<p>This paper presents verbal working memory test results towards establishing the effects of menstrual cycle on working memory of women. The study comprised of a subject-set of twenty healthy young women with a regular 28 – 32 day menstrual cycles. Subjects were tested twice, once during their menstrual phase and second during their ovulation phase (on approximately day 12). Working memory tests were performed in a random sequence i.e. for some subjects during the menstrual phase (low estrogen level) working memory test occurred before their ovulation phase (high estrogen level) memory test and vice versa for other subjects. Study revealed that the test scores in the ovulatory phase were significantly higher than those in the menstrual phase. These findings suggest that higher levels of estrogen may improve working memory. Moreover, effects of estrogen on mood were also considered during both phases of menstruation. The fluctuation in estrogen levels seems to have an effect on women’s mood during menstrual and ovulation phases.</p>

<p>Proteases of the plasminogen activator (PA) and the matrix metalloproteinase (MMP) enzyme systems are expressed in the ovulatory follicle and in the developing corpus luteum (CL). However, the functional role of these extracellular degrading protease systems in the ovulatory and CL development processes remains elusive. The first aim of this thesis was to develop a mouse model to study gonadotropin-induced CL formation. The second aim was to study the involvement of the PA and the MMP systems in gonadotropin-induced ovulation, and in CL formation and function.</p><p>A mouse model for gonadotropin-induced CL formation was developed in order to control the timing of CL formation. In this model, immature mice were induced to ovulate by administrating gonadotropins and the endogenous prolactin surges were mimicked by administration of prolactin twice daily from day 2 of CL development. We observed that steroidogenic acute regulatory protein (StAR) mRNA was highly expressed at days 3 and day 6 of CL development and the levels remained high until late stages of CL regression.</p><p>Since mice lacking plasminogen (plg-/-) only have a 14% reduction of ovulation efficiency, our hypothesis was that the MMP system could compensate for the loss of plasminogen. When administrating the MMP-inhibitor galardin to gonadotropin-primed ovulating mice, we found that wild-type mice (plg+/+ and C67BL/J6) and heterozygous mice (plg+/-) had an 18-20% reduction in ovulation efficiency as compared to untreated mice.</p><p>Two models for CL formation, the adult pseudopregnant (psp) mouse model and a model whereby immature gonadotropin-primed mice were treated with prolactin, were used to study the formation and function of the CL in plg-/- mice treated with galardin. At day 3 of CL development, we found no alterations other than a slightly lower number of CL in plg-/- mice. This is most likely a secondary effect of the lower ovulation efficiency found in these mice. On the other hand, we found a 54% reduction in serum progesterone levels in plg-/- mice and a 37% reduction in the plg+/- mice as compared to wild type mice. At day 6 of CL development we saw a 45 % reduction of serum progesterone level in the plg-/- mice and a 22 % reduction in the plg+/- mice. A similar trend was observed at day 3 of CL development in immature gonadotropinprimed mice treated with prolactin. Galardin treatment did not alter the results significantly and the CLs were healthy and viable in these mice.</p><p>In conclusion, our data suggest that both plasminogen and MMPs, alone or in combination, are dispensable for ovulation and for the formation of a viable CL under the conditions used in this study. The reduced serum progesterone levels observed in the plg-/- mice did not appear to be a result of defective CL formation. Instead, plasmin may have a novel role in the maintenance of luteal function. StAR expression may also be a good marker for CL development and regression in mice.</p>

Thesis (Ph. D.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.

This paper presents verbal working memory test results towards establishing the effects of menstrual cycle on working memory of women. The study comprised of a subject-set of twenty healthy young women with a regular 28 – 32 day menstrual cycles. Subjects were tested twice, once during their menstrual phase and second during their ovulation phase (on approximately day 12). Working memory tests were performed in a random sequence i.e. for some subjects during the menstrual phase (low estrogen level) working memory test occurred before their ovulation phase (high estrogen level) memory test and vice versa for other subjects. Study revealed that the test scores in the ovulatory phase were significantly higher than those in the menstrual phase. These findings suggest that higher levels of estrogen may improve working memory. Moreover, effects of estrogen on mood were also considered during both phases of menstruation. The fluctuation in estrogen levels seems to have an effect on women’s mood during menstrual and ovulation phases.

