Disabled children suffer not only from their primary disease, but also from other complications, including food refusal. The purpose of this study was to elucidate the relationship between these conditions and food refusal in disabled children. The effectiveness of feeding therapy in treating food refusal was also examined. The study subjects were 67 disabled children (35 boys and 32 girls; mean age at initial examination: 6.5 years, SD: 6.0 years) who attended the Nippon Dental University Hospital between April 2004 and August 2008. Of them, the 13 subjects who were diagnosed as those who refused food received feeding therapy combined with desensitization therapy for hypersensitivity. Approximately 20% of the subjects showed food refusal symptoms. Primary disease, respiratory impairment and gastroesophageal reflux were not causes of food refusal in this population. There was a significant relationship between food refusal and hypersensitivity (p = 0.021). After receiving feeding therapy, six of the seven subjects with hypersensitivity but without dysphagia at initial examination recovered from food refusal. Food refusal did not significantly correlate with tube feeding. Hypersensitivity and/or tube feeding may induce food refusal. For subjects with these conditions, feeding therapy combined with desensitization therapy is effective in achieving recovery from food refusal.
Uptake of P(i) at the cellular membrane is essential for the maintenance of cell viability. However, phosphate overload is also stressful for cells and can result in cellular damage. In the present study, we investigated the effects of the transgenic overexpression of type III P(i) transporter Pit-1 to explore the role of extracellular P(i) in glomerular sclerosis during chronic renal disease. Pit-1 transgenic (TG) rats showed progressive proteinuria associated with hypoalbuminemia and dyslipidemia. Ultrastructural analysis of TG rat kidney by transmission electron microscopy showed a diffuse effacement of the foot processes of podocytes and a thickening of the glomerular basement membrane, which were progressively exhibited since 8 wk after birth. TG rats died at 32 wk of age due to cachexia. At this time, more thickening of the glomerular basement membrane and segmental sclerosis were observed in glomeruli of the TG rats. Immunohistochemical examination using anti-connexin 43 and anti-desmin antibodies suggested the progressive injury of podocytes in TG rats. TG rats showed higher P(i) uptake in podocytes than wild-type rats, especially under low P(i) concentration. When 8-wk-old wild-type and TG rats were fed a 0.6% normal phosphate (NP) or 1.2% phosphate (HP) diet for 12 wk, HP diet-treated TG rats showed more progressive proteinuria and higher serum creatinine levels than NP diet-treated TG rats. In conclusion, our findings suggest that overexpression of Pit-1 in rats induces phosphate-dependent podocyte injury and damage to the glomerular barrier, which result in the progression of glomerular sclerosis in the kidney.
The type III inorganic phosphate (Pi) transporter Pit-1 was previously found to be preferentially expressed in developing long bones. Several studies also described a regulation of its expression in cultured bone cells by osteotropic factors, suggesting a role of this transporter in bone metabolism. In the present study, we investigated the effects of the transgenic overexpression of Pit-1 in Wistar male rats on calcium phosphate and bone metabolism. A threefold increase and doubling of Pi transport activity were recorded in primary cultured osteoblastic cells derived from calvaria of two transgenic (Tg) lines compared with wild-type littermates (WT), respectively. Skeletal development was not affected by the transgene, and bone mass, analyzed by DXA, was slightly decreased in Tg compared with WT. Enhanced Pi uptake in calvaria-derived osteoblasts from Pit-1 Tg was associated with a significantly decreased expression of alkaline phosphatase activity and a normal deposition and calcification of the collagenous matrix. In 4-month-old adult Tg rats, serum Pi and renal Pi transport were increased compared with WT. The decrease of serum Ca concentration was associated with increased serum parathyroid hormone levels. Variations in serum Pi in Pit-1 Tg rats were negatively correlated with serum fibroblast growth factor-23, whereas 1,25-dihydroxyvitamin D(3) was not affected by Pit-1 overexpression. In conclusion, transgenic Pit-1 overexpression in rats affected bone and calcium phosphate metabolism. It also decreased alkaline phosphatase activity in osteoblasts without influencing bone matrix mineralization as well as skeletal development.
Inorganic phosphate (Pi) transport probably represents an important function of bone-forming cells in relation to extracellular matrix mineralization. In the present study, we investigated the effect of prostaglandin D2 (PGD2) on Pi transport activity and its intracellular signaling mechanism in MC3T3-E1 osteoblast-like cells. PGD2 stimulated Na-dependent Pi uptake time- and dose-dependently in MC3T3-E1 cells during their proliferative phase. A protein kinase C (PKC) inhibitor calphostin C partially suppressed the stimulatory effect of PGD2 on Pi uptake. The selective inhibitors of mitogen-activated protein (MAP) kinase pathways such as ERK, p38 and Jun kinases suppressed PGD2-induced Pi uptake. The inhibitors of phosphatidylinositol (PI) 3-kinase and S6 kinase reduced this effect of PGD2, while Akt kinase inhibitor did not. These results suggest that PGD2 stimulates Na-dependent Pi transport activity in the phase of proliferation of osteoblasts. The mechanisms responsible for this effect are activation of PKC, MAP kinases, PI 3-kinase and S6 kinase.
This study was performed to ascertain the relationships between oral motor functions, such as those of the tongue and lips, and age in the community-dwelling elderly, as well as to investigate the effects of these factors on masticatory performance. The subjects were 268 healthy elderly Japanese living in Kyoto. They were divided into four age groups and further classified into the following two groups by the presence or absence of posterior occlusal support: Eichner A or B1-B3 (group A), and Eichner B4 or C (group B). They were wearing removable or fixed dentures if they had missing teeth. Oral function evaluation items included (1) masticatory performance and (2) oral motor skills. Significant differences were noted among the age groups in tongue pressure within group A (P < 0.01) and group B (P < 0.05), and in the number of repetitions of the syllables /ta/ and /ka/ in group B (/ta/: P < 0.05, /ka/; P < 0.01). The number of natural teeth (beta = 0.463, P < 0.001) in group A and tongue pressure (beta = 0.436, P < 0.001) in group B were the only predictors of masticatory performance when the data were analyzed by multiple regression analysis. The tongue may compensate for the missing teeth in masticatory performance of those elderly who have lost their natural teeth. The results of this study highlight the importance of tongue function in masticatory performance.
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