bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long‐Term Follow‐Up of Overweight Children: After Training, After a Single Consultation Session, and Without Treatment
Authors: Reinehr Thomas , Kersting Mathilde , Alexy Ute , Andler Werner 
Published: January 2024

ABSTRACTBackground:A satisfactory treatment of childhood obesity has not yet been found. An individual consultation session is the usual practice while experts recommend an outpatient training program consisting of a combination of physical exercise, nutrition education, and behavior therapy.Methods:We analyzed degree of overweight (SDS‐BMI) after one and two years in overweight children (aged 6‐15 years) who had had a single consultation session (n = 66) and who had finished a one‐year, structured outpatient training program consisting of physical exercise, nutrition education, and behavior therapy (n = 81). Furthermore we collected data on changes in weight for a control group of overweight children not receiving any treatment (n = 100) over the same period of time.Results:There was no significant change in the degree of overweight over the period of two years either for the control group or for those having received single consultation. The participants of the training were in mean significantly less overweight than at the beginning of the training (P < 0.001), both after one year (mean change in SDS‐BMI ‐0.38) and after the second year (mean change in SDS‐BMI ‐0.30).Conclusions:Overweight children not receiving treatment do not reduce in weight. A single consultation session is not sufficient to achieve weight reduction in children. Weight reduction over at least two years can be achieved in part of the participants of a long‐term, specialized treatment. JPGN 37:72‐74, 2003.
Dietary Nucleotides Modulate Mitochondrial Function of Intestinal Mucosa in Weanling Rats with Chronic Diarrhea
Authors: Arnaud Alexandra , López‐Pedrosa José María , Torres María Isabel , Gil Ángel 
Published: January 2024

ABSTRACTBackgroundChronic diarrhea during early infancy is characterized by intestinal mucosal injury, and as a consequence, the mitochondrial system of oxidation and reduction and energy production is altered. Since dietary nucleotides have been associated with the process of intestinal mucosal repair in rats with chronic diarrhea, the aim of this study was to examine the effects of dietary nucleotides on the functioning of mucosal mitochondria.MethodsWeanling rats were fed with a semipurified synthetic diet (C) or the same diet in which carbohydrates were substituted by lactose (L), resulting in chronic diarrhea. During recovery, rats were fed with the semipurified synthetic diet (LC) or the same diet supplemented with nucleotides (LN). The activities of adenosine triphosphate synthase (ATPase), cytochrome c oxidase, citrate synthase, and malate dehydrogenase were measured in mitochondria from ileum and colon mucosa.ResultsThese enzymatic activities rose in rats with chronic diarrhea, possibly to compensate for the drastic decline in adenosine triphosphate (ATP) synthesis. Dietary nucleotide supplementation allowed normalizing of the activities of ATPase (C: 0.37 ± 0.16 μg/min/mg protein; L: 0.68 ± 0.25 μg/min/mg protein; LC: 0.60 ± 0.20 μg/min/mg protein; LN: 0.42 ± 0.22 μg/min/mg protein), citrate synthase (C: 0.12 ± 0.05 mM/min/mg protein; L: 0.21 ± 0.07 mM/min/mg protein; LC: 0.21 ± 0.06 mM/min/mg protein; LN: 0.12 ± 0.02 mM/min/mg protein), and malate dehydrogenase (C: 0.77 ± 0.48 mM/min/mg protein; L: 3.08 ± 0.85 mM/min/mg protein; LC: 2.11 ± 0.44 mM/min/mg protein; LN: 1.13 ± 0.51 mM/min/mg protein) in the ileum mitochondria of the diarrheic rats. In colonic mucosa, mitochondrial enzymatic activities were restored after eliminating lactose from the diet.ConclusionThese results suggest that dietary nucleotides promote earlier restoration of the ileal mitochondrial function after chronic diarrhea.
Gastrointestinal Motility and Sensory Abnormalities May Contribute to Food Refusal in Medically Fragile Toddlers
Authors: Zangen Tsili , Ciarla Carla , Zangen Samuel , Di Lorenzo Carlo , Flores Alex F. , Cocjin Jose , Reddy Sarabudla Narasimha , Rowhani Anita , Schwankovsky Lenore , Hyman Paul E. 
Published: January 2024

