Dechlorination Helps Defluorination: Insights into the Defluorination Mechanism of Florfenicol by S-nZVI and DFT Calculations on the Reaction Pathways.

Defluorination is essential to eliminate the antibiotic resistance and detrimental effects of florfenicol (C12H14Cl2FNO4S, FF), which is achievable by sulfidated nanoscale zerovalent iron (S-nZVI), yet a comprehensive understanding of the mechanism is lacking. Herein, we used experimental data and density functional theory calculations to demonstrate four dechlorination-promoted defluorination pathways of FF, depending on S-nZVI or not. FF was defluorinated in a rapid and then slow but continuous manner, accompanying a consecutive dechlorination to deschloro (dFF) and dideschloro FF (ddFF). Unexpectedly, the predominant defluorination occurs by spontaneous hydrolysis of ddFF to form the hydrolyzed byproduct (HO-ddFF), i.e., independent of S-nZVI, which is initiated by intramolecular attack from carbonyl O to alkyl F and is thus limited for FF and dFF owing to the diminished nucleophilicity by electron-withdrawing Cl. The removal of Cl also makes the reductive defluorination of ddFF by S-nZVI amenable. The other two minor but more rapid defluorination pathways occur in synergy with the dechlorination of FF and dFF, which are mediated by the reactive carbanion intermediates and generate HO-dFF and HO-ddFF, respectively. The reliability of these dechlorination-facilitated defluorination pathways was verified by the consistency of theoretical calculations with experimental data, providing valuable insights into the degradation of fluorinated contaminants.

JinJiang ablation catheter is no inferior than Johnson ablation catheter in radiofrequency ablation of paroxysmal supraventricular tachycardia.

BACKGROUND: Paroxysmal supraventricular tachycardia (PSVT) is characterized by episodes of rapid tachycardia with sudden onset and sudden termination. PSVT treatment has evolved considerably over the past 30 years. Currently, radiofrequency catheter ablation is the first-line treatment. HYPOTHESIS: We conducted a randomized controlled trial to compare safety and effectiveness of PSVT ablation between the Jinjiang and Johnson (J&J) catheters in 57 patients in our hospital. METHODS AND RESULTS: Patients were randomly assigned to ablation procedures using either the Jinjiang system or the J&J Carto system. Follow-up was performed 3 days, 1, and 6 months after the procedure. Success rate, ablation time, frequency of ablation, and rates of complications and recurrence did not significantly differ between the groups. One Jinjiang group patient (3.6%) experienced arrhythmia recurrence during the 6-month follow-up. CONCLUSIONS: The Jinjiang catheter for radiofrequency ablation of PSVT is as safe and effective as the J&J catheter.

Antihypertrophic Memory After Regression of Exercise-Induced Physiological Myocardial Hypertrophy Is Mediated by the Long Noncoding RNA Mhrt779.

BACKGROUND: Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5 to 6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress. METHODS: C57BL/6 mice were submitted to 21 days of swimming training to develop PMH. After termination of exercise, PMH regressed within 1 week. PMH regression mice (exercise hypertrophic preconditioning [EHP] group) and sedentary mice (control group) then underwent transverse aortic constriction or a sham operation for 4 weeks. Cardiac remodeling and function were evaluated with echocardiography, invasive left ventricular hemodynamic measurement, and histological analysis. LncRNA sequencing, chromatin immunoprecipitation assay, and comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot were used to investigate the role of Mhrt779 involved in the antihypertrophic effect induced by EHP. RESULTS: At 1 and 4 weeks after transverse aortic constriction, the EHP group showed less increase in myocardial hypertrophy and lower expression of the Nppa and Myh7 genes than the sedentary group. At 4 weeks after transverse aortic constriction, EHP mice had less pulmonary congestion, smaller left ventricular dimensions and end-diastolic pressure, and a larger left ventricular ejection fraction and maximum pressure change rate than sedentary mice. Quantitative polymerase chain reaction revealed that the long noncoding myosin heavy chain-associated RNA transcript Mhrt779 was one of the markedly upregulated lncRNAs in the EHP group. Silencing of Mhrt779 attenuated the antihypertrophic effect of EHP in mice with transverse aortic constriction and in cultured cardiomyocytes treated with angiotensin II, and overexpression enhanced the antihypertrophic effect. Using chromatin immunoprecipitation assay and quantitative polymerase chain reaction, we found that EHP increased histone 3 trimethylation (H3K4me3 and H3K36me3) at the a4 promoter of Mhrt779. Comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot showed that Mhrt779 can bind SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 (Brg1) to inhibit the activation of the histone deacetylase 2 (Hdac2)/phosphorylated serine/threonine kinase (Akt)/phosphorylated glycogen synthase kinase 3ß(p-GSK3ß) pathway induced by pressure overload. CONCLUSIONS: Myocardial hypertrophy preconditioning evoked by exercise increases resistance to pathological stress via an antihypertrophic effect mediated by a signal pathway of Mhrt779/Brg1/Hdac2/p-Akt/p-GSK3ß.

