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PubMedDate not supplied

Physiological effect of the alterations of plasmids derived from Neisseria gonorrhoeae.

Transfer of plasmid DNA from penicillinase-producing Neisseria gonorrhoeae to Escherichia coli produced relatively small colonies that became pigmented in the presence of the dye, congo red. Mutations to large, non-pigmented colonies were frequent, and were the result of a variety of alterations in these plasmids. Miniplasmid formation was the major alteration that led to non-pigmented colonies. However, deletions in any of three putative replication regions resulted in non-pigmented colonies. These altered plasmids mediated significantly less beta-lactamase production than that of the parent plasmid. A new origin of replication was discovered and mapped within the miniplasmid. This origin was responsible for: 1) high plasmid copy number, 2) stability of inheritance, and 3) the majority of beta-lactamase produced in culture. The evolution of gonococcal plasmids may be followed in E. coli, since less defective plasmids produce nonpigmented colonies on congo red agar medium.

Congo Red↗

PubMed1981

Polyps in the acid-secreting area of the stomach.

The relation of gastric polyps to acid-secreting mucosa was examined in 120 patients with gastric polyps. Studies were made by the endoscopic Congo red test developed in this clinic. In 23 patients (19.1%) gastric polyps were located in acid-secreting mucosa and may have arisen from normal oxyntic mucosa. These polyps were of two histological types: oxyntic gland polyps containing many parietal cells, and nonoxyntic gland polyps without parietal cells. Only the former type appeared to secrete acid, judging endoscopically from the change of Congo red from red to blue-black on the surface of the polyps after administration of gastrin.

Adult↗

PubMed2003

Temperature-dependent, irreversible formation of amyloid fibrils by a soluble human ataxin-3 carrying a moderately expanded polyglutamine stretch (Q36).

The protein ataxin-3 is responsible for Machado-Joseph disease/spinocerebellar ataxia type 3, a neurodegenerative disorder caused by the presence of an expanded polyglutamine tract. A previous investigation [Bevivino, A. E., and Loll, P. J. (2001) Proc. Natl. Acad. Sci. U.S.A. 98, 11955-11960] showed that a nonexpanded ataxin-3 (Q27) was fully soluble, whereas an expanded form (Q78) gave rise to amyloid fibrils. Here, we report investigations on three forms of ataxin-3 (i.e., human nonexpanded (Q26), moderately expanded (Q36) ataxins-3, and the murine protein (Q6)). Far-UV circular dichroism spectra at room temperature were substantially similar, with a relatively high helical content. On heating to 96 degrees C, human Q26 and murine proteins did not display large structural changes, nor did they undergo any precipitation, which highlights their amazing heat-resistance. In contrast, human Q36 ataxin-3 underwent a progressive increase in the beta-sheet and a concomitant decrease in helical content when the temperature was shifted from 37 to 80 degrees C, followed by the irreversible formation of aggregates above 80 degrees C. They were shown to consist of amyloid fibrils, as supported by both electron microscopy images and the typical spectral shift displayed by Congo red when it was added to the protein at growing temperatures. We also found that protein precipitation could be prevented by mixing the dye with Q36 ataxin-3 prior to heating, which also confirms that the precipitates do represent authentic amyloid fibrils. In contrast, other compounds structurally related to Congo red did not exert significant effects. Our observations suggest that the temperature of the observed transition is inversely related to the length of the expansion. Finally, we suggest that antiamyloidogenic compounds might be selected on the basis of their ability to block or retard human Q36 ataxin-3 precipitation on heat-treatment.

Amyloid↗

PubMed1997

SEF17 fimbriae are essential for the convoluted colonial morphology of Salmonella enteritidis.

