Enhanced aerobic granular sludge with micro-electric field for sulfamethoxazole degradation: Efficiency, mechanism, and microbial community.

In this study, an aerobic granular sludge electrochemical system (AGES) was established by applying the micro-electric field to an aerobic granular sludge (AGS) reactor for the degradation of sulfamethoxazole (SMZ). Under the stimulation of the micro-electric field, the granulation of sludge was improved and the degradation rate of SMZ was enhanced. The features of granular sludge were characterized by scanning electron microscopy and X-ray diffraction. The optimal degradation rate of SMZ (88%) was obtained at the voltage of 3 V and the effective electrode area of 800 mm2. The results of kinetics analyses revealed that the degradation of SMZ by AGES can be fitted with the second-order kinetic equation, showing a degradation rate constant (k) of 0.001 L mol-1·min-1. The degradation products of SMZ in the AGES system were detected by LC-MS and their possible degradation routes were elucidated. The micro-electric field in the AGES system played a selective role in microbes' enrichment and growth, changing the diversity of the microbial community. Pseudomonas, Tolumonas, and Acidovorax were the dominant bacteria in the AGES system, which is accountable for the abatement of SMZ and nutrients. This work provides a green means for improving AGS and paves the way for applying the AGS process to real-world wastewater treatment.

Characteristics of Cu(II)-modified aerobic granular sludge biocarbon in removal of doxycycline hydroxide.

In this study, the biocarbon derived from aerobic granular sludge with different nutritive proportions was modified by Cu(NO3)2•3H2O (Cu-BC) to improve its adsorption capacity of doxycycline hydrochloride (DOX). The surface area, pores, functional groups, and element composition of biocarbon were characterized by scanning electron microscopy (SEM), Brunauer-Emmett-Teller (BET) surface area, X-ray photoelectron spectrometer, X-ray diffraction (XRD), the X-ray photoelectron spectrometer, and Fourier transform infrared spectrometry (FT-IR), respectively. Effects of DOX concentration, initial pH, and background electrolyte on adsorption effects of composite were analyzed. Furthermore, the adsorption kinetics, isotherm, thermodynamics, and diffusion model were investigated. Results demonstrated that biocarbons which were prepared with aerobic granular sludge under different nutritive proportions presented different performances. The BET specific surface area of Cu-NaAC/AGS-BC was 260.1592 m2/g, and the micropore volume was 0.054101 cm3/g. The BET specific surface area of Cu-GLC /AGS-BC was only 10.6821 m2/g, and the micropore volume was 0.008687 cm3/g. Both kinds of modified biochar contain a large number of oxygen-containing functional groups. The highest adsorption efficiency of Cu-BC could reach 99.54%. The adsorption of DOX on two modified biocarbons conforms to the pseudo-second-order dynamic model and Temkin isothermal model.

Acetylbritannilactone attenuates contrast-induced acute kidney injury through its anti-pyroptosis effects.

Contrast-induced acute kidney injury (CI-AKI) is a severe complication caused by intravascular applied radial contrast media (CM). Pyroptosis is a lytic type of cell death inherently associated with inflammation response and the secretion of pro-inflammatory cytokines following caspase-1 activation. The aim of the present study was to investigate the protective effects of acetylbritannilactone (ABL) on iopromide (IOP)-induced acute renal failure and reveal the underlying mechanism. In vivo and in vitro, IOP treatment caused renal damage and elevated the caspase-1 (+) propidium iodide (PI) (+) cell count, interleukin (IL)-1ß and IL-18 levels, lactate dehydrogenase (LDH) release, and the relative expression of nucleotide-binding domain, leucine-rich repeat containing protein 3 (NLRP3), apoptosis-associated speck-like protein (ASC), and gasdermin D (GSDMD), suggesting that IOP induces AKI via the activation of pyroptosis. Furthermore, the pretreatment of ABL partly mitigated the CI-AKI, development of pyroptosis, and subsequent kidney inflammation. These data revealed that ABL partially prevents renal dysfunction and reduces pyroptosis in CI-AKI, which may provide a therapeutic target for the treatment of CM-induced AKI.

