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At least 1,243 records · Page 69Linked to original sources
PubMed1984

Comparison of 7 azo dyes and their azo reduction products in the rat and hamster hepatocyte primary culture/DNA-repair assays.

Pursuant to the characterization of species differences in the effects of chemical carcinogens, several studies have demonstrated that hamster hepatocytes are more effective than rat hepatocytes in mediating the metabolic activation of certain chemicals to their genotoxic (i.e., mutagenic) derivatives. In the present investigation, a comparison of the amount of DNA repair induced in rat and hamster hepatocytes by 7 azo dyes and 7 aromatic amine azo reduction products of the dyes was performed using the primary hepatocyte culture/DNA repair (HPC/DR) assay. Congo Red and its azo reduction product, benzidine, were more potent inducers of DNA repair in hamster than in rat hepatocytes, whereas Trypan Blue and its reduction product, o-tolidine, were equipotent in the 2 hepatocyte systems. Evans Blue, another o-tolidine-based dye, elicited a greater DNA-repair response in hamster hepatocytes. The absolute potency of these dyes, however, was much less than their reduction products. o-Aminoazotoluene was the most potent of the dyes tested, and its DNA repair-inducing activity was much greater than that of its azo reduction products, o-toluidine and 2,5-diaminotoluene. Ponceau SX, which is carcinogenic in hamsters, but not in rats, was inactive in both hepatocyte systems. Dimethylaminobenzeneazo-1-naphthalene and its 2-naphthalene congener, as well as the 1- and 2-naphthylamine azo reduction products of these dyes, were more potent in hamster than in rat hepatocytes. However, the DNA repair-inducing activities of the parent dyes could not be entirely accounted for by the potencies of their respective naphthylamine derivatives. Taken together, these findings extend previous observations of the superior metabolic activation capabilities of hamster, relative to rat hepatocytes, and further demonstrate the utility of testing chemicals in both the hamster and rat HPC/DR assays.

Animals↗
PubMed1995

beta-Amyloid 25-35 and/or quinolinic acid injections into the basal forebrain of young male Fischer-344 rats: behavioral, neurochemical and histological effects.

beta-Amyloid peptides have been shown to potentiate the neurotoxic effect of excitatory amino acids in vitro. In order to determine if this occurs in vivo, four experiments were performed. We injected beta-amyloid 25-35 (beta A 25-35) and/or quinolinic acid (QA) bilaterally into the ventral pallidum/substantia innominata (VP/SI) of rats. Control rats received vehicle infusions. A high dose of QA (75.0 nmol/3 microliters) increased open field activity and impaired spatial learning in the Morris water maze, but did not affect the acquisition of a one-way conditioned avoidance response. These changes were associated with histological evidence of neurotoxicity and a reduction in amygdaloid but not frontal cortical or hippocampal choline acetyltransferase (ChAT) activity. A lower dose of QA (37.5 nmol/3 microliters) produced no behavioral effects. It reduced amygdaloid ChAT activity to a lesser extent than the higher dose (15% vs. 29-37%), and caused less histological damage. beta A 25-35 (1.0 or 8.0 nmol/3 microliters) failed to produce behavioral, histological or neurochemical signs of toxicity. Neither dose of beta A 25-35 potentiated the effects of QA (37.5 nmol) on behavior or amygdaloid ChAT activity, and did not appear to increase the histological damage caused by QA. These results suggest that in vivo beta A 25-35 is not neurotoxic and does not potentiate the neurotoxicity of QA in the VP/SI. Further, the histological effects of a high dose of beta A 25-35 (8.0 nmol/3 microliters; a cavitation containing a Congo red positive proteinaceous material) are quite distinct from those produced by a high dose of QA (75.0 nmol/3 microliters; widespread neuronal loss and gliosis).

Amyloid beta-Peptides↗
PubMed1995

Characterization of Yersinia enterocolitica isolated from the oral cavity of swine in Slovakia.

