Visual-vestibular interaction in early infancy.

The development of visual and vestibular control of smooth gaze adjustments was studied longitudinally in 3- to 18-week-old infants. Eye and head movements were measured with electro-oculography (EOG) and an optoelectronic system, respectively. The infant was placed in a chair providing full support to the trunk but allowing relatively free head movements. The chair was positioned at the center of a striped-patterned drum. The chair and the drum were oscillated sinusoidally, either individually or in synchrony at 0.25 Hz. When the drum oscillated around the infant (the optokinetic response condition, OKR), the gain of both smooth eye and head tracking components was low up to 6 weeks of age, after which the eye gain increased dramatically and the lag decreased. The most substantial increase in head gain was observed at 13-18 weeks of age. When only the chair was oscillated (visual VOR, VVOR), the compensatory eye gain was high at 3 weeks and the head contributed significantly to the compensation (vestibulocollic reflex, VCR). The head gain increased significantly at 13-18 weeks of age as in the OKR case. When the drum and the chair were oscillated synchronously (inhibition of VOR, VORINHIB), the compensatory eye gain was significantly lower than in the VVOR, indicating suppression of VOR. This effect was considerable at 3 weeks. However, VCR was not suppressed but comparable to the VVOR condition at all ages studied. In summary, we found that the vestibular control of smooth gaze adjustment functions earlier than the visual control. At 2 months, the visual control improves dramatically and at 3-4 months head participation increases considerably. The eye gain in the VORINHIB condition could be well predicted by vector addition of the eye position signals in the OKR and VVOR conditions.

Predictive action in infancy: tracking and reaching for moving objects.

Because action plans must anticipate the states of the world which will be obtained when the actions take place, effective actions depend on predictions. The present experiments begin to explore the principles underlying early-developing predictions of object motion, by focusing on 6-month-old infants' head tracking and reaching for moving objects. Infants were presented with an object that moved into reaching space on four trajectories: two linear trajectories that intersected at the center of a display and two trajectories containing a sudden turn at the point of intersection. In two studies, infants' tracking and reaching provided evidence for an extrapolation of the object motion on linear paths, in accord with the principle of inertia. This tendency was remarkably resistant to counter-evidence, for it was observed even after repeated presentations of an object that violated the principle of inertia by spontaneously stopping and then moving in a new direction. In contrast to the present findings, infants fail to extrapolate linear object motion in preferential looking experiments, suggesting that early-developing knowledge of object motion, like mature knowledge, is embedded in multiple systems of representation.

Development of smooth pursuit tracking in young infants.

Eye and head movements were measured in a group of infants at 2, 3, and 5 months of age as they were attentively tracking an object moving at 0.2 or 0.4 Hz in sinus or triangular mode. Smooth pursuit gain increased with age, especially until 3 months. At 2-3 months, the lag of the smooth pursuit was small for the sinusoidal motion but large for the triangular one. At 5 months, smooth pursuit was leading the sinusoidal motion and the lag for the triangular one was small. Head tracking increased substantially with age and its lag was always large.

The development of gaze control and predictive tracking in young infants.

Eye and head tracking of an oscillating visual flow was studied in 1-, 2-, and 3-month-old infants using EOG and an opto-electronic system. A pronounced decrease in phaselag of gaze velocity was observed over this age period, from 170 to 70 msec, but gain changed only marginally. Latency of the onset of tracking decreased with age from 860 to 560 msec. During tracking, the velocity of the head showed high frequency components in the 1-6 Hz range, to which the eye movements were reciprocal and without systematic phase lag. This coordination improved with age.

DNA damage in human endothelial cells after irradiation in anoxia.

Endothelial cells and fibroblasts have been reported to respond differently to oxidative stress. Both the effects of high oxygen tension and radiation involve the action of free radicals. DNA damage (single strand breaks, SSB, and double strand breaks, DSB) was assayed in human umbilical cord vein (HUV) cells and in Chinese hamster fibroblasts (V79) after irradiation under oxic or anoxic conditions. The cells were exposed to single doses in the range of 2-18 Gy of gamma-radiation from 60Co. Significantly more DNA damage was induced in the V79 cells than in the HUV cells. As a consequence, a higher oxygen enhancement ratio was obtained for the HUV cells (6.3) as compared to the V79 cells (2.8). The repair of SSB was slower in the HUV cells than in the V79 cells, irrespective of oxic state. For the higher doses, the damage remaining at 60 min after anoxic irradiation, i.e. DSB, was only detected in the V79 cells.

The effect of cold after whole-body irradiation of the mouse.

Mice were placed in a cold environment (4 degrees C) directly after whole-body irradiation. Those irradiated with a lethal dose showed higher lethality than mice irradiated with the same dose but placed in room temperature. The response was also altered after irradiation with a sublethal dose. At various periods after irradiation mice were injected with 125IUdR, the tissue uptake of which is an index of DNA synthesis. The result showed that cold treatment after irradiation caused slower cell renewal in the spleen and bone marrow, but that the thymus was only marginally affected. Furthermore, the concentrations of erythrocytes in the peripheral blood reached a lower level in the cold-treated group. Finally, the levels of the thyroid hormones T3 and T4 in the blood were measured and it was found that the T3/T4 ratio was higher in the cold-treated mice. It is suggested that during prolonged exposure to cold after irradiation the cell recovery in the haemopoietic system is exposed to hormonal action that induces significant alterations in the postirradiation cell kinetics.

