Ultra-small-angle X-ray scattering from dislocation structures.

Ultra-small-angle X-ray scattering data were obtained from deformed single-crystal aluminium samples. These data are consistent with recent theoretical predictions of scattering from dislocation walls, allowing quantitative microstructural parameters to be extracted.

P53+/- hemizygous knockout mouse: overview of available data.

The performance of the p53-/- transgenic (knockout) mouse model was evaluated through review of the data from 31 short-term carcinogenicity studies with 21 compounds tested as part of the International Life Sciences Institute's (ILSI) Alternatives to Carcinogenicity Testing (ACT) project, together with data from other studies which used comparable protocols. As expected based on the hypothesis for the model, a significant number (12/16 or 75%) of the genotoxic human and/or rodent carcinogens tested were positive and the positive control, p-cresidine, gave reproducible responses across laboratories (18/19 studies positive in bladder). An immunosuppressive human carcinogen, cyclosporin A, was positive for lymphomas but produced a similar response in wild type mice. Two hormones that are human tumorigens, diethylstilbestrol and 17beta-estradiol, gave positive and equivocal results, respectively, in the pituitary with p53-deficient mice showing a greater incidence of proliferative lesions than wild type. None of the 22 nongenotoxic rodent carcinogens that have been tested produced a positive response but 2 compounds in this category, chloroform and diethylhexylphthalate, were judged equivocal based on effects in liver and kidney respectively. Four genotoxic noncarcinogens and 6 nongenotoxic, noncarcinogens were also negative. In total (excluding compounds with equivocal results), 42 of 48 compounds or 88% gave results that were concordant with expectations. The technical lessons learned from the ILSI ACT-sponsored testing in the p53+/- model are discussed.

Proliferative lesions of ovarian granulosa cells and reversible hormonal changes induced in rats by a selective estrogen receptor modulator.

This study assessed the effects of raloxifene, a selective estrogen receptor modulator (SERM), on ovarian morphology and circulating hormone levels in rats. Female Fischer-344 rats (65/group) were given dietary raloxifene for 6 months at average daily doses of 0, 15, 75, and 365 mg/kg. Morphologic evaluation of ovaries was conducted on 25 rats/group at the end of the treatment period and from 20 rats per group after 1 and 3 months withdrawal from treatment. Plasma hormone analyses were conducted on 10 rats pergroup at the end of the treatment period and aftereach withdrawal period. Treatment with raloxifene for 6 months resulted in disruption of the hypothalamic-pituitary-ovarian axis, manifested by increased plasma concentrations of luteinizing hormone (LH) and estradiol-17beta (E2), and failure of ovulation, manifested by ovarian follicular prominence (retained anovulatory follicles), lack of corpora lutea (CL), and depressed plasma progesterone (P4). Many (56% to 80%) rats in all raloxifene treated groups had focal, minimal to slight hyperplasia of granulosa cells within individual retained follicles. A few treated rats in the mid- and high-dose groups (2 of 25 and 3 of 25, respectively) had more extensive focal proliferation of granulosa cells. These foci were approximately 3 to 6 mm in overall size and were characterized by moderate papillary proliferation of large granulosa cells associated with cystic spaces, often with hemorrhage. In 4 of the 5 rats with this focal cystic granulosa cell hyperplasia, the remainder of the involved ovary and the contralateral ovary were atrophic. After 1 or 3 months of drug withdrawal, most previously treated rats examined had morphologic evidence of ovarian cyclic changes. including developing follicles, various stages of CL, and normal plasma levels of LH, E2, and P4. Continued lack of cyclic changes was limited to 4 of 20 rats from the low-dose group after 1 month of recovery and to 1 low dose rat after 3 months. Intrafollicular granulosa cell hyperplasia was not seen in rats in the reversibility phase. Areas of prior focal cystic granulosa cell hyperplasia were represented by focal sclerosis that included hemorrhage and/or hemosiderin. The foci of sclerosis were associated with cystic spaces after 1 month and were solid after 3 months. A granulosa cell tumor, approximately 12-13 mm diameter, was present in a high-dose rat in the 3-month reversibility group. This tumor effaced 1 ovary and was characterized by proliferative granulosa cells, usually in papillary formations and cords within cystic spaces. This rat had atrophy of the uninvolved ovary, excessive plasma levels of E2 and prolactin, and high P4 levels considering the absence of CL. The results of this study indicate that ovarian granulosa cells in rats are susceptible to proliferative changes when stimulated chronically with excessive trophic hormones. Most of these proliferative changes were reversible upon cessation of the hormonal stimulation. However, the proliferative lesion in one treated rat progressed to apparent autonomous (neoplastic) growth.

