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Biomedical subjects

G B Ryan

Publications and source records attributed to G B Ryan.

At least 73 records · Page 4Linked to original sources
PubMed1983

Acute renal failure and tubular necrosis associated with hematuria due to glomerulonephritis.

A 16 year old male with a history of recurrent synpharyngitic macroscopic hematuria presented with severe loin pain, macroscopic hematuria and oliguric acute renal failure. Although renal biopsy showed mesangial IgA nephropathy with focal and segmental proliferation with crescents, the extent of glomerular involvement could not explain the severe functional disturbance. Intratubular obstruction and tubular necrosis secondary to the presence of severe glomerular bleeding provide a better explanation. Although renal failure resolved spontaneously, the long-term effects of episodes of this type on structure and function is unknown.

Acute Kidney Injury↗
PubMed1982

Ultrastructure of the pars intermedia of the developing sheep hypophysis.

Using light and electron microscopy, the morphogenesis of the pars intermedia of the sheep pituitary gland was examined in developing lambs between 26 days of gestation and the newborn stage. Following the establishment of contact between the anterior and posterior lobe primordia seen at 26 days, the connection with the pharyngeal roof disappeared by 31 days. The lumen of Rathke's pouch, which was a prominent cavity at the earlier stages, became inconspicuous by 40 days but progressively increased in size during gestation and, in some newborn animals, contained colloid material. At 40 days the pars intermedia consisted of a uniform population of undifferentiated cells. Cells with cytoplasmic granules were first identified at 50 days. The cytological appearance of granular cells at 70 days indicated increased synthetic activity and by 80 days they closely resembled adult glandular cells. At 100 days, membrane activity suggestive of exocytosis was first observed in granular cells; fenestrated capillaries were present, and early follicle formation between adjacent non-granular cells was seen. This apparent exocytotic release of granules was observed much more frequently between 100 days of gestation and the newborn stage than in adult pars intermedia cells. These findings indicate that glandular cells of the developing pars intermedia are actively engaged in synthesis, storage and secretion from an early stage.

Animals↗
PubMed1982

Morphogenesis of the renal juxtaglomerular apparatus and peripolar cells in the sheep.

The morphogenesis of the juxtaglomerular apparatus and peripolar cells was studied in the metanephros of fetal sheep (from 24 to 147 days of gestation) using light and electron microscopy. The first juxtaglomerular apparatus was detected at 45 days of gestation, following constriction of the edges of Bowman's capsule and formation of the vascular pole of the renal corpuscle. Mesenchymal cells gave rise to lacis cells and to smooth muscle and epithelioid cells of the juxtaglomerular arterioles. Epithelioid cells developed only sparse cytoplasmic granulation, first detectable at 92 days. The macula densa developed from tubular cells at the junction of the middle and upper limbs of the S-shaped body of the developing nephron. Peripolar cells arose from epithelial cells in the lower limb of the S-shaped body, at the constricting edges of Bowman's capsule, and formed a cuff around the origin of the glomerular tuft. Cytoplasmic granules were first detected in peripolar cells at 53 days, and remained more prominent than epithelioid cell granulation throughout gestation.

Animals↗
PubMed1982

Ultrastructural morphology of granule release from juxtaglomerular myoepithelioid and peripolar cells.

The morphology of granule release from juxtaglomerular myoepithelioid and peripolar cells has been examined. Renin release occurs from myoepithelioid granules by an unusual form of exocytosis via deep channel-like invaginations of the plasma membrane. Such release occurs towards the juxtaglomerular interstitium as well as towards the arteriolar lumen. Peripolar cell granule exocytosis occurs directly into the urinary space in sodium-depleted sheep, tentatively supporting the speculation that it may be the source of an intrarenal sodium-retaining hormone.

Animals↗
PubMed1981

Ultrastructure of the pars intermedia of the adult sheep hypophysis.

Light microscopy of coronal sections of the sheep pars intermedia revealed a compact, incompletely lobulated V-shaped region about 15-20 cells thick, situated between the pars distalis and the pars nervosa. A prominent hypophysial cleft and follicles containing a colloid-like substance were seen. Using electron microscopy, five cell types could be distinguished: pars intermedia glandular cells, pars distalis-like glandular cells, interstitial cells, follicular cells and cleft lining cells. The polyhedral to pear-shaped pars intermedia glandular cells predominated. They contained dense-cored, membrane-bound granules near the Golgi complex, and larger, irregular vesicles with finely granular contents of varying electron density throughout the remaining cytoplasm; exocytotic release of granules was occasionally observed. Smaller numbers of cells resembling those seen in the pars distalis were scattered throughout the pars intermedia. Interstitial cells usually possessed elongated cytoplasmic processes which extended between the glandular cells, and were characterized by deeply indented nuclei, elaborate junctional complexes and an absence of cytoplasmic granules. Cells lining the follicles resembled the interstitial cells. The major cells bordering the hypophysial cleft were triangular in section and bore irregular microvilli on their free surface. The pars intermedia appeared to be less vascular than the remainder of the hypophysis and only occasional fenestrated capillaries were seen. Nerve profiles were rare.

