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

Lewis (LEW) rats immunized with Brown Norway (BN) rat renal basement membrane (RBM) and adjuvants produce high titer circulating anti-BN tubular basement membrane (TBM) antibodies, in addition to developing an autoimmune cell-mediated form of nodular tubulointerstitial nephritis (TIN). This immune LEW serum, which reacted with BN TBM but not LEW TBM by immunofluorescence, was capable of passively transferring TIN as early as 24 hr after administration of volumes as low as 3 ml i.v. to normal BN recipients, producing focal lesions histologically and immunopathologically similar but less extensive than those studied previously in this strain after active immunization with heterologous RBM. In contrast, a total of 45 ml of serum (in multiple doses) from BN rats immunized with bovine RBM and adjuvants produced only one small lesion of TIN in a recipient BN rat. This difference in serum transferability of anti-TBM-associated TIN appears to relate to quantitative differences in anti-particulate and soluble (collagenase-extracted) BN RBM antigen reactivity measured by radioimmunoassay. Paired-label quantitative studies of passively transferred LEW anti-BN RBM IgG demonstrated a slow accumulation of renal-bound antibody over 6 days, and corresponded with kidney elution and immunofluorescence studies after transfer of immune LEW sera to normal BN rats. Approximately 167 micrograms of kidney-fixing antibody per gram of kidney were calculated to be required for the development of the earliest cellular infiltration. C3 depletion with cobra venom factor greatly diminished the development of destructive TIN lesions associated with multinucleate giant cells after passive transfer of LEW anti-BN RBM antibody to BN rats. This study, using immune LEW sera containing high levels of anti-BN RBM antibody, has defined and quantitated a role for anti-TBM antibody and complement in the initiation of TIN in BN rats.
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PMID:Transfer of tubulointerstitial nephritis in the Brown Norway rat with anti-tubular basement membrane antibody: quantitation and kinetics of binding and effect of decomplementation. 387 59

Brown adipose tissue (BAT), obtained from the axillary and perirenal regions of newborns 24-48 h after death, was digested with collagenase and the free cells were cultured. Only the cultures of cells from tissue obtained later than 24 h post mortem were successful. These cells grew slowly to reach confluence. Their typical mitochondria gradually disappeared, being replaced by untypical mitochondria. After confluence, the cells accumulated large amounts of lipid in non-coalescent multivacuolar depots. This model can be useful for the study of the metabolic and morphological features of human brown fat cells.
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PMID:Human brown adipose cells in culture. 402 66

Suspensions of freshly isolated hepatocytes were prepared by collagenase perfusion of livers of adult Fischer 344 female rats. The cells were injected into the dorsal fascia of 2/3 partially hepatectomized syngeneic hosts (10(6) cells per injection site) and were monitored from 3 days to 3 months after injection. Brown nodules developed at the transplantation site. Histologic examination of the nodules revealed that the hepatocytes were arranged in cords and clusters surrounded by fibrovascular connective tissue. Bile ductules were also seen. Hepatocytes were positive for glucose-6-phosphatase. Staining for gamma-glutamyltranspeptidase showed that the parenchymal hepatocytes were mostly (approximately 95%) negative, whereas bile ductules were positive. These histochemical findings were seen in hepatocytes up to 3 months after transplantation and did not vary with the age of the transplants. Electron-microscopic examination of the transplanted nodules demonstrated that the cells maintained the characteristics of hepatocellular cytoplasmic structure. The relationship between the bile canaliculi and the stromal vessels was found to be similar to the bile canaliculi and hepatic sinusoid polarity seen in the normal liver. Autoradiographic analysis showed that a fraction of the transplanted cells was active in DNA synthesis. This system may become a tool in the study of survival and neoplastic transformation of hepatocytes as a result of exposure to X-irradiation and chemical carcinogens.
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PMID:Morphologic and histochemical analysis of hepatocytes transplanted into syngeneic hosts. 610 19