Proliferative lesions of ovarian granulosa cells and reversible hormonal changes induced in rats by a selective estrogen receptor modulator.

This study assessed the effects of raloxifene. a selective estrogen receptor modulator (SERM), on ovarian morphology and circulating hormone levels in rats. Female Fischer-344 rats (65/group) were given dietary raloxifene for 6 months at average daily doses of 0, 15, 75, and 365 mg/kg. Morphologic evaluation of ovaries was conducted on 25 rats/group at the end of the treatment period and from 20 rats per group after 1 and 3 months withdrawal from treatment. Plasma hormone analyses were conducted on 10 rats per group at the end of the treatment period and after each withdrawal period. Treatment with raloxifene for 6 months resulted in disruption of the hypothalamic-pituitary-ovarian axis, manifested by increased plasma concentrations of luteinizing hormone (LH) and estradiol-17beta (E2), and failure of ovulation, manifested by ovarian follicular prominence (retained anovulatory follicles), lack of corpora lutea (CL), and depressed plasma progesterone (P4). Many (56% to 80%) rats in all raloxifene treated groups had focal, minimal to slight hyperplasia of granulosa cells within individual retained follicles. A few treated rats in the mid- and high-dose groups (2 of 25 and 3 of 25, respectively) had more extensive focal proliferation of granulosa cells. These foci were approximately 3 to 6 mm in overall size and were characterized by moderate papillary proliferation of large granulosa cells associated with cystic spaces, often with hemorrhage. In 4 of the 5 rats with this focal cystic granulosa cell hyperplasia, the remainder of the involved ovary and the contralateral ovary were atrophic. After 1 or 3 months of drug withdrawal, most previously treated rats examined had morphologic evidence of ovarian cyclic changes, including developing follicles, various stages of CL, and normal plasma levels of LH, E2, and P4. Continued lack of cyclic changes was limited to 4 of 20 rats from the low-dose group after 1 month of recovery and to 1 low dose rat after 3 months. Intrafollicular granulosa cell hyperplasia was not seen in rats in the reversibility phase. Areas of prior focal cystic granulosa cell hyperplasia were represented by focal sclerosis that included hemorrhage and/or hemosiderin. The foci of sclerosis were associated with cystic spaces after 1 month and were solid after 3 months. A granulosa cell tumor, approximately 12-13 mm diameter, was present in a high-dose rat in the 3-month reversibility group. This tumor effaced 1 ovary and was characterized by proliferative granulosa cells, usually in papillary formations and cords within cystic spaces. This rat had atrophy of the uninvolved ovary, excessive plasma levels of E2 and prolactin, and high P4 levels considering the absence of CL. The results of this study indicate that ovarian granulosa cells in rats are susceptible to proliferative changes when stimulated chronically with excessive trophic hormones. Most of these proliferative changes were reversible upon cessation of the hormonal stimulation. However, the proliferative lesion in one treated rat progressed to apparent autonomous (neoplastic) growth.

National Institute of Standards and Technology Synchrotron Radiation Facilities for Materials Science.

Synchrotron Radiation Facilities, supported by the Materials Science and Engineering Laboratory of the National Institute of Standards and Technology, include beam stations at the National Synchrotron Light Source at Brookhaven National Laboratory and at the Advanced Photon Source at Argonne National Laboratory. The emphasis is on materials characterization at the microstructural and at the atomic and molecular levels, where NIST scientists, and researchers from industry, universities and government laboratories perform state-of-the-art x-ray measurements on a broad range of materials.

The reversible effects of raloxifene on luteinizing hormone levels and ovarian morphology in mice.

