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Biomedical subjects

R R Brown

Publications and source records attributed to R R Brown.

At least 91 records · Page 5Linked to original sources
PubMed1983

Can antibody responses in cattle vaccinated with a multivalent leptospiral bacterin interfere with serologic diagnosis of disease?

A commercially available leptospiral bacterin containing 5 serovars (canicola, grippotyphosa, hardjo, icterohemorrhagiae, pomona) was used per label directions to vaccinate 45 steers and bulls. In animals in which the prevaccination sera were negative for microscopic agglutinating antibody, the increase and decrease of titers were similar among all serovars. A serologic response was stimulated by a single dose and enhanced by the 2nd dose. Most titers peaked at 2 weeks and then fell rapidly by 15 weeks after the 2nd dose. Thirty-four animals with prevaccinal titers to serovar hardjo responded with high microscopic agglutinating titers for a sustained period. Of these cattle, 31 still had titers between 200 and 400 by 29 weeks after the 2nd dose. These results were interpreted as representing an anamnestic response initiated by the bacterin to a sensitization that had followed natural exposure.

Agglutination Tests↗
PubMed1983

Determination and pharmacology of a new hydroxylated metabolite of tamoxifen observed in patient sera during therapy for advanced breast cancer.

A new hydroxylated metabolite of tamoxifen, Metabolite Y [trans-1-(p-beta-hydroxyethoxyphenyl)-1,2-diphenylbut-1-ene] was characterized and subsequently measured by high-performance liquid chromatography in serum from patients receiving normal (10 mg twice daily) and high dose (greater than or equal to 150 mg twice daily) tamoxifen therapy for treatment of advanced breast cancer. In normal-dose patients, the serum level of Metabolite Y ranged between 6 and 60 ng/ml. This contrasted with serum levels of 80 to 180 ng/ml for tamoxifen and 200 to 300 ng/ml for N-desmethyltamoxifen, the major metabolite of tamoxifen. Serum levels of all three components were unchanged in one patient during the 24 hr after the cessation of tamoxifen therapy. Maximum serum levels of Metabolite Y were 800 ng/ml with concentrations of 1 micrograms/ml for tamoxifen and 2 micrograms/ml for N-desmethyltamoxifen in a patient on a 2-year course of high-dose therapy. Metabolite Y inhibited the binding of 17 beta-[3H]-estradiol to rat uterine and human breast carcinoma estrogen receptor. However, this metabolite was only weakly active: monohydroxytamoxifen [relative binding affinity (RBA) = 280]; tamoxifen (RBA = 6); Metabolite E (RBA = 3); N-desmethyltamoxifen (RBA = 4); Metabolite Y (RBA = 0.5). In 3-day immature rat uterine weight tests, Metabolite Y was a partial agonist with weak antiestrogenic activity. Although Metabolite Y has only weak activity, this compound would be expected to contribute to the overall antiestrogenic and antitumor properties of tamoxifen during therapy.

Animals↗
PubMed1982

Arthropathic properties related to the molecular weight of peptidoglycan-polysaccharide polymers of streptococcal cell walls.

The covalently bound polymers of peptidoglycan and group-specific polysaccharide (PG-APS) were isolated from the cell walls of group A streptococci. Arthritis was induced in rats with a single intraperitoneal injection of an aqueous suspension of PG-APS fragments derived by sonication. The joint lesions induced with this polydisperse suspension followed a bimodal pattern consisting of an acute phase, which reached a peak 5 days after injection and then receded, followed by a chronic, remittent, erosive arthritis lasting several months. The relative severities of the acute and chronic phases could be manipulated by selection of the size of PG-APS fragments. The fragments of PG-APS obtained by sonic treatment were resolved on the basis of size into three major populations by sucrose gradient or differential centrifugation. Based upon light scattering and gel filtration, the average molecular weight of the largest family of fragments was estimated to be about 500 x 10(6), the intermediate fragments were 50 x 10(6) daltons, and the predominant size in the smallest population was 5.3 x 10(6) daltons. The larger fragments induced negligible acute inflammation, but chronic disease became apparent 5 to 9 weeks after injection. The smallest fragments induced the most severe acute inflammation, with relatively little late, chronic joint disease. The particles of intermediate size induced moderate acute inflammation and the most severe chronic, erosive joint lesions. A single injection of fragments of the isolated peptidoglycan moiety of the PG-APS induced only a moderate acute inflammation of joints, with no apparent capacity to maintain the injury and induce chronic disease.

Animals↗
PubMed1981

Safety aspects in preparing suspensions of field strains of Brucella abortus for serological identification.

Forty field strains of Brucella abortus, obtained from milk and vaginal samples of naturally infected cattle, were heated in a waterbath at 65 degrees C, 75 degrees C, 80 degrees C for 60 to 120 minutes. Ninety-five per cent survived 65 degrees C for 120 minutes, 55 per cent survived 75 degrees C for 120 minutes, 25 per cent survived 80 degrees C for 120 minutes and 12.5 per cent survived 85 degrees C for 60 minutes. No isolates survived 85 degrees C for 75 minutes.

