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Environmental Science and Pollution... May 2024Developing the Co-based catalysts with high reactivity for the sulfate radical (SO·)-based advanced oxidation processes (SR-AOPs) has been attracting numerous...
Developing the Co-based catalysts with high reactivity for the sulfate radical (SO·)-based advanced oxidation processes (SR-AOPs) has been attracting numerous attentions. To improve the peroxymonosulfate (PMS) activation process, a novel Co-based catalyst simultaneously modified by bamboo carbon (BC) and vanadium (V@CoO-BC) was fabricated through a simple solvothermal method. The atenolol (ATL) degradation experiments in V@CoO-BC/PMS system showed that the obtained V@CoO-BC exhibited much higher performance on PMS activation than pure CoO, and the V@CoO-BC/PMS system could fully degrade ATL within 5 min via the destruction of both radicals (SO· and O·) and non-radicals (O). The quenching experiments and electrochemical tests revealed that the enhancing mechanism of bamboo carbon and V modification involved four aspects: (i) promoting the PMS and Co ion adsorption on the surface of V@CoO-BC; (ii) enhancing the electron transfer efficiency between V@CoO-BC and PMS; (iii) activating PMS with V species; (iv) accelerating the circulation of Co and Co, leading to the enhanced yield of reactive oxygen species (ROS). Furthermore, the V@CoO-BC/PMS system also exhibited satisfactory stability under broad pH (3-9) and good efficiency in the presence of co-existing components (HCO, NO, Cl, and HA) in water. This study provides new insights to designing high-performance, environment-friendly bimetal catalysts and some basis for the remediation of antibiotic contaminants with SR-AOPs.
Topics: Atenolol; Catalysis; Carbon; Peroxides; Vanadium; Oxidation-Reduction; Water Pollutants, Chemical
PubMed: 38753235
DOI: 10.1007/s11356-024-33657-4 -
Applied Microbiology and Biotechnology Sep 2023Pharmaceuticals are of concern to our planet and health as they can accumulate in the environment. The impact of these biologically active compounds on ecosystems is...
Pharmaceuticals are of concern to our planet and health as they can accumulate in the environment. The impact of these biologically active compounds on ecosystems is hard to predict, and information on their biodegradation is necessary to establish sound risk assessment. Microbial communities are promising candidates for the biodegradation of pharmaceuticals such as ibuprofen, but little is known yet about their degradation capacity of multiple micropollutants at higher concentrations (100 mg/L). In this work, microbial communities were cultivated in lab-scale membrane bioreactors (MBRs) exposed to increasing concentrations of a mixture of six micropollutants (ibuprofen, diclofenac, enalapril, caffeine, atenolol, paracetamol). Key players of biodegradation were identified using a combinatorial approach of 16S rRNA sequencing and analytics. Microbial community structure changed with increasing pharmaceutical intake (from 1 to 100 mg/L) and reached a steady-state during incubation for 7 weeks on 100 mg/L. HPLC analysis revealed a fluctuating but significant degradation (30-100%) of five pollutants (caffeine, paracetamol, ibuprofen, atenolol, enalapril) by an established and stable microbial community mainly composed of Achromobacter, Cupriavidus, Pseudomonas and Leucobacter. By using the microbial community from MBR1 as inoculum for further batch culture experiments on single micropollutants (400 mg/L substrate, respectively), different active microbial consortia were obtained for each single micropollutant. Microbial genera potentially responsible for degradation of the respective micropollutant were identified, i.e. Pseudomonas sp. and Sphingobacterium sp. for ibuprofen, caffeine and paracetamol, Sphingomonas sp. for atenolol and Klebsiella sp. for enalapril. Our study demonstrates the feasibility of cultivating stable microbial communities capable of degrading simultaneously a mixture of highly concentrated pharmaceuticals in lab-scale MBRs and the identification of microbial genera potentially responsible for the degradation of specific pollutants. KEY POINTS: • Multiple pharmaceuticals were removed by stable microbial communities. • Microbial key players of five main pharmaceuticals were identified.
