Objective: To investigate the use of glutamine administered orally during Methotrexate chemotherapy to prevent oral mucositis and reduce hospital costs in children with acute lymphoblastic leukemia (ALL). Methods: Twenty-four children received oral glutamine (400 mg/kg body weight per day) and twenty four received placebo on days of chemotherapy administration and for at least 14 additional days. Oral mucositis was graded daily at each day of treatment till completion of therapy. The study groups were compared for the oral mucositis development using the WHO scale. Results: Oral mucositis occurred in 4.2 % of the glutamine group and 62.5% in the placebo group. The use of glutamine was directly associated with prevention of oral mucositis than placebo (OR 0,026; 95% CI: 0,003-0,228). The duration of length hospital stay was lower in the glutamine group than in the placebo group ((8 vs 12 days); p = 0,005). Hospital cost per day for glutamine group was 40 USD per day while placebo group was 48 USD per day. Conclusions: There was significant difference in the prevention of oral mucositis by oral glutamine vs placebo. The hospital cost for glutamine supplementation was lower than control group.

Aim: Glutamine is needed for optimal cell growth and for the immune system, especially in the enterocytes of gut mucosal immune responses. Low birth weight makes infants susceptible to glutamine depletion because nutrition is limited in the first week of life. To determine the effect of enteral glutamine supplementation on weight gain patterns and fecal secretory immunoglobulin A. Material and Methods:This study is a double-blind, randomized controlled trial. Infants were randomly assigned to the glutamine group and placebo group. The glutamine group was supplemented with glutamine 400 mg/kg/day for 14 days, and placebo group received glucose 400 mg/kg/day for 14 days. The infants were observed for 30 days. Return-to-birth-weight, weight gain velocity, and fecal secretory immunoglobulin A levels were monitored during the study. Results: Thirty-seven low-birth-weight infants were randomly assigned to the glutamine and placebo groups. The glutamine group had a shorter return-to-birth-weight time than the placebo group (8.1±0.9 vs. 11.0±1.6 days) and faster weight gain velocity (20.0±1.8 vs. 15.5±2.2 g/ kg/day) (p<0.001). Secretory immunoglobulin A levels after glutamine supplementation were higher than in the placebo group (0.456±0.057 vs. 0.376±0.035 mg/g) (p<0.001). Levels of secretory immunoglobulin A after treatment in each group were increased. However, there was a significant difference before and after supplementation between the glutamine and placebo groups (0.247±0.024 vs. 0.140±0.016 mg/g) (p<0.001). Conclusion: Enteral glutamine supplementation in low-birth-weight infants accelerates return to birth weight, increases the weight gain velocity, and the levels of fecal secretory immunoglobulin A.

IntroductionAtopic dermatitis (AD) is the most common skin disorder in young children worldwide, with a high impact on morbidity and quality of life. To date, no prospective study has been published on the incidence and potential predictors of AD in South East Asian populations. The Indonesian Prospective Study of Atopic Dermatitis in Infants (ISADI) will address the genetic, metabolic and dietary characteristics of mothers and their offspring, as well as potential determinants of AD within the first year of infant life.Methods and analysisThis prospective study will be undertaken in about 400 infants to investigate the direct and indirect effects of filaggrin (FLG) gene mutations, the genetic variants of FADS1, FADS2 and FADS3 and the role of long-chain polyunsaturated fatty acids (LCPUFA) on the development of AD. We will use standardised protocols for subject recruitment, umbilical artery plasma analysis, buccal cell sampling for genotyping, fatty acid analysis, physical exams, 3-day food-intake recall of mothers and children, as well as comprehensive questionnaires on environmental, socioeconomic and AD-related factors, including family history. Monthly monitoring by telephone and physical exams every 3 months will be carried out to assess participants' anthropometry, medical history and incidence of AD diagnosis during the first year of life. Hypotheses-driven analyses of quality-controlled dietary, genetic and metabolic data will be performed with state-of-the-art statistical methods (eg, AD-event history, haplotype, dietary or metabolic factor analysis). Direct and indirect effects of genetics and LCPUFA in buccal cell and cord plasma glycerophospholipids as potential mediators of inflammation on AD development will be evaluated by path analysis.Ethics and disseminationThe Permanent Medical Research Ethics Committee in Medicine and Health/Faculty of Medicine Universitas Indonesia/Dr Cipto Mangunkusumo Hospital (No. 47/H2.F1/ETIK/2014) approved the study protocol (extended by the letter no. 148/UN2.F1/ETIK/2015). We aim to disseminate our findings via publication in an international journal with high impact factor.

This study aims to determine the effect of high glycemicindex (GI) diet on blood glucose, serum insulin, number of islet cells, Akt, and Pdx1 expression in beta cells. Eight weeks-old healthy male Balb/c mice were divided into two groups. The control group was given standard diet. The high glycemic index (highGI) group was given standard diet added with oral gavage of glucose solution everyday for 4 weeks. The dose of glucose solution was 0.013 g/gBW or 3-5% additional calories each day. Random blood glucose (BG) was taken before (pre) and after (post) treatment from tail vein. Serum insulin (SI) was taken after treatment from blood cardiac. Islet was removed after treatment. The number of islet cells was counted in HE staining. Akt and Pdx1 were analyzed in IHC staining. The results revealed that the changes of body weight before and after treatment were significantly different between groups (P=0.025). BG post in the highGI increased significantly compared to that in the control (P= 0.032). However, SI in the highGI decreased significantly compared to that in the control (P=0.003). The number of islet cells in the highGI decreased insignificantly (P=0.346). Meanwhile, Akt and Pdx1 in the highGI increased slightly (P=0.729; P=0.701). It can be concluded that a high GI diet can increase blood glucose level but reduce serum insulin level. However, there is no evidence of underlying mechanism of this chronic condition via Akt and Pdx1. Thus, further research is needed, especially for observing apoptosis and other modulators on beta cells.

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