Exploring the impact of the COVID-19 epidemic on the medical emergency calls and calls for cardiovascular diseases in Hangzhou, China.

AIMS: We aimed to evaluate the impact of the COVID-19 epidemic on emergency and cardiovascular disease-related calls in Hangzhou, China. METHODS: We conducted a single-center retrospective study, collecting data on emergency calls to the Hangzhou Emergency Center (HEC) during the COVID-19 epidemic (January 20, 2020, to March 15, 2020). Data were compared with the same period in 2019. RESULTS: Compared to 2019, the number of emergency calls has dropped by 21.63%, ambulance calls by 29.02%, rescue calls by 22.57%, and cardiovascular disease-related emergency calls by 32.86%. The numbers of emergency, ambulance, and rescue calls in 2020 were significantly lower than in 2019. CONCLUSIONS: During the COVID-19 epidemic in Hangzhou, the numbers of emergency and cardiovascular disease-related calls have decreased significantly. These results point to a severe social problem that requires the attention of the medical community and the government.

Isofraxidin Alleviates Myocardial Infarction Through NLRP3 Inflammasome Inhibition.

Isofraxidin is a well-known coumarin compound refined from traditional Chinese medicines. It has been previously demonstrated to play an anti-inflammatory role in various inflammatory conditions. However, the effect of isofraxidin on myocardial infarction (MI) remains uncovered. In this study, we aimed to investigate the effect of isofraxidin on MI. MI mice was created and triphenyltetrazolium chloride (TTC) staining as well as echocardiographic evaluation were conducted to analyze the severity of MI. Oxygen-glucose deprivation (OGD) was used for the mimics of ischemic stress in murine cardiomyocytes, and Cell Counting Kit-8 (CCK-8), Annexin V, and lactate dehydrogenase (LDH) release assays were conducted for cell viability. Western blot was used for the detection of NOD-like receptor family, pyrin domain containing 3 (NLRP3), and adapter protein apoptosis-associated speck-like protein (ASC) in heart tissues and cardiomyocytes. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) were applied for the detection of proinflammatory cytokines. We found that isofraxidin alleviated the severity of MI and produced a cardio-protective effect against OGD damage. Isofraxidin also decreased the overall and local inflammatory reaction in MI. Those effects were through the inhibition of the NLRP3 inflammasome. Taken together, we initially reported the cardio-protective and alleviative effect of isofraxidin on MI and uncovered its underlying mechanism related to the NLRP3 inflammasome inhibition.

Association between TGF-ß1 -913G/C polymorphism and myocardial infarction risk in a Chinese Han population: a case-control study.

Transforming growth factor (TGF)-ß1 contributed to angiotensin II (Ang II)-mediated collagen accumulation after myocardial infarction (MI). The present study aimed to investigate the association of genetic variant of TGF-ß1 gene with the risk of MI. The present study recruited a total of 530 MI patients and 651 healthy controls. The genomic DNA was extracted and subjected into polymerase chain reaction (PCR) and Sanger sequencing. The present study indicated that TGF-ß1 -913G/C polymorphism was associated with increased risk for MI under the co-dominant, dominant and allelic models. The increased risk effect was also evident among the females, younger subjects (age < 60 years), smokers, non-drinkers and individuals with hypertension. Additionally, the present study observed significant differences among cases and controls in terms of total cholesterol (TC). In conclusion, TGF-ß1 -913G/C polymorphism is associated with increased risk for MI. TGF-ß1 -913G/C polymorphism may be a potential prognostic biomarker for MI.

Gr-1⁺CD11b⁺ immature myeloid cells (IMC) promote resistance of pro-inflammatory T cells to suppression by regulatory T cells in atherosclerotic Apo E- deficient mice.

Accumulating evidence indicates that both defects in Treg numbers and/or function as well as resistance of effector T cells to suppression may contribute to the development of human chronic inflammatory diseases. However, which mechanism involved in the progression of atherosclerosis remains unclear. In this study, we evaluated the production and function of CD4⁺ inflammatory and regulatory T cells in atherosclerosis-prone mice. We found that the hyperactivity and unresponsiveness to Treg-mediated suppression of inflammatory CD4⁺ T cells occurred in the progression of atherosclerosis, though Treg cells were present in very large numbers and fully functional. We further found that Gr-1⁺CD11b⁺ immature myeloid cells were significantly accumulated in atherosclerotic Apo E⁻/⁻ mice, and they promoted resistance of inflammatory CD4⁺ T cells to Treg-mediated suppression in vitro and in vivo. we further confirmed that Gr-1⁺CD11b⁺ immature myeloid cells produced high level of interleukin 6 which was at least partially responsible for inducing unresponsiveness of inflammatory CD4⁺ T cells to suppression via activation of Jak/Stat signaling pathway. Taken together, these findings might provide new insights to explore potential targets for immune therapeutic intervention in atherosclerosis.

[Role of the Th17/Treg functional imbalance on the development of atherosclerosis in apo E knockout mice].

OBJECTIVE: To investigate the role of the helper T cells (Th) 17/Treg cell imbalance on the development of atherogenesis in apo E knockout mice. METHODS: Apo E(-/-) mice were examined at age of 6, 12, 24 and 48 weeks (n = 10 each). Age matched C57/B6 mice served as controls. The number of Th17, Treg and dendritic cell (DC) was detected by flow cytometry. The levels of interleukin(IL)-6, IL-17A and transforming growth factor(TGF)-ß1 were detected by ELISA. The suppression ability of Treg was evaluated by mixed lymphocyte reaction. RESULTS: With increasing ages, the frequencies of Th17 and Treg in CD4(+) T cells were increased (Th17 ratio from 1.00% to 3.14%; Treg ratio from 8.08% to 27.80%) and the level of IL-17A was up-regulated [from (87 ± 15) pg/ml to (191 ± 26) pg/ml], but the rate of Th17/Treg cell and the level of TGF-ß1 remained stable during atherogenesis in apo E knockout mice. Furthermore, the phenotype of splenic DC was matured and the blood level of IL-6 was up-regulated [from (43 ± 5) pg/ml to (104 ± 11) pg/ml] with aging in apo E(-/-) mice. Addition of IL-6 to T cells reversed the ability of Treg to suppress the proliferation of effective T cells. CONCLUSION: DC overactivation, subsequent increased secretion of IL-6, inhibition of Treg cell function and the Th17/Treg cell imbalance play key roles on the atherogenesis in apo E(-/-) mice.