Trans-sulphuration in primate brain: regional distribution of s stages of development.
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Biomedical subjects
Publications and source records attributed to J J Volpe.
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The development of activity of methionine-activating enzyme was studied in four organs of the rat. Three different patterns were observed: (a) in the liver, specific activity began to increase in late fetal life and reached a maximum 2 days after birth; (b) in the small intestine, specific activity began to rise in the 2nd wk after birth and reached a maximum at age 18 days; and (c) in the brain and kidney, specific activity did not change markedly from the earliest stage of fetal development studied to adult life. Hydrocortisone increased hepatic methionine-activating enzyme activity as much as 55% in the young rat. However, adrenalectomy in the newborn rat did not prevent the postnatal rise in hepatic methionine-activating enzyme activity, nor did adrenalectomy at age 10 days prevent the developmental rise of intestinal activity at age 18 days. Conjugated estrogens partially inhibited both the neonatal rise in hepatic methionine-activating enzyme activity and the rise in activity after adrenal steroid injection. Injection of L-methionine did not increase hepatic methionine-activating enzyme activity in the developing or adult rat.
We describe the association of brain death in an infant with a large cutaneous hemangioma of the forearm. The irreversible cerebral injury is presumed to be secondary to cerebral hypoperfusion as a result of a combination of systemic hypotension and a systemic vascular "steal" phenomenon caused by the cutaneous hemangioma.
A newborn with bilateral uncal herniation secondary to acute bacterial meningitis is reported. The findings of previous neuropathologic studies of neonatal bacterial meningitis are reviewed and the factors most likely responsible for the relative rarity of herniation in this disease in newborns are discussed.
A child developed acute fulminant viral hepatitis and cerebral edema confirmed on postmortem examination. Clinical evidence of herniation, effacement of cortical sulci on computed tomography, and elevated cerebrospinal fluid pressure preceded complicating terminal events, demonstrated that cerebral edema was associated with acute hepatic failure, rather than complicating factors, and led to the patient's death. The mechanism is unknown.
Seizures in the neonatal period are usually concomitants of serious neurological disease. The convulsive phenomena take certain distinctive and often subtle forms because of the status of the neuroanatomical and neurophysiological development of the neonatal brain. The predominant etiological process is hypoxic-ischemic encephalopathy, but intracranial hemorrhage, intracranial infection, development defects and metabolic disorders are also responsible for a considerable proportion of cases. Prognosis is related primarily to the neurological disease that underlies the seizures. Treatment may be specific for the underlying disorder, e.g., glucose, calcium, magnesium, pyridoxine, but whatever the cause, urgent control of the convulsions is important because they may have deleterious consequences. Phenobarbital is the single, most important anticonvulsant in the management of neonatal seizures.
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