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Improving the selectivity in the oxidative coupling of methane to ethane/ethylene poses a significant challenge for commercialization. The required improvements are hampered by the uncertainties associated with the reaction mechanism due to its complexity. Herein, we report about 90 % selectivity to the target products at 11 % methane conversion over Gd2O3‐based catalysts at 700 °C using N2O as the oxidant. Sophisticated kinetic studies have suggested the nature of adsorbed oxygen species and their binding strength as key parameters for undesired methane oxidation to carbon oxides. These descriptors can be controlled by a metal oxide promoter for Gd2O3. [ABSTRACT FROM AUTHOR]

The present study of oxidative coupling of methane (OCM) over MnOx−Na2WO4/support catalysts demonstrated that the selectivity to C2H6 and C2H4 (C2‐hydrocarbons) is affected by the kind of support, co‐fed water, and the kind of oxidant (O2 vs. N2O). In addition to previous studies with MnOx−Na2WO4/SiO2, an enhancing water effect was obtained using catalysts based on TiO2‐ or ZrO2‐containing supports. However, a negative effect on methane conversion was established for SiO2−Al2O3‐supported catalysts. Temporal analysis of products with isotopic tracers suggests that the ability of MnOx−Na2WO4 to generate diatomic adsorbed oxygen species depends on the kind of support and is the key property for the water effect. The strength of the water effect on the activity decreases with an increase in the surface area of working catalysts. The kind of support also affects products selectivity due to its influence on the mobility/releasability of lattice oxygen in supported MnOx−Na2WO4. Among the prepared catalysts, MnOx−Na2WO4/TiO2 was found to be promising for H2O‐assisted OCM. The use of N2O instead of O2 further increases the selectivity to C2‐hydrocarbons to 84 % at 6.8 % CH4 conversion due to the formation of predominantly monoatomic oxygen species from N2O that selectively convert CH4 into C2H6. [ABSTRACT FROM AUTHOR]

Nocturnal hypertension is highly prevalent among Chinese and Asian populations, which is mainly attributed to high salt intake and high salt sensitivity. Nocturnal hypertension increases the risk of cardiovascular and all‐cause mortality, independent of daytime blood pressure (BP). However, it can usually be detected by 24‐h ambulatory BP monitoring, rather than routine office or home BP measurement, thus is often underdiagnosed in clinical practice. Currently, no specific guidance is available for the management of nocturnal hypertension in China or worldwide. Experts from the Chinese Hypertension League summarized the epidemiologic and pathophysiologic characteristics and clinical phenotype of nocturnal hypertension and provided consensus recommendations on optimal management of nocturnal hypertension, with the goal of maximally reducing the cardiovascular disease risks. In this consensus document, 24‐h ABPM is recommended for screening and diagnosis of nocturnal hypertension, especially in the elderly, patients with diabetes, chronic kidney diseases, obstructive sleep apnea and other conditions prone to high nocturnal BP. Lifestyle modifications including salt intake restriction, exercise, weight loss, sleep improvement, and mental stress relief are recommended. Long‐acting antihypertensive medications are preferred for nocturnal and 24‐h BP control. Some newly developed agents, renal denervation, and other device‐based therapy on nocturnal BP reduction are evaluated. [ABSTRACT FROM AUTHOR]

