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Biomedical subjects

C E Brown

Publications and source records attributed to C E Brown.

At least 127 records · Page 7Linked to original sources
PubMed1979

Hormonally induced tumors of the reproductive system of parabiosed male rats.

Parabiosis of intact male rats to castrated males or oophorectomized females for a period of approximately 20 months resulted in three interstitial cell tumors of the testis. When unilateral nephrectomy was added to the parabiotic procedure in ten pairs, eight interstitial cell tumors of the testis and four adenocarcinomas of the prostate occurred in the target male parabionts. These changes were preceded by elevations in luteinizing and follicle-stimulating hormone levels in the serum of the castrates and high levels of testosterone and, to a lesser degree, of androstenedion in the target partners developing the tumors.

Adenocarcinoma↗
PubMed1978

Late effects of successive massive doses of radiation on parabiont rat pairs.

Parabiosis of rats permits one partner to survive 1000 R X-radiation if the other is shielded. This dose to the previously shielded partner after intervals of 5, 10 or 30 days tests the ability of the first irradiated partner to recover and, in turn, support the second. The effectiveness of this can be measured by the late effects induced in the pair. Lifespan was shortened by 100--150 days following a 5-day interval, by 30 days following a 10-day interval and not shortened following a 30-day interval. The incidence of leukaemia was about 6 per cent in each group, close to that in control pairs. Shortening the interval between the irradiations decreased the average age of death from leukaemia. No solid lymphoid tumours were induced in the doubly irradiated pairs. The incidence of osteogenic sarcoma was 1.6 per cent in controls and 12.9 per cent in the pairs with both partners irradiated.

Animals↗
PubMed1978

Mammary and other tumors as a response to radiation and multiple stresses.

Parabiosis of paired NEDH rats and subsequent irradiation of one produced multiple stresses, particularly altered hormonal milieu. Benign mammary tumors developed in 8.6% of the control pairs, 12.7% of the shielded partners, and 19.7% of the irradiated rats. Mammary cancers developed in 5% of control pairs, 14.2% of the shielded partners, and 11.9% of the irradiated rats. With increased amounts of prolactin, the rate was 50% in shielded partner, 10% in the irradiated rats. Mesenchymal sarcoma develop at the anastomosis in parabiont rats. Their incidence rate in single controls is 3.1%, in parabiont control pairs 12.5%, in pairs with one partner irradiated 16.6%, and with both irradiated 23.1%. The incidence rate in other parts was increased threefold over controls in the irradiated partners. Radiation appears to be the dominant factor in both mammary and anastomotic tumors.

Adenofibroma↗
PubMed1978

Carcinoma of the prostate in irradiated parabiotic rats.

Twelve hundred fifty-two pairs of male NEDH rats were parabiosed, one partner received a single dose of 1000 R X-radiation, and the other rat was shielded with lead. Eleven hundred twenty pairs survived over 200 days and constitute the basis of this report. Twenty-five of the irradiated partners developed malignant tumors of the prostate, 19 of which were adenocarcinomas. One adenocarcinoma appeared in the shielded partners and one in a control group of 586 parabiosed and single rats. The long-term effect of a single dose of 1000 R whole-body X-radiation is weakly carcinogenic for the rat prostate.

Adenocarcinoma↗
PubMed1975

The effect of nephrectomy on the incidence of breast carcinoma in irradiated parabiosed rats.

The incidence of carsinoma the breast in parabiosed female NEDH rats is 2.5%. When one member of such a pair is irradiated, the incidence rises to 11% in the irradiated partner and 10% in the nonirradiated partner. If in such a pair of rats one kidney is removed from each partner, the incidence of breast carcinoma rises fivefold in the nonirradiated partner. The factors involved in such an increase probably have to do with alteration in retention, interchange, and feedback of the pituitary and ovarian hormones.

Adenocarcinoma↗
PubMed1972

The biosynthesis of vitamin B 12 : a study by 13 C magnetic resonance spectroscopy.

The origin of the methyl group on C-1 of Ring A of the corrin ring of vitamin B(12) was investigated by (13)C magnetic resonance spectroscopy. The proton-decoupled (13)C spectra of vitamin B(12) synthesized from [5-(13)C]delta-aminolevulinic acid by Propionibacteria were obtained by Fourier-transform nuclear magnetic resonance of high resolution, and spectra of high-resolution proton magnetic resonance of the (13)C-labeled B(12) were also taken. The delta-carbon atom of delta-aminolevulinic acid is the source of seven or eight known positions of vitamin B(12), depending on whether the C-1 methyl group is also derived from the labeled substrate. We have found seven resonances whose chemical shifts enable us to identify the position of the (13)C atoms in the molecule from the assignment of Dodderell and Allerhand. We observed no (13)C resonance corresponding to the C-1 methyl group of Ring A. Furthermore, the proton magnetic resonance spectrum showed no spin-spin splitting of the proton peak at the tau values assigned for the H atoms in this methyl group. It would thus appear that the methyl group at C-1, which has been considered to have the same origin as the delta-methine bridge of porphyrins, does not originate from the delta-carbon atom of delta-aminolevulinic acid. This finding may aid in elucidation of the mechanism of synthesis of the functional isomer of vitamin B(12) and porphyrins. The (13)C-labeled vitamin B(12) enabled us to make further assignments to the (13)C magnetic resonance of the vitamin.

Carbon Isotopes↗
PubMed1972

A second transport system for L-arabinose in Escherichia coli B-r controlled by the araC gene.

Escherichia coli B/r possesses two active transport systems for l-arabinose, both of which are regulated by araC, the regulatory gene for the l-arabinose operon. The system with the higher affinity for l-arabinose has a K(m) for initial uptake of l-arabinose of 8.3 x 10(-6)m; the system of lower affinity has a K(m) of 1.0 x 10(-4)m. The two systems can also be distinguished by differences in their response to analogues that act as competitive inhibitors of initial uptake. d-Galactose strongly inhibits l-arabinose uptake by the high affinity system but only weakly inhibits such uptake by the low affinity system. d-Fucose, d-xylose, and beta-methyl-l-arabinoside competitively inhibit the uptake of l-arabinose by both systems to approximately the same extent. d-Glucose and l-lyxose do not inhibit either system. On the basis of kinetic evidence and the properties of mutants lacking one or the other of the two systems, it has been concluded that the high affinity uptake system involves the l-arabinose binding protein. Kinetic studies have shown that the K(m) for l-arabinose uptake by the high affinity system resembles the K(m) for binding of l-arabinose by the binding protein, and both have similar K(i) values for the inhibitory substrates tested. A consideration of l-arabinose transport-deficient mutants has demonstrated that the previously described araE mutants lack the low affinity system but retain the high affinity system and have normal levels of the l-arabinose binding protein. Mutants described in this communication which lack only the high affinity system either contain no detectable l-arabinose binding protein or possess an immunologically cross-reacting material that is reduced in its ability to bind l-arabinose. These observations support a role for the binding protein in l-arabinose uptake.

Arabinose↗