A new cooperative approach for ST-elevation myocardial infarction patients to receive timely and effective percutaneous coronary reperfusion in China.

BACKGROUND: Acute myocardial infarction (AMI) is the most serious type of coronary heart disease. However, less than 30% of these patients have been treated effectively in China. Delayed treatment is a leading cause. This study aimed to evaluate a new regional cooperative model for improving the first medical contact-to-device time and the therapeutic effects on AMI patients. METHODS: A retrospective analysis of 458 ST-elevation myocardial infarction (STEMI) patients was performed. Patients were divided into two groups in terms of before or after the model were implemented. First medical contact-to-device time (FMC2D), Door to device time (D2D), referral time, cardiac functions, mean cost, days of hospitalization, and major adverse cardiac events (MACE) were analyzed. RESULTS: The mean FMC2D time, D2D time and referral time of the model group were significantly lower than the control group. The left ventricular ejection fraction of the model group increased but the left ventricular end-diastolic dimension decreased compared with the control group at 6 months after discharge. These results also showed that mean costs and days of hospitalization were reduced. The MACE rate was reduced in the model group. CONCLUSIONS: These results suggested that the new model decreased the FMC2D time, which could improve the cardiac function and therapeutic effect of STEMI patients as well as decreased the financial burden.

Effects of OX40-OX40L interaction on the nuclear factor of activated T cells c1 in ApoE-deficient mice.

We previously reported the emerging role of OX40-OX40L interaction in inflammation and atherosclerosis. However, the mechanism by which OX40-OX40L interaction contributes to pathogenesis is poorly understood. This study investigated the effects of OX40-OX40L interaction on the nuclear factor of activated T cells c1 (NFATc1) in ApoE(-/-) mice. Atherosclerotic plaque was induced via rapid perivascular carotid collar placement in ApoE(-/-) mice. The expression levels of OX40, OX40L, and NFATc1 in the lymphocytes were measured via real-time polymerase chain reaction and flow cytometry. The presence of NFATc1 in the atherosclerotic plaque was detected via immunohistochemistry, and the level of IL-4 was measured via enzyme-linked immunosorbent assay. The expression level of NFATc1 significantly increased in atherosclerotic lesion and in the leukocytes from the ApoE(-/-) mice. After stimulating OX40-OX40L interaction, the mRNA and protein expression levels of NFATc1 in the lymphocytes significantly increased. Meanwhile, anti-OX40LmAb significantly suppressed the expression of NFATc1 in the leukocytes and substantially elevated the level of IL-4. NFATc1 inhibitor markedly suppressed IL-4 production. This study suggests that OX40-OX40L interaction regulates the expression of NFATc1, which may play a critical role in atherosclerotic plaque formation, and may therefore have implications with pathophysiology of atherosclerosis.

[The effect of CD137-CD137 ligand interaction on the expression of nuclear factor of activated T cells c1 in apolipoprotein E-deficient mice atherosclerotic plaque model].

OBJECTIVE: To investigate the effects of CD137-CD137L interaction on the nuclear factor of activated T cells c1 (NFATc1) in apolipoprotein E knockout (ApoE(-/-)) mice. METHODS: Atherosclerotic plaque model was produced by rapid perivascular carotid collar placement in ApoE(-/-) mice. In vivo, the expression of NFATc1 in mice plaque and lymphocytes was detected by immunohistochemical and flow cytometry, respectively. In vitro, the NFATc1 mRNA and protein expressions in cultured lymphocytes of ApoE(-/-) mice were measured by RT-PCR and flow cytometry, respectively. RESULTS: In vivo, after stimulating CD137-CD137L signal pathway, the expression of NFATc1 was significantly upregulated in the atherosclerotic plaques and lymphocytes. In vitro, the mRNA and protein expressions of NFATc1 in cultured leukocytes of ApoE(-/-) mice were also significantly increased, the maximal effect appeared post 20 µg/ml anti-CD137 mAb-stimulation and reached maximum at 24 h at any concentrations. Anti-CD137L mAb significantly downregulated the mRNA and protein expressions of NFATc1 in lymphocytes of ApoE(-/-) mice, maximal effect appeared at 20 µg/ml anti-CD137L mAb and reached minimum at 24 h. CONCLUSION: CD137-CD137L interactions can modulate the expression of NFATc1 in this ApoE(-/-) mice atherosclerotic plaque model.

[Effect of the costimulatory molecules OX40-OX40 ligand interaction on the expression of NFATc1 in leukocytes of apolipoprotein E-deficient mice].

OBJECTIVE: To investigate the effect of OX40/OX40L interaction on the nuclear factor of activated T cells c1 (NFATc1) in ApoE-/- mice. METHODS: Lymphocytes were prepared from mouse spleens after Collar-treated Surgery, then incubated with a range of agonistic anti-OX40 mAbs and inhibitory anti-OX40L mAb to stimulate or inhibit OX40-OX40L interaction in vitro. The expression of NFATc1 mRNA and protein in lymphocytes of ApoE-/- mice was measured by Real Time PCR and flow cytometry, respectively. RESULTS: (1) After stimulating OX40-OX40L signal pathway, the expression of NFATc1 mRNA and protein in leukocytes of ApoE-/- mice was significantly increased, with maximal effect occurring at 20 µg/ml anti-OX40 mAb-stimulated, and peaked at 24 h at any concentration (P < 0.01). (2) Anti-OX40L mAb significantly suppressed the expression of NFATc1 in leukocytes of ApoE-/- mice, with maximal effect occurring at 20 µg/ml anti-OX40L mAb, and peaked at 24 h (P < 0.001). CONCLUSIONS: OX40-OX40L interaction can regulate the mRNA and protein expressions of NFATc1 in lymphocytes of ApoE-/- mice.