IGF-1 deletion affects renal sympathetic nerve activity, left ventricular dysfunction, and renal function in DOCA-salt hypertensive mice.

To determine the influence of IGF-1 deletion on renal sympathetic nerve activity (RSNA), left ventricular dysfunction, and renal function in deoxycorticosterone acetate (DOCA)-salt hypertensive mice. The DOCA-salt hypertensive mice models were constructed and the experiment was classified into WT (Wild-type mice) +sham, LID (Liver-specific IGF-1 deficient mice) + sham, WT + DOCA, and LID+ DOCA groups. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum IGF-1 levels in mice. The plasma norepinephrine (NE), urine protein, urea nitrogen and creatinine, as well as RSNA were measured. Echocardiography was performed to assess left ventricular dysfunction, and HE staining to observe the pathological changes in renal tissue of mice. DOCA-salt induction time-dependently increased the systolic blood pressure (SBP) of mice, especially in DOCA-salt LID mice. Besides, the serum IGF-1 levels in WT mice were decreased after DOCA-salt induction. In addition, the plasma NE concentration and NE spillover, urinary protein, urea nitrogen, creatinine and RSNA were remarkably elevated with severe left ventricular dysfunction, but the creatinine clearance was reduced in DOCA-salt mice, and these similar changes were obvious in DOCA-salt mice with IGF-1 deletion. Moreover, the DOCA-salt mice had tubular ectasia, glomerular fibrosis, interstitial cell infiltration, and increased arterial wall thickness, and the DOCA-salt LID mice were more serious in those aspects. Deletion of IGF-1 may lead to enhanced RSNA in DOCA-salt hypertensive mice, thereby further aggravating left ventricular dysfunction and renal damage.

C-reactive protein aggravates myocardial ischemia/reperfusion injury through activation of extracellular-signal-regulated kinase 1/2.

BACKGROUND: Ischemia/reperfusion injury (IRI) is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein (CRP) might play an important role in inducing IRI. However, the effects of CRP on myocardial IRI and the underlying mechanisms have not been fully elucidated. This study aimed to investigate the association between CRP and myocardial IRI and the underlying mechanisms. METHODS: We simulated ischemia/reperfusion using oxygen-glucose deprivation/ reoxygenation (OGD/R) in neonatal Sprague-Dawley rat cardiomyocytes; reperfusion injury was induced by three hours of hypoxia with glucose and serum deprivation followed by one hour of reperfusion. Cell viability was tested with MTS assays, and cardiomyocyte damage was evaluated by lactate dehydrogenase (LDH) leakage. Mitochondrial membrane potential was measured using tetramethylrhodamine ethyl ester (TMRE) and mitochondrial permeability transition pore (mPTP) opening was measured using calcein/AM; both TMRE and caocein/AM were visualized with laser scanning confocal microscopy. In addition, we studied the signaling pathways underlying CRP-mediated ischemia/reperfusion injury via Western blot analysis. RESULTS: Compared with the simple OGD/R group, after intervention with 10 µg/mL CRP, cell viability decreased markedly (82.36 % ± 6.18% vs. 64.84% ± 4.06%, P = 0.0007), and the LDH leakage significantly increased (145.3 U/L ± 16.06 U/L vs. 208.2 U/L ± 19.23 U/L, P = 0.0122). CRP also activated mPTP opening and reduced mitochondrial membrane potential during myocardial ischemia/reperfusion. Pretreatment with 1 µM atorvastatin (Ator) before CRP intervention protected cardiomyocytes from IRI. Mitochondrial KATP channel opener diazoxide and mPTP inhibitor cyclosporin A also offset the effects of CRP in this process. The level of phosphorylated extracellular-signal-regulated kinase (ERK) 1/2 was significantly higher after pre-treatment with CRP compared with the OGD/R group (170.4% ± 3.00% vs. 93.53% ± 1.94%, P < 0.0001). Western blot analysis revealed that Akt expression was markedly activated (184.2% ± 6.96% vs. 122.7% ± 5.30%, P = 0.0003) and ERK 1/2 phosphorylation significantly reduced after co-treatment with Ator and CRP compared with the level after CRP pretreatment alone. CONCLUSIONS: Our results suggested that CRP directly aggravates myocardial IRI in myocardial cells and that this effect is primarily mediated by inhibiting mitochondrial ATP-sensitive potassium (mitoKATP) channels and promoting mPTP opening. Ator counteracts these effects and can reduce CRP-induced IRI. One of the mechanisms of CRP-induced IRI may be related to the sustained activation of the ERK signaling pathway.