To investigate the physiological action of follistatin in the swine ovary a recombinant porcine follistatin (rpFS) with apparent molecular weights of 39, 46, 48, and 50 kDa was expressed and characterized. The rpFS crossreacted with antibodies against native porcine follistatin and with activin A. One rpFS isotype was purified by monoclonal antibody affinity chromatography (rp-305 a.a. FS). In porcine granulosa cell cultures, rp-305 a.a. FS suppressed estradiol-17<math> <f> <g>b</g></f> </math> accumulation (ED50 = 0.9 <math> <f> <g>m</g></f> </math>g/ml) independent of activin. Gilts were vaccinated against rpFS to determine the effect of follistatin immunoneutralization on litter size or ovulation rate. In Experiment 1, forty-seven gilts were vaccinated four times with rpFS (FS n = 23) or with a control vaccine (CTL n = 24). The naturally matured, cycling gilts were bred and piglet numbers were recorded at farrowing. FS vaccination did not increase total litter size. However, grouping by low (<math> <f> <=</f> </math>1:400 n = 16) or high anti-follistatin antibody titer (>1:400 n = 7) responses showed an increased litter size in gilts with a high titer (total piglets: FS high titer = 13.0 ± 0.8; FS low titer = 10.8 ± 0.6; CTL 11.4 ± 0.5; p = 0.08). In Experiment 2, sixty-nine gilts were vaccinated three times with rpFS (n = 35) or CTL (n = 34) vaccines. The gilts were induced and synchronized into estrus using PG600, <math> <f> <rm>PGF<inf>2<g>a</g></inf></rm></f> </math> and boar exposure; cycling gilts received a fourth vaccination. Reproductive tracts were collected two weeks after the second observed estrus (FS n = 14, CTL n = 15). FS vaccination did not increase the number of corpora lutea (FS = 13.2 ± 0.5, CTL = 14.5 ± 0.7) or corpora albicantia (FS = 12.1 ± 1.9, CTL = 12.3 ± 2.0), but appeared to effect normal ovarian morphology increasing the number of blood-filled follicles and corpora lutea. In conclusion, rp-305 a.a. FS appears to negatively affect estradiol accumulation 'in vitro'. Vaccination against follistatin in naturally cycling gilts enhanced litter size. Follistatin vaccination of pharmacologically induced gilts did not increase ovulation rate, but biological effects were apparent suggesting that pharmacological induction of estrus may have confounded the follistatin vaccination treatment.

Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 161-197). Also available in print.

Proteases of the plasminogen activator (PA) and the matrix metalloproteinase (MMP) enzyme systems are expressed in the ovulatory follicle and in the developing corpus luteum (CL). However, the functional role of these extracellular degrading protease systems in the ovulatory and CL development processes remains elusive. The first aim of this thesis was to develop a mouse model to study gonadotropin-induced CL formation. The second aim was to study the involvement of the PA and the MMP systems in gonadotropin-induced ovulation, and in CL formation and function. A mouse model for gonadotropin-induced CL formation was developed in order to control the timing of CL formation. In this model, immature mice were induced to ovulate by administrating gonadotropins and the endogenous prolactin surges were mimicked by administration of prolactin twice daily from day 2 of CL development. We observed that steroidogenic acute regulatory protein (StAR) mRNA was highly expressed at days 3 and day 6 of CL development and the levels remained high until late stages of CL regression. Since mice lacking plasminogen (plg-/-) only have a 14% reduction of ovulation efficiency, our hypothesis was that the MMP system could compensate for the loss of plasminogen. When administrating the MMP-inhibitor galardin to gonadotropin-primed ovulating mice, we found that wild-type mice (plg+/+ and C67BL/J6) and heterozygous mice (plg+/-) had an 18-20% reduction in ovulation efficiency as compared to untreated mice. Two models for CL formation, the adult pseudopregnant (psp) mouse model and a model whereby immature gonadotropin-primed mice were treated with prolactin, were used to study the formation and function of the CL in plg-/- mice treated with galardin. At day 3 of CL development, we found no alterations other than a slightly lower number of CL in plg-/- mice. This is most likely a secondary effect of the lower ovulation efficiency found in these mice. On the other hand, we found a 54% reduction in serum progesterone levels in plg-/- mice and a 37% reduction in the plg+/- mice as compared to wild type mice. At day 6 of CL development we saw a 45 % reduction of serum progesterone level in the plg-/- mice and a 22 % reduction in the plg+/- mice. A similar trend was observed at day 3 of CL development in immature gonadotropinprimed mice treated with prolactin. Galardin treatment did not alter the results significantly and the CLs were healthy and viable in these mice. In conclusion, our data suggest that both plasminogen and MMPs, alone or in combination, are dispensable for ovulation and for the formation of a viable CL under the conditions used in this study. The reduced serum progesterone levels observed in the plg-/- mice did not appear to be a result of defective CL formation. Instead, plasmin may have a novel role in the maintenance of luteal function. StAR expression may also be a good marker for CL development and regression in mice.

