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Two studies were conducted with beef steers to compare the effects of long-acting implants Synovex One (SYN-ONE) and Revalor-XS with each other and with the shorter-acting implant Synovex Plus (SYN-PLUS) on growth performance and carcass quality. Steers (n = 240, initial BW = 384 ± 4.0 kg) in Nebraska were administered SYN-ONE, SYN-PLUS, or Revalor-XS 161 d before slaughter. Steers (n = 300, initial BW = 262 ± 3.6 kg) in Texas were administered the same implants 200 d before slaughter. Each experiment was conducted according to a randomized complete block design with 10 blocks of 3 treatments and pen as the experimental unit. Blocking was based on pretreatment BW, and treatments within a block were assigned to contiguous pens. On d 0, steers were weighed and received assigned implants. Steers were fed finishing diets and were weighed twice more during each experiment and on 2 consecutive days before slaughter in commercial facilities for carcass evaluation. Statistical-analysis models included the fixed effect of treatment and random effects of block and block by treatment interaction and residual; BW and ADG were analyzed as repeated measures. Overall growth performance did not differ (P > 0.05) among implant groups in either location. However, there were differences (P 0.05) among implant groups. It was concluded that the 3 implants were equally efficacious.

Approximately 4,000 yearling heifers (initial BW = 306 ± 1.9 kg) were randomly allotted into 4 treatment groups to determine the effect of melengestrol acetate (MGA) on feedlot performance and carcass parameters. Treatments included a diet containing monensin (Rumensin) and tylosin (Tylan; RT) fed during the entire feeding period; RT plus MGA (RTM) also fed during the entire feeding period; RT withdrawn 35 d preslaughter (RTwd); and RTM withdrawn 35 d preslaughter (RTMwd). All cattle were implanted at arrival with Revalor-IH and reimplanted with Revalor-200, and were fed a standard feedlot finishing diet (that met or exceeded 1996 NRC requirements) for approximately 150 d. Final BW, ADG, hot carcass weight (HCW), DMI, and percentage of cattle grading Choice were greater (P < 0.05) for RTM than for all other treatments. Withdrawal of MGA (RTMwd) significantly (P < 0.01) decreased ADG, HCW, 12th-rib fat thickness, calculated YG, and percentage of carcasses grading Choice, but significantly increased the percentage of dark-cutting carcasses, LM area, and YG 1, 2, or 3 carcasses compared with RTM. There were no significant differences (except for dressing percentage) between RT and RTwd. Heifers continuously fed MGA increased in ADG, HCW, and carcass quality traits of economic importance compared with other treatments. Withdrawal of MGA, Rumensin, and Tylan 35 d preslaughter adversely affected carcass weight and carcass quality traits of economic importance when compared with a feeding program including MGA, Rumensin, and Tylan.

Two commercial feedlot experiments were conducted to determine the effects of feeding melengestrol acetate (MGA) or MGA plus ractopamine (MGA+OPT) on the performance and carcass characteristics of finishing heifers. In Nebraska (Exp. 1), 1,807 heifers (337.3 ± 20.0 kg) and in Texas (Exp. 2), 1,964 heifers (331.5 ± 6.1 kg) were fed 0.4 mg of MGA daily. For heifers fed MGA+OPT, 200 mg of ractopamine was fed daily the last 29 (Exp. 2) or 36 d (Exp. 1). Live and carcass-adjusted performance data were collected. On a carcass-adjusted basis, G:F for the entire feeding period was improved (P 0.47) between treatments in Exp. 1. Carcasses from heifers fed MGA+OPT had decreased marbling scores (P = 0.01) and greater LM area (P = 0.01) than carcasses from heifers fed MGA in Exp. 2. In Exp. 1, in which G:F was improved by 8.1%, no effect on QG was observed. In Exp. 2, in which G:F was improved by 27.2%, QG decreased. Based on these results, feeding MGA+OPT increased ADG and improved G:F, with variable effects on carcass characteristics.

