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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. [ABSTRACT FROM AUTHOR]

This paper presents novel empirical evidence on the welfare impacts of forest protection programs, focusing on both income and material welfare at the household level. Specifically, we conduct a household survey of 1271 households in forestry communities that participate in the Natural Forest Protection Program (NFPP) in China. The survey data are collected from 56 state forest enterprises (SFEs) across three provinces in China. We employ the Alkire–Foster method to calculate and decompose the material deprivation index based on household income levels. Our analysis reveals that forestry communities exhibit a significant proportion of households in low-income welfare states, comprising nearly one-fourth (25.41%) of the sample. Furthermore, we observe that the percentage of households in a low-material welfare state is nearly one-fifth (21.70%), with 7.79% of households experiencing both low-income and low-material welfare. Importantly, we find that welfare disparities persist across population subgroups based on occupation and geography. In addition, we assess the impact of the NFPP on household welfare outcomes and identify an elite group of technicians residing in urban communities down the hill who experience positive welfare effects from the program. These findings provide critical insights beyond a single welfare dimension and contribute to the growing literature on evaluating forest protection policies. Furthermore, the results offer valuable lessons for designing and implementing forest protection programs in other developing countries. [ABSTRACT FROM AUTHOR]

Calcareous sand is a special marine soil rich in calcium carbonate minerals, characterized by brittle particles. It is, therefore, widely used as a filling material in the construction of islands and reefs. In this study, a series of cyclic tri-axial tests were conducted on calcareous sand taken from a reef in the South China Sea under different confining pressures and cyclic stress ratio (CSR). Then, applying the shakedown theory, the cumulative deformation of calcareous sand under a long-term cyclic load of aircraft was evaluated. Results showed that with the increase in the effective confining pressure, the stress–strain curves of calcareous sand showed a change from the strain-softening to the strain-hardening state; the volumetric strain of calcareous sand showed a change from shear shrinkage and then shear expansion to continuous shear shrinkage. Calcareous sand showed three different response behaviors under cyclic load: plastic shakedown, plastic creep and incremental plastic failure. With the plastic strain rate as the defining index, this study determined the critical CSR of calcareous sand under different shakedown response statuses and found them to increase with the effective confining pressure. The empirical formula for critical stress was established based on the fitting analysis of critical CSR under different confining pressures, taking the confining pressure as the variable. At the early stage of the cyclic load, calcareous sand samples were under compression. When the resilient modulus grew rapidly and the number of loading cycles continued to increase, the particles of calcareous sand samples were crushed, causing the fine particles to fill the voids among coarse particles, further compacting the samples and increasing the resilient modulus of calcareous sand samples. Hardin's breakage potential model was adopted to quantitatively describe the particle breakage of calcareous sand samples before and after tests. The results indicated that calcareous sand samples produced obvious particle breakage when the CSR was small. As the CSR increased, the extent of the breakage of the sample particles first increased and thereafter stabilized. This study provides a theoretical reference for the assessment of the dynamic stability of calcareous sand subgrade subjected to traffic loads. [ABSTRACT FROM AUTHOR]

Whether financial inclusion and economic growth can sustainably release poverty alleviation effects in long term has been the focus of academia and government sector. This article uses provincial panel data from 2004 to 2019 to examine the dynamic nonlinear connectedness between the financial inclusion, economic growth, income inequality, and poverty alleviation; the main objective is to reveal the direction and intensity of the long-term and short-term impact of each factor on poverty alleviation. By building a panel vector autoregression model (PVAR), the comparison analyses of national, eastern, central, and western sample groups verify the existence of dynamic nonlinear connectedness among the four variables. The study found that there is complex bidirectional causality between these variables, financial inclusion has the long-term impact on promoting poverty alleviation in China, the impact of economic growth is relatively weak, and income inequality has weakened the positive impact of financial inclusion on poverty alleviation. Through the analysis of impulse response function, variance decomposition, and time-varying nonparametric estimates in different economic regions, we find that the impact of financial inclusion on poverty alleviation presents a U-shaped characteristic, and the contribution of financial inclusion to poverty alleviation in western regions is significant, but poverty reduction in eastern and central region mainly depends on economic growth. For policymakers, financial inclusion can be an effective way to alleviate relative poverty, but the poverty governance should focus more on reducing income inequality in China. [ABSTRACT FROM AUTHOR]

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-β/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. [ABSTRACT FROM AUTHOR]

