Medical Treatment for Burn Patients with Eating Disorders: A Case Report

There have been many cases of burn patients who also suffer from psychiatric problems, including eating disorders. We present a case of a 38-year-old female with an eating disorder and depression who became light-headed and fell, spilling boiling water from a kettle on herself at home sustaining partial thickness and full thickness burns over 5% of her total body surface area: left buttock and right thigh and calf. Eating disorders (in the present case, anorexia nervosa) cause emaciation and malnutrition, and consent for hospitalization from the patient and/or family is often difficult. During the medical treatment of burns for these patients, consideration not only of physical symptoms caused by malnutrition but also the psychiatric issues is required. Therefore, multifaceted and complex care must be given to burn patients with eating disorders

Effects of High Phosphorus Diet on Bone Metabolism-Related Gene Expression in Young and Aged Mice

In this study, the effects of high phosphorus (P) diet on bone metabolism-related gene expression were investigated in young and aged mice. Twelve- and 80-week-old ddY male mice were divided into two groups, respectively, and fed a control diet containing 0.3% P or a high P diet containing 1.2% P. After 4 weeks of treatment, serum parathyroid hormone (PTH) concentration was significantly higher in the high P groups than in the control groups in both young and aged mice and was significantly higher in aged mice than in young mice fed the high P diet. High P diet significantly increased receptor activator of NF-κB ligand (RANKL) mRNA in the femur of both young and aged mice and significantly increased the RANKL/osteoprotegerin (OPG) mRNA ratio only in aged mice. High P diet significantly increased mRNA expression of transient receptor potential vanilloid type 6, calbindin-D9k, and plasma membrane Ca2+-ATPase 1b in the duodenum of both young and aged mice. These results suggest that high P diet increased RANKL mRNA expression in the femur and calcium absorption-related gene expression in the duodenum regardless of age. Furthermore, the high P diet-induced increase in PTH secretion might increase the RANKL/OPG mRNA ratio in aged mice

Bioavailability of prenyl quercetin

Prenyl flavonoids are widely distributed in plant foods and have attracted appreciable attention in relation to their potential benefits for human health. Prenylation may enhance the biological functions of flavonoids by introducing hydrophobic properties in their basic structures. Previously, we found that 8-prenyl naringenin exerted a greater preventive effect on muscle atrophy than nonprenylated naringenin in a mouse model. Here, we aimed to estimate the effect of prenylation on the bioavailability of dietary quercetin (Q). The cellular uptake of 8-prenyl quercetin (PQ) and Q in Caco-2 cells and C2C12 myotube cells was examined. Prenylation significantly enhanced the cellular uptake by increasing the lipophilicity in both cell types. In Caco-2 cells, efflux of PQ to the basolateral side was <15% of that of Q, suggesting that prenylation attenuates transport from the intestine to the circulation. After intragastric administration of PQ or Q to mice or rats, the area under the concentration-time curve for PQ in plasma and lymph was 52.5% and 37.5% lower than that of Q, respectively. PQ and its O-methylated form (MePQ) accumulated at much higher amounts than Q and O-methylated Q in the liver (Q: 3400%; MePQ: 7570%) and kidney (Q: 385%; MePQ: 736%) of mice after 18 d of feeding. These data suggest that prenylation enhances the accumulation of Q in tissues during long-term feeding, even though prenylation per se lowers its intestinal absorption from the diet

Single-Cell Expression Profiling Reveals a Dynamic State of Cardiac Precursor Cells in the Early Mouse Embryo

In the early vertebrate embryo, cardiac progenitor/precursor cells (CPs) give rise to cardiac structures. Better understanding their biological character is critical to understand the heart development and to apply CPs for the clinical arena. However, our knowledge remains incomplete. With the use of single-cell expression profiling, we have now revealed rapid and dynamic changes in gene expression profiles of the embryonic CPs during the early phase after their segregation from the cardiac mesoderm. Progressively, the nascent mesodermal gene Mesp1 terminated, and Nkx2-5+/Tbx5+ population rapidly replaced the Tbx5low+ population as the expression of the cardiac genes Tbx5 and Nkx2-5 increased. At the Early Headfold stage, Tbx5-expressing CPs gradually showed a unique molecular signature with signs of cardiomyocyte differentiation. Lineage-tracing revealed a developmentally distinct characteristic of this population. They underwent progressive differentiation only towards the cardiomyocyte lineage corresponding to the first heart field rather than being maintained as a progenitor pool. More importantly, Tbx5 likely plays an important role in a transcriptional network to regulate the distinct character of the FHF via a positive feedback loop to activate the robust expression of Tbx5 in CPs. These data expands our knowledge on the behavior of CPs during the early phase of cardiac development, subsequently providing a platform for further study

Iron deficiency decreases renal 25-hydroxyvitamin D3-1α-hydroxylase activity and bone formation in rats

BACKGROUND: Dietary iron intake is associated with bone metabolism in human and animals. Previous studies have suggested that iron deficiency diminishes bone formation and causes bone loss in rats, however, the detailed mechanisms remain unclear. To clarify the mechanism of the diminishing bone formation in iron deficiency, we examined the renal 25-hydroxyvitamin D3-1α-hydroxylase (1α-hydroxylase) activity and femoral expression of bone formation-related genes in iron-deficient rats. METHODS: Male Wistar rats (n = 18) at 3 weeks of age were divided into three groups of six rats each. Two groups of rats were given free access to a control diet or an iron-deficient diet for 4 weeks. Rats in the third group were pair-fed the control diet, calculated as the mean food intake of the iron-deficient group. RESULTS: Following the treatment, compared with the control and pair-fed groups, hemoglobin and liver iron concentrations were significantly lower and heart weight was significantly higher in the iron-deficient group. Serum 1,25-dihydroxyvitamin D3 concentration and renal 1α-hydroxylase activity were significantly lower in the iron-deficient group compared with the control and pair-fed groups. Serum osteocalcin concentration and bone mineral density of the femur were also significantly lower in the iron-deficient group compared with the control and pair-fed groups. Furthermore, iron-deficient diet decreased runt-related transcription factor 2, osteocalcin, and type I collagen mRNA expression in the femur. CONCLUSIONS: Our findings indicate that iron deficiency reduces renal 1α-hydroxylase activity, leading to a decreased bone formation in rats