Little research has focused on treatment of cows with subclinical mastitis during lactation. Ceftiofur is a new broad-spectrum, third-generation cephalosporin antibiotic for veterinary use that inhibits bacterial cell wall synthesis by interfering with enzymes essential for peptidoglycan synthesis. Ceftiofur should be effective against a wide range of contagious and environmental mastitis pathogens. Objectives of the present study were to evaluate the efficacy of ceftiofur for treatment of subclinical mastitis in lactating dairy cows, and to determine if extended therapy regimens enhanced efficacy of ceftiofur. Holstein and Jersey dairy cows (n = 88) from 3 dairy research herds were used. Cows were enrolled in the study based on milk somatic cell counts >400,000/mL and isolation of the same mastitis pathogen in 2 samples obtained 1 wk apart. Cows with one or more intramammary infections (IMI) were blocked by parity and DIM and allocated randomly to 1 of 3 different ceftiofur treatment regimens: 2-d (n = 49 IMI), 5-d (n = 41 IMI), and 8-d (n = 38 IMI) treatment regimens. For all groups, 125 mg of ceftiofur hydrochloride was administered via intramammary infusion. Eighteen cows with 38 IMI were included as an untreated negative control group. A bacteriological cure was defined as a treated infected mammary quarter that was bacteriologically negative for the presence of previously identified bacteria at 14 and 28 d after the last treatment. Efficacy of ceftiofur therapy against all subclinical IMI was 38.8, 53.7, and 65.8% for the 2-, 5-, and 8-d ceftiofur treatment regimens, respectively. Four of 38 (10.5%) IMI in control cows were cured spontaneously without treatment. All 3 ceftiofur treatment regimens were significantly better than the negative control, and the 8-d extended ceftiofur treatment regimen treatment group was significantly better than the standard 2-d treatment group. Pathogen groups had significantly different cure rates from one another. The cure rate for the 8-d extended ceftiofur treatment regimen was 70% for Corynebacterium bovis, 86% for coagulase-negative Staphylococcus species, 36% for Staph. aureus, 80% for Streptococcus dysgalactiae ssp. dysgalactiae, and 67% for Strep. uberis.

Growth hormone-releasing factor is the main endogenous stimulator of somatotropin secretion. Our objective was to compare the effects of recombinant growth hormone-releasing factor and recombinant bST on somatotropin secretion, mammary function, and body composition of lactating, primiparous dairy cows. Cows (118 d of lactation) served as uninfused controls or were infused for 63 d with 12 mg/d of releasing factor or with 29 mg/d of bST. These doses elevated somatotropin in serum to concentrations of similar magnitude. The releasing factor and bST each similarly increased milk yield, yield of milk components, weight of most organs, mobilization of adipose tissue, accretion of lean tissue in the carcass, and metabolic activity (RNA) of mammary tissue. Relative to controls, neither releasing factor nor bST significantly affected cell numbers (DNA) in mammary glands or concentrations of plasmin in milk. None of the variables measured provided evidence for galactopoietic effects of releasing factor independent of somatotropin.

Two experiments were conducted to determine the galactopoietic effects of an analog of growth hormone-releasing factor. Specific replacements were made in the AA sequence of growth hormone-releasing factor to produce a growth hormone-releasing factor analog with enhanced stability in vivo. In Experiment 1, 24 Holstein cows were infused i.v. with 0, .33, 1, or 3 mg/d of growth hormone-releasing factor analog for 20 d. Infusion of the analog increased mean serum concentrations of somatotropin, IGF-I, and NEFA. The analog also increased milk yield as much as 44% relative to that of controls. In Experiment 2, 24 Holstein cows were infused i.v. with 0, .11, .33, or 1 mg/d of analog for 60 d. Infusion of analog increased serum concentrations of somatotropin, IGF-I, and NEFA in a dose-dependent manner. At 1 mg/d, the analog increased SCM yield 28% throughout the infusion period relative to the 0 mg/d controls. In summary, a growth hormone-releasing factor analog increased milk yield and serum concentrations of somatotropin and IGF-I. Furthermore, this galactopoietic activity was mediated through the somatotropic axis.

Eight Holsteins per group received 12 mg/d of recombinant growth hormone-releasing factor or 29 mg/d of recombinant bST or served as untreated controls for 60 d. Milk yield and composition were measured for 10 d before infusion, during infusion (d 0 to 59), and for 20 d after infusion ended. Compared with controls, bST and growth hormone-releasing factor increased SCM during infusion. The SCM yield of cows treated with growth hormone-releasing factor was greater than that of bST-treated cows during the final 20 d of infusion. Relative to controls, bST and growth hormone-releasing factor increased serum concentrations of somatotropin and IGF-I during infusion. Concentrations of somatotropin and IGF-I in serum of bST- and growth hormone-releasing factor-treated cows did not differ during infusion. In summary, growth hormone-releasing factor increased SCM yield more than bST, despite similar serum concentrations of somatotropin and IGF-I. Thus, the galactopoietic action of growth hormone-releasing factor was not explained solely by elevation of total radioimmunoassayable somatotropin and IGF-I in serum.

