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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our previous studies showed that 54 kD and 48 kD tubular basement membrane (TBM) proteins were the major form of the target antigen involved in anti-TBM antibody-mediated tubulo-interstitial nephritis in humans. In those studies, we isolated the 54 kD glycoprotein (named gp54) from collagenase-digested bovine TBM. NH2-terminal amino acid sequencing indicated that gp54 represented a newly defined glycoprotein. In this study, we further characterized the target antigen, using mouse monoclonal antibodies to gp54 and polyclonal anti-gp54 peptide antibody. Two monoclonal antibodies (H79 and H80) were established, and they reacted, by immunofluorescence, predominantly with the proximal TBM of humans, rabbits, and Wistar, Sprague-Dawley, and Brown-Norway rats, but not with that of Lewis rats. They were also fixed by blotting intensely to the 54 kD component and weakly to the 48 kD component of collagenase-digested human TBM. In vivo transfer of H79 to Wistar rats showed extensive linear binding of mouse IgG to the TBM and the basal membrane of the small intestine; however, no pathologic changes were seen by light microscopy. The anti-gp54 peptide antibody reacted with both the 54 kD and 48 kD TBM components of human TBM. mRNA was prepared from rabbit kidneys, and fractionated to enrich mRNA encoding the 54 kD and 48 kD peptides. On in vitro translation experiments with the mRNA fraction, the 54 kD and 48 kD peptides were immunoprecipitated with anti-gp54 antibodies. These findings indicate that the 54 kD and 48 kD components are encoded with different mRNA, but that they share the same antigenic epitope.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The target antigen of anti-tubular basement membrane antibody-mediated interstitial nephritis. 785 11

Brown adipose tissue and collagenase-isolated brown adipocytes were investigated in rats by means of 1H and 13C nuclear magnetic resonance spectroscopy. After chloroform-methanol extraction of brown adipose tissue, proton and natural abundance 13C spectra of the chloroform fraction showed resonances attributable to triglycerides, and were qualitatively similar to those of the corresponding fraction of white adipose tissue. By means of quantitative analysis of 1H spectra, fatty acid unsaturation and polyunsaturation in triglycerides were found to be lower in brown than white adipose tissue; moreover, unsaturation parameters decreased in triglyceride fatty acids of brown adipose tissue upon norepinephrine administration or cold acclimatization of rats, and were affected by the age of donors. The molar percentage of mono- and polyunsaturated C18 fatty acids in triglycerides was determined from 13C spectra and found to change in the early post-natal period. Isolated, agarose-embedded brown adipocytes from 4-day-old rats showed a number of peaks in the carbohydrate region of 1H spectra that were not present in spectra of white adipocytes and almost disappeared in brown fat cells of older animals. These peaks could be restored by insulin exposure. Natural abundance 13C spectra of isolated brown adipocytes were resolved enough to allow unambiguous assignment of resonances to carbons of fatty acids, glycerol, glucose, ethanolamine, and choline. Calculation of the mono- to polyunsaturated fatty acids ratio in the cells was also performed. Nuclear magnetic resonance spectroscopy is a useful tool for the investigation of brown adipose tissue and adipocytes therefrom.
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PMID:Magnetic resonance spectroscopy investigations of brown adipose tissue and isolated brown adipocytes. 789 17

Some forms of glomerulonephritis (GN) in humans appear consequent to autoimmunity. Experimental autoimmune GN (EAG) has been described in sheep, but attempts to develop EAG in other mammals have resulted only in antibody and proteinuria but no GN. We have developed a model of EAG in an inbred mammalian species to further study pathogenetic mechanisms. We immunized Brown Norway (BN) and Wistar-Kyoto (WKY) rats with glomerular basement membrane (GBM) or collagenase solubilized GBM (csGBM). Circulating and bound anti-GBM antibody developed in all rats. Only interstitial nephritis occurred in BN rats despite amounts of glomerular and serum anti GBM antibodies similar to WKY animals. One hundred percent of WKY rats immunized with csGBM/acid developed reproducible severe GN at two to three weeks with proteinuria and decreased kidney function which progressed to glomerulosclerosis and interstitial fibrosis. Antigen in acid was a requisite for induction of EAG. EAG rats had positive tests for delayed type hypersensitivity, their T cells underwent antigen specific transformation, and T cells and macrophages were present histologically. Passive transfer of EAG serum to naive rats resulted in fixation to recipient GBM but no proteinuria or GN. This new model of EAG in rats appears dependent on genetic factors, may involve cellular immunity in pathogenesis, requires exposure of the nephritogenic antigen, and is highly similar to rapidly progressive GN in humans.
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PMID:Proliferative autoimmune glomerulonephritis in rats: a model for autoimmune glomerulonephritis in humans. 837 73

