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The authors present the case of a child aged 7 years who suffered from relapsing acute lymphocytic leukemia. Treatment consisting mainly of oral and intrathecal methotrexate and x‐ray therapy produced remission of the hematologic symptoms. Three years after the onset of the leukemia, mental deterioration gradually appeared. Radiography of the skull revealed diffuse bilateral calcium deposits in both cerebral and cerebellar hemispheres. Four years after the onset of the disease, a hematologic relapse occurred. Behavioral disorders became more severe and the child died after a period of seizures and unconsciousness. The main pathologic data obtained by the study of a brain biopsy and after a complete postmortem examination consisted of calcifications located bilaterally in the cerebral and cerebellar cortex. No signs of leukemia were present. Cerebral calcification is an extremely rare complication in the course of the therapy of lymphocytic leukemia. Its possible causes are discussed.

Hyperactive dog thyroids were prepared by repeated TSH stimulation in vivo. Butanol-extractable 125I (BE125I) release in vitro from slices and hormonal secretion in vivo in the thyroid vein was enhanced. Apical pseudopods and colloid droplets were very infrequent in such hyperactive thyroids. Moreover, BE125I release was insensitive to cytochalasin B, to inhibitors of microtubules, and to metabolic inhibitors, and decreased only with temperature. Our data demonstrate that hormonal secretion by hyperactive thyroids is not secondary to apical phagocytosis (i.e. macropinocytosis). Micropinocytosis or intraluminal hydrolysis of thyroglobulin are suggested as first step of the secretory process.

cAMP accumulation and pseudopod formation have been studied in dog thyroid slices stimulated by thyrotropin. lt is shown that the kinetics and concentration effeet re lationship support the validity of Sutherltmd's model of hormone action through cAMP for thyrotropin and thyroid secretion.