Yersinia enterocolitica was detected in 160 of 2760 examined samples that were prepared from dental cavity of 920 pigs. From the isolates 49 strains were characterized with respect to their genetic and phenotypic markers of virulence. All strains were belonging to serogroup 0:3, biovar 4. Forty-one isolates (84%) harboured the virulence plasmid detected by DNA colony hybridization. Of the other assays of virulence--autoagglutination, binding of crystal violet, pyrazinamidase activity, calcium dependence and Congo red binding--the latter two exhibited the best correlation with the detected presence of plasmid DNA.

Animals↗
PubMed1995

Kinetics of interactions of lactic acid, pH and atmosphere on the growth and survival of Yersinia enterocolitica IP 383 O:9 at 4 degrees C.

The influence of different lactic acid concentrations (0.1, 0.3, 0.5, 0.7, 0.9, 1.1% v/v), within pH range of 3.9 to 5.8 on the aerobic and anaerobic growth and survival kinetics of the virulent strain of Y. enterocolitica IP 383 O:9, was determined in Tryptone Soy Broth at 4 degrees C. Growth and survival data were analyzed and fitted by a modification of the Whiting and Cygnarowicz-Provost model, using the Minpack software library. Initial generation times, initial specific growth rates, lag times and death rates were subsequently calculated from the model parameters. The stability of the virulence plasmid in growing and surviving cells was examined using crystal violet binding, low-calcium response and congo red uptake. The results demonstrate the dependancy of the growth and survival kinetics on the interaction between the three variables. The effect of lactic acid on Y. enterocolitica is greater under anaerobic than aerobic conditions. Nevertheless, the organism was found to be more tolerant of low pH conditions under anaerobic atmosphere than under an aerobic atmosphere in the absence of lactic acid. The interaction between the variables did not lead to loss of the virulence plasmid in growing or non-growing cells.

Aerobiosis↗
PubMed1995

Secondary amyloidosis complicating psoriasis.

BACKGROUND: Amyloidosis is a heterogeneous group of disorders characterized by extracellular deposition of fibrillar protein. Secondary amyloidosis occurs in patients with chronic infectious or inflammatory processes. Only 18 cases of secondary amyloidosis complicating psoriasis have been reported. OBJECTIVE: We characterized secondary amyloidosis complicating psoriasis. METHODS: We reviewed all cases of coexisting psoriasis and amyloidosis seen at the Mayo Clinic from 1950 to 1992. The clinical characteristics were summarized, and the literature was reviewed. RESULTS: There were 28 cases of coexistent disease, and in five of these psoriasis was the only inflammatory condition preceding the development of secondary amyloidosis. Histopathologic confirmation with Congo red staining was available in four cases, and immunohistochemical confirmation of the characteristic amyloid A subtype was performed in two. CONCLUSION: Follow-up of four patients supports the view that amyloidosis associated with psoriasis is an aggressive disease that may be fatal.

Aged↗
PubMedDate not supplied

Chrysamine-G binding to Alzheimer and control brain: autopsy study of a new amyloid probe.

Chrysamine-G (CG) is a carboxylic acid analogue of Congo red, a histologic dye which stains amyloid. CG binds to the beta-amyloid protein of Alzheimer's disease (AD) in vitro and partitions into the brain of normal mice. In this study, we demonstrate increased binding of [14C]CG to homogenates of several regions of AD brain as compared to control. The total binding of CG to AD brain was approximately two- to three-fold that of control brain. The cerebellum could be used as an internal standard for each brain as CG binding to cerebellum did not differ between AD and control. The binding of [14C]CG correlated with numbers of senile plaques and neurofibrillary tangles. In addition, CG could be used to stain cerebrovascular amyloid in tissue sections. These results suggest that CG may prove useful as an in vivo probe of amyloid deposition in AD.

Adult↗
PubMed1995

[Primary AL-type amyloidosis disclosed by Horton disease].

Primary systemic amyloidosis rarely affects the walls of small and medium-sized vessels. We report a case of primary AL amyloidosis masquerading as giant cell arteritis at the onset of the disease, revealed by the temporal arteritis biopsy, and successfully treated by corticotherapy for three years. Histology of temporal arteritis confirms the diagnosis of amyloidosis (characteristic birefringence with Congo red). We discuss in this case the diagnosis of primary amyloidosis revealed by Horton disease, or the coincidental association of these two diseases.

