Phosphate solubilizing fungi (PSF) have huge potentials in enhancing release of phosphorus from fertilizer. Two PSF (NJDL-03 and NJDL-12) were isolated and identified as Penicillium oxalicum and Aspergillus niger respectively in this study. The quantification and identification of organic acids were performed by HPLC. Total concentrations of organic acids secreted by NJDL-03 and NJDL-12 are ~4000 and ~10,000 mg/L with pH values of 3.6 and 2.4 respectively after five-days culture. Oxalic acid dominates acidity in the medium due to its high concentration and high acidity constant. The two fungi were also cultured for five days with the initial pH values of the medium varied from 6.5 to 1.5. The biomass reached the maximum when the initial pH values are 4.5 for NJDL-03 and 2.5 for NJDL-12. The organic acids for NJDL-12 reach the maximum at the initial pH = 5.5. However, the acids by NJDL-03 continue to decrease and proliferation of the fungus terminates at pH = 2.5. The citric acid production increases significantly for NJDL-12 at acidic environment, whereas formic and oxalic acids decrease sharply for both two fungi. This study shows that NJDL-12 has higher ability in acid production and has stronger adaptability to acidic environment than NJDL-03.
Factor XI deficiency is an autosomal bleeding disorder of variable severity. It is particularly common in the Ashkenazi Jewish population, the result of two founder mutations -E117X and F283L. Recent studies have shown the causative mutations of Factor XI deficiency, outside the Ashkenazi Jewish population, to be highly heterogeneous. We have studied 116 index cases, mostly from an ethnically diverse UK population, in order to better understand the spectrum of mutations responsible for factor XI deficiency. A total of 140 causative mutations of the F11 gene were identified in 109 patients. Fifty-five (39.3%) of the mutations were one of three common mutations -E117X (Type II), F283L (Type III), or C128X. The remaining 85 (60.7%) mutations comprised at least 57 variants including 31 novel mutations and whole gene deletions. This large study reconfirms that, despite the presence of founder mutations in discrete populations, factor XI deficiency remains a highly heterogeneous disease at the molecular level.
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