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Biomedical subjects

W Young

Publications and source records attributed to W Young.

At least 163 records · Page 9Linked to original sources

Effect of high-dose corticosteroid therapy on blood flow, evoked potentials, and extracellular calcium in experimental spinal injury.

High-dose methylprednisolone (15 to 30 mg/kg), administered 45 minutes after severe contusion injury (400 gm-cm) to cat spinal cords, rapidly reverses the typical posttraumatic ischemia that occurs in spinal injuries. White matter blood flow improves despite the systemic hypotension associated with bolus intravenous injections of such massive corticosteroid doses. In addition, this treatment facilitates extracellular calcium ionic recovery in contused spinal cords, and salvages evoked potential activity that is lost in untreated cats. These data suggest that high-dose corticosteroid treatment causes local vasodilation of spinal cord blood vessels. The consequent blood flow increase may account for the beneficial effects of high-dose corticosteroid treatment on both functional recovery and histopathological appearance of injured spinal cords.

Animals↗

Experimental spinal cord injury: treatment with naloxone.

We studied the effect of the opiate antagonist naloxone on the recovery of cats injured with a 400-g-cm impact injury to T-9. The animals were evaluated by recording somatosensory evoked potentials and performing weekly neurological examinations. Several dose schedules were followed. Six of eight cats that received an intravenous or intraperitoneal bolus of naloxone (10 mg/kg) 45 minutes after injury regained the ability to walk. Recovery occurred in only one of five animals that were treated with an infusion of naloxone, 10 mg/kg/hour, and in none of five animals given 1 mg/kg as a bolus. Because these results are not related to any observed change in blood pressure, we believe that naloxone may be achieving its effect through the preservation of spinal cord blood flow, as well as other mechanisms that have yet to be defined.

Animals↗

Acute physiological effects of ultrasonic vibrations on nervous tissue.

We investigated the acute effects of ultrasonically induced lesions on action potential conduction and blood flow in nervous tissues. A Cavitron ultrasonic surgical aspirator (CUSA) was used to emulsify small areas of cat thoracic spinal cord while hydrogen clearance, somatosensory evoked potentials, and vestibulospinal evoked potentials wee monitored. In addition, we examined the effect of direct and indirect application of the vibrating probe on rat sciatic nerves. The CUSA created localized lesions of the spinal cord, sparing the function and blood flow of immediately adjacent white structures. Histological studies revealed a sharp demarcation of the lesion sites with little morphological evidence of tissue injury beyond the borders of the lesions. The rat sciatic nerve experiments showed that, as long as the probe tip did not touch the nerve, ultrasonic vibrations had little effect on the nerve. These results suggest that the destructive effects of the ultrasonic vibrating probe are limited to a small volume at the probe tip. We conclude that, at low power levels sufficient to cause tissue emulsification at the probe tip, the CUSA does not acutely affect the function of nearby white matter. However, our results may not be extendable to higher intensity levels and do not rule out chronic effects.

Action Potentials↗

Intraspinal localization of the somatosensory evoked potential.

Somatosensory evoked potentials (SEPs) are used widely for monitoring neurophysiological function in experimental spinal injury. Yet the spinal pathways for SEP conduction remain unclear. Consequently, we sought to define specific changes in the SEP after interruption of selected spinal pathways. We activated cortical SEPs with sciatic nerve stimulation in 11 anesthetized (25 mg of pentobarbital per kg) cats after a multilevel thoracic laminectomy. The most consistent wave from component was an initial positivity (IP) at a 17- to 19-ms onset latency. We then used a Cavitron ultrasonic surgical aspirator to interrupt specific spinal pathways. A unilateral dorsal column lesion abolished the ipsilateral IP, but did not affect conduction in the contralateral column. Bilateral dorsal column lesions obliterated the IP, but sometimes left some longer latency components. Interruption of all but the ventral columns abolished the SEPs. When we interrupted all spinal pathways but the dorsal columns, an intact IP remained. In fact, a distinct IP was conducted through a single dorsal column after the division of all other spinal cord pathways. We concluded that, in the barbiturate-anesthetized cat: (a) the most consistent SEP wave form is an initial positivity at a 17- to 19-ms onset latency, (b) the integrity of the dorsal columns is both necessary and sufficient to conduct a normal-appearing IP component of the SEP, (c) the lateral columns may carry some longer latency component of the SEP, (d) the ventral columns carry no component of the SEP, and (e) bilateral recording may be useful for detecting asymmetry of injury.

Animals↗

Effect of naloxone on posttraumatic ischemia in experimental spinal contusion.