The objective of this study was to determine the ability of a passive temperature monitoring system consisting of radio frequency identification (RFID) boluses with thermistors and receiver panels to detect ovulation in high performing dairy cows. The twice-daily reticulo-rumen temperature (Trr) acquisitions of 41 early-lactation Holstein dairy cows were analyzed. The data were analyzed using two criteria: six baseline days (2d, 3d, 4d, 5d, 6d, 7d) and four temperature deviations (0.2°C, 0.3°C, 0.4°C, 0.5°C). The best criteria were chosen by selecting the baseline/deviation combination that gave the best positive predictive value (PPV). The system detected 93 true positive and 267 false positive alerts of ovulation, with a monitoring rate (MR) of 47% and a PPV of 46.2%. There were indications that the Cow Temperature Monitoring System could have a future as an ovulation detection aid, but due to the unreliability of the Wi-Fi transmission of acquisitions, more research needs to be conducted before definite conclusions can be drawn.

Factors affecting bovine ovarian responsiveness to stimulation by pregnant mare's serum gonadotropin (PMSG) were studied. Initially, the effects of plasma progesterone concentration on the response were considered using a progesterone-releasing intravaginal device (PRID) to provide an artificial source of the hormone. Due to inherent biological variation in vivo, in vitro methods were developed in which cAMP and progesterone production by granulosa cells were measured. Regardless of the size of the follicles from which the cells originated, PMSG stimulated significant cAMP accumulation. Cyclic AMP production was similar between aspirated granulosa cells and those scraped from the follicle wall, between ovaries with and without a corpus luteum from the same animal, and between follicles from animals early ( 10 days) in their estrous cycles. The PMSG failed to stimulate bovine granulosa cells to synthesize significantly more progesterone than untreated cells. Unlike porcine granulosa cells, bovine cells from antral follicles of any size appeared to luteinize spontaneously in culture. / Hormonal changes in the preovulatory follicle were measured using the PMSG/hCG-treated prepubertal gilt as a model. After hCG administration, follicular fluid levels of cAMP peaked at 4 hr followed 24 hr later by a rise in prostaglandins F and E (PGF, PGE) concentrations which peaked near the expected time of ovulation. Indomethacin injection blocked ovulation and the prostaglandin rise, although the inhibition could be reversed by the administration of PGF(,2)(alpha). Temporal changes in estrone, estradiol-17(beta), progesterone, androstenedione, testosterone and 5 (alpha)-dihydrotestosterone were also measured. / In an effort to decrease endogenous levels of inhibin, thereby increasing endogenous FSH and thence follicular development, heifers, ewes and does were actively immunized against porcine follicular fluid or proteinaceous fractions of bovine seminal plasma. In some animals, plasma FSH concentrations were elevated although ovulation rates and estrous cycle lengths were not altered. / A culdoscopy technique was developed for repeated monitoring of ovarian morphological changes in cows.

It is widely accepted that prostaglandins (PGs), produced via the cyclooxygenase pathway from arachidonic acid, are essential to the ovulatory process in the pig. In support of this, ovulation is preceded by an increase in follicular fluid (FF) PG concentration, indomethacin (INDO) suppresses both the PG increase and ovulation, and ovulation can be restored by administration of exogenous PGs (Downey and Ainsworth, 1980; Prostaglandins 19: 17-22). Recent studies in the rat have shown that ovulation is also preceded by a rise in ovarian concentrations of 15-hydroxyeicosatetraenoic acid (15-HETE), a product of the lipoxygenase pathway (Tanaka et al., 1989; Endocrinology