We conducted a systematic review and meta‐analysis to evaluate postoperative seizure and memory outcomes of temporal lobe epilepsy with different hippocampal sclerosis (HS) subtypes classified by International League Against Epilepsy (ILAE) Consensus Guidelines in 2013. Following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta‐Analyses) and MOOSE (Meta‐Analysis of Observational Studies in Epidemiology) guidelines, we searched PubMed, Embase, Web of Science, and Cochrane Library from January 1, 2013 to August 6, 2023. Observational studies reporting seizure and memory outcomes among different HS subtypes were included. We used the Newcastle–Ottawa scale to assess the risk of bias and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach to grade the quality of evidence. Seizure freedom and improved outcome (Engel 1 or ILAE class 1–2) ≥1 year after surgery were defined as the primary and secondary seizure outcome. A random‐effects meta‐analysis by DerSimonian and Laird method was performed to obtain pooled risk ratio (RRs) with 95% confidence interval (CIs). The memory impairment was narratively reviewed because of various evaluation tools. Fifteen cohort studies with 2485 patients were eligible for the meta‐analysis of seizure outcome. Six cohorts with detailed information on postoperative memory outcome were included. The pooled RRs of seizure freedom, with moderate to substantial heterogeneity, were.98 (95% CI =.84–1.15) between HS type 2 and type 1, 1.11 (95% CI =.82–1.52) between type 3 and type 1, and.80 (95% CI =.62–1.03) between the no‐HS and HS groups. No significant difference of improved outcome was found between different subtypes (p >.05). The quality of evidence was deemed to be low to very low according to GRADE. The long‐term seizure outcome (≥5 years after surgery) and memory impairment remained controversial. [ABSTRACT FROM AUTHOR]

Fully densified (transparent) ceramic with small grain size is highly desired to improve the field breakdown strength (BDS) and its scattering. Sintering behavior, microstructural evolution, electric, dielectric, and energy storage properties of (Ba0.6Sr0.4)1‐1.5xBixTi1‐x(Mg1/3Nb2/3)xO3 (x =.04–.10) ceramics have been studied in this paper. Phase pure cubic perovskite is observed for the x =.04 composition. Nb‐rich tungsten bronze type and Ti‐rich barium titanate secondary phases are present in the x >.05 compositions. A multiphasic transparent ferroelectric ceramic with ∼74.2% (780 nm) transmittance and a high refractive index of ∼2.3 within the visible region could be successfully obtained for the x =.10 composition by traditional ceramic process. The x =.09 composition demonstrates good energy storage performance (recoverable energy density Wrec = 3.74J/cm3, efficiency η = 77% and BDS = 390kV/cm) with extremely low scattering in BDS, suggesting potential application in large sized energy storage capacitor. [ABSTRACT FROM AUTHOR]

This work built a molecular‐level kinetic model for hydrocarbon catalytic cracking, incorporating the catalyst acidity as the parameter to estimate reaction rates. The n‐decane and 1‐hexene co‐conversion catalytic cracking process was chosen as the studying case. The molecular reaction network was automatically generated using a computer‐aided algorithm. A modified linear free energy relationship was proposed to estimate the activation energy in a complex reaction system. The kinetic parameters were initially regressed from the experimental data under several reaction conditions. On this basis, the product composition was evaluated for three catalytic cracking catalysts with different Si/Al. The Bronsted acid and Lewis acid as the key catalyst properties were correlated with kinetic parameters. The built model can calculate the product distribution, gasoline composition, and molecular distribution at different reaction conditions for different catalysts. This sensitive study shows that it will facilitate the model‐based optimization of catalysts and reaction conditions according to product demands. [ABSTRACT FROM AUTHOR]

Chiral phosphoric acid‐catalyzed couplings of C‐alkynyl N,N′‐di‐(tert‐butoxycarbonyl)‐aminals with β‐naphthols led to chiral propargylamines in moderate to high yields with high to excellent enantioselectivity, in which the reactions underwent sequential chiral phosphoric acid‐catalyzed in situ formation of N‐(tert‐butoxycarbonyl)‐imines (N‐Boc‐imines) from the aminals, and 1,2‐addition of β‐naphthols to the N‐Boc‐imines. Chiral 1,2‐dihydronaphtho[2,1‐b]furans and naphtho[2,1‐b]furans were prepared with satisfactory results when 10 mol% AgOAc and 20 mol% 2,6‐lutidine or 1.2 equiv. of 1,8‐diazabicyclo[5.4.0]undec‐7‐ene (DBU) were added to the resulting chiral propargylamines solution, respectively. [ABSTRACT FROM AUTHOR]

