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Diabetic pregnancy and perinatal morbidity.
Failure of Premature Rabbits to Increase Antioxidant Enzymes During Hyperoxic Exposure: Increased Susceptibility to Pulmonary Oxygen Toxicity Compared with Term Rabbits
TLDR
This first reported comparison of prematurely born versus full-term animal responses to hyperoxia might help to explain the clinical observation that the very prematurely born infant is excessively prone to the development of O2-induced lung injury and the progressive development of bronchopulmonary dysplasia.
Relation of kidney tissue somatomedin-C/insulin-like growth factor I to postnephrectomy renal growth in the rat.
TLDR
The increased tissue levels of SmC in the regenerating kidney, with a return to baseline levels within 30 days, along with the absence of elevated serum levels suggest a local role for this mitogen in organ growth.
The infant of the diabetic mother: correlation of increased cord C-peptide levels with macrosomia and hypoglycemia.
TLDR
C peptide levels in infants of diabetic mothers were elevated at the earliest gestational age studied and were directly related to the severity of maternal diabetes, as assessed by the White classification.
DEXAMETHASONE STIMULATES FETAL RAT LUNG ANTIOXIDANT ENZYME ACTIVITY IN PARALLEL WITH SURFACTANT STIMULATION
TLDR
Pregnant DEX treatment results in an acceleration of the normal developmental increase in lung antioxidant enzyme activity which occurs late in gestation in the rat (as in the rabbit), and the DEX-treated prematurely-born may be in a more favorable biochemical state to avoid toxic lung changes associated with the relatively O2-rich ex utero environment and any supplemental hyperoxic treatment it may require.
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