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Neonatal development

Deficiency of manganese may lead to vitamin K deficiency (Chiswell and Johnson 1994) and to problems in prenatal and neonatal development of the brain. [Pg.203]

Holtzman D.A. and Halpem M. (1990). Embryonic and neonatal development of the vomeronasal and olfactory systems in garter snakes. J Morphol 203, 123-140. [Pg.212]

Massaro EJ, Massaro TF. 1987. Low level lead exposure during neonatal development perturbs cognitive function. Am Coll Toxicol 6 441-449. [Pg.548]

Overmann SR. 1977. Behavioral effects of asymptomatic lead exposure during neonatal development in rats. Toxicol Appl Pharmacol 41 459-471. [Pg.561]

Essential fatty adds in foetal and neonatal development... [Pg.238]

Short CL, Kinden DA, Stith R. 1976. Fetal and neonatal development of the microsomal monooxygenase system. Drug Metab Rev 5 1-42. [Pg.183]

Fig. 5. Schematic illustration of adjustments in titin expression that decrease titin-based passive myocardial stiffness during DCM heart failure (A) and increase titin-based passive myocardial stiffness during normal neonatal development (B). Titin gels are shown in the inset. They reveal that normal adult myocardium (control in A) expresses more N2B titin than N2BA titin and that N2BA titin in upregulated in myocardium of heart failure (HF) patients. In fetal myocardium (inset of B), N2BA titin also dominates. (Figure based on Nagueh et al, 2004 and Lahmers et at, 2004.)... Fig. 5. Schematic illustration of adjustments in titin expression that decrease titin-based passive myocardial stiffness during DCM heart failure (A) and increase titin-based passive myocardial stiffness during normal neonatal development (B). Titin gels are shown in the inset. They reveal that normal adult myocardium (control in A) expresses more N2B titin than N2BA titin and that N2BA titin in upregulated in myocardium of heart failure (HF) patients. In fetal myocardium (inset of B), N2BA titin also dominates. (Figure based on Nagueh et al, 2004 and Lahmers et at, 2004.)...
Calamandrei G, Ricceri L, Santucci D, et al. 1996. Neurobehavioural abnormalities during neonatal development in a rodent model The role of neurotrophic factors. Teratology 53 22A. [Pg.298]

S8) to be located in the microsome fraction of the liver. The neonatal development of this conjugating system has been studied by Brown et al. (B17) in the guinea pig. They were unable to detect the presence of bilirubin glucuronyl transferase in liver microsomes from fetal and newborn animals and, using o-aminophenol as a glucuronyl acceptor, were... [Pg.277]

RE Peterson University of Wisconsin-Madison, Madison, Wl Determine the mechanisms by which 2,3,7,8-TCDD adversely affects the male reproductive system of rats exposed in adulthood or during fetal and neonatal development ... [Pg.376]

Behne, M.J. et al., Neonatal development of the stratum corneum pH gradient localization and mechanisms leading to emergence of optimal barrier function, J. Invest. Dermatol., 120, 998, 2003. [Pg.168]

During neonatal development, the brain possesses the striking ability to transfer initially lost functions to new, unaffected cortical areas when irreversible lesions prohibit function of the original representation fields - an ability that is still to a lesser degree present in mature brain. This type of plastic response has been studied in rats with a well defined lesion of the somatosensory cortex that was induced 1 day after birth. Six months later functional MRI (fMRI) was performed with a forepaw stimulation paradigm when the animals showed no neurological... [Pg.65]

Alpha 1 FetoProtein (AFP) is normally produced during fetal and neonatal development by the liver, yolksac, and in small concentrations by the gastrointestinal tract. After birth, serum AFP concentration decreases rapidly, and by the second year of life and thereafter only trace amounts are normally detected in serum. [Pg.524]

Simmons RA Cell glucose transport and glucose handling during fetal and neonatal development, in Polin RA, FoxWW, Abman SH (edsy.Fetal and Neonatal Physiology. Saunders, Philadelphia, 2004, pp. 487-493. [Pg.119]

Carlock L, Oneda S, Bussiere J. An assessment of the effects of human soluble IL-4 receptor on reproduction and neonatal development when administered intravenously to pregnant cynomolgus monkeys. Toxicologist 2003 72 327. [Pg.397]

Manganese deficiency results in a wide variety of structural, physiological and biochemical defects, for it has been implicated in a number of metabolic and enzymatic processes (5-15). Hurley has summarized the evidence that manganese is essential for normal prenatal and neonatal development, with deficiency resulting in a variety of congenital malformations (16). [Pg.68]

Expression later in neonatal development, e.g. CYP1A2 [21], CYP3A4 [15, 16]. [Pg.115]

The efficacy and safety of fluconazole in neonates with Candida fungemia has been evaluated in a multicenter prospective study (65). Fluconazole was safe and effective even in complicated cases, including infants of very low birth weights. Two of 50 neonates developed raised liver enzymes during fluconazole therapy and two others had raised serum creatinine concentrations. In none of them did these abnormalities necessitate discontinuation of antifungal therapy. [Pg.1381]


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See also in sourсe #XX -- [ Pg.65 ]




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