eIF3a is a N ⁶-methyladenosine (m⁶A) reader that regulates mRNA translation by recognizing m⁶A modifications of these mRNAs. It has been suggested that eIF3a may play an important role in regulating translation initiation via m⁶A during infection when canonical cap-dependent initiation is inhibited. However, the death of animal model studies impedes our understanding of the functional significance of eIF3a in immunity and regulation in vivo. In this study, we investigated the in vivo function of eIF3a using eIF3a knockout and knockdown mouse models and found that eIF3a deficiency resulted in splenic tissue structural disruption and multi-organ damage, which contributed to severe sepsis induced by Lipopolysaccharide (LPS). Ectopic eIF3a overexpression in the eIF3a knockdown mice rescued mice from LPS-induced severe sepsis. We further showed that eIF3a maintains a functional and healthy immune system by regulating B cell function and quantity through m⁶A modification of mRNAs. These findings unveil a novel mechanism underlying sepsis, implicating the pivotal role of B cells in this complex disease process regulated by eIF3a. Furthermore, eIF3a may be used to develop a potential strategy for treating sepsis.

Objective To determine whether the 12-lead-resting electrocardiogram(ECG) is a predictor of left vertricular(LV) recovery after successful recanalization of chronic total coronary occlusions(CTO).Methods The 12-lead-resting ECG was evaluated for Q-wave areas and parameters of QT dispersion.Impairment of regional wall motion was evaluated by real-time three-dimensional echocardiography(RT-3DE) at baseline and at follow-up.Results The wall motion score index(WMSI) was improved from 1.56?0.31 to 1.12?0.21(P0.05).Conclusion In patients with recanalization of CTO,recovery of regional wall motion is reliably predicted by analysis of the12-lead-resting ECG.