Salmonella enteritidis isolated from poultry infections generated a convoluted colonial morphology after 48 h growth on colonisation factor antigen (CFA) agar at 25 degrees C. A mutant S. enteritidis defective for the elaboration of the SEF17 fimbrial antigen, in which the agf gene cluster was inactivated by insertion of an ampicillin resistance gene cassette, and other wild-type S. enteritidis transduced to this genotype failed to produce convoluted colonies. However, growth of SEF17- mutants at 25 degrees C on CFA agar supplemented with 0.001% Congo red resulted in partial recovery of the phenotype. Immunoelectron microscopy demonstrated that copious amounts of the SEF17 fimbrial antigen were present in the extracellular matrix of convoluted colonies of wild-type virulent S. enteritidis isolates. Bacteria were often hyperflagellated also. Immunoelectron microscopy of SEF17- mutants grown on CFA agar+0.001% Congo red demonstrated the elaboration of an as yet undefined fimbrial structure. Isolates of S. enteritidis which were described previously as avirulent and sensitive to environmental stress failed to express SEF17 or produce convoluted colonies. These data indicate an essential role for SEF17, and possibly for another fimbria and flagella, in the generation of the convoluted colonial phenotype. The relationship between virulence and colonial phenotype is discussed.

Animals↗

PubMed1987

Variations on the standard protocol design of the hepatocyte DNA repair assay.

Several variations on the standard primary rat hepatocyte DNA/repair assay were evaluated for their ability to enhance the sensitivity of this genotoxicity test system. The use of hamster hepatocytes proved to be a much more sensitive system than rat hepatocytes for detecting the DNA repair inducing ability of the nitrosamines, dimethylnitrosamine and diethylnitrosamine, and the aromatic amines, 2-acetylaminofluorene, 9-aminoacridine, 1-naphthylamine and benzidine. In addition, hamster hepatocytes were a more sensitive indicator of the genotoxicity of the azo dyes, o-aminoazotoluene, Congo Red and Evans Blue. However, the azo reduction product of the azo dyes Congo Red, Trypan Blue and Evans Blue, benzidine and o-tolidine, respectively, were active in both rat and hamster hepatocytes at concentrations that were 10-100 fold lower than the parent dyes. This suggests that little or no azo reduction of the dyes occurred in the in vitro assay systems. The in vivo-in vitro variation of the rat hepatocytes DNA/repair assay exhibited a positive DNA repair response with the azo dye solvent Yellow 5, which was negative in the standard in vitro assay. The in vivo-in vitro hepatocyte DNA repair assay was also more sensitive for detecting the genotoxic activity of Evans Blue, which was positive in the in vivo-in vitro assay and equivocal in the standard in vitro assay. Also, Solvent Yellow 14 was negative in the in vitro assay, but induced an equivocal DNA repair response in the in vivo-in vitro assay system. A treatment/3H-thymidine labeling period of approximately 18 hours, compared to 4 hours, was demonstrated to be superior for detecting the DNA repair elicited by the mutagens 4-nitroquinoline-1-oxide, mitomycin C, dimethylnitrosamine and methyl methanesulfonate in the in vitro rat hepatocyte assay. There was little or no difference observed between the 4 hour and 18 hour treatment/labeling incubation periods for the detection of DNA repair induced by 2-acetylaminofluorene, aflatoxin B1, and benzidine. The data suggest that these several variations on the standard rat hepatocyte DNA/repair assay should be considered when evaluating the genotoxicity of chemicals for safety purposes.

Animals↗

PubMed1994

Fibril formation from recombinant human serum amyloid A.

Three isotypes of human serum amyloid A (SAA), SAA1, SAA2 beta, and SAA4 were expressed at high levels in Escherichia coli (E. coli) using a pET vector expression system. Each SAA cDNA was ligated to the vector pET-21a(+) and transformed into E. coli, strain BL21(DE3)pLysS. Expression conditions required high concentrations of antibiotics in order to obtain a high ratio of synthesized SAA to total E. coli proteins. Each recombinant SAA (rSAA) was purified by molecular sieve chromatography followed by chromatofocusing or hydrophobic interaction chromatography. The yield of purified protein was 5-10 mg per 11 of culture. When subjected to in vitro fibril forming conditions, rSAA1 formed amyloid-like fibrils confirmed by Congo red staining and electron microscopy. In contrast, rSAA2 beta and rSAA4 showed negative Congo red staining and curvilinear or flattened fibrillar structures on electron microscopy. This suggests that SAA1 has greater potential for forming amyloid fibrils than either SAA2 beta or SAA4.