The spatial spillover effect and nonlinear relationship analysis between land resource misallocation and environmental pollution: Evidence from China.

Compared with other countries, China's local governments often adopt the land supply strategy of "low price and sufficient supply" for industrial land and "high price and limited supply" for commercial land in the allocation of land resources. The allocation of land resources is an important means to promote the rapid development of China's economy, and the impacts of land resource misallocation (LRM) on environmental pollution are increasingly apparent. This paper uses panel data from 30 provinces in China from 2009 to 2018 to discuss the relationship between LRM and environmental pollution. The ratio of the average price of commercial land to the average price of industrial land is used to measure the degree of LRM. The Ordinary Least Squares (OLS), spatial Durbin model (SDM), threshold model, and mediation effect model are used to study the direct effect, spatial spillover effect, nonlinear relationship, and conduction mechanism of LRM on environmental pollution. The results show that LRM significantly aggravated environmental pollution. This conclusion still holds after robustness tests including the substitution of dependent variables and IV estimates. The LRM aggravates environmental pollution through industrial structure and technological progress. Interestingly, the impact of LRM on environmental pollution also has a significant positive spatial spillover effect in adjacent regions. In addition, there is also evidence that the adverse effect of LRM on environmental pollution is nonlinear at different levels of industrial structure and technological progress. The threshold model shows that with the optimization of the industrial structure, the impact of LRM on environmental pollution shows a weakening trend of "inverted V-shaped", and with the advancement of technology, the impact of LRM on environmental pollution presents an "S-shaped" changing trend of "strong-weak-strong".

Unraveling the High-Activity Origin of Single-Atom Iron Catalysts for Organic Pollutant Oxidation via Peroxymonosulfate Activation.

Single-atom catalysts (SACs) have emerged as efficient materials in the elimination of aqueous organic contaminants; however, the origin of high activity of SACs still remains elusive. Herein, we identify an 8.1-fold catalytic specific activity (reaction rate constant normalized to catalyst's specific surface area and dosage) enhancement that can be fulfilled with a single-atom iron catalyst (SA-Fe-NC) prepared via a cascade anchoring method compared to the iron nanoparticle-loaded catalyst, resulting in one of the most active currently known catalysts in peroxymonosulfate (PMS) conversion for organic pollutant oxidation. Experimental data and theoretical results unraveled that the high-activity origin of the SA-Fe-NC stems from the Fe-pyridinic N4 moiety, which dramatically increases active sites by not only creating the electron-rich Fe single atom as the catalytic site but also producing electron-poor carbon atoms neighboring pyridinic N as binding sites for PMS activation including synchronous PMS reduction and oxidation together with dissolved oxygen reduction. Moreover, the SA-Fe-NC exhibits excellent stability and applicability to realistic industrial wastewater remediation. This work offers a novel yet reasonable interpretation for why a small amount of iron in the SA-Fe-NC can deliver extremely superior specific activity in PMS activation and develops a promising catalytic oxidation system toward actual environmental cleanup.

New Insights into the Generation of Singlet Oxygen in the Metal-Free Peroxymonosulfate Activation Process: Important Role of Electron-Deficient Carbon Atoms.