We examined the effects of sensitization and antigen challenge on the cellular populations retrieved from the large airways (LA) (generations zero to 5 approximately) and small airways and parenchyma (S/P) of the rat. Male Brown-Norway rats, 7 to 8 wk of age, were either actively sensitized to ovalbumin (n = 24) or sham-sensitized to saline (n = 9), and, 14 days later, they were anesthetized with urethane, intubated endotracheally, and challenged. Aerosols of ovalbumin (5% wt/vol in saline for 5 min) or saline were administered to 12 and six rats, respectively, and measurements of pulmonary resistance (RL) were made for 8 h. The early airway response (ER) was calculated as the highest value of RL in the first hour after challenge, and the late response (LR) was calculated as an increase in RL to greater than 200% of the baseline value in the 4- to 8-h period after challenge. Rats were killed by exsanguination, LA were separated from S/P, and cells were isolated after tissue mincing and digestion with collagenase. Total and differential cell counts and lymphocyte subsets were determined. Antigen challenge significantly increased the cellular yield (mostly neutrophils) from the LA and S/P. Animals with a LR had a lower total cellular yield from the LA and S/P than did animals without a LR. The animals with a LR also had a lower yield of eosinophils and lymphocytes from the S/P than did animals challenged with saline alone. Cellular yields were not lower in the animals with an isolated ER after antigen challenge.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inflammatory cell populations in the airways and parenchyma after antigen challenge in the rat. 846 35

In the present study, hypertriglyceridemia was induced by feeding S. D. rats with high carbohydrate diet (carbohydrate accounting for 80% of total calorie) for 5 days. Rat liver parenchymal cells (PC) and non-parenchymal cells (NPC) were prepared by collagenase method. Human plasma LDL, VLDL and HDL were isolated by density gradient ultracentrifugation method. 125I-LDL was labelled by ICI method. 125I-LDL binding to rat liver PC and NPC were measured by Goldstein and Brown's method. The results showed that both rat liver PC and NPC had LDL receptors to bind, uptake and degradate 125I labelled human plasma LDL. The Bmax of 125I-LDL binding to NPC was 7-fold higher than that of PC (P < 0.01), but the Kd values remained unchanged. The Bmax of 125I-LDL binding to liver NPC from hypertriglyceridemic rats was significantly higher than that of NPC from the normal diet (carbohydrate accounting for 60% of total calorie) rats (435.4 + 100.0 vs 307.1 +/- 76.8 ng/mg cell protein, n = 6, P > 0.05), but there was no difference in Kd between the HTG rats and normal rats (18.1 +/- 4.1 vs 17.2 +/- 4.0 micrograms/ml n = 6, P > 0.05). These results suggest that the increase in fractional catabolic rate of LDL in patients with hypertriglyceridemia reported by Vega and Grundy might be induced by the increase in number of LDL receptor on liver non-parenchymal cells.
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PMID:[Study on LDL receptors of liver non-parenchymal cells in hypertriglyceridemic rats induced by high carbohydrate diet]. 858 86

