Oral progestagen treatment extends the weaning-to-estrus interval (WEI) in weaned sows. Particularly in lower parity sows, this allows recovery from lactational catabolism and improves sow productivity. However, the optimal duration of progestagen treatment in contemporary dam-line sows is unclear. Therefore, sows (n = 749) weaned over consecutive 3-wk periods in June and July and classified as parity 2 and 3 (P2-3); 4, 5, and 6 (P4-6); or parity 7 or higher (P7+) were organized into 2 breeding groups using 1 of 3 strategies: 1) oral progestagen for 2 d before and 12 d after weaning (M14; n = 249); 2) oral progestagen for 2 d before and 5 d after weaning (M7; n = 250); or 3) no progestagen treatment (M0; n = 250). Progestagen (altrenogest) was administered directly into the sow's mouth at a dosage of 6.8 mL (15 mg of altrenogest) daily. Sows were bred using artificial insemination at first detection of estrus after weaning (M0) or altrenogest withdrawal, and every 24 h thereafter, until they no longer exhibited the standing reflex. The WEI for M0 sows was 5.1 +/- 0.1 d. Estrus was recorded sooner (P < 0.001) after withdrawing treatment in M14 than in M7 sows (6.9 +/- 0.1 vs. 7.4 +/- 0.1 d, respectively). More (P < 0.001) M14 sows (88.6 +/- 2.5%) were bred within 10 d of altrenogest withdrawal than M7 (72.8 +/- 2.8%) sows, or within 10 d of weaning in M0 sows (78.8 +/- 2.6%). Reproductive tracts were recovered after slaughter at d 30 or 50 of gestation. For P2-3 sows, ovulation rate (least squares mean +/- 95% confidence interval) in M7 (23.1 +/- 1.0) was greater (P < 0.001) than in M14 (20.7 +/- 1.0) or M0 (19.7 +/- 1.0) sows; no differences were detected in P4-6 and P7+ sows. At d 30, M7 and M14 sows had more (P < 0.01) embryos (16.4 +/- 0.6 and 15.8 +/- 0.4, respectively) than M0 (13.9 +/- 0.5) sows. At d 50 of gestation, number of fetuses in M14 sows (13.6 +/- 0.4) was greater (P < 0.001) than in M0 (11.8 +/- 0.4) and M7 (12.2 +/- 0.3) sows. Use of oral progestagen to delay the return to postweaning estrus for greater than 18 d appears to have potential for improving weaned sow productivity. Given the incidence of high ovulation rates and associated evidence of intrauterine crowding of embryos around d 30 of gestation, the changing dynamics of prenatal loss resulting from longer periods of progestagen treatment may represent an additional production advantage.

The effects of feed restriction (60% of anticipated feed intake; Restrict; n=60) during the last week of a 21-day lactation in primiparous sows compared with feeding at 90% of anticipated feed intake (Control; n=60) on sow metabolic state, litter growth and sow reproductive performance after weaning were compared. Metabolisable energy (ME) derived from feed was lower, ME derived from body tissues was higher and litter growth rate was reduced (all P<0.05) in Restrict sows during the last week of lactation. Treatment did not affect weaning-to-oestrus interval, pregnancy rate, ovulation rate, embryonic survival or the number of live embryos (P>0.05) at Day 30 of gestation: However, embryo weight was greater (P<0.05) in Control than in Restrict sows (1.55±0.04vs 1.44±0.04g, respectively). These data suggest the biology of the commercial sow has changed and reproductive performance of contemporary primiparous sows is increasingly resistant to the negative effects of lactational catabolism. Overall, catabolism negatively affected litter weaning weight and embryonic development of the next litter, but the extent to which individual sows used tissue mobilisation to support these litter outcomes was highly variable.

e17528 Background: First primary tumors (FPT) generally are associated with decreased survival and, thus, reduced risk of second primary tumors (SPT). A greater than expected incidence of SPT may indicate causal factors shared in common with a particular FPT, especially if the converse also is observed, i.e. if incidence is also greater than expected when tumor sequence is reversed. We analyzed the Surveillance, Epidemiology, and End Results (SEER) cancer registry to identify tumors with higher than expected incidence in relation to PCa, both as FPT and SPT. Methods: We searched the SEER18 cancer database covering 18 geographical regions of the U.S. from 2000 to 2016. SEER*Stat software v.8.3.6 was used to calculate standardized incidence ratios (SIR) of various SPT after defined FPT. SIR compare the incidence of a particular cancer within subsets of the registry population as a ratio to the expected incidence from a comparable matched group derived from the general population. 813,712 men with prostatic FPT (1° PCa) were included in the analysis for SIR of any SPT, while 2,554,835 men with any FPT were included in the analysis for SIR of prostatic SPT (2° PCa). Results were stratified by race and latency. Reciprocal SIR (1° PCa; 2° PCa) for values with p < 0.05 are reported. Results: Aggregate analysis of all tumors demonstrated lower than expected SIR for SPT, both for any SPT after 1° PCa and for 2° PCa after any FPT (0.69; 0.53). By contrast, six tumor subtypes – small intestine (1.17; 1.19), melanoma (1.05; 1.23), bladder (1.14; 2.02), kidney (1.22; 1.36), thyroid (1.27; 1.36), and chronic myelogenous leukemia (1.10; 1.15) – had bidirectionally increased secondary SIR in relation to PCa. The reciprocal increases were detected across racial subgroups for bladder, kidney and thyroid cancers. SIR tended to be highest in the early post-FPT period (2-11 mo.) with significant increases for bladder (1.49; 6.75), kidney (2.66; 1.87), and thyroid (1.61; 1.65) cancers. These three tumor types retained bidirectional increases in relation to PCa over intermediate latencies (12-119 mo.), but not beyond 120 mo. Conclusions: Overall, FPT were associated with lower than expected incidence of SPT, most likely as a result of shortened life expectancy. However, several tumors were identified that 1). occurred with higher than expected incidence after 1° PCa and 2). were associated with higher than expected incidence of 2° PCa. Further examination of the relationship of these tumors with PCa may identify mutual intrinsic or extrinsic factors that contribute to tumor development.