ABSTRACT
Tomato yellow leaf curl virus (TYLCV) is a prominent viral pathogen that adversely affects tomato plants. Effective strategies for mitigating the impact of TYLCV include isolating tomato plants from the whitefly, which is the vector of the virus, and utilizing transgenic lines that are resistant to the virus. In our preliminary investigations, we observed that the use of growth retardants increased the rate of TYLCV infection and intensified the damage to the tomato plants, suggesting a potential involvement of gibberellic acid (GA) in the conferring of resistance to TYLCV. In this study, we employed an infectious clone of TYLCV to inoculate tomato plants, which resulted in leaf curling and growth inhibition. Remarkably, this inoculation also led to the accumulation of GA3 and several other phytohormones. Subsequent treatment with GA3 effectively alleviated the TYLCV-induced leaf curling and growth inhibition, reduced TYLCV abundance in the leaves, enhanced the activity of antioxidant enzymes, and lowered the reactive oxygen species (ROS) levels in the leaves. Conversely, the treatment with PP333 exacerbated TYLCV-induced leaf curling and growth suppression, increased TYLCV abundance, decreased antioxidant enzyme activity, and elevated ROS levels in the leaves. The analysis of the gene expression profiles revealed that GA3 up-regulated the genes associated with disease resistance, such as WRKYs, NACs, MYBs, Cyt P450s, and ERFs, while it down-regulated the DELLA protein, a key agent in GA signaling. In contrast, PP333 induced gene expression changes that were the opposite of those caused by the GA3 treatment. These findings suggest that GA plays an essential role in the tomato's defense response against TYLCV and acts as a positive regulator of ROS scavenging and the expression of resistance-related genes.
ABSTRACT
AIMS: The short-term mortality of heart failure (HF) patients admitted to the intensive care unit (ICU) is reported to be high. This study aims to explore the association between white blood cell-to-haemoglobin ratio (WHR) and 30 day mortality from the admission to the ICU. METHODS AND RESULTS: This retrospective cohort study was performed based on the Medical Information Mart for Intensive Care III (MIMIC-III) database (2001-12) and MIMIC-IV database (2008-19). Covariables were selected using the least absolute shrinkage and selection operator regression. Based on the optimal cutoff point selected using the survminer package, WHR was divided into high-ratio group (≥1.6) and low-ratio group (<1.6). The association between WHR and the risk of 30 day mortality was explored using univariate and multivariable Cox regression models. The area under the receiver operating characteristic curve (AUC) was calculated to evaluate the prediction performance of WHR. A total of 13 702 patients were included. After adjusting the potential covariates, high WHR was associated with a greater risk of 30 day mortality compared with low WHR [hazard ratio = 1.16, 95% confidence interval (CI): 1.07-1.27, P < 0.001]. WHR also showed a good performance for the prediction of risk of 30 day mortality (AUC = 0.751, 95% CI: 0.746-0.756). CONCLUSIONS: WHR was positively associated with and performed well to predict 30 day mortality, indicating that WHR may be a reliable index to assess the prognosis of HF patients admitted to the ICU.
Subject(s)
Heart Failure , Intensive Care Units , Humans , Retrospective Studies , Critical Care , PrognosisABSTRACT
OBJECTIVE: To assess the predictive value of heart rate turbulence (HRT) in patients with acute myocardial infarction. METHODS: One hundred and twenty-five patients with acute myocardial infarction were enrolled in this study. During the period from 6 to 21 days after onset of acute myocardial infarction, they were undergone 24-hour Holter recordings to collect the mean RR interval and heart rate variability (HRV) SDNN. The Holter files were processed with software of "HRT! View V0.60-1" to obtain the value of Turbulence Onset (TO) and Turbulence Slope (TS) and the value of "heart rate variability (HRV) SDNN". LVEF and EDD were measured by Ultrasonic Cardiography. Endpoint of follow-up was cardiac death. According to the results, patients were divided into two groups (the "survivors" and the "nonsurvivors"). The predictive value for high-risk patients with acute myocardial infarction was assessed by variables between the two groups. RESULTS: In the period of follow-up (mean 225.4 +/- 99.8 days), 14 patients died and 111 patients survived. In the univariate Cox regression analysis, "TS" was a strong univariate predictor of mortality (hazard ratio 11.46, P < 0.01); "TO" was a relatively weak predictor and the hazard ratio was 2.76 (P > 0.05). Combination of abnormal TO and abnormal TS was the strongest mortality predictor (hazard ratio 26.70, P < 0.01); in the multivariate Cox regression analysis, TS < or = 2.5 ms/RR and EDD > or = 5.6 cm were the independent predictors of mortality with hazard ratios 9.49 (P < 0.01) and 3.64 (P < 0.05), respectively. CONCLUSIONS: The absence of the heart rate turbulence after ventricular premature beats is a very potent post-infarction risk predictor which is independent of and stronger than other known risk predictors.