A series of core‐shell HZSM‐5@mesoSiO2 with tunable shell thickness from 10 to 70 nm was prepared and studied for n‐butane catalytic cracking. With introducing of SiO2 shell, the catalytic performance of HZSM‐5@mesoSiO2 was largely enhanced, and n‐butane conversion rate per Al site reached to 2.43 min−1 over HZSM‐5@mesoSiO2(1:4) at 675°C which is nearly twice to that of HZSM‐5 (1.34 min−1). The diffusion property of n‐butane over as‐prepared sample was quantified by measuring the diffusional time constants using zero length column chromatography technique (ZLC). Combining with chemical reaction kinetic analysis, the quantitative relationship between diffusion property and catalytic performance was effectively established for the first time in n‐butane catalytic cracking. Positive linear correlation between diffusional time constant (D/R2) and n‐butane conversion rate per Al site could be found, which confirms that diffusion enhancement by hierarchical structure is an effective strategy to improve the activity of HZSM‐5 in catalytic cracking. [ABSTRACT FROM AUTHOR]

The Front Cover depicts the main products of the oxidative coupling of methane reaction over MnOx‐Na2WO4/support catalysts. In their Research Article, G. Jian, E. V. Kondratenko and co‐workers established that low catalyst surface area and low reactivity of support lattice oxygen are advantageous for achieving high selectivity to C2H6 and C2H4. The TiO2 support fulfills these requirements, whereas the use of Al2O3‐ or ZrO2‐containing supports leads to the predominant formation of CO or CO2. In addition, the selectivity to the desired products over TiO2‐supported catalysts can be improved by replacing O2 with N2O and/or through co‐fed H2O due to reducing the concentration of adsorbed diatomic oxygen species. More information can be found in the Research Article by G. Jian, E. V. Kondratenko and co‐workers. [ABSTRACT FROM AUTHOR]

Background: Increasing numbers of studies have demonstrated that circulating tumor cells (CTCs) undergo a phenotypic change termed epithelial‐mesenchymal transition (EMT), and researchers have proposed that EMT might provide CTCs with increased potential to survive in the different microenvironments encountered during metastasis through various ways, such as by increasing cell survival and early colonization. However, the exact role of EMT in CTCs remains unclear. Methods: In this study, we identified CTCs of 41 patients with gastric cancer using Cyttel‐CTC and im‐FISH (immune‐fluorescence in situ hybridization) methods, and tested the expression of EMT markers and ULBP1 (a major member of the NKG2D—natural killer [NK] group 2 member D—ligand family) on CTCs. Moreover, we investigated the relationship between the expression of EMT markers and ULBP1 on CTCs and gastric cancer cell lines. Results: Our results showed that the CTCs of gastric cancer patients exhibited three EMT marker subtypes, and that the expression of ULBP1 was significantly lower on mesenchymal phenotypic CTCs (M+CTCs) than on epithelial phenotypic CTCs (E+CTCs). EMT induced by TGF‐β in vitro produced a similar phenomenon, and we therefore proposed that EMT might be involved in the immune evasion of CTCs from NK cells by altering the expression of ULBP1. Conclusions: Our study indicated that EMT might play a vital role in the immune invasion of CTCs by regulating the expression of ULBP1 on CTCs. These findings could provide potential strategies for targeting the immune evasion capacity of CTCs. [ABSTRACT FROM AUTHOR]

A simple solvent‐free method for the regioselective synthesis of pyrazoline derivatives via the annulation reactions of α‐cyano‐α,β‐unsaturated ketones and β‐carboxylic ester‐α,β‐unsaturated ketone with Huisgen zwitterions was developed. Interestingly, the reaction substrate is identified as a critical factor to control the final products. This method features simplicity, high efficiency, environmentally benign, and broad substrate scope. The gram scale applicability also points towards its possible implementation in industrial use. [ABSTRACT FROM AUTHOR]

