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The Animal Sciences Academic Quadrathlon (AQ) provides opportunities for teams of undergraduate animal and dairy science students to participate in regional American Society of Animal Science (ASAS)/American Dairy Science Association (ADSA) meetings and to collectively exhibit their knowledge and talents competitively in 4 categories: 1) solving practical, hands-on, laboratory-type problems; 2) providing written answers to essay-type questions about principles and concepts; 3) preparing and communicating orally and extemporaneously topics of current animal science interest; and 4) quickly responding to short-answer questions provided in the form of double-elimination quiz bowls. Each team is selected by winning the local AQ at their university. Overall and individual category winning teams are recognized, but team rankings are not emphasized. The ASAS/ADSA members provide leadership for organizing and conducting the AQ, and ASAS and each university provide travel expenses for students. The ultimate purpose is to stimulate academic excellence among undergraduate students and for the students to attend ASAS/ADSA regional scientific meetings to meet faculty and students and to attend scientific research presentations. The purpose of this document was to provide a history of the event and to make recommendations for its improvement. The AQ was conceived in 1967. During the next 10 yr, an ASAS committee developed procedures for a trial AQ held in 1980 at the ASAS Midwestern Section, Kansas State University-Manhattan, and in the next year the first official AQ was held at the ASAS Midwestern Section at the University of Nebraska-Lincoln. Starting in 1985, AQ programs were initiated at the other 3 ASAS sectional meetings, and an estimated 50,000 students representing 60 universities have participated in AQ programs since that time. If the AQ is to continue its improvement over time, it will greatly depend on sustained ASAS/ADSA faculty interest and support, as well as greater adherence to the original AQ procedures.

The object of this study was to investigate the role of epidermal growth factor (EGF) and IGF-I in the regulation of preantral follicular growth, antrum formation, and granulosal cell proliferation/ apoptosis. Porcine preantral follicles were manually dissected and cultured for up to 8 d in Waymouth's (Exp. 1) or alpha-minimum Eagle's essential medium (Exp. 2 and 3) supplemented with 10 microg/mL of transferrin, 100 microg/mL of L-ascorbic acid, and 2 mU/mL of ovine FSH, in the presence (Exp. 1 and 3) or absence (Exp. 2) of 7.5% fetal calf serum. According to the experimental protocol, IGF-I (0, 1, 10, or 100 ng/mL; Exp. 1), or IGF-I (50 ng/mL), EGF (10 ng/mL) and EGF+IGF-I (Exp. 2 and 3) were added to the culture media. In Exp. 1, follicles exhibited a concentration-dependent response (P0.05) to IGF-I, with the highest rates of granulosal cell proliferation, follicular integrity, and recovery rate of cumulus cell-oocyte complexes and lowest incidence of apoptosis occurring at the highest IGF-I dose. In Exp. 2 serum-free medium, granulosal cell proliferation was low (1 to 5%), irrespective of whether EGF and/or IGF-I were present and cellular apoptosis was increased (P0.05) on d 4 and 8 in the EGF+IGF-I group compared with the addition of either factor alone. In Exp. 3, granulosal cell proliferation was high in all follicles cultured in serum-containing medium for the first 3 d, but fell sharply (P0.05) on d 4, except in media containing IGF-I. Collectively, EGF and IGF-I increased granulosal cell proliferation, decreased apoptosis, and promoted follicular antrum formation. These results may provide useful information for developing a preantral follicular culture system in which the oocytes are capable of fertilization and embryonic development.

