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Biomedical subjects

D Lin

Publications and source records attributed to D Lin.

At least 235 records · Page 13Linked to original sources
PubMed1981

Comprehensive analysis of urinary metabolites of N'-nitrosonornicotine.

A detailed study of the urinary metabolites of N'-nitrosonornicotine has been performed, employing a simple high pressure liquid chromatographic method. The percentage excretion of the principal urinary metabolites was determined over a dose range of 3-300 mg/kg in the F-344 rat, as follows: 4-hydroxy-4-(3-pyridyl)butyric acid (37.1-53.3%, respectively, of the dose), N'-nitrosonornicotine-I-N-oxide (6.7-10.7%), norcotinine (3.2-5.1%), 4-oxo-4-(3-pyridyl)butyric acid (31.1-12.8%), N'-nitrosonornicotine (3.3-5.2%). In the strain A mouse and Syrian golden hamster, the urinary metabolites were qualitatively similar to those observed in the F-344 rat. The interrelationships of the various metabolites of N'-nitrosonornicotine which have been observed in vitro and in vivo were established. The in vitro metabolites resulting from 2'-hydroxylation by liver microsomes, myosmine and 4-hydroxy-I-(3-pyridyl)-1-butanone were converted, by the F-344 rat, primarily to 4-oxo-4-(3-pyridyl)butyric acid as a urinary metabolite. The in vitro metabolite resulting from 5'-hydroxylation by liver microsomes, 2-hydroxy-5-(3-pyridyl)tetrahydrofuran, gave 4-hydroxy-4-(3-pyridyl)butyric acid as its major urinary metabolite, apparently via 5-(3-pyridyl)-tetrahydrofuran-2-one. N'-nitrosonornicotine-I-N-oxide, the remaining major in vitro metabolite, was excreted to a large extent unchanged in F-344 rat urine. The urinary metabolites from 2'-hydroxylation and 5'-hydroxylation of N'-nitrosonornicotine, 4-oxo-4-(3-pyridyl)butyric acid and 4-hydroxy-4-(3-pyridyl)butyric acid, respectively, were not formed from the in vivo metabolite norcotinine and were ot interconverted significantly by the F-344 rat. Thus, these metabolites appear to be reliable indicators for the two possible in vivo alpha-hydroxylations of N'-nitrosonornicotine.

Animals↗
PubMed1981

Studies on mechanism of action of luteinizing releasing hormone (LH-RH) in ovulation of fish--intracellular distribution of LH-RH-A in pituitary gonadotrophs as revealed by electron-microscopic autoradiography.

The results of competitive bending experiment and the electron-microscopic autoradiographic studies show that the peptide hormone, LH-RH-A (a nonapeptide), could be internalized into the gonadotrophs of the pituitary gland of the mud-carp (Cirrhrinus molitorella). It is demonstrated that the labeled peptide, 125I-LH-RH-A, is internalized not only into the cytoplasm, but also into the nucleus, apparently via the nuclear pores. It is, therefore, suggested that the peptide hormone might act directly on the genome either in the form of a hormone-receptor complex or of a single molecule.

Animals↗
PubMed1980

Progesterone administration in vivo stimulates release of luteinizing hormone-releasing hormone in vitro.

The release of luteinizing hormone-releasing hormone (LHRH) from tissue from the mediobasal hypothalamic-anterior hypothalamic-preoptic area of prepuberal female rats was measured in a perfusion system. Measurements were also made of the concentrations of LHRH in these tissue fragments and of luteinizing hormone in serum obtained when the rats were killed. Four groups of immature rats were studied: intact, ovariectomized, ovariectomized and implanted with estradiol-containing capsules, and ovariectomized rats primed with estradiol and injected with progesterone. The release of LHRH from the tissue of ovariectomized animals was significantly less than that of intact females and was not modified when the ovariectomized rats received estradiol. However, there was a four- to fivefold increase in LHRH release from tissue of ovariectomized rats primed with estradiol when they were killed 6 hours after they received an injection of progesterone. The concentrations of LHRH in tissue and of luteinizing hormone in serum varied among groups and with the time of day that the animals were killed. The interactions among luteinizing hormone, gonadal steroids, and the photoperiod seem to set the appropriate conditions for neural processes triggering a complete and normal release of luteinizing hormone.

Animals↗
PubMed1980

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↗
PubMed1980

"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↗
PubMed1980

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↗
PubMed1979

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↗
PubMed1977

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↗
PubMed1976

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↗
PubMed1976

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↗
PubMed1970

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↗
PubMedDate not supplied

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↗