Topics: Ibuprofen; RNA, Ribosomal, 16S; Atenolol; Acetaminophen; Caffeine; Microbiota; Bioreactors; Biodegradation, Environmental; Environmental Pollutants; Water Pollutants, Chemical; Pharmaceutical Preparations
PubMed: 37436483
DOI: 10.1007/s00253-023-12677-z -
Biochimica Et Biophysica Acta.... Oct 2023Decreased autophagic flux in cardiomyocytes is an important mechanism by which the β-adrenoreceptor (β-AR) autoantibody (β-AA) induces heart failure. A previous study...
Decreased autophagic flux in cardiomyocytes is an important mechanism by which the β-adrenoreceptor (β-AR) autoantibody (β-AA) induces heart failure. A previous study found that β-AA imparts its biological effects via the β-AR/Gs/AC/cAMP/PKA canonical signaling pathway, but PKA inhibition does not completely reverse β-AA-induced reduction in autophagy in myocardial tissues, suggesting that other signaling molecules participate in this process. This study confirmed that Epac1 upregulation is indeed involved β-AA-induced decreased cardiomyocyte autophagy through CE3F4 pretreatment, Epac1 siRNA transfection, western blot and immunofluorescence methods. On this basis, we constructed β-AR and β-AR knockout mice, and used receptor knockout mice, β-AR selective blocker (atenolol), and the β-AR/Gi-biased agonist ICI 118551 to show that β-AA upregulated Epac1 expression through β-AR and β-AR to inhibit autophagy, and biased activation of β-AR/Gi signaling downregulated myocardial Epac1 expression to reverse β-AA-induced myocardial autophagy inhibition. This study aimed to test the hypothesis that Epac1 acts as another effector downstream of cAMP on β-AA-induced reduction in cardiomyocyte autophagy, and β-AA upregulates myocardial Epac1 expression through β-AR and β-AR, and biased activation of the β-AR/Gi signaling pathway can reverse β-AA-induced myocardial autophagy inhibition. This study provides new ideas and therapeutic targets for the prevention and treatment of cardiovascular diseases related to dysregulated autophagy.
Topics: Animals; Mice; Autoantibodies; Autophagy; Mice, Knockout; Myocytes, Cardiac; Signal Transduction
PubMed: 37315585
DOI: 10.1016/j.bbamcr.2023.119512 -
Frontiers in Immunology 2023Severe inflammation via innate immune system activation causes organ dysfunction. Among these, the central nervous system (CNS) is particularly affected by...
Severe inflammation via innate immune system activation causes organ dysfunction. Among these, the central nervous system (CNS) is particularly affected by encephalopathies. These symptoms are associated with the activation of microglia and a potential infiltration of leukocytes. These immune cells have recently been discovered to have the ability to produce extracellular traps (ETs). While these components capture and destroy pathogens, deleterious effects occur such as reduced neuronal excitability correlated with excessive ETs production. In this study, the objectives were to determine (1) whether immune cells form ETs in the CNS during acute inflammation (2) whether ETs produce neuromuscular disorders and (3) whether an immunomodulatory treatment such as β1-adrenergic blockers limits these effects. We observed an infiltration of neutrophils in the CNS, an activation of microglia and a production of ETs following lipopolysaccharide (LPS) administration. Atenolol, a β1-adrenergic blocker, significantly decreased the production of ETs in both microglia and neutrophils. This treatment also preserved the gastrocnemius motoneuron excitability. Similar results were observed when the production of ETs was prevented by sivelestat, an inhibitor of ET formation. In conclusion, our results demonstrate that LPS administration increases neutrophils infiltration into the CNS, activates immune cells and produces ETs that directly impair neuromuscular function. Prevention of ETs formation by β1-adrenergic blockers partly restores this function and could be a good target in order to reduce adverse effects in severe inflammation such as sepsis but also in other motor related pathologies linked to ETs production.
Topics: Mice; Animals; Extracellular Traps; Lipopolysaccharides; Neutrophils; Inflammation; Leukocytes
PubMed: 37809074
DOI: 10.3389/fimmu.2023.1228374 -
European Journal of Internal Medicine Jan 2024Arterial hypertension is the most common cardiovascular comorbidity in atrial fibrillation (AF). Few studies investigated management strategies of hypertension in AF.
