The possibility of developing deep-sowing tolerant (DST) maize to absorb moisture from subsoil zones is crucial to maize adaptation to water-stressed environments. The function of the mesocotyl in field emergence of seedlings is established in grasses. However, information is scarce on the extent of genetic variability for mesocotyl length (ML) in maize. Sixty-eight maize genotypes were studied using Completely Randomised Design in a laboratory experiment to investigate the extent of genetic variability for ML, and the relationship of seed biochemical components with ML. Ten seeds of each genotype were germinated for 10 days in the dark. Mesocotyl length was determined by placing cut mesocotyl against a flexible measuring tape. Biochemical contents of seeds were determined at a standard diagnostic laboratory. Analysis of variance revealed highly significant (p ≤ 0.01) genotype mean square, indicating sufficient variability for genetic improvement. Broad-sense heritability and genetic advance were high and implied that ML was heritable. Mean ML for genotypes ranged from 0.58 to 9.02 cm; thus, planned crosses can be made for ML improvement. A dendrogram from cluster analysis based on Ward’s minimum variance cluster analysis classified 65 of the genotypes into clusters I, II, and III with ML (mean ± standard deviation) of 0.49 ± 0.18, 4.25 ± 0.96, and 9.16 ± 0.93 cm, respectively. All the measured biochemical parameters, except selenium, showed significant (p ≤ 0.05/0.01) associations with ML. Crosses can be planned involving genotypes from clusters 1 and III, to exploit heterosis for ML in a hybrid program. The results obtained from this study provide a basis for the development of DST maize for drought-prone environments.
Background: High-density lipoprotein cholesterol (HDL-C) and other lipoproteins are metabolized in part by the cholesteryl ester transport protein (CETP). Cardiovascular risk and the occurrence of ischemic stroke are linked to polymorphism in the CETP gene. Methodology: For the study, 100 ischemic stroke patients and 100 controls with matched sexes and ages ranging from 46 to 87 were chosen. Lipoprotein ratios were computed using Excel software, and lipid parameters were evaluated using Randox diagnostic kits. Polymerase Chain Reaction and Restriction Fragment Length Polymorphism (PCR-RFLP) and 2% gel electrophoresis were used to genotype the CETP gene. The genotyping of the CETP gene were performed by Polymerase Chain Reaction and Restriction Fragment Length Polymorphism (PCR-RFLP) combined with 2% gel electrophoresis. Results: There were significant difference (P<0.0001) in the genotypic and allelic frequencies of CETP SNP between the healthy and patients with ischemic stroke. The frequencies of I/I, I/V and V/V genotypes of the CETP gene were 48%, 37% and 15% for the control and 17%, 33% and 50%, for the stroke subjects, respectively. The frequencies of I and V alleles were 67% and 33% for the control and 37.5% and 62.5% for the stroke subjects, respectively. The V allele carriers of CETP gene had higher plasma TC, TG, VLDL-C, LDL-C, Non-HDL-C, defective HDL-C, HDL2-C and HDL3-C when compared to the I allele carriers for both subjects. The V allele carriers were responsible for the increase in dyslipidemia for both subjects. Conclusion: The results of this study show that mutation of CETP I405V (rs5882) polymorphism causes an increased in plasma TC, TG, VLDL-C, LDL-C, Non-HDL-C, defective HDL-C, HDL2-C and HDL3-C concentration and is associated with an increased risk of ischemic stroke.
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