Corresponding to the pronounced amplitude asymmetry for the central Pacific (CP) and eastern Pacific (EP) types of El Niño, an asymmetry in the strength of the Bjerknes positive feedback is found between these two types of El Niño, which is manifested as a weaker relationship between the zonal wind anomaly and the zonal gradient of sea surface temperature (SST) anomaly in the CP El Niño. The strength asymmetry mainly comes from a weaker sensitivity of the zonal gradient of sea level pressure (SLP) anomaly to that of diabatic heating anomaly during CP El Niño. This weaker sensitivity is caused by (1) a large cancelation induced by the negative SST-cloud thermodynamic feedback to the positive dynamical feedback for CP El Niño, (2) an off-equator shift of the maximum SLP anomalies during CP El Niño, and (3) a suppression of the mean low-level convergence when CP El Niño events occur more often. Key Points Asymmetry of the Bjerknes positive feedback exits between the CP and EP El NiñosThe strength of the Bjerknes positive feedback acts to induce the ENSO diversityThe asymmetry is caused by a different response of zonal SLP to diabatic heating

Clear decadal variations exist in the predictability of the El Niño–Southern Oscillation (ENSO), with the most recent decade having the lowest ENSO predictability in the past six decades. The Bjerknes Feedback (BF) intensity, which dominates the development of ENSO, has been proposed to determine ENSO predictability. Here we demonstrate that decadal variations in BF intensity are largely a result of the sensitivity of the zonal winds to the zonal sea level pressure (SLP) gradient in the equatorial Pacific. Furthermore, the results show that during low-ENSO predictability decades, zonal wind anomalies over the equatorial Pacific are more linked to SLP variations in the off-equatorial Pacific, which can then transfer this information into surface temperature and precipitation fields through the BF, suggesting a weakening in the ocean-atmosphere coupling in the tropical Pacific. This result indicates that more attention should be paid to off-equatorial processes in the prediction of ENSO.

Epoxyeicosatrienoic acids (EETs), the metabolites of arachidonic acid derived from the cytochrome P450 (CYP450) epoxygenases, are mainly metabolized by soluble epoxide hydrolase (sEH) to their corresponding diols. EETs but not their diols, have anti-inflammatory properties and inhibition of sEH might provide protective effects against inflammatory fibrosis. We test the effects of a selected sEH inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), on bleomycin-induced pulmonary fibrosis (PF) in mice. A mouse model of PF was established by intratracheal injection of bleomycin and TPPU was administered for 21 days after bleomycin injection. We found TPPU treatment improved the body weight loss and survival rate of bleomycin-stimulated mice. Histological examination showed that TPPU treatment alleviated bleomycin-induced inflammation and maintained the alveolar structure of the pulmonary tissues. TPPU also decreased the bleomycin-induced deposition of collagen and the expression of procollagen I mRNA in lung tissues of mice. TPPU decreased the transforming growth factor-β1 (TGF-β1), interleukin-1β (IL-1β) and IL-6 levels in the serum of bleomycin-stimulated mice. Furthermore, TPPU inhibited the proliferation and collagen synthesis of mouse fibroblasts and partially reversed TGF-β1-induced α-smooth muscle actin expression. Our results indicate that the inhibition of sEH attenuates bleomycin-induced inflammation and collagen deposition and therefore prevents bleomycin-induced PF in a mouse model.