Correlation of radionuclide scintigraphy and gray-scale ultrasonography in the evaluation of hepatic disorders.
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Adult↗
Biomedical subjects
D Lin
Publications and source records attributed to D Lin.
Dorsal noradrenergic bundle and selective attention in the rat.
The role for the dorsal noradrenergic bundle (DNB) in selective attention and stimulus filtering was tested in several situations. The DNB was damaged by stereotaxically guided injections of 4 microgram of the neurotoxin 6-hydroxydopamine (6-OHDA). The latent inhibition effect was blocked by 6-OHDA-induced depletion of forebrain noradrenaline, whereas nonreversal shift performance was better in noradrenaline-depleted rats than controls. These data are interpreted to indicate that animals with DNB lesions are imparied in ignoring irrelevant stimuli. However, in situations in which control animals did not learn to ignore irrelevant stimuli, no lesion-induced difference was found. Thus, controls and animals with DNB lesions learned equally about each of two dimensions of a multiple-redundant discrimination task. This was assessed both by interpolated trials with only one dimension present and by shifts in which only one of the previous two dimensions remained relevant. It is concluded that the DNB lesion does not increase stimulus sampling globally but that it impairs performance only in those cases in which normal rats learn to ignore irrelevant stimuli.
Animals↗
"Hot spot" on liver scan due to tricuspid insufficiency.
A patient with a diagnosis of tricuspid insufficiency was found to have a small focal area of increased activity, or "hot spot," in the liver on a Tc-99-sulfur colloid scan. This "hot spot" was in the superior central portion of the liver in the region of the junction of the hepatic veins and inferior vena cava. Its presence was confirmed on a dynamic study of the liver, which showed appearance of the activity in the abnormal area at the same time as in the right atrium. The finding was thought to be the result of reflux of blood from the right atrium into the vena cava and hepatic veins due to tricuspid insufficiency.
Humans↗
Metabolism of the tobacco specific nitrosamines, N'-nitrosonornicotine and 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone.
The metabolism, in the F-344 rat, of the tobacco-specific carcinogens, N'-nitrosonornicotine (NNN) and 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was studied. NNN was hydroxylated at each position of the pyrrolidine ring; 2'-hydroxylation gave 4-hydroxy-1-(3-pyridyl)-1-butanone in vitro and the corresponding acid in vivo, 3'-hydroxylation gave 3'-hydroxyNNN, 4'-hydroxylation gave 4'-hydroxy-NNN and 5'-hydroxylation gave 4-hydroxy-4-(3-pyridyl)butanal (in vitro) and 4-hydroxy-4-(3-pyridyl) butanoic acid (in vivo). The principle ring hydroxylation in the untreated F-344 rat was 5'-hydroxylation. Pyridine N-oxidation was also observed, giving NNN-1-N-oxide as a major metabolite. The principle urinary metabolites of NNN were formed by 5'-hydroxylation and pyridine-N-oxidation. For NNK, a major process was reduction of the carbonyl to give 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanol. alpha-Hydroxylation of both the N-methyl and N-methylene groups was also observed, as was formation of NNK-N-oxide in vitro and in vivo.
Animals↗
Protein and RNA synthesis in kainic acid-injected striata.
Injections of kainic acid into rat neostriata destroy neuronal soma in the injected area. Kainic acid-injected neostriata show a significant increase (as compared with control) in the incorporation in vitro of label from radioactive leucine into the TCA-insoluble protein fraction at all time periods studied (from 1 to 80 days after the kainic acid injection), with the greatest stimulation ((6-7-fold) occurring between the third and eighth day. At 1-5 days there was also increased incorporation in vitro of label from uridine into RNA. The increased protein synthesis is probably due to the astrocytes which invade the injected area and are still seen in electron microscopic studies 2-3 months after the injections.
Animals↗
Oxygen tension under a hard, gas-permeable contact lens.
Oxygen tension under a hard, gas-permeable contact lens is calculated. The gas permeability of the lens is taken from the engineering literature and is shown to be 10 times smaller than claimed in the optometric literature. The engineering data are supported by new measurements of gas permeability. Calculations using the new data show that the oxygen tension under the lens is at the lower end of the range of acceptable values.
Contact Lenses↗
Histones bind more tightly to bromodeoxyuridine-substituted DNA than to normal DNA.
