The neonatal intensive parenting unit: an introduction.

This paper describes a paradigm shift occurring in neonatal intensive care. Care teams are moving from a focus limited to healing the baby's medical problems towards a focus that also requires effective partnerships with families. These partnerships encourage extensive participation of mothers and fathers in their baby's care and ongoing bi-directional communication with the care team. The term Newborn Intensive Parenting Unit (NIPU) was derived to capture this concept. One component of the NIPU is family-integrated care, where parents are intimately involved in a baby's care for as many hours a day as possible. We describe six areas of potentially better practices (PBPs) for the NIPU along with descriptions of NIPU physical characteristics, operations, and a relationship-based culture. Research indicates the PBPs should lead to improved outcomes for NIPU babies, better mental health outcomes for their parents, and enhanced well-being of staff.

Insulin stimulation of glycogen synthase in cultured human diploid fibroblasts.

The effect of insulin on glycogen synthase activity in human diploid fibroblasts has been studied. As little as 2 X 10(-10) M insulin increased the glycogen synthase / activity without changing the total activity. Stimulation occurred within 5 min and became maximal in 30 min. A half-maximal increase of / activity was achieved at 3 X 10(-9) M insulin. Glucose starvation increased the magnitude of response of glycogen synthase to insulin but did not change the insulin concentration necessary to give a half-maximal stimulation. Glucose increased the basal level of / activity in human diploid fibroblasts; the effect of insulin was additive. During in vitro senescence the total glycogen synthase activity declined, but the concentration of insulin that produced a half-maximal stimulation remained unchanged. These data indicate that regulation of glycogen synthase activity in human diploid fibroblasts is responsive to physiologic insulin levels and that the system provides a useful model for the in vitro study of insulin sensitivity.

Effect of pH and 3-hydroxybutyrate on insulin binding and action in cultured human fibroblasts.

The influence of pH and 3-hydroxybutyrate on insulin binding and action has been studied in cultured human fibroblasts. When the pH of the incubation medium was decreased from 7.6 to 6.8, insulin stimulation of glycogen synthase and total glucose uptake was decreased. The decreased pH induced both an increase in the insulin concentration for half-maximal response, and a decrease in maximal responsiveness. When insulin binding was measured at lower pH, receptor affinity was decreased. The effect of 3-hydroxybutyrate on insulin binding and action was assessed at pH 7.4 and 6.9. In the presence of 3-hydroxybutyrate, insulin binding increased, but insulin action on glycogen synthase and total glucose uptake was unaffected. The data show that insulin action is impaired at lower pH. The decreased sensitivity is probably related to the decrease in insulin binding affinity at lower pH, but decreased maximal responsiveness implies that postreceptor components are also affected by lower pH. The results also suggest that 3-hydroxybutyrate induced a dissociation between binding and response, since an increase of insulin binding was not accompanied by changes in the regulation of glycogen synthase and total glucose uptake.

NICU discharge planning and beyond: recommendations for parent psychosocial support.

Parents will interact with a multitude of teams from various disciplines during their child's admission to the neonatal intensive care unit. Recognition of the emotional stressors experienced by these parents is a first step in working to provide the crucial support and parenting skills needed for bonding and caring for their infant from admission through discharge and beyond. Family-centered care involves time-sensitive two-way communication between parents and the multidisciplinary team members who coordinate care transition by providing emotional, educational, medical and home visitor support for these families. To do this well, a thoughtful exchange of information between team members and parents is essential to identify psychosocial stress and ameliorate family concerns. Parents will need emotional and educational support and follow-up resources. Establishing individualized, flexible but realistic, pre- and post-discharge plans with parents is needed to start their healthy transition to home and community.

Recommendations for involving the family in developmental care of the NICU baby.

Family involvement is a key to realize the potential for long-lasting positive effects on physical, cognitive and psychosocial development of all babies, including those in the neonatal intensive care unit (NICU). Family-centered developmental care (FCDC) recognizes the family as vital members of the NICU health-care team. As such, families are integrated into decision-making processes and are collaborators in their baby's care. Through standardized use of FCDC principles in the NICU, a foundation is constructed to enhance the family's lifelong relationship with their child and optimize development of the baby. Recommendations are made for supporting parental roles as caregivers of their babies in the NICU, supporting NICU staff participation in FCDC and creating NICU policies that support this type of care. These recommendations are designed to meet the basic human needs of all babies, the special needs of hospitalized babies and the needs of families who are coping with the crisis of having a baby in the NICU.