The objective of this study was to determine the effects of recombinant porcine somatotropin (rpST) on placental size, fetal growth, and maternal and fetal IGF-I and IGF-II concentrations. Twenty-four pregnant gilts received daily injections of either 1 mL of saline (control) (n = 12) or 5 mg of rpST (n = 12) from d 30 to 43 of gestation. Gilts were slaughtered on d 44 of gestation, reproductive tracts were removed, and fetal weight and length, placental weight, and implantation length were recorded. There was no effect of rpST on fetal or implantation length. Placental weight increased with rpST administration (71.20 +/- 3.52 vs 58.35 +/- 3.41 g; P.02), as did fetal weight (18.06 +/- .55 vs 16.44 +/- .53 g; rpST vs control, respectively; P.05). Implantation lengths were partitioned into quartiles to determine the effect of rpST on fetuses with different implantation lengths. The effect of rpST of fetal weight was greater in the first quartile (137.5 mm) than in the fourth quartile (240 mm) (16.04 vs 13.86 g compared with 19.47 vs 18.21 g, respectively). Analysis using a modified Brody curve suggests that the effect of rpST treatment on fetal weight is equivalent to the effect of increasing implantation length by 58.8 mm. Administration of rpST numerically raised IGF-I (P = .07) and IGF-II (P = .12) concentrations in fetal serum. Although maternal serum IGF-I concentrations were similar at d 30, treatment with rpST increased these concentrations over time (77.76, 247.75, 267.85 vs 82.59, 79.59, 77.97 ng/mL on d 30, 37, 43, respectively; P.001, SE = 14.09). Maternal IGF-II concentrations were also similar at d 30 but decreased over time with rpST treatment (265.78, 219.61, 191.05 vs 285.44, 284.72, 283.05 ng/mL; P.03, SE = 14.03). Increased maternal IGF-I concentrations may exhibit negative feedback on maternal IGF-II concentrations. The more pronounced effect of rpST on growth in fetuses with shorter implantation lengths suggests that rpST may increase uptake or utilization of nutrients by fetuses. In addition, nutrient transfer across placental membranes may be enhanced by rpST.

The cervix is a barrier for transferring porcine embryos non-surgically. A non-surgical embryo transfer instrument composed of four parts has been developed that allows the delivery of embryos into the lumen of one uterine horn. Part 1, a modified artificial insemination spirette, is used to produce a cervical lock and to assist in manipulating Part 2 through the cervix. Part 2 is made of stainless steel tubing with a unique curved tip that can be manipulated through the folds of the cervix. Part 3 is a testing bar to ensure that the tip of Part 2 reaches the bifurcation of the uterus. Part 4, a disposable tubing complex for embryo delivery, is composed of a soft plastic leader tubing, a double opened connector for embryo loading and unloading, a semi-hard plastic tubing, and a hard tubing with a water-sealable plunger. Embryos (4-cell to blastocyst stages) were surgically collected and maintained in vitro up to 5 h before the non-surgical embryo transfer. Five of 16 recipients became pregnant (31%) and farrowed an average of 6.2 +/- 3.1 pigs per litter. This easily learned non-surgical embryo transfer technique will simplify embryo transfer in the swine industry and may lead to improvements in swine breeding and scientific research.

The effects of somatotropin (ST) on functions of porcine corpora lutea (CL) during pregnancy were investigated. Twenty-four crossbred (Yorkshire/Landrace) gilts from d 30 to 43 of pregnancy were injected daily with 5 mg of recombinant porcine somatotropin (rpST; n = 12) or 1 mL of saline (control, n = 12). Blood was collected on d 30, 37, and 43 for analyses of plasma progesterone. Gilts were killed on d 44 of pregnancy, and mRNA were isolated from CL, ovary, and liver. Messenger RNA expression for LH receptor, FSH receptor, ST receptor, 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), and cytochrome P450 side-chain cleavage enzyme (SCC) were measured. Liver, CL, and ovary contained a 4.7-kb mRNA of ST receptor, but the liver contained more mRNA for ST receptor than did CL or ovary (.97 +/- .18, .47 +/- .04, and .25 +/- .04 units, respectively). There were two variants of LH receptor mRNA in CL (6.8 and 4.4 kb). The CL also contained a 1.8-kb mRNA of SCC and a 1.7-kb mRNA of 3 beta-HSD. No FSH receptor mRNA was detected in CL of the pig. The rpST treatment did not affect the mRNA level of ST receptor, 3 beta-HSD, SCC, or 4.4-kb mRNA of the LH receptor. The 6.8-kb mRNA for the LH receptor was decreased (P < .05) by rpST (.56 +/- .04 vs .78 +/- .05 units). Furthermore, concentrations of plasma progesterone decreased (P < .001) in gilts treated with rpST. Decreased luteal function was associated with decreased expression of LH receptor in rpST-treated gilts. The luteotropic effects of ST observed in vitro do not necessarily occur in vivo when gilts are administered rpST during pregnancy.