Using a membrane filter assay, we have obtained results from both kinetic and competition experiments indicating that histones bind more strongly to bromodeoxyuridine-substituted DNA than to normal DNA. At 37 degrees C in our standard buffer of 0.2 M ionic strength, the rate of dissociation of histones H1, H2, and h4 from BrdU-substituted DNA is respectively 7, 4, and 2 times slower than it is from normal DNA. Competition experiments show an even greater difference between BrdU-substituted and normal DNA with respect to histone binding. The tighter binding of histones to BrdU-substituted DNA is of interest because of the known effects of BrdU on eukaryotic chromosome condensation and staining, virus induction, and the inhibition of differentiation.
Binding Sites↗
Oxygen tension under a soft or hard, gas-permeable contact lens in the presence of tear pumping.
The oxygen tension under hard or soft, oxygen-permeable contact lenses is calculated. The calculation recognizes delivery of oxygen to the tear fluid under the contact lens by diffusion through the lens material and by entrance of fresh, air-saturated tears at each blink. The results show that oxygen diffusion through the lens material is much more effective than tear pumping in maintaining a useful oxygen tension under the lens.
Contact Lenses↗
Oxygen tension distributions in the cornea: a re-examination.
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Animals↗
[Etiology of post-traumatic osteomyelitis].
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Adolescent↗
Effect of cellulose in the diet on the recovery of dietary plant sterols from the feces.
In one normal subject, J.S., fed several formula diets in a sterol balance study, only 25-58% of the ingested plant sterols were recovered from the stool. The dietary plant sterols were completely recovered from the stools of five other men. Plant sterol recovery was complete in all men when a diet of mixed general foods was consumed. Since the chief differences in composition of the formula and the diet of mixed general foods were related to the different contents of cellulose and lactose, these components were added to the formula diet of J.S., and plant sterol balance studies were then carried out. The addition of fresh celery or pulverized cellulose to the formula diet partially corrected the usual fecal loss of plant sterols (80% being recovered). Lactose in the formula was only slightly corrective. However, the addition of both cellulose and lactose led to complete recovery of the ingested plant sterols in the feces. Bacterial cultures of stools were incubated with added cholesterol-4-(14)C, and a linear relationship between losses of sterol during balance studies and in vitro incubations was observed; that is, a considerable loss of the labeled cholesterol from cultures after the formula diet, but not after the diet of mixed general foods. This in vitro loss was also corrected by the addition of cellulose and lactose to the formula diet. The loss of the sterol nucleus in the intestinal tract may occur at times because of the lack of certain dietary constituents. It is hypothesized that the metabolism of intestinal tract bacteria is altered when certain constituents are not present in the diet, and that these bacteria may then degrade the sterol nucleus.
Carbon Isotopes↗
Hypoxia after prenatal cocaine attenuates striatal dopamine and neurotrophic activity.
We have previously shown that newborn rabbits exposed to cocaine prenatally have an altered cardiorespiratory response to hypoxia. We report the effect of postnatal hypoxia on brain DA and neurotrophic activity in New Zealand White rabbit pups (n = 41) born to cocaine-exposed does (30 mg/kg/day SC from days 7-15 of a 32-day gestation = COCaine) and control does (sterile H2O = VEHicle). Four to 6-day-old pups were exposed to 20 min of room air (0.21 fractional inspired oxygen tension, FIO2). One third of each group was then exposed to 20 min of either 0.15 (moderate hypoxia) or 0.08 (severe hypoxia) FIO2. Immediately following hypoxic challenge the pups were sacrificed. Striatal tissue extracts were subsequently assessed for DA and striatal trophic activity by monitoring the number of neuron specific enolase immunoreactive (NSEir) cells in mesencephalic culture following incubation with striatal extracts. Increasing the severity of hypoxia increased DA content (p < 0.005), but reduced DA activity (p < 0.0001) and trophic activity (p < 0.001). Cocaine exposure reduced striatal DA (p < 0.005) as well as NSEir (p < 0.001) in all conditions relative to vehicle-treated controls. These data suggest that prenatal cocaine exposure enhances the vulnerability of the DA system to the stress of hypoxia, possibly through alterations in neurotrophic activity.
3,4-Dihydroxyphenylacetic Acid↗
Analysis for N2-(pyridyloxobutyl)deoxyguanosine adducts in DNA of tissues exposed to tritium-labeled 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and N'-nitrosonornicotine.