A nonradical oxidation process via metal-free peroxymonosulfate (PMS) activation has recently attracted considerable attention for organic pollutant degradation; however, the origin of singlet oxygen (1O2) generation still remains controversial. In this study, nitrogen-doped carbon nanosheets (NCN-900) derived from graphitic carbon nitride were developed for activation of PMS and elucidation of 1O2 production. With a large specific surface area (1218.7 m2 g-1) and high nitrogen content (14.5 at %), NCN-900 exhibits superior catalytic activity in PMS activation, as evidenced by complete degradation of bisphenol A within 2 min using 0.1 g L-1 NCN-900 and 2 mM PMS. Moreover, the reaction rate constant fitted by pseudo-first-order kinetics for NCN-900 reaches an impressive value of 3.1 min-1. Electron paramagnetic resonance measurements and quenching tests verified 1O2 as the primary reactive oxygen species in the NCN-900/PMS system. Based on X-ray photoelectron spectroscopy analysis and theoretical calculations, an unexpected generation pathway of 1O2 involving PMS oxidation over the electron-deficient carbon atoms neighboring graphitic N in NCN-900 was unraveled. Besides, the NCN-900/PMS system is also applicable for remediation of actual industrial wastewater. This work highlights the important role of electron-deficient carbon atoms in 1O2 generation from PMS oxidation and furnishes theoretical support for further relevant studies.

Acute hyperglycemia suppresses left ventricular diastolic function and inhibits autophagic flux in mice under prohypertrophic stimulation.

BACKGROUND: Left ventricular (LV) dysfunction is closely associated with LV hypertrophy or diabetes, as well as insufficient autophagic flux. Acute or chronic hyperglycemia is a prognostic factor for patients with myocardial infarction. However, the effect of acute hyperglycemia on LV dysfunction of the hypertrophic heart and the mechanisms involved are still unclear. This study aimed to confirm our hypothesis that either acute or chronic hyperglycemia suppresses LV diastolic function and autophagic flux. METHODS: The transverse aortic constriction (TAC) model and streptozocin-induced type 1 diabetic mellitus mice were used. LV function was evaluated with a Millar catheter. Autophagic levels and autophagic flux in the whole heart and cultured neonatal rat cardiomyocytes in response to hyperglycemia were examined by using western blotting of LC3B-II and P62. We also examined the effect of an autophagic inhibitor on LC3B-II and P62 protein expression and LC3 puncta. RESULTS: In mice with TAC, we detected diastolic dysfunction as early as 30 min after TAC. This dysfunction was indicated by a greater LV end-diastolic pressure and the exponential time constant of LV relaxation, as well as a smaller maximum descending rate of LV pressure in comparison with sham group. Similar results were also obtained in mice with TAC for 2 weeks, in addition to increased insulin resistance. Acute hyperglycemic stress suppressed diastolic function in mice with myocardial hypertrophy, as evaluated by invasive LV hemodynamic monitoring. Mice with chronic hyperglycemia induced by streptozocin showed myocardial fibrosis and diastolic dysfunction. In high glucose-treated cardiomyocytes and streptozocin-treated mice, peroxisome proliferator-activated receptor-γ coactivator 1α was downregulated, while P62 was upregulated. Autophagic flux was also significantly inhibited in response to high glucose exposure in angiotensin-II treated cardiomyocytes. CONCLUSIONS: Acute hyperglycemia suppresses diastolic function, damages mitochondrial energy signaling, and inhibits autophagic flux in prohypertrophic factor-stimulated cardiomyocytes.

Exploring new frontiers: a rare case of catheter ablation for persistent atrial fibrillation in a patient with cor triatriatum sinister guided by intracardiac echocardiography.

BACKGROUND: Cor triatriatum sinister (CTS) is an uncommon congenital cardiac anomaly. Atrial fibrillation (AF) is commonly the initial symptom in patients with CTS, occurring in approximately 32% of the cases. The complexity of performing AF catheter ablation, particularly in cases with persistent AF, increases in patients with CTS due to its unique structural challenges. CASE PRESENTATION: We report the treatment course of a 60-year-old male patient diagnosed with CTS, who underwent catheter ablation of drug-refractory, persistent AF. The complex anatomical structure of the condition made catheter ablation of AF challenging. To navigate these challenges, we performed comprehensive assessments using transthoracic echocardiography and transesophageal echocardiography, along with cardiac computed tomography angiography, prior to treatment initiation. The intricate anatomy of CTS was further clarified during the procedure via intracardiac echocardiography (ICE). Additionally, the complexity of catheter manipulation was further reduced with the aid of the VIZIGO sheath and the vein of Marshall ethanol infusion to achieve effective mitral isthmus blockage, thereby circumventing the impact of the CTS membrane. CONCLUSIONS: This case underscores the complexity and potential of advanced ablation techniques in managing cardiac arrhythmias associated with unusual cardiac anatomies. During the procedure, ICE facilitated detailed modeling of the left atrium, including the membranous structure and its openings, thus providing a clearer understanding of CTS. It is noteworthy that the membrane within the CTS may serve as a potential substrate for arrhythmias, which warrants further validation through larger sample studies.

