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C K Henrikson

Publications and source records attributed to C K Henrikson.

14 recordsLinked to original sources
PubMed1993

Pancreatic splenic lobe organ culture system: viability and amylase release.

An organ explant culture system for the intact chick pancreatic splenic lobe (SL) was characterized for exocrine function. Organ cultures were prepared using the pancreatic splenic lobe from 9- and 15-day-old male broiler chicks (Arbor Acres x Arbor Acres) to characterize amylase release as well as tissue integrity during 2, 4, 8, and 12 h of incubation. Light microscopy studies indicated necrosis of the exocrine pancreatic acini after 4 h of incubation. Changes in islets of Langerhans were noted 4 h after incubation, but islet structural integrity remained intact for up to 12 h of incubation. Lactate dehydrogenase (LD) levels measured in the culture medium did not increase significantly from 2 to 4 h of incubation. After 4 h of incubation, total LD levels increased (P < .05) for the 9-day-old SL cultures, and LD levels increased (P < .01) per unit weight of SL for the 15-day-old cultures. Medium amylase activity did not increase after 2 h of incubation. Large increases occurred for total amylase activity and amylase activity per unit weight of SL between 4 and 12 h of incubation for both 9- and 15-day-old cultures. Histological examination as well as increases in LD and amylase activities for total and per unit weight of SL in the incubation medium suggest that the viability of the 9- and 15-day-old SL organ incubation system decreases after 4 h.

Aging↗
PubMed1989

Effect of prostaglandin inhibitors on bile salt-induced mucosal damage of porcine colon.

The effect of endogenous prostaglandin inhibition on bile salt-induced colonic injury and secretion was studied microscopically and by measurements of [14C]mannitol clearance and transmural potential difference in vivo. Bile salt-induced mucosal damage and permeability increased sequentially with concentration, and these degenerative changes were accelerated with the cyclooxygenase inhibitor indomethacin. Mepacrine, a phospholipase inhibitor, gave similar results, whereas nordihydroguaiaretic acid, a lipoxygenase inhibitor, was ineffective. The effect of indomethacin was abolished by prostaglandin E2 replacement; however, exogenous prostaglandin or prior bile salt exposure failed to result in additional protection. Concentrations of bile salts below the threshold for damage elicited net secretion in the presence or absence of indomethacin, and indomethacin was also without effect on the bile salt-induced secretion at damaging concentrations. Restitution of a completely denuded surface was unaffected by indomethacin, and occurred within 30 min of recovery. The present evidence suggests that endogenous prostaglandins render the mucosa more resistant to acute injury by events independent of the repair process. In addition, the bile salt-induced secretion, which can be dissociated from increased mucosal permeability and microscopic damage, is unlikely to be the result of increased mucosal synthesis of prostaglandins.

Animals↗
PubMed1989

Morphologic and functional effects of bile salt on the porcine colon during injury and repair.

Deoxycholate-induced colonic injury and repair were studied both functionally and morphologically utilizing in vivo loop preparations of the porcine colon. The mucosa was exposed to (a) varying doses (1.5 to 21 mM) of deoxycholate for 30 minutes, (b) 15 mM deoxycholate for varying times and (c) 15 mM deoxycholate for 30 minutes with varying times of recovery. Colonic permeability was assessed by mannitol clearance from blood to lumen and transmural potential difference. After colonic perfusion, tissue samples were collected for light and electron microscopy. Both the degree of mucosal permeability and the amount of superficial epithelial damage increased with increasing concentrations of bile salt culminating in cell necrosis and epithelial sloughing. Denuded colonic surfaces became reepithelialized by migrating, flattened cells in as little as 15 minutes of recovery. Relatively normal appearing columnar epithelium was restituted within 2 hours. Mannitol clearance returned to control values after 30 minutes of recovery, whereas it took potential difference 2 hours of recovery to return to normal. The results of these experiments suggest that (a) the permeability changes measured are most likely due to the lytic action of bile salts which leads to cell degeneration and sloughing of the superficial epithelium, (b) epithelial restitution after superficial damage is remarkably rapid, (c) the formation of a flattened epithelium of immature cells is adequate for restoration of the barrier to macromolecules but ion transport or resistance is slower to recover and (d) repair is due to an active ameboid movement of viable cells out of the crypts onto the surface of the colon.

Animals↗
PubMed1988

Restitution of barrier and transport function of porcine colon after acute mucosal injury.