Raloxifene is a selective estrogen receptor modulator that has estrogen agonist effects on bone and serum lipids and estrogen antagonist effects on breast and uterine tissues. This study assessed the effects of raloxifene hydrochloride (HCl) treatment on circulating luteinizing hormone (LH) levels and ovarian morphology in sexually mature, 15-week-old, female CD-1 mice. Mice were maintained on diets providing average daily doses of 0 or 233 mg/kg raloxifene for 2 weeks (Study 1) or 0, 7.9, or 236 mg/kg raloxifene for 4 weeks (Study 2). At the end of the treatment period, blood samples were collected every 2 hours for 24 h in Study 1 (5 mice per group) and at 10:00 a.m. and 10:00 p.m. in Study 2 (8 mice per group). Serum LH levels were measured by radioimmunoassay. Ovarian histomorphology was evaluated in the 10 mice per group (Study 1) and the 8 mice per group (Study 2). For the reversibility phase (Study 2), mice were fed untreated diets for 3 weeks; serum LH levels and ovarian histomorphology were then assessed. Raloxifene treatment at 233 mg/kg/day for 2 weeks (Study 1) significantly elevated circulating LH levels by 4- to 7-fold compared with control. Raloxifene-treated mice had elevated LH levels sustained over the 24-h sampling period and did not exhibit the preovulatory LH surge evident in some control mice at the 4:00 p.m., 6:00 p.m., and 8:00 p. m. time points. Mice treated with 236 mg/day raloxifene for 4 weeks (Study 2) had elevated LH levels (4.4-fold compared to control), whereas mice exposed to 7.9 mg/kg/day raloxifene had a slight, nonsignificant increase in LH (2-fold compared to control). In both dose groups, LH levels were indistinguishable from controls 3 weeks after raloxifene treatment was discontinued. The ovaries in six of the eight mice treated with 7.9 mg/kg/day raloxifene had dilated and/or anovulatory follicles. One mouse in this group had a single hemorrhagic follicle; however, corpora lutea distribution was normal, indicating that ovulation was occurring. Raloxifene-treated mice in Study 1 and mice treated with a comparable raloxifene dose (236 mg/day) in Study 2 had histomorphological changes in the ovary indicative of arrested follicular maturation, including anovulatory hemorrhagic follicles, some developing follicles, and very few corpora lutea. At the end of the reversibility phase, hemorrhagic follicles were no longer evident and follicular maturation and corpora lutea distribution were normal. Raloxifene treatment in mice produces a dose-dependent, sustained elevation in serum LH levels and is associated with changes in ovarian follicular morphology. These changes are reversible upon discontinuation of raloxifene treatment.

Incidence of spontaneous neoplastic and nonneoplastic lesions in Charles River CD-1 mice varies with breeding origin.

Three separate control lifetime studies were conducted with untreated Crl:CD-1 (ICR)BR mice using a total of 400 mice/sex maintained to 21 mo of age. Similar husbandry practices and environmental conditions were used for all 3 studies. It was noted after study initiation that the Charles River breeding facility of origin was different for each study. The aggregate range of survival and incidence of neoplasms for the combined studies was similar to that previously reported. However, these 3 groups of mice had prominent variation in survival and in the incidence of pulmonary adenomas and systemic amyloidosis in males and females, and in the incidence of hepatocellular neoplasms in males. The present studies indicate that consistent procurement of test animals is an additional variable to be considered in the establishment of a valid database within a test facility when using an outbred mouse.

Neuronal vacuolization and necrosis induced by the noncompetitive N-methyl-D-aspartate (NMDA) antagonist MK(+)801 (dizocilpine maleate): a light and electron microscopic evaluation of the rat retrosplenial cortex.

MK(+)801 (dizocilpine maleate) is a noncompetitive antagonist at the N-methyl-D-aspartate (NMDA) receptor, the major glutamate receptor at excitatory synapses in the central nervous system. Since NMDA antagonists are neuroprotective, there is interest in their development for treatment of cerebral ischemia. Unfortunately, many of these compounds also induce vacuole formation in neurons of the rat retrosplenial cortex (Olney et al., Science 244: 1360-1362, 1989). Although vacuolization was initially reported to be reversible with MK(+)801, preliminary data later suggested that higher doses might produce neuronal necrosis. To explore this issue, young male Sprague-Dawley rats were given a single subcutaneous dose of vehicle or 1, 5, or 10 mg/kg MK(+)801. At 4 h and 1, 2, 3, 4, 7, and 14 days postdose (DPD), the retrosplenial cortex was examined by light and electron microscopy. At 4 h, vacuoles occurred in neurons of retrosplenial cortical layers 3 and 4 in all rats given MK(+)801. Mitochondria and endoplasmic reticulum contributed to vacuole formation. At 1 DPD, vacuoles or necrotic neurons were rarely observed. At all subsequent time points, necrotic neurons were readily evident in rats given 5 or 10 mg/kg MK(+)801, but only rarely evident in rats given 1 mg/kg. Necrotic neurons were associated with reactive microglial cells that contained electron-dense debris ultrastructurally. If similar dose-dependent neuronal necrosis proves to be a feature of other NMDA antagonists, such effects might raise concerns for the development and use of these compounds in human cerebrovascular diseases.