ABSTRACTBackgroundIn chronically ill children who refuse to eat, surgery to correct anatomic problems and behavioral treatments to overcome oral aversion often succeed. A few patients fail with standard treatments. The aims of the study were to: 1) investigate motility and gastric sensory abnormalities and 2) describe treatment that was individualized based on pathophysiology in children who failed surgery and behavioral treatments.MethodsWe studied 14 patients (age 1.5–6; mean 2.5; M/F: 7/7). All had a lifelong history of food aversion and retching or vomiting persisting after feeding therapy and fundoplication. All were fed through gastrostomy or gastro‐jejunostomy tubes. We studied esophageal and antroduodenal manometry, and gastric volume threshold for retching. We identified when gastric antral contractions were associated with retching and pain. A multidisciplinary treatment program included a variable combination of continuous post‐pyloric feedings, drugs to decrease visceral pain, drugs for motility disorders, and behavioral, cognitive, and family therapy. We interviewed parents 2–6 months following testing to evaluate symptoms, mode of feeding and emotional health.ResultsWe found a motility disorder alone in 2, decreased threshold for retching alone in 5 and both motility and sensory abnormalities in 7. After treatment, 6 of 14 (43%) began eating orally and 80% had improved emotional health. Retching decreased from 15 episodes per day to an average of 1.4 per day (p <0.01).ConclusionsUpper gastrointestinal motor and/or sensory disorders contributed to reduced quality of life for a majority of children and families with persistent feeding problems. A multidisciplinary approach improved symptoms and problems in these children
Can Pre‐Neoplastic Lesions be Detected in Gastric Biopsies of Children with Helicobacter pylori Infection?
Authors: Guarner Jeannette , Bartlett Jeanine , Whistler Toni , Pierce‐Smith Daphne , Owens Marilyn , Kreh Rachel , Czinn Steven , Gold Benjamin D. 
Published: January 2024

ABSTRACTBackgroundActive gastritis, gastric mucosal atrophy and intestinal metaplasia are lesions associated with Helicobacter pylori infection. Atrophy and intestinal metaplasia are only seen in adults.ObjectivesWe describe pediatric patients with atrophy and metaplasia, and compare the inflammatory response in these patients to controls.MethodsAs part of a multicenter study of pediatric H. pylori infection, gastric biopsy specimens obtained during diagnostic upper endoscopy of 19 H. pylori‐infected children and 45 uninfected controls were reviewed and graded by using the updated Sydney system. The inflammatory response was characterized using immunohistochemistry for T lymphocytes, B lymphocytes, and macrophages, and TUNEL assay for apoptosis.ResultsHistology of H. pylori‐infected and control biopsy specimens showed active gastritis in 32% and 2% respectively (P = 0.002). Mild intestinal metaplasia was found in 4 H. pylori‐infected children, in two of whom it appeared to be accompanied by atrophy. Specimens from patients with H. pylori infection contained increased numbers of B lymphocytes in lymphoid nodules, and apoptosis in the superficial epithelium and inflammatory cells. T lymphocytes and macrophages appeared in similar numbers in specimens from controls and infected patients.ConclusionsWe describe intestinal metaplasia associated with H. pylori infection in children. Since atrophy usually precedes intestinal metaplasia in adults, we suggest that atrophy exists in children. High numbers of B lymphocytes and apoptosis in the surface epithelium are seen in patients with H. pylori infection and may be related to the development of atrophy and intestinal metaplasia.
Maternal Education and the Incidence and Duration of Breast Feeding: A Prospective Study
Authors: Bertini Giovanna , Perugi Silvia , Dani Carlo , Pezzati Marco , Tronchin Michele , Rubaltelli Firmino F. 
Published: January 2024

