PubMed · 10503511
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N Ohya. 1999. [Galactose].. https://pubmed.ncbi.nlm.nih.gov/10503511/
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Four neoglycolipids having 2-amino-2-deoxy-D-glucose or D-galactose moieties linked to the lipidic part by a glucitol or a mannitol spacer-arm have been synthesized. The key step of the synthetic strategy was the regiospecific or regioselective beta-glycosylation of partially protected glucitol or mannitol acceptors by either 3,4,6-tri-O-acetyl-2-deoxy-2-iodo-alpha-D-mannopyranosyl azide or 2,3,4,6-tetra-O-benzoyl-alpha-D-galactopyranosyl trichloroacetimidate donors.
BACKGROUND: Because a large amount of serum alpha-fetoprotein (alpha-FP) is synthesized in the liver of the fetus or premature newborn, high concentrations or delayed degradation of serum alpha-FP during the neonatal period may reflect hepatic immaturity. METHODS: In order to evaluate the relationship between transient neonatal galactosemia and delay of liver maturation, the concentration and half-life of serum alpha-FP during the neonatal period were measured in patients with transient galactosemia and in normal neonates. RESULTS: No significant differences were observed in the serum concentration of alpha-FP between normal and galactosemic patients less than 1 month of age. However, the half-life of serum alpha-FP was significantly longer in galactosemic patients between 15 and 60 days of age compared with age-matched normal neonates. CONCLUSION: Based on these results, we hypothesize that delay of liver maturation during the neonatal period, especially during the first 2 months after birth, can be a cause of transient neonatal galactosemia.
In yeast, trehalose accumulation and its hydrolysis, which is catalyzed by neutral trehalase, are believed to be important for thermotolerance. We have shown that trehalose is one of the important factors for barotolerance (resistance to hydrostatic pressure); however, nothing is known about the role of neutral trehalase in barotolerance. To estimate the contribution of neutral trehalase in resisting high hydrostatic pressure, we measured the barotolerance of neutral trehalase I and/or neutral trehalase II deletion strains. Under 180 MPa of pressure for 2 h, the neutral trehalase I deletion strain showed higher barotolerance in logarithmic-phase cells and lower barotolerance in stationary-phase cells than the wild-type strain. Introduction of the neutral trehalase I gene (NTH1) into the deletion mutant restored barotolerance defects in stationary-phase cells. Furthermore, we assessed the contribution of neutral trehalase during pressure and recovery conditions by varying the expression of NTH1 or neutral trehalase activity with a galactose-inducible GAL1 promoter with either glucose or galactose. The low barotolerance observed with glucose repression of neutral trehalase from the GAL1 promoter was restored during recovery with galactose induction. Our results suggest that neutral trehalase contributes to barotolerance, especially during recovery.