Aged↗
PubMed1991

Interspecies comparisons of A/D ratios: A/D ratios are not constant across species.

The hypothesis that the ratio of the adult (A) and developmental (D) toxicity of a chemical is constant across animal species has been proposed as the basis for identifying developmental hazards, both from traditional developmental toxicity screens using laboratory mammals and from alternative systems such as the coelenterate Hydra attenuata. The purpose of this study was to determine whether A/D ratios are constant across species. The developmental and adult toxicity of 14 chemicals was assessed in four phylogenetically different species. The chemicals tested were aminopterin, bromodeoxyuridine, cadmium chloride, caffeine, congo red, dinocap, dinoseb, diphenylhydantoin, epinephrine, ethylenethiourea, 2-methoxyethanol, mirex, all-trans-retinoic acid, and trypan blue. These chemicals are representative of a variety of toxic mechanisms and a range of potencies. Species used were the CD-1 mouse (Mus musculus), South African clawed frog (Xenopus laevis), fathead minnow (Pimephales promelas), and fruit fly (Drosophila melanogaster). The mouse is a commonly used model for developmental toxicity. The other species are known to be sensitive to mammalian toxicants and have well-studied embryologies. Mice were exposed to chemicals either po or by sc injection using a standard Segment II protocol in which pregnant mice are administered the test agent on a daily basis from Gestation Days 6 to 15, adult toxicity is evaluated during and after treatment, and developmental toxicity is evaluated in fetuses at term. The exposure duration spans the period of organ formation in the embryo. The other species were exposed to test agents for a developmentally comparable period. This was from blastulation (shortly after fertilization) to the free-swimming tadpole stage in Xenopus (4 days); from blastulation to the free-swimming fry stage in Pimephales (7 days); and for the entire larval period, the period of development of the imaginal discs, in Drosophila (6 days). Adults of each species were exposed to test agents for 4, 7, and 6 days, respectively. The route of exposure was via the water column in the two aquatic species and via the diet in Drosophila. Statistical lowest observed effect level (LOEL) and no observed effect level (NOEL) values were generated for adult and developmental toxicity in each species. A/D ratios were calculated using both LOEL and NOEL values.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1991

Cerebral amyloid angiopathy in Chinese: incidence and significance.

Histological sections of 210 randomly selected autopsy brains and 49 consecutive autopsy cases of spontaneous intracerebral haemorrhage in the Chinese population aged over 40 years were examined by H&E and congo red stain with and without polarized light. In the randomly selected group, 10% of cases are positive for cerebral amyloid angiopathy (CAA) while 8.2% of cases are positive in the group with haemorrhage. The incidence is strongly age-related. Compared with Western figures. Chinese are less frequently and less severely affected by CAA. Although CAA does account for some cases of spontaneous intracerebral haemorrhage, it cannot account for the high incidence of cerebral haemorrhage among Chinese. Its significance in Chinese is much lower than in Caucasians.

Adult↗
PubMed1989

Tau-reactive neurofibrillary tangles in cerebellar cortex from patients with Alzheimer's disease.

In 4 cases of Alzheimer's disease (AD) a tau antiserum immunostained thin, round or flame-shaped profiles disposed around the nuclei of the cerebellar fusiform-type Golgi cells. In adjacent sections either a Bodian silver method or Congo red failed to reveal any abnormal structures. Since normal tau immunoreactivity is located on axons and is absent in formalin-fixed tissue, the tau-reactive profiles are likely to correspond to small masses of abnormal filaments, antigenically similar to those composing neurofibrillary tangles (NFT). This observation indicates that in AD the NFT formation is more diffuse than that showed with conventional histological methods.

Aged↗
PubMed1989

Alzheimer patients: preamyloid deposits are more widely distributed than senile plaques throughout the central nervous system.

