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Background: Hyperglycemia is a common complication of prematurity, which requires attention because of its high prevalence and multiple consequences. Serum fructosamine used in diabetic patients provides information about the average glucose concentration in the preceding period of 2–3 weeks. Objective: We investigated the physiologic characteristics of a glycemic marker, fructosamine, in preterm and term neonates. We also studied its association with hyperglycemia and related morbidities of preterm infants. Method: Fructosamine levels of 22 extremely premature (gestational age, GA: 25.8 ± 1.0 weeks), 36 moderately premature (GA: 29.8 ± 1.3 weeks) and 26 term infants (GA: 39.1 ± 1.3 weeks) were determined in the 1st week of life. Fructosamine assay was repeated in all preterm neonates in the 4th and 7th postnatal weeks. Hyperglycemic episodes and main morbidities of preterm infants were recorded and analyzed in association with fructosamine levels. Results: Preterm infants had higher fructosamine levels after birth compared to term infants and a postnatal fall was observed. Serum fructosamine did not show association with the occurrence of hyperglycemia or its main morbidities in preterm infants. Conclusion: In the framework of our study, we could not confirm the usefulness of fructosamine determination in the glycemic control of preterm neonates during the perinatal period.

Summary Saccharomyces cerevisiae responds to environ- mental stimuli such as an exposure to pheromone or to hexoses after carbon source limitation with a tran- sient elevation of cytosolic calcium (TECC) response. In this study, we examined whether hexose transport and phosphorylation are necessary for the TECC response. We found that a mutant strain lacking most of the known hexose transporters was unable to carry out the TECC response when exposed to glucose. A mutant strain that lacked the ability to phosphorylate glucose was unable to respond to glucose addition, but displayed a normal TECC response after the addi- tion of galactose. These results indicate that hexose uptake and phosphorylation are required to trigger the hexose-induced TECC response. We also found that the TECC response was significantly smaller than normal when the level of environmental calcium was reduced, and was abolished in a mid1 mutant that lacked a subunit of the high-affinity calcium channel of the yeast plasma membrane. These results indicate that most or all of the TECC response is mediated by an influx of calcium from the extracellu- lar space. Our results indicate that this transient increase in plasma membrane calcium permeability may be linked to the accumulation of Glc-1-P (or a related glucose metabolite) in yeast.

A PMMA (polymethyl-methacrylate)-sorbitol-based capsule system was recently developed, and the permeability of 16 types of capsules with different wall thicknesses and sorbitol contents tested. By optimizing these two parameters, we showed that capsule permeability could be controlled. Promising preliminary data obtained using BPB (Bromophenol Blue) as diffusion marker prompted us to further investigate the antibiotic release of capsules showing the most appropriate release characteristics. PMMA-sorbitol capsules were prepared with wall thickness of 0.5 or 0.6 mm and 60 or 70 w/w% (weight percent) of sorbitol content. In vitro gentamicin, amikacin, tobramycin releases were determined by using a microbiological agar plate diffusion assay. Capsules released 70-100% of their gentamicin load, substantially superior to Septopal, and showed preferable, extended release profiles when compared with the beads. The release kinetics of amikacin and tobramycin closely resembled those of gentamicin. PMMA-sorbitol capsules have been developed and tested, which make them promising devices for local antibiotic delivery.

d -Glucose is the preferred carbon and energy source for most eukaryotic cells. Immediately following its uptake, glucose is rapidly phosphorylated to glucose-6-phosphate (Glc-6-P). The yeast Saccharomyces cerevisiae has three enzymes (Hxk1p, Hxk2p, and Glk1p) that convert glucose to Glc-6-P. In the present study, we found that yeast mutants lacking any two of these enzymes retain the ability to efficiently convert glucose to Glc-6-P and thus maintain a low level of cellular glucose. However, a mutant strain lacking all three glucose-phosphorylating enzymes contained up to 225-fold more intracellular glucose than normal. Drugs that inhibit the synthesis or the trimming of the lipid-linked core oligosaccharide Glu 3 Man 9 GlcNac 2 effectively reduced the accumulation of glucose. Similarly, mutations that block the addition of glucose residues to the core oligosaccharide moiety, such as alg5Δ or alg6Δ , also diminished glucose accumulation. These results indicate that the intracellular glucose accumulation observed in the glucose phosphorylation mutant results primarily from the trimming of glucose residues from core oligosaccharide chains within the endoplasmic reticulum (ER). Consistent with this conclusion, both [ 14 C]glucose exchange and subcellular fractionation experiments indicate that much of the accumulated glucose is retained within an intracellular compartment, suggesting that the efficient transport of glucose from the ER to the cytosol in yeast may be coupled to its rephosphorylation to Glc-6-P. The high level of cellular glucose was associated with an increased level of protein glycation and the release of glucose into the culture medium via its transit through the secretory pathway. Finally, we also found that the accumulation of glucose may lead to a subtle alteration in ion homeostasis, particularly Ca 2+ uptake. This suggests that this mutant strain may serve as a useful model to study the consequences of excessive glucose accumulation and protein glycation.