Teneligliptin mitigates diabetic cardiomyopathy by inhibiting activation of the NLRP3 inflammasome.

BACKGROUND: Diabetic cardiomyopathy (DCM), which is a complication of diabetes, poses a great threat to public health. Recent studies have confirmed the role of NLRP3 (NOD-like receptor protein 3) activation in DCM development through the inflammatory response. Teneligliptin is an oral hypoglycemic dipeptidyl peptidase-IV inhibitor used to treat diabetes. Teneligliptin has recently been reported to have anti-inflammatory and protective effects on myocardial cells. AIM: To examine the therapeutic effects of teneligliptin on DCM in diabetic mice. METHODS: Streptozotocin was administered to induce diabetes in mice, followed by treatment with 30 mg/kg teneligliptin. RESULTS: Marked increases in cardiomyocyte area and cardiac hypertrophy indicator heart weight/tibia length reductions in fractional shortening, ejection fraction, and heart rate; increases in creatine kinase-MB (CK-MB), aspartate transaminase (AST), and lactate dehydrogenase (LDH) levels; and upregulated NADPH oxidase 4 were observed in diabetic mice, all of which were significantly reversed by teneligliptin. Moreover, NLRP3 inflammasome activation and increased release of interleukin-1ß in diabetic mice were inhibited by teneligliptin. Primary mouse cardiomyocytes were treated with high glucose (30 mmol/L) with or without teneligliptin (2.5 or 5 µM) for 24 h. NLRP3 inflammasome activation. Increases in CK-MB, AST, and LDH levels in glucose-stimulated cardiomyocytes were markedly inhibited by teneligliptin, and AMP (p-adenosine 5'-monophosphate)-p-AMPK (activated protein kinase) levels were increased. Furthermore, the beneficial effects of teneligliptin on hyperglycaemia-induced cardiomyocytes were abolished by the AMPK signaling inhibitor compound C. CONCLUSION: Overall, teneligliptin mitigated DCM by mitigating activation of the NLRP3 inflammasome.

Simulating wood companies development considering the effect of ethical marketing.

Dedicating oneself to a greater good is one of the secret ingredients to business success in an evolving and highly interconnected markets environment. For wood companies, this is even more needed to face the overwhelming ongoing environmental crisis affecting business practices and customers' behavior in general. To build solid reputation and increase one's presence on competing markets, wood companies should not only care about products competitiveness, but also customers' perception, environmental awareness and ethical marketing. In this article, we simulated the effect of ethical commerce on wood companies' reputation using a modified competitive and cooperative model based on differential equations considering wood type, products categories and companies brand score or reputation as function of their commitment to social and environmental causes. The qualitative analysis and results of numerical experiment show that, focusing on sharing values, and building strong relationship with customers are highly important for long-term development. Moreover, reducing environmental impact by shifting production strategy towards man-made materials could meet today customers' demands for ethically and environmentally aware manufactured wood products.

The Role of Government Innovation Support in the Process of Urban Green Sustainable Development: A Spatial Difference-in-Difference Analysis Based on China's Innovative City Pilot Policy.

The role of government support in sustainable urban development has always been a research topic of scholars, but research focusing on the relationship between government innovation support and urban green sustainable development is still relatively rare. This article uses China's innovative city pilot policy (ICPP) to represent the innovation support provided by the government and address the interaction mechanism and the spatial spillover effect of China's innovative city pilot policy (ICPP), green technology innovation (GTI), and green sustainable development performance (GSDP) with the support of the mediating effect model and the spatial econometric model. Based on panel data of 24 cities in the Yangtze River Delta urban agglomeration from 2001 to 2020, this paper establishes an evaluation index system of green sustainable development performance (GSDP), measuring with the SBM directional distance function based on the undesired output. This paper adopts the spatial difference-in-difference model (SDID) to study the impact mechanism of the ICPP on the GSDP in the Yangtze River Delta. The results show that (i) there is a positive spatial spillover effect of GSDP in the urban agglomeration of the Yangtze River Delta urban agglomeration; (ii) ICPP has a significantly positive effect on GSDP, as verified by several robustness checks; (iii) green technology innovation plays a partial mediating effect in the relationship of the ICPP and GSDP.