ABSTRACTIntroductionDuration of breast feeding and factors possibly affecting duration were studied in a population of 2174 newborn infants, with gestational age of >37 weeks, who were born in the Department of Obstetrics and Gynaecology at the University of Florence Hospital between November 15, 1997, and November 14, 1998.Patients and MethodsNine hundred mothers agreed to participate in the study. Five questionnaires were completed at the end of the 1st, 3rd, 6th, 9th, and 12th postpartum month. These dealt with infant feeding practices, including breast feeding during the previous week. Breast feeding duration was defined as short (1 month); medium‐short (>1 month–<3 months); medium (>3–<6 months); medium‐long (>6–<9 months), and long (>9 months).ResultsThe authors found that 76.3%, 64.7%, 42.3%, 26.4%, and 17% of mothers were still breast feeding at 1, 3, 6, 9, and 12 months after delivery, respectively. The multivariate analysis of the correspondence shows that lack of breast feeding is associated with a birth weight of less than 3000 g, a low level of maternal education, and maternal profession as a housewife or blue collar worker in the commercial sector. A period of breast feeding defined as short or medium‐short is associated with mothers who smoke, primiparous mothers, and absence of maternal allergy. The survival curves highlight how the single factor of smoking is an element that leads to a significant difference in the duration of breast feeding. The multiple Cox regression analysis shows a significant negative influence associated with birth weight of less than 3000 g, maternal smoking, and first parity. Above all, among low–birth‐weight infants of mothers who smoke, there is a strong correlation with a shorter duration of breast feeding.DiscussionThere is still a need for programs that support and encourage breast feeding, focusing particularly on mothers with a low level of education who give birth to a low‐weight infant, primiparous mothers, and smokers.
Dietary Nucleotides Accelerate Changes in Intestinal Lymphocyte Maturation in Weanling Mice
Authors: Manzano Manuel , Abadía‐Molina Ana Clara , Olivares Enrique‐García , Gil Angel , Rueda Ricardo 
Published: January 2024

ABSTRACTObjectiveNucleotides, the building blocks of nucleic acids, are normal components of the mammalian diet. These molecules have been implicated in biologic processes, such as the stimulation of the immunologic response. Nucleotides have also been considered as conditionally essential nutrients for infant formulas. The authors evaluated the influence of dietary nucleotides on the expression of several surface antigens by different intestinal lymphocyte populations in weanling mice.MethodsMice at weaning were fed a semipurified diet with or without 3 g/kg of each of the following nucleotides: adenosine monophosphate, cytosine monophosphate, guanosine monophosphate, and uridine monophosphate. Animals were killed at different times (0, 4, 7, 12, and 18 days) after weaning, and lymphocytes from intestinal Peyer's patches, epithelium, and lamina propria were isolated. The expression of different antigens (CD3, CD4, CD8α, CD8β, TCRαβ, TCRγδ, CD5, CD22 and CD45R) was analyzed by flow cytometry.ResultsThe expression of these antigens changed parallel to the maturation of the lymphocytes from Peyer's patches, epithelium, and lamina propria. However, developmental changes of expression for most of the antigens occurred sooner in the animals fed the diet supplemented with nucleotides. The expression of T and B antigens was different in the lymphocyte populations analyzed and also changed according to the diet within each population. In general, nucleotides promoted the expression of B‐ and T‐helper cell antigens.ConclusionsThe authors conclude that dietary nucleotides may affect the process of maturation and differentiation of intestinal lymphocytes, which usually takes place at weaning.
Leptin and Cytokines Levels in Children with Failure to Thrive
Authors: Shaoul Ron , Kessel Aharon , Toubi Elias , Lanir Amos , Glazer Oded , Jaffe Michael 
Published: January 2024

ABSTRACTBackgroundThe majority of cases of failure to thrive (FTT) are non‐organic. Many of these patients present with significant decreased caloric intake. It appears as if the appetite regulation center in the hypothalamus is not attuned to the calorie requirements of the infant.ObjectiveOur hypothesis was that some cases of non‐organic FTT might be caused by abnormalities in hunger/satiety control secondary to neuroendocrine or cytokine imbalance. The aim of this study was to investigate which hormonal/cytokine profiles could be assigned to a defined category of FTT, namely organic, psychosocial and idiopathic subgroups.Study design34 patients were enrolled and 32 completed the study (12 controls, 12 idiopathic FTT, 5 organic FTT, and 3 psychosocial FTT). Each child was assessed by a pediatric gastroenterologist, dietician, and social worker and underwent appropriate laboratory investigation during which leptin, IL1, IL6 and TNF‐α levels were determined. The Mann‐Whitney U test was used to compare the groups.ResultsIL6 was the only cytokine that showed significant differences between FTT patients (4.06 ± 6.3 pg/ml) and normal controls (0.0 pg/ml (p = 0.028). Leptin values were significantly higher in the normal control group (1632 ± 483 pg/ml) as compared to FTT patients (685 ± 687 pg/ml) (p = 0.001).ConclusionsOur results indicate that leptin does not play a role in the pathogenesis of anorexia in children with FTT. It is however, possible that IL6 may be an important factor in the etiology of anorexia in patients with FTT.
CARD15 Genotype and Phenotype Analysis in 55 Pediatric Patients With Crohn Disease From Saxony, Germany
Authors: Sun Liping , Roesler Joachim , Rösen‐Wolff Angela , Winkler Ulf , Koch Rainer , Thürigen Anett , Henker Jobst 
Published: January 2024