The occurrence of hypertension is influenced by combined actions of genetic and environmental factors. Among environmental factors, high salt intake is considered as one of the most important and critical dietary factors. High salt intake is closely related to the incidence and mortality of cardiac and cerebrovascular events, as well as ventricular hypertrophy, renal damage, and other target organ damages. The existing data show that the daily sodium salt intake of Chinese population is significantly higher than that of European and American populations, and it generally exceeds the standard. Therefore, sodium and potassium intake in patients with hypertension should be actively assessed to carry out targeted treatment, which is an important strategy in blood pressure management. According to the characteristics of high prevalence of hypertension, high sodium salt intake, and low blood pressure control rate in China, Chinese Medical Association Hypertension Professional Committee believes that it is necessary to promote salt restriction and formulate the assessment of salt intake and clinical process of blood pressure management according to the current status of sodium intake. [ABSTRACT FROM AUTHOR]

Abstract: Gastric cancer (GC) is one of the most common malignancies worldwide. TGF‐β1 induces the epithelial–mesenchymal transition (EMT) in GC, mainly through Smad‐dependent pathways. Nevertheless, few studies have focused on the activation of non‐canonical transduction pathways. TRPC, Ca2+ entry channels, are ubiquitously expressed in various cell types and are involved in many cellular functions. However, their roles in GC are not well elucidated. This study aimed to determine whether TRPC participates in the TGF‐β1‐induced EMT of GC and to investigate the potential mechanisms. Immunofluorescence staining was performed to examine the distribution and expression of TRPCs and EMT‐related proteins in SGC‐7901 cells incubated with or without TGF‐β1. The expression of TRPC1/3/6 and EMT‐related molecules, including E‐cadherin, vimentin, and α‐SMA, was detected by qRT‐PCR and Western blotting. Additionally, the underlying mechanism was determined by treating cells with pharmacological inhibitors and examining the levels of proteins involved in the main signaling cascades using Western blotting. TRPC1/3/6 were expressed at high levels in SGC‐7901 cells. Following TGF‐β1 stimulation, the expression of vimentin, α‐SMA, and TRPC1/3/6 increased and E‐cadherin expression decreased, accompanied by activation of the Ras/Raf1/ERK1/2 signaling pathway. Notably, activation of the Ras/Raf1/ERK1/2 signaling cascade was suppressed by SKF96365 and 2‐APB. Both TRPC and ERK inhibitors mitigated EMT progression. Based on these results, TRPC1/3/6 inhibition attenuated the TGF‐β1‐induced EMT in GC by suppressing Ras/Raf1/ERK signal transduction. [ABSTRACT FROM AUTHOR]

