Screening and Resistance Locus Identification of the Mutant fcrZ22 Resistant to Crown Rot Caused by Fusarium pseudograminearum.

Crown rot caused by Fusarium pseudograminearum is a devastating wheat disease worldwide. In addition to yield losses, the fungi causing Fusarium crown rot (FCR) also deteriorate the quality and safety of food because of the production of mycotoxins. Planting resistant cultivars is an effective way to control FCR. However, most wheat cultivars are susceptible to FCR. Therefore, development of new sources and detection of loci for FCR resistance are necessary. In the present study, a resistant mutant, fcrZ22, was identified from an ethyl methane sulfonate (EMS)-mutagenized population of the cultivar Zhoumai 22, and then fcrZ22 was crossed with the wild type to produce an F2 population. Genetic analysis of the F2 population was carried out by the mixed inheritance model of major genes plus polygenes, and 20 resistant and 20 susceptible plants were selected to assemble mixed pools. Combining 660K SNP arrays, the resistance loci were detected by bulked segregant analysis. The resistance to FCR caused by F. pseudograminearum in the F2 population was in accordance with the "mixed model with two major genes of additive-epistasis effect + additive-dominant polygenes," and the heritability of the major gene was 0.92. Twenty-one loci were detected, which were located on 10 chromosomes, namely, 1B (1), 1D (1), 2A (3), 1B (1), 3A (3), 3B (3), 4A (2), 5A (2), 7A (3), and 7B (2). Among the 21 loci, eight were new loci for FCR resistance. This is the first report of detecting loci for FCR resistance from a mutant. The results of the present study provided excellent germplasm resources for breeding wheat cultivars with FCR resistance and laid the foundation for fine mapping of FCR resistance loci.

Correlation between glycaemic variability and prognosis in diabetic patients with CKD.

INTRODUCTION: Glycaemic variability (GV), rather than glucose level, has been shown to be an important factor associated with in-hospital mortality. The coefficient of variation of glucose (GLUCV) is one of the methods used to evaluate GV. However, the clinical significance of GLUCV in diabetes mellitus (DM) patients diagnosed with chronic kidney disease (CKD) as a risk factor for long-term adverse changes is unknown. MATERIAL AND METHODS: In this retrospective study, we extracted data of adult DM patients diagnosed with CKD from the Medical Information Mart for Intensive Care (MIMIC-IV). We sought to investigate the relationship between GV and in-hospital mortality as well as 30-day mortality. A non-parametric test was used to compare baseline characteristics between groups. Kaplan-Meier analysis and Cox regression model were used to analyse the risk factors associated with in-hospital and 30-day mortality. RESULTS: A total of 1572 DM patients with CKD were included in our data analysis. The quartile of the GLUCV values was used to assign subjects to 4 groups: GLUCV1 (GLUCV < 24), GLUCV2 (24 ≤ GLUCV < 31), GLUCV3 (31 ≤ GLUCV < 39) and GLUCV 4 (GLUCV ≥ 39). COX regression analysis revealed that the GLUCV was an independent risk factor for in-hospital and 30-day mortality [GLUCV2 group (HR = 0.639, 95% CI: 0.454-0.899, p = 0.010), GLUCV3 group (HR = 0.668, 95% CI: 0.476-0.936, p = 0.019), and GLUCV3 group (HR = 0.726, 95% CI: 0.528-0.999, p = 0.049)]. The Kaplan-Meier survival curve was steeper in the GLUCV1 and GLUCV4 groups, and the survival rate decreased in a time-dependent manner. CONCLUSIONS: Herein, we validated GV as a mortality risk factor for DM patients with CKD. Therefore, monitoring and adjusting GV in hospitalized patients might have a significant treatment benefit.