The Feulgen Reaction after Glutaraldehyde Fixation

Kasten, Frederick H.; Lala, Raymond

doi:10.3109/10520297509117057

Cited by 22 publications

(8 citation statements)

References 6 publications

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“…Thin sections (60-80 nm) were stained with 4% aqueous uranyl acetate and lead citrate, and examined with an AEI electron microscope. Midcoronal sections of the whole kidney were embedded in paraffin, treated with sodium borohydride (22), and then stained with periodic acid-Schiff (PAS) or phosphotungstic acidhematoxylin.…”

Section: Methodsmentioning

confidence: 99%

Mechanisms underlying transition from acute glomerular injury to late glomerular sclerosis in a rat model of nephrotic syndrome.

Anderson¹,

Diamond²,

Karnovsky³

et al. 1988

J. Clin. Invest.

118

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Functional and morphologic measurements were performed in Munich-Wistar rats after a single central venous injection of puromycin aminonucleoside (PA) or saline vehicle (sham). During phase I, PA rats exhibited overt nephrotic syndrome and impaired glomerular filtration, primarily due to a reduction in the glomerular capillary ultrafiltration coefficient. The morphologic counterpart of the latter consisted of effacement of glomerular epithelial cell foot processes and decrease in the number of filtration slit diaphragms. Administration of the angiotensin I converting enzyme inhibitor (CEI) enalapril to PA rats did not ameliorate glomerular dysfunction. During phase II, PA rats exhibited spontaneous resolution of proteinuria, impaired function, and morphologic abnormalities. However, PA rats now demonstrated marked glomerular capillary hypertension and continued, albeit lesser, reductions in the ultrafiltration coefficient. Concurrent CEI administration modestly lowered systemic arterial pressure, and normalized the glomerular capillary hydraulic pressure and ultrafiltration coefficient. Additional rats were studied during phase III, 70 wk after injection. In PA rats, prior glomerular hypertension was associated with development of recurrent proteinuria and extensive glomerular sclerosis, whereas concurrent CEI administration limited these parameters to values comparable to those in sham rats. Glomerular hypertension thus may explain the development of glomerular sclerosis and renal failure long after an episode of acute glomerular injury.

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Section: Methodsmentioning

confidence: 99%

Mechanisms underlying transition from acute glomerular injury to late glomerular sclerosis in a rat model of nephrotic syndrome.

Anderson¹,

Diamond²,

Karnovsky³

et al. 1988

J. Clin. Invest.

118

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“…The nuclei and chromosomes of the cultured soybean cells were stained by a modification of the Feulgen procedure (22). Cells were collected by filtration and resuspended in SCF medium containing 2% glutaraldehyde.…”

Section: Methodsmentioning

confidence: 99%

Polyribosome Formation in Relation to Cytokinin-induced Cell Division in Suspension Cultures of Glycine max [L.] Merr.

Fosket¹,

Volk²,

Goldsmith³

1977

Plant Physiol.

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We have investigated the relationship between cell proliferation and protein synthetic capacity in a cytokinin-requiring strain of cultured soybean ceUls (Glycine max IL.] Menf. cv. Sodffuri, of cotyledonary origin) in suspension culture. When transferred to a defined medium lacking cytokinin, very little cell division or cell enlrgement took place over the course of a 6-day culture period. Cells transferred to medium of the same composition, but containing 0.5 jM zeatin, exhibited rapid initial growth, with maimum mitotic activity occurring after 24 hours in culture, and a doubling of the cell population within the first 36 hours of the culture period. The polyribosomal RNA content of the cells decreased over the course of the first 24 hours of the growth cycle while the polyribosome to monoribosome (P/M) ratio increased. The increase in the P/M ratio was greater in the cytokinin-treated cels. This apparent relationship between cytokinin-induced ceUl proliferation and polyribosome formation was examined further. Polyribosome formation was stimulated when zeatin was added directly to cel populations which had been cultured for 24 hours in medium lacking a cytokinin. Transfer to fresh medium alone also stimulated polyribosome formation, whether this medium contained a cytokinin or not. The magnitude of transferinduced polyribosome formation depended upon the initial cell density (number of cells/mi of medium). Regardiess of the initial cell density and independent of the P/M ratios attained, the cytokinin-treated cell populations divided while the cytokinin-deprived cell populations did not. In vivo labeling with [uSImethionine and slab gel electrophoretic separation of sodium dodecyl sulfate derivatives of the labeled polypeptides demonstrated qualitative changes in the spectrum of proteins synthesized by the cytokinin-treated cells. These qualitative changes were independent of the cell density (and hence, independent of the P/ M ratio) but they preceded cytokinin-induced ceUl division.

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“…Sections, approximately I -pm thick, were stained with either 1% loluidine blue or periodic acid-Schiff (PAS) reagent [24j. Midcoronal sections of the whole kidney were treated with sodium borohydride [25] and stained with the PAS reagent. Tissue was examined and photographed with a Leitz photomicroscope.…”

Section: Preparation For Light Microscopymentioning

confidence: 99%

Nonanticoagulant Protective Effect of Heparin in Chronic Aminonucleoside Nephrosis

Diamond¹,

Karnovsky²

1986

Kidney Blood Press Res

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Aminonucleoside nephrosis progresses over an 18-week period to focal and segmental glomerulosclerosis (FSGS). Whole heparin has been shown to blunt the extent of renal injury in another model of FSGS, renal ablation; however, the precise mechanism of protection has remained uncertain. Since heparin has a variety of physiologie actions unrelated to anticoagulation, we administered three different heparin compounds, each with a distinct profile of biological properties, to groups of rats given a single intravenous dose of puromycin aminonucleoside (PA). In the absence of a prolongation of the activated partial thromboplastin time (aPTT), both whole heparin (WH) and a 7,000- to 11,000-dalton-molecular-weight nonanticoagulant heparin (NAH) ameliorated the functional and histologic abnormalities of chronic aminonucleoside nephrosis as evidenced by significant reductions in 24-hour urine protein excretion while preserving the glomerular filtration rate and blunting the rise in serum creatinine as compared to untreated PA control animals at the conclusion of the study. In addition, the NAH and WH groups exhibited significantly fewer glomeruli with either segmental mesangial proliferative areas or glomerulosclerosis/hyalinosis lesions 18 weeks after PA administration. A fragment of heparin (HF) was ineffective. We conclude that heparin may exert its beneficial effect in chronic aminonucleoside nephrosis through a biologic action, other than anticoagulation, perhaps by inhibition of mesangial cell proliferation.

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The Feulgen Reaction after Glutaraldehyde Fixation

Cited by 22 publications

References 6 publications

Mechanisms underlying transition from acute glomerular injury to late glomerular sclerosis in a rat model of nephrotic syndrome.

Mechanisms underlying transition from acute glomerular injury to late glomerular sclerosis in a rat model of nephrotic syndrome.

Polyribosome Formation in Relation to Cytokinin-induced Cell Division in Suspension Cultures of Glycine max [L.] Merr.

Nonanticoagulant Protective Effect of Heparin in Chronic Aminonucleoside Nephrosis

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