Animals↗
PubMed1981

The metabolism of 3H-pyridoxine in rat liver and brain.

A study of the metabolism and distribution of 3H-pyridoxine in normal rat liver and brain was done in animals given small single doses of the labeled vitamin intraperitoneally. Liver and brain tissues were collected from 1 h to 14 days. Perchloric acid extracts of tissues were fractionated by an ion exchange chromatographic procedure and six B6 vitamers were separated and assayed for radioactivity and microbiological activity. In liver 3H-pyridoxal phosphate peaked at 1 h after the administration of 3H-pyridoxine; however, the accumulation of total isotope in combined vitamers continued slowly until 4 h. During the first 4 h, about 50% of the tritium resided in the supernatant fraction of liver. In the brain, tritium accumulated slowly and reached a peak at day 7. Nearly 90% of the vitamin in the brain was in the form of pyridoxal phosphate and pyridoxamine phosphate. The concentrations of the total microbiologically active vitamin in the liver and brain were 35 to 40 and 20 to 25 nmol/g, respectively. However, the maximum amount of tritium in the brain was less than 10% of that in the liver. These data indicate that uptake and turnover of vitamin B6 in brain studied with tracer doses was very much slower than previously reported from studies with larger doses.

Animals↗
PubMed1981

Effects of dietary fat on incidence of spontaneous and induced cancer in mice.

A study was done to evaluate the effect of quantity and degree of saturation of dietary fat on the incidence of spontaneous tumors in male and female Swiss mice and in female C3H mice and on the incidence of tumors induced by s.c. administration of 1,2-dimethylhydrazine (DMH) in Swiss mice. Diets contained 5 or 17% fat substituted isocalorically for sucrose in a semipurified diet. Gross autopsy results suggest that the quantity of dietary fat, when fed isocalorically, did not appreciably influence the incidence of spontaneous or DMH-induced tumors in these mouse strains. Mice fed 17% of the triene fat generally had a higher incidence of liver tumors than corresponding groups fed the saturated fat. High levels (0.5%) of butylated hydroxyanisole protected female C3H mice from spontaneous liver tumors, but low levels of butylated hydroxyanisole (200 ppm of fat) did not protect. Neither level of butylated hydroxyanisole influenced tumor incidence in CD-1 mice. The absence of gross bowel tumors in animals given DMH was unexpected but may be related to the levels of cholesterol and fiber in the diets, since these factors are reported to influence the effects of DMH.

Animals↗
PubMed1980

Tryptophan and lysine metabolism in alpha-aminoadipic aciduria.

Two brothers previously diagnosed as having alpha-aminoadipic aciduria (alpha-AA) were subjected to a tryptophan loading test to determine if their condition resulted from a defect in the alpha-aminoadipate aminotransferase (kynurenine aminotransferase) system. Normal increases in kynurenic and xanthurenic acids eliminated this possibility. Further analyses of their urines revealed that both boys had measurable amounts of previously undetected alpha-ketoadipic acid (alpha-KA) before and after the loading test. A reexamination of speciments from a prelysine and postlysine loading test reconfirmed the existence of alpha-KA in their urines at the time the original observation of alpha-AA was made. The response to the lysine load was a predictable increase in both alpha-AA and alpha-KA. The boy who had been referred to this institution with a learning defect responded to the tryptophan load with a slight decrease in alpha-AA and an unpredicted decrease in alpha-KA and 3-hydroxykynurenine. His mentally normal brother showed a significant decrease in alpha-AA and major increases in all other measured metabolites including alpha-KA. The latter results were compatible with a defect in the oxidative decarobxylation of alpha-KA. A comparison of the urinary alpha-AA and alpha-KA concentrations in our subjects with comparable data in mentally normal and mentally retarded patients with this condition suggested that the retardation may result from other causes.

2-Aminoadipic Acid↗
PubMed1980

Analysis of mepivacaine, bupivacaine, etidocaine, lidocaine, and tetracaine.

A GLC method, employing a nitrogen-phosphorus-sensitive detector, is described for the analysis of mepivacaine, bupivacaine, etidocaine, lidocaine, and tetracaine in biological fluids. The method is simple, reliable, and sensitive, with a practical limit of sensitivity of approximately 2.5 ng/ml, well below therapeutic plasma levels. Extensive start-up procedures and sample preparation are not required.

Acetanilides↗
PubMed1980

Excretion of tryptophan-niacin metabolites by young men: effects of tryptophan, leucine, and vitamin B6 intakes.