Animals↗
PubMed1981

Selective distal nephron damage during isolated kidney perfusion.

The morphologic characteristics of the isolated perfused rat kidney were examined by light and electron microscopy. Following perfusion for 90 min, the cortex appeared normal except for the development of spaces in glomerular mesangial regions and ultrastructural abnormalities in very few proximal tubular cells. In the medulla, descending limbs of the loops of Henle and Collecting tubules appeared normal. During perfusion, however, even under optimal conditions, consistent and reproducible changes rapidly developed in cells of the thick ascending limb of Henle's loop, more specifically, in cells of the straight portion of the distal tubule in the inner stripe of the outer medulla. The changes became progressively more severe as perfusion continued and ranged from swelling of mitochondria at 15 min to complete cellular disruption by 90 min. Horseradish peroxidase added to the perfusion medium was found in and between damaged cells and in the interstitial tissue adjacent to affected areas. The pathogenesis of these selective medullary distal tubular abnormalities may relate to the specialized functional activity of this segment of the nephron. Such abnormalities may contribute to the specific functional defects of the preparation.

Animals↗
PubMed1981

The glomerular sieve and the mechanisms of proteinuria.

The glomerular capillary wall acts as a sieve, allowing the passage of water and small solutes but holding up circulating macromolecules the size of albumin or larger. Recent studies indicate that such macromolecules are held up at the level of the endothelial fenestrae by a functional barrier which depends critically upon the maintenance of normal haemodynamic conditions. The effectiveness of this barrier probably relates to molecular sieving phenomena across the basement membrane, perhaps in conjunction with the formation of a concentration-polarisation layer beneath the endothelium, and possibly in association with charge effects. Accordingly, proteinuria may result not only from structural damage to the capillary wall in glomerular disease but also from general or local changes in glomerular blood flow or ultrafiltration flux, causing disturbances in the functional barrier at the endothelial fenestrae. Because it appears that the epithelial layer offers the major restriction to water flux across the wall, protein leakage at sites of focal loss of the epithelial layer (as found in a variety of human and experimental proteinuric states) may result from a focal "blow-out" of ultrafiltration flux, thereby disrupting the functional barrier at the endothelial fenestrae and dragging macromolecules across to the urinary space.

Albumins↗
PubMed1981

Functional properties of hormonally responsive cultured normal and malignant rat osteoblastic cells.

Certain metabolic properties of hormonally responsive osteogenic sarcoma cells derived from a transplantable rat tumor have been compared with those of related normal rat bone cells. All studies were carried out on cells grown in monolayer culture. Normal rat bone cells derived by repeated collagenase/trypsin digestion of newborn rat calvaria. Bone cells selected for comparison were thought to be osteoblast-like, as judged by enrichment of alkaline phosphatase and adenylate cyclase responsiveness to parathyroid hormone and prostaglandin E2. The adenylate cyclases of the two cell strains were similarly stimulated by a range of prostanoids and their metabolites and analogs. Morphology showed the two cell strains to be similar; the only obvious difference was a multilayering of cells in the sarcoma cultures, while the normal cultures showed abundant extracellular fibril formation which was not seen in the tumor cells. Investigation of the cAMP-dependent protein kinase isoenzymes showed the presence of two forms in both cell types, one eluting at a low salt concentration and the other at a high salt concentration. There was approximately twice the amount of the first isoenzyme compared to the second isoenzyme. The results indicate the usefulness of the two cell strains to elucidate further the molecular mechanisms of action of parathyroid hormone and prostaglandins.

Acid Phosphatase↗
PubMed1981

Distribution of anionic groups in the glomerular capillary wall in rat nephrotoxic nephritis and aminonucleoside nephrosis.

It is widely believed that polyanionic plasma proteins, such as albumin, are normally prevented from penetrating the glomerular capillary wall by the presence of intrinsic fixed negative charges in the wall. There is also strong support for the corollary that proteinuria occurs in glomerular disease as a result of loss of such charges. Morphologic studies using cationic 'stains' have indicated that anionic groups can be detected in normal glomeruli and that, in proteinuric states, there is an apparent reduction in such staining. Because most of the latter claims are based largely upon light microscopic studies, critical reassessment at the electron microscopic level is necessary, particularly using the recently developed technique of in situ drip-fixation of superficial glomeruli during good blood flow. In normal rats, this technique results in heavy cationic colloidal iron staining of podocytic epithelial surfaces but little or no staining in the basement membrane or within endothelial fenestrae. In two experimental proteinuric models, rat nephrotoxic nephritis and aminonucleoside nephrosis, there was no loss of colloidal iron staining on podocytic epithelial surfaces at any stage. There was, however, a striking alteration in glomerular architecture in each model, particularly affecting podocytic epithelium. Thus, there was extensive replacement of foot processes by flattened expanses of epithelial cytoplasm, associated with scattered focal gaps in the epithelial covering of the basement membrane. It therefore appears that the reduction of glomerular polyanion seen by light microscopy in glomerular disease results simply from a decrease in visceral epithelial surface area rather than a loss of intrinsic polyanion from the filtering portion of the glomerular capillary wall.

