Traumatic axolemmal and cytoskeletal derangement in myelinated axons of human oedematous cerebral cortex and loss of consciousness. An electron microscopic study using cortical biopsies.

Cortical biopsies of 7 patients with clinical diagnosis of severe head trauma and complicated brain trauma with subdural and epidural hematoma, and loss of consciousness were examined with the transmission electron microscope to study axolemmal and cytoskeletal damage in myelinated axons. Granular disintegration of microtubules and misaligned and fragmented neurofilaments, and fragmentation of axolemmal membrane were observed in most patients studied. In some cases a differential response characterized by increased number of neurofilaments and decreased number or disappearance of microtubules was found. In few cases apparently intact microtubules coexisting with fragmented ones were found. These findings are discussed in relation with traumatic brain edema and associated anoxic-ischemic conditions, the Hameroff-Penrose hypothesis relating microtubules and consciousness, and the existing and contemporary knowledge on neural correlates of consciousness.

Iron absorption by humans and swine from Fe(III)-EDTA. Further studies.

Studies on iron absorption from Na59Fe-EDTA in humans have shown that only a small proportion of the iron absorbed is excreted by the kidney, less than 1% of the dose administered. The pathway of Na55Fe-[2-14C]EDTA absorption and excretion when administered orally was studied in swine. A certain proportion (about 5%) of the 55Fe is split from the EDTA complex in the lumen of the gut, absorbed mainly from the pylorus and upper jejunum, transferred to plasma transferrin and then incorporated into the circulating hemoglobin. A small proportion of the iron absorbed, less than 1% of the dose administered, is excreted by the kidney, to a degree similar to that excreted by humans. The rest of the iron is eliminated in the feces, about 3% in a soluble form possibly still bound to EDTA and the greater part, about 92%, in an insoluble form. About 5% of the 14C is absorbed almost uniformly along the pyloric duodenal and jejunal mucosa, then transferred slowly to the plasma and excreted by the kidney within 48 hours. The rest of the 14C was excreted in the feces, about 80% in a soluble form and 20% in the insoluble fraction.