF generation; whereas, intensive involvements of these two pathways (up to 49.2% and 61.0%, respectively) were observed for GAOs, highlighting a major and community-level difference in their VFA uptake biogenetics in full-scale systems. However, different from VFAs, the uptake of glutamate and aspartate by both PAOs and GAOs commonly involved fumarate reductase and F1, F0-ATPase activities. Apart from these major and community-level differences, high level fine-scale micro-diversity in carbon uptake bioenergetics was observed within PAO and GAO lineages, probably resulting from their versatilities in employing different pathways for reducing power generation. Ca. Accumulibacter and Halomonas seemed to show higher dependency on the reverse operation of F1, F0-ATPase than other PAOs, likely due to the low involvement of glyoxylate shunt pathway. Unlike Tetrasphaera, but similar to Ca. Accumulibacter, Microlunatus phosphovorus took up glutamate and aspartate via the proton/glutamate-aspartate symporter driven by PMF. This feature was testified using a pure culture of Microlunatus phosphovorus stain NM-1. The major difference between PAOs and GAOs highlights the potential to selectively suppress GAOs for community regulation in EBPR systems. The finer-scale carbon uptake bioenergetics of PAOs or GAOs from different lineages benefits in understanding their interactions in community assembly in complex environment.


Asunto(s)
Actinomycetales , Betaproteobacteria , Acetatos , Actinomycetales/metabolismo , Adenosina Trifosfatasas/metabolismo , Ácido Aspártico , Betaproteobacteria/metabolismo , Reactores Biológicos , Carbono/metabolismo , Metabolismo Energético , Ácido Glutámico/metabolismo , Glucógeno/metabolismo , Fósforo/metabolismo , Polifosfatos/metabolismo , Propionatos , Propionibacteriaceae , ARN Ribosómico 16S/genética , ARN Ribosómico 16S/metabolismo , Succinato Deshidrogenasa/metabolismo
2.
Bioresour Technol ; 337: 125452, 2021 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-34186332

RESUMEN

This first-attempt study illustrated the microbial cooperative interactions related to bioelectricity generation from the mixture of sludge fermentation liquid (SFL) and fruit waste extracts (FWEs) via microbial fuel cells (MFCs). The optimal output voltages of 0.65 V for SFL-MFCs, 0.51 V for FWEs-MFCs and 0.75 V for mixture-MFCs associated with bioelectricity conversion efficiencies of 1.061, 0.718 and 1.391 kWh/kg COD were reached, respectively. FWEs addition for substrates C/N ratio optimization contributed considerably to increase SFL-fed MFCs performance via triggering a higher microbial diversity, larger relatively abundance of functional genes and microbial synergistic interactions with genera enrichment of Clostridium, Alicycliphilus, Thermomonas, Geobacter, Paludibaculum, Pseudomonas, Taibaiella and Comamonas. Furthermore, a conceptual illustration of co-locating scenario of wastewater treatment plant(s), waste sludge in situ acidogenic fermentation, fruit waste collection/crushing station and MFC plant was proposed for the first time, which provided new thinking for future waste sludge treatment toward maximizing solid reduction and power recovery.


Asunto(s)
Fuentes de Energía Bioeléctrica , Electricidad , Electrodos , Fermentación , Frutas , Extractos Vegetales , Aguas del Alcantarillado , Aguas Residuales
3.
Neuropharmacology ; 158: 107682, 2019 11 01.
Artículo en Inglés | MEDLINE | ID: mdl-31278927

RESUMEN

Yin-Yang 1 (YY1) has been identified as playing critical roles in multiple diseases. However, little is known regarding its roles and mechanisms in cerebral ischemia/reperfusion (I/R) injury. This study is aimed to explore the roles of YY1 in regulating neuronal apoptosis in cerebral I/R injury and its underlying mechanisms. Primary mouse cerebral cortical neurons were isolated and subjected to OGD/R to mimic cerebral I/R injury in vitro. The roles of YY1 on OGD/R-induced neuronal injury were investigated by performing western blotting, quantitative real-time polymerase chain reaction, TUNEL, RNA-binding protein immunoprecipitation, chromatin immunoprecipitation, chromatin isolation by RNA purification assay, glucose uptake assay, lactate production assay, and extracellular acidification rate assay. YY1-binding long non-coding RNAs (LncRNAs) in neurons subjected to OGD/R were identified by RIP and RNA sequencing. The roles of YY1 on cerebral I/R in vivo were detected by assessing neuronbehaviour, infarct size, and neuronal apoptosis. We found that YY1 expression is downregulated, and LncRNA GAS5 is upregulated in neurons subjected to OGD/R. OGD/R treatment promotes YY1 interacting with GAS5 in neurons, and YY1 negatively regulates GAS5 expression by binding to GAS5 promoter to repress its transcription. Besides, YY1 and GAS5 bind to the same region of PFKFB3 promoter to promote PFKFB3 expression and strengthen neuronal glycolysis, resulting in aggravating OGD/R-induced neuronal apoptosis. Knockdown of YY1 or GAS5 protects against I/R-induced ischemic brain damage and improves overall neurological functions in vivo. Overall, YY1 interacts with LncRNA GAS5 to promote PFKFB3 transcription to enhance neuronal glycolysis, resulting in aggravating cerebral I/R injury.


