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Aims: Left ventricular (LV) remodelling after acute myocardial infarction (AMI) is associated with heart failure and increased mortality. There was no consensus on the definition of LV remodelling, and the prognostic value of LV remodelling with different definitions has not been compared. We aimed to find the optimal definition and develop a prediction nomogram as well as online calculator that can identify patients at risk of LV remodelling. Methods and results: This prospective, observational study included 829 AMI patients undergoing percutaneous coronary intervention from January 2015 to January 2020. Echocardiography was performed within the 48 h of admission and at 6 months after infarction to evaluate LV remodelling, defined as a 20% increase in LV end‐diastolic volume (LVEDV), a 15% increase in LV end‐systolic volume (LVESV), or LV ejection fraction (LVEF) < 50% at 6 months. The impact of LV remodelling on long‐term outcomes was analysed. Lasso regression was performed to screen potential predictors, and multivariable logistic regression analysis was conducted to establish the prediction nomogram. The area under the curve, calibration curve and decision curve analyses were used to determine the discrimination, calibration and clinical usefulness of the remodelling nomogram. The incidences of LV remodelling defined by LVEDV, LVESV and LVEF were 24.85% (n = 206), 28.71% (n = 238) and 14.60% (n = 121), respectively. Multivariable Cox regression models demonstrated that different definitions of LV remodelling were independently associated with the composite endpoint. However, only remodelling defined by LVEF was significantly connected with long‐term mortality (hazard ratio = 2.78, 95% confidence interval 1.41–5.48, P = 0.003). Seven variables were selected to construct the remodelling nomogram, including diastolic blood pressure, heart rate, AMI type, stent length, N‐terminal pro brain natriuretic peptide, troponin I, and glucose. The prediction model had an area under the receiver operating characteristics curve of 0.766. The calibration curve and decision curve analysis indicated consistency and better net benefit in the prediction model. Conclusions: LV remodelling defined by LVEDV, LVESV and LVEF were independent predictors for long‐term mortality or heart failure hospitalization in AMI patients after percutaneous coronary intervention. However, only remodelling defined by LVEF was suitable for predicting all‐cause death. In addition, the nomogram can provide an accurate and effective tool for the prediction of postinfarct remodelling. [ABSTRACT FROM AUTHOR]

Soil salinity impairs plant growth reducing crop productivity. Toxic accumulation of sodium ions is counteracted by the Salt Overly Sensitive (SOS) pathway for Na+ extrusion, comprising the Na+ transporter SOS1, the kinase SOS2, and SOS3 as one of several Calcineurin‐B‐like (CBL) Ca2+ sensors. Here, we report that the receptor‐like kinase GSO1/SGN3 activates SOS2, independently of SOS3 binding, by physical interaction and phosphorylation at Thr16. Loss of GSO1 function renders plants salt sensitive and GSO1 is both sufficient and required for activating the SOS2‐SOS1 module in yeast and in planta. Salt stress causes the accumulation of GSO1 in two specific and spatially defined areas of the root tip: in the endodermis section undergoing Casparian strip (CS) formation, where it reinforces the CIF‐GSO1‐SGN1 axis for CS barrier formation; and in the meristem, where it creates the GSO1‐SOS2‐SOS1 axis for Na+ detoxification. Thus, GSO1 simultaneously prevents Na+ both from diffusing into the vasculature, and from poisoning unprotected stem cells in the meristem. By protecting the meristem, receptor‐like kinase‐conferred activation of the SOS2‐SOS1 module allows root growth to be maintained in adverse environments. Synopsis: Salt extrusion through the SOS (salt overly sensitive) pathway is essential for plant salt tolerance. This study identifies the receptor‐like kinase GSO1 as a direct activator of the protective SOS2‐SOS1 module that promotes cellular Na+ extrusion from the meristem to maintain root growth. The receptor‐like kinase mutant gso1 is hypersensitive to salt stress.GSO1 expression is strongly upregulated in the meristem under salt stress.GSO1 phosphorylates SOS2 at T16 to activate the SOS2‐SOS1 module for salt extrusion.The GSO1‐SOS2‐SOS1 axis promotes salt extrusion for meristem protection. [ABSTRACT FROM AUTHOR]