The selective catalytic reduction technology has the potential hazards of NH3 escape while catalytically reducing NOx. The HCl in the flue gas can react with the NH3 under certain conditions to form NH4Cl and deposit in the appropriate temperature range. In this study, the deposition behavior of fly ash and NH4Cl was studied by a charge‐coupled device (CCD) camera in a drop tube furnace under the condition of the NH4Cl atmosphere. To investigate the effect of surface temperature on the deposition characteristics, we set the surface temperature at 363 K for Case 1, 373 K for Case 2, and 383 K for Case 3, respectively. The CCD camera monitored the morphology of ash deposit growth, and two type‐K thermocouples measured the temperature of the inner and outer surfaces of the deposition probe. Collected deposit samples were analyzed by scanning electron microscopy and X‐ray diffraction. The results showed that the primary substance of the deposited sediments was salammoniac (NH4Cl). The crystal granules of NH4Cl in the deposited sediment were disconnected, and they were denser under the lower surface temperatures. The deposited layer caused a declination in the heat flux through the deposition probe, and the lower surface temperature was more conducive to the growth of the deposition. This work contributes to a deeper understanding of the characteristics of NH4Cl deposition, which has practical utility in preventing the formation of the NH4Cl deposition in the precipitator and induced draft fans. [ABSTRACT FROM AUTHOR]

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 3β, and active β-catenin in TAC mice and in angiotensin II-stimulated cardiomyocytes. After overexpression of active β-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/GSK3β/β-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. [ABSTRACT FROM AUTHOR]

High-mobility group box1 (HMGB1) exerts effects on inflammation by binding to receptor for advanced glycation end products (RAGE) or Toll-like receptor 4. Considering that inflammation is involved in pressure overload-induced cardiac hypertrophy, we herein attempted to investigate whether HMGB1 plays a role in myocardial hypertrophy in RAGE knockout mice as well as in the growth and apoptosis of cardiomyocytes. The myocardial expression of RAGE was not significantly changed while TLR4 mRNA was upregulated in response to transverse aortic constriction (TAC) for 1 week. The myocardial expression of HMGB1 protein was markedly increased in TAC group when compared to the sham group. Heart weight to body weight ratio (HW/BW) and lung weight to body weight ratio (LW/BW) were evaluated in RAGE knockout (KO) and wild-type (WT) mice 1 week after TAC. Significant larger HW/BW and LW/BW ratios were found in TAC groups than the corresponding sham groups, but no significant difference was found between KO and WT TAC mice. Similar results were also found when TAC duration was extended to 4 weeks. Cultured neonatal rat cardiomyocytes were treated with different concentrations of recombinant HMGB1, then cell viability was determined using MTT and CCK8 assays and cell apoptosis was determined by Hoechst staining and TUNEL assay. The results came out that HMGB1 exerted no influence on viability or apoptosis of cardiomyocytes. Besides, the protein expression levels of Bax and Bcl2 in response to different concentrations of HMGB1 were similar. These findings indicate that HMGB1 neither exerts influence on cardiac remodeling by binding to RAGE nor induces apoptosis of cardiomyocytes under physiological condition. [ABSTRACT FROM AUTHOR]

China's forest products manufacturing industry is experiencing the dual pressure of forest protection policies and wood scarcity and, therefore, it is of great significance to reveal the spatial agglomeration characteristics and evolution drivers of this industry to enhance its sustainable development. Based on the perspective of large-scale agglomeration in a continuous space, in this study, we used the spatial Gini coefficient and standard deviation ellipse method to investigate the spatial agglomeration degree and location distribution characteristics of China's forest products manufacturing industry, and we used exploratory spatial data analysis to investigate its spatial agglomeration pattern. The results show that: (1) From 1988 to 2018, the degree of spatial agglomeration of China's forest products manufacturing industry was relatively low, and the industry was characterized by a very pronounced imbalance in its spatial distribution. (2) The industry has a very clear core–periphery structure, the spatial distribution exhibits a "northeast-southwest" pattern, and the barycenter of the industrial distribution has tended to move south. (3) The industry mainly has a high–high and low–low spatial agglomeration pattern. The provinces with high–high agglomeration are few and concentrated in the southeast coastal area. (4) The spatial agglomeration and evolution characteristics of China's forest products manufacturing industry may be simultaneously affected by forest protection policies, sources of raw materials, international trade and the degree of marketization. In the future, China's forest products manufacturing industry should further increase the level of spatial agglomeration to fully realize the economies of scale. [ABSTRACT FROM AUTHOR]

