Design, construction, and validation of a large capacity rodent magnetic field exposure laboratory.

A magnetic field exposure laboratory has been constructed to support National Toxicology Program studies for the evaluation of the toxicity and carcinogenicity of pure, linearly polarized, 60 Hz magnetic fields in rodents. This dual corridor, controlled access facility can support the simultaneous exposure of 1200 rats and 1200 mice. The facility contains fully redundant electrical and environmental control systems and was constructed using non-metallic materials to maintain low levels of background (ambient), stray, and cross-talk magnetic fields. The exposure module design provides for large uniform exposure volumes with good control of stray and cross-talk fields, while allowing the use of roll-around cage racks for simplified animal husbandry. Stray fields and cross-talk have been further reduced by the inclusion of "steering coils" in each exposure module. Ambient 60 Hz fields (less cross-talk) in all exposure rooms are <0.1 microT (1 mG), and static magnetic fields have been mapped extensively. Magnetic field strength, waveform, temperature, relative humidity, light intensity, noise level, vibration, and air flow in all animal holding areas are tightly regulated, and are monitored continuously during all studies. Field uniformity in the animal exposure volumes is better than -/+l0%; a systematic program of cage, rack, and room rotation controls for possible positional effects within the exposure system. Magnetic fields are turned on and off over multiple cycles to prevent the induction of transients associated with abrupt field level changes. Total harmonic distortion is <3% at all field strengths. The facility has been used to study magnetic field bioeffects in rodent model systems in experiments ranging in duration from 8 weeks to 2 years.

High autopsy rates at a university medical center. What has gone right?

OBJECTIVE: Identification of factors that contribute to a high autopsy rate at our institution. DESIGN: An objective analysis of the Autopsy Service's organization, functions, and process flow to identify factors that impact the autopsy rate. SETTING: The University of Texas Medical Branch at Galveston, Tex. METHODS: Statistics were collected using the autopsy log book and computerized data bank. The events starting at the time of a patient's death through the completion of the autopsy report were reviewed. The role of each significant event was analyzed. RESULTS AND CONCLUSIONS: The annual autopsy rates between 1981 and 1995 ranged between 45% and 59%. The largest number of nonmedicolegal autopsies were received from the Department of Internal Medicine. The Texas Department of Criminal Justice Hospital contributed the largest number of medicolegal autopsies. We conclude that the following key factors contribute to our high autopsy rates: (1) the organization and multiple functions of the Autopsy Service, particularly the presence of a Decedent Affairs Office, dedicated resident assignments, and internal and external quality control of the autopsies; (2) close interactions with clinicians, including timely communication of autopsy results to clinicians and a fostering of positive attitude among clinical residents and faculty; and (3) other factors such as the contributions to hospital risk management, disproving the idea that there may be increased litigation related to high autopsy rates, and support by the hospital administration.

General practitioners' perceptions of the effects of a distance learning programme.

A postal/telephone survey of 400 general dental practitioners working in the Greater Glasgow and Lanarkshire Health Board areas was carried out between May and September 1990. The aims were to monitor any changes in the use of sealant restoration techniques in the last year, to investigate the practitioners' perception of the effects of a distance learning programme on their techniques and to provide data on the use of the techniques in the final months of the 'old contract'. A response rate of 66.7% was achieved. Eighty-eight per cent of the group were placing sealant restorations. Dentists' perceptions of the impact of the distance learning programme were encouraging. In key areas of practice, 16-44% of the group reported changes in their clinical techniques as a result of reading the programme.

Rat Schwann cell remyelination of demyelinated cat CNS axons: evidence that injection of cell suspensions of CNS tissue results in Schwann cell remyelination.

Injection of a suspension of embryonic rat central nervous system (CNS) cells into an area of persistent demyelination, produced in the cat spinal cord by injecting ethidium bromide into an area previously exposed to 40 Grays of x-irradiation, results, initially, in Schwann cell remyelination of the demyelinated axons. However, the Schwann cells are subsequently rejected; a response which confirms that the remyelinating cells are of rat origin.

Schwann cell remyelination of CNS axons following injection of cultures of CNS cells into areas of persistent demyelination.

The injection of suspensions of central nervous system (CNS) cells, prepared by standard methods from 4-day-old rat brain and maintained in vitro for 10 days, into areas of persistent demyelination in rat spinal cord resulted in extensive remyelination of axons by Schwann cells. As control lesions injected with medium showed no remyelination, the most likely explanation of this finding is that 'CNS cultures' contain a small population of Schwann cells which are stimulated to proliferate by the demyelinated axons.