Pirfenidone attenuates cardiac hypertrophy against isoproterenol by inhibiting activation of the janus tyrosine kinase-2/signal transducer and activator of transcription 3 (JAK-2/STAT3) signaling pathway.

Cardiovascular risk factors have attracted increasing attention in recent years with the acceleration of population aging, amongst which cardiac hypertrophy is the initiating link to heart failure. Pirfenidone is a promising agent for the treatment of idiopathic pulmonary fibrosis and has recently proven to exert inhibitory effects on the inflammatory response. This study proposes to explore the potential pharmacological action of Pirfenidone in treating cardiac hypertrophy in a rodent model. Four groups of mice were used in the present study: the control, ISO (5 mg/kg/day) for 7 days, Pirfenidone (200 mg/kg/day) for 14 days, and Spironolactone (SPI) (200 mg/kg/day) for 14 days groups. Increased heart weight index, left ventricle (LV) weight index, LV wall thickness, declined LV volume, and elevated serum levels of CK-MB, AST, and LDH were observed in ISO-challenged mice, all of which were dramatically reversed by the administration of Pirfenidone or SPI. Furthermore, an elevated cross-sectional area of cardiomyocytes in the wheat germ agglutinin (WGA) staining of heart cross-sections, upregulated atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), ß Myosin Heavy Chain (ß-MHC), and excessively released tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) in cardiac tissues were observed in the ISO group but greatly alleviated by Pirfenidone or SPI. Lastly, the promoted expression levels of p-JAK-2/JAK-2 and p-STAT3/STAT-3 in the cardiac tissues of ISO-challenged mice were significantly repressed by Pirfenidone or SPI. Collectively, our data reveals a therapeutic property of Pirfenidone on ISO-induced cardiac hypertrophy in mice.

CX3CL1 Worsens Cardiorenal Dysfunction and Serves as a Therapeutic Target of Canagliflozin for Cardiorenal Syndrome.

The prognosis of cardiorenal dysfunction induced by diabetes mellitus (DM), which belongs to cardiorenal syndrome type 5, is poor and its pathogenesis remains elusive. We have reported that CX3CL1 exacerbated heart failure and direct inhibition of CX3CL1 improved cardiac function. Emerging evidence supports that CX3CL1 is involved in renal impairment. Here we attempt to clarify whether CX3CL1 might be a therapeutic target for cardiorenal dysfunction in diabetes. We found that cardiac and renal CX3CL1 protein levels were significantly increased in both streptozotocin-induced diabetic mice and in non-obese diabetic mice, and that hyperglycemia led to persistent CX3CL1 expression in the heart and kidneys even after it was controlled by insulin. In cultured cardiac and renal cells, soluble CX3CL1 accelerated mitochondrial-dependent apoptosis via activation of the RhoA/ROCK1-Bax signaling pathway and promoted fibrosis through cellular phenotypic trans-differentiation mediated by the TGF-ß/Smad pathway. In the two diabetic mouse models, knockout of CX3CL1 receptor CX3CR1 or treatment with an CX3CL1 neutralizing antibody significantly improved cardiorenal dysfunction by inhibiting apoptosis, mitochondrial dysfunction, and fibrosis. Moreover, sodium glucose cotransporter 2 inhibitor canagliflozin significantly downregulated cardiac and renal CX3CL1 expression and improved cardiorenal dysfunction. These findings indicate that CX3CL1 could be a new therapeutic target for diabetes-induced cardiorenal dysfunction.

Growth differentiation factor 11 attenuates cardiac ischemia reperfusion injury via enhancing mitochondrial biogenesis and telomerase activity.

It has been reported that growth differentiation factor 11 (GDF11) protects against myocardial ischemia/reperfusion (IR) injury, but the underlying mechanisms have not been fully clarified. Considering that GDF11 plays a role in the aging/rejuvenation process and that aging is associated with telomere shortening and cardiac dysfunction, we hypothesized that GDF11 might protect against IR injury by activating telomerase. Human plasma GDF11 levels were significantly lower in acute coronary syndrome patients than in chronic coronary syndrome patients. IR mice with myocardial overexpression GDF11 (oe-GDF11) exhibited a significantly smaller myocardial infarct size, less cardiac remodeling and dysfunction, fewer apoptotic cardiomyocytes, higher telomerase activity, longer telomeres, and higher ATP generation than IR mice treated with an adenovirus carrying a negative control plasmid. Furthermore, mitochondrial biogenesis-related proteins and some antiapoptotic proteins were significantly upregulated by oe-GDF11. These cardioprotective effects of oe-GDF11 were significantly antagonized by BIBR1532, a specific telomerase inhibitor. Similar effects of oe-GDF11 on apoptosis and mitochondrial energy biogenesis were observed in cultured neonatal rat cardiomyocytes, whereas GDF11 silencing elicited the opposite effects to oe-GDF11 in mice. We concluded that telomerase activation by GDF11 contributes to the alleviation of myocardial IR injury through enhancing mitochondrial biogenesis and suppressing cardiomyocyte apoptosis.

