Xanthan- and Rice Cereal-Based Thickeners in Infants: A Multidisciplinary Single-Center Experience.

Some infants aspirate thin liquids and must be fed thickened liquids in order to protect the lungs. However, thickeners have not been fully studied for safety. Xanthan-based thickeners have been implicated in the development of necrotizing enterocolitis and rice cereal-based thickeners have been associated with constipation and excessive weight gain. The aim of this study was to compare rates of adverse events between both thickeners. Methods: Single-center retrospective chart review conducted at a tertiary pediatric care center between January 2013 and July 2017. All infants deemed unsafe for oral feeding and treated with xanthan- or rice cereal-based milk thickeners were included. Data were extracted from the medical records and patients categorized according to the type of thickener. Primary outcome was the occurrence of diarrhea, constipation, overweight, and obesity at 3-6 and 6-12 months after thickener initiation. Appropriate statistical tests were used. In addition, an e-mail was sent to 14 level III Canadian Pediatric hospitals inquiring about their practice. Results: We identified 53 patients to be included in the study; 20 used xanthan-based- and 33 used rice cereal-based milk thickeners. Rates of diarrhea, constipation, overweight, and obesity at 3-6 and 6-12 months after initiation were not different between thickeners. Important variability concerning thickening practices was reported by the 8 centers that responded. Conclusions: In infants treated with milk thickeners, xanthan-based or rice cereal-based thickeners may have similar safety profiles that require further investigation including a larger number of patients.

The plant-based by-product diets for the mass-rearing of Acheta domesticus and Gryllus bimaculatus.

Edible insect rearing could provide one alternative for protein production by having a smaller environmental impact than traditional livestock farming due to insects' ability to convert organic side streams. Currently, the insect rearing industry utilizes soybeans as a major source of protein in the feeds. Protein-rich by-products of food industry could be used to replace them in insect feeds, but it is not known if they also meet the insects' nutritional requirements. Our study evaluated the growth performance of two widely used edible cricket species, Acheta domesticus and Gryllus bimaculatus (Orthoptera: Gryllidae), on 18 experimental diets. The experimental diets included commercial chicken feeds and cricket diets, where soybean was partly and completely replaced with by-products from food industry: potato protein, barley mash, barley feed, compressed leftover of turnip rape and mix of broad bean and pea on three levels of protein. We found that the high- and medium-protein turnip rape and barley mash diets produced the highest yield and an increase in all performance variables. Overall, the high- and medium-protein diets produced the highest yield, growth and fastest development. Our results showed that by-products of food industry could be utilized as a part of the cricket feeds and thus advance the goals of circular economy.

Doubles game: Src-Stat3 versus p53-PTEN in cellular migration and invasion.

We have recently shown that Src induces the formation of podosomes and cell invasion by suppressing endogenous p53, while enhanced p53 strongly represses the Src-induced invasive phenotype. However, the mechanism by which Src and p53 play antagonistic roles in cell invasion is unknown. Here we show that the Stat3 oncogene is a required downstream effector of Src in inducing podosome structures and related invasive phenotypes. Stat3 promotes Src phenotypes through the suppression of p53 and the p53-inducible protein caldesmon, a known podosome antagonist. In contrast, enhanced p53 attenuates Stat3 function and Src-induced podosome formation by upregulating the tumor suppressor PTEN. PTEN, through the inactivation of Src/Stat3 function, also stabilizes the podosome-antagonizing p53/caldesmon axis, thereby further enhancing the anti-invasive potential of the cell. Furthermore, the protein phosphatase activity of PTEN plays a major role in the negative regulation of the Src/Stat3 pathway and represses podosome formation. Our data suggest that cellular invasiveness is dependent on the balance between two opposing forces: the proinvasive oncogenes Src-Stat3 and the anti-invasive tumor suppressors p53-PTEN.

p53 suppresses Src-induced podosome and rosette formation and cellular invasiveness through the upregulation of caldesmon.

The tumor-suppressive role of p53 at the level of tumor initiation is well documented. It has also been shown previously that p53 acts against tumor progression/metastasis. However, its role in modulating cell migration and invasion leading to metastasis is poorly understood. In this study, using vascular smooth muscle cells and NIH 3T3 fibroblast cells, we have shown that p53 potently suppresses Src-induced podosome/rosette formation, extracellular matrix digestion, cell migration, and invasion. The overexpression of exogenous wild-type p53 or the activation of the endogenous p53 function suppresses, while the short hairpin RNA-mediated knockdown of p53 expression or the pageing of its function exacerbates, Src-induced migratory and invasive phenotypes. We have also found that p53 expression and function are downregulated in cells stably transformed with constitutively active Src that exhibit aggressive invasive properties. Lastly, p53 upregulates the expression of caldesmon, an actin-binding protein that has been shown to be an inhibitor of podosome/invadopodium formation. The ability of p53 to suppress Src phenotypes in transformed cells was largely abolished by knocking down caldesmon. This study reports a novel molecular mechanism (caldesmon), as well as a structural basis (podosomes/rosettes), to show how p53 can act as an anti-motility/invasion/metastasis agent.