Amino Acid Sequence↗

PubMed2003

Longterm complete remission of AL-amyloid-related nephrotic syndrome.

We describe a 59-year-old man with nephrotic syndrome that was diagnosed as suspected minimal change nephrotic syndrome by the routine examination of renal tissues at first biopsy, because renal histology showed segmental mild mesangial expansion with argyrophilic staining and partial foot process fusion without any deposition. Prednisolone therapy induced complete remission of nephrotic syndrome. Relapse occurred after 4 years of complete remission, and the second renal biopsy revealed amyloid light-chain (AL)-amyloidosis. Re-examination of the first biopsy tissues by Congo red staining confirmed a small amount of amyloid deposition in the mesangial areas although the mesangial areas showed argyrophilic staining, which is atypical for amyloid deposition. This case raises a caution that even when renal histology is not suggestive of amyloidosis and prednisolone therapy is very effective, when a renal histology diagnosis is not confirmed, the clinician should suspect amyloidosis and should, at least, undertake Congo red staining to definitively rule out amyloidosis.

Amyloidosis↗

PubMed1988

Aging and cerebral amyloid: early detection of amyloid in the human brain using biochemical extraction and immunostain.

To search for relationships between aging and cerebral amyloid, the brains of 66 clinically nondemented individuals were investigated, using the following three approaches for verification of the amyloid: Congo red staining as a histochemical method; immunostaining using anti-beta protein antiserum as an immunohistochemical identification; and biochemical extraction of amyloid from nonfixed brain tissues. That the incidence of cerebral amyloid increased with aging was determined using all three approaches. Immunostaining using anti-beta protein antiserum was more sensitive than Congo red staining. The biochemical extraction was most sensitive for detection of amyloid, and revealed that amyloid was extracted initially from more than half (67%) of the brains of 9 persons in their 50s and from almost all (97%) brains of 35 persons over 60 years of age. Amyloid was extracted even from brains in which amyloid deposits were not detected by histochemical or immunohistochemical methods. This result shows early appearance of the age-related cerebral amyloid.

Aging↗

PubMed1995

A simple and rapid semiquantitative method for measuring cellulase activity in agar media.

A simple and rapid semiquantitative technique for the determination of fungal cellulytic activities in solid (agar slant) media has been developed. This method is a combination of Congo-red staining widely used for qualitative cellulase detection and common cellulase activity tests. Previous investigation on the adsorptive effect of cellulose content of media showed that the real enzyme activity values can be measured with minimum loss by means of agar discs cut from the most active zones of slants visualized by Congo-red staining. Different cellulase activity tests (FPase, CMCase and beta-glucosidase by PNPG-method) of seven cellulolytic fungal strains were investigated by this technique. Data give information on the different enzyme profiles of the species. The method can be regarded as very simple and suitable for simultaneous rapid comparison of cellulase components of greater series of fungal strains from agar slant cultures. It can also be used in the case of fungi unable to grow in liquid cultures.

Agar↗

PubMed1994

Estimates of antagonist affinities at P2X purinoceptors in rat vas deferens.