Acute injury of the porcine colonic epithelium was induced in vivo with the bile salt, deoxycholate. A concentration of 15 mM for 30 min completely destroyed the surface epithelium and induced a marked increase in mucosal permeability to mannitol. The crypt epithelium however was not significantly affected. Within 8 min of recovery, the colonic surface was reepithelialized with flattened, migrating cells, and within 40 min, mucosal permeability to mannitol was normalized. In vitro studies showed that in these early stages of recovery, NaCl transport, short-circuit current, and resistance were markedly impaired, whereas the theophylline-induced secretory response remained intact. Recovery of absorptive function paralleled the transition from flattened to columnar surface epithelium and was complete within 2 h. Results suggest that 1) active migratory events play an important role in rapid restitution of an epithelial barrier, 2) active absorption of ions is much slower to recover, and 3) active secretory events are intact and probably originate in the crypt epithelium.

Animals↗
PubMed1986

The ultrastructure of osteochondrosis of the articular-epiphyseal cartilage complex in growing swine.

Osteochondrosis of the articular-epiphyseal cartilage complex (A-E complex) is a significant clinical disease in swine. It has been suggested that osteochondrosis is the underlying cause of osteochondritis dissecans in humans. The purpose of this investigation was to characterize the ultrastructural changes in the earliest macroscopically visible lesion of the epiphyseal cartilage in osteochondrosis of the A-E complex in swine. Osteochondritic epiphyseal cartilage from the distal femora and humeri of growing crossbred boars was collected, embedded in plastic, and studied light and electron microscopically. The predominant lesion was chondronecrosis, characterized by chondrocyte death and loss of matrical proteoglycan. Transition from normal to abnormal cartilage was abrupt. Lipid accumulated in chondrocytes within and adjacent to lesions, but not in chondrocytes distant from lesions. Intracellular lipid accumulation was an important feature of the lesion and may play a role in its initiation. It is hypothesized that intracellular lipid accumulation results from hypoxia/anoxia and may precede matrix degeneration, which precedes cell death.

Animals↗
PubMed1985

Ultrastructure of normal epiphyseal cartilage of the articular-epiphyseal cartilage complex in growing swine.

Normal epiphyseal cartilage from the articular-epiphyseal cartilage complex (A-E complex) of the distal parts of the femur and humerus of growing commercial crossbred boars was collected, embedded in plastic, and studied by light and electron microscopies. The morphology of this cartilage was determined to provide a basis for comparison with cartilage affected with osteochondrosis, an important clinical disease in swine. Normal epiphyseal cartilage from the A-E complex in growing swine was divided into 4 major regions of cells: resting, proliferating, hypertrophic, and calcifying regions. Cells in the resting zone contained prominent lipid and densely aggregated glycogen. As the cells proliferated and matured, the lipid and glycogen became less prominent. The lipid droplets became smaller and scarcer, and the glycogen became dispersed in the cytoplasm. Proliferating and hypertrophic cells clustered in roughly egg-shaped groups of 4 to 8 cells/plane of section. In the calcifying region, the interterritorial matrix (between cell clusters) calcified, and the territorial matrix (uniting cells in a cluster) remained uncalcified. Calcified matrix extended the depth of one cell group from the area of capillary penetration, and the capillaries invaded by entering a cluster of cells. Territorial matrices in all regions of A-E complex epiphyseal cartilage were composed of randomly oriented collagen fibrils with a granular fibrillar proteoglycan network dispersed between the fibrils. Heterogeneity of chondrocytes was characterized by the presence of both light- and dark-staining cells in the proliferating through calcifying regions and by 3 morphologically distinct light cell types in the late hypertrophic and calcifying regions.

Aging↗
PubMed1981

Ultrastructural lesions of pyridoxine toxicity in beagle dogs.

Three adult Beagle dogs given pyridoxine hydrochloride orally at a dose of 150 mg/kg body weight/day for about 100 days developed ataxia and had spastic, dysmetric leg movements. Ultrastructural alterations in the dorsal funiculus of the spinal cord were degeneration and loss of axons and myelin, and secondary changes of the myelin sheaths. Possible pathogenic mechanisms of pyridoxine neurotoxicity are discussed.

Animals↗
PubMed1976

Alterations in the hippocampus of aged mice.

The hippocampus of C57B1/6 mice was examined histologically and electron microscopically. Male and female mice at 3 and 8 months of age and female mice at 16 months of age were studied. PAS positive foci, containing particles 1-2 mu in diameter, were observed in the hippocampal region of 8 and 16 month old mice. These particles were diastase sensitive. Electron microscopically, in similar mice, a vacuolating change was observed in the cytoplasm of perithelial cells (pericytes) in the same area.

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PubMed1976

Surface specializations of neurites in embryonic mouse spinal cord.