Asunto(s)
Isquemia Encefálica/genética , Glucosa/metabolismo , Glucólisis/genética , Neuronas/metabolismo , Fosfofructoquinasa-2/genética , ARN Largo no Codificante/genética , Daño por Reperfusión/genética , Factor de Transcripción YY1/genética , Animales , Apoptosis/genética , Isquemia Encefálica/metabolismo , Corteza Cerebral/citología , Inmunoprecipitación de Cromatina , Inmunoprecipitación , Etiquetado Corte-Fin in Situ , Masculino , Ratones , Cultivo Primario de Células , ARN Largo no Codificante/metabolismo , Reacción en Cadena en Tiempo Real de la Polimerasa , Daño por Reperfusión/metabolismo , Regulación hacia Arriba , Factor de Transcripción YY1/metabolismo
4.
Zhonghua Nan Ke Xue ; 24(11): 1041-1044, 2018 Nov.
Artículo en Chino | MEDLINE | ID: mdl-32212481

RESUMEN

The incidence of sexual dysfunction is higher in men with chronic kidney disease (CKD) than in those without, of which ED is the most common clinical manifestation. Sexual dysfunction is closely related to malfunction of the endocrine system in CKD males, mainly including the disorder in the hypothalamus-pituitary-gonadal axis and hyperprolactinemia. Besides, blood vessels, the nervous system, psychological status, trace elements, and drugs are also contributory factors. At present, sexual dysfunction in CKD males is diagnosed chiefly by scale assessment, clinical manifestation and special examination, and its treatment focuses on the correction of the endocrine system malfunction, as by kidney transplantation or by drug therapy with recombinant human erythropoietin, 1,25- (OH)2 D3, bromocriptine, losartan, or zinc preparation. In addition, conventional treatment with phosphodiesterase-5 inhibitors can be used as a supplement. This paper outlines the recent progress in the studies of sexual dysfunction in CKD males, covering its risk factors, etiology, pathophysiology, diagnosis and treatment.


Asunto(s)
Insuficiencia Renal Crónica , Disfunciones Sexuales Fisiológicas , Suplementos Dietéticos , Humanos , Incidencia , Masculino , Inhibidores de Fosfodiesterasa 5/uso terapéutico , Insuficiencia Renal Crónica/complicaciones , Disfunciones Sexuales Fisiológicas/complicaciones
5.
J Pharmacol Sci ; 135(1): 1-7, 2017 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-28939129

RESUMEN

Drug resistance is one of the leading causes of chemotherapy failure in non-small cell lung cancer (NSCLC) treatment. The purpose of this study was to investigate the role of c-met in human lung cancer cisplatin resistance cell line (A549/DDP) and the reversal mechanism of salvianolic acid A (SAA), a phenolic active compound extracted from Salvia miltiorrhiza. In this study, we found that A549/DDP cells exert up-regulation of c-met by activating the Akt/mTOR signaling pathway. We also show that SAA could increase the chemotherapeutic efficacy of cisplatin, suggesting a synergistic effect of SAA and cisplatin. Moreover, we revealed that SAA enhanced sensitivity to cisplatin in A549/DDP cells mainly through suppression of the c-met/AKT/mTOR signaling pathway. Knockdown of c-met revealed similar effects as that of SAA in A549/DDP cells. In addition, SAA effectively prevented multidrug resistance associated protein1 (MDR1) up-regulation in A549/DDP cells. Taken together, our results indicated that SAA suppressed c-met expression and enhanced the sensitivity of lung adenocarcinoma A549 cells to cisplatin through AKT/mTOR signaling pathway.