ABSTRACTObjectivesCrohn disease is a chronic inflammatory bowel disorder that is caused by environmental and genetic factors. Mutations in the CARD15 gene have been recently identified to be associated with the disease. Until now no genetic study has focused directly on a pediatric population.MethodsThe authors sequenced all 12 exons of the CARD15 gene in 55 pediatric patients with Crohn disease from Saxony. Their average age at onset was 11.2 years (1–17.5 years). The authors also evaluated the genotype‐phenotype relationship in the patients.ResultsFourteen different polymorphic and/or disease‐related nucleotide alterations have been identified in the patients. Sixty‐five percent of their genomic DNA samples harbored at least one of six mutations within the CARD15 gene, which previously has been identified as being associated with Crohn disease. The authors found that the cytosine insertion mutation 3020insC was significantly more common in their pediatric population than in patients with Crohn disease (26% versus 11% of the alleles) whose results were reported in the literature. The genotype–phenotype analysis showed that the authors' patients with at least one of the six CARD15 disease‐associated mutations had a high risk of inflammation located in the terminal ileum and ascending colon. In 10 of 19 patients with two mutations, intestinal resection surgery was necessary because of stricturing.ConclusionsIn the authors' pediatric patients, the genetic influence on Crohn disease was more pronounced than that reported in any other study, and it strongly affected the clinical phenotype.
Establishing Enteral Feeding in Preterm Infants with Feeding Intolerance: A Randomized Controlled Study of Low‐dose Erythromycin
Authors: Ng Steven Chin‐Yuen , Gomez Joseph Manuel , Rajadurai Victor Samuel , Saw Seang‐Mei , Quak Seng‐Hock 
Published: January 2024

ABSTRACTObjectiveA prospective, double‐blind, randomized, controlled trial was conducted to evaluate the effect of low‐dose erythromycin on the time taken to attain full enteral feedings in preterm infants with very low birth weight and feeding intolerance.MethodsTwo groups of preterm infants (birth weight ≤ 1500 g) with feeding intolerance were randomized to either low‐dose erythromycin (5 mg/kg every 8 hours) or 5% dextrose placebo, both of which were discontinued 1 week after full enteral feedings were tolerated. The primary outcome variable was the time taken to attain full enteral feedings of at least 130 mL/kg/d.ResultsThe gestational age at birth was similar in the two groups (erythromycin, 27.1 ± 1.9 weeks; placebo, 27.5 ± 2.9 weeks). The mean birth weight of the erythromycin group was lower (806.3 ± 215.6 g) than the placebo group (981.4 ± 285.4 g; P = 0.18), and included more infants who were small for gestational age (4/13 = 31% versus 1/11 = 9%; P = 0.224). There was no difference between the two groups with regard to the volume of feedings they were receiving at the time of enrollment. Reduction in symptoms of gastroesophageal reflux was similar in the two groups. 3 of 13 in the erythromycin group and 4 of 11 in the placebo group improved during the study (P = 0.565). The mean time to attain full enteral feedings after enrollment was 24.9 + 2.9 days in the erythromycin group and 30.8 ± 4.1 days in the placebo group, a difference that did not reach statistical significance (P = 0.17).ConclusionsLow‐dose erythromycin did not reduce the time taken to attain full enteral feedings in preterm infants with very low birth weight and feeding intolerance. Gastroesophageal reflux decreased as a consequence of maturation of the gastrointestinal tract and not because of erythromycin. These preliminary results justify verification in larger multicenter trials.
Increased Levels of Hemostatic Proteins are Independent of Inflammation in Glycogen Storage Disease Type Ia
Authors: Marfaing‐Koka Anne , Wolf Martine , Boyer‐Neumann Catherine , Meyer Dominique , Odievre Michel , Labrune Philippe 
Published: January 2024

