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Limited and selective adduction of carboxyl-terminal lysines in the high molecular weight neurofilament proteins by 2,5-hexanedione in vitro.
DeCaprio AP, Fowke JH
(1992) Brain Res 586: 219-28
MeSH Terms: Animals, Binding Sites, Carbon Radioisotopes, Electrophoresis, Polyacrylamide Gel, Hexanones, Kinetics, Lysine, Macromolecular Substances, Microscopy, Electron, Neurofilament Proteins, Neurotoxins, Peptide Fragments, Rats
Show Abstract · Added December 10, 2013
2,5-Hexanedione (2,5-HD) induces a toxic neuropathy characterized by massive, focal axonal neurofilament (NF) accumulation. Covalent interaction of 2,5-HD with NF protein amines, resulting in pyrrole adduct formation, has been proposed as a critical step in its mechanism. The present study was undertaken to evaluate the hypothesis of selective 2,5-HD/lysine modification, by quantitating in vitro adduction in the NF proteins and in specific polypeptide domains of each protein. Native rat spinal cord NFs were exposed to 0-212.5 mM [14C]2,5-HD for 2-16 h (37 degrees C under argon), followed by removal of non-covalently bound radioactivity. Incorporation of radioactivity and pyrrole formation in NFs increased linearly with 2,5-HD concentration and biphasically with time. SDS-PAGE and fluorography demonstrated prominent labeling of the three NF subunit proteins (H, M, and L), in addition to high-MW, crosslinked material derived from NF-H and -M. Mild chymotryptic cleavage was employed to isolate the carboxyl-terminal 'tail' domains of NF-H and -M, and the pooled amino-terminal NF 'rod' regions, all of which were radiolabeled. Specific activity (mol adduct/mol protein) of adducted NF proteins and polypeptide domains was determined by scintillation counting of electroeluted proteins. Stable binding in the NF-H and -M proteins was 4- to 6-fold higher than in the NF-L protein at all 2,5-HD concentrations, with specific activities of approximately 6.9, 4.7, and 1.3 mol/mol protein, respectively, at 212.5 mM. Approximately 70-80% of NF-H and -M binding was localized to the tail domains. In contrast, NF-L and pooled rod domain adduction did not substantially exceed 1 mol/mol protein. These findings provide the first direct evidence for limited and selective pyrrole adduction in the NF proteins following 2,5-HD exposure.
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13 MeSH Terms
Interstitial nephritis associated with glomerulonephritis in a patient with Hashimoto's disease and idiopathic portal hypertension.
Sasaki H, Joh K, Ohtsuka I, Ohta H, Ohhashi T, Hoashi S, Takahashi T, Tokuda T, Koyama K, Isogai Y
(1992) Intern Med 31: 641-8
MeSH Terms: Female, Glomerulonephritis, Humans, Hypertension, Portal, Immunoglobulin A, Kidney Glomerulus, Microscopy, Electron, Middle Aged, Nephritis, Interstitial, Thyroiditis, Autoimmune
Show Abstract · Added August 27, 2013
A middle-aged women with hypothyroidism, idiopathic portal hypertension and nephrotic syndrome is presented. This unusual clinical appearance could not be explained as SLE by serological examinations. Pathohistological examinations showed "Banti's liver", Hashimoto's thyroiditis and diffuse proliferative glomerulonephritis with severe tubulo-interstitial nephritis. Immunohistochemical studies revealed IgA deposits in glomeruli. Electron microscopic study disclosed peculiar lucent areas of rarefaction with osmiophilic particles in tubular basement membranes. This tubulointerstitial nephritis was considered to be related to the immunological mechanism involving thyroid gland, liver and kidney disorders. This case thus had a clinically rare combination of these three.
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10 MeSH Terms
Ultrastructural localization of peroxidase in atherosclerotic lesions of pigeons.
Taylor RG, Jerome WG, Lewis JC
(1992) Exp Mol Pathol 57: 167-79
MeSH Terms: Animals, Aorta, Arteries, Arteriosclerosis, Cell Nucleus, Columbidae, Coronary Vessels, Endoplasmic Reticulum, Endothelium, Vascular, Histocytochemistry, Lipids, Microscopy, Electron, Muscle, Smooth, Vascular, Peroxidase
Show Abstract · Added December 10, 2013
Atherosclerotic lesions are known to have metabolic alterations which are associated with progressive lipid accumulation. Among the changes, lysosomal enzyme activity has been extensively characterized and at the ultrastructural level has been correlated with the amount of foam cell lipid. In a fashion paralleling lysosomal change, artery wall peroxidase activity is also altered during disease progression. The present study focuses upon the ultrastructural localization of peroxidase activity in atherosclerotic lesions of the aorta and coronary arteries from White Carneau pigeons fed a cholesterol-supplemented (0.3%) diet for 3 years. This resulted in fibrous lesions, rich in smooth muscle cells. The birds were necropsied by perfusion fixation, and peroxidase cytochemistry was carried out using the diaminobenzidine reaction. Peroxidase activity was found within endothelial cells and smooth muscle cells in both the media and intima, but cytochemically demonstrable activity was not found in macrophage foam cells. Peroxidase was localized within the nuclear envelope and endoplasmic reticulum, especially within cells that had lipid inclusions. The degree of peroxidase positivity varied within and among the arteries. In nonlesion regions of the aorta 20% of medial smooth muscle cells was peroxidase positive; the value for coronary artery smooth muscle cells was less. The peroxidase activity within aortic lesions was increased with 44% of intimal smooth muscle cells being positive. Notably, 85-90% of the lipid-containing intimal smooth muscle cells were positive. In contrast, intimal smooth muscle cells in the coronary artery lacked peroxidase reaction product, even in cells containing lipid. We conclude from these studies that aortic lesions contain a cytochemically differentiated subset of lipid-containing, peroxidase-positive smooth muscle cells; but coronary lesions lack a comparable subset of smooth muscle cells.