Abstract: Autophagy modulation is a potential therapeutic strategy for tongue squamous cell carcinoma (TSCC). Melatonin possesses significant anticarcinogenic activity. However, whether melatonin induces autophagy and its roles in cell death in TSCC are unclear. Herein, we show that melatonin induced significant apoptosis in the TSCC cell line Cal27. Apart from the induction of apoptosis, we demonstrated that melatonin‐induced autophagic flux in Cal27 cells as evidenced by the formation of GFP‐LC3 puncta, and the upregulation of LC3‐II and downregulation of SQSTM1/P62. Moreover, pharmacological or genetic blockage of autophagy enhanced melatonin‐induced apoptosis, indicating a cytoprotective role of autophagy in melatonin‐treated Cal27 cells. Mechanistically, melatonin induced TFE3(Ser321) dephosphorylation, subsequently activated TFE3 nuclear translocation, and increased TFE3 reporter activity, which contributed to the expression of autophagy‐related genes and lysosomal biogenesis. Luzindole, a melatonin membrane receptor blocker, or MT2‐siRNA partially blocked the ability of melatonin to promote mTORC1/TFE3 signaling. Furthermore, we verified in a xenograft mouse model that melatonin with hydroxychloroquine or TFE3‐siRNA exerted a synergistic antitumor effect by inhibiting autophagy. Importantly, TFE3 expression positively correlated with TSCC development and poor prognosis in patients. Collectively, we demonstrated that the melatonin‐induced increase in TFE3‐dependent autophagy is mediated through the melatonin membrane receptor in TSCC. These data also suggest that blocking melatonin membrane receptor‐TFE3‐dependent autophagy to enhance the activity of melatonin warrants further attention as a treatment strategy for TSCC. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to evaluate vascular function, including arterial resistance and endothelial function, by high‐resolution sonography in an Nω‐nitro‐ l‐arginine methyl ester hydrochloride ( l‐NAME)‐induced mouse model of preeclampsia‐like symptoms. Methods: Pregnant mice were subcutaneously injected with a saline solution (control; n = 10) or l‐NAME (n = 10) between the 7th and 18th days of gestation. The resistive index and pulsatility index (RI and PI, indicators of arterial resistance) of the uteroplacental, umbilical, femoral, and common carotid arteries and the flow‐mediated dilatation (index of endothelial function) of the femoral artery were measured by high‐frequency sonography in both groups. Results: We noted significant increases in the RI and PI of the uteroplacental and umbilical arteries and a decrease in the flow‐mediated dilatation of the femoral artery in the l‐NAME group compared with the control group. We also found that the RI and PI of the uteroplacental and umbilical arteries were negatively correlated with fetal weight and crown‐rump length. The results of the multivariate analysis using a logistic regression model indicated that the flow‐mediated dilatation at 120 seconds was an independent diagnostic criterion for the l‐NAME‐induced preeclampsia‐like model. A receiver operating characteristic analysis showed that flow‐mediated dilatation at 120 seconds had the greatest area under the curve of 0.934, with an optimal cutoff point of 11.1%, yielding sensitivity of 100% and specificity of 84.6%. Conclusions: The PI and RI of the fetomaternal vasculature can identify fetuses in “high‐risk” pregnancies, and flow‐mediated dilatation is a reliable indicator for predicting preeclampsia. Assessment of vascular function by high‐resolution sonography provides a useful platform for preeclampsia‐related basic research with high reproducibility. [ABSTRACT FROM AUTHOR]

A cascade aza-Michael/Aldol annulation of 2-arylideneindane-1,3-diones with in situ generated Huisgen zwitterions has been developed. This reaction afforded the desired products in moderate to good yields (up to 87%) with excellent chemo- and diastereoselectivity (up to 20:1). This strategy allows facile diastereoselective preparation of biologically important indenopyrazoline derivatives containing two contiguous chiral centers including a quaternary stereogenic center. [ABSTRACT FROM AUTHOR]