[Cardioprotective effects of limb ischemic postconditioning by different strength and time in rabbits].

OBJECTIVE: In this study, we try to find the better protocol of limb ischemia postconditioning by observing different protective effects of limb ischemic postconditioning (different strength and time windows in rabbits). METHODS: 42 healthy New Zealand rabbits were randomly divided into 7 groups (n = 6): Sham; Control (CON); Skeletal muscle postconditioning (SP); 6 min-delayed skeletal muscle postconditioning (6M-DSP); 1 min-delayed skeletal muscle postconditioning (1M-DSP); Strengthen skeletal muscle postconditioning (SSP); Weakened skeletal muscle postconditioning (WSP). Acute ischemia/reperfusion (I/R) model was induced by 45 minutes occlusion on left circumflex coronary artery (LCX) and 2 hours reperfusion in all anesthetized open-chest rabbits except the Sham. Limb ischemia was induced by external iliac arteries occlusion and reperfusion through artery clamps. The extent of myocardial infarction was assessed by triphenyltetrazolium (TTC) staining. Blood serum creatine kinase (CK) activity and lactate dehydrogenase (LDH) activity were measured at baseline,the end of ischemia, after 1 hour and 2 hours of reperfusion respectively. RESULTS: Compared with the CON, the weight ratio and area ratio of myocardial infarction size were significantly decreased by 49.97% and 43.78% in SP, by 42.32% and 42.68% in 1M-DSP, by 48.36% and 48.86% in SSP (P < 0.05). But there was no significant difference between SP and 1M-DSP and SSP (P > 0.05). Otherwise, compared with the CON, myocardial infarct size was not significantly reduced in 6M-DSP or WSP (P > 0.05). The change of CK was similar to the trend of myocardial infarct size. CONCLUSION: The limb ischemia strength of 5 mini/1 minR x 1 cycle could significantly reduce the myocardial ischemia/ reperfusion injury in rabbits, if it was achieved before myocardial reperfusion.

Statin therapy shortens QTc, QTcd, and improves cardiac function in patients with chronic heart failure.

Although some data suggest that statins can improve cardiac mechanical function in some patients with chronic heart failure (CHF), the effects of long-term statin therapy on cardiac electrical instability remain unclear. We performed a randomized perspective analysis of the effects of 10 mg/d (statin group 1, n=40), 20 mg/d (statin group 2, n=38) of atorvastatin and controls (control group, n=41) on corrected QT intervals (QTc), corrected QT dispersion (QTcd) and cardiac function in patients with CHF secondary to coronary artery disease (CAD) for one year. At 6 and 12 months, the statin groups displayed lower QTc and QTcd compared with controls. The changes were becoming more distinct in statin group 2, (P<0.05). In statin groups, the changes of QTc and QTcd were independent of changes of plasma low-density lipoprotein cholesterol and total cholesterol levels, and the decrease of QTcd was correlated with the increase of LVEF within 12 months. Atorvastatin shortens QTc, QTcd and improves cardiac function, and might thereby be parts of the mechanisms which atorvastatin benefited CHF patients secondary to CAD.