ALBERT

Description: This technical paper discusses the following: (1) The VOR of two rhesus monkeys was studied before and after 14 days of spaceflight to determine effects of microgravity on the VOR. Horizontal, vertical and roll eye movements were recorded in these and six other monkeys implanted with scleral search coils. Animals were rotated about a vertical axis to determine the gain of the horizontal, vertical and roll VOR. They were rotated about axes tilted from the vertical (off-vertical axis rotation, OVAR) to determine steady state gains and effects of gravity on modulations in eye position and eye velocity. They were also tested for tilt dumping of post-rotatory nystagmus. (2) The gain of the horizontal VOR was close to unity when animals were tested 15 and 18 hours after flight. VOR gain values were similar to those registered before flight. If the gain of the horizontal VOR changes in microgravity, it must revert to normal soon after landing. (3) Steady state velocities of nystagmus induced by off-vertical axis rotation (OVAR) were unchanged by adaptation to microgravity, and the phase of the modulations was similar before and after flight. However, modulations in horizontal eye velocity had more variation after landing and were on mean about 50% larger for angles of tilt of the axis of rotation between 50 and 90?/s after flight. This difference was similar in both animals and was significant. (4) A striking finding was that tilt dumping was lost in the one animal tested for this function. This loss persisted for several days after return. This is reminiscent of the loss of response to pitch while rotating in the M-131 experiments of Skylab, and must be studied in detail in future spaceflights. (5) Thus, two major findings emerged from these studies: after spaceflight the modulation of horizontal eye velocity was larger during OVAR, and one animal lost its ability to tilt-dump its nystagmus. Both findings are consistent with the postulate that adaptation to microgravity causes alterations in the way that otolith information is processed in the central nervous system. The experiments lay the groundwork for studying the vertical and roll VOR before and after future space flights, as well as for studying modulations in vertical and roll eye position during OVAR and tilt dumping.

Description: We recorded the horizontal (yaw), vertical (pitch), and torsional (roll) eye movements of two rhesus monkeys with scleral search coils before and after the COSMOS Biosatellite 2229 Flight. The aim was to determine effects of adaptation to microgravity on the vestibulo-ocular reflex (VOR). The animals flew for 11 days. The first postflight tests were 22 h and 55 h after landing, and testing extended for 11 days after reentry. There were four significant effects of spaceflight on functions related to spatial orientation: (1) Compensatory ocular counterrolling (OCR) was reduced by about 70% for static and dynamic head tilts with regard to gravity. The reduction in OCR persisted in the two animals throughout postflight testing. (2) The gain of the torsional component of the angular VOR (roll VOR) was decreased by 15% and 50% in the two animals over the same period. (3) An up-down asymmetry of nystagmus, present in the two monkeys before flight was reduced after exposure to microgravity. (4) The spatial orientation of velocity storage was shifted in the one monkey that could be tested soon after flight. Before flight, the yaw axis eigenvector of optokinetic afternystagmus was close to gravity when the animal was upright or tilted. After flight, the yaw orientation vector was shifted toward the body yaw axis. By 7 days after recovery, it had reverted to a gravitational orientation. We postulate that spaceflight causes changes in the vestibular system which reflect adaptation of spatial orientation from a gravitational to a body frame of reference. These changes are likely to play a role in the postural, locomotor, and gaze instability demonstrated on reentry after spaceflight.

Description: No abstract available

Description: No abstract available

Description: With our stimulus conditions we were unable to record more than 2-3 beats of OKAN; therefore direct comparison to the data recorded from monkeys is not possible. We did, however, see cross-coupling in OKN. In monkeys, cross-coupling predominates in OKAN, indicating that velocity storage underlies this phenomenon. We consistently saw the axis of response shift towards the spatial vertical. This implies that although OKAN was weak, velocity storage contributed a representation of the spatial vertical to OKN that is dependent on the axis of the head or body with respect to gravity.

Description: Background and Purpose: An association between atrial septal aneurysm and embolic events has been suggested. Atrial septal aneurysm has been shown to be associated with patent foramen ovale and,.in some reports, with mitral valve prolapse. These two latter cardiac disorder; have been identified as potential risk factors for ischemic stroke. The aim of this prospective study was to assess the role of atrial septal aneurysm as an independent risk factor for stroke, especially for cryptogenic stroke. Methods: We studied the prevalence of atrial septal aneurysm, patent foramen ovale, and mitral valve prolapse in 100 consecutive patients 〈55 years of age with ischemic stroke who underwent extensive etiological investigations. We compared these results with those in a control group of 50 consecutive patients. The diagnosis of atrial septal aneurysm and patent foramen ovale relied on transesophageal echocardiography with a contrast study and that of mitral valve prolapse, on two-dimensional transthoracic echocardiography. Results: Stepwise logistic regression analysis showed that atrial septal aneurysm (odds ratio, 4.3; 95% confidence interval, 1.3 to 14.6; P=.01) and patent foramen ovale (odds ratio, 3.9; 95% confidence interval, 1.5 to 10; P=.003) but not mitral valve prolapse were significantly associated with the diagnosis of cryptogenic stroke. The stroke odds of a patient with both atrial septal aneurysm and patent foramen ovale were 33.3 times (95% confidence interval, 4.1 to 270) the stroke odds of a patient with neither of these cardiac disorders. For a patient with atrial septal aneurysm of 〉lo-mm excursion, the stroke odds were approximately 8 times the stroke odds of a patient with atrial septal aneurysm of 〈10 mm. Conclusions: This study shows that atrial septal aneurysm and patent foramen ovale are both significantly associated with cryptogenic stroke and that their association has a marked synergistic effect. Atrial septal aneurysms of 〉lo-mm excursion are associated with a higher risk of stroke. (Stroke. 1993;24:1865-1873.) KEY WORDS aneurysm echocardiography foramen ovale, patent mitral valve prolapse o young adults