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14 MeSH Terms
Evidence for transforming growth factor-beta expression in human leptomeningeal cells and transforming growth factor-beta-like activity in human cerebrospinal fluid.
Johnson MD, Gold LI, Moses HL
(1992) Lab Invest 67: 360-8
MeSH Terms: Agar, Arachnoid, Blotting, Northern, Cells, Cultured, Culture Media, Conditioned, Gene Expression, Humans, Immunohistochemistry, Isomerism, Microscopy, Electron, Pia Mater, RNA, Messenger, Receptors, Cell Surface, Receptors, Transforming Growth Factor beta, Transforming Growth Factor beta
Show Abstract · Added February 17, 2014
BACKGROUND - Little is known about the factors regulating growth and maintenance of human leptomeningeal cells. The influence of cerebrospinal fluid on these functions is also unknown. Possible mediators include the transforming growth factor-beta (TGF beta) family, three closely related peptides that regulate proliferation and numerous other physiologic processes in most mesenchymal cells.
EXPERIMENTAL DESIGN - Expression of both mRNA and protein for TGF beta isoforms TGF beta 1, TGF beta 2, and TGF beta 3 as well as TGF beta-competing activity were evaluated in primary human leptomeningeal cultures by Northern blot analysis, immunohistochemistry, and a radioreceptor assay, respectively. TGF beta 1, TGF beta 2, and TGF beta 3 immunoreactivity was also evaluated in brain sections containing leptomeninges from which these cell cultures were established. An additional study analyzed human cerebrospinal fluid for TGF beta-like activity.
RESULTS - Transcripts for TGF beta 1, TGF beta 2 and TGF beta 3 were detected in RNA from each of the eight leptomeningeal cultures. Significant TGF beta 1 immunoreactivity was detected in leptomeningeal tissue from five of eight cases. TGF beta 2 and TGF beta 3 immunostaining was seen in eight and seven of the cases, respectively. Similarly, cells cultured from these meninges exhibited variable TGF beta 1 and extensive TGF beta 2 and TGF beta 3 immunoreactivity. Radioreceptor assays of conditioned media from four cultures demonstrated significant latent TGF beta-like activity. TGF beta radioreceptor competing activity was also detected by radioreceptor assay in normal blood-free cerebrospinal fluid from 32 patients without neurological disease. In addition, pooled cerebrospinal fluid (from six additional patients) exhibited dose dependent TGF beta-like activity in the radioreceptor assay, stimulation of AKR-2B cell growth in soft agar and inhibition of growth in CCL-64 cell assays suggesting that cerebrospinal fluid contains TG beta-like activity.
CONCLUSIONS - These findings suggest that the human leptomeninges synthesize TGF beta 1, TGF beta 2 and TGF beta 3 and secrete latent TGF beta s at least in vitro. Human cerebrospinal fluid may also contain TGF beta isoforms. Collectively, these observations raise the possibility that members of the TGF beta family contribute to biologic processes of the leptomeninges.
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15 MeSH Terms
Distinctive patterns of hyperplasia in transgenic mice with mouse mammary tumor virus transforming growth factor-alpha. Characterization of mammary gland and skin proliferations.
Halter SA, Dempsey P, Matsui Y, Stokes MK, Graves-Deal R, Hogan BL, Coffey RJ
(1992) Am J Pathol 140: 1131-46
MeSH Terms: Animals, Cysts, Hyperplasia, Immunohistochemistry, Mammary Glands, Animal, Mammary Tumor Virus, Mouse, Mice, Mice, Transgenic, Microscopy, Electron, Nucleic Acid Hybridization, RNA, Messenger, Radioimmunoassay, Skin, Transforming Growth Factor alpha
Show Abstract · Added March 27, 2014
Eight lines of transgenic mice expressing a mouse mammary tumor virus (MMTV) human transforming growth factor-alpha (TGF alpha) fusion gene were established. Three lines with distinctive phenotypes are presented. All have proliferative changes of the mammary gland. One line has sebaceous gland hyperplasia of the skin. Five histologic patterns of mammary gland hyperplasia based on two of these lines were identified: cystic hyperplasia, solid hyperplasia, dysplasia, adenoma, and adenocarcinoma. Human TGF alpha mRNA and protein were produced in all patterns but appeared reduced in solid hyperplasia, dysplasia, and adenocarcinoma. TGF alpha immunoreactivity in the mammary tissue, cystic fluid, and serum did not show significant differences; hyperplasia developed in 65% of multiparous mice and 45% of virgin mice by 12 months of age. Adenocarcinoma developed in 40% of multiparous mice and 30% of virgin mice by 16 months of age. These transgenic lines may provide useful models of mammary and sebaceous gland hyperplasia analogous to human disease.
