FUEL
·
2024
·
IF 6.7
Zongyang Zhang,Yuping Li,Ze Chen,Fuchao Ji,Xiaohong Liang,Haicheng Xuan,Lina Han,Peide Han
Developing an economical and high-efficiency synthesis pathway of SSZ-13 zeolite is of great significance for the ammonia selective catalytic reduction of nitrogen oxides (NH 3 -SCR of NO x ) reactions. Herein, SSZ-13 zeolite were synthesized using L zeolite as the aluminum source in the presence of a mixed structure directing agent (SDA) composed of N,N,N, trimethtyl-1-adamantammonium hydroxide (TMAdaOH) and tetraethylammonium hydroxide (TEAOH). This synthesis strategy aims to accelerate the crystallization rate through interzeolite transformation, while less expensive TEAOH can play a cooperative structure-directing role, thus reducing the consumption of expensive TMAdaOH template. The results showed that pure SSZ-13 zeolites with high crystallinity can be obtained from L zeolite within 12 h at 160 ℃ under low TMAdaOH/SiO 2 ratio of 0.05 (too low to carry out the synthesis on its own in the current synthesis system) in the presence of TEAOH. Moreover, the crystallization mechanism was also investigated by XRD, FT-IR, SEM and TG-DTG techniques. It was proposed that the crystallization of SSZ-13 occurs through the formation of SSZ-13 nuclei under the direction of TMAdaOH and promotion of TEAOH, subsequently TMAdaOH was incorporated in the framework to further induce the crystal growth of SSZ-13. Especially, the zeolite crystal size can be modulated by the amount of TEAOH added. In addition, After Cu 2+ exchange, the obtained Cu-SSZ-13 sample exhibits superior catalysis performance in the NH 3 -SCR of NO x reaction, and the NO x conversion rate remained over 90 % across a broad range from 200 to 600 °C, demonstrating its significant application potentials in NO x removal from diesel vehicle exhausts.
研究领域:
材料科学
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环境科学
·
催化化学
✓ 已验证
DOI
高影响因子
BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES
·
2017
·
IF 3.498
Zhuo Fan,Nanying Lv,Xiao Luo,Wen Tan
Cardiac hypertrophy is a thickening of the heart muscle that is associated with cardiovascular diseases such as hypertension and myocardial infarction. It occurs initially as an adaptive process against increased workloads and often leads to sudden arrhythmic deaths. Studies suggest that the lethal arrhythmia is attributed to hypertrophy-induced destabilization of cardiac electrical activity, especially the prolongation of the action potential. The reduced activity of I to is demonstrated to be responsible for the ionic mechanism of prolonged action potential duration and arrhythmogeneity. Isosteviol (STV), a derivative of stevioside, plays a protective role in a variety of stress-induced cardiac diseases. Here we report effects of STV on rat ISO-induced hypertrophic cardiomyocytes. STV alleviated ISO-induced hypertrophy of cardiomyocytes by decreasing cell area of hypertrophied cardiomyocytes. STV application prevented the prolongation of action potential which was prominent in hypertrophied cells. The decrease and increase of current densities for I to and I CaL observed in hypertrophied myocytes were both prevented by STV application. In addition, the results of qRT-PCR suggested that the changes of electrophysiological activity of I to and I CaL are correlated to the alterations of the mRNA transcription level.
研究领域:
药理学
·
心血管病学
✓ 已验证
DOI
PubMed
高影响因子
Cell Reports Methods
·
2024
·
IF 4.3
Jinli Geng,Yaxiong Yang,Boying Li,Zhen Yu,Shuang Qiu,Wen Zhang,Shixin Gao,Nan Liu,Yi Liu,Bo Wang,Yubo Fan,Chengfen Xing,Xiaodong Liu
Genetically encoded inhibitors of Ca V 1 channels that operate via C-terminus-mediated inhibition (CMI) have been actively pursued. Here, we advance the design of CMI peptides by proposing a membrane-anchoring tag that is sufficient to link the inhibitory modules to the target channel as well as chemical and optogenetic modes of system control. We designed and implemented the constitutive and inducible CMI modules with appropriate dynamic ranges for the short and long variants of Ca V 1.3, both naturally occurring in neurons. Upon optical (near-infrared-responsive nanoparticles) and/or chemical (rapamycin) induction of FRB/FKBP binding, the designed peptides translocated onto the membrane via FRB-Ras, where the physical linkage requirement for CMI could be satisfied. The peptides robustly produced acute, potent, and specific inhibitions on both recombinant and neuronal Ca V 1 activities, including Ca 2+ influx-neuritogenesis coupling. Validated through opto-chemogenetic induction, this prototype demonstrates Ca 2+ channel modulation via membrane-assisted molecular linkage, promising broad applicability to diverse membrane proteins.
研究领域:
神经科学
·
分子生物学
·
生物工程
✓ 已验证
DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2025
·
IF 4.7
Guo-Xuan Liu,Fan Diao,Guang Lu,Qiang Zheng,Bin Fu,Hua-Chen Jiao,Ke-Zhou Wang,Dong-Hai Liu
Alectinib is the first-line therapy for anaplastic lymphoma kinase rearranged non-small cell lung cancer globally. Sinus bradycardia, as the major adverse cardiac events of alectinib, still widely impact patient’s quality of life. However, its underlying mechanism remains elusive. The aim of this study was to reveal the pathogenesis of the alectinib induced sinus bradycardia (AISB) in a rat model, including the electrophysiology alterations and the molecular mechanism. SD rats were administered alectinib (10 mg / kg / day) by gavage for 7 to 10 days to mimic the clinical AISB. 3-days alectinib treatment did not change heart rate and sinus node recovery time (SNRT) as assessed through in vivo electrophysiology study. Also, alectinib didn’t influence automaticity in isolated heart or single sinus node cardiomyocytes, indicating alectinib cannot decrease sinus node function rapidly. The decreased heart rate and prolonged SNRT was found after 7-days alectinib treatment. The inducibility of atrial fibrillation was not affected under the same condition. The RNA-seq assay revealed the transcriptomic alterations in sinus node of alectinib treated rats, and the dysregulation of genes in cardiac function were observed. The decreased expression of L-type calcium channel Cacna1d was confirmed among the channel candidates identified from RNA-seq assay. Subsequently, the patch-clamp test revealed the reduction in the corresponding L-type calcium current density in 7-days alectinib treated rats. These findings revealed that the AISB was caused by the reduction in Cacna1d expression which resulted in the electro-dysfunction mediated by the suppressed I CaL .
研究领域:
肿瘤学
·
心脏病学
·
分子生物学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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