Richardson ground squirrels are hibernators with seasonal changes in the thermogenic capacity of brown adipose tissue (BAT). The objective of this work was to evaluate whether norepinephrine (NE) acts both as a thermogenic and a growth factor in BAT. Brown adipocytes were isolated by collagenase digestion of axillary BAT and kept in a tissue culture incubator in methionine-free Dulbecco's modified Eagle's medium supplemented with albumin, antibiotics, and calf serum with or without NE for up to 24 h. For short-term incubations (<6 h), calf serum was omitted. Freshly isolated brown adipocytes responded to NE with 10- to 20-fold increases in rates of oxygen uptake. This ability to respond calorigenically to NE was maintained over a 24-h period. However, no significant increase in [35S]methionine incorporation into cellular proteins was observed when brown adipocytes were incubated for 1-6 or 24 h with NE. When labeled cell proteins were separated by SDS-PAGE and visualized by autoradiography, no selective change in protein labeling, particularly in the uncoupling protein (32 kDa) region was observed. Likewise, [35S]methionine incorporation into immunoprecipitable uncoupling protein was not affected by the presence of NE. These results suggest a dissociation between the thermogenic and growth effects of NE in BAT of Richardson ground squirrels.
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PMID:Dissociation of thermogenic and trophic actions of norepinephrine in brown adipocytes of Richardson ground squirrels. 874 38

Using Brown Norway (BN) rats, we isolated and characterized the tubular basement membrane (TBM) antigens that are immunologically common to humans. The renal basement membrane (RBM) of BN rat, as an antigen source, was solubilized with 8 M urea instead of collagenase followed by extraction with 0.5 M NaCl. On frozen section-immunohistochemistry, the autoantibody obtained from BN rats, which had been immunized with human RBM and showed tubulointerstitial nephritis, bound to the TBM, the basement membrane of the Bowman's capsule, and the brush border of the proximal tubules, but not to the GBM of the normal BN rat kidney. Nephritogenic antigens were isolated by immunoaffinity chromatography using Sepharose-bound purified autoantibody. By Western blot analysis of the eluate, bands with molecular weight of 200 kDa and 180 kDa were positively reacted to anti-FX1A (brush border antigen) antibody and were apparently different from the major bands with molecular weight of 145 kDa and 130 kDa. The bands with molecular weight of 145 and 130 kDa showed major cross reactivity with antibodies to fibronectin and laminin. In contrast with these high molecular weight (HMW) bands, the major 60 kDa band with three minor bands showed no reactivity with any type of antibody tested. These results indicated that the non-enzymatic solubilization of RBM is one of the possible procedures for isolating the HMW form of antigens. These antigens may be epitopically modified pre-existing constitutions of the basement membrane and may play a role in the induction of tubulointerstitial nephritis.
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PMID:Isolation and characterization of tubular basement membrane antigen common to humans and rats. 985 23

Short-term exposure of rats to ozone results in lung inflammation characterized by increased permeability damage and the infiltration of neutrophils into the airways. The present study compared these ozone-induced inflammatory responses in different strains of male rat, Brown Norway rats from Charles River Laboratories, Inc. (BN-CRL), and Harlan Sprague Dawley, Inc. (BN-HSD), and Fischer 344 (F344), Sprague-Dawley (SPD), and Wistar (WSTR) male rats from Hilltop Lab Animals, Inc. Ozone-induced permeability damage was indicated by recoveries of bronchoalveolar lavage fluid (BALF) albumin 20 h following single exposures of 6 h to either air or 1 ppm or 2 ppm O3. Although BALF albumin recoveries from air-exposed rats were not significantly different between strains, ozone exposures resulted in a range of enhancements of BALF albumin of 2-, 9-, 17-, 7-, and 20-fold following exposures of BN-CRL, BN-HSD, F344, SPD, and WSTR rats to 2 ppm ozone, respectively. Concomitant strain differences in the number of ozone-induced BAL-recoverable neutrophils were not observed, except for BN-CRL rats, which demonstrated significantly lower numbers. However, the degree of ozone-induced permeability damage did directly correspond to differences observed in the numbers of neutrophils and eosinophils in the peripheral blood and collagenase tissue digest of lavaged and perfused lungs prior to ozone exposure. Ozone-resistant BN-CRL rats exhibited the highest numbers of blood and lung tissue neutrophils and eosinophils when compared with ozone-susceptible WSTR rats exhibiting the lowest number of these granulocytes. These data suggested that the presence of high numbers of blood and tissue granulocytes at the onset of short-term ozone exposures might provide a certain degree of protection against subsequent pathological events.
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PMID:Lung tissue neutrophil content as a determinant of ozone-induced injury. 1098 20


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