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E R Feringa

Publications and source records attributed to E R Feringa.

At least 37 records · Page 2Linked to original sources
PubMed1984

Histologic evidence for death of cortical neurons after spinal cord transection.

Dying cortical neurons, identified by standard histologic criteria, were observed in the rat sensory/motor cortex after spinal cord transection. The peak incidence of these changes was 10 weeks after injury. At that time, spinal-cord-injured animals showed 10 times as many abnormal cells as were found in matched controls (p less than or equal to 0.05). Dying cells were found in the same anatomic location as corticospinal neurons axotomized by the experimental injury, and at the expected time after injury. The survival of corticospinal neurons in these young adult rats may be dependent on obtaining a crucial input from an appropriate target cell (neuron).

Animals↗
PubMed1983

Retrograde transport in corticospinal neurons after spinal cord transection.

Complete spinal cord transection at T-6/T-7 in rats caused a decrease in the number of surviving corticospinal neurons. Cell death began 5 and 10 weeks after cord injury. The number of surviving cells decreased progressively for at least 25 weeks after injury. Surviving cells were identified by their ability to transport horseradish peroxidase (HRP) retrograde from a T-1/T-2 insertion site to cortical cell somas. Therapy aimed at promoting corticospinal tract regeneration must be started early after spinal cord injury.

Animals↗
PubMed1981

Axoplasmic flow of tritiated proline in the corticospinal tract of the rat.

The rates of axoplasmic transport were studied in the corticospinal tract of the rat by injecting tritiated proline into the sensory-motor cortex and subsequently analyzing the distribution of incorporated label in the spinal cord at intervals after injection. A mathematical model of the anatomy of the corticospinal tract was developed and used in analysis of the data. The rate of a fast component was calculated to be 240-420 mm per day, which is comparable with rates of fast components in the peripheral nervous system (PNS), but considerably greater than rates in other tracts in the central nervous system. A slow component was calculated to have a transport rate of 3-8 mm per day which is greater than rates found either in the CNS or PNS. This higher rate may be related to the greater length of the corticospinal tract as compared to other CNS tracts studied.

Animals↗
PubMed1981

The adrenoleukomyeloneuropathy complex: expression in four generations.

Varying combinations of leukodystrophy, myeloneuropathy, peripheral neuropathy, and primary Addison disease were identified in 14 members of four generations of a kindred of 49 persons. Of these, 26 persons from three generations were evaluated clinically. We propose that adrenoleukomyeloneuropathy (ALMN) is a rare, progressive, presumably biochemical disorder of uncertain inheritance. ALMN is expressed clinically by dysfunction of the central nervous system, peripheral nervous system, and endocrine system. We stress that suspicion of this disorder be high in evaluating uncertain neurologic disorders, and that identification of one manifestation of this complex should alert the clinician to the possibility of a different expression of the same complex in other family members.

Adolescent↗
PubMed1980

Basal lamina formation at the site of spinal cord transection.

The pia-glial basal lamina (BL) at the site of spinal cord injury could be an important physical impediment to central nervous system regeneration. We used an epithelial BL-specific immunohistochemical stain to determine the location of the pia-glial BL after spinal cord transection. Small segments of BL were found at the margin of the lesion 5 days after transection. After 10 days, longer and more numerous segments were seen. At 20 days, the entire transected end of the spinal cord was capped by a layer of BL.

Animals↗
PubMed1980

Light microscopic, immunohistochemical localization of the pia-glial basal lamina.

The current histologic methods for studying the pia-glial basal lamina (BL) are inappropriate for high contrast, permanent light microscopy preparation. We have developed a staining technique for epithelial BL which is highly specific, extremely sensitive, permanent, relatively inexpensive, and suitable for light or electron microscopy (EM). Central nervous system (CNS) basement membrane zone (BMZ) antigens were isolated by the technique of Meezan (1975) from female albino Wistar rats. Using this CNS BMZ preparation as an antigenic source, a hyperimmune rabbit serum was developed. This serum was exhaustively adsorbed with rat splenic pulp to remove undesirable antibodies to endothelial BL and collagen. The peroxidase-antiperoxidase indirect antibody technique was used to test the staining specificity of this splenic adsorbed serum on different tissues containing BLs of known origin and/or function. The results indicated that this BL staining technique was specific for epithelial BL of the rat and of some other species.

Animals↗
PubMed1979

Enzyme treatment of spinal cord transected rats.

Russian investigators have recently reported clinical recovery of enzyme treated, spinal cord transected rats. Using the exact protocols of Matinian and Andreasian's two most successful treatment regimens, we repeated their experiments using United States produced pure hyaluronidase and trypsin or trypsin and elastase. Animals were evaluated for return of bladder function, clinical evidence of hind limb motor function, cortical evoked response after sciatic nerve stimulation, and axonal transport of cortically injected tritiated proline by regenerated corticospinal axons. None of the treated animals differed from control animals treated only with the enzyme vehicle. No animals walked, had return of voluntary motor activity, showed cortical evoked response, or had evidence for transport of tritiated proline over regenerated corticospinal axons.

Animals↗
PubMed1979

Lidase treatment of spinal cord transected rats.

Russian investigators have recently reported clinical recovery of enzyme treated, spinal cord transected rats. Using the exact protocols outlined by Matinian and Andreasian, we repeated a portion of their experiment using a Lidase preparation manufactured in the USSR. Animals were evaluated for return of bladder function, clinical evidence of hind limb motor function, cortical evoked response after sciatic nerve stimulation, and axonal transport of cortically injected tritiate proline by regenerated corticospinal axons. The only difference between treated and control animals was that the mean total body weight of the treated animals increased more than that of controls (p less than 0.05). No animal walked, had return of voluntary motor activity, showed cortical evoked response, or had evidence for transport of tritiated proline over regenerated corticospinal axons.