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14 MeSH Terms
A role for the passage helix in the DNA cleavage reaction of eukaryotic topoisomerase II. A two-site model for enzyme-mediated DNA cleavage.
Corbett AH, Zechiedrich EL, Osheroff N
(1992) J Biol Chem 267: 683-6
MeSH Terms: Animals, Base Sequence, DNA, DNA Topoisomerases, Type II, Drosophila melanogaster, Electrophoresis, Polyacrylamide Gel, Microscopy, Electron, Molecular Sequence Data, Nucleic Acid Conformation, Oligonucleotides, Substrate Specificity
Show Abstract · Added March 5, 2014
Eukaryotic topoisomerase II is capable of binding two separate nucleic acid helices prior to its DNA cleavage and strand passage events (Zechiedrich, E. L., and Osheroff, N (1990) EMBO J. 9, 4555-4562). Presumably, one of these helices represents the helix that the enzyme cleaves (i.e. cleavage helix), and the other represents the helix that it passes (i.e. passage helix) through the break in the nucleic acid backbone. To determine whether the passage helix is required for reaction steps that precede the enzyme's DNA strand passage event, interactions between Drosophila melanogaster topoisomerase II and a short double-stranded oligonucleotide were assessed. These studies employed a 40-mer that contained a specific recognition/cleavage site for the enzyme. The sigmoidal DNA concentration dependence that was observed for cleavage of the 40-mer indicated that topoisomerase II had to interact with more than a single oligonucleotide in order for cleavage to take place. Despite this requirement, results of enzyme DNA binding experiments indicated no binding cooperativity for the 40-mer. These findings strongly suggest a two-site model for topoisomerase II action in which the passage and the cleavage helices bind to the enzyme independently, but the passage helix must be present for efficient topoisomerase II-mediated DNA cleavage to occur.
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11 MeSH Terms
Transforming growth factor alpha protection against drug-induced injury to the rat gastric mucosa in vivo.
Romano M, Polk WH, Awad JA, Arteaga CL, Nanney LB, Wargovich MJ, Kraus ER, Boland CR, Coffey RJ
(1992) J Clin Invest 90: 2409-21
MeSH Terms: Animals, Aspirin, Dinoprostone, Ethanol, Ethylmaleimide, Gastric Mucins, Gastric Mucosa, Image Processing, Computer-Assisted, Indomethacin, Microscopy, Electron, Scanning, Necrosis, Ornithine Decarboxylase, Phosphorylation, Phosphotyrosine, Rats, Rats, Sprague-Dawley, Sulfhydryl Compounds, Time Factors, Transforming Growth Factor alpha, Type C Phospholipases, Tyrosine
Show Abstract · Added March 5, 2014
This study was designed to determine whether transforming growth factor alpha (TGF alpha) protects rat gastric mucosa against ethanol- and aspirin-induced injury. Systemic administration of TGF alpha dose-dependently decreased 100% ethanol-induced gastric mucosal injury; a dose of 50 micrograms/kg delivered intraperitoneally 15 min before ethanol decreased macroscopic mucosal injury by > 90%. At the microscopic level, TGF alpha prevented deep gastric necrotic lesions and reduced disruption of surface epithelium. Pretreatment with orogastric TGF alpha (200 micrograms/kg) only partially (40%) decreased macroscopic ethanol damage. Intraperitoneal administration of TGF alpha at a dose of 10 micrograms/kg, which does not significantly inhibit gastric acid secretion, decreased aspirin-induced macroscopic damage by > 80%. TGF alpha protection does not seem to be mediated by prostaglandin, glutathione, or ornithine decarboxylase-related events, as evidenced by lack of influence of the inhibition of their production. Pretreatment with the sulfhydryl blocking agent N-ethylmaleimide partially abolished (40%) the protective effect of TGF alpha. In addition, systemic administration of TGF alpha resulted in a two-fold increase in tyrosine phosphorylation of phospholipase C-gamma 1 and in a time- and dose-dependent increase in levels of immunoreactive insoluble gastric mucin; these events occurred in a time frame consistent with their participation in the protective effect of TGF alpha.
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21 MeSH Terms
Molecular aspects of sickle cell disease.
Waterman MR, Cottam GL
(1976) Angew Chem Int Ed Engl 15: 749-57
MeSH Terms: Anemia, Sickle Cell, Electron Spin Resonance Spectroscopy, Erythrocytes, Gels, Glutamates, Hemoglobin A, Hemoglobin, Sickle, Kinetics, Macromolecular Substances, Microscopy, Electron, Oxygen, Protein Conformation, Thermodynamics, Valine, X-Ray Diffraction
Added February 12, 2015
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15 MeSH Terms