Effect of zearalenone on days 7 to 10 post-mating on blastocyst development and endometrial morphology in sows.

First litter sows in naturally occurring post-weaning estrus were hand mated to proven boars and were fed a diet supplemented with zearalenone, an estrogenic mycotoxin (1 mg zearalenone/kg body weight), or a control diet on days 7 through 10 after mating. Embryos (blastocysts) and endometrial biopsies were collected from control and treated sows on days 9, 11, and 13 after mating. All blastocysts harvested on day 9 were spherical; treatment of sows with zearalenone had no effect on blastocyst development. Blastocysts collected from treated sows on day 11 were in stages of elongation comparable to those of blastocysts from control sows but had mild degenerative changes in the embryonic disks, characterized by slightly retarded development and an increase in the number of necrotic cells. Blastocysts collected from treated sows on day 13 were in an advanced stage of degeneration, characterized by circumferential constrictive division, fragmentation, and degeneration and disorganization of the embryonic disk. Feeding zearalenone to pregnant sows had no effect on the normal decrease in height of the endometrial luminal epithelium on days 9 through 13 after mating and no effect on morphologic appearance of secretory vesicles in the endometrial glandular epithelium. The dosage scheme of zearalenone used in this study did not cause any morphologic changes in the endometrium that could be associated with hyperestrogenism.

Evaluation of use of progesterone to counteract zearalenone toxicosis during early pregnancy in gilts.

It has been shown that zearalenone disrupts early pregnancy in swine without altering intrauterine content of estradiol 17 beta or progesterone, embryo migration, or estradiol-17 beta synthesis by blastocysts. However, serum concentrations of progesterone were reduced 2 to 3 weeks after mating in gilts that ingested zearalenone. Therefore, progesterone was administered to gilts during early pregnancy to determine whether it could counteract the detrimental actions of zearalenone on embryonic development. Thirty-two crossbred gilts (Hampshire x Chester White x Yorkshire x Duroc) were assigned randomly to a 2 x 2 factorial arrangement of treatments: zearalenone (Z); zearalenone plus progesterone (ZP); progesterone (P); or control (C). From postmating days 4 to 15, Z- and ZP-treated gilts were fed 1 mg of Z/kg of body weight, and P-treated and C gilts were fed ethanol as vehicle in a corn-soybean diet. On postmating days 3 to 15, P- and ZP-treated gilts were injected IM with 100 mg of progesterone, and C and Z-treated gilts were injected with progesterone carrier (15% ethanol, 15% benzyl alcohol, 70% propylene glycol). Blood was collected from gilts by puncture of the jugular vein daily from days 3 to 15, on alternate days from days 17 to 31, and then twice weekly until the end of the experiment. Fetal development was assessed in Z- and ZP-treated gilts on postmating day 47.6 +/- 2.9 by cesarean section and in P-treated and C gilts at slaughter on postmating days 51.2 +/- 3.2. Serum concentrations of progesterone in P-treated gilts were greater on days 7 to 8, 10 to 15, 17, and 19 than in C gilts. Serum concentrations of progesterone were greater on days 8, 10, and 12 in ZP-treated than in C gilts. However, serum concentrations of progesterone were lower in ZP-treated gilts than in C gilts on postmating days 19 to 31.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of prepubertal consumption of zearalenone on puberty and subsequent reproduction of gilts.