Animals↗
PubMed1979

Spinal cord regeneration in rats made immunologically unresponsive to CNS antigens.

Seventy days after complete spinal cord transection, both treated and untreated rats showed evidence that some corticospinal axons had regenerated. Rats made immunologically unresponsive to CNS tissue showed no increase in corticospinal regeneration as measured by orthograde axoplasmic flow of tritated proline or retrograde axoplasmic labelling with horeseradish peroxidase. However, treated rats did demonstrate electrophysiological evidence of regeneration of long ascending sensory pathways. Tolerant animals additionally treated with cyclophosphamide showed corticospinal axonal regeneration by tritated proline transport and electrophysiological techniques and also showed electrophysiological evidence of ascending sensory tract regeneration.

Afferent Pathways↗
PubMed1978

Fink-Heimer/Nauta demonstration of regenerating axons in the rat spinal cord.

Six months after complete spinal cord transection, regenerated descending motor axons can be found by electrophysiologic testing and can also be demonstrated anatomically using the Fink-Heimer/Nauta technique. Regeneration was found in all animals, treated or control, but statistically significant increased regeneration as measured by the Fink-Heimer/Nauta technique was found in animals treated with a single injection of 75 mg/kg of cyclophosphamide 24 hours after the original spinal cord transection. This result is similar to those of another study using the orthograde axonal transport of tritiated proline as a measure of axonal regeneration. The mode of action of cyclophosphamide may be by its immunosuppressive properties because this drug is most effective when administered 24 hours after cord transection, a time when its effects as an immunosuppressant would be maximal.

Animals↗
PubMed1978

A mask for the artificial respiration of rats.

A simple artificial respiration mask for rats was constructed from the drip chamber of an intravenous solution administration set. The mask was held in place by means of straps and a hole through which the maximillary incisors protruded. This mask permitted artificial ventilation during drug-induced respiratory paralysis, was easily and inexpensively constructed, and may be used with a variety of positive pressure respirators.

Animals↗
PubMed1977

Axon regeneration across the site of injury in the optic nerve of the newt Triturus pyrrhogaster.

The process by which axons regenerate following a freeze injury to the optic nerve of the newt was analyzed by light and electron microscopy. Freezing destroys cellular constituents in a one millimeter segment of the nerve, leaving intact the basal lamina and the blood supply to the eye. No axons are seen at the site of injury one to seven days post lesion. This contrasts with the persistence of normal-appearing but severed unmyelinated axons within the cranial stump which thus give a false appearance of early regeneration. The first axon sprouts traverse the lesion and enter the cranial strump by ten days. The number of regenerating axons increases rapidly thereafter with no signs of random growth at the site of injury. These axon sprouts tend to be somewhat larger than normal unmyelinated axons and contain dense core vesicles and abnormal organelles similar to those in growing axons in tissue culture. The persisting basal lamina inside the optic sheath appears to provide continuity across the site of injury, to orient axon sprouts, and to favor an orderly process of axon regeneration without neuroma formation.

Animals↗
PubMed1977

Cyclophosphamide-induced abnormalities in the incisors of the rat.

A single injection of 75 mg/kg cyclophosphamide caused gross dental abnormalities in rats. Broken, malformed, overgrown, and "extra" incisors developed several weeks after drug treatment. Radioautographic investigations show no unusual features in the morphology or labeling with H3-thymidine in the odontogenic cells. The results suggest that the cytotoxic effect of the drug is a temporary one which induces a residual alteration of tooth growth.

Animals↗
PubMed1976

Recovery in rats after spinal cord injury.

Previous studies from this laboratory have shown evidence of regeneration of long descending spinal motor tracts in rats after spinal cord transection and treatment to modify the animals' immune response. In this study, less extensive surgical lesions were combined with the most favorable drug treatment (75 mg per kilogram of cyclophosphamide in a single dose) in an effort to improve the prospects for regeneration. Less than complete spinal cord transections in the rat were frequently followed by clinical and electrophysiologic evidence of return of function. Such return of function appears to depend on a reorganization of the nervous system that results in the use of the few remaining fibers to transmit motor information rather than on regeneration. Immunosuppressive treatment had no effect on these results.

Animals↗
PubMed1975

Spinal cord regeneration in rats after immunosuppressive treatment. Theoretic considerations and histologic results.

Some species of animals and some early developmental stages of other species are capable of central nervous system (CNS) regeneration. These species and developmental stages also have reduced or absent allergic reaction to tissue homografts. Mammals are allergic to their own brain antigens, and experimental allergic encephalomyellitis (EAE) can be produced when they are exposed to parenterally administered brain antigen. Immunosuppressive treatment will delay or prevent the production of EAE in rats. In our experiments, immunosuppressive treatment made possible the electrophysiologic study of regeneration of long descending motor tracts of the spinal cord in rats six months after spinal cord transection. Histologic evaluation showed no comparative difference in scar at the site of transection when treated animals were compared with controls. Neither was any difference noted between animals in which regeneration was shown electrophysiologically and those without such regeneration. Perhaps humoral antibodies play a role in the prevention of functional regeneration in the rat.

Animals↗
PubMed1975

Hypertrophic granulomatous cranial pachymeningitis causing progressive blindness in a chronic dialysis patient.

A patient on chronic haemodialysis because of renal failure developed progressive visual field loss and eventual blindness. A postmortem examination indicated that the blindness was caused by granulomatous thickening of the pachymeninges which constricted the optic nerves as they passed through the optic foramina. Exhaustive bacteriological and histopathological studies failed to identify a specific cause for this hypertrophic cranial pachymeningitis.

Adult↗