Biomedical subjects

S B Plurad

Publications and source records attributed to S B Plurad.

24 records · Page 2Linked to original sources

PubMed1985

Retrograde axonal transport of 125I-nerve growth factor in rat ileal mesenteric nerves. Effect of streptozocin diabetes.

The retrograde axonal transport of intravenously (i.v.) administered 125I-nerve growth factor (125I-NGF) was examined in mesenteric nerves innervating the small bowel of rats with streptozocin (STZ) diabetes using methods described in detail in the companion article. The accumulation of 125I-NGF distal to a ligature on the ileal mesenteric nerves of diabetic animals was 30-40% less than in control animals. The inhibition of accumulation of 125I-NGF in diabetic animals was greater at a ligature tied 2 h after i.v. administration than at a ligature tied after 14 h, which suggests that the diabetic animals may have a lag in initiation of NGF transport in the terminal axon or retardation of transport at some site along the axon. The 125I-NGF transport defect was observed as early as 3 days after the induction of diabetes, a time before the development of structural axonal lesions, and did not worsen at later times when dystrophic axonopathy is present. Both the ileal mesenteric nerves, which eventually develop dystrophic axonopathy in experimental diabetes, and the jejunal mesenteric nerves, which never develop comparable structural alterations, showed similar 125I-NGF transport deficits, suggesting that the existence of the transport abnormality does not predict the eventual development of dystrophic axonal lesions. Autoradiographic localization of 125I-NGF in the ileal mesenteric nerves of animals that had been diabetic for 11-13 mo demonstrated decreased amounts of 125I-NGF in transit in unligated paravascular nerve fascicles. There was, however, no evidence for focal retardation of transported 125I-NGF at the sites of dystrophic axonal lesions.

Animals↗

PubMed1983

Neuroaxonal dystrophy in the autonomic ganglia of aged rats.

Distinctive axonal abnormalities in selected sympathetic ganglia of male and female Sprague-Dawley and male Fischer 344 rats have been characterized as a function of increasing age. Dilated intraganglionic axons contained a variety of unusual subcellular organelles, including large numbers of compact or loosely aggregated tubulovesicular profiles, layered membranous loops, and collections of normal and degenerating organelles, identical to those described in clinical and experimental neuroaxonal dystrophy. Although occasional dystrophic axons were encountered free within the ganglionic neuropil, the majority were intimately associated with the surface of major dendrites or perikarya of principal sympathetic neurons and presumably represent terminal preganglionic axons. However, neither synaptic vesicles in dystrophic axons nor the association of dystrophic axons with post-synaptic densities were demonstrated. Dystrophic axons were infrequent within the prevertebral superior mesenteric and celiac ganglia before one year of age, but increased substantially in numbers thereafter. Similar findings expressed as lesions per mm2 were approximately tenfold less frequent in the paravertebral superior cervical ganglia of the same animals.

Aging↗

PubMed1983

The effect of pancreatic islet transplantation and insulin therapy on experimental diabetic autonomic neuropathy.

Rats with chronic streptozotocin (SZ) diabetes develop dilatation of the alimentary tract, loss of fecal consistency, and autonomic neuropathy involving unmyelinated axons of the extrinsic innervation of the small bowel. Diabetic autonomic neuropathy involving the ileal mesenteric nerves is characterized by modest to marked dilatation of axons by distinctive subcellular organelles identical to those described in experimental and clinical axonal dystrophies. Axonopathy is confined to the alimentary tract; examination of myelinated and unmyelinated axons of the sciatic (midthigh level) and distal somatic nerves of the tail of diabetic animals with prominent ileal axonopathy failed to demonstrate significant numbers of dystrophic axons. The prevention or reversal of diabetic autonomic neuropathy by a variety of experimental manipulations clearly indicates that the lesions we have demonstrated in chronically SZ-induced diabetic animals were produced by diabetes and were not the result of a direct neurotoxic effect of the diabetogenic agent streptozotocin. Animals did not develop axonopathy after simultaneous administration of SZ and nicotinamide, a procedure which prevents pancreatic beta-cell necrosis and induction of diabetes while exposing the nervous system to a possible neurotoxic agent. Selected animals that were given SZ, became diabetic, and subsequently received daily insulin therapy or pancreatic islet transplantation also did not develop axonopathy. Transplantation of pancreatic islets 6 mo after induction of diabetes, a time at which mesenteric axonopathy was well developed, quickly reestablished normoglycemia, and within 3 mo resulted in nearly complete resolution of the neuropathy. Mild chronic diabetes maintained for 5-6 mo failed to produce significant levels of axonopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1983

Experimental diabetic autonomic neuropathy characterization in streptozotocin-diabetic Sprague-Dawley rats.

