The effect of different postweaning altrenogest treatments of primiparous sows on follicular development, pregnancy rates, and litter sizes.

This study investigated follicular development during and after postweaning altrenogest treatment of primiparous sows in relation to subsequent reproductive performance. Primiparous sows (n = 259) were randomly assigned at weaning (d 0) to 1 of 4 groups: control (no altrenogest, n = 71), RU4 (20 mg of altrenogest from d -1 to 2, n = 62), RU8 (20 mg of altrenogest from d -1 to 6, n = 65), or RU15 (20 mg of altrenogest from d -1 to 13, n = 61). Average follicular size (measured by ultrasound) increased during altrenogest treatment and resulted in larger follicles at the start of the follicular phase for RU4, RU8, and RU15 compared with controls (5.3 ± 0.9, 5.5 ± 1.3, 5.1 ± 1.2, and 3.4 ± 0.6 mm, respectively; P < 0.0001). Farrowing rate was greater in RU15 (95%) than in RU8 (76%; P = 0.04). The RU15 group also had more piglets (2 to 3 more piglets total born and born alive; P < 0.05) than the other treatment groups. Follicular development at weaning clearly affected reproductive performance. At weaning, average follicular size: small (<3.5 mm), medium (3.5 to 4.5 mm), or large (≥ 4.5 mm), was associated with farrowing rates of 86, 78, and 48%, respectively (P < 0.001). Sows with large follicles at weaning had low farrowing rates (71%) in RU4, very low farrowing rates (22%) in RU8, but normal farrowing rates in RU15 (83%). In conclusion, this study showed that 15 d of postweaning altrenogest treatment of primiparous sows may allow follicle turnover in sows that had large follicles at weaning and that this was associated with an improved reproductive performance. It also showed that shorter treatment with altrenogest (4 or 8 d) is beneficial for sows with small follicles at weaning, but is not recommendable for sows with large follicles at weaning.

Post-weaning Altrenogest treatment in primiparous sows; the effect of duration and dosage on follicular development and consequences for early pregnancy.

Our objective was to investigate follicle development in sows during and after different Altrenogest treatments post-weaning and relate this to subsequent ovulation rate and embryonic development. Primiparous UPB sows (n=47) were randomly assigned to (weaning=Day 0): control (no Altrenogest, n=12), RU8-15 (15 mg of Altrenogest, Day-1 till Day 7, n=12), RU8-20 (20 mg of Altrenogest, Day-1 till Day 7, n=12) or RU15-15 (15 mg of Altrenogest, Day-1 till Day 14, n=11). From weaning onwards, trans-abdominal ultrasound was performed daily. Sows were slaughtered on Day 4 or 5 after ovulation. Follicle size increased during Altrenogest treatment and reached a plateau around Day 6, regardless of dose (4.6+/-1.5, 4.6+/-1.6 and 4.6+/-1.6 mm for RU8-15, RU8-20 and RU15-15, respectively). This increase resulted in larger follicles (P=0.0002) at the onset of the follicular phase (i.e. time of weaning for control sows and 24h after last administration of Altrenogest for treated sows); 4.8+/-1.8, 4.8+/-1.4, 4.9+/-0.9 mm and 2.9+/-0.8, for RU8-15, RU8-20, RU15-15 and controls, respectively. Pre-ovulatory follicle size tended (P=0.07) to be larger for treated animals (7.9+/-2.4, 7.9+/-0.7, 8.6+/-1.3 and 6.9+/-0.9 mm for RU8-15, RU8-20, RU15-15 and controls, respectively). The interval follicular phase-oestrus was shorter (P=0.005) for treated animals. Treatment did not affect ovulation rate or early embryonic development. However, for treated animals, the increase in follicle size during treatment was positively related with ovulation rate (P=0.05). In conclusion, post-weaning treatment with Altrenogest of first litter sows influenced follicle size and shortened the follicular phase, but did not affect ovulation rate or early embryonic development.

Ligand-based histochemical localization and capture of cells expressing heat-stable enterotoxin receptors.

The heat stable enterotoxins (ST) of enterotoxigenic Escherichia coli (ETEC) cause diarrhoea by binding specific intestinal receptors. Precise histochemical localization of ST receptors could provide more information about the pathophysiology of secretory diarrhoea and the role of ST receptors in normal biology. To accomplish this, we quantitatively coupled biotin to the N-terminus of ST1b using biotin-X-X-N-hydroxysuccinimide ester. The derivatized toxin (BST) has an apparent Kd of 11.7 +/- 10 nM for rat brush border receptors. We used BST in an affinity panning cell-capture system, to validate its ability to discriminate between receptor-positive and receptor-negative cells. Cell lines expressing ST receptors (human colon carcinoma T84, and COS cells transfected with guanylyl cyclase-C (GC-C) ST receptor cDNA) were captured to streptavidin and anti-biotin-coated plates with high efficiency and specificity. This system provides a novel approach to screening cells for the presence of unique ST-binding proteins. BST was then used with streptavidin-gold to demonstrate the cellular topography of ST receptors at the light microscopic level. Villus enterocytes were intensely stained, but only a faint signal was observed in upper crypts of rat small intestine. Thus, a gradient of increasing receptor density was seen as upper crypt cells matured into villus enterocytes. Higher magnification revealed that ST receptors are concentrated at the apical aspect of villus enterocytes. Recently, guanylin, a putative endogenous ligand for ST receptors, has been localized to Paneth cells, at the base of intestinal crypts. Thus, ST receptors are concentrated in villus enterocytes, while guanylin appears to be produced at the base of the crypts.(ABSTRACT TRUNCATED AT 250 WORDS)