The tobacco-specific carcinogens 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN) are metabolically activated to DNA binding intermediates, partially via 4-(3-pyridyl)-4-oxobutanediazohydroxide (7) or related carbonium ions. Previous studies have shown that generation of 7 from 4-(carbethoxynitrosamino)-1-(3-pyridyl)-1-butanone (11) in the presence of deoxyguanosine yields a major adduct identified as 2'-deoxy-N-[1-methyl-3-oxo-3-(3-pyridyl)propyl]guanosine (adduct 1). These results suggested that adduct 1 should be present in DNA of tissues that can metabolically activate NNK and NNN. In the present study, we evaluate the formation of adduct 1 and its structurally related straight-chain analogue 2'-deoxy-N-[4-oxo-4-(3-pyridyl)butyl]guanosine (adduct 2) in DNA of tissues of rats treated with [5-3H]NNK or [5-3H]NNN, and in DNA of nasal mucosa that had been cultured in medium containing [5-3H]NNK or [5-3H]NNN. Hepatic DNA from rats treated with [5-3H]NNK was enzymatically hydrolyzed to deoxyribonucleosides and analyzed by HPLC. One of the radioactive peaks, peak E, coeluted with adduct 1. However, treatment of peak E with NaBH4 resulted in the formation of products different from those produced by NaBH4 treatment of adduct 1, demonstrating that adduct 1 could not be detected under these conditions. Hydrolysis of peak E with acid produced 4-hydroxy-1-(3-pyridyl)-1-butanone (9), suggesting that peak E might be adduct 2. Therefore, adduct 2 was synthesized by reaction of deoxyguanosine with 1-(3-pyridyl)butane-1,4-dione (5) in the presence of NaCNBH3.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Identification of N-(Deoxyguanosin-8-yl)-2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine as the major adduct formed by the food-borne carcinogen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, with DNA.
The covalent binding of the N-acetoxy-, N-hydroxy-, and nitro derivatives of the food-borne carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) to 2'-deoxyribonucleosides or DNA was investigated in vitro and in vivo. N-Acetoxy-PhIP reacted with deoxyguanosine (dG), but not with the other deoxyribonucleosides, to form N-(deoxyguanosin-8-yl)-PhIP (dG-C8-PhIP), whose structure was determined by NMR and mass spectral analyses and by ultraviolet absorption and pH-solvent partitioning characteristics. While reaction of N-acetoxy-PhIP with calf thymus DNA at pH 5.0 yielded 5.38 +/- 1.16 nmol of bound PhIP residues/mg of DNA, N-hydroxy-PhIP gave only 0.13-0.23 nmol binding/mg of DNA under identical reaction conditions. Nitro-PhIP produced no detectable binding under these conditions. HPLC analysis of 1-butanol extracts of enzymatically hydrolyzed DNA that had been modified by N-acetoxy-PhIP in vitro showed a major adduct which coeluted with and had an ultraviolet absorption and a mass spectrum that were identical to that of authentic dG-C8-PhIP. 32P-Postlabeling analysis of DNA isolated from colon, pancreas, lung, heart, and liver of rats treated orally with PhIP revealed the presence of a major PhIP-DNA adduct. This adduct had chromatographic properties identical to that of the 32P-labeled bis(phosphate) derivative of dG-C8-PhIP and represented 35-45% of the total adducts.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Analysis of DNA adducts of 2-amino-1-methyl-6-phenylimidazo[4,5- b]pyridine in rat and human tissues by alkaline hydrolysis and gas chromatography/electron capture mass spectrometry: validation by comparison with 32P-postlabeling.
A sensitive and specific method has been developed to measure levels of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) adducted to DNA in tissues. The method is based on alkaline hydrolysis of PhIP from DNA, followed by organic solvent extraction, derivatization to form the electron-capturing bis(pentafluorobenzyl) derivative, and analysis by gas chromatography/electron capture mass spectrometry (GC/MS) using a deuterium-labeled internal standard. The method can detect PhIP-DNA adducts at levels down to 0.03 fmol of PhIP/micrograms of DNA (1 PhIP adduct/10(8) normal nucleotides) for a 100 micrograms sample of DNA. The method is reproducible for sample sizes ranging up to at least 1000 micrograms of DNA. A series of 20 DNA samples from 5 tissues of rats treated with a single oral dose of PhIP were analyzed both by alkaline hydrolysis-GC/MS and by 32P-postlabeling. Results from the two methods were highly correlated (r2 = 0.83), with adduct levels determined by alkaline hydrolysis-GC/MS averaging about 60% of the levels determined by 32P-postlabeling. A pilot survey of 24 individual human tissue DNA samples, including pancreas (n = 12), colon mucosa (n = 6), and urinary bladder epithelium (n = 6), was carried out by alkaline hydrolysis-GC/MS and 32P-postlabeling. Both methods provided evidence for PhIP-DNA adducts in two of the colon samples, but not in the samples from human pancreas or urinary bladder.