Streptococcus uberis is an important cause of mastitis in dairy cows throughout the world, particularly during the dry period, the period around calving, and during early lactation. Strategies for controlling Strep. uberis mastitis are poorly defined and are currently inadequate. Objectives of the present study were to evaluate efficacy of ceftiofur, a new broad-spectrum cephalosporin antibiotic, for treatment of experimentally induced Strep. uberis intramammary infections (IMI) in lactating dairy cows during early lactation and to determine whether extended therapy regimens enhanced efficacy of ceftiofur. Efficacy of extended ceftiofur intramammary therapy regimens was investigated in 37 mammary quarters of 23 dairy cows that developed clinical mastitis following experimental infection with Strep. uberis during early lactation. Cows that developed clinical mastitis during the challenge period were allocated randomly to 3 groups representing 3 different ceftiofur treatment regimens: 2-d (n = 7 mammary quarters), 5-d (n = 16 mammary quarters), and 8-d (n = 14 mammary quarters) treatment regimens. For all groups, 125 mg of ceftiofur hydrochloride was administered via intramammary infusion. A bacteriological cure was defined as an experimentally infected quarter that was treated and was bacteriologically negative for the presence of Strep. uberis at 7, 14, 21, and 28 d posttreatment. Percentage of Strep. uberis IMI eliminated was 43, 88, and 100% for the 2-, 5-, and 8-d ceftiofur treatment regimens, respectively. Both the 5- and 8-d ceftiofur extended therapy treatment regimens had significantly higher bacterial cure rates than the standard 2-d ceftiofur treatment regimen. The bacterial cure rate of the 8-d ceftiofur extended therapy group was marginally better (P = 0.052) than the 5-d ceftiofur extended therapy group. Results of this study indicate that ceftiofur therapy was effective for eliminating Strep. uberis experimental IMI, and 5- and 8-d extended ceftiofur therapy regimens were more effective than the standard 2-d treatment.

The hormonal and nutritional modulation of hepatic arginase activity (HARG) was characterized in growing cattle in two studies. In the first study, 20 steers (initial weight, 182 ± 2 kg) were assigned in equal numbers to either Synovex-S (SYN) (ear implant), recombinant bovine somatotropin (Somavubove; SbV; 0.1 mg/kg intramuscularly daily), SYN + SbV, or nothing (control). Steers were individually fed, for 56 d, a concentrate (80% diet dry matter [DM]) and silage (20% diet DM) diet providing 20 g of crude protein (CP) and 252 kcal metabolizable energy (ME) per kg body weight 0.75 . On Day 57, samples of liver were obtained at slaughter and subsequently assayed for HARG by the incubation of a tissue homogenate for 2 hr with 250 mM arginine, with and without Mn 2+ and heat activation, and the measurement of the resulting urea. HARG was uniformly increased by divalent cation (Mn 2+) and heating. SYN had no effect on HARG, whereas SbV treatment resulted in an overall 34% decrease in HARG. Plasma urea nitrogen (PUN) was decreased by SbV but not consistently affected by SYN. In the second study, 16 steers (avg. initial weight, 284 ± 5 kg) were initially fed a concentrate basal diet consisting of 11% CP and 1.96 Mcal ME for 21 d. Steers were then assigned to one of four dietary treatments (6.4 kg DM/hr per day) in a factorial arrangement of high and low CP (8 and 14%) and two levels of energy (1.96 and 2.67 Meal ME/kg of diet DM) for 210 d and slaughtered. HARG and PUN were higher in steers fed 14% CP but were lower at each level of CP fed at the higher level of ME. The data suggest that hormonal repartitioning compounds and diet composition may modulate nitrogen metabolism by affecting the activity of arginase in the liver as well as by affecting the total content of arginase in association with changes in organ size.

Lactating, primiparous Holstein cows were continuously infused for 63 d with either recombinant growth hormone-releasing factor or recombinant bST or were not infused (control). The releasing factor and bST treatments reduced fat synthesis from acetate and lipoprotein lipase activity in omental adipose tissue. Also, both treatments increased hormone-sensitive lipase activity per gram of adipose tissue and reduced fatty acid esterification per milligram of protein in adipose tissue. Protein concentration in adipose tissue with both treatments was greater than that of the control, although the protein concentration was less in adipose tissue from cows treated with the releasing factor than from those treated with bST. In mammary tissue, releasing factor increased fat synthesis from acetate more than did bST treatment, but percentages of fat or short-chain fatty acids in milk were not different between treatments, nor were differences significant between treatments and control for fatty acid esterification or lipoprotein lipase activity in mammary tissue or gluconeogenesis and fatty acid esterification in liver. We conclude that protein concentration was lower in omental adipose tissue of cows treated with releasing factor than that in tissue of cows treated with bST, although both treatments similarly suppressed synthesis of fat from acetate and activity of lipoprotein lipase.