MiR-206 has been found to play a critical role in skeletal muscle proliferation, differentiation, and regeneration. However, little is known about the function of miR-206 in vascular smooth muscle cells (VSMCs) biology. In this study, we will investigate its roles in phenotypic switching of VSMCs and neointimal lesion formation. First, we identified the expression of miR-206 in VSMCs treated with various concentrations of TGFβ1 and in rat carotid arteries after angioplasty by using qPCR. TGFβ1 inhibited the expression of miR-206 and TGFβ1 inhibitor induced miR-206 expression. In VSMCs of injured vascular walls, miR-206 expression was upregulated. Then, we overexpressed miR-206 using lentivirus Lv-rno-mir-206 and knocked down miR-206 using LV-rno-mir-206-inhibitor in rat carotid arteries after angioplasty. Overexpression of miR-206 resulted in decreasing SM22α expression in VSMCs in vitro and knockdown of miR-206 suppressed neointimal lesion formation in vivo. Finally, ZFP580 (zinc finger protein 580) was identified as the direct target of miR-206 in VSMCs by using luciferase report assay. The results indicate that miR-206 is involved in phenotypic switching of VSMCs and neointimal lesion formation after angioplasty through targeting ZFP580. These findings may provide a novel therapeutic target in post-angioplasty restenosis. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a persistent environmental and occupational contaminant that accumulates in the liver and induces oxidative stress and inflammation. Melatonin possesses potent hepatoprotective properties against the development and progression of acute and chronic liver injury. Nevertheless, the molecular mechanism underlying the protective effects of melatonin against Cd-induced hepatotoxicity remains obscure. In this study, we aimed to investigate the effects of melatonin on Cd-induced liver inflammation and hepatocyte death. Male C57BL/6 mice were intraperitoneally injected with melatonin (10 mg/kg) once a day for 3 days before exposure to CdCl2 (2.0 mg/kg). We found that Cd induced hepatocellular damage and inflammatory infiltration as well as increased serum ALT/AST enzymes. In addition, we showed that Cd triggered an inflammatory cell death, which is mediated by the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Moreover, melatonin treatment significantly alleviated Cd-induced liver injury by decreasing serum ALT/AST levels, suppressing pro-inflammatory cytokine production, inhibiting NLRP3 inflammasome activation, ameliorating oxidative stress, and attenuating hepatocyte death. Most importantly, melatonin markedly abrogated Cd-induced TXNIP overexpression and decreased the interaction between TXNIP and NLRP3 in vivo and in vitro. However, treatment with siRNA targeting TXNIP blocked the protective effects of melatonin in Cd-treated primary hepatocytes. Collectively, our results suggest that melatonin confers protection against Cd-induced liver inflammation and hepatocyte death via inhibition of the TXNIP-NLRP3 inflammasome pathway. [ABSTRACT FROM AUTHOR]

Cadmium (Cd), a highly ubiquitous heavy metal, induces neurotoxicity. Melatonin, a major secretory product of the pineal gland, protects against Cd-induced neurotoxicity. However, the mechanism that accounts for this protection remains to be elucidated. Herein, we exposed mouse neuroblastoma cells (Neuro-2a cells) to different concentrations of cadmium chloride (CdCl2) (12.5, 25, and 50 μ mol L−1) for 24 hours. We showed that Cd inhibits autophagosome-lysosome fusion and impairs lysosomal function, subsequently leading to nerve cell death. In addition, Cd decreases the level of transcription factor EB ( TFEB) but induces the nuclear translocation of TFEB, associated with compromised lysosomal function or a compensatory effect after the impairment of the autophagic flux. Moreover, compared to the 50-μ mol L−1 Cd group, administration of 1 μ mol L−1 melatonin increased ' TFEB-responsive genes' ( P<.05) and the levels of lysosomal-associated membrane protein (0.57±0.06 vs 1.00±0.11, P<.05), preserved lysosomal protease activity (0.52±0.01 vs 0.90±0.02, P<.05), maintained the lysosomal pH level (0.50±0.01 vs 0.87±0.05, P<.01), and enhanced autophagosome-lysosome fusion (0.05±0.00 vs 0.21±0.01, P<.01). Notably, melatonin enhanced TFEB expression (0.37±0.04 vs 0.72±0.07, P<.05) and nuclear translocation (2.81±0.08 vs 3.82±0.05, P<.05). Tfeb si RNA blocked the melatonin-mediated elevation in autophagy-lysosome machinery in Cd-induced neurotoxicity ( P<.01). Taken together, these results uncover a potent role for TFEB-mediated autophagy in the pathogenesis of Cd-induced neurotoxicity, suggesting that control of the autophagic pathway by melatonin might provide an important clue for exploring potential targets for novel therapeutics of Cd-induced neurotoxicity. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a persistent environmental toxin and occupational pollutant that is considered to be a potential risk factor in the development of neurodegenerative diseases. Abnormal mitochondrial dynamics are increasingly implicated in mitochondrial damage in various neurological pathologies. The aim of this study was to investigate whether the disturbance of mitochondrial dynamics contributed to Cd-induced neurotoxicity and whether melatonin has any neuroprotective properties. After cortical neurons were exposed to 10 μM cadmium chloride (CdCl2) for various periods (0, 3, 6, 12, and 24 hr), the morphology of their mitochondria significantly changed from the normal tubular networks into punctuated structures within 3 hr. Following this pronounced mitochondrial fragmentation, Cd treatment led to signs of mitochondrial dysfunction, including excess reactive oxygen species ( ROS) production, decreased ATP content, and mitochondrial membrane potential (▵Ψm) loss. However, 1 mM melatonin pretreatment efficiently attenuated the Cd-induced mitochondrial fragmentation, which improved the turnover of mitochondrial function. In the brain tissues of rats that were intraperitoneally given 1 mg/kg CdCl2 for 7 days, melatonin also ameliorated excessive mitochondrial fragmentation and mitochondrial damage in vivo. Melatonin's protective effects were attributed to its roles in preventing cytosolic calcium ([Ca2+]i) overload, which blocked the recruitment of Drp1 from the cytoplasm to the mitochondria. Taken together, our results are the first to demonstrate that abnormal mitochondrial dynamics is involved in cadmium-induced neurotoxicity. Melatonin has significant pharmacological potential in protecting against the neurotoxicity of Cd by blocking the disbalance of mitochondrial fusion and fission. [ABSTRACT FROM AUTHOR]