Forty-eight prepubertal gilts (178.7 +/- 4.1 d; 94.2 +/- 4.1 kg), 16 in each of three trials, were assigned randomly to receive 0 (C) or 10 ppm zearalenone (Z) daily in 2.5 kg of a 14% protein finishing ration for 2 wk. Blood samples were collected at 20-min intervals for 4 h 1 wk after the start of the experiment and 1 wk after Z was withdrawn. Two weeks after Z was withdrawn, gilts were exposed to mature boars 15 min per day for 3 wk. Gilts in estrus were mated to two different boars 12 h apart. Twice each week, blood was sampled and analyzed for progesterone to establish age of puberty. Age at puberty differed (P = .008) among replicates but was similar (P = .13) between Z and C gilts within each replicate. Mean serum concentrations of LH were suppressed (P = .025) during consumption of Z (.25 vs .42 ng/ml) but were similar (P = .16) to concentrations in C gilts 1 wk after Z was withdrawn (.35 vs .45 ng/ml). Frequency and amplitude of LH secretory spikes did not differ (P greater than .50) between Z and C gilts during either sampling period. Mean serum concentrations of FSH were similar (P = .25) between Z and C gilts. Number of corpora lutea and live fetuses were similar (P = .29 and P = .94, respectively) between Z and C gilts. Fetal weights were greater (P = .025) and crown to rump length tended to be greater (P = .10) in fetuses from Z gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of zearalenone on early pregnancy in guinea pigs.

Female guinea pigs were tested to determine whether they could serve as a model of zearalenone (ZEN) toxicosis during early pregnancy, as observed in domestic swine. Only 1 of 4 female guinea pigs that were given 21 mg of ZEN/kg of body weight orally during the first 8 days after mating was pregnant when examined 22 days after mating. Guinea pigs that were given 7 or 14 mg of ZEN/kg had normal fetal development. Serum concentrations of progesterone were less than 12 ng/ml in all guinea pigs 8 and 15 days after mating. Serum concentrations of progesterone were greater than 100 ng/ml in pregnant guinea pigs on day 22, but remained less than 12 ng/ml in nonpregnant guinea pigs. Three of 5 guinea pigs treated with 20 mg of ZEN/kg and only 1 of 4 guinea pigs given 30 mg of ZEN/kg on days 1 to 3 after mating were pregnant 22 days after mating. Female guinea pigs treated with 20 or 30 mg of ZEN/kg on days 4 to 5 or 6 to 8 after mating and female guinea pigs treated with 60 or 90 mg of ZEN/kg on days 4 and 5 after mating had normal pregnancies. Serum concentrations of progesterone were less than 10 ng/ml in all guinea pigs on day 15 and remained low on day 22 only in nonpregnant guinea pigs.(ABSTRACT TRUNCATED AT 250 WORDS)

Blastocyst development on days 10 or 14 after consumption of zearalenone by sows on days 7 to 10 after breeding.

Sixteen primiparous sows were bred and fed either a control ration (n = 8) or a diet containing purified zearalenone (n = 8; 1 mg/kg of body weight) from days 7 to 10 after breeding. On day 7 after breeding, the jugular vein of each sow was cannulated and blood was collected at 20-minute intervals for 4 hours before feeding and 4 hours after feeding. On day 10 after breeding, blood samples were collected from 4 control sows and 4 zearalenone-fed sows at 20-minute intervals for 4 hours before collection of blastocysts. A similar blood sampling schedule was followed for the remaining 4 control and 4 zearalenone sows on day 14 after breeding. On day 10 after breeding, spherical blastocysts were recovered from all control sows and from 3 of 4 zearalenone-treated sows. Average diameter of blastocysts from zearalenone-treated sows were similar to that of control sows. On day 14 after breeding, blastocysts were recovered from all control sows and 3 of 4 zearalenone-treated sows. Blastocysts from the control sows were filamentous, whereas blastocysts from zearalenone-treated sows were fragmented and contained foci of necrosis. Incidence of luteinizing hormone (LH) secretory spikes per sow was less (P less than 0.01) in zearalenone-treated sows (0.25 +/- 0.25/4 h) than control sows (1.75 +/- 0.25/4 h) on day 10 after breeding. Incidence of follicle-stimulating hormone (FSH) secretory spikes was similar (P = 0.45) among treatments on days 7, 10, and 14 after breeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of zearalenone and estradiol benzoate on serum concentrations of LH, FSH and prolactin in ovariectomized gilts.