During the summer and fall of 1987, sows from eight herds in three states were assigned randomly to receive either a combination of 400 IU of pregnant mare's serum gonadotropin with 200 IU of hCG (P.G. 600) or no treatment at weaning. A treatment x parity interaction was observed for days to first estrus after treatment and percentage anestrus (percentage of sows not achieving estrus within 10 d after weaning). Relative to primiparous control sows, primiparous sows given P.G. 600 expressed estrus sooner (P less than .02) after weaning (6.0 vs 7.8 +/- .6 d) and exhibited less (P less than .02) postweaning anestrus (15.6 vs 29.2 +/- 4.0%). Second parity sows that received P.G. 600 showed estrus sooner (P less than .06) than second-parity control sows (4.7 vs 6.4 +/- .7 d). Days to first estrus after treatment did not differ between groups for parity-three and older sows, and percentage anestrus was not different between treatments for parity-two and older sows. The herd X treatment interaction was significant for percentage recycled (percentage of successfully mated sows that returned to estrus), subsequent farrowing rate, and subsequent number of pigs born dead. Number of pigs born alive was lower for sows treated with P.G. 600 than for control sows (10.55 vs 10.10 +/- .18; P less than .02). In summary, treatment of sows weaned in the summer and fall with P.G. 600 had decreased days to postweaning estrus in parity-one and -two sows and reduced frequency of postweaning anestrus in primiparous sows.

To examine the effect of housing on the ovarian response to exogenous gonadotropins, 51 crossbred gilts were reared in confinement and assigned to a control or a treatment group at an average age of 212 days. Gilts in the control group were maintained in confinement and those in the treatment group were relocated to pasture lots. All gilts were fed a synthetic progestin for at least 19 days, given 1,000 IU pregnant mare serum gonadotropin (PMSG), checked for estrus and then laparotomized 1 to 5 days after estrus for examination of ovarian morphology. After withdrawal of the synthetic progestin and administration of PMSG, 24 of 26 treated gilts and 24 of 25 control gilts exhibited estrus. Single injections of 1,000 IU PMSG resulted in similar numbers of induced follicles and (or) corpora lutea in teated and control gilts. In the second experiment, 43 gilts reared in confinement were assigned to a control or treatment group at an average age of 180 days. Gilts in the control group were maintained in confinement, while gilts in the treatment group were relocated to pasture lots. All gilts were bilaterally ovariectomized, given .25 mg estradiol benzoate and checked twice daily for estrus. The proportion of gilts exhibiting estrus in the control and treatmet groups was 7 of 22 and 15 of 21, respectively (P < .01). The interval from injection of estradiol benzoate to the first day of estrus did not differ significantly between groups. The results indicate that housing in confinement does not affect the ovarian response of gilts to exogenous gonadotropin but that it may reduce the ability of gilts to respond to marginal levels of exogenous estrogen.

To examine the effect of housing on the ovarian response to exogenous gonadotropins, 51 crossbred gilts were reared in confinement and assigned to a control or a treatment group at an average age of 212 days. Gilts in the control group were maintained in confinement and those in the treatment group were relocated to pasture lots. All gilts were fed a synthetic progestin for at least 19 days, given 1,000 IU pregnant mare serum gonadotropin (PMSG), checked for estrus and then laparotomized 1 to 5 days after estrus for examination of ovarian morphology. After withdrawal of the synthetic progestin and administration of PMSG, 24 of 26 treated gilts and 24 of 25 control gilts exhibited estrus. Single injections of 1,000 IU PMSG resulted in similar numbers of induced follicles and (or) corpora lutea in teated and control gilts. In the second experiment, 43 gilts reared in confinement were assigned to a control or treatment group at an average age of 180 days. Gilts in the control group were maintained in confinement, while gilts in the treatment group were relocated to pasture lots. All gilts were bilaterally ovariectomized, given .25 mg estradiol benzoate and checked twice daily for estrus. The proportion of gilts exhibiting estrus in the control and treatmet groups was 7 of 22 and 15 of 21, respectively (P.01). The interval from injection of estradiol benzoate to the first day of estrus did not differ significantly between groups. The results indicate that housing in confinement does not affect the ovarian response of gilts to exogenous gonadotropin but that it may reduce the ability of gilts to respond to marginal levels of exogenous estrogen.

