Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Functional renal compensatory hypertrophy (RCH) in the uninephrectomized rat is completely reversible by transplantation in Brown Norway (BN) rats, while anatomic RCH is not. To determine the nephron element(s) responsible for persistent anatomic RCH, we performed morphometric analysis on perfusion fixed rat kidneys following renal function studies. In this model the function of renal transplants is not different from contralateral and unmanipulated control kidneys, and there is no histological evidence of rejection. Rats uninephrectomized for three or six weeks had larger glomeruli than controls, and after transplantation of a previously hypertrophied kidney into a rat with a normal or a solitary hypertrophied kidney, glomerular size returned to control levels. Increased glomerular capillary volume (CVCP) in kidneys with RCH was due to increased capillary length (LCP; 13.1 +/- 1.0 mm cf. 10.3 +/- 0.9, P < 0.01) without increase in capillary radius (RCP; 3.26 +/- 0.33 microM cf. 3.28 +/- 0.24). In contrast, return of CVCP to control levels in kidneys undergoing regression was associated with persistently elevated LCP (13.0 +2- 2.9 mm; native previously hypertrophied kidney; 12.2 +/- 0.9; transplanted previously hypertrophied kidney vs. 10.3 +/- 0.9, P < 0.01) and decreased RCP (2.79 +/- 0.10 microM and 2.73 +/- 0.09, cf 3.28 +/- 0.24, P < 0.01). RCH was associated with proportional increases in glomerular, tubular, and vascular-interstitial volumes while only elevated tubular volume persisted during regression. Altered glomerular capillary dimensions and increased tubular volumes acquired during renal RCH induced by unilateral nephrectomy persisted during complete functional regression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversible compensatory hypertrophy in rat kidneys: morphometric characterization. 845 59

Brown rust, caused by Puccinia melanocephala, can cause severe epidemics in susceptible sugarcane cultivars during spring and early summer in Louisiana. The effect of the disease on yield was evaluated in field experiments conducted during three growing seasons. A mixture of three fungicides-azoxystrobin, propiconazole, and tebuconazole-applied biweekly during the spring epidemic period kept brown rust severity low (<5%), and plants protected by fungicide applications throughout the epidemic provided an estimate of attainable yield for comparison with plants naturally infected with rust. A combined analysis over three seasons estimated brown rust caused reductions of 16 and 14% in cane tonnage and total amount of sucrose produced, respectively, in cv. LCP 85-384. The greatest reduction in total sucrose yield of 22% resulted from the epidemic of longest duration, and stalk weight was negatively correlated with rust severity. Comparisons of the yields obtained from plots in which brown rust was controlled early versus late in the epidemic suggested that the impact of the disease is greatest from the middle to late epidemic period when stem elongation has begun.
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PMID:Effect of Brown Rust on Yield of Sugarcane in Louisiana. 3075 85