In Alzheimer's disease, anti-beta-protein antisera label not only amyloid deposits accompanied by degenerating neurites (neuritic and mature plaques) and amyloid deposits without degenerating neurites, but also preamyloid deposits lacking the optical properties of amyloid fibrils. We have carried out a study of the brains of 13 patients with Alzheimer's disease (one with the familial and 12 with the sporadic form), using anti-beta-protein and anti-paired helical filament antisera, thioflavine S, Congo red and Gallyas' silver impregnation, in order to determine whether the distribution of preamyloid deposits and amyloid deposits without degenerating neurites differs from that of amyloid deposits with degenerating neurites. Preamyloid deposits and amyloid deposits with or without degenerating neurites were present in cortex, neostriatum, medial geniculate body and thalamic (anterior and extralaminar) nuclei, whereas preamyloid deposits and amyloid deposits without degenerating neurites, but not amyloid deposits with degenerating neurites, were present in other thalamic nuclei, in the globus pallidus, brainstem, cerebellar cortex and upper spinal cord. These results support the view that preamyloid deposits evolve to senile (neuritic and mature) plaques only in specific brain regions, where neurites vulnerable to amyloid fibrils are widely distributed.

Adult↗
PubMed1989

Down patients: extracellular preamyloid deposits precede neuritic degeneration and senile plaques.

Using anti-SP28 (a polyclonal antibody to a 28 residue synthetic peptide homologous to the NH2-terminal region of the Alzheimer amyloid beta-protein) to investigate the cerebral cortex of 6 Down patients aged 6-55 y, we found that, besides senile plaques and congophilic vessels, extracellular deposits unrelated to degenerating neurites, tangle-bearing neurons or congophilic vessels were labelled. These deposits were similar to the extracellular deposits previously observed in the cerebral cortex of Alzheimer patients and non-demented individuals. The material accumulated in the deposits did not react with Congo red, thioflavine S or, on some occasions, silver salts and therefore might have been constituted by beta-protein precursors lacking the molecular conformation of amyloid fibrils. Age-related analysis of the cortical lesions in Down patients suggested that such extracellular deposits precede degenerating neurites and evolve into senile plaques.

Adult↗
PubMed1989

Alzheimer's disease: mismatch between amyloid plaques and neuritic plaques.

Isocortical amyloid deposits and neurofibrillary changes were studied using selective silver staining methods. Amyloid was found in plaque-like formations varying in size and shape. The distribution pattern of these plaques as seen in the silver-stained preparations was identical to that recognized by A4 protein (amyloid) immunostaining. Consecutive sections stained for amyloid and neurofibrillary changes revealed the absence of intraneuronal cytoskeleton abnormalities within the boundaries of many of the amyloid plaques. Congo red preparations did not show these plaques and the tissue within the range of the plaques did not reveal any conspicuous neuropil distortions and/or glial cell accumulations. Hence, a considerable proportion of the amyloid plaques do not correspond to and should carefully be distinguished from 'primitive', 'mature', and 'burned out' types of neuritic (senile) plaques.

Aged↗
PubMed1989

Alzheimer patients and Down patients: cerebral preamyloid deposits differ ultrastructurally and histochemically from the amyloid of senile plaques.

The preamyloid deposits found in the cerebral grey matter of Alzheimer patients and Down patients following immunostaining with anti-beta-protein antisera are neither birefringent following Congo red staining nor fluorescent after thioflavine S treatment. Further, they contain small amounts of alpha 1-antichymotrypsin, sulfated glycosaminoglycans and complement fraction C3d, but not the P component. As suggested previously, the material accumulated in these deposits may lack the molecular conformation responsible for the properties of amyloid fibrils. To test this hypothesis, we selected cortical samples from 6 Alzheimer and 4 Down patients for an electronmicroscopical study of senile plaques and of preamyloid deposits, both identified by indirect immunogold staining with anti-beta-protein antiserum. We observed the labelling of 4-8 nm wide amyloid fibrils in the plaque cores and of extracellular electrondense, flaky and irregularly distributed material in the preamyloid deposits. In the latter, amyloid fibrils were very rarely detected. These findings support the view that preamyloid deposits mostly contain amyloid precursors that are not yet organized in fibrils.

