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This study investigated the transcriptomic mechanisms underlying melatonin accumulation and the enhancement of salt tolerance in hull-less barley seeds subjected to zinc sulphate stress. Following zinc sulphate treatment, hull-less barley seeds demonstrated increased melatonin accumulation and improved salt tolerance. Through transcriptome analysis, the study compared gene expression alterations in seeds (using the first letter of seed, this group is marked as 'S'), seeds treated with pure water (as the control group, is marked as 'C'), and germinated seeds exposed to varying concentrations of zinc sulphate (0.2 mM and 0.8 mM, the first letter of zinc sulphate, 'Z', is used to mark groups 'Z1' and 'Z2'). The analysis revealed that 8176, 759, and 622 differentially expressed genes (DEGs) were identified in the three comparison groups S.vs.C, C.vs.Z1, and C.vs.Z2, respectively. Most of the DEGs were closely associated with biological processes, including oxidative-stress response, secondary metabolite biosynthesis, and plant hormone signaling. Notably, zinc sulphate stress influenced the expression levels of Tryptophan decarboxylase 1 (TDC1), Acetylserotonin O-methyltransferase 1 (ASMT1), and Serotonin N-acetyltransferase 2 (SNAT2), which are key genes involved in melatonin synthesis. Furthermore, the expression changes of genes such as Probable WRKY transcription factor 75 (WRKY75) and Ethylene-responsive transcription factor ERF13 (EFR13) exhibited a strong correlation with fluctuations in melatonin content. These findings contribute to our understanding of the mechanisms underlying melatonin enrichment in response to zinc sulphate stress. [ABSTRACT FROM AUTHOR]

Few studies expressed the β-galactosidase encoding gene from L. plantarum in E. coli so far. In the present study, the recombinant β-galactosidase from L. plantarum FMNP01 was used as a catalyst in transgalactosylation to form tri-GOS and lactosucrose. In the presence of lactose and sucrose, six transfer products were formed in the transgalactosylation reaction with recombinant β-galactosidase L.pFMNP01Gal as a catalyst. Three transfer products were tri-galacto-oligosaccharides (tri-GOS), lactosucrose, and lactulose; the other three transfer products needed to be identified further. Based on a single factor test and response surface methodological approach, the optimal transgalactosylation conditions of the production of tri-GOS and lactosucrose were determined as initial sugar concentration of 50%, lactose: sucrose ratio of 1:2, enzyme concentration of 3 U/mL, and reaction time of 6 h at 50 °C resulting in a maximum tri-GOS concentration of 47.69 ± 1.36 g/L and a maximum lactosucrose concentration of 8.18 ± 0.97 g/L. [ABSTRACT FROM AUTHOR]

Background and Objectives: With the increasing number of patients with febrile neutropenia (FN), voriconazole (VRC) has been widely used in hospitals for first-line treatment of FN. The study was designed for evaluating the influence of FMO3 mutation on the plasma disposition and adverse reactions of VRC in FN. Materials and Methods: A single-center observational study was conducted in the inpatient ward for 4 years. The genotypes of FMO3 and cytochrome P450 (CYP) 2C19 were detected by PCR-restriction fragment length polymorphism. Patients with neutropenia were screened according to the CYP2C19 metabolic phenotype and other inclusion criteria. Five days after empirical administration of VRC, blood concentrations of VRC and nitrogen oxides in patients' blood were determined by liquid chromatography-electrospray tandem mass spectrometry (LC-ESI MS/MS). Serum parameters and clinical adverse reaction symptoms in the medical records were collected and statistically analyzed. Results: A total of 165 patients with neutropenia with the intermediate metabolic phenotype of CYP2C19 were screened. At the initial stage of oral VRC treatment, patients with the FMO3 E308G genotype had a poorer plasma disposal ability to VRC than those with the wide type of FMO3 (WT) genotype (p = 0.0005). Moreover, patients with the FMO3 E308G genotype were more likely to have adverse drug reactions and abnormal serum parameters after receiving VRC treatment. For example, the serum potassium level in the FMO3 E308G genotype group was significantly lower than that in the WT group (p = 0.028), the abnormal level of total bilirubin in the FMO3 E308G genotype group was significantly higher than that in the WT group (p = 0.049), and the aspartate aminotransferase level in the E308G group was significantly higher than that in the WT group (p = 0.05). The incidence of atopic dermatitis and visual impairment in the FMO3 E308G genotype group was 67 and 75%, respectively, and the incidences of peripheral neuroedema, headache, and diarrhea were 57, 50, and 60%, respectively, which were significantly different from those in the WT group. Conclusion: FMO3 E308G reduces the activity of the FMO3 enzyme by decreasing the metabolic ability of VRC, which increases the plasma concentration of VRC and may also lead to adverse reactions in patients with FN. [ABSTRACT FROM AUTHOR]