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Aim: Cardiac arrhythmias are among the most important pathologies that cause sudden death. The exploration of new therapeutic options against arrhythmias with low undesirable effects is of paramount importance. Methods: However, the convenient and typical animal model for screening the potential lead compound becomes a very critical modality, particularly in anti-arrhythmia. In this study, mice were intraperitoneally (i.p.) injected with BaCl2, CaCl2, and adrenaline to induce arrhythmia, and simultaneously compared with BaCl2-induced rats. Results: Electrocardiogram (ECG) showed that the majority of mice repeatedly developed ventricular bigeminy, ventricular tachycardia (VT), and ventricular fibrillation (VF) after BaCl2-injection as seen in rats. The ECG of mice developed ventricular bigeminy and VT after CaCl2 and AT after adrenaline i.p. injection. Additionally, acute cardiac arrhythmia after BaCl2 i.p. injection could be reverted by drugs (lidocaine and amiodarone) administration. Additionally, the different routes of administration for various chemical-induced arrhythmia in both mice and rats were also retrieved from PubMed and summarized. Comparing this approach with previous studies after the literature review reveals that arrhythmia of BaCl2-induced i.p. mice is compatible with the induction of other routes. Conclusions: This study brings an alternative experimental model to investigate antiarrhythmic theories and provides a promising approach to discovering new interventions for acute arrhythmias. [ABSTRACT FROM AUTHOR]

AbstractObjectiveMaterials and methodsResultsConclusionsPM2.5 is closely linked to vascular endothelial injury and has emerged as a major threat to human health. Our previous research indicated that exposure to PM2.5 induced an increased release of miR-421 from the bronchial epithelium. However, the role of miR-421 in PM2.5-induced endothelial injury remains elusive.We utilized a subacute PM2.5-exposure model in mice in vivo and an acute injury cell model in vitro to simulate PM2.5-associated endothelial injury. We also used quantitative real-time polymerase chain reaction, western blot, enzyme-linked immunosorbent assay, and immunohistochemistry to investigate the role of miR-421 in PM2.5-induced endothelial injury.Our findings reveal that inhibition of miR-421 attenuated PM2.5-induced endothelial injury and hypertension. Mechanistically, miR-421 inhibited the expression of angiotensin-converting enzyme 2 (ACE2) in human umbilical vein endothelial cells and upregulated the expression of the downstream molecule inducible nitric oxide synthase (iNOS), thereby exacerbating PM2.5-induced endothelial injury.Our results indicate that PM2.5 exposure facilitates crosstalk between bronchial epithelial and endothelial cells via miR-421/ACE2/iNOS signaling pathway, mediating endothelial damage and hypertension. MiR-421 inhibition may offer a new strategy for the prevention and treatment of PM2.5-induced vascular endothelial injury. [ABSTRACT FROM AUTHOR]

Objective: PM 2.5 is closely linked to vascular endothelial injury and has emerged as a major threat to human health. Our previous research indicated that exposure to PM 2.5 induced an increased release of miR-421 from the bronchial epithelium. However, the role of miR-421 in PM 2.5 -induced endothelial injury remains elusive., Materials and Methods: We utilized a subacute PM 2.5 -exposure model in mice in vivo and an acute injury cell model in vitro to simulate PM 2.5 -associated endothelial injury. We also used quantitative real-time polymerase chain reaction, western blot, enzyme-linked immunosorbent assay, and immunohistochemistry to investigate the role of miR-421 in PM 2.5 -induced endothelial injury., Results: Our findings reveal that inhibition of miR-421 attenuated PM 2.5 -induced endothelial injury and hypertension. Mechanistically, miR-421 inhibited the expression of angiotensin-converting enzyme 2 (ACE2 ) in human umbilical vein endothelial cells and upregulated the expression of the downstream molecule inducible nitric oxide synthase (iNOS) , thereby exacerbating PM 2.5 -induced endothelial injury., Conclusions: Our results indicate that PM 2.5 exposure facilitates crosstalk between bronchial epithelial and endothelial cells via miR-421 / ACE2 / iNOS signaling pathway, mediating endothelial damage and hypertension. MiR-421 inhibition may offer a new strategy for the prevention and treatment of PM 2.5 -induced vascular endothelial injury.

Background and Objective: Research on allergic rhinitis (AR) immunotherapy has increased in recent decades. This study conducted a bibliometric and visualization analysis of studies related to AR immunotherapy to identify research trends and highlight current research foci., Methods: Relevant original publications were obtained from the Science Citation Index-Expanded and Social Sciences Citation Index in the Web of Science Core Collection databases between 2002 and 2021. CiteSpace and VOSviewer software were used to identify and analyze the research foci and emerging trends in the field of AR immunotherapy., Results: Over the last two decades, the number of publications related to AR immunotherapy has increased markedly. With regard to publications and access to collaborative networks, the leading country was the USA. Inspection of keyword bursts suggested that "subcutaneous immunotherapy", "quality of life", "prevalence", "rhino-conjunctivitis", and "mechanism" are emerging research hotspots. The timeline of the co-cited references cluster diagram revealed that the mechanism of allergen immunotherapy has emerged as a main topic in AR immunotherapy., Conclusion: Over the past 20 years, scholars have significantly improved their understanding of AR immunotherapy. The current research hotspots of AR immunotherapy in the health promotion domain lie in "subcutaneous immunotherapy", "quality of life", and "rhino-conjunctivitis". In addition, the mechanism of allergen immunotherapy has emerged as a frontier and focus of this field., Competing Interests: None., (AJTR Copyright © 2022.)