Animals↗
PubMed1980

Ultrastructure of the renal juxtaglomerular complex and peripolar cells in the axolotl (Ambystoma mexicanum) and toad (Bufo marinus).

Renal juxtaglomerular regions were examined in the axolotl (Ambystoma mexicanum and toad (Bufo marinus). Prominent granulated peripolar epithelial cells were found surrounding the origin of the glomerular tuft in the axolotl. These cells resembled the peripolar cells recently discovered in mammalian species. They contained multiple electron-dense cytoplasmic granules, some of which showed a paracrystalline substructure and signs of exocytoxic activity. Such cells were difficult to find and smaller in the toad. In contrast, granulated juxtaglomerular arteriolar myoephithelial cells were much more readily found and larger in the toad than in the axolotl. No consistent differences were noted in juxtaglomerular cells or their granules in response to changes in environmental chloride concentration.

Ambystoma↗
PubMed1978

Membranous glomerulonephritis associated with sarcoidosis.

Two patients with sarcoidosis involving pulmonary hilar lymph nodes developed the nephrotic syndrome. Renal biopsy in both cases showed membranous glomerulonephritis. In one patient, there was an associated renal vein thrombosis.

Adult↗
PubMed1978

The distribution of albumin and immunoglobulin G in the glomerular capillary wall in aminonucleoside nephrosis.

Using an ultrastructural immunoperoxidase technique, the distribution of endogenous albumin and immunoglobulin G was examined in superficial glomeruli of Munich-Wistar rats with aminonucleoside nephrosis. In glomerular capillaries in which the external surface of the glomerular basement membrane (GBM) was completely covered with spread expanses of epithelial cytoplasm, albumin and IgG were distributed normally, with no detectable penetration beyond the endothelial fenestrae. However, at sites of focal loss of the epithelial covering of the GBM, both albumin and IgG were found to penetrate the GBM. These results suggest that, in this experimental model, plasma proteins leak into the urine at sites of glomerular epithelial denudation.

Albumins↗
PubMed1977

Binding of anti-actin autoantibodies to platelets.

Normal platelets incubated with anti-actin autoantibodies (AAA) (from the serum of patients with chronic aggressive hepatitis) do not show binding of these antibodies as seen by indirect immunofluorescence. AAA serum does not inhibit thrombin-induced clot retraction, despite the binding of the antibodies to platelets in the clot. Similarly, AAA serum does not affect "reversible" or "irreversible" aggregation (induced by ADP, collagen or epinephrine), despite the binding of the antibodies to platelet actin under such circumstances. AAA also bind to platelets when aggregation is inhibited by EDTA. The incubation of "reversibly" aggregated platelet with AAA results in a small but definite binding of AAA to platelets. These findings suggest that during "irreversible" and/or "reversible" aggregation, changes take place at the surface of platelets which expose the antigen at the surface of the cell.

Actins↗
PubMed1977

An ultrastructural study of the mechanisms of proteinuria in rat nephrotoxic nephritis.

Nephrotoxic nephritis was induced in Sprague-Dawley and Munich-Wistar rats by the injection of rabbit antirat kidney serum. A biphasic pattern of proteinuria was induced: the heterologous phase with a peak of proteinuria occurring at 10 to 16 hours, and the autologous phase with a peak at 10 to 15 days. For morphologic studies, glomeruli were fixed by perfusion, or by drip-fixation during good blood flow. In the heterologous phase, glomerular endothelial detachment or loss and leukocytic infiltration were prominent. In the autologous phase, focal detachment of glomerular endothelium and epithelium was commonly found. At sites of endothelial loss, in both phases, endogenous albumin (demonstrated by an ultrastructural immunoperoxidase technique), but not intravenously injected ferritin, showed abnormally deep penetration into the glomerular basement membrane. At sites of epithelial loss, found in the autologous phase, both albumin and ferritin were detected throughout the glomerular basement membrane. It is proposed that, in glomerular disease, leakage of plasma proteins may occur across the glomerular basement membrane at sites of endothelial or epithelial detachment.

Albumins↗