Excessive fibroblast growth factor 23 promotes renal fibrosis in mice with type 2 cardiorenal syndrome.

Cardiorenal syndrome (CRS) has a high mortality, but its pathogenesis remains elusive. Fibroblast growth factor 23 (FGF23) is increased in both renal dysfunction and cardiac dysfunction, and FGF receptor 4 (FGFR4) has been identified as a receptor for FGF23. Deficiency of FGF23 causes growth retardation and shortens the lifespan, but it is unclear whether excess FGF23 is detrimental in CRS. This study sought to investigate whether FGF23 plays an important role in CRS-induced renal fibrosis. A mouse model of CRS was created by surgical myocardial infarction for 12 weeks. CRS mice showed a significant increase of circulatory and renal FGF23 protein levels, as well as an upregulation of p-GSK, active-ß-catenin, TGF-ß, collagen I and vimentin, a downregulation of renal Klotho expression and induction of cardiorenal dysfunction and cardiorenal fibrosis. These changes were enhanced by cardiac overexpression of FGF23 and attenuated by FGF receptor blocker PD173074 or ß-catenin blocker IGC001. In fibroblasts (NRK-49F), expression of FGFR4 rather than Klotho was detected. Recombinant FGF23 upregulated the expression of p-GSK, active-ß-catenin, TGF-ß, collagen I and vimentin proteins. These changes were attenuated by FGFR4 blockade with BLU9931 or ß-catenin blockade with IGC001. We concluded that FGF23 promotes CRS-induced renal fibrosis mediated by partly activating FGFR4/ß-catenin signaling pathway.

General synthesis of carbon and oxygen dual-doped graphitic carbon nitride via copolymerization for non-photochemical oxidation of organic pollutant.

Earth-abundant, environmental-benign and durable catalysts are of paramount importance for remediation of organic pollutants, and graphitic carbon nitride (g-C3N4) is a promising nonmetallic material for this application. However, the catalytic oxidation on g-C3N4 suffers from low efficiency because of its chemical inertness if not irradiated with light. Herein, we develop a facile copolymerization strategy for the synthesis of carbon and oxygen dual-doped g-C3N4 using urea as g-C3N4 precursor and ascorbic acid (AA) as carbon and oxygen sources, which induces electronic structure reconfiguration. By replacing AA with other organic precursors, a series of C and O dual-doped g-C3N4 are successfully prepared, demonstrating the generality of the developed methodology. As a demonstration, the C and O dual-doped g-C3N4 using AA as the organic precursor (CN-AA0.3) exhibits pronouncedly enhanced catalytic activity in peroxymonosulfate (PMS) activation for organic pollutant degradation without light irradiation compared with pristine g-C3N4 and single oxygen-doped g-C3N4. Experimental and theoretical results revealed the electron-poor C atoms and electron-rich O atoms as active sites for PMS activation in terms of simultaneous PMS oxidation and reduction. This work offers a universal approach to synthesize nonmetal dual-doped g-C3N4 with reconfigured electronic structure, stimulating the development of g-C3N4-based materials for diverse environmental applications.

Highly nitrogen-doped porous carbon transformed from graphitic carbon nitride for efficient metal-free catalysis.

Nitrogen-doped carbon materials are proposed as promising metal-free catalysts for persulfate-mediated catalytic oxidation process, yet the nitrogen content in the final carbon products is typically low. Moreover, controversies remain in the unambiguous identification of active sites in nitrogen-doped carbons for persulfate activation. Here we report the facile synthesis of nitrogen-doped carbon material via one-step pyrolysis of urea and D-mannitol, which simultaneously combine ultrahigh nitrogen content (up to 33.75 at%) with apparent porous structure via transformation from graphitic carbon nitride. With this strategy, the highly nitrogen-doped porous carbon (NC1.0) exhibits excellent catalytic activity toward peroxymonosulfate (PMS) activation for oxidation of organic pollutants. Both experiments and density functional theory (DFT) calculations, for the first time, revealed that the electron-rich graphitic N and electron-deficient carbon atom adjacent to graphitic N in NC1.0 served as active sites for PMS reduction and oxidation toward the generation of hydroxyl radical (OH) and singlet oxygen (1O2), respectively, in which PMS oxidation was the main reaction in the course of PMS activation rendering 1O2 the dominant reactive oxygen species (ROS) in the NC1.0/PMS system. More importantly, NC1.0 presents robust stability in PMS activation, superior to most reported nitrogen-doped carbon-based catalysts, offering great promise for practical environmental remediation.

