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Biomedical subjects

B Cohen

Publications and source records attributed to B Cohen.

At least 253 records · Page 14Linked to original sources

Vestibuloocular reflex of rhesus monkeys after spaceflight.

The vestibuloocular reflex (VOR) of two rhesus monkeys was recorded before and after 14 days of spaceflight. The gain (eye velocity/head velocity) of the horizontal VOR, tested 15 and 18 h after landing, was approximately equal to preflight values. The dominant time constant of the animal tested 15 h after landing was equivalent to that before flight. During nystagmus induced by off-vertical axis rotation (OVAR), the latency, rising time constant, steady-state eye velocity, and phase of modulation in eye velocity and eye position with respect to head position were similar in both monkeys before and after flight. There were changes in the amplitude of modulation of horizontal eye velocity during steady-state OVAR and in the ability to discharge stored activity rapidly by tilting during postrotatory nystagmus (tilt dumping) after flight: OVAR modulations were larger, and tilt dumping was lost in the one animal tested on the day of landing and for several days thereafter. If the gain and time constant of the horizontal VOR change in microgravity, they must revert to normal soon after landing. The changes that were observed suggest that adaptation to microgravity had caused alterations in way that the central nervous system processes otolith input.

Animals↗

Stabilization of gaze during circular locomotion in light. I. Compensatory head and eye nystagmus in the running monkey.

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.

Adaptation, Physiological↗

Stabilization of gaze during circular locomotion in darkness. II. Contribution of velocity storage to compensatory eye and head nystagmus in the running monkey.

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)

Adaptation, Physiological↗

Ocular motor function in motor neuron disease.

We studied ocular motor function in 34 patients with motor neuron disease (MND) and in 18 age-matched controls. This included the latency, accuracy, and amplitude-velocity relationships of saccades. We also examined ocular pursuit, the slow phases of optokinetic nystagmus, and the ability to suppress the vestibulo-ocular reflex (VOR) with visual fixation of a head-mounted target. Five of the subjects with MND had pronounced parkinsonian features on neurologic examination. The nonparkinsonian MND subjects had normal ocular motor function for all measures. Most subjects suppressed the VOR completely. The parkinsonian-MND patients had impairment of both saccadic and pursuit eye movements, and one parkinsonian-MND patient with poor pursuit was unable to suppress the VOR. We conclude that ocular motor function is generally spared in MND. The occasional appearance of ocular motor dysfunction probably reflects the incidence of secondary abnormalities such as parkinsonism.

Adult↗

The Wilfred Fish memorial lecture. The Hunterian tradition in dentistry.

The influence of William and John Hunter upon the development of Medicine and Dentistry in Britain has endured for more than two centuries. John Hunter's first book set out the morphological details of the teeth and their associated structures. From this basis he sought to attain an understanding of physiological and pathological processes by studies of the entire animal kingdom and by experimentation. His foundations of scientific dentistry were built upon by John Tomes and Wilfred Fish in subsequent centuries, both invoking the use of microscopy to enhance Hunter's naked eye descriptions and to interpret the results of experiments. Both, too, are inseparably linked with the history of the Royal College of Surgeons of England by the parts they played in establishing and preserving the place of their profession in that great repository of Hunter's teachings.

History of Dentistry↗

Effects of midline medullary lesions on velocity storage and the vestibulo-ocular reflex.

1. Crossing fibers were sectioned at the midline of the medulla caudal to the abducens nucleus in four cynomolgus monkeys. In two animals the lesions caused the time constant of horizontal and vertical per- and post-rotatory nystagmus to fall to 5-8 s. The slow rise in optokinetic nystagmus (OKN), as well as optokinetic after-nystagmus (OKAN) and cross-coupling of horizontal to vertical OKN and OKAN were abolished. Steady state velocities could not be maintained during off-vertical axis rotation (OVAR). Pitch and yaw nystagmus were affected similarly. We conclude that the ability to store activity related to slow phase eye velocity, i.e., "velocity storage", was lost in these monkeys for nystagmus about any axis. Velocity storage was partially affected by a small midline lesion in the same region in a third animal. There was no effect of a more superficial midline section in a fourth monkey, and it served as a control. 2. The gain (eye velocity/head velocity) of the vestibulo-ocular reflex (VOR) was unaffected by the midline lesions. Saccades were normal, as was the ability to hold the eyes in eccentric gaze positions. The gain of the fast component of OKN increased in one monkey to compensate for the loss of the slow component. 3. One animal was tested for its ability to adapt the gain of the VOR due to visual-vestibular mismatch after lesion. Average changes in gain in response to wearing magnifying (2.2x) and reducing (0.5x) lenses, were +35% and -30%, respectively. This is within the range of normal monkeys. Thus, a midline lesion that abolished velocity storage did not alter that animal's ability to adapt the gain of the VOR. 4. Lesions that reduced or abolished velocity storage interrupted crossing fibers in the rostral medulla, caudal to the abducens nuclei. Cells that contributed axons to this portion of the crossing fibers are most likely located in central portions of the medial vestibular nucleus (MVN) and/or in rostral portion of the descending vestibular nucleus (DVN). The implication is that velocity storage arises from neurons in MVN and DVN whose axons cross the midline.