Three human metabolic studies, each 35 days in length, were performed to investigate the relationship between tryptophan intake and the proportion of dietary tryptophan converted to niacin and the effect of supplements of L-leucine and vitamin B6 on this conversion. Nine college men consumed a basal diet that provided 8 mg of niacin, 1 mg of vitamin B6, and either 245, 548, or 845 mg of tryptophan from proteins per day. During each 35-day study, for one 15-day period basal diet alone was consumed, for another 15-day period basal diet plus 10 g of L-leucine per day was consumed, and for the last 5-day period, 20 mg of vitamin B6 per day was added to the diets of both groups. N1-methylnicotinamide, N1-methyl-2-pyridone-5-carboxamide, and quinolinic acid were measured in 24-hr urine samples. There were no significant or consistent effects of L-leucine or vitamin B6 supplements on the excretin of any of the metabolites measured. The proportion of tryptophan converted to niacin tended to increase as tryptophan consumption increased; however, this change was small and was probably not significant over the range of tryptophan intakes studied. The average conversion ration of tryptophan to niacin was approximately 72:1 in these subjects.

Adult↗
PubMed1980

Affinity of phytoestrogens for estradiol-binding proteins and effect of coumestrol on growth of 7,12-dimethylbenz[a]anthracene-induced rat mammary tumors.

A number of nonsteroidal estrogens, which are common naturally occurring substances in human foods, were examined for competitive binding to estrogen receptor proteins. These compounds bound competitively to estrogen receptor proteins in rat uterine cytosol, in tissue from 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat mammary tumors, and in human mammary tumor tissue. The relative affinity of these estrogens for rat uterine cytosol receptors paralleled closely the affinities reported for other receptors. Oral administration of coumestrol did not appear to support the growth of DMBA-induced rat mammary tumors, nor did coumestrol act as an antiestrogen when administered orally in combination with 17 beta-estradiol. Coumestrol administered sc might, however, be able to support the growth of these tumors.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1980

The kynurenine load test, an adjunct to the tryptophan load test.

The kynurenine load test was introduced to distinguish, in vivo, between abnormal tryptophan metabolism caused by induction of tryptophan oxygenase or by impaired kynureninase function. This test was carried out by giving a loading dose of 700 mumol L-kynurenine sulphate followed by determination of urinary metabolites of the tryptophan-nicotinic acid ribonucleotide pathway. The results of the kynurenine load test in a group of healthy post-menopausal female subjects show a consistant increase in urinary excretion of some metabolites of the tryptophan-nicotinic acid ribonucleotide pathway (kynurenine, 3-hydroxy-kynurenine, and 3-hydroxyanthranilic acid) of a magnitude comparable to the increase seen after a loading dose of 9800 mumol L-tryptophan (the tryptophan load test).

3-Hydroxyanthranilic Acid↗
PubMed1980

Effect of natural oestrogens on tryptophan metabolism: evidence for interference of oestrogens with kynureninase.

Urinary excretion of metabolites of the tryptophan-nicotinic acid ribonucleotide pathway, urinary excretion of 4-pyridoxic acid and blood concentrations of oestradiol and pyridoxal phosphate were studied in groups of post-menopausal women before or during treatment with natural oestrogens, i.e. oestradiol and oestriol, before and after loading doses of 9800 mumol L-tryptophan or 700 mumol L-kynurenine sulphate. Natural oestrogens induced abnormalities of tryptophan metabolism similar to those induced by synthetic oestrogens, and there was a dose related increase in urinary excretion of metabolites of the tryptophan-nicotinic acid ribonucleotide pathway before the kynureninase step. The increase in urinary excretion of these metabolites also after a loading dose of 700 mumol L-kynurenine indicates an inhibitory effect of oestrogens on kynureninase in vivo. Evidence is presented that this inhibition is an effect mediated through decreased availability of vitamin B6, the coenzyme of kynureninase, although the possibility of a direct effect of oestrogens on kynureninase can not be excluded.

Aged↗
PubMed1980

Cell-mediated immune response during experimental arthritis induced in rats with streptococcal cell walls.

Chronic, remittent, erosive arthritis was produced in rats by a single intraperitoneal injection of an aqueous suspension of cell wall fragments isolated from group A streptococci. Arthritis could be induced in rats which had been immunologically compromised by neonatal thymectomy. Delayed hypersensitivity to cell wall peptidoglycan could not be elicited in these rats, although progressive joint disease was obvious by clinical and radiological measurements. A delayed skin test was elicited with peptidoglycan in non-thymectomized rats at 6 to 14 days after injection of low doses of cell wall fragments. Between 2 to 4 weeks after cell wall injection the skin test could not be elicited and these rats could not be sensitized again with peptidoglycan. After a high dose of cell wall the skin test could not be elicited at any time. These non-thymectomized rats which had been injected with cell walls remained hyporesponsive to peptidoglycan for at least 3 months. Lymphocytes from non-thymectomized cell wall-injected rats also showed a non-specific depression of lymphocyte response to phytohaemagglutinin in vitro, but this function was recovered between 2 to 4 weeks after cell wall injection. We conclude that cell-mediated immunity against bacterial cell wall antigens is not a pathogenetic factor in this experimental model of arthritis.

Animals↗