Six ovariectomized gilts were given zearalenone (Z), estradiol benzoate (EB) or vehicle in a replicated 3 x 3 Latin square design. Zearalenone was added to 2.3 kg of a corn-soybean ration at a dose of 1 mg Z/kg body weight; EB was given intramuscularly at 0.1 mg EB/kg body weight. Control gilts received vehicle solvent for both Z and EB. Blood samples were collected from indwelling jugular cannulas at 6-h intervals for 48 h before Z, EB or vehicle was given. After treatment, blood samples were drawn at 6-h intervals for an additional 84 h. Serum concentrations of luteinizing hormone (LH) decreased (P<0.001) from 4.67 ng/ml to 0.29 ng/ml within 6 h of EB. From 54 to 84 h after EB, serum concentrations of LH rose to 15.60 ng/ml (P<0.001). Serum concentrations of LH were reduced (P<0.001) in a similar pattern after Z (3.70 ng/ml to 0.49 ng/ml), but a rise in serum LH was not observed 54 to 84 h after Z (1.30 ng/ml). Serum concentrations of LH remained unchanged (P=0.55) in gilts given vehicle. Serum concentrations of follicle stimulating hormone (FSH) were suppressed (P<0.03) at 6 h in EB (19.10 vs 11.35 ng/ml) and Z gilts (16.16 vs 11.41 ng/ml) but remained unchanged in vehicle gilts. Serum concentrations of FSH did not change in EB or Z gilts during the next 36 h. These data indicate that the suppressive action of Z on serum concentrations of LH and FSH was similar to that of EB, while the biphasic stimulatory effect of EB for LH was not manifested by Z.

Effect of zearalenone on the growth of mouse embryos from blastocysts to the egg cylinder stage in vitro.

Embryos were harvested at the blastocyst stage from nontreated outbred mice and were grown in vitro for 4 days. Embryos cultured in control medium hatched and grew to the egg cylinder stage. Purified zearalenone (ZEN) added to the culture medium at concentrations of 8.5 to 68 micrograms/ml decreased the number of embryos growing, with a 50% decrease in the number growing in 32 micrograms of ZEN/ml of medium. Embryos growing in ZEN had decreased numbers of cells derived from the inner cell mass, normal growth of the trophoblast, less cellular differentiation than was seen in control embryos, and increased numbers of phagosomes. Undifferentiated cells of the inner cell mass of control and treated embryos were of the same size, as determined by morphometric analysis. Addition of 25 micrograms of estradiol/ml of culture medium caused no decrease in number of embryos growing or in embryonic size. Saturation of culture medium with ZEN (68 micrograms/ml) did not inhibit the growth of a tissue culture line of goat synovial cells. Seemingly, ZEN at concentrations near saturation inhibited the growth of mouse embryos in vitro. This effect was not duplicated with similar concentrations of estradiol and was not manifested in culture-adapted cells.

Effect of zearalenone on days 7 to 10 postmating on intrauterine environment and migration of embryos in sows.

On d 7 to 10 postmating, first-litter sows were fed either a control diet or a diet containing zearalenone (ZEN; 1 mg/kg body weight). Surgery was performed on either d 9, 11 or 13 postmating to collect blastocysts and uterine flushings. The rostral and caudal portion of each uterine horn was flushed with phosphate buffered saline, and the blastocysts were separated from the recovered solution. Uterine flushings were analyzed for total Ca, Mg, Zn, estradiol-17 beta (E2 17 beta) and progesterone (P4). Administration of ZEN did not affect the number of blastocysts recovered or the position of embryos within the uterus on d 9 or 11. Blastocysts recovered on d 13 were filamentous and could not be enumerated. Total Ca in uterine flushings of control sows was higher (P less than .001) on d 11 than on d 9 or 13, but intrauterine Ca of ZEN-treated sows did not vary by sampling day (P greater than .05) and was lower (P = .01) than that of controls on d 11. Total intrauterine Mg of ZEN sows was greater (P = .002) than of control sows on d 11 and 13, and total intrauterine Zn of ZEN sows was greater than that in control sows on d 13. There were no differences in total intrauterine P4 or E2 17 beta among ZEN-treated and control sows on d 9, 11 or 13 postmating. Serum concentrations of 13, 14-dihydro-15-ketoprostaglandin F2 alpha (PGFM) increased from d 9 to 13 in control and ZEN-treated sows, but there were no differences between treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)