In functional studies pyridoxalphosphate-6-azophenyl-2',5'-disulphonic acid (iso-PPADS), suramin, GR200282 (4,4'-[carbonyl-bis(imino-3- benzoylimino)]-bis[5-hydroxy-naphthalene-2,7-disulfonic acid] tetrapotassium salt), cibacron blue, trypan blue and congo red, each produced specific antagonism of the contractile responses of isolated rat vas deferens, induced by alpha,beta-methylene ATP (alpha,beta-meATP), with antagonist pKB estimates of 6.6 +/- 0.3, 5.5 +/- 0.2, 5.1 +/- 0.3, 5.8 +/- 0.2, 4.7 +/- 0.2 and 4.6 +/- 0.2, respectively. In radioligand binding studies, iso-PPADS, suramin, cibacron blue, GR200282, trypan blue and congo red competed for the high affinity [3H]alpha,beta-meATP binding sites in rat vas deferens membranes with pKi estimates of 5.6 +/- 0.04, 5.5 +/- 0.08, 5.6 +/- 0.15, 5.6 +/- 0.04, 4.3 +/- 0.06 and 4.9 +/- 0.10, respectively. Comparison of pKB and pKi estimates revealed a good agreement between the two approaches for estimating measures of affinity for the putative antagonists, except in the case of iso-PPADS. However, we found that two populations of [3H]alpha,beta-meATP binding sites can be identified by iso-PPADS, 26.4% of these having low affinity (pKi of 4.4 +/- 0.2), and 73.6% having high affinity (pKi of 6.5 +/- 0.02) for iso-PPADS. The pKi of 6.5 obtained at the high affinity sites identified by iso-PPADS was close to the equivalent pKB value of 6.6 from functional studies. These studies therefore show a good agreement between pKB and pKi estimates for several antagonists, and suggest that the high affinity binding sites labelled with [3H]alpha,beta-meATP in rat vas deferens represents binding to functional P2X purinoceptors.

Adenosine Triphosphate↗

PubMed1998

Rimmed vacuoles with beta-amyloid and ubiquitinated filamentous deposits in the muscles of patients with long-standing denervation (postpoliomyelitis muscular atrophy): similarities with inclusion body myositis.

In the chronically denervated muscles of patients with prior paralytic poliomyelitis, there are secondary myopathic features, including endomysial inflammation and rare vacuolated fibers. To assess the frequency and characteristics of the vacuoles and their similarities with those seen in inclusion body myositis (IBM), we examined 58 muscle biopsy specimens from patients with prior paralytic poliomyelitis for (1) the presence of rimmed vacuoles; (2) acid-phosphatase reactivity; (3) Congo-red-positive amyloid deposits; (4) electron microscopy, searching for tubulofilaments; and (5) immunoelectron microscopy, using antibodies against beta-amyloid and ubiquitin. We found vacuolated muscle fibers in 18 of 58 (31%) biopsies, with a mean frequency of 2.06 +/- 0.42 fibers per specimen. The vacuoles contained acid phosphatase-positive material in 6 of the 18 (33.30%) specimens and stained positive for Congo red in five (27.80%). By immunoelectron microscopy, the vacuoles contained 5.17 +/- 0.13 nm fibrils and 14.9 +/- 0.31 nm filaments that immunoreacted with antibodies to beta-amyloid and ubiquitin in a pattern identical to the one seen in IBM. We conclude that vacuolated muscle fibers containing filamentous inclusions positive for amyloid and ubiquitin are not unique to IBM and the other vacuolar myopathies but can also occur in a chronic neurogenic condition, such as postpoliomyelitis. The chronicity of the underlying disease, rather than the cause, may lead to vacuolar formation, amyloid deposition, and accumulation of ubiquitinated filaments.

Amyloid beta-Peptides↗

PubMed2002

A pulse-chase study tracking the conversion of macrophage-endocytosed serum amyloid A into extracellular amyloid.

OBJECTIVE: To determine whether serum amyloid A (SAA) is internalized by and processed in macrophages en route to deposition as extracellular amyloid. METHODS: SAA was tracked in cultures of peritoneal macrophages, using a pulse-chase protocol. Macrophages were pulsed with either fluorescently (with Texas Red) tagged SAA (TxR-SAA) or iodinated SAA ((125)I-SAA). Cells were then rinsed and shifted to chase medium containing unlabeled SAA and amyloid-enhancing factor (AEF) to induce amyloid formation. At selected times, TxR-SAA in living cells was observed by confocal scanning microscopy. (125)I-SAA was visualized and quantified in cell lysates and medium by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and phosphorimaging. The presence of amyloid was confirmed by Congo red staining. RESULTS: Confocal microscopy immediately after the pulse revealed TxR-SAA in endosomal vesicles, with no extracellular or cell surface accumulation. After 24 hours and 72 hours of chase, virtually all TxR-SAA remained intracellular. By 10 days, extracellular fluorescence was very strong, indicating that SAA had moved out of cells. Congo red staining revealed amyloid colocalized with areas of extracellular fluorescence. Experiments using (125)I-SAA showed that while 90-95% of internalized (125)I-SAA was degraded within 24 hours, 5-10% persisted as intact SAA or SAA peptides. Immediately after the pulse, SAA was full-length, but within 24 hours, discrete (125)I-SAA peptides were seen. Each peptide had an intact SAA amino-terminus, as expected for AA protein. Amyloid was detected in cultures as early as 24 hours after initiation of treatment with SAA and AEF and appeared to be intracellular. CONCLUSION: The results of this study provide direct evidence that SAA internalized by and processed in macrophages forms extracellular amyloid. Based on the presence of (125)I-AA protein in macrophage lysates prior to the appearance of extracellular TxR-labeled amyloid, it was concluded that cleavage of SAA to AA occurs intracellularly.