Focal surface specializations occur upon axons, axon growth cone filopodia and, somewhat less frequently, upon dendrites as well as dendritic growth cones in embryonic mouse spinal cord. These surface specializations are observed during the early synaptogenic period (embryonic days 12-16) when the axons of the marginal zone are forming synaptic junctions with motor neuron dendrites growing into their domain. At relatively low electron microscopic magnifications, the specializations appear as discrete patches of electron-dense material located just outside the plasma membrane. Higher resolution and an optimum section plane reveal the following ultrastructural characteristics of these specializations. There is a narrow (approximately 5 nm) less dense layer between the outer surface of the plasms membrane and the thicker (approximately 11.5-15 nm) electron-dense, distal layer of the specializations. The dense layer contains spherical profiles (approximately 10-15 nm in diameter) which have relatively clear centers and non-laminar, opaque perimeters. The surface specializations are commonly associated with an accumulation of dense, fibrillar cytoplasmic material that undercoats the cytoplasmic surface of the plasma membrance directly opposite to the external specializations. Furthermore, some of these surface specializations appear to be forming or merging with the cleft material of protosynaptic junctions and primitive puncta adhaerentia-like contacts. We have also examined the pattern of concanavalin A-peroxidase staining on the cell surfaces in embryonic spinal cord. At embryonic day 13, the earliest stage examined in the concanavalin A-peroxidase experiments, there is already an ubiquitous staining around all the cellular processes in the marginal zone as well as around the perikarya and processes of cells located in the intermediate and ventricular zones. No selective enhancement of neurite surfaces occurred which might have correlated with the surface specializations described above. Finally, the possibility is discussed that the neurite surface specializations might play some role in intercellular recognition phenomena leading to the formation of synaptic junctions and puncta adhaerentia.

Age Factors↗
PubMed1975

Genetically-associated variations in the development of reflex movements and synaptic junctions within an early reflex pathway of mouse spinal cord.

The embryonic development of reflex forelimb movements produced by cutaneous stimulation of the forepaw was examined in five inbred strains of the house mouse, Mus musculus. A quantitative electron microscopic study of synapse formation between the neurons that comprise the spinal cutaneous reflex arc was also carried out on specimens from three of the strains subjected to reflex testing. This investigation provides evidence that there is significant genetically-associated variability in the developmental timing of synapse formation within this disynaptic pathway and in the reflex behavior which it mediates. Specifically, it was found that C57BL/6J embryos had greater numbers of synaptic junctions in the reflex pathway at embryonic days 14-16, and they also showed reflex movements earlier than LP/J embryos. C57BL/6J embryos also showed a more rapid increase in the number of boutons during this embryonic period. CBA/CaJ embryos displayed a temporal pattern of development that differed from both C57BL/6J and LP/J. At E15, CBA/CaJ embryos were more similar to LP/J with regard to both reflex activity and synapse number, but by E16, CBA/CaJ values for both of these measures were more similar to C57BL/6J. On the basis of the data detailed in the text, we suggest that the strains differ in the following manner: C57BL/6J embryos develop boutons rapidly but appear to be relatively inefficient in the actual formation of synaptic junctions; CBA/CaJ embryos develop boutons at a slower rate than C57BL/6J but form synaptic junctions more efficiently; LP/J embryos develop boutons slowly and are also relatively inefficient in forming synaptic junctions. The genetic implications of--and some developmental processes which might be responsible for--the observed strain differences in the timing of synaptic development are discussed in the text. There was no detectable genetic variability of the basic sequence in which the neurons of the cutaneous reflex arc develop their synaptic connections. For all three strains examined, the data indicated that synaptic closure occurred in a retrograde sequence with respect to the direction that neurotransmission normally flows between the neurons of this pathway. This finding agrees with results obtained by other investigators from a number of diverse vertebrate species, and such a widespread lack of variability implies that a retrograde sequencing of synapse formation is involved in the development of specific neuronal connectivities.

Age Factors↗
PubMed1974

A quantitative study of synapses on motor neuron dendritic growth cones in developing mouse spinal cord.

The proportion of synaptic contacts occurring on dendrites as well as on dendritic growth cones and filopodia was determined from electron micrographs of developing mouse (C57BL/6J) spinal cord. Comparable areas of the marginal zone adjacent to the lateral motor nucleus were sampled from specimens on the 13th-16th days of embryonic development (E13-E16). At the beginning of this period, synapses upon growth cones and filopodia comprise about 80% of the observed synaptic junctions, but this proportion decreases with developmental time so that in E16 specimens growth cone synapses account for slightly less than 30% of the synaptic population. Conversely, at E13, synapses upon dendrites comprise less than 20% of the total number of synapses, but increase with developmental time so that they account for about 65% of the synaptic population of E16 specimens. From these data, we suggest the following temporal sequence for the formation of synaptic junctions on motor neuron dendrites growing into the marginal zone. New synapses are initially made upon the filopodia of dendritic growth cones. A synaptically contacted filopodium expands to become a growth cone while the original growth cone begins to differentiate into a dendrite. This process is repeated as the dendrite grows farther into the marginal zone so that synapses originally made with filopodia come to be located upon dendrites. This speculation is briefly discussed in relation to the work and ideas of others concerning synaptogenesis and dendritic development.

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