The effect of naloxone on blood flow and somatosensory evoked potentials was studied in cats subjected to 400 gm-cm contusion injuries of the thoracic spinal cord. Eight cats were treated with 10 mg/kg naloxone 45 to 60 minutes after injury, 11 cats were given 10 ml of saline instead of naloxone, and six cats were neither injured nor treated. Hydrogen clearance was used to measure blood flow in the lateral white columns at the contusion site. Naloxone, given intravenously, significantly inproved the blood flow rates in the lateral column white matter. At 2 hours after injury, the mean blood flow in the saline-treated cats fell to 50% (p greater than 0.01) of preinjury flow rates, whereas it increased 6% (p greater than 0.50) in naloxone-treated cats, and 12% (p greater than 0.50) in uninjured cats. At the 3rd hour after injury, the respective flows fell 47% (p less than 0.01), and 6% (p greater than 0.50), and increased 15% (p greater than 0.50) of the preinjury flow rates. The naloxone-treated cats had striking preservation of sensory function and somatosensory evoked potentials at 24 hours after injury. At 24 hours, responses had returned in all the naloxone-treated cats and in only 11% of the saline-treated cats. The probability of this combination of events occurring by chance is 0.0030. The authors conclude that naloxone may be useful for the treatment of spinal cord injury. The mechanism of the effect is unknown.

Animals↗

Human monoclonal antibody against Forssman antigen.

Hybrid cells formed between human lymphocytes and mouse myeloma cells produce human immunoglobulin in culture. Stable antibody-producing cell lines can be isolated after multiple cycles of low-density passage, cloning, and continued selection for immunoglobulin production. The origin and characteristics of a hybrid of human and mouse cells is described. This hybrid produces high concentrations (8.3 micrograms per milliliter) of human immunoglobulin M reactive with the terminal disaccharide of the Forssman glycolipid. These findings point to the potential use of human-mouse hybrid cells as a source of human monoclonal antibodies for therapeutic and diagnostic purposes.

Animals↗

Field potential analysis in elasmobranch cerebellum.

Stimulation of cerebellar white matter (WM) in the skate, an elasmobranch fish, evokes a distinctive set of cortical field potentials characterized by 3 negativities and a positivity. The first negativity (N1) has 1 msec latency and is largest in the lateral regions of the corpus cerebelli where Purkinje cells and white matter are most densely congregated. The second negativity (N2) occurs at 2--4 msec latency and is localized to the granular layer. The third negativity (N3) follows with a latency of 4--6 msec and is prominent in the molecular layer. The positivity (P) correlates with N2 in time course and dominates in the midline where granule cell axons ascend en masse to form parallel fibers in the molecular layer. A preceding WM stimulus blocks the N1 potential for 20 msec and the N2 potential for 60 msec and the N2 potential for 20 msec. A conditioning stimulus, applied to the parallel fibers in the dorsal midline (LOC), suppresses the N1 potential for 20 msec and the N2 potential for 40 msec. Intracellular recordings from the Purkinje cell layer reveals short latency action potentials correlating in time with N1. These findings suggest that N1 derives from antidromic Purkinje cell activation and mossy fiber excitation, that N2 represents orthodromic granule cell excitation by white matter fibers, and that N3 stems from parallel fiber activity. Because of its close association with parallel fibers and the similarity of its time course to N2, the positivity is attributed to current sources in parallel fibers generated by granule cell current sinks. Differences between the cerebellar field potentials found in elasmobranchs and mammals can be explained by the unique anatomic arrangement of granule cell axons in the former.

Animals↗

Spreading depression in elasmobranch cerebellum.

Spreading depression (SD) occurs in the cerebellum of an elasmobranch fish, the skate (Raja erinacea, Raja ocellata). The elasmobranch cerebellum, because of its unique separation of granular form molecular layer, provides an excellent opportunity to study the characteristics of SD in two distinct neuronal populations. Both the DC potential shifts and changes in neuronal activity effected by SD were analyzed. The SD DC potential shifts in both layers closely resembled those in mammalian cerebral cortices. Consisting of a predominantly negative extracellular potential shift, they were typically 1--10 min in duration and reached 5--40 mV peak amplitudes. The largest negative shifts were found in the granular layer, without any consistent positive phases in the white matter, molecular, or granular layers. The SD propagated radially from surface electrical stimulation at 0.78 mm/min (+/- 0.16, n = 8) in the molecular layer and 0.43 mm/min (+/- 0.17, n = 8) in the granular layer at 15 degrees C. At 18 degrees C, the molecular layer propagatory velocity was 1.1 mm/min (+/- 0.12, n = 20) while, at 10 degrees C, it was 0.52 mm/min (+/- 0.21, n = 20), suggesting a temperature-dependent Q10 factor of 2. A profound depression of both spontaneous and evoked neuronal activity accompanied the DC potential shift. Activation of Purkinje cells antidromically, white matter, and granular layer neurons was typically abolished by the peak of the negative DC shift. However, a significant increase in granular layer excitability often followed the neuronal depression, remaining so far up to an hour. Repeated waves of SD sometimes occurred in the absence of neuronal recovery. A similar post-SD excitability increase was not seen in molecular layer neurons. Intracellular recordings from Purkinje cells revealed a spontaneous burst of action potentials at the onset of SD, closely followed by a depolarization of membrane potential from an average of -64 mV (+/- 12 mV, n = 3) to -11 mV (+/- 5 mV, n = 3).

