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Biomedical subjects

B J Furr

Publications and source records attributed to B J Furr.

At least 37 records · Page 2Linked to original sources

Endocrine and ovarian changes in dairy cattle fed a low beta-carotene diet during an oestrus synchronisation regime.

Twelve Friesian cows, 76 to 110 days calved, with blood cell counts and Compton metabolic profile values in the normal range throughout, were housed and fed a marginal diet for varying periods before being injected twice, 11 days apart, with cloprostenol. Artificial insemination was carried out 72 and 96 hours after the second injection. Plasma concentrations of progesterone, oestradiol 17 beta, luteinising hormone, follicle stimulating hormone, and beta-carotene were monitored during this regime as were uterine and ovarian changes. Progesterone profiles were followed for a further 21 days by assay of milk samples. Subsequent rectal examinations showed that five of the 12 cows conceived at controlled oestrus and another four within 52 days of this time. No correlation was observed between time of conception and condition score, metabolic profiles or haematological parameters; there was a correlation between time of conception and plasma beta-carotene concentrations and cows with lower beta-carotene values showed cyclic irregularities or appeared to have depressed steroid hormone production.

Animals↗

Influence of stage of oestrous cycle on time of oestrus following cloprostenol treatment in the bovine.

The first of 2 injections of 0.5 mg cloprostenol (PG1 and PG2) eleven days apart was given to 19 Friesian-Hereford cross heifers between days 8-14 of their cycle (Treatment A) and 16 similar animals between days 0-4 (Treatment B). Oestrus show was monitored by Kamar Heat Mount detectors and vasectomised bulls with chin-ball markers. Blood samples taken at PG1, six days later, at PG2 and four days later were assayed for progesterone to confirm that luteolysis had occurred as expected. Four hourly rectal examinations of the ovaries were carried out from 56-112 hours after PG2 and four hourly blood samples from 36-96 hours after PG2 were collected for FSH and LH assay. Mean time in hours from PG2 to oestrus onset, LH peak and ovulation respectively was 57.4 +/- 2.9, 60.2 +/- 2.0, 91.7 +/- 1.8 for Treatment A and 64.9 +/- 4.1, 68.9 +/- 2.4, 96.7 +/- 1.3 for Treatment B. Treatment A animals showed significantly higher (p<0.01) FSH levels at PG2 than Treatment B. Time from PG2 to LH peak was significantly shorter in animals treated either on days 7 and 8 (p<0.01) or days 15-16 (p<0.05) of their cycle compared with treatment on days 12-14 and it is suggested that these shorter response times correspond to an early and late cycle wave of follicular growth. Secondary FSH peaks some 28 hours after that occurring synchronously with the pre-ovulatory LH peak were observed to be significantly (p<0.01) higher at oestrus associated with the early cycle follicular growth wave as compared with that later in the cycle which may argue a difference in endocrine control of the two periods of follicular maturation.

Journal Article↗

Separate roles of androgen and oestrogen in the manipulation of growth and efficiency of food utilization in female rats.

The roles of androgen and oestrogen in the perinatal and postpubertal stages of development on the masculinization of female patterns of growth have been investigated in several experiments in rats. A stimulatory effect of testosterone on subsequent growth and efficiency of food utilization was only observed when administered perinatally to intact females as the propionate ester. Thus females which were untreated (or androgenized) perinatally and ovariectomized at weaning failed to grow more rapidly or utilize food more efficiently when treated with mixed testosterone esters from 36 to 38 days of age. Also autoimmunity to luteinizing hormone releasing hormone (LH-RH) had little effect on the growth or efficiency of food utilization of male rats, although testicular development was grossly affected. An inhibitory effect of oestrogen on subsequent growth and efficiency of food utilization was demonstrated by surgical ovariectomy and by autoimmunity to LH-RH. Also perinatal administration of oestradiol benzoate to intact female rats depressed growth below that of untreated intact litter-mate females until about 50 days of age. Then oestradiol benzoate-treated female rats grew to a larger size than untreated intact litter-mates but not to a heavier weight than untreated litter-mate females which like the oestradiol benzoate-treated females, were ovariectomized at 18-21 days of age. Both of these groups of female rats differed markedly in weight gain from females which were perinatally androgenized and ovariectomized at weaning. The effects of androgenization and ovariectomy on weight gain were comparable and additive in female rats fed restrictedly or ad libitum. Nevertheless, androgenized + ovariectomized female rats fed restrictedly or ad libitum failed to grow as rapidly as male rats. Some additional factor(s) prevents complete masculinization of the female pattern of development. The stimulatory effects of androgenization and ovariectomy on the growth of females appear to be related to endocrine mechanisms controlling the onset of pubertal changes in somatic development.

Androgens↗

Synthesis and biological activity of highly active alpha-aza analogues of luliberin.

Analogues of luliberin containing an alpha-azaamino acid in position 6, 9, or 10 (I--XIV) have been synthesized by the solution method of peptide synthesis. Two nonaza analogues, [D-Phe6]- and [D-Ser(But)6,des-Gly-NH2(10),Pro-ethylamide9]luliberin, were also synthesized for comparison. The ovulation-inducing activity of the compounds was evaluated in androgen-sterilized constant-estrus rats. A combination of D-amino acid replacement in position 6 with an azaglycine residue at position 10 resulted in highly active compounds which were superior to the corresponding nonaza analogues. The most active compoungs, [D-Phe6,Azgly10-a1-, [D-Tyr(Me)6,Azgly10]-, and [D-Ser(But)6,Azgly10]luliberin, were about 100 times as potent as luliberin. N-Methylleucine substitution in position 7 in these compounds resulted in decreased activity; [D-Phe6,MeLeu7,Azgly10]- and [D-Tyr(Me)6,MeLeu7,Azgly10]luliberin were only 50 times as active as luliberin. The presence of either an azaproline residue in position 9, an azaphenylalanine or azaglycine residue in positions 6 and 10, or a tert-butyl ether protecting group on the hydroxyl group of the tyrosine residue in position 5 resulted in compounds with significantly reduced biological activity.

Amino Acid Sequence↗