Animals↗

PubMed1998

Characteristics of Yersinia pseudotuberculosis isolated from animals in Brazil.

Strains (105) of Yersinia pseudotuberculosis isolated in Brazil between 1982 and 1990 were bio-serotyped. They were also studied for plasmid profile, autoagglutination and calcium dependence at 37 degrees C, Congo red uptake, pyrazinamidase activity, esculin hydrolysis, salicin fermentation and drug sensitivity: 95.24% were biotype 2, serogroup O:3; 2.86% were biotype 1, serogroup O:1; and 1.90% were biotype 2, non-agglutinable. Plasmids were found in 77.14% of the strains (one in each strain). There was total correlation between the presence of the virulence plasmid and autoagglutination, calcium dependence at 37 degrees C and Congo red uptake. The esculin, salicin and pyrazinamidase tests were not efficient in differentiating pathogenic from non-pathogenic Y. pseudotuberculosis isolates. All strains were highly sensitive to the drugs used. These results indicate that Y. pseudotuberculosis is a potential pathogen for humans in Brazil, especially because the bio-serogroups detected among animals are those most frequently associated with human diseases.

Amidohydrolases↗

PubMed1986

Minimal renal amyloidosis with nephrotic syndrome.

Two patients older than age 50 years had minimal amyloidosis in association with the nephrotic syndrome. The amyloid deposits in each case were so inconspicuous as to have been initially overlooked, and both biopsy specimens were thought to show minimal glomerular changes. A few, widely scattered, silver-positive, epimembranous spicules were found on reexamination by light microscopy, and Congo red and thioflavin T stains and electron microscopy confirmed the presence of small glomerular amyloid deposits. Both patients have since died of renal failure. In our series of biopsy specimens, amyloidosis was found in 14.2% of patients older than age 50 years presenting with nephrotic syndrome or severe proteinuria, over 1 1/2 times the frequency of minimal-change nephrotic syndrome. We therefore urge careful examination for amyloid deposits of all kidney biopsy specimens with the appearance of minimal-change nephrotic syndrome in older patients. Fluorescence microscopy of Congo red- and thioflavin T-stained sections is very helpful in the detection of small deposits.

Amyloidosis↗

PubMed2003

The native-like conformation of Ure2p in fibrils assembled under physiologically relevant conditions switches to an amyloid-like conformation upon heat-treatment of the fibrils.

The [URE3] phenotype in the yeast Saccharomyces cerevisiae is inherited by a prion mechanism involving self-propagating Ure2p aggregates. It is believed that assembly of intact Ure2p into fibrillar polymers that bind Congo Red and show yellow-green birefringence upon staining and are resistant to proteolysis is the consequence of a major change in the conformation of the protein. We recently dissected the assembly process of Ure2p and showed the protein to retain its native alpha-helical structure upon assembly into protein fibrils that are similar to amyloids in that they are straight, bind Congo red and show green-yellow birefringence and have an increased resistance to proteolysis (). Here we further show using specific ligand binding, FTIR spectroscopy and X-ray fiber diffraction that Ure2p fibrils assembled under physiologically relevant conditions are devoid of a cross-beta core. The X-ray fiber diffraction pattern of these fibrils reveals their well-defined axial supramolecular order. By analyzing the effect of heat-treatment on Ure2p fibrils we bring evidences for a large conformational change that occurs within the fibrils with the loss of the ligand binding capacity, decrease of the alpha helicity, the formation of a cross-beta core and the disappearance of the axial supramolecular order. The extent of the conformational change suggests that it is not limited to the N-terminal part of Ure2p polypeptide chain. We show that the heat-treated fibrils that possess a cross-beta core are unable to propagate their structural characteristic while native-like fibrils are. Finally, the potential evolution of native-like fibrils into amyloid fibrils is discussed.