Our objective was to compare the effects of recombinant bovine growth hormone-releasing factor and recombinant bST on the somatotropic cascade in lactating dairy cows. Primiparous cows were killed after 63 d of continuous daily infusion with 12 mg of releasing factor or 29 mg of bST or no infusion (controls). Both hormone infusions similarly increased mean concentration of somatotropin in serum, but pulsatility of somatotropin in serum was greater for cows given releasing factor. Both hormone infusions increased the amounts of IGF-I in serum, IGF-I mRNA in liver, and IGF-binding protein-3 in serum and decreased IGF binding protein-2 in serum, but these effects were less for cows given releasing factor than for those given bST. Both infusions decreased the number of free binding sites for IGF-I in mammary tissue. In liver, treatment did not alter the abundance of mRNA for the somatotropin receptor or the number of free binding sites for somatotropin. Results suggest that endogenous somatotropin is less effective as an IGF-I secretagogue than is exogenous bST infused continuously, yet the releasing factor and bST increased milk yield similarly. We conclude that growth hormone-releasing factor stimulates milk synthesis mostly through the same mechanisms as bST, but that serum IGF-I alone is not a good indicator of the galactopoietic potency of the two hormones.

Holstein cows received 12mg/d of growth hormone-releasing factor (continuous i.v. infusion, n=5), 14mg/d of bST (single daily i.m. injection, n=8), or no treatment (controls, n=8) for 60 d. Compared with controls (31.6kg/d), bST and growth hormone-releasing factor increased milk yield to 34.2 and 37.0kg/d, respectively. The increase in milk yield induced by the growth hormone-releasing factor was greater than that for bST. Milk yield was not different among groups following cessation of treatment. Milk energy output was 24.2Mcal/d in controls, and growth hormone-releasing factor increased milk energy output to 28.5Mcal/d. Milk energy output of cows receiving bST was 26.1Mcal/d. Growth hormone-releasing factor increased DMI (23.2kg/d) over that of controls (21.1kg/d), whereas bST (21.5kg/d) did not. Relative to controls, bST increased averaged daily serum somatotropin from 1.3 to 7.6ng/ml and insulin-like growth factor-I from 67.5 to 116.0ng/ml. Relative to bST, growth hormone-releasing factor increased serum somatotropin to 16.3ng/ml and insulin-like growth factor-I to 202.6ng/ml. Relative to control (115.8meq/dl) and bST (158.1meq/dl), growth hormone-releasing factor increased plasma NEFA (230.3meq/dl). During treatment, calculated energy balance was negative for cows receiving growth hormone-releasing factor but positive for bST and control cows. Milk composition, body condition score, BW, and apparent digestibility of DM were not different among treatments. We conclude that i.v. infusion of 12mg/d mg of growth hormone-releasing factor has greater galactopoietic activity than i.m. injections of 14mg/d of bST. These data support the concept that the galactopoietic effects of growth hormone-releasing factor are mediated via increased secretion of somatotropin and insulin-like growth factor-I.

Twenty-four Holstein cows were infused intravenously with sterile water (placebo) or 1, 3, or 12 mg of recombinant bovine somatotropin-releasing factor 1-45-homoserine lactone/d for 60 d. Relative to placebo (22.8 kg/d), 3 and 12 mg of somatotropin-releasing factor increased yield of milk to 28.8 and 33.3 kg/d during infusion. At 1 mg of somatotropin-releasing factor, milk averaged 27.5 kg/d during infusion but was increased above placebo only through 39 d. After infusion of 12 mg somatotropin-releasing factor ended, milk (26.4 kg/d) remained above placebo amounts (20.6 kg/d) for 15 d. Three and 12 mg of somatotropin-releasing factor increased serum somatotropin from .7 (placebo) to 8.2 and 10.3 mg/ml when averaged across 1, 30, and 59 d, whereas 1 mg increased somatotropin to 5.8 ng/ml after 1 d but had no effect at 30 or 59 d. Within 17 h of cessation of somatotropin-releasing factor infusion, serum concentrations of somatotropin were similar across all groups. On d 59, 3 and 12 mg infusions increased insulin-like growth factor I from 115.8 (placebo) to 204.7 and 261.4 ng/ml of serum. We conclude that somatotropin-releasing factor increased serum concentrations of somatotropin and milk yield in a dose-dependent manner for at least 60 d. Also, galactopoietic effects of somatotropin-releasing factor persisted for 15 d independent of increased concentrations of somatotropin in serum following withdrawal of somatotropin-releasing factor.

