Background: During critical care in neonatal intensive care units (NICU), infants experience stressors and treatments that may produce lasting effects on adult health. An animal model simulating the NICU experience is needed to understand the impact of specific neonatal stressors. Objective: We combined approaches to develop a neonatal rat model simulating NICU stressors in order to examine the hypothesis that early stress and morphine sulfate (MS) exposure would affect development and alter adult behavior. Methods: Rat pups were exposed to stressors and given twice daily MS injections (2 mg/kg s.c.) for 5 days (postnatal days 3–7). Stress included daily maternal separation (from 08.00 to 16.00 h), hand feedings, a daily hypoxia/hyperoxia episode (100% N₂ for 8 min, then 100% O₂ for 4 min), and cold exposure (4°C for 20 min/day). Five treatment groups were formed: (1) ‘control control’ (dam reared and untreated); (2) control vehicle; (3) stress vehicle; (4) control morphine, and (5) stress morphine. Early growth and developmental indices were measured. Adult neurobehavioral tests were paw flick, passive avoidance, and forced swimming. Neonatal MS pharmacokinetics, neonatal and adult corticosterone levels, and adult hematocrit and blood pressure values were measured. Results: Neonatal stress significantly increased the mortality. Neonatal stress and MS treatment slowed early growth. Neonatal MS impaired passive avoidance learning and increased frequency, duration, and distance of forced swimming. There were no differences in corticosterone, hematocrit, or blood pressure values. Conclusions: This model simulates NICU stressors and enables measurement of acute physiological and long-term neurobehavioral indices. Neonatal MS treatment impaired the adult cognitive functioning.

Fetal or early postnatal stressors may predispose infants to develop diabetes, metabolic syndrome, or stroke. We hypothesized that postnatal stress will predispose animals to develop metabolic syndrome and impair the physiologic response to hypoxic-ischemic brain injury. We characterized the short-and long-term physiologic responses to postnatal stress by examining corticosterone (CS), glucose metabolism, and brain injury in neonatal and adult rats exposed to hypoxiaischemia (H-I). Rat pups were divided into three levels of postnatal stress from postnatal day (P) 3 to P7. All rats underwent unilateral brain injury on either P7 or P134. We measured brain injury, growth, blood pressure, urine/plasma CS, plasma leptin, insulin, and glucose before and after H-I. Postnatal stress increased neonatal CS production, exacerbated neonatal white matter injury, and was associated with adult hyperglycemia after H-I despite increased insulin production. There were no group differences in adult weight, blood pressure, or leptin. Postnatal stress exacerbated brain injury and produced adult hyperglycemia, triggered after hypoxia exposure, consistent with the hypotheses that neonates exposed to early stress are more vulnerable to hypoxia and may be predisposed to develop metabolic syndrome in adulthood. Prolonged maternal separation produced more hyperglycemia than did brief daily handling. (Pediatr Res 66: 278-282, 2009) P rolonged hospitalization in a neonatal intensive care unit is stressful because preterm infants experience prolonged isolation, gavage feedings, and multiple painful procedures. These postnatal stressors may perturb early brain development and permanently impact brain function by affecting neuronal apoptosis, neurogenesis, synaptogenesis, or vascular development. For example, neonatal isolation permanently impairs hippocampus-dependent learning and memory (1), promotes depression (2), and disrupts fear conditioning in rats (3). In addition, because prenatal events can exacerbate neonatal brain injury (4), it is possible that postnatal stress may also exacerbate neonatal H-I. Surprisingly, it is still unknown whether postnatal stress has acute or lasting effects on physiologic responses to H-I.Heart disease, cerebrovascular disease, and diabetes are among the top causes of death in the United States (CDC), and these disease processes can be influenced by early life experiences. The observation that diabetes is more prevalent in infants born to diabetic mothers (5-7) has prompted the development of models of gestational diabetes. A variety of experimental manipulations find that prenatal hyperglycemia leads to abnormal glucose homeostasis in the adult animal (8 -11). Moreover, experimental IUGR produces defects in insulin secretion and hyperglycemia in the exposed adult rats (12,13). The fact that prenatal exposure to dexamethasone increases fetal hepatic glucocorticoid receptor expression and produces adult hyperglycemia in rats strongly suggests that fetal stress may program adult function (14). Alth...

A nasal swab specimen was collected for culture within 48 hours of admission and a questionnaire was completed using a convenience sample of 350 patients admitted to Driscoll Children's Hospital between February 15 and March 15, 2005. Of the 350 patients enrolled, 125 (36%) patients were colonized with Staphylococcus. aureus and 76 (61%) of the 125 S. aureus isolates were methicillin-resistant.

Background: Erythropoietin (Epo) receptors (EpoR) are present in embryonic and postnatal mammalian bowel, and activation of EpoR signaling with recombinant Epo (rEpo) has trophic effects. Transgenic mice with absent Epo function are embryonic lethal, so it is not known whether Epo function is required for bowel development. Objective: To characterize bowel structure in the absence of EpoR signaling. Methods: Heterozygous EpoR knockout mice were mated. Bowel segments from their embryos were dissected and transplanted beneath the renal capsule of adult wild-type mice and residual embryo tissue was excised for genotyping. Transplants were harvested at 7, 14 or 21 days. The transplanted bowel segments were immunostained to identifyproliferation (BrdU+), as well as neuronal (PGP9.5+), endothelial (vWF+), and neuroendocrine (synaptophysin+) cells. Gross and microscopic characteristics of intestinal differentiation were evaluated. Results: 50 transplants were performed: bowel from 49 embryos survived to harvest and 43 showed evidence of bowel development with appropriate small or large intestinal features. No differences in morphology, immunolabeling, or BrdU incorporation were observed between homozygous-null, heterozygote or wild-type bowel. Smooth muscle and mucosal cells were present, along with neuronal, endothelial, and neuroendocrine cells in all genotypes. Conclusions: Enteric EpoR signaling is not essential for intestinal morphogenesis.