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Objective Human milk (HM) has antibacterial properties due to the presence of immune-modulators, including lactoferrin (LF). This study will determine effect(s) of HM maturation, fortification, and storage conditions on LF levels and its antibacterial properties. Study Design HM samples (n = 30) were obtained from preterm and term mothers. The LF levels were analyzed by ELISA, and the antibacterial activity was measured after inoculation with Escherichia coli. Results The highest level of LF in preterm HM was observed in the first week of lactation. However, storage of preterm HM at 4°C decreased LF levels significantly. Both LF levels and antibacterial activity in preterm HM was lower compared with term HM, but significantly higher than donor HM even after HM-based fortification. LF supplementation of donor HM improved its antibacterial activity. Conclusion Preterm infants fed donor HM, formula, or stored HM at 4°C may benefits from LF supplementation to improve HM antibacterial properties. Key Points Milk LF levels vary with storage and maturity. Donor milk is deficient in LF even after adding HM-based fortification. Donor HM and formula fed infants may benefit from LF. [ABSTRACT FROM AUTHOR]

Powell, Saul R., Ellen M. Gurzenda, Mark A. Wingertzahn, and Raul A. Wapnir. Promotion of copper excretion from the isolated rat heart attenuates postischemic cardiac oxidative injury. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H956-H962, 1999.--This study examined the role of Cu as a mediator of cardiac postischemic oxidative injury. Isolated rat hearts were subjected to 20 rain of normothermic global ischemia, followed by 30 rain of reperfusion; after 20 rain of preischemic loading with Krebs-Henseleit buffer [+ or -] 20 or 30 [micro]M zinc-bis-histidinate (Zn-[His.sub.2]), 0.5 mM deferoxamine (DEF) or 42 [micro]M neocuproine (NEO). Postischemic developed systolic pressure and rate-pressure product were highest and postischemic end-diastolic pressure was lowest in hearts treated with 20 or 30 [micro]M Zn-[His.sub.2] and 0.5 mM DEF. Cu efflux was significantly increased by 225 and 290% (end of preischemic loading), and 325 and 375% (immediate postischemic period) of control basal rates in hearts treated with 30 [micro]M Zn-[His.sub.2] and 0.5 mM DEF, respectively. NEO did not effect any of these parameters. By the end of ischemia, protein carbonyls were lowest in Zn-[His.sub.2]-treated hearts and highest in DEF-treated hearts when compared with control hearts. The results of this study suggest that removal of redox-active Cu before ischemia has beneficial effects, indicating a mediatory role in postischemic cardiac oxidative injury. iron; protein carbonyls; ischemia-reperfusion; zinc

Problem: Placental infection induces increased levels of pro‐inflammatory cytokines, which have been implicated in the pathogenesis of pre‐term labor. Endotoxin tolerance is a phenomenon in which exposure to a dose of endotoxin makes tissue less responsive to subsequent exposures. The objective of our study was to determine whether repeated exposure to endotoxin will induce a tolerant phenotype in normal human second‐trimester placental tissue. Methods of study: Human second‐trimester placental explants from elective termination of pregnancy were cultured and exposed to endotoxin (LPS). After 24 hours, the media was collected for analysis, and the explants were re‐exposed to LPS after adding fresh media for another 24 hours. This process was repeated for a total of 4 LPS doses. The media was collected from each day and analyzed for cytokine levels. Results: The first LPS treatment stimulated the secretion of the pro‐inflammatory cytokines IL‐1β and TNF‐α. However, their production was significantly diminished with repeated LPS doses. Production of the anti‐inflammatory cytokines, IL‐1ra and IL‐10, was also stimulated by the first LPS treatment, but secretion was more gradually and moderately decreased with repeated LPS doses compared to the pro‐inflammatory cytokines. The ratios of the anti‐inflammatory/pro‐inflammatory mediators (IL‐1ra/IL‐1β and IL‐10/TNF‐α) indicate a progressively more anti‐inflammatory milieu with repeated LPS doses. Conclusion: Repeated LPS exposure of human second‐trimester placental tissues induced endotoxin tolerance. We speculate that endotoxin tolerance at the maternal‐fetal interface will protect the fetus from exaggerated inflammatory responses after repeated infectious exposure. [ABSTRACT FROM AUTHOR]