Quasi-10-day waves in temperature and polar mesospheric clouds: Results of AIM/SOFIE and Aura/MLS observations.

Planetary waves, including quasi-2, -5, -10, -16-day waves, play significant roles in stratospheric dynamics. However, the existing knowledge on quasi-10-day waves (Q10DWs) at high latitudes is limited. This paper investigated the interannual and seasonal variations of Q10DWs with zonal wave numbers varying from the -3 (westward propagation) to 3 (eastward propagation) modes from 2008 to 2022, using temperature data measured by the Microwave Limb Sounder instrument (316-0.001 hPa, corresponding to an altitude of approximately 8-97 km) and temperature/ice water content data measured by the Solar Occultation for Ice Experiment (SOFIE) instrument (10-100 km at latitudes >55°). The findings revealed that the amplitude of Q10DWs in winter was higher than that in other seasons. The amplitude of Q10DWs was observed to substantially decrease with an increase in wavenumber. In addition, the amplitude of stationary Q10DWs in the northern polar region exceeded that in the southern polar region. Moreover, we used observational data from the SOFIE instrument, which simultaneously measures temperature and ice water content (IWC) in the mesosphere, to examine the variations of Q10DWs with respect to the temperature and IWC. Our findings suggest that in the northern polar region, the maximum value of Q10DWs in IWC was occasionally observed earlier than the lowest value of Q10DWs in temperatures.

Shexiang Tongxin Dropping Pill alleviates M1 macrophage polarization-induced inflammation and endothelial dysfunction to reduce coronary microvascular dysfunction via the Dectin-1/Syk/IRF5 pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Shexiang Tongxin Dropping Pill (STDP), a traditional Chinese medicine compound, is fragrant, invigorates the qi, unblocks pulses, activates the blood circulation, removes blood stasis, and relieves pain. It is used clinically to treat coronary heart disease and angina pectoris. Coronary microvascular dysfunction (CMD) is associated with increased morbidity and mortality from cardiovascular events. Endothelial dysfunction and inflammation have been verified as its underlying causes. STDP can ameliorate CMD, but the mechanism has not been fully elucidated. AIM OF THE STUDY: To explore the effects of STDP on M1 macrophage polarization-induced inflammation and endothelial dysfunction as an inhibitor of CMD, and to determine its mechanisms of action. MATERIALS AND METHODS: The CMD rat model was established by left anterior descending artery (LAD) ligation. The efficacy of STDP against CMD was evaluated by echocardiography, optical microangiography, Evans blue staining, and histological examination. The OGD/R-induced endothelial injury model, the endothelial injury-induced sterile inflammation model, the Dectin-1 overexpression model, and the Dectin-1-overexpressing RAW264.7 macrophage supernatant-stimulated HUVEC-induced secondary injury of endothelial function model were established to confirm the efficacy of STDP against M1 macrophage polarization-induced inflammation and endothelial dysfunction. RESULTS: STDP blunted the deterioration of cardiac function and ameliorated CMD by reducing inflammatory cell infiltration and endothelial dysfunction in CMD rats. Endothelial injury and Dectin-1 overexpression induced M1 macrophage polarization and inflammation. Mechanically, STDP hindered M1 macrophage polarization and inflammation by inhibiting the Dectin-1/Syk/IRF5 pathway both in vivo and in vitro. STDP alleviated endothelial dysfunction induced by Dectin-1 overexpression in macrophages. CONCLUSION: STDP can alleviate M1 macrophage polarization-induced inflammation and endothelial dysfunction against CMD via the Dectin-1/Syk/IRF5 pathway. Dectin-1-associated M1 macrophage polarization might be developed as a novel target for ameliorating CMD.

Transcriptional regulation of macrophages in heart failure.

Adverse cardiac remodeling after acute myocardial infarction is the most important pathological mechanism of heart failure and remains a major problem in clinical practice. Cardiac macrophages, derived from tissue resident macrophages and circulating monocyte, undergo significant phenotypic and functional changes following cardiac injury and play crucial roles in inflammatory response and tissue repair response. Currently, numerous studies indicate that epigenetic regulatory factors and transcription factors can regulate the transcription of inflammatory and reparative genes and timely conversion of inflammatory macrophages into reparative macrophages and then alleviate cardiac remodeling. Accordingly, targeting transcriptional regulation of macrophages may be a promising option for heart failure treatment. In this review, we not only summarize the origin and function of cardiac macrophages, but more importantly, describe the transcriptional regulation of macrophages in heart failure, aiming to provide a potential therapeutic target for heart failure.