Effects of estradiol benzoate (EB) and zearalenone (Z) on luteal maintenance and plasma hormone concentrations were studied in 45 gilts. Gilts were allocated to receive either 20 mg Z, 2 mg EB or no treatment (C) on d 1 to 5 (T1), 6 to 10 (T2) or 11 to 15 (T3) of an estrous cycle (five per treatment). Onset of estrus was designated as d 0 of the estrous cycle. Zearalenone was added to the daily ration and EB was administered via an intramuscular injection. Blood samples were collected every 10 min over a 4-h period on the first 2 d prior to onset of treatment; the first, third and fifth days of treatment; and the first two and the fifth day after the end of the treatment periods. Gilts receiving EB and Z during T2 and T3 had longer (P less than .05) inter-estrous intervals than C gilts. The range in inter-estrous intervals for Z and EB treatments was 28 to 74 and 27 to 63 d, respectively. Mean plasma progesterone concentrations were elevated (P less than .05) during T2 and T3 in EB and Z-treated gilts when compared with C females. Estradiol benzoate treatment during T2 and T3 reduced (P less than .05) mean plasma luteinizing hormone (LH) concentrations more than C or Z treatments. Mean plasma concentrations of 13, 14-dihydro-, 15-keto-prostaglandin F2 alpha (PGFM) during T3 were higher (P less than .05) in C and Z gilts on d 13 and 15 post-estrus when compared with EB gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

A study was conducted to establish the profile of reproductive hormones and the degree of ovarian activity in gilts fed either 2.5 or 15.0 mg of allyl trenbolone (AT) daily. Progesterone levels following regression of corpora lutea remained low (less than 1 ng/Ml) during progestin treatment. In gilts given 2.5 mg AT, plasma estradiol (E2) levels fluctuated between 7 and 13 pg/ml during treatment and began to decrease by day 2 after withdrawal of AT. Gilts given 15 mg of AT had lower (P less than .01) plasma concentrations of E2 (2.5 pg/ml) during treatment; concentrations began to increase the day after withdrawal of AT, reaching a maximum of 13.1 pg/Ml in 3.5 to 4.0 days. Luteinizing hormone (LH) levels were low (less than 1.5 ng/ml) during AT treatment. Daily feeding of AT prevented estrus in all gilts. A preovulatory surge of LH (4 ng/ml) was observed on the first day of the first post-treatment estrus. Gilts given 2.5 mg of AT daily had more (P less than .01) follicles of ovulatory size during treatment and a higher frequency of cystic follicles after withdrawal than gilts given 15 mg of AT daily. Estrus was effectively synchronized in gilts given 15 mg of AT daily, whereas the feeding of 2.5 mg AT daily resulted in an increased incidence of anestrus.

Hormonal changes during the follicular phase of gilts exhibiting their first estrus were examined in response to either relocation and boar exposure or treatment with pregnant mare serum gonadotropin (PMSG). In the first experiment, blood was collected from nine gilts from 6 d before to 6 d after the onset of first estrus. Mean estradiol-17 beta (E2 beta) concentrations increased from d -6 to a peak on d -2 of 20 pg/ml (d 0 = of estrus) and then declined gradually over the next 6 d until basal levels (2.4 pg/ml) were reached. Mean concentrations of luteinizing hormone (LH) fluctuated between .5 to 1 ng/ml before d 1.5 and after d 1.5, with the ovulatory surge occurring on either d -1 or d 0 and averaging 6.2 ng/ml. Progesterone (P) concentrations were less than .3 ng/ml until formation of corpora lutea, while concentrations of glucocorticoids (CORT) ranged from 7.4 to 24.5 ng/ml. In Exp. 2, blood was collected every 6 h from d -2 to d 14 from eight gilts that were exposed to boars on d 0. Four of the gilts exhibited estrus and had a hormonal profile similar to that of gilts in Exp. 1. Concentrations of E2 beta were elevated in two gilts after exposure to a boar, but concentrations of LH were not altered. The remaining two gilts had basal concentrations of E2 beta and LH throughout the blood sampling period. In Exp. 3, blood was sampled from five gilts twice daily for 8 d following the administration of 1,000 IU PMSG. Estrus was exhibited by all gilts on the fifth day after PMSG. Circulating concentrations of total estrogens peaked on -1 while concentrations of LH peaked on d 0. Concentrations of P were low until after estrus and CORT levels displayed a diurnal pattern throughout. The results indicate that the hormonal profiles during the pubertal follicular phase of gilts induced by relocation and boar exposure or PMSG are similar. Furthermore, no changes were observed in P concentrations immediately before or during the pubertal follicular phase, suggesting that progesterone priming may not be prerequisite to puberty in gilts.

