Neonates/newborns

Neonate. Newborn baby, from immediately after birth through the first 28 days of life. 

The question of whether genetic screening should be voluntary or mandatory is controversial. So is the goal of the screening— whether to detect afflicted individuals or carriers. Screening can be performed at various life stages, such as prenatal, neonatal, newborn, or premarital. 

Hormone Neonates with hypothyroidism pefore therapy, 5-7 days of age) (n = 8) Healthy neonates (newborn 5-7 days of age) (n = 8) p value Neonates with hypothyroidism (after 8 weeks of therapy) (n = 8) Healthy neonates (after 8 weeks of therapy) (n = 8) p value... 

It has the ability to cross the placenta and therefore provides a major line of defence against infection for the newborn. This can be reinforced by transfer ofcolostral IgG across the gut mucosa of the neonate. It diffuses readily into the extravascular spaces where it can act in the neutralization of bacterial toxins and can bind to microorganisms enhancing the process of phagocytosis (opsonization). This is due to the presence on the phagocytic cell surface of a receptor for Fc. 

Necheles et al. (N4) first reported a genetically determined homozygous GSH-Px deficiency associated with neonatal jaundice and mild hemolysis. Spontaneous recovery from hemolysis was noted 3 months after birth. Thereafter, several cases with GSH-Px deficiency were reported. Newborn infants exhibit significantly lower red blood cell GSH-Px activity and serum selenium concentrations than adult control subjects, and a significantly positive correlation between selenium concentration and GSH-Px activity has been observed. Furthermore, the addition of selenium stimulates, both in vivo and in vitro, the GSH-Px activity. The neonatal red blood cell GSH-Px deficiency may be partially due to insufficient availability of selenium during pregnancy (P9). Therefore, the diagnosis of GSH-Px deficiency in newborn infants must be made carefully. 

Infant respiratory distress syndrome (IRDS), also known as hyaline membrane disease, is one of the most common causes of respiratory disease in premature infants. In fact, it occurs in 30,000 to 50,000 newborns per year in the U.S. — most commonly in neonates bom before week 25 of gestation. IRDS is characterized by areas of atelectasis, hemorrhagic edema, and the formation of hyaline membranes within the alveoli. IRDS is caused by a deficiency of pulmonary surfactant. Alveolar type II cells, which produce surfactant, do not begin to mature until weeks 25 to 28 of... 

The forms of phototherapy in common use include (i) the phototherapy of jaundice (neonatal hyperbilirubinemia) in the newborn, and especially in the prematurely born 5 (ii) the treatment of psoriasis using light in the UV-A range (320 100 nm) and an administered photosensitizer, such as 8-methoxypsoralen 6 (iii) the treatment of the wet form of age-related macular degeneration with a photosensitizer such as a benzoporphyrin derivative (VISUDYNE ), and a laser light source 7 and (iv) the treatment of certain cancers with a photosensitizer such as a porphyrin derivative, and red light.8... 

Urea cycle defects Failure to convert ammonia to urea via urea cycle (Fig. 40-5). Coma, convulsions, vomiting, respiratoryfailure in neonate. Often mistaken for sepsis of the newborn. Mental retardation, failure to thrive, lethargy, ataxia and coma in the older child. Associated with hyperammonemia and abnormalities of blood aminogram Low protein diet Acylation therapy (sodium benzoate, sodium phenylacetate) Arginine therapy in selected syndromes Hepatic transplantation... 

Bakka, A. and M. Webb. 1981. Metabolism of zinc and copper in the neonate changes in the concentrations and contents of thionein-bound Zn and Cu with age in the livers of the newborn of various mammalian species. Biochem. Pharmacol. 30 721-725. 

Kotiranta-Ainamo, A., Rautonen, J., and Rautonen, N. Imbalanced cytokine secretion in newborns, Biol. Neonate, 85, 55, 2004. 

Over the past three decades, several studies have assessed neonatal responses to odors naturally emitted from the breasts by lactating women (e.g., Macfar-lane 1975 Russell 1976 Schaal, Montagner, Herding, Bolzoni, Moyse and Qui-chon 1980 Schaal 1986 Makin and Porter 1989). The odour of the whole breast, collected on a cotton pad applied on the areola, reduces arousal in active newborns (Schaal et al. 1980 Schaal 1986 Sullivan and Toubas 1998) and increases it... 

In the same way as volatiles from the whole breast, odorants carried in human colostrum/milk are arousing and attractive to newborns (Mizuno, Mizuno, Shino-hara and Noda 2004 Marlier and Schaal 2005). Interestingly, neonatal responsiveness to these milk cues does not seem to depend on breastfeeding experience as term-born infants exclusively fed formula (Marlier and Schaal 2005), and premature infants (Bingham et al. 2003), react to them in the same way as regularly breast-fed infants. 

Sullivan, R.M., and Toubas, P. (1998). Clinical usefulness of maternal odor in newborns soothing and feeding preparatory responses. Biol. Neonate 74, 402-408. 

Fitzgerald (1954) injected newborn mice (less than 12 h old) and adult mice subcutaneously with sodium cyanide (NaCN). The threshold for lethality was the same in newborn and adult male and female male mice, NaCN at 2 mg/kg. The dose-response curve for neonatal mice was much steeper than for adult mice, which resulted in a lower LC50 value. The LC50 for adult male mice was approximately 5 mg/kg for female mice it was 3.5 to 3.7 mg/kg and for neonatal mice it was between 2.0 and 2.5 mg/kg. On the basis of the threshold for lethality, newborn and adult mice were equally sensitive to HCN, but on the basis of LC50 values, newborn mice were approximately two to three times more sensitive than adult male mice. 

Bilirubin is a product of the breakdown of haemoglobin in red blood cells. Neonatal jaundice occurs when bilirubin builds up faster than a newborn baby s liver is able to break it down. This results in the deposition of water-insoluble bilirubin in the skin (giving the skin a yellow colour) and untreated it can lead to damage of the central nervous system by deposition in brain cells. 

Akisu M, Kultursay N, Coker I, Huseyinov A. (1998). Platelet-activating factor is an important mediator in hypoxic ischemic brain injury in the newborn rat. Flunarizine and Ginkgo biloba extract reduce PAF concentration in the brain. Biol Neonate. 74(6) 439-44. 

Neonates have diminished nicotine metabolism, as demonstrated by a nicotine half-life of three to four times longer in newborns exposed to tobacco smoke than in adnlts (Dempsey et al. 2000). Cotinine half-life is reported to be similar in neonates, older children, and adults in two studies (Dempsey et al. 2000 Leong et al. 1998). Other studies found that the half-life of urine cotinine was about three times longer in children less than one year old than to the cotinine half-life in adults (Collier et al. 1994). Urine cotinine half-life can be influenced by variations in urine volume and excretion of creatinine. The study by Dempsey et al. was the only one in which the half-life of cotinine was calculated based on both the blood and urine cotinine concentrations (Dempsey et al. 2000). In that study, both the blood and urine half-lives were similar to adult values, supporting the notion that neonates have the same cotinine half-life as older children and adults. 

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