Food fussiness is associated with family environmental factors in 1-3-year-old children: A large-scale cross-sectional study.

The effects of environmental factors on eating behavior and food intake are not well-known during toddlerhood. This is a cross-sectional study exploring the association between family environmental factors, food fussiness and poorly diversified diet. N = 1679 healthy children aged 1-3 years were recruited by general practitioners and pediatricians. Two validated questionnaires were used: the Children's Eating Behavior Questionnaire (CEBQ), which includes a food fussiness (FF) dimension, and the Infant and Child Feeding Index (ICFI) which assesses diet diversification. Factors associated with FF and diet diversification were identified by multivariate logistic regression. Of the 1356 analyzed children, 19.5% were fussy (CEBQ-FF subscore >3). Food fussiness was significantly more common in older children (25.1% of 2-3-year-olds, versus 15.2% of 1-2-year-olds; OR = 1.7) and those conceived with medical assistance (OR = 3.2). Food fussiness was also observed more often in children exposed to distractions during meals (OR = 1.8), rewarded by parents to finish meals (OR = 3.9), free to eat at will (OR = 3.7), or who ate only occasionally with the whole family (OR = 2.0). Unsatisfactory dietary diversification (ICFI≤13.8) was observed in 21.8% of children and was not significantly associated with any variable. No association was found between eating behavior and dietary diversification level. This study showed that food mistrust tends to increase with age in 1-3-year-old children. It highlighted the influence of environmental factors on FF, including family habits during meals. Assisting parents with child food fussiness may help reduce later unhealthy dietary patterns.

Complementary bottles during the first month and risk of cow's milk allergy in breastfed infants.

AIM: To assess the impact of complementary feeding bottles given at maternity hospital and/or over the first month after discharge from the maternity ward on cow's milk allergy (CMA) risk in breastfed infants. METHODS: Case-control study involving infants aged 6-9 months and who were breastfed for at least 1 month. RESULTS: In 554 cases with a diagnosis of CMA and 211 controls, feeding bottles at maternity hospital, feeding bottles during the first month of life, avoidance of dairy products during pregnancy or breastfeeding, family history of allergy, intake of antibiotics and consumption of proton-pump inhibitors or antacids by the infant during the first month of life were associated with increased risk of CMA in a univariate model. In a multivariate model, only feeding bottle at maternity hospital (OR = 1.81 [1.27; 2.59]), family history of allergy (OR = 2.83 [2.01; 3.99]) and avoidance of dairy products during pregnancy or breastfeeding (OR = 5.62 [1.99; 15.87]) were independent risk factors of CMA. CONCLUSION: Complementary bottles given at maternity hospital to newborns who will be exclusively breastfed increases the later risk of CMA. Similarly, avoidance of dairy products during pregnancy or breastfeeding should be discouraged.

Functional Gastrointestinal Disorders in Outpatients Aged up to 12 Months: A French Non-Interventional Study.

BACKGROUND: The aim of this study was to estimate the frequency of functional gastrointestinal disorders (FGIDs) in infants aged up to 12 months according to the new ROME IV criteria defining these disorders, and to describe the management of FGIDs in France. METHODS: This French non-interventional, cross-sectional, and multicenter study was conducted among private-outpatient physicians who each included four consecutive patients aged up to 12 months. The frequency of FGIDs was described using the ROME IV criteria versus clinicians' diagnosis. The characteristics of infants with and without FGID were compared, and the management of the FGIDs was described. RESULTS: In the 1722 infants analyzed, the following frequencies were observed according to the ROME IV criteria versus the physicians' diagnosis: regurgitation 41% versus 45%; colic 18% versus 30%; constipation 9% versus 19%; diarrhea 3% versus 8%. Of note, FGID infants were less frequently exclusively breastfeeding at the maternity hospital (p < 0.001), were introduced to cow's milk earlier after leaving the maternity hospital (p < 0.001), and more frequently had symptoms suggestive of cow's milk protein allergy (p < 0.001). Physicians frequently recommended an adapted infant formula (in 77% to 82% of cases depending on the FGID diagnosed) and prescribed a specific treatment in 51% to 66% of infants (probiotics: 35% to 64%). CONCLUSIONS: This real-world study confirms the high frequency of FGIDs in infants in France, and provides new information regarding the characteristics of FGID infants.

Nardilysin, a basic residues specific metallopeptidase that mediates cell migration and proliferation.

Nardilysin (NRDc), a metallopeptidase of the M16 family, presents, in vitro, cleavage specificity for basic residues. Depending on the cell type, it is cytoplasmic, exported or cell surface associated. As a new receptor for heparin-binding EGF-like growth factor (HB-EGF), NRDc was recently shown to be involved in cellular migration and proliferation. Since for those processes its enzymatic activity is not required, it is now evident that nardilysin fulfills at least two distinct functions, i.e. an HB-EGF modulator and a peptidase.

Serine/threonine protein phosphatases PP1 and PP2A are key players in apoptosis.

The reversible phosphorylation of proteins controlled by protein kinases and protein phosphatases is a major mechanism that regulates a wide variety of cellular processes. In contrast to C. elegans, recent studies in mammalian cells have highlighted a major role of serine/threonine protein phosphorylation in apoptosis. To illustrate the importance of dephosphorylation processes in apoptosis, this review will focus on recent studies suggesting that the interaction of the serine/threonine protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A) with certain regulators of the Bcl-2 family is critically involved in the control of apoptosis.

Cell death and inflammation during infection with the obligate intracellular pathogen, Chlamydia.

Infections by Chlamydia are followed by a strong inflammatory response, which is necessary to eliminate the infection, but at the same time is responsible for the pathology of infection. Resistance of infected cells against apoptosis induced by external ligands, together with the effects of IFNgamma secreted during infection, would be expected to contribute to persistence of infection. Secretion of TNFalpha plays an important role during clearance of the chlamydiae, but also triggers apoptosis of uninfected cells in infected tissues. Apoptosis of infected host-cells towards the end of the infection cycle is thought to participate in the release of chlamydiae from infected cells and propagation of the infection. Dysregulation of the apoptotic program during infection leads to a less efficient infection, but paradoxically, results in a higher inflammatory response and more severe pathology.

The metalloendopeptidase nardilysin (NRDc) is potently inhibited by heparin-binding epidermal growth factor-like growth factor (HB-EGF).

Nardilysin (N-arginine dibasic convertase, or NRDc) is a cytosolic and cell-surface metalloendopeptidase that, in vitro, cleaves substrates upstream of Arg or Lys in basic pairs. NRDc differs from most of the other members of the M16 family of metalloendopeptidases by a 90 amino acid acidic domain (DAC) inserted close to its active site. At the cell surface, NRDc binds heparin-binding epidermal growth factor-like growth factor (HB-EGF) and enhances HB-EGF-induced cell migration. An active-site mutant of NRDc fulfills this function as well as wild-type NRDc, indicating that the enzyme activity is not required for this process. We now demonstrate that NRDc starts at Met(49). Furthermore, we show that HB-EGF not only binds to NRDc but also potently inhibits its enzymic activity. NRDc-HB-EGF interaction involves the 21 amino acid heparin-binding domain (P21) of the growth factor, the DAC of NRDc and most probably its active site. Only disulphide-bonded P21 dimers are inhibitory. We also show that Ca(2+), via the DAC, regulates both NRDc activity and HB-EGF binding. We conclude that the DAC is thus a key regulatory element for the two distinct functions that NRDc fulfills, i.e. as an HB-EGF modulator and a peptidase.