Animals↗

Vestibulospinal monitoring in experimental spinal trauma.

Vestibulospinal tract function was monitored in experimental contusion of the spinal cord in cats, and compared with somatosensory cortical evoked potentials. Both white and gray matter portions of the vestibular and somatosensory pathways were evaluated in cord injuries at T-7 and L-4. Severe contusions of 20 gm-20 cm force impact resulted in a rapid (less than 1 second) abolition of thoracic white matter conductivity, but a somewhat slower (4 to 5 minutes) loss of lumbar gray matter responses. A paradoxical transient recovery of white matter conductivity occurred 1 to 2 hours after injury, despite eventual progression to central hemorrhagic necrosis at the contusion site. In contrast, mild contusions (20 gm-10 cm force impact) produced only a temporary loss of neuronal activity: white matter for 1 to 2 hours, and gray matter for 30 to 40 minutes. In general, vestibular and somatosensory potentials showed similar sensitivity to contusion, although the former tended to recover earlier. We conclude that contusion injury causes two types of neuronal dysfunction in spinal cord: 1) a low-threshold concussion-related loss of activity lasting 30 to 120 minutes; and 2) a higher threshold necrotic process, requiring 1 to 2 hours to develop, which apparently spreads from gray to white matter.

Animals↗

The role of the sympathetic nervous system in pressor responses induced by spinal injury.

Spinal cord injury consistently evokes a transient 3- to 4-minute rise is systemic pressure, followed by prolonged hypotension. Because the role of the sympathetic nervous system in these blood pressure changes is not clear, the pressure responses were studied using systematic ablation of the peripheral sympathetic nervous system. In total, 24 cats were subjected to bilateral thoracic sympathectomy, adrenalectomy, splanchnicectomy, combinations of the preceding, sham operation, or no treatment. Either 3 or 24 hours after the ablations, the blood pressure responses were evoked by 400 gm-cm contusions of the thoracic cord. Although neither thoracic sympathectomy nor adrenalectomy alone abolished the hypertensive phase, the combination of the two procedures did. This suggests that both the thoracic sympathetic ganglia and the adrenal glands participate in the pressor response. Thoracic sympathectomy affected primarily the early part, whereas adrenalectomy diminished the later part of the hypertensive response. This correlates with the function of the former being neurally and the latter being humorally mediated. None of the sympathetic lesions consistently affected the hypotensive phase. Spinal contusion injury produces widespread sympathetic activation, mediating the hypertensive changes.

Adrenal Medulla↗

Prolonged increases in paradoxical sleep during and after avoidance-task acquisition.

Rats were trained in a two-way shock-avoidance task, either in a single training session of 100 trials or over a 5 day period with 20 trials per day. Electroencephalograph and electromyograph recordings were continuous for 2 days prior (base line), during, and following the experiments, except during the actual training sessions. Animals that learned the task showed marked increases in PS. Rats that learned the distributed trials training task showed PS increases in the 24 hr period prior to a maximum increase in correct performance. These PS elevations appeared after a 10 hr latency following the training session. The animals that learned the single training session exhibited PS increases that persisted for a period of 6 days, which appeared daily in a cyclic manner. The latency to onset of these PS changes was less than 1 hr. The PS increases in both types of training were due to an increase in the number of PS periods and are believed to be different manifestations of the same flexible mechanism. This mechanism is considered to be involved with some aspect of learning other than the acquisition process, such as retention.

Animals↗

Determining continuing education interests of medical technologists: an initial step.

Continuing education is an ever-increasing need for medical technologists who want to maintain and upgrade their professional knowledge and skills. Professional groups strive to develop programs to meet a diversity of needs. Planning groups often encounter difficulty during the program development process as they identify topics and select effective educational strategies for presentation. In order to help identify topics of interest and desirable educational methods for the continuing education of laboratory personnel, a continuing medical technology education interest assessment tool was developed and used by a medical technology continuing education committee. Development and use of this assessment tool and resulting statistical survey results formed the basis for two continuing education courses, both considered highly successful.

Education, Continuing↗