BACKGROUND
Arterial hypertension is the most common cardiovascular comorbidity in atrial fibrillation (AF). Few studies investigated management strategies of hypertension in AF.
MATERIALS AND METHODS
We included 5769 AF patients on oral anticoagulants from the nationwide ongoing Italian START registry. We investigated the prescription of antihypertensive drugs and mortality risk. Subgroup analyses according to sex and major cardiovascular comorbidities were performed.
RESULTS
Mean age was 80.8 years, 46.1% were women; 80.3% of patients were hypertensive. Furosemide (30.1%) was the most frequent diuretic followed by hydrochlorothiazide (15.4%) and potassium canrenoate (7.9%). 61.1% received β-blockers: 34.2% bisoprolol, 6.2% atenolol. Additionally, 36.9% were on angiotensin converting enzyme inhibitors (ACE-I): ramipril (20.9%), enalapril (5.3%) and perindopril (2.8%); 31.7% were on angiotensin receptors blockers (ARBs): valsartan (7.6%) and irbesartan (6.4%). Amlodipine and lercanidipine were prescribed in 14.0% and 2.3%, respectively. ACE-I (p < 0.001), α-blockers (p = 0.020) and Dihydropyridines calcium channel blockers (p = 0.004) were more common in men, while ARBs (p = 0.008), thiazide diuretics (p < 0.001) and β-blockers (p < 0.001) in women. During 22.61 ± 17.1 months, 512 patients died. Multivariable Cox regression analysis showed that ACE-I (Hazard ratio [HR] 0.758, 95% Confidence Interval [95%CI] 0.612-0.940, p = 0.012) and ARBs (HR 0.623, 95%CI 0.487-0.796, p < 0.001) inversely associated with mortality. ACE-I/ARBs inversely associated with mortality in both sexes and in patients with diabetes. This associastion was evident for ACE-I in patients with previous cardiovascular disease, and for ARBs in HF.
CONCLUSION
A lower mortality risk was found in AF patients on ACE-I/ARBs. Different prescription patterns of antihypertensive drugs between men and women do exist.
Topics: Male; Humans; Female; Aged; Aged, 80 and over; Antihypertensive Agents; Angiotensin-Converting Enzyme Inhibitors; Renin-Angiotensin System; Atrial Fibrillation; Angiotensin Receptor Antagonists; Hypertension; Adrenergic beta-Antagonists
PubMed: 37648584
DOI: 10.1016/j.ejim.2023.08.019 -
Chemosphere Sep 2023Herein, BiFeO nanorods (BFO NRs) was synthesized as the piezoelectric catalyst. The synergistic mechanism of sonolysis and sono-induced BFO-piezocatalysis in atenolol...
Insight into the synergistic mechanism of sonolysis and sono-induced BiFeO nanorods piezocatalysis in atenolol degradation: Ultrasonic parameters, ROS and degradation pathways.
Herein, BiFeO nanorods (BFO NRs) was synthesized as the piezoelectric catalyst. The synergistic mechanism of sonolysis and sono-induced BFO-piezocatalysis in atenolol degradation was revealed and the effect of ultrasonic parameters on it was investigated for the first time. The results indicated that 100 kHz was the optimal frequency for the sonolytic and sono-piezocatalytic degradation of atenolol in ultrasound/BFO nanorods (US/BFO NRs) system, with the highest synergistic coefficient of 3.43. The piezoelectric potential differences of BFO NRs by COMSOL Multiphysics simulations further distinguishing that the impact of cavitation shock wave and ultrasonic vibration from sonochemistry reaction (i.e., 2.48, -2.48 and 6.60 V versus 0.008, -0.008 and 0.02 V under tensile, compressive and shear stress at 100 kHz). The latter piezoelectric potentials were insufficient for reactive-oxygen-species (ROS) generation, while the former contributed to 53.93% •OH yield in US/BFO NRs system. Sono-piezocatalysis was found more sensitive to ultrasonic power density than sonolysis. The quenching experiments and ESR tests indicated that the ROS contribution in atenolol degradation followed the order of •OH > O > h > O in US/BFO NRs system and O generation is exclusively dissolved-oxygen dependent. Four degradation pathways for atenolol in US/BFO NRs system were proposed via products identification and DFT calculation. Toxicity assessment by ECOSAR suggested the toxicity of the degradation products could be controlled.