Glucose kinetics in leprechaunism: accelerated fasting due to insulin resistance.

Postprandial and postabsorptive glucose metabolism was studied in a 3-yr-old girl with leprechaunism by substrate and hormonal measurements and by quantifying hepatic glucose output during continuous infusion of D-[6-6-2H2]-glucose. Hepatic glucogen content and the activity of glycogen synthase and phosphorylase were also measured in the post-prandial state on a separate occasion. During the 4-h postprandial state, plasma glucose, alanine, lactate, beta-hydroxybutyrate, and glycerol were normal, as were hepatic glycogen, glycogen synthase, phosphorylase, and hepatic glucose output of 7.5 mg kg-1 min-1. Intravenous injection of glucagon (30 micrograms kg-1) caused an immediate almost 3-fold rise in glucose production consistent with brisk glycogenolysis. During the 8- to 12-h postabsorptive state, however, the patient had elevated levels of glycerol (330-508 microM) and beta-hydroxybutyrate (3291-3801 microM) and decreased levels of glucose 24-29 mg/dl) and alanine (121-135 microM) consistent with a much longer period of fasting in the normal child. Furthermore, hepatic glucose output was reduced to 3.9 mg kg-1 min-1, and iv glucagon injection failed to increase this rate; both of these observations are consistent with a hepatic state generally found only later in fasting in the normal child. From these observations we conclude that the hypoglycemia reported in the leprechaunism syndrome is due to an accelerated fasting state secondary to insulin resistance. As with long-fasted, glycogen-depleted normal children, gluconeogenesis alone is often not capable of adequately meeting the child's large noninsulin-dependent cerebral glucose requirements.

Mechanisms of insulin resistance in cultured fibroblasts from a patient with leprechaunism: impaired post-binding actions of insulin and multiplication-stimulating activity.

The binding and action of insulin and of the insulin-like growth factor, multiplication-stimulating activity (MSA), were studied in cultured skin fibroblasts from an infant with leprechaunism and associated insulin resistance. Three actions of insulin were reduced in the leprechaun cells: activation of glycogen synthase was 30% as great as in control fibroblasts, the increase in 2-deoxyglucose transport was 33% of the control value, and the uptake of alpha-aminoisobutyric acid was sevenfold less sensitive to enhancement. On a molar basis, MSA was at least as effective as insulin in activating glycogen synthase in control fibroblasts; in the patient's cells there was a reduction in activation that paralleled the changes observed with insulin. To localize the site of insulin resistance, the binding of both [125I]-insulin and [125I]-MSA to fibroblasts was measured and found to be reduced in the leprechaun cells. However, the impairment of the actions of insulin and MSA in the patient's cells was not explained solely by the diminished binding of the two polypeptides. Since the hexose transport system and the terminal enzymes studied thus far are intact, the defect is postulated to involve the post-binding coupling mechanism and mediator formation.

Induced rhinovirus infection under controlled exposure to sulfur dioxide.

The interaction between short-term sulfur dioxide (SO2) exposure and experimentally induced rhinovirus infection was studied in thirty-two volunteers divided into two groups balanced with respect to age, antibody levels, and nasal mucus flow rates. One group was exposed to SO2 exposure at the threshold limit value (TLV) of 5 ppm during 4 hours; the other group served as controls exposed to pollution-free air under the same conditions. The SO2 exposure caused a 50% decrease in nasal mucus flow rate in the anterior parts of the nose, but there was no difference in the number of colds which developed in the two groups. The group exposed to SO2 had fewer symptoms and a possibly shorter incubation period (P = .06), and virus shedding was at a lower level but more persistent than in the control group. No differences were found in antibody response. The rhinovirus infection in the control group caused a gradual decrease in nasal mucus flow rate starting 2 days after the virus instillation, and after 5 days the rate was less than half its initial value. For future experiments on the interaction between airborne pollutants and rhinovirus infections, a virus challenge by aerosol inhalation is recommended. Our study supports an earlier observation that growth of influenza virus in the nasal cavity of mice was inhibited by exposure to SO2 concentrations of 6 or 20 ppm.