Rats with chronic streptozotocin-induced diabetes develop enlargement of the alimentary tract, loss of fecal consistency, and autonomic neuropathy involving the extrinsic innervation of the ileum. In this study we have continued the characterization of the unmyelinated axonopathy involving the ileal mesenteric nerves of outbred Sprague-Dawley rats diabetic for 1.5 to 10 months using ultrastructural methods. Axonopathy in the alimentary tract of chronically diabetic rats is characterized by modest to marked dilation of axons by distinctive subcellular organelles identical with those described in experimental and clinical axonal dystrophies. Lesions are infrequent 1.5 and 3 months after induction of diabetes, increasing rapidly in numbers thereafter. Axonal lesions are reproducibly encountered in the ileum, cecum, and rectum but not in the proximal jejunum of chronically diabetic rats. Sectioning of mesenteric nerves along their longitudinal axes demonstrates the focal and in some instances apparent terminal nature of the axonal dilation. Disappearance of dystrophic axons distal (peripheral) to mesenteric crush injury confirms the origin of the axons extrinsic to the gut wall. Only rare examples of dystrophic diabetic axonopathy were detected within the wall of the ileum, presumably representing involvement of terminal axonal segments within the intrinsic ganglia. Examination of the mesenteric nerves of 18- and 30-month-old control rats failed to demonstrate dystrophic axonopathy, providing evidence that diabetic axonopathy does not represent premature development of an aging change in mesenteric nerves. Examination of the autonomic innervation of various other tissues including spleen, bladder, vas deferens, and iris, as well as the phrenic, sciatic, vagus, and tail nerves of 4- to 12-month diabetic animals, failed to demonstrate reproducible axonopathy comparable to that involving the alimentary tract of the same animals. The paravascular fascicles of ileal mesenteric nerves of 6- to 7-month diabetic and age-matched control rats were examined by morphometric methods and failed to demonstrate significant loss of axons or an appreciable shift in mean fiber diameter.

Aging↗

PubMed1982

A cellular investment of bone marrow.

We describe a method for clearly separating the cell layers at the bone-marrow interface, which reveals that the myeloid tissue is invested by an epithelial-like layer of specialized squamous cells we call the marrow sac. The scanning electron microscope showed that the sac was fenestrated and that some of its cells pass as perivascular elements with the marrow capillaries that penetrate the bony cortex. The transmission electron microscope (TEM) showed that the cells comprising the marrow sac are less than 0.1 micrometer thick, overlap at their margins without specialized cell junctions, and are more electron dense than the reticular or fibroblastic cells of the marrow stroma. The fenestrations in the sac were intercellular and were usually occupied by cells having an ultrastructure compatible with an osteoprogenitor cell (OPC) lineage. The observation of a close proximity between the cells of the marrow sac and the osteogenic cells that line the endosteal surfaces of bone suggest that the sac cells, along with the OPCs of the superficial marrow stroma, should be included in any morphological or functional definition of an endosteum.

Animals↗

PubMed1972

Fine structure of ascosporogenesis in Nematospora coryli Peglion, a pathogenic yeast.

Observations with the electron microscope of the early stages of ascospore formation in Nematospora coryli Peglion reveal the following sequence of events. Partial dissociation of the nuclear membrane is followed by the appearance of unit membranes. Each unit membrane gives rise to two pairs of double membranes delimiting the ascospores from the epiplasm of the ascus. Enlarged mitochondria which have a granular matrix and limited cristae development are also regularly seen.

Cell Membrane↗