Brown adipocytes can be readily isolated by collagenase digestion of perirenal adipose tissue from fetal lambs. In isolated cells the addition of phenylephrine in the presence of alprenolol (to specifically stimulate alpha adrenoceptors) resulted in an increase in de novo synthesis of phosphatidylinositol and phosphatidic acid. The stimulatory effects were preferentially inhibited by prazosin while yohimbine had little effect, indicating that the adrenoceptors were alpha 1 in character. Isoproterenol stimulated cyclic adenosine monophosphate (AMP) accumulation and lipolysis as well as respiration. Forskolin also mimicked the effects of beta adrenergic stimulation. Clonidine, a specific alpha 2 adrenergic agonist, inhibited lipolysis and cyclic AMP accumulation. Insulin inhibited cyclic AMP accumulation and stimulated glucose metabolism in the adipocytes. The present studies indicate that beta, alpha 1, and alpha 2 adrenergic as well as insulin responses can be detected in ovine perirenal adipocytes.
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PMID:Metabolic effects of beta, alpha 1, and alpha 2 adrenoceptor activation on brown adipocytes isolated from the perirenal adipose tissue of fetal lambs. 614 21

Autoimmune tubulointerstitial nephritis was induced in Brown-Norway (BN) rats by immunization with bovine (Bov) tubular basement membrane (TBM) in complete Freund's adjuvant. Serum antibodies thus produced reacted to a greater extent with Bov than BN TBM antigens by indirect immunofluorescence and by radioimmunoassay with particulate (P) and collagenase-solubilized (CS) TBM. The quantities of antibodies reactive with CS TBM correlated with the intensity of tubulointerstitial pathologic changes. Antibodies eluted from kidneys reactive with BN TBM by indirect immunofluorescence were 508 times more concentrated in the kidney than in the serum, compared with 15 times for Bov TBM-reactive antibodies. The reactivity of eluted antibodies to P BN TBM was inhibited by 70% after absorption with BN CS TBM. A major CS TBM antigen of 42,000 m.w. was identified by polyacrylamide gel electrophoresis. This antigen was present in both Bov and BN TBM, and may be important in triggering autoantibody formation in this model. Lewis rats immunized under the same conditions produced antibodies reactive with BN TBM by immunofluorescence but failed to develop immune deposits in TBM of their own kidneys. Analysis of serum anti-TBM antibodies in Lewis rats revealed a selective lack of reactivity with either homologous or autologous CS TBM. These results suggest that the ability to make an immune response to one or more elements of CS TBM plays a major role in the development of autoimmune tubulointerstitial nephritis in rats.
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PMID:Characterization of anti-tubular basement membrane antibodies in rats. 630 Feb 40

We have studied the compartmentation of cyclic AMP action in purified ventricular cardiomyocytes prepared by collagenase perfusion of adult rabbit hearts. Incubation of purified adult myocytes with 1 microM isoproterenol causes rapid accumulation of intracellular cyclic AMP in both soluble (2.3 leads to 7.7 pmol/ mg of protein) and particulate (3.0 leads to 9.2) fractions of cell homogenates (3000 X g for 5 min), increases in the total activity and activity ratio of soluble cyclic AMP-dependent protein kinase (0.21 leads to 0.66), a decrease in protein kinase activity remaining in the particulate fraction (47 leads to 30%), and an increase in the activity ratio of glycogen phosphorylase (0.15 leads to 0.47). Incubation of myocytes with 10 microM prostaglandin E1 (PGE1) leads to a comparable increase in soluble cyclic AMP (2.3 leads to 5.8 pmol/mg of protein) and activation of soluble cyclic AMP-dependent protein kinase (0.21 leads to 0.39) but does not result in any change in cAMP or protein kinase in the particulate fraction and fails to cause an activation of glycogen phosphorylase. PGE1 does not inhibit the effects of isoproterenol; when myocytes are incubated with both isoproterenol and PGE1, the accumulation of cyclic AMP, activation of cAMP-dependent protein kinase and phosphorylase b leads to a conversion are equal to that achieved with isoproterenol alone. Perturbation of cellular calcium using the ionophore A23187, verapamil, or high or low extracellular calcium did not alter the ability of isoproterenol to cause activation of particulate cAMP-dependent protein kinase or influence the inability of PGE1 to do so. Activation of adenylate cyclase by forskolin (30 microM) caused immediate activation of both soluble and particulate cAMP-dependent protein kinase leading to rapid activation of phosphorylase. We conclude that the hormonally specific compartmentation of cyclic AMP and cAMP-dependent protein kinase that occurs in intact heart (Hayes, J. S., Brunton, L. L., Brown, J. H., Reese, J. B., and Mayer, S. E. (1979) Proc. Natl. Acad. Sci. U.S.A. 76, 1570-1574) is not explained on the basis of cellular heterogeneity but has a subcellular basis within the cardiomyocyte.
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PMID:Compartments of cyclic AMP and protein kinase in mammalian cardiomyocytes. 630 96