Topics: Reactive Oxygen Species; Atenolol; Ultrasonics; Oxygen; Nanotubes
PubMed: 37263504
DOI: 10.1016/j.chemosphere.2023.139084 -
European Heart Journal Apr 2024Visit-to-visit systolic blood pressure variability (BPV) is an important predictor of cardiovascular (CV) outcomes. The long-term effect of a period of blood pressure...
BACKGROUND AND AIMS
Visit-to-visit systolic blood pressure variability (BPV) is an important predictor of cardiovascular (CV) outcomes. The long-term effect of a period of blood pressure (BP) control, but with differential BPV, is uncertain. Morbidity and mortality follow-up of UK participants in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure-Lowering Arm has been extended for up to 21 years to determine the CV impact of mean systolic blood pressure (SBP) control and BPV during the trial, and amongst those allocated to amlodipine- and atenolol-based treatment.
METHODS
Eight thousand five hundred and eighty hypertensive participants (4305 assigned to amlodipine ± perindopril-based and 4275 to atenolol ± diuretic-based treatment during the in-trial period (median 5.5 years) were followed for up to 21 years (median 17.4 years), using linked hospital and mortality records. A subgroup of participants (n = 2156) was followed up 6 years after the trial closure with a self-administered questionnaire and a clinic visit. In-trial mean SBP and standard deviation of visit-to-visit SBP as a measure of BPV, were measured using >100 000 BP measurements. Cox proportional hazard models were used to estimate the risk [hazard ratios (HRs)], associated with (i) mean with SBP and BPV during the in-trial period, for the CV endpoints occurring after the end of the trial and (ii) randomly assigned treatment to events following randomization, for the first occurrence of pre-specified CV outcomes.
RESULTS
Using BP data from the in-trial period, in the post-trial period, although mean SBP was a predictor of CV outcomes {HR per 10 mmHg, 1.14 [95% confidence interval (CI) 1.10-1.17], P < .001}, systolic BPV independent of mean SBP was a strong predictor of CV events [HR per 5 mmHg 1.22 (95% CI 1.18-1.26), P < .001] and predicted events even in participants with well-controlled BP. During 21-year follow-up, those on amlodipine-based compared with atenolol-based in-trial treatment had significantly reduced risk of stroke [HR 0.82 (95% CI 0.72-0.93), P = .003], total CV events [HR 0.93 (95% CI 0.88-0.98), P = .008], total coronary events [HR 0.92 (95% CI 0.86-0.99), P = .024], and atrial fibrillation [HR 0.91 (95% CI 0.83-0.99), P = .030], with weaker evidence of a difference in CV mortality [HR 0.91 (95% CI 0.82-1.01), P = .073]. There was no significant difference in the incidence of non-fatal myocardial infarction and fatal coronary heart disease, heart failure, and all-cause mortality.
CONCLUSIONS
Systolic BPV is a strong predictor of CV outcome, even in those with controlled SBP. The long-term benefits of amlodipine-based treatment compared with atenolol-based treatment in reducing CV events appear to be primarily mediated by an effect on systolic BPV during the trial period.
Topics: Humans; Blood Pressure; Atenolol; Antihypertensive Agents; Hypertension; Amlodipine; Risk Factors
PubMed: 38291599
DOI: 10.1093/eurheartj/ehad814 -
BMJ Supportive & Palliative Care Jan 2024This case report describes the care of a 75-year-old gentleman with metastatic head and neck cancer who was highly symptomatic with intractable tenacious oropharyngeal... (Review)
Review
This case report describes the care of a 75-year-old gentleman with metastatic head and neck cancer who was highly symptomatic with intractable tenacious oropharyngeal secretions. The patient reported subjective benefit from oral atenolol. A literature review was undertaken and identified no previous studies on the use of β-blockers for secretions in malignant disease, although some anecdotal evidence for their use in motor neuron disease. The proposed underlying mechanism is that β1-blockade reduced the protein content of salivary secretions, hence reducing its viscosity. Further studies of both the role of β-adrenoreceptors in the control of secretion viscosity and the potential role of β-blockers in alleviating symptomatic tenacious secretions are warranted.