Animals↗
Quantitative immunohistochemical analysis of 4-aminobiphenyl-DNA in cultured cells and mice: comparison to gas chromatography/mass spectroscopy analysis.
Two monoclonal antisera, 4C11 and 3C8, recognizing 4-aminobiphenyl (4-ABP)--DNA adducts were developed and characterized by competitive enzyme-linked immunosorbent assay (ELISA). Both antisera are highly specific for 4-ABP-DNA and, at the highest concentration tested, do not recognize the DNA adducts of several other aromatic amines tested including 1-aminopyrene, 8-nitro-1-aminopyrene, and 6-nitro-1-aminopyrene. An immunohistochemical method for detecting adducts was developed in R52 cells, a mouse NIH3T3 cell line expressing high levels of cytochrome P450 1A2. Quantitation of fluorescence labeling indicated a dose-related increase in staining in cells treated with 0, 6, 30, 60, and 300 microM 4-ABP. To apply the method to tissue samples, Balb/c mice were treated with 0, 4, 10, 20, 40, and 80 mg/kg 4-ABP and liver, bladder, and lung tissue analyzed by immunohistochemical staining of tissue sections. There was a dose-related increase in specific nuclear staining in liver and bladder tissues with no detectable staining in lung tissue. DNA from liver tissue was also analyzed by alkaline hydrolysis of 4-ABP, derivatization with pentafluoropropionic anhydride, and gas chromatography/mass spectroscopy analysis. A good correlation (r = 0.98, p < 0.0001) was found between DNA damage levels determined by the two methods. Based on adduct levels determined by GC/MS in both R52 cells and liver tissue, the immunohistochemical method has a limit of sensitivity of approximately 1 adduct/10(7-8) nucleotides. Immunohistochemistry should be useful for analysis of 4-ABP-DNA adducts in human tissue biopsies as well as exfoliated cells from the oral mucosa and urinary bladder.
3T3 Cells↗
Random amplified polymorphic DNA for strain delineation within Candida tropicalis.
Candida tropicalis DNA was used as a template in a polymerase chain reaction (PCR) utilizing a 10-mer primer to generate random amplified polymorphic DNA (RAPD). RAPD patterns associated with 25 primers were obtained for six epidemiologically-unrelated isolates, then a subset of six primers were selected to screen a panel of 18 isolates of C. tropicalis and six isolates of Candida paratropicalis, a species that resembles C. tropicalis but has a sucrose-negative phenotype. The panel, which included nine epidemiologically-related isolates from an outbreak of sternal wound infections, was typed without knowledge of each isolate's origin. The RAPD profiles of the epidemiologically-related isolates were identical to very similar; in contrast, the profiles of most unrelated isolates showed more dissimilarity. While RAPD profiles of C. albicans and Candida parapsilosis differed substantially from those of C. tropicalis, the profiles obtained for C. paratropicalis were consistent with it being a variant of C. tropicalis.
Base Sequence↗
Small subunit ribosomal RNA sequence of Henneguya exilis (class Myxosporea) identifies the actinosporean stage from an oligochaete host.
Several transmission studies, as well as recent molecular data, have indicated that the two classes Myxosporea and Actinosporea represent different life cycle stages of Myxozoa. To evaluate the life cycles of myxozoa in catfish aquaculture systems, the small subunit (18S) ribosomal RNA gene sequences of Henneguya exilis, a myxosporean from channel catfish Ictalurus punctatus, and an actinosporean (previously designated as Aurantiactinomyxon janiszewskai) from the aquatic oligochaete Dero digitata were determined. The sequences were identical, indicating that H. exilis and the actinosporean are alternate life stages of a single species. This is the first report identifying the actinosporean stage of the genus Henneguya.
Animals↗