Intravenous infusion of growth hormone (GH)-releasing factor (GRF) sustains elevated serum GH for at least 5 days in young Holstein steers, but the effects of extended infusion of GRF on serum GH and nitrogen (N) metabolism have not been determined. Thirteen Dutch-Friesian bull calves (148 +/- 1.5 kg) were assigned randomly to receive daily either 0 or 3.6 mg GRF (hGRF1-44NH2; U-68420) in saline as a continuous infusion for 20 days. Calves were fed milk replacer twice daily while housed indoors in wooden-slatted floor box crates (metabolism cages). Nitrogen determinations were made on daily feed, feces, and urine samples which were pooled for days 9 to 14 of treatment. Concentrations of GH were quantified in blood samples collected at 20 min intervals for 8 hr on day 1, 10 and 20. The infusion of GRF increased baseline GH (P less than .07), the number of GH pulses (P less than .0001), the amplitude of the GH pulses (P less than .001), and area under the GH response curve (P less than .0002). Within GRF-infused calves baseline GH (P less than .0001) and area under the GH response curve (P less than .006) were greater on day 20 than on day 1 or 10 (day X treatment interaction, P less than .04). Area under the GH response curve was similar on each sampling day in saline-infused calves, but baseline GH was higher (P less than .03) on day 20 than either day 1 or 10. Infusion of GRF increased episodic GH secretion in spite of limited pulsatile activity in saline-infused calves.(ABSTRACT TRUNCATED AT 250 WORDS)

In a first experiment growth hormone was determined in serum of lactating cows infused intravenously with bovine growth hormone-releasing factor for 24 h. Concentrations of growth hormone increased 5 times above placebo after 3.125, 6.25, 12.5, 25.0, or 50.0 mg releasing factor/cow per 24 h. Releasing factor increased the pulsatile nature of growth hormone release. In a second experiment we determined effects of intravenous infusions of releasing factor for 20 d on growth hormone and lactation in primiparous cows (n = 5/treatment; 144 +/- 7 d after parturition). Milk yield of placebo-infused cows averaged 26.5 +/- 1.7 kg/d during d 6 to 20 of infusion. Infusions of 1 and 3 mg releasing factor/cow per 24 h increased milk yield 11 and 23%, respectively. Releasing factor had only small effects on milk composition, net energy intake, and BW. Releasing factor did not affect energy efficiency of milk production (energy output in milk per unit of net energy intake) when corrected for BW changes. Average growth hormone across d 1, 10, and 19 of infusion was 2.1, 4.1, and 6.8 ng/ml serum for placebo, 1, and 3 mg releasing factor, respectively. Infusions of bovine growth hormone-releasing factor: 1) increased mean and pulsatile release of growth hormone during 24 h and 20 d, 2) increased milk yield in a dose-dependent manner, and 3) did not affect BW-corrected energy efficiency of milk production.

Serum growth hormone was determined in lactating cows following repeated intravenous injections of growth hormone-releasing factor. A given dose was injected every 4 h for 24 h in a 4 (cow) X 4 (d) Latin square. Growth hormone increased similarly above controls after 10, 20, or 40 micrograms releasing factor/100 kg body weight. In another experiment the effects on lactational performance and growth hormone responses of cows to repeated injections of releasing factor for 10 d were determined in a 2 (cow) X 2 (period) Latin square crossover. Administration of 20 micrograms releasing factor/100 kg body weight to 16 Holstein cows (lactating 4.5 to 7.5 mo) every 4-h for 10 d increased milk yield from 25.4 to 27.7 kg/d and increased total fat, protein, and lactose 11% above controls. Releasing factor did not affect milk composition or feed intake. Peak growth hormone response to releasing factor was similar between d 1 (19.9 ng/ml) and 10 (24.4 ng/ml). Exogenous growth hormone-releasing factor administered to lactating Holstein cows at the doses tested: 1) increases growth hormone consistently, although the response is not dose dependent, 2) is galactopoietic, 3) causes an apparent increase in feed to milk conversion, and 4) increases growth hormone to at least the same magnitude on d 10 as on d 1.

(1823). LXXVII. On Mr. Groombridge's Tables of Vesta. The Philosophical Magazine: Vol. 61, No. 301, pp. 375-375.