Background and Objective: Intestinal permeability in preterm infants represents a critical balance between absorption of nutritional agents and protection from dangerous pathogens. This study identified the relationship between feeding type (human milk and formula) and intestinal permeability as measured by lactulose to mannitol ratio in preterm infants in the first postnatal month. Study Design: Sixty-two preterm (Յ32 weeks of gestation) infants had assessment of feeding type and evaluation with enteral lactulose and mannitol administration and urinary measurement at three time points in the first postnatal month. Results: Infants who received the majority of feeding as human milk (Ͼ75%) demonstrated significantly lower intestinal permeability when compared to infants receiving minimal or no human milk (Ͻ25% or none) at postnatal days 7, 14, and 30 (p ϭ 0.02, 0.02, and 0.047, respectively). When infants receiving any human milk were compared to infants receiving formula only, a significant difference existed at day 7 and day 14 but not for day 30 (p ϭ 0.04, 0.02, and 0.15, respectively). With evaluation over the complete study period, exclusively formulafed infants demonstrated a 2.8-fold higher composite median lactulose/mannitol ratio when compared with those who received any human milk. Infants who received Ͼ75% of enteral feeding as mother's milk demonstrated a 3.8-fold lower composite median ratio when compared to infants receiving Ͻ25% or no mother's milk. Conclusion: Preterm infant intestinal permeability was significantly decreased for those receiving human milk versus formula in a dose-related manner in the first postnatal month.

High-dose vitamin D was effective in increasing 25(OH)D levels in fully breastfeeding mothers to optimal levels without evidence of toxicity. Breast milk [Ca] and its decline in both groups during 1 to 4 months were independent of maternal vitamin D status and regimen. Both the mother and her infant attained improved vitamin D status and maintained normal [Ca].

Objective: With vitamin D deficiency as a serious public health problem, vitamin D status at birth was measured in neonates at latitude 32172 0 (southeastern United States).Study Design: In umbilical cord blood, vitamin D status, demonstrated by circulating 25-hydroxyvitamin D, was measured and related to race and season of birth.Result: The mean±standard deviation of 25-hydroxyvitamin D in 100 cord blood samples was 13.5±8.3 ng/ml for the cohort. African-American infants, with a mean±standard deviation of 10.5±6.0 ng/ml, demonstrated significantly lower vitamin D status than Caucasian infants, with a mean±standard deviation of 19.5±9.6 ng/ml (P<0.0001). By season, the mean 25-hydroxyvitamin D level at birth in NovemberMarch compared to April-October was 11.3 ng/ml lower in Caucasian infants (from 29.0 to 17.7 ng/ml) and 3 ng/ml lower in African-American infants (from 13.1 to 10.1 ng/ml).

Although Bordetella pertussis contains and transcribes loci encoding type III secretion system (TTSS) homologues, expression of TTSS-associated proteins has been reported only for non-laboratory-adapted Irish clinical isolates. Here we confirm such a result for clinical isolates obtained from patients treated in Argentinean hospitals. Moreover, we demonstrate that the expression of TTSS-associated proteins is independent both of the year in which the isolate was obtained and of the types of polymorphic alleles for other virulence factors but is dependent on environmental growth conditions. Interestingly, we observed that TTSS-associated protein expression is lost after successive in vitro passages but becomes operative again when bacteria come into contact with the host. This in vivo activation of TTSS expression was observed not only for clinical isolates previously adapted to the laboratory after successive in vitro passages but also for vaccine strains that did not express the system in vitro. The reversibility of TTSS expression, demonstrated by its switching off-on when the bacterium comes into contact with the host, appears to be an adaptive response of this pathogen.