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W J Niklowitz

Publications and source records attributed to W J Niklowitz.

11 recordsLinked to original sources

Immobilization-associated osteoporosis in primates.

The progressive osteopenic changes in tibial compact bone in adult male monkeys (Macaca nemestrina) were examined histologically during chronic studies of immobilization. The animals were restrained in a semirecumbent position, which reduces normally occurring stresses in the lower extremities and results in bone mass loss. The longest immobilization studies were of 7 months duration. Losses of haversian bone tended to occur predominantly in the proximal tibia and were characterized by increased activation with excessive depth of penetration of osteoclastic activity. There was no apparent regulation of the size and orientation of resorption cavities. Rapid bone loss seen during 10 weeks of immobilization appeared to be due to unrestrained osteoclastic activity without controls and regulation, which are characteristic of adaptive systems. The general pattern of loss persisted throughout 7 months of immobilization. Clear-cut evidence of a formation phase in haversian bone was seen only after 2 months of reambulation. During this period osteoblasts accumulated within resorption cavities, and there was matrix apposition. Within 6 months of recovery there was increased bone turnover, and resorption cavities with diameters of 500-1500 micron were filled partially with new bone; the mean wall thickness of new bone was 2 to 3 times larger than normal. In addition there were numerous remodeling sites that were of normal size and orientation. Trabecular bone was lost during immobilization, and it is probable that losses of large trabecular plates are not replaced, and consequently original bone volume in the cross section is not recovered. In this immobilization model we observed bone resorption occurring for long periods without apparent interruption.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Tibial changes in experimental disuse osteoporosis in the monkey.

We studied the mechanical properties and structural changes in the monkey tibia with disuse osteoporosis and during subsequent recovery. Bone bending stiffness was evaluated in relationship to microscopic changes in cortical bone and Norland bone mineral analysis. Restraint in the semireclined position produced regional losses of bone most obviously in the anterior-proximal tibiae. Following 6 months of restraint, the greatest losses of bone mineral in the proximal tibiae ranged from 23% to 31%; the largest changes in bone stiffness ranged from 36% to 40%. Approximately 8 1/2 months of recovery were required for restoration of normal bending properties. However, even after 15 months of recovery, bone mineral content did not necessarily return to normal levels. Histologically, resorption cavities in cortical bone were seen within 1 month of restraint; by 2 1/2 months of restraint there were large resorption cavities subperiosteally, endosteally, and intracortically. After 15 months of recovery, the cortex consisted mainly of first-generation haversian systems. After 40 months, the cortex appeared normal with numerous secondary and tertiary generations of haversian systems.

Animals↗

Ultrastructural changes in alveolar macrophages of rats exposed to nickel oxide by inhalation.

Alveolar macrophages recovered from rats exposed to nickel oxide (NiO) showed distinct changes in cell size and presence of viscous substances surrounding the cells. Both alveolar macrophages and lung washout fluid (LWF) exhibited alterations in the cytoplasmic inclusion bodies by the presence of parallel, concentric lamellar structures or formations, osmiophilic inclusions, matrix formations and obvious degenerative changes. In addition, alveolar macrophages showed eccentrically placed nucleus with peripheral chromatinization, elongated outline and cytoplasmic projections of different sizes.

Animals↗

Neurofibrillary changes following childhood lead encephalopathy.

This report details the findings in a patient who survived severe lead encephalopathy at age 2 1/4 years, to die 42 years later in a state of severe mental deterioration. The brain revealed diffuse cortical atrophy, most severe in the temporal lobes, followed by hippocampi, amygdaloid nuclei and frontal cortex. Numerous pyramidal cells of the forebrain grisea contained Alzheimer's neurofibrillary tangles. The remaining pyramidal cells of the hippocampi exhibited granulo-vacuolar degeneration. Many senile plaques were present predominantly in the atrophic temporal cortex. Electron microscopic examination revealed many 800 A twisted tubules in the tangles. Atomic absorption spectrophotometry disclosed a tenfold increase of lead in frontal and temporal cortices as compared to suitable controls. The possibility that toxic levels of lead in any form could result in the formation of Alzheimer's fibrillary tangles is discussed.

Adult↗

Neurofibrillary changes after acute experimental lead poisoning.

Following acute tetraethyllead intoxication in rabbits classic neurofibrillary tangles develop. As studied by electron microscopy, such tangles develop in hydropic degenerating neurons and consist primarily of bundles of 200 A diameter smooth tubules of enormous length. In two of 16 animals a few twisted tubules (periodicity of 800 A) also could be found. The significance of these lead-induced twisted tubules, so characteristic of Alzheimer's pre-senile dementia in man, is discussed.

Acute Disease↗