Lansoprazole alleviates pressure overload-induced cardiac hypertrophy and heart failure in mice by blocking the activation of ß-catenin.

AIMS: Proton pump inhibitors (PPIs) are widely used in patients receiving percutaneous coronary intervention to prevent gastric bleeding, but whether PPIs are beneficial for the heart is controversial. Here, we investigated the effects of lansoprazole on cardiac hypertrophy and heart failure, as well as the underlying mechanisms. METHODS AND RESULTS: Adult male C57 mice were subjected to transverse aortic constriction (TAC) or sham surgery and then were treated with lansoprazole or vehicle for 5 weeks. In addition, cultured neonatal rat ventricular cardiomyocytes and fibroblasts were exposed to angiotensin II in the presence or absence of lansoprazole. At 5 weeks after TAC, the heart weight/body weight ratio was lower in lansoprazole-treated mice than in untreated mice, as was the lung weight/body weight ratio, while left ventricular (LV) fractional shortening and the maximum and minimum rates of change of the LV pressure were higher in lansoprazole-treated mice, along with less cardiac fibrosis. In cultured cardiomyocytes, lansoprazole inhibited angiotensin II-induced protein synthesis and hypertrophy, as well as inhibiting proliferation of fibroblasts. Lansoprazole decreased myocardial levels of phosphorylated Akt, phosphorylated glycogen synthase kinase 3ß, and active ß-catenin in TAC mice and in angiotensin II-stimulated cardiomyocytes. After overexpression of active ß-catenin or knockdown of H+/K+-ATPase α-subunit, lansoprazole still significantly attenuated myocyte hypertrophy. CONCLUSION: Lansoprazole inhibits cardiac remodelling by suppressing activation of the Akt/GSK3ß/ß-catenin pathway independent of H+/K+-ATPase inhibition, and these findings may provide a novel insight into the pharmacological effects of PPIs with regard to alleviation of cardiac remodelling.

Overexpression of Na+-HCO3- cotransporter contributes to the exacerbation of cardiac remodeling in mice with myocardial infarction by increasing intracellular calcium overload.

The role of the cardiac isoform of the electrogenic sodium-bicarbonate ion cotransporter (NBCe1) in cardiac remodeling is not fully understood. The aim of this study was to assess the effects of NBCe1 overexpression on cardiac remodeling induced by myocardial infarction (MI) in mice. We generated NBCe1 transgenic (Tg) mice and NBCe1 overexpressing adult mouse ventricular myocytes (AMVMs) to investigate the role of NBCe1 on post-MI remodeling and calcium kinetics. Tg mice showed a markedly higher mortality rate and larger infarct size after MI. At 6 weeks after MI, the maximum rising rates of left ventricular pressure (dp/dt), contractility index, and the exponential time constant of relaxation (τ) were markedly lower, and there was higher cardiomyocyte apoptosis, in Tg mice compared with WT mice. In cultured AMVMs, overexpression of NBCe1 decreased sarcomere shortening and calcium amplitude. In WT AMVMs, the rates of the rise and decay phase of calcium transients, indicated by the rising time (Tpeak, time to peak) and decay time constant (τd), and the number of apoptotic cells, were increased following hypoxia, while overexpression of NBCe1 further increased Tpeak and cellular apoptosis, but not τd. Intracellular resting calcium and sodium concentrations were significantly increased following both hypoxia and NBCe1 overexpression. Co-treatment with S0859, an NBCe1 antagonist, blocked the hypoxia-induced increase in Tpeak, τd, intracellular resting calcium and sodium concentrations, and apoptosis in cardiomyocytes. These findings indicate that NBCe1 overexpression promotes cardiac remodeling by increasing intracellular calcium overload. Therefore, NBCe1 should be a potential target for treatment of cardiac remodeling.