ABSTRACTObjectivesGlycogen storage disease type Ia (GSD‐Ia), a congenital deficiency of hepatic glucose‐6‐phosphatase activity, is often associated with hyperproteinemia. To document the mechanism of hyperproteinemia, the proteins of the hemostatic system were analyzed according to their site of synthesis: hepatocyte, endothelial cell, or both. The role of inflammation was investigated by the measurement of tumor necrosis factor alpha (TNF‐α) and interleukin‐6 (IL‐6) levels in plasma.MethodsTwenty‐seven patients with GSD‐Ia were evaluated, as were 14 patients with other types of GSD and 30 healthy control subjects. Of the 41 patients with GSD, 15 also had hepatic adenoma (14 patients with GSD‐Ia and 1 with GSD type III).ResultsIn patients with GSD‐Ia, there was a two‐fold increase in all hepatocyte‐synthesized proteins (i.e., factor VII, protein C, C4b binding protein) compared with control subjects and patients with other types of GSD. The proteins with mixed endothelial and hepatocyte origin (i.e., antithrombin and protein S) also were significantly increased but to a lesser extent. In contrast, the mean concentration of von Willebrand factor, which is exclusively synthesized in endothelial cells, was normal, as was the concentration of TNF‐α and IL‐6.ConclusionsThese results suggest that the hyperproteinemia of GSD‐Ia (including hemostatic proteins) is attributable to hepatocyte dysfunction and not related to an inflammatory process.
Effects of Highly Purified Eicosapentaenoic Acid on Erythrocyte Fatty Acid Composition and Leukocyte and Colonic Mucosa Leukotriene B4 Production in Children With Ulcerative Colitis
Authors: Shimizu Toshiaki , Fujii Tohru , Suzuki Ryuyo , Igarashi Jun , Ohtsuka Yoshikazu , Nagata Satoru , Yamashiro Yuichiro 
Published: January 2024

ABSTRACTBackgroundn‐3 Polyunsaturated fatty acids (PUFAs) have been suggested as a treatment for ulcerative colitis (UC). However, the efficacy of n‐3 PUFAs against UC has not been examined in children. Therefore, the authors investigated the effects of eicosapentaenoic acid (EPA) on fatty acid composition and leukotriene (LT) production in children with UC.MethodsFor 2 months the authors administered highly purified EPA ethyl ester (EPA‐E) (1.8 g/d) to children with UC in remission. Colonic mucosal histology, fatty acid composition of erythrocyte membrane phospholipids, and LTB4 production by leukocytes and colonic mucosa were measured before and 2 months after the initiation of EPA‐E treatment.ResultsNo patients relapsed during the study period, and no significant differences were detected in laboratory findings obtained before and 2 months after the initiation of EPA‐E ingestion. There were no significant differences in mucosal histologic scores before and 2 months after EPA‐E treatment. The EPA levels in erythrocyte membranes 2 months after the initiation of EPA‐E treatment were significantly higher than before treatment, but the other fatty acids showed no significant changes. LTB4 production by leukocytes and rectal mucosa after 2 months of EPA‐E treatment was significantly lower than before treatment.ConclusionEPA‐E treatment increased the levels of EPA in erythrocytes and decreased LTB4 levels produced by leukocytes and colonic mucosa. To assess the concomitant clinical changes, we should examine the long‐term effects of EPA‐E ingestion on the maintenance of remission in children with UC.
Hyperhomocystinemia in Children With Inflammatory Bowel Disease
Authors: Nakano Emi , Taylor Christopher J. , Chada Lavleen , McGaw Jean , Powers Hilary J. 
Published: January 2024

ABSTRACTObjectivesThromboembolism is a significant cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). Plasma total homocysteine (tHcy) is a risk factor for vascular disease and has been implicated as a mediator of thromboembolic events in adults with IBD. The authors studied the link between tHcy and IBD in children, in whom associations may be clearer, and investigated associations with plasma von Willebrand factor antigen, a marker of vascular damage.MethodsThis cross‐sectional study included 43 patients with IBD (27 Crohn disease, 9 ulcerative colitis, and 7 indeterminate colitis) and 46 control subjects from a pediatric gastroenterology clinic. Plasma tHcy, plasma 5‐methyl tetrahydrofolate, red cell folate, plasma vitamin B12, plasma von Willebrand factor antigen, and methylene tetrahydrofolate reductase (MTHFR) genotype (for the C677T mutation) were measured.ResultsPlasma tHcy concentrations were higher in children with IBD than in control subjects, when corrected for age (P < 0.05), and plasma tHcy was negatively correlated with plasma 5 methyl tetrahydrofolate (P < 0.0005). Plasma 5 methyl tetrahydrofolate and age were the main predictors of plasma tHcy. Neither MTHFR genotype nor von Willebrand factor showed any association with any other measure, and there were no differences between children with IBD and control subjects.ConclusionsElevated plasma tHcy is a consequence of IBD in children, probably mediated by poor folate status associated with diet or the pathophysiology of the disease.