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Objective: Preterm infants often show intolerance to the first enteral feeds, and the structural and functional basis of this intolerance remains unclear. We hypothesized that preterm and term neonates show similar gut trophic responses to feeding but different expression of intestinal functional proteins, thus helping to explain why preterm neonates are more susceptible to feeding-induced disorders such as necrotizing enterocolitis (NEC)., Methods: Incidence of feeding-induced NEC, intestinal mass, and brush border enzyme activities, and the intestinal proteome in preterm cesarean-delivered pigs were compared with the corresponding values in pigs delivered spontaneously at term., Results: For both preterm and term pigs, mucosal mass and maltase activity increased (50%-100%), whereas lactase decreased (-50%), relative to values at birth. Only preterm pigs were highly NEC sensitive (30% vs 0% in term pigs, P < 0.05). By gel-based proteomics, 36 identified proteins differed in expression, with most proteins showing downregulation in preterm pigs, including proteins related to intestinal structure and actin filaments, stress response, protein processing, and nutrient metabolism., Conclusions: Despite that enteral feeding induces rapid gut tropic response in both term and preterm neonates, the expression level of cellular proteins related to mucosal integrity, metabolism, and stress response differed markedly (including complement 3, prohibitin, ornithine carbamoyltransferase, and arginosuccinate synthetase). These proteins may play a role in the development of functional gut disorders and NEC in preterm neonates.

As of 1991 we had ascertained 42 native resident Faroese plus 12 non-resident "migrant" Faroese with clinical onset of MS in this century. The resident series comprised four successive epidemics beginning in 1943 and then at 13-year intervals thereafter, a separation of very high statistical significance (p < 0.00001). We concluded that the first epidemic in the Faroes resulted from the introduction of a specific but unknown infection which we call the "primary MS affection" (PMSA) by occupying British troops during World War II. Clinical neurologic MS (CNMS) is then the rare late sequel of infection with PMSA. The first epidemic defined age of susceptibility to PMSA as age 11 to 45 at onset of exposure. Models of transmission used for the first three epidemics included the need for two years of exposure before PMSA acquisition and limitation of transmissibility of PMSA to age 13 to 26. With these conditions successive cohorts of susceptible Faroese were defined to account for the second and third epidemics, and they also predicted the occurrence of the fourth epidemic. Further consideration of these models suggests transmissibility is even more limited, perhaps to age 20 to 26 or so.