Description: We examined the changes in the levels of indoleacetic acid (IAA), IAA esters, and a 22-kilodalton subunit auxin-binding protein (ABP1) in apical mesocotyl tissue of maize (Zea mays L.) during continuous red light (R) irradiation. These changes were compared with the kinetics of R-induced growth inhibition in the same tissue. Upon the onset of continuous irradiation, growth decreased in a continuous manner following a brief lag period. The decrease in growth continued for 5 hours, then remained constant at 25% of the dark rate. The abundance of ABP1 and the level of free IAA both decreased in the mesocotyl. Only the kinetics of the decrease in IAA within the apical mesocotyl correlated with the initial change in growth, although growth continued to decrease even after IAA content reached its final level, 50% of the dark control. This decrease in IAA within the mesocotyl probably occurs primarily by a change in its transport within the shoot since auxin applied as a pulse move basipetally in R-irradiated tissue at the same rate but with half the area as dark control tissue. In situ localization of auxin in etiolated maize shoots revealed that R-irradiated shoots contained less auxin in the epidermis than the dark controls. Irradiated mesocotyl grew 50% less than the dark controls even when incubated in an optimal level of auxin. However, irradiated and dark tissue contained essentially the same amount of radioactivity after incubation in [14C]IAA indicating that the light treatment does not affect the uptake into the tissue through the cut end, although it is possible that a small subset of cells within the mesocotyl is affected. These observations support the hypothesis that R causes a decrease in the level of auxin in epidermal cells of the mesocotyl, consequently constraining the growth of the entire mesocotyl.

Description: 1. A rhesus and cynomolgus monkey were trained to run around the perimeter of a circular platform in light. We call this "circular locomotion" because forward motion had an angular component. Head and body velocity in space were recorded with angular rate sensors and eye movements with electrooculography (EOG). From these measurements we derived signals related to the angular velocity of the eyes in the head (Eh), of the head on the body (Hb), of gaze on the body (Gb), of the body in space (Bs), of gaze in space (Gs), and of the gain of gaze (Gb/Bs). 2. The monkeys had continuous compensatory nystagmus of the head and eyes while running, which stabilized Gs during the slow phases. The eyes established and maintained compensatory gaze velocities at the beginning and end of the slow phases. The head contributed to gaze velocity during the middle of the slow phases. Slow phase Gb was as high as 250 degrees/s, and targets were fixed for gaze angles as large as 90-140 degrees. 3. Properties of the visual surround affected both the gain and strategy of gaze compensation in the one monkey tested. Gains of Eh ranged from 0.3 to 1.1 during compensatory gaze nystagmus. Gains of Hb varied around 0.3 (0.2-0.7), building to a maximum as Eh dropped while running past sectors of interest. Consistent with predictions, gaze gains varied from below to above unity, when translational and angular body movements with regard to the target were in opposite or the same directions, respectively. 4. Gaze moved in saccadic shifts in the direction of running during quick phases. Most head quick phases were small, and at times the head only paused during an eye quick phase. Eye quick phases were larger, ranging up to 60 degrees. This is larger than quick phases during passive rotation or saccades made with the head fixed. 5. These data indicate that head and eye nystagmus are natural phenomena that support gaze compensation during locomotion. Despite differential utilization of the head and eyes in various conditions, Gb compensated for Bs. There are various frames of reference in which an estimate of angular velocity that drives the head and eyes could be based. We infer that body in space velocity (Bs) is likely to be represented centrally to provide this signal.

Description: 1. Yaw eye in head (Eh) and head on body velocities (Hb) were measured in two monkeys that ran around the perimeter of a circular platform in darkness. The platform was stationary or could be counterrotated to reduce body velocity in space (Bs) while increasing gait velocity on the platform (Bp). The animals were also rotated while seated in a primate chair at eccentric locations to provide linear and angular accelerations similar to those experienced while running. 2. Both animals had head and eye nystagmus while running in darkness during which slow phase gaze velocity on the body (Gb) partially compensated for body velocity in space (Bs). The eyes, driven by the vestibuloocular reflex (VOR), supplied high-frequency characteristics, bringing Gb up to compensatory levels at the beginning and end of the slow phases. The head provided substantial gaze compensation during the slow phases, probably through the vestibulocollic reflex (VCR). Synchronous eye and head quick phases moved gaze in the direction of running. Head movements occurred consistently only when animals were running. This indicates that active body and limb motion may be essential for inducing the head-eye gaze synergy. 3. Gaze compensation was good when running in both directions in one animal and in one direction in the other animal. The animals had long VOR time constants in these directions. The VOR time constant was short to one side in one animal, and it had poor gaze compensation in this direction. Postlocomotory nystagmus was weaker after running in directions with a long VOR time constant than when the animals were passively rotated in darkness. We infer that velocity storage in the vestibular system had been activated to produce continuous Eh and Hb during running and to counteract postrotatory afterresponses. 4. Continuous compensatory gaze nystagmus was not produced by passive eccentric rotation with the head stabilized or free. This indicates that an aspect of active locomotion, most likely somatosensory feedback, was responsible for activating velocity storage. 5. Nystagmus was compared when an animal ran in darkness and in light. the beat frequency of eye and head nystagmus was lower, and the quick phases were larger in darkness. The duration of head and eye quick phases covaried. Eye quick phases were larger when animals ran in darkness than when they were passively rotated. The maximum velocity and duration of eye quick phases were the same in both conditions. 6. The platform was counterrotated under one monkey in darkness while it ran in the direction of its long vestibular time constant.(ABSTRACT TRUNCATED AT 400 WORDS).

Description: No abstract available