Ultrastructure of motor endplates in canine congenital myasthenia gravis.

Morphometric analysis was carried out on electron micrographs of motor endplates from three Jack Russell terriers affected with congenital myasthenia gravis (CMG) aged 10 weeks, 12 weeks and 22 weeks, respectively. Control endplates from age-matched pups and an adult Jack Russell were also examined. The results showed that postsynaptic membrane density was significantly increased in affected animals and secondary fold length was decreased. The ratio of postsynaptic to presynaptic membrane length was normal in the 10 and 12-week-old pups, but reduced in the 22-week-old CMG animal. These changes were unrelated to muscle fibre diameter and there was no evidence of a destructive process. It is suggested that the alteration in membrane folding pattern in this condition may be related to abnormal trophic influences during synaptogenesis.

Morphologic evaluation of vitreous collagen after penetrating ocular injury.

Condensation and contraction of the vitreous have been implicated in the development of vitreoretinal traction and traction retinal detachment after penetrating ocular injury. In this study, using the inorganic dye ruthenium-red, we studied ultrastructural changes in vitreous in the rabbit eye after standard penetrating injury and intravitreal blood injection. In normal rabbit vitreous the collagen fibrils have a regular arrangement. In contrast, after a penetrating injury the collagen fibrils appear focally condensed. While it appears unlikely that such a network could alone produce tractional or directional forces, these alterations along the collagen fibrils could provide a scaffold along which contractile cells migrate into the vitreous.

Internodal myelin volume and axon surface area. A relationship determining myelin thickness?

Internodes from normal, remyelinated and regenerated nerve fibres have been isolated from rat spinal roots and sciatic nerve. The internodes have been examined quantitatively by light and electron microscopy to determine their internodal length, myelin thickness, and the circumference and cross-sectional area of both the axons and fibre. Comparison of these measurements of the axon and myelin sheath has revealed a close relationship between the volume of myelin comprising the internode and the area over which the Schwann cell and axon are in close proximity, i.e. the surface area of the axolemma beneath the internodal myelin sheath. The same relationship described not only the internodes on normal nerve fibres, where internodal length is proportional to axon diameter, but also the short and thinly myelinated internodes formed in the adult animal on remyelinated and on regenerated axons. Examination of data presented by Berthold (1978) revealed that a closely similar relationship is also present in feline nerve fibres. In view of the constancy of the relationship between such different types of internode it is suggested that the regulation of myelin volume, and thereby of myelin thickness, may be mediated via the area of the axolemma or of the Schwann cell membrane beneath the myelin sheath.

Suppression of remyelination in the CNS by X-irradiation.

Rat and cat spinal cords were exposed to 2000, 3000 or 4000 rads of x-irradiation prior to producing an area of primary demyelination in the dorsal columns by the injection of lysolecithin. In animals irradiated with 4000 rads no remyelination by either Schwann cells or oligodendrocytes occurred. With 2000 rads both types of remyelination occurred, but when compared to unirradiated controls, central remyelination was less extensive, while Schwann cells remyelinated a greater percentage of axons. With 3000 rads the results were variable, some animals responded similarly to those in the 4000 rad group, whereas others responded as the 2000 rad animals. Oligodendrocytes were found among the persistently demyelinated axons in the 4000 rad animals and their processes were associated with, but only rarely formed a myelin sheath round, the demyelinated axons. It was concluded that irradiation damage to local cells was responsible for the inhibition of remyelination but it could not be determined if this was due to its effect on the oligodendrocytes alone. The origin of the oligodendrocytes found among the demyelinated axons is discussed in this context.

Observations on the interactions of Schwann cells and astrocytes following X-irradiation of neonatal rat spinal cord.

Myelination was inhibited in the spinal cord of three day-old rats with 2000 rads of X-irradiation. Myelination subsequently occurred as a result of caudal migration of oligodendrocytes and extensive invasion of the cord by Schwann cells. Although oligodendrocytes were present in areas containing Schwann cells, astrocytes were absent. The presence of Schwann cells in the neuropil of the spinal cord did not stimulate production of basement membrane by astrocytes, so no new glial limiting membrane was formed. Evidence is presented which suggests that if astrocytes do not form a glial limiting membrane when opposed by large numbers of Schwann cells they are destroyed by the invading cells. It is suggested that the glial limiting membrane normally inhibits entry of Schwann cells into the central nervous system; if this is destroyed and not reconstituted, Schwann cells can migrate freely into the neuropil.