Alleviation by abscisic acid of Al toxicity in rice bean is not associated with citrate efflux but depends on ABI5-mediated signal transduction pathways.

Under conditions of aluminum (Al) toxicity, which severely inhibits root growth in acidic soils, plants rapidly alter their gene expression to optimize physiological fitness for survival. Abscisic acid (ABA) has been suggested as a mediator between Al stress and gene expression, but the underlying mechanisms remain largely unknown. Here, we investigated ABA-mediated Al-stress responses, using integrated physiological and molecular biology approaches. We demonstrate that Al stress caused ABA accumulation in the root apex of rice bean (Vigna umbellata [Thunb.] Ohwi & Ohashi), which positively regulated Al tolerance. However, this was not associated with known Al-tolerance mechanisms. Transcriptomic analysis revealed that nearly one-third of the responsive genes were shared between the Al-stress and ABA treatments. We further identified a transcription factor, ABI5, as being positively involved in Al tolerance. Arabidopsis abi5 mutants displayed increased sensitivity to Al, which was not related to the regulation of AtALMT1 and AtMATE expression. Functional categorization of ABI5-mediated genes revealed the importance of cell wall modification and osmoregulation in Al tolerance, a finding supported by osmotic stress treatment on Al tolerance. Our results suggest that ABA signal transduction pathways provide an additional layer of regulatory control over Al tolerance in plants.

Interleukin-18 levels on admission are associated with mid-term adverse clinical events in patients with ST-segment elevation acute myocardial infarction undergoing percutaneous coronary intervention.

The long-term prognostic value of interleukin (IL)-18 in patients with ST-segment elevation acute myocardial infarction (STEMI) has been conflicting. Thus, the purpose of this study was to test whether the level of interleukin-18 measured on admission can predict long-term adverse clinical events in patients with STEMI who were undergoing percutaneous coronary intervention (PCI). We recruited 288 consecutive STEMI patients (210 men, average age [71.42 +/- 10.32] years) with onset < 6 hours who were undergoing primary PCI, and 148 age- and gender-matched control subjects. Plasma levels of IL-18 were measured by enzyme-linked immunosorbent assay (ELISA) in all subjects. The patients with STEMI were then followed prospectively over 434 days (range, 0 to 642 days) for the occurrence of composite major adverse clinical events (MACE) (cardiac mortality, recurrent myocardial infarction, or readmission due to advanced heart failure). Patients with STEMI exhibited higher levels of plasma IL-18 (P < 0.001) compared with the control subjects. Positive correlations between IL-18 and cardiac troponin-I (cTnI) (r = 0.353, P = 0.0004) and IL-18 and high-sensitivity C-reactive protein (hs-CRP) (r = 0.420, P < 0.001) were observed by Spearman's correlations analysis. Logistic regression analysis demonstrated that IL-18 >/= 450 pg/mL (OR 10.854, 95% CI 2.328 to 50.594, P < 0.0001) was a significant independent predictor of composite MACE at 60 days. Cox regression analysis demonstrated that high plasma IL-18 levels were not correlated with the occurrence of long-term composite MACE. The level of plasma IL-18 on admission may predict 60-day adverse clinical outcome, but not the long-term adverse clinical events in patients with STEMI undergoing PCI, and may be useful for mid-term risk stratification.

[Changes of serum hepatocyte growth factor before and after percutaneous coronary intervention in patients with unstable angina pectoris and significance there].

OBJECTIVE: To investigate the effect of unfitrate heparin (UFH) and low molecular weight heparin (LMWH) on the expression of serum hepatocyte growth factor (HGF) during percutaneous coronary intervention (PCI). METHODS: Seventy patients with chronic unstable angina pectoris were divided into 2 groups: PCI group (n = 49, with at least one main coronary artery branch with stenosis > or = 70%) and non-PCI group (n = 21, with the main coronary artery branch with stenosis < 70%). UFH was used at the beginning of coronary angiography in both groups and LMWH was used after PCI only in the PCI group. The serum level of HGF was measured before, during, and 1 and 7 days after PCI; and cardiac troponin 1 (cTnI) was measured before and 1 day after PCI in all 70 patients. RESULTS: The serum level of HGF of the PCI group increased during and immediately after PCI (12 322 +/- 3723 ng/L and 13 566 +/- 3767 ng/L respectively), both significantly higher than that before the procedure (1736 +/- 604 ng/L, both P < 0.0001), The serum level of HGF of the non-PCI group increased during and immediately after the procedure (10 928 +/- 2196 ng/L and 11 457 +/- 2298 ng/L respectively), both significantly higher than that before the procedure (967 +/- 349 ng/L, both P < 0.01). However, there were no significant differences in the HGF levels during and after the procedure between the PCI and non-PCI groups. The serum HGF returned to the normal level 24 h after the procedure in both groups. The serum GHF 7 days after the procedure of the cTnI (-) PCI group was significantly lower than that before the procedure (P < 0.01), however, the serum GHF 7 days after the procedure of the cTnI (+) PCI group remained relatively high, not significantly different from that before the procedure. CONCLUSION: There is an enhanced secretion of cardiac HGF in the patients with severe coronary artery disease. UFH promotes the release of serum HGF in the patients with chronic unstable angina pectoris undergoing PCI, which indicates some other biological effects in addition to its anticoagulant property. The delayed fall of serum HGF after PCI has relationship with minor myocardial infarction.