Tissues neonatal

Although mast cells and basophils probably account for >90% of stored histamine in the body, histamine is also present in platelets, enterochromaffin-like cells, endothelial cells, and neurons. Histamine can act as a neurotransmitter in the brain. Histaminergic nerves have their cell bodies within a very small area of the brain (the magnocellular nuclei of the posterior hypothalamus) but have axons in most areas of the forebrain. There is also evidence for axons projecting into the spinal (Fig. 1) cord. Finally, there is evidence that histamine synthesis can be induced in tissues undergoing rapid tissue growth and repair. In certain neonatal tissues (e.g. liver), the rate of synthesis of this unstored diffusable histamine (termed nascent histamine) is profound and may point to a role for histamine is cell proliferation. 

This complex contains 11 polypeptide subunits of which only one is encoded by mtDNA. Defects of complex III are relatively uncommon and clinical presentations vary. Fatal infantile encephalomyopathies have been described in which severe neonatal lactic acidosis and hypotonia are present along with generalized amino aciduria, a Fanconi syndrome of renal insufficiency and eventual coma and death. Muscle biopsy findings may be uninformative since abnormal mitochondrial distribution is not seen, i.e., there are no ragged-red fibers. Other patients present with pure myopathy in later life and the existence of tissue-specific subunits in complex III has been suggested since one of these patients was shown to have normal complex 111 activity in lymphocytes and fibroblasts. 

Duo S, Lea TC, Stipanuk MH. 1983. Developmental pattern, tissue distribution, and subcellular distribution of cysteine -ketoglutarate aminotransferase and 3-mercaptopyruvate sulfurtransferase activities in the rat. Biol Neonat 43 23-32. 

Miller GD, Massaro TF, Granlund RW, et al. 1983. Tissue distribution of lead in the neonatal rat exposed to multiple doses of lead acetate. J Toxicol Environ Health 11 121-128. 

An aminoaciduria usually results from the congenital absence of an enzyme needed for metabolism of an amino acid. Aminoacidopathies typically involve an inherited deficiency of an enzyme that is important for the metabolism of a particular amino acid (Table 40-1). The concentration of that amino acid and its metabolites consequently rise sharply in blood, urine and body tissues, including the brain. When the enzymatic deficiency is nearly complete, the onset of disease tends to occur in infancy, even in the neonatal period. Partial enzyme deficiencies may not become apparent until later in life [1,2]. 

Glutaric aciduria type II, which is a defect of P-oxida-tion, may affect muscle exclusively or in conjunction with other tissues. Glutaric aciduria type II, also termed multiple acyl-CoA dehydrogenase deficiency (Fig. 42-2), usually causes respiratory distress, hypoglycemia, hyperammonemia, systemic carnitine deficiency, nonketotic metabolic acidosis in the neonatal period and death within the first week. A few patients with onset in childhood or adult life showed lipid-storage myopathy, with weakness or premature fatigue [4]. Short-chain acyl-CoA deficiency (Fig. 42-2) was described in one woman with proximal limb weakness and exercise intolerance. Muscle biopsy showed marked accumulation of lipid droplets. Although... 

Moorhouse KG, Logan CJ, Hutson DH, Dodds PF (1990) The incorporation of 3-phenoxybenzoic acid and other xenobiotics acids into xenobiotic lipids by enzymes of the monoacylglycerol pathway in microsomes from adult and neonatal tissues. Biochem Pharmacol 39 1529-1536... 

Since the early 90s, noninvasive functional brain imaging of humans using NIR methods have been slowly gaining momentum despite existence of more established imaging modailties, such as PET, fMRI, and EEG. Part of the reason as stated previously, is because of its relatively high temporal resolution and its ability to monitor multiple tissue chromophores. The technique has been applied to adult as well as infant studies. NIR method is particularly suited for infant studies as the equipment, at least the CW kind, are minimally restraining, relatively safe, and portable [67]. Most neonatal studies focus on sensory stimulation such as visual, auditory and olfactory stimulations [69] [101] [89] [115] [6] [5], and cerebral disfunction [70, 71]. Our review will focus primarily on adult studies with some emphasis on defense and security applications. 

Kavlock RJ, Chemoff N, Rogers E, et al. 1980. Comparative tissue distribution of mirex and chlordecone in fetal and neonatal rats. Pestic Biochem Physiol 14(3) 227-235. 

The over-production of bilirubin to the point at which the liver s capacity to metabolize is exceeded or if there is dysfunction of the liver itself due to damage or metabolic immaturity, can lead to a yellow discolouration of tissues called jaundice. The accumulation of unconjugated bilirubin in neonates, often as a result of antibody-mediated destruction of the baby s red cells is dangerous as serious and irreversible brain damage can occur. Acute or chronic damage to the adult liver (hepatitis) may cause jaundice but not brain damage. 

---