Animals↗

Failure to awaken after general anaesthesia secondary to paradoxical venous embolus.

A patient is presented who failed to regain consciousness after an apparently uneventful nine-hour revision of a total hip replacement. There were no clinically important haemodynamic changes during the operation, and oxygen saturation, capnography and acid base balance were normal throughout. Postop CT of the head showed a large left MCA infarct with midline shift. At autopsy, the patient was found to have a previously unsuspected patent foramen ovale, and a venous embolus in the left internal carotid artery, which probably had originated from the periprostatic venous plexus with a large infarct in the distribution of the left anterior and middle cerebral arteries. The authors conclude that massive paradoxical venous emboli can occur during surgery with minimal haemodynamic changes.

Anesthesia, General↗

Early development of leg and wing primordia in the Drosophila embryo.

The development of the leg and wing primordia in the Drosophila embryo has been traced using molecular markers. Distal-less and disconnected gene expression provide molecular labels for the leg primordia throughout embryonic development, disconnected expression in the developing leg primordia depends on Distal-less activity. The leg primordia arise as discrete clusters of cells that occupy well defined positions in the embryonic ectoderm. At later stages of embryogenesis the primordia become morphologically recognizable and are intimately associated with the development of the Keilin's organs. The presumptive leg disc and the Keilin's organ appear to derive from a common primordium. Similarly the Abnormal leg pattern gene provides a molecular label for the wing and haltere primordia. The dorsal thoracic primordia appear to be of independent origin from the legs.

Animals↗

Interleukin-6 induces the (2'-5') oligoadenylate synthetase gene in M1 cells through an effect on the interferon-responsive enhancer.

Interleukin-6 (IL-6) activates (2'-5') A synthetase (2'-5' AS) gene expression in differentiating myeloleukemic M1 cells. Antibodies to type I interferon (IFN) inhibit 2'-5' AS induction but not differentiation. Analysis of the mechanism of 2'-5' AS induction shows that it does not result from increased IFN formation, but from a synergism between IL-6 and endogenously secreted IFN. IL-6 can activate expression of a CAT construct fused to the interferon response sequence (IRS) of the 2'-5' AS gene. In extracts of IL-6-treated M1 cells, changes in protein binding to IRS DNA can be demonstrated. One of the effects of IL-6 on M1 cells is, therefore, to induce DNA binding factors, some of which act on the same enhancer sequence as IFNs, resulting in a synergistic gene activation. M1 variants resistant to differentiation by IL-6 have lost the ability to induce the 2'-5' AS gene.

2',5'-Oligoadenylate Synthetase↗

Metacognition in HIV-1 seropositive asymptomatic individuals: self-ratings versus objective neuropsychological performance. Multicenter AIDS Cohort Study (MACS).

This study examined the relationship between actual and self-reported neuropsychological deficits, depression, and HIV-1 serostatus. The subjects, who consisted of 479 individuals, 256 who were HIV seronegative (SN) and 233 who were HIV-1 seropositive though still asymptomatic (ASP), were administered a standardized neuropsychological screening battery consisting of measures of attention, motor speed, psychomotor speed, verbal memory, verbal fluency, and depression. To assess subjects' subjective sense of their cognitive status, the Cognitive Failures Questionnaire (CFQ), a 25-item self-report questionnaire, was also administered. The results of MANOVA failed to reveal group differences between the SN and ASP groups on the measures of neuropsychological function. Similarly, the ASP and SN groups did not differ on the number or severity of reported cognitive failures. However, a positive correlation was found between CFQ scores and level of depression. These results do not support the hypothesis that ASP individuals are aware of cognitive decline prior to detection using standard neuropsychologic screening instruments. The data do suggest that the presence of depressed mood, independent of serostatus or actual neuropsychological impairment, is associated with increased cognitive complaints.

Adult↗

Spinal cord compression from a thoracic paraganglioma: case report.

A 34-year-old man with a 4-month history of midthoracic back pain sought treatment for a recent onset of lower extremity paresthesia and stiffness. A myelogram and computed tomographic myelogram disclosed an extradural block at the level of the 8th thoracic vertebral body with involvement of the pedicles, lamina, and spinous process. A posterior decompression of the spinal cord with subtotal resection of a highly vascular tumor was performed. The tumor was identified as a paraganglioma. In a second stage, the remainder of the tumor was embolized preoperatively, and gross total excision and sequential stabilization of the spine with a Luque rectangle and sublaminar wires were performed. The patient has been symptom free and without signs of a recurrence in the spine for over 13 months. A large abdominal paraganglioma was recently resected from its probable origin from the adventitia of the abdominal aorta.

Abdominal Neoplasms↗