Oral Feeding Assessment Predicts Length of Hospital Stay in Late Preterm Infants.

BACKGROUND: When compared with term infants, late preterm (LP) infants have greater morbidity and mortality, longer hospital stay, and greater rate of hospital readmission. Oral feeding difficulty is one of the prominent reasons for delayed discharge in LP infants. OBJECTIVE: To identify the maturity levels of LP infants' oral feeding skills (OFS) at the time of their first oral feeding and to determine the relationship between OFS maturity levels and length of hospital stay. METHODS: OFS was assessed in 48 LP infants born between 340/7 and 356/7 weeks gestational age at the time of their first oral feeding within 24 h of birth. The intake at 5 minutes, at completion of the feeding, and the duration of feeding a 15 mL prescribed volume of milk were tabulated. Proficiency expressed as percent mL consumed in the first 5 min/15 mL prescribed and rate of milk transfer over the entire feeding (mL/min) were recorded. OFS were assessed using a novel 4-level scale defined by the combined proficiency and rate of milk transfer. RESULTS: When compared with their 35-week counterparts, infants born at 34 weeks gestation had poorer OFS profiles (p = 0.035) and longer hospital stay (p < 0.001). Additionally, further analyses demonstrated that, independently, LOS was associated negatively with both GA and OFS. CONCLUSION: Assessment of OFS levels in LP infants at their first oral feeding can help identify infants at risk of oral feeding issues that may delay hospital discharge. For those infants, we speculate that provision of evidence-based efficacious interventions that improve OFS may shorten hospital stay and decrease hospital re-admissions.

Effect of food service nutrition improvements on elementary school cafeteria lunch purchase patterns.

BACKGROUND: Schools can play a major role in prevention and intervention for childhood obesity. We describe changes in elementary school cafeteria lunch sales patterns resulting from nutritional improvements in menu offerings that were part of a community-wide focus on health. METHODS: Elementary school lunch sales data were collected for 1 week in each of 7 years in a district serving a predominantly poor, rural, and Caucasian student population, with high rates of obesity. Post hoc data analyses described lunch sales patterns and related food service costs over the project years. RESULTS: The percentage of high calorie/low nutrition foods sold decreased from 22% of all sales in 2005 to 0% in 2011. High-calorie snack purchases decreased from 535 items to 0 items. The sale of fresh fruits increased by 12%. There was only a slight decline in the percentage of children who purchased cafeteria lunches over the years and a 15.2% cost increase for purchasing healthier food supplies. CONCLUSIONS: Elementary school children purchased healthier lunches when healthier menu items were offered and when less healthy foods were eliminated from the menu. There was no significant decline in the number of students who purchased lunches as nutritional improvements were made.

Reciprocal modifications of CLIC4 in tumor epithelium and stroma mark malignant progression of multiple human cancers.

PURPOSE: CLIC4, a member of a family of intracellular chloride channels, is regulated by p53, c-Myc, and tumor necrosis factor-alpha. Regulation by factors involved in cancer pathogenesis, together with the previously shown proapoptotic activity of CLIC4, suggests that the protein may have a tumor suppressor function. To address this possibility, we characterized the expression profile, subcellular localization, and gene integrity of CLIC4 in human cancers and determined the functional consequences of CLIC4 expression in tumor epithelium and stromal cells. EXPERIMENTAL DESIGN: CLIC4 expression profiles were analyzed by genomics, proteomics, bioinformatics, and tissue microarrays. CLIC4 expression, as a consequence of crosstalk between stroma and epithelium, was tested in vitro by coculture of breast epithelial tumor cells and normal fibroblasts, and the functional consequences of CLIC4 expression was tested in vivo in xenografts of human breast tumor cell lines reconstituted with CLIC4 or mixed with fibroblasts that overexpress CLIC4 transgenically. RESULTS: In cDNA arrays of matched human normal and tumor tissues, CLIC4 expression was reduced in renal, ovarian, and breast cancers. However, CLIC4 protein levels were variable in tumor lysate arrays. Transcript sequences of CLIC4 from the human expressed sequence tag database and manual sequencing of cDNA from 60 human cancer cell lines (NCI60) failed to reveal deletion or mutations in the CLIC4 gene. On matched tissue arrays, CLIC4 was predominantly nuclear in normal human epithelial tissues but not cancers. With advancing malignant progression, CLIC4 staining became undetectable in tumor cells, but expression increased in stromal cells coincident with up-regulation of alpha-smooth muscle actin, suggesting that CLIC4 is up-regulated in myofibroblasts. Coculture of cancer cells and fibroblasts induced the expression of both CLIC4 and alpha-smooth muscle actin in fibroblasts adjacent to tumor nests. Introduction of CLIC4 or nuclear targeted CLIC4 via adenovirus into human breast cancer xenografts inhibited tumor growth, whereas overexpression of CLIC4 in stromal cells of xenografts enhanced tumor growth. CONCLUSION: Loss of CLIC4 in tumor cells and gain in tumor stroma is common to many human cancers and marks malignant progression. Up-regulation of CLIC4 in tumor stroma is coincident with myofibroblast conversion, generally a poor prognostic indicator. Reactivation and restoration of CLIC4 in tumor cells or the converse in tumor stromal cells could provide a novel approach to inhibit tumor growth.