Asunto(s)
Adenocarcinoma/patología , Alquenos/farmacología , Antineoplásicos/farmacología , Cisplatino/farmacología , Resistencia a Antineoplásicos/efectos de los fármacos , Neoplasias Pulmonares/patología , Polifenoles/farmacología , Proteínas Proto-Oncogénicas c-met/metabolismo , Transducción de Señal/efectos de los fármacos , Subfamilia B de Transportador de Casetes de Unión a ATP/genética , Subfamilia B de Transportador de Casetes de Unión a ATP/metabolismo , Adenocarcinoma/tratamiento farmacológico , Alquenos/aislamiento & purificación , Línea Celular Tumoral , Resistencia a Múltiples Medicamentos/efectos de los fármacos , Resistencia a Múltiples Medicamentos/genética , Sinergismo Farmacológico , Humanos , Neoplasias Pulmonares/tratamiento farmacológico , Fitoterapia , Polifenoles/aislamiento & purificación , Proteínas Proto-Oncogénicas c-akt/metabolismo , Salvia miltiorrhiza/química , Serina-Treonina Quinasas TOR/metabolismo , Regulación hacia Arriba/efectos de los fármacos , Regulación hacia Arriba/genética
6.
Molecules ; 17(3): 2271-82, 2012 Feb 24.
Artículo en Inglés | MEDLINE | ID: mdl-22367023

RESUMEN

The volatile compounds from brown millet (BM), milled millet (MM) and millet bran (MB) were extracted using simultaneous distillation/extraction with a Likens-Nickerson apparatus. The extracts were analysed using gas chromatography coupled with mass spectrometry (GC-MS). A total of 65 volatile compounds were identified in all of the samples. Among these compounds, 51, 51 and 49 belonged to BM, MM and MB, respectively. Aldehydes and benzene derivatives were the most numerous among all of the compounds. Three compounds (hexanal, hexadecanoic acid and 2-methylnaphthalene) were dominant in the BM and MM materials. Eight compounds (hexanal, nonanal, (E)-2-nonenal, naphthalene, 2-methylnaphthalene, 1-methylnaphthalene, hexadecanoic acid and 2-pentylfuran) were dominant in the MB materials. Apart from the aromatic molecules, which were present in all fractions, compounds present only in BM, MM or MB were also identified.


Asunto(s)
Extractos Vegetales/aislamiento & purificación , Setaria (Planta)/química , Compuestos Orgánicos Volátiles/aislamiento & purificación , Destilación , Cromatografía de Gases y Espectrometría de Masas , Extractos Vegetales/química , Compuestos Orgánicos Volátiles/química
7.
Am J Chin Med ; 37(4): 785-96, 2009.
Artículo en Inglés | MEDLINE | ID: mdl-19655415

RESUMEN

Oxidative stress plays a significant role in the progression of cataract. We aimed to investigate the protective effect of magnolol, a compound extracted from the Chinese herb Magnolia officinalis, against oxidative stress in human lens epithelial (HLE) cells as well as the possible molecular mechanism involved. In this study, magnolol was observed to protect against H2O2-induced cytotoxicity in HLE B-3 cells. Magnolol inhibited the generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential (Delta psi m) and release of cytochrome c from mitochondria caused by H2O2 into cytosol in HLE B-3 cells. Magnolol also inhibited H2O2-induced expressions of caspase-9 and caspase-3 and reduction of Bcl-2/Bax ratio. Moreover, magnolol attenuated the deactivation of ERK/MAPK (extracellular signal-regulated kinase/mitogen activated protein kinase) and the enhanced activation of p38, JNK (c-Jun N-terminal kinase) induced by H2O2. Magnolol could be useful in protecting against oxidative stress in HLE cells, suggesting a potential protective effect against cataractogenesis effect against cataractogenesis.


Asunto(s)
Compuestos de Bifenilo/farmacología , Células Epiteliales/efectos de los fármacos , Peróxido de Hidrógeno/farmacología , Lignanos/farmacología , Estrés Oxidativo/efectos de los fármacos , Western Blotting , Caspasa 3/metabolismo , Caspasa 9/metabolismo , Línea Celular , Supervivencia Celular/efectos de los fármacos , Citocromos c/metabolismo , Relación Dosis-Respuesta a Droga , Activación Enzimática/efectos de los fármacos , Células Epiteliales/citología , Células Epiteliales/metabolismo , Citometría de Flujo , Humanos , Cristalino/citología , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Magnolia/química , Potencial de la Membrana Mitocondrial/efectos de los fármacos , Oxidantes/farmacología , Sustancias Protectoras/farmacología , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Proteína X Asociada a bcl-2/metabolismo
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