A solid-phase radioimmunoassay (RIA) is described for the detection of IgG autoantibodies to glomerular basement membrane (GBM) induced in the Brown Norway rat by mercuric chloride. The assay involves the adsorption of a collagenase digest of GBM to plastic microtitre plates and detection of bound antibody with affinity purified radiolabelled rabbit anti-rat IgG. Comparison with existing immunofluorescence methods for detection of anti-GBM antibody showed that the solid-phase RIA is highly sensitive, allowing detection of antibody in solutions with as low as 0.5 ng protein/ml. The assay is suitable for detection of anti-GBM antibody both in serum and in eluates from nephritic kidneys. The assay proved to be specific in competitive studies of inhibition brought by GBM, keyhole limpet antigen and ovalbumin. This solid-phase RIA is reproducible, robust and easy to perform.
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PMID:Anti-glomerular basement membrane autoantibodies in the Brown Norway rat: detection by a solid-phase radioimmunoassay. 634 63

Rabbit antibodies specific for the idiotype (Id) of autoantibodies to tubular basement membrane (TBM) eluted from kidneys of Brown Norway rats with tubulointerstitial nephritis (TIN) were used to analyze the immune response to TBM antigens at the humoral and cellular levels. These antibodies appeared to recognize Id determinants associated with the antigen combining site on the anti-TBM Id as well as on splenic lymphocytes. However, efforts to detect Id-positive cells in the interstitial infiltrates of kidneys with TIN failed. In contrast, in vivo injection of anti-Id serum before immunization with TBM resulted in a) significant selective suppression of antibodies to the autologous collagenase-solubilized TBM moiety but not to antigenic determinants of the intact TBM nor to those of heterologous TBM, and b) a corresponding decrease of TIN. These results suggest that anti-Id antibodies of this type can be useful as a probe for further dissecting the pathogenetic mechanisms underlying these complex autoimmune responses.
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PMID:Anti-idiotype as a probe in the analysis of autoimmune tubulointerstitial nephritis in the Brown Norway rat. 635 Apr 53

Monoclonal anti-glomerular basement membrane (GBM) antibodies were obtained by fusing spleen cells from Brown-Norway (BN) rats injected with mercuric chloride with IR 983 F, a nonsecreting rat myeloma cell line. These antibodies showed the same pattern of fixation on renal basement membranes by indirect immunofluorescence. One of them was developed. It reacted both in vivo and in vitro with GBM but failed to react with collagenase-digested GBM, laminin, and collagen IV. This monoclonal antibody which resembles the kidney acid eluate obtained from BN rats injected with mercuric chloride induced a weak and transient proteinuria when intravenously injected into normal BN rats.
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PMID:Production of monoclonal anti-glomerular basement membrane antibodies during autoimmune glomerulonephritis. 638 29

The immunogenicity of allogeneic cardiac valves (ACV) has not been previously demonstrated in vitro, though valve failure due to tissue degeneration has been attributed to adverse immunological reactions. A novel in vitro assay has been developed in a Brown Norway (BN; RT1n)-Lewis (RT1; donor-recipient) rat model system that demonstrates the immunogenicity of ACVs. A single cell suspension of viable cardiac valve conduit (CVC) cells was obtained by collagenase treatment of BN rat aortic valve conduits. Brown Norway rat CVC cells (5 x 10(4)) and Lewis responder lymphocytes (10(5)) were co-cultured in 96 well plates in RPMI 1640 plus 2.5% (v/v) non heat-inactivated Lewis rat serum and supplements with appropriate controls. Stimulation of responder lymphocytes by CVC cells was measured by 3H-thymidine incorporation into DNA. The counts obtained between 96-192 h of co-culture in the CVC cell/responder lymphocyte reaction were significantly higher (P < 0.05) than those of responder cell controls as assessed by analysis of variance. These results indicate the presence of potent immunostimulatory cells in viable ACVs and the possibility of using a sensitive and reproducible in vitro assay to evaluate ACV immunogenicity.
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PMID:In vitro immunogenicity of allogeneic cardiac valves. 782 53


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