Topics: Male; Humans; Aged; Saliva; Adrenergic beta-Antagonists; Atenolol
PubMed: 35332025
DOI: 10.1136/bmjspcare-2022-003615 -
Journal of Chromatographic Science Mar 2024Two rapid, smart and validated stability indicating HPLC and TLC techniques were developed to determine atenolol (ATE) and lercanidipine HCl (LER) simultaneously in...
Comprehensive and Validated Chromatographic Techniques for the Estimation of Lercanidipine Hydrochloride and Atenolol in Bulk and Combined Dosage Form in the Presence of Lercanidipine Degradation Products with LC/MS Characterization.
Two rapid, smart and validated stability indicating HPLC and TLC techniques were developed to determine atenolol (ATE) and lercanidipine HCl (LER) simultaneously in their pharmaceutical formulation. HPLC chromatographic separation was implemented by using Microsorb C18 (250 × 4.6 mm, 5 μm) column, with mobile phase of acetonitrile and 20 mM potassium dihydrogen phosphate buffer pH 3.5 adjusted by orthophosphoric acid in the ratio of (65:35, v/v) at a flow rate of 1.2 mL/min at 240 nm also the injection volume adjusted to be 30 μL. These selected conditions effectively separated ATE and LER at a retention time of 2 and 6.7 min, respectively, by isocratic elution mode without any interference from the obtained degradation products of LER. The densitometric determination was performed by using precoated silica gel 60F254 aluminum plates and chloroform, methanol and triethylamine (11.3:1.3: 0.3, by volume) as a developing system. The detection wavelength for simultaneous estimation of both drugs was 240 nm in the presence of the oxidative product of LER. The RF values for ATE and LER were 0.22 and 0.78, respectively. The calibration curves of both techniques were constructed with linearity ranges of (5-55) μg.mL-1 and (1-55) μg.mL-1 for both ATE and LER, respectively, for HPLC determination. While for TLC, the linearity ranges were (1-4) μg/band and (0.2-1.4) μg/band for ATE and LER, respectively. LER degradation products were characterized using UPLC/MS and the suggested mechanisms and degradation pathways were introduced.
Topics: Atenolol; Chromatography, Thin Layer; Reproducibility of Results; Dihydropyridines; Chromatography, High Pressure Liquid
PubMed: 36929845
DOI: 10.1093/chromsci/bmad018 -
Scientific Reports Jul 2023Familial hypertrophic cardiomyopathy (FHC) patients are advised to avoid strenuous exercise due to increased risk of arrhythmias. Mice expressing the human FHC-causing...
Familial hypertrophic cardiomyopathy (FHC) patients are advised to avoid strenuous exercise due to increased risk of arrhythmias. Mice expressing the human FHC-causing mutation R403Q in the myosin heavy chain gene (MYH6) recapitulate the human phenotype, including cytoskeletal disarray and increased arrhythmia susceptibility. Following in vivo administration of isoproterenol, mutant mice exhibited tachyarrhythmias, poor recovery and fatigue. Arrhythmias were attenuated with the β-blocker atenolol and protein kinase A inhibitor PKI. Mutant cardiac myocytes had significantly prolonged action potentials and triggered automaticity due to reduced repolarization reserve and connexin 43 expression. Isoproterenol shortened cycle length, and escalated electrical instability. Surprisingly isoproterenol did not increase Ca1.2 current. We found alterations in Ca1.2-β1 adrenergic receptor colocalization assessed using super-resolution nanoscopy, and increased Ca1.2 phosphorylation in mutant hearts. Our results reveal for the first time that altered ion channel expression, co-localization and β-adrenergic receptor signaling associated with myocyte disarray contribute to electrical instability in the R403Q mutant heart.
Topics: Humans; Animals; Mice; Isoproterenol; Cardiomyopathy, Hypertrophic; Arrhythmias, Cardiac; Heart; Cardiomyopathy, Hypertrophic, Familial
PubMed: 37438479
DOI: 10.1038/s41598-023-38296-2