Refeeding Hypophosphatemia in Anorexia Nervosa

Objective: Refeeding in patients with anorexia nervosa (AN) is associated with a risk of refeeding syndrome (RS), which is a disruption in metabolism with a variety of features including hypophosphatemia. We evaluated the risk factors for refeeding hypophosphatemia (RH) during nutritional replenishment in Japanese patients with AN. Methods: We retrospectively examined clinical data for 99 female inpatients (mean age 30.9 ± 10.7 years, range: 9 to 56 years). Results: RH (phosphate <2.3 mg/dL) occurred within 4.8 ± 3.7 days of hospital admission and was still observed at 28 days after admission in 21 of the 99 cases (21.2%). Oral or intravenous phosphate was given to some patients to treat or prevent RH. Patients with RH had a significantly lower body mass index, were older, and had higher blood urea nitrogen than those without RH. Severe complications associated with RH were recorded in only one patient who showed convulsions and disturbed consciousness at day 3 when her serum phosphate level was 1.6 mg/dL. Conclusion: The significant risk factors for RH that we identified were lower BMI, older age, and higher blood urea nitrogen at admission. No significant difference in total energy intake was seen between the RH and no RH groups, suggesting that RH may not be entirely correlated with energy intake. Precisely predicting and preventing RH is difficult, even in patients with AN who are given phosphate for prophylaxis. Thus, serum phosphate levels should be monitored for at least 5-10 days after admission

双極性障害におけるグルタミン酸神経伝達異常に関するMRS研究

Background: Previous studies of patients with bipolar disorder (BD) using magnetic resonance spectroscopy (MRS) have shown neurophysiological abnormalities related to the glutamate (Glu)-glutamine (Gln) cycle, membrane turnover, and neuronal integrity, although the results were neither consistent nor conclusive. Recently it has been reported the Gln/Glu ratio is the most useful index, quantifying neuronal-glial interactions and the balance of glutamatergic metabolites In this MRS study, we elucidated the abnormalities of metabolites in a larger sample of patients with BD with a high-field MRI system. Methods: Sixty-two subjects (31 patients with BD and 31 healthy controls [HC]) underwent 3T proton MRS (1H-MRS) of the anterior cingulate cortex (ACC) and left basal ganglia (ltBG) using a stimulated echo acquisition mode (STEAM) sequence. Results: After verifying the data quality, 20 patients with BD and 23 age- and gender-matched HCs were compared using repeated-measures analysis of covariance (ANCOVA). Compared to the HC group, the BD group showed increased levels of Gln, creatine (Cr), N-acetyl aspartate (NAA), choline (Cho), and an increased ratio of Gln to Glu in the ACC, and increased Gln and Cho in the ltBG. These findings remained after the participants with BD were limited to only euthymic patients. After removing the influence of lithium (Li) and sodium valproate (VPA), we observed activated glutamatergic neurotransmission in the ACC but not in the ltBG. Limitations: The present findings are cross-sectional and metabolites were measured in only two regions. Conclusions: Our results support a wide range of metabolite changes in patients with BD involved in glutamatergic neurotransmission, membrane turnover, and neuronal integrity. Moreover, the elevation of Gln/Glu ratio suggested that hyperactivity of glutamatergic neurotransmission in the ACC is a disease marker for BD

Dipeptidyl peptidase IV is involved in the cellulose-responsive induction of cellulose biomass-degrading enzyme genes in <i>Aspergillus aculeatus</i>

<p>We screened for factors involved in the cellulose-responsive induction of cellulose biomass-degrading enzyme genes from approximately 12,000 <i>Aspergillus aculeatus</i> T-DNA insertion mutants harboring a transcriptional fusion between the FIII-avicelase gene (<i>cbhI</i>) promoter and the orotidine 5′-monophosphate decarboxylase gene. Analysis of 5-fluoroorodic acid (5-FOA) sensitivity, cellulose utilization, and <i>cbhI</i> expression of the mutants revealed that a mutant harboring T-DNA at the dipeptidyl peptidase IV (<i>dppIV</i>) locus had acquired 5-FOA resistance and was deficient in cellulose utilization and <i>cbhI</i> expression. The deletion of <i>dppIV</i> resulted in a significant reduction in the cellulose-responsive expression of both <i>cbhI</i> as well as genes controlled by XlnR-independent and XlnR-dependent signaling pathways at an early phase in <i>A. aculeatus</i>. In contrast, the <i>dppIV</i> deletion did not affect the xylose-responsive expression of genes under the control of XlnR. These results demonstrate that DppIV participates in cellulose-responsive induction in <i>A. aculeatus</i>.</p> <p>Dashed lines with arrows indicate putative signaling pathways.</p