Lead-inducing hyperactivity. Chronic exposure during the neonatal period in the rat.

The effects of chronic exposure to low levels of lead via maternal milk during the neonatal period in the rat were evaluated by means of several activity measures, spontaneous alternation in the Y-maze, and weight data. Animals reared at the highest concentrations of lead showed retarded body growth. Lead-treated rats were found to be more active in the Y-maze and in the tilt-box, but not in the running wheel. Lead-treated rats showed lowered spontaneous alternation and increased squealing; results were dependent upon the concentration of lead on which the animals were reared. Activity and alternation data provide suggestive evidence of lead-induced damage of the hippocampus, a structure which undergoes much of its development during the stage in which the lead was administered. Behavioral parallels found between lead poisoning and childhood hyperactivity were discussed with respect to the utility of chronic low level lead administration as an animal model of minimal brain dysfunction hyperactivity.     

Prolonged neonatal alloimmune thrombocytopenic purpura associated with anti-Bak(a). Two cases in siblings

Two cases of prolonged neonatal alloimmune thrombocytopenic purpura in siblings due to anti-Bak(a) are reported. The first case was complicated by an intracranial hemorrhage due to severe thrombocytopenia, but the second case had no untoward complications. Delivery by cesarean section and immediate platelet support from "compatible" (nonmaternal) donors may have contributed to the more favorable outcome in the second case. An analysis of the gene frequencies of platelet-specific antigens suggests that factors other than the potential for maternal exposure to antigen determine the incidence of affected births. Knowledge of gene frequencies may, however, permit a priori prenatal calculation of the probability of an affected birth for couples with a previously affected child even if the genotype of the father is unknown.     

Pulmonary atelectasis: signal patterns with MR imaging

To assess the signal characteristics of different types of pulmonary atelectasis on magnetic resonance (MR) images, the authors studied obstructive atelectasis (OA) in 17 patients and nonobstructive atelectasis (NOA) in 25 patients. All patients underwent electrocardiographically gated MR imaging studies of the thorax with standard spin-echo sequences. No signal differences were observed between either type of atelectasis on T1-weighted images. Conversely, OA and NOA appeared significantly different on spin-density-weighted images (P less than .001) and on T2-weighted studies (P less than .0001). On T2-weighted images, all 17 cases of OA appeared hyperintense, whereas 22 of 25 cases of NOA demonstrated a very low signal intensity. Differences in the pathophysiology of OA and NOA presumably account for this observation. In OA, alveolar air is totally resorbed and secretions accumulate in the obstructed lung. The resulting increase in free fluid prolongs the T2 relaxation times and leads to high signal intensity on T2-weighted images. In NOA, the short T2 relaxation time of lung tissue in the absence of secretions and potential magnetic susceptibility effects due to residual air are likely to be responsible for the low T2 signal pattern.     

Host genetics and the behavioral sequelae to herpes encephalitis in mice

The effects of intracerebral infection with herpes simplex virus on the subsequent behavior of two strains of mice were examined. Infected Nya: NYLAR mice were hyperactive and did not show any deficits in the acquisition or reversal of a spatial learning task. In contrast, infected Nya: (SW) mice were hypoactive and made more errors than controls during both phases of the learning tasks. These differences in the nature of the sequelae to infection were related to an overall higher virus titer in the brains of Nya:(SW) mice, an effect particularly marked in the cerebral hemispheres. The results suggest that herpes encephalitis may produce a variety of behavioral syndromes, depending in part on the genetic background of the host. The relevance of these findings to clinical disorders produced by viral infection is discussed.