To compare 2 hormonal protocols for submission of lactating dairy cows for timed artificial insemination (TAI), nonpregnant lactating Holstein cows (n = 269) >60 d in milk were randomly assigned to each of 2 treatments to receive TAI (TAI = d 0). Cows assigned to the first treatment (Ovsynch, n = 134) received 50 microg of GnRH (d -10), 25 mg of PGF2alpha (d -3), and 50 microg of GnRH (d -1) beginning at a random stage of the estrous cycle. Cows assigned to the second treatment (Presynch, n = 135) received Ovsynch but with the addition of 2 PGF2alpha (25 mg) injections administered 14 d apart beginning 28 d (d -38 and -24) before initiation of Ovsynch. All cows received TAI 16 to 18 h after the second GnRH injection. Ovulatory response after each GnRH injection for a subset of cows (n = 109) and pregnancy status 42 d after TAI for all cows were assessed using transrectal ultrasonography. Based on serum progesterone (P4) profiles determined for a subset of cows (n = 109), P4 concentrations decreased for Presynch cows after the first 2 PGF2alpha injections, and Presynch cows had greater P4 concentrations at the PGF2alpha injection on d -3 compared with Ovsynch cows. Although the proportion of cows ovulating after the first and second GnRH injections did not differ statistically between treatments (41.1 and 69.6% vs. 35.9 and 81.1% for Ovsynch vs. Presynch, respectively), pregnancy rate per artificial insemination (PR/AI) at 42 d post TAI was greater for Presynch than for Ovsynch cows (49.6 vs. 37.3%). Parity, DIM, and body condition score (BCS) at TAI did not affect PR/AI to TAI. These data support use of this presynchronization protocol to increase PR/ AI of lactating dairy cows receiving TAI compared with Ovsynch.

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The time-course of uterine growth, cell proliferation, and microvascular development was evaluated during the first 72 h after implanting estradiol-17beta (E2) into ovariectomized (OVX) ewes. Uterine fresh weight increased 2.3-fold by 24 h and increased further (3.3-fold) by 48 h. The majority (approximately 75%) of this growth response was associated with tissue growth rather than a change in the tissue dry weight:fresh weight ratio. Both uterine cell number (DNA content) and cell size (RNA:DNA ratio) increased from 0 to 24 h (1.8-fold and 1.7-fold, respectively). Cell proliferation also increased dramatically between 8 h and 24 h after E2 implantation. Endometrial microvascular volume density (percentage of tissue volume occupied by microvessels) increased approximately 1.8-fold by 24 h and then remained constant or declined slightly through 72 h. The total endometrial microvascular volume, however, increased approximately 5-fold from 0 to 24 h and increased further by 72 h. Thus, treatment of OVX ewes with E2 caused a dramatic increase in uterine fresh and dry weights by 24 h, due primarily to hyperplasia and hypertrophy, with only a relatively small change in tissue dry weight:fresh weight ratio. This dramatic uterine growth was associated with a profound increase in endometrial microvascular volume.

Uterine expression of angiogenic factors (vascular endothelial growth factor [VEGF] and basic fibroblast growth factor [bFGF]) was evaluated in ovariectomized ewes at 0, 2, 4, 8, 24, 48, or 72 h after estradiol (E2) treatment. Endometrial VEGF mRNA increased more than 5-fold from 0 to 4 h, remained elevated at 8 h, and then declined through 72 h after E2 treatment. In contrast, endometrial bFGF mRNA remained constant from 0 to 4 h, increased 2.2-fold from 4 to 8 h, remained elevated at 24 h, and then declined through 72 h. Immunostaining for VEGF was present in myometrial and endometrial microvessels (arterioles, venules, and/or capillaries) and also in myometrial smooth muscle; the pattern of VEGF immunostaining followed that of mRNA expression, being elevated at 4 and 8 h after E2 treatment. Immunostaining for bFGF was present exclusively in uterine glands; the pattern of bFGF immunostaining also followed that of its mRNA, being elevated at 8 and 24 h after E2. On the basis of these observations, we suggest that VEGF and bFGF are probably important factors responsible for the dramatic uterine microvascular response that occurs 8 to 24 h after E2 treatment in ovariectomized ewes.

In the present study, we evaluated whether the nasopharyngeal, ruminal, and vaginal microbiota would diverge (1) in virgin yearling beef heifers (9 months old) due to the maternal restricted gain during the first trimester of gestation; and (2) in pregnant beef heifers in response to the vitamin and mineral (VTM) supplementation during the first 6 months of pregnancy. As a secondary objective, using the microbiota data obtained from these two cohorts of beef heifers managed at the same location and sampled at the same time, we performed a holistic assessment of the microbial ecology residing within the respiratory, gastrointestinal, and reproductive tract of cattle. Our 16S rRNA gene sequencing results revealed that both α and β-diversity of the nasopharyngeal, ruminal and vaginal microbiota did not differ between virgin heifers raised from dams exposed to either a low gain (targeted average daily gain of 0.28 kg/d, n = 22) or a moderate gain treatment (0.79 kg/d, n = 23) during the first 84 days of gestation. Only in the vaginal microbiota were there relatively abundant genera that were affected by maternal rate of gain during early gestation. Whilst there was no significant difference in community structure and diversity in any of the three microbiota between pregnant heifers received no VTM (n = 15) and VTM supplemented (n = 17) diets, the VTM supplementation resulted in subtle compositional alterations in the nasopharyngeal and ruminal microbiota. Although the nasopharyngeal, ruminal, and vaginal microbiota were clearly distinct, a total of 41 OTUs, including methanogenic archaea, were identified as core taxa shared across the respiratory, gastrointestinal, and reproductive tracts of both virgin and pregnant heifers.