Two trials were conducted to evaluate the effectiveness of a synthetic progestogen, allyl trenbolone, for control of estrus and ovulation in gilts. Estrus was effectively synchronized with 33 of 38 gilts exhibiting estrus 2 to 7 days after last progestogen feeding. There was no effect on fertilization rate in gilts free of ovarian abnormalities. Ovulation rate was higher in gilts fed the progestogen in both Trial 1 (P less than .01) and Trial 2 (P less than .10). Progestogen treatment caused an increase (P less than .01) in the incidence of cystic follicles which resulted in a decrease (P less than .01) in conception rate in Trial 1.

Three experiments were conducted to examine the effect of adrenal corticoids on occurrence of estrus in gilts. In the first experiment, 10 mg of triamcinolone acetonide (TA), a synthetic glucocorticoid, were given to four ovariectomized and five diestrous gilts. Plasma glucocorticoid concentration declined to non-detectable levels within 5 hr of TA administration and remained at this level for 4 days in diestrous gilts and for 6 days in ovariectomized gilts. The second experiment examined the relationship between glucocorticoids and the expression of estrus in thirty-eight ovariectomized gilts. Seven of nine control gilts given .4 mg estradiol benzoate (EB) and three of four gilts given 10 mg TA 2 days before administration of .4 mg EB exhibited estrus. However, only one of four gilts displayed estrus when 10 mg TA were given simultaneously with EB, and none of seven gilts showed estrus after receiving 10 mg TA on days -7, -4, 0 and 4 (day 0 = the day of EB administration). The third experiment was conducted to determine the effect of TA on the expression of first estrus following relocation and exposure to a boar of gilts reared in confinement. Forty-three gilts were randomly assigned to a treatment or control group. Gilts in the treatment group were given 10 mg TA, and gilts in the control group received saline on days -3, 0, 4 and 8 (day 0 = the day of relocation and initial exposure to a boar). Gilts not exhibiting behavioral estrus by day 10 were given 80 IU ACTH. On day 20, all gilts failing to exhibit estrus were subjected to a laparoscopic examination of the reproductive tract and ovaries. Within 20 days after relocation and exposure to a boar, 15 of 21 control gilts and six of 22 treated gilts displayed first estrus (P.01). However, ovarian stimulation had occurred in 10 treated gilts prior to laparoscopic examination. Seven of these gilts had corpora lutea present on the ovaries, two had cystic follicles and one had mature follicles. Therefore, treatment with TA did not alter the proportion of gilts demonstrating ovarian stimulation following relocation and exposure to a boar but significantly reduced the proportion of gilts exhibiting behavioral estrus.

Ten trials involving 678 presumed prepuberal gilts (5.5 to 7.5 mo old) were conducted in North Carolina, Illinois and Missouri to evaluate the reproductive performance of gilts given a combination of 400 IU of pregnant mare's serum gonadotropin and 200 IU of human chorionic gonadotropin (P. G. 600). Gilts that were presumed to be prepuberal received P. G. 600 or no treatment (control) on the day of movement from finishing facilities to pens for breeding. Detection of estrus, with the aid of mature boars, was conducted daily for 28 d; gilts in estrus were mated naturally. Treatment with P. G. 600 increased the percentage in estrus within 7 (57.5 vs 40.9%) or 28 d (72.9 vs 59.5%); average interval to estrus was reduced (P less than .05) from 10.4 to 7.5 d. Farrowing rate (78.5 +/- 3.1%), number of pigs born alive (8.6 +/- .2) or dead (.26 +/- .06) and number of pigs weaned (8.0 +/- .2) were unaffected by treatment. Gilts that were heavier than the median for each farm were in heat sooner and more were detected in heat, but no other reproductive traits differed between heavy and light gilts. Overall, the results reveal that P. G. 600 was useful for induction of fertile estrus in prepuberal gilts.

Records on age at puberty from 1,555 gilts and total number of pigs born in litters of 1,187 gilts from the Nebraska gene pool population were used to evaluate the effects of uterine environment on subsequent reproductive performance. Independent variables were line, year, line x year, proportion of males in the birth litter (sex ratio), number born in the birth litter (fraternity size) and sex ratio x fraternity size. Sex ratio, fraternity size and their interaction influenced age at puberty (P less than .01) but not number born (P greater than .2). Partial regression coefficients indicated that age at puberty tended to decrease as sex ratio increased, particularly in small litters. Although the regression coefficients were relatively large, sex ratio, fraternity size and their interaction accounted for only 1.3% of the variation in age at puberty within line x year subclass. These results offer little encouragement for the use of sex ratio as a phenotypic selection criterion for improvement of reproductive performance in gilts. Results suggest that female swine are similar to rodents in response to uterine environmental effects.