Central nervous system radiation syndrome in mice from preferential 10B(n, alpha)7Li irradiation of brain vasculature.

Ionizing radiations were directed at the heads of anesthetized mice in doses that evoked the acute central nervous system (CNS) radiation syndrome. Irradiations were done using either a predominantly thermal neutron field at a nuclear reactor after intraperitoneal injection of 10B-enriched boric acid or 250-kilovolt-peak x-rays with and without previous intraperitoneal injection of equivalent unenriched boric acid. Since 10B concentrations were approximately equal to 3-fold higher in blood than in cerebral parenchyma during the reactor irradiations, more radiation from alpha and 7Li particles was absorbed by brain endothelial cells than by brain parenchymal cells. Comparison of the LD50 dose for CNS radiation lethality from the reactor experiments with the LD50 dose from the x-ray experiments gives results compatible with morphologic evidence that endothelial cell damage is a major determinant of acute lethality from the CNS radiation syndrome. It was also observed that boric acid is a low linear energy transfer radiation-enhancement agent in vivo.

DNA damage in irradiated endothelial cells of the rat cerebral cortex. Protective action of cysteamine in vivo.

The induction and repair of DNA damage in single endothelial cells of rat cerebral cortex capillaries were studied in vivo and in vitro. Capillaries from the cerebral cortex were prepared in suspension, embedded in agarose on microscope slides, and treated with alkaline solution (unwinding of DNA). After neutralization the slides were stained with the fluorescent dye acridine orange and endothelial cell nuclei were evaluated in a microscope photometer. The intensity of the red fluorescence (from single-stranded DNA) divided by the green fluorescence (from double-stranded DNA) was used as a measured of DNA strand breaks. The results showed that most DNA strand breaks were repaired within 30 min postirradiation. A linear dose-effect relationship was found up to 18 Gy. Similar results were obtained from in vitro and in vivo experiments. Cysteamine administered 20 min before irradiation in vivo gave a protective effect on the cells studied. An EMF of 1.3 was determined.

Permeability of the blood-brain barrier in the rat after local proton irradiation.

Rats were irradiated laterally through the brain with 200 MeV protons. The beam was of circular cross-section with a diameter of 5 or 7 mm. The doses were 50, 70, 100 and 150 Gy. After irradiation the rats were examined several times by use of injected 99Tcm-pertechnetate. The uptake of the substance increased to a maximum after 20 to 30 days and then decreased to a normal level. Differences in maximum uptake with respect to dose were significant only for the smaller beam diameter.

Effects of proton irradiation of the lumbar intumescence on intra-axonal transport of acetylcholine and cholinergic enzymes in rat sciatic nerve.

The content and intra-axonal transport of acetylcholine (ACh) and the cholinergic enzymes cholineacetyltransferase (CAT) and ACh-esterase (AChE) in sciatic nerve were investigated in rats following single dose proton irradiation of the lumbar intumescence of the spinal cord with 60 Gy or 200 Gy. One, 7 or 30 days after irradiation nerve-crush operations were performed 12 hours before killing and the levels of ACh and enzyme activities in nerve segments relative to the crushes were estimated by biologic (ACh) or chemical (enzyme) methods. The results indicate that alterations in intraneuronal dynamics of ACh and related enzymes are not a major cause for the development of neurologic symptoms of the motor system after irradiation, and that descending myelinated axons are of minor importance for the regulation of cholinergic substances in rat motor nerves.

Radiation-induced DNA strand breaks and their repair in the developing rat brain.

Rats, 5, 10 or 25 days old, were 60 Co gamma irradiated. The induction of DNA strand breaks was studied after killing the rats within 1 min after irradiation, and the repair of the induced breaks after various intervals up to 180 min. Cell suspensions were prepared from the brain and samples were transferred into alkaline solutions. The fraction of DNA remaining double-stranded after 30 min alkali treatment was estimated after separation of single- and double-stranded DNA on hydroxylapatite. The amount of DNA strand breaks induced per Gray (1--8 Gray) was found to be in accordance with earlier in vivo studies of the mouse small intestine and mouse spleen. The DNA strand breaks in the rat brain induced by 4 Gray 60Co gamma irradiation were repaired 30 min after irradiation in all age groups studied.

Influence of absorbed dose and field size on the geometry of the radiation-surgical brain lesion.

Specimens from a number of patients locally irradiated in the thalamus for intractable pain with a multiple gamma beam technique have been examined. The geometry of well circumscribed necrotic lesions was ascertained. No correlation was seen between the dimensions of the lesions and the size of the field, 3 mm X 5 mm or 3 mm X 7 mm, within the clinically useful dose range, 16 to 25 krad.