Alzheimer Disease↗
PubMed1990

Large amounts of neocortical beta A4 deposits without neuritic plaques nor tangles in a psychometrically assessed, non-demented person.

An 88-year-old mentally normal woman (Blessed test score = 27) had very large amounts (397/mm2) of deposits stained by anti-beta A4 serum in the first temporal gyrus. Senile plaques and neurofibrillary tangles were lacking on sections stained with the Bodian's silver method, with anti-tau and anti-paired helical filament (anti-PHF) antibodies. The following beta A4 deposits were found in decreasing order of frequency: diffuse (64.8%), stellate (24.4%), primitive (10.2%), classic (0.6%) plaques. Compact plaques were not observed. Diffuse deposits predominated in layers I, III and IV. On the contrary, the rare classic plaques were located in layers II and III. No amyloid angiopathy was seen with Congo red stain although beta A 4 deposits were seen in vessel walls with immunocytochemistry. These data indicate that severe diffuse beta A4 deposits in the neocortex do not induce dementia. They suggest that the development of senile plaques composed of beta A4 amyloid and of degenerating neurites is not related solely to the density of the diffuse beta A4 deposits. Nor does it depend on the regional susceptibility of the nervous tissue since beta A4 deposits were seen in highly vulnerable cortical areas. Some other, as yet unknown, factors seem necessary. In addition, determination of beta A4 level in the neocortex is not sufficient for the diagnosis of dementia of Alzheimer type.

Aged↗
PubMed1993

Toxic effect of a beta-amyloid peptide (beta 22-35) on the hippocampal neuron and its prevention.

A synthetic truncated beta-amyloid peptide, beta 22-35, was shown to have a cytotoxic effect on cultured neurons from the rat hippocampus in serum-free medium. The peptide formed aggregates and typical amyloid fibrils resembling those of the beta-amyloid protein (AP) in neutral buffer solution and showed characteristic staining with Congo red and thioflavin-S. The neurotoxicity of beta 22-35 was suppressed by addition of calf serum, dibutyryl cAMP or insulin to culture medium, but not by addition of NGF or substance P. beta 22-35 had no effect on the glial cells. These results suggest that the AP can induce neurotoxicity in the hippocampal cells in vitro and the toxicity may involve a disorder in the intracellular signal transduction.

Amyloid beta-Peptides↗
PubMed1990

A neutral thiol protease secreted from newly excysted metacercariae of trematode parasite Paragonimus westermani: purification and characterization.

1. A neutral thiol protease was purified from the culture filtrate of newly excysted metacercariae of Paragonimus westermani to homogeneity as judged by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, having a monomeric form with mol. wt 22,000. 2. It expressed activity on t-butyloxycarbonyl-valyl-leucyl-lysyl-4-methyl-coumaryl-7-amide in the presence of cysteine at an optimal pH of 7.5, and also the activity was significantly affected by thiol protease inhibitors, indicating that the enzyme belongs to a neutral thiol protease family. 3. The enzyme hydrolyzed protein substrates, azocoll, casein and fluorescein isothiocyanate-labeled collagen, and showed low specificity toward hemoglobin, but no activity with elastin Congo Red and bovine serum albumin. 4. Catalytic property on fluorogenic substrates demonstrated that the enzyme cleaved preferentially the carboxylic side of the basic residue in N-substituted peptides.

Amino Acid Sequence↗
PubMed1988

Multigene families of Cellulomonas flavigena encoding endo-beta-1,4-glucanases (CM-cellulases).

Multiple genes coding for endo-beta-1,4-glucanases (CM-cellulases) have been isolated from a newly discovered highly cellulolytic strain of Cellulomonas flavigena. Clones of C. flavigena DNA were isolated in Escherichia coli and screened for gene expression on CM-cellulose plates staining with congo red. Six clones produced CM-cellulase activity as detected in liquid assays, and on activity gels. They fell into three groups within which the sequences cross-hybridised. There were small differences in the pH and temperature optima of the enzymes encoded by representatives of the three groups of clones.

Bacteria↗