In real options models, investment can increase under some conditions when interest rates rise. This research tests for these positive interest rate responses in the context of the Capozza-Li model of land development. In the model variable capital intensity is a sufficient condition for positive responses to interest rates that can occur when growth rates are high or uncertainty is high. The empirical analysis uses a panel data set on residential investment in the 1980s and finds that 25-50% of the sample lies in the positive response region. [ABSTRACT FROM AUTHOR]

Chemical equations are presented for article "Regioselective BF3.Et2O-Catalyzed C-H Functionalization of Indoles and Pyrrole with Reaction of α-Diazophosphonates. " by Y. Cai and colleagues which was published in periodical "Royal Society of Chemistry (RSC) Advances."

Background Autoantibodies against the second extracellular loop of the β 1 -adrenoceptor (β 1 - AA ) act similarly to agonist of β 1 -adrenergic receptor, which plays an important role in the pathophysiological characteristics of ventricular remodeling. Recently, considerable lines of evidence have suggested that CTRP9 (C1q tumor necrosis factor-related protein 9) is a potent cardioprotective cardiokine and protects the heart from ventricular remodeling. The aim of this study was to determine the role of CTRP 9 in ventricular remodeling induced by β 1 - AA . Methods and Results Blood samples were collected from 131 patients with coronary heart disease and 131 healthy subjects. The serum levels of β 1 - AA and CTRP 9 were detected using ELISA . The results revealed that CTRP 9 levels in β 1 - AA -positive patients were lower than those in β 1 - AA -negative patients, and serum CTRP 9 concentrations were inversely correlated with β 1 - AA . β 1 - AA monoclonal antibodies (β 1 - AA mAbs) were administered in mice with and without rAAV 9- cTnT -Full Ctrp9- FLAG virus for 8 weeks. Reverse transcription-polymerase chain reaction/Western analysis showed that cardiomyocyte CTRP 9 expression was significantly reduced in β 1 - AA mAb-treated mice. Moreover, compared with the β 1 - AA mAb alone group, cardiac-specific CTRP 9 overexpression improved cardiac function, attenuated adverse remodeling, and ameliorated cardiomyocyte apoptosis and fibrosis. Mechanistic studies demonstrated that CTRP 9 overexpression decreased the levels of G-protein-coupled receptor kinase 2 and promoted the activation of AMP-dependent kinase pathway. However, cardiac-specific overexpression of CTRP 9 had no effect on the levels of  cAMP and protein kinase A activity elevated by β 1 -AAmAb. Conclusions This study provides the first evidence that the long-term existence of β 1 - AA mAb suppresses cardiac CTRP 9 expression and exaggerates cardiac remodeling, suggesting that CTRP 9 may be a novel therapeutic target against pathologic remodeling in β 1 - AA -positive patients with coronary heart disease.