Understanding the reduction mechanism of additives on ammonium bisulfate (ABS) fouling formation can alleviate ABS fouling problems. This paper presents an investigation of the influence of Na2SO3/NaHSO3 on the formation process of ABS fouling with an in situ measurement technique. According to the thickness curves, both Na2SO3 and NaHSO3 can control the growth of ABS fouling, but Na2SO3 shows a better inhibitory effect on the growth of ABS fouling. Meanwhile, the mitigation effect of the additive on ABS fouling increases with the increasing injection quantity of the additive. The results of the heat flux show that the heat transfer performance of the fouling probe becomes better with the injection of additives, whereas the heat transfer performance becomes worse with the increasing injection quantity of additives. The thermal resistance of ABS fouling provides a reasonable agreement with the results of the heat flux. The SEM‐EDX results show that the additives have an effect on the formation of ABS fouling by controlling the ABS concentration, which can increase the viscosity of the particle, promote the agglomeration of the fouling particle, and enhance the heat transfer of the ABS fouling, providing a rational explanation for the experimental results. [ABSTRACT FROM AUTHOR]

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), β Myosin Heavy Chain (β-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.

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-β-catenin, TGF-β, 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 β-catenin blocker IGC001. In fibroblasts (NRK-49F), expression of FGFR4 rather than Klotho was detected. Recombinant FGF23 upregulated the expression of p-GSK, active-β-catenin, TGF-β, collagen I and vimentin proteins. These changes were attenuated by FGFR4 blockade with BLU9931 or β-catenin blockade with IGC001. We concluded that FGF23 promotes CRS-induced renal fibrosis mediated by partly activating FGFR4/β-catenin signaling pathway.

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 ( 1 O 2 ) 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 1 O 2 production. With a large specific surface area (1218.7 m 2 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 1 O 2 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 1 O 2 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 1 O 2 generation from PMS oxidation and furnishes theoretical support for further relevant studies.

Either angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor 1 blocker (ARB) attenuates cardiac remodeling. However, the overall molecular modulation of the reversing remodeling process in response to the ACEI or ARB treatment is not yet well determined. In this study, we examined whether gene expressions are modulated by ACEI (temocapril), ARB (olmesartan) or both in a murine model with transverse aortic constriction (TAC) and confirm whether periostin is a target gene of olmesartan in mice with myocardial infarction (MI). We detected 109 genes that were significantly up-regulated in TAC mice and a majority of these were down-regulated in response to temocapril, olmesartan or their combination which significantly attenuated cardiac remodeling at one or four weeks. Real-time RT-PCR demonstrated that olmesartan, temocapril or their combination down-regulated the expression of periostin. In MI mice treated with olmesartan for 4 weeks, the left ventricular end-diastolic and systolic dimensions measured with echocardiography were lower, whereas maximum rate of rise and fall rate of LV pressure (±dp/dt max) were greater, and Azan-staining cardiac fibrotic area was smaller. Furthermore, periostin was upregulated in response to MI, whereas olmesartan blocked this upregulation. Post-MI fibrosis was smaller in periostin knockout adult mice than in wildtype mice, while glycogen synthase kinase 3β was increased and cyclin D1 was decreased in periostin knockout mice. These findings indicate that periostin is a target gene of ARB and olmesartan reverses cardiac remodeling at least partially through the downregulation of periostin., Competing Interests: CONFLICTS OF INTEREST The authors declare no conflicts of interest.

Fibroblast growth factor 23 (FGF23) has been reported to induce left ventricular hypertrophy, but it remains unclear whether FGF23 plays a role in cardiac fibrosis. This study is attempted to investigate the role of FGF23 in post-infarct myocardial fibrosis in mice. We noted that myocardial and plasma FGF23 and FGF receptor 4 were increased in mice with heart failure as well as in cultured adult mouse cardiac fibroblasts (AMCFs) exposed to angiotensin II, phenylephrine, soluble fractalkine. Recombinant FGF23 protein increased active β-catenin , procollagen I and procollagen III expression in cultured AMCFs. Furthermore, intra-myocardial injection of adeno-associated virus-FGF23 in mice significantly increased left ventricular end-diastolic pressure and myocardial fibrosis, and markedly upregulated active β-catenin, transforming growth factor β (TGF-β), procollagen I and procollagen III in both myocardial infarction (MI) and ischemia/reperfusion (IR) mice, while β-catenin inhibitor or silencing of β-catenin antagonized the FGF23-promoted myocardial fibrosis in vitro and in vivo. These findings indicate that FGF23 promotes myocardial fibrosis and exacerbates diastolic dysfunction induced by MI or IR, which is associated with the upregulation of active β-catenin and TGF-β.

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.