Amyloid↗

PubMed1998

Postantibiotic effects of norfloxacin and netilmicin and their influence on the biological properties of Salmonella strains.

The postantibiotic effect (PAE) and the postantibiotic sub-MIC effect (PA SME) of norfloxacin and netilmicin on two clinical strains--Salmonella typhimurium and Salmonella enteritidis was investigated. After both PAE and PA SME of antibiotics were studied, we determined their effect on the induction of a prophage in the lysogenic S. typhimurium and on Congo red binding by both serovars, as an indicator of invasive ability in vitro. The PAE was induced by 2.MIC and 4.MIC of norfloxacin and netilmicin for 0.5 h. Norfloxacin induced a longer lasting PAE on both Salmonella serovars as compared to netilmicin. Supra-subinhibitory concentrations (PA SMEs) delayed regrowth of tested strains. The PA SMEs of norfloxacin as well as of netilmicin (except 2.MIC + 0.1.MIC concentration) did not allow regrowth of S. enteritidis. The prophage-inductive ability of norfloxacin was more expressive after PA SMEs than PAE. The PA SMEs of netilmicin caused loss of Congo red binding by S. typhimurium cells and decreased this binding by S. enteritidis cells.

Anti-Bacterial Agents↗

PubMed2002

Evaluation of different detection methods of biofilm formation in Staphylococcus aureus.

The icaADBC gene locus of Staphylococcus aureus and its polysaccharide intercellular adhesin (PIA/PNSG) were recently identified, but biofilm formation has rarely been detected in vitro. In this study we evaluated a tissue culture plate (TCP) assay and a tube test, as well as Congo red agar, using the two basic media trypticase soy broth (TSB) and brain heart infusion (BHI) broth with different sugar supplements for detection of biofilm formation in 128 ica-positive S. aureus isolates. Of the S. aureus strains, 57.1% displayed a biofilm-positive phenotype under optimized conditions in the TCP test. The tube test correlated well with the TCP test for strongly biofilm-producing strains, whereas weak producers were not safely discriminated from biofilm-negative strains. Screening on Congo red agar displayed a strong correlation with the TCP and the tube test for only 3.8%, and is therefore not recommended for investigation of biofilm formation in S. aureus.

Agar↗

PubMed2000

Inhibition of huntingtin fibrillogenesis by specific antibodies and small molecules: implications for Huntington's disease therapy.

The accumulation of insoluble protein aggregates in intra and perinuclear inclusions is a hallmark of Huntington's disease (HD) and related glutamine-repeat disorders. A central question is whether protein aggregation plays a direct role in the pathogenesis of these neurodegenerative diseases. Here we show by using a filter retardation assay that the mAb 1C2, which specifically recognizes the elongated polyglutamine (polyQ) stretch in huntingtin, and the chemical compounds Congo red, thioflavine S, chrysamine G, and Direct fast yellow inhibit HD exon 1 protein aggregation in a dose-dependent manner. On the other hand, potential inhibitors of amyloid-beta formation such as thioflavine T, gossypol, melatonin, and rifampicin had little or no inhibitory effect on huntingtin aggregation in vitro. The results obtained by the filtration assay were confirmed by electron microscopy, SDS/PAGE, and MS. Furthermore, cell culture studies revealed that the Congo red dye at micromolar concentrations reduced the extent of HD exon 1 aggregation in transiently transfected COS cells. Together, these findings contribute to a better understanding of the mechanism of huntingtin fibrillogenesis in vitro and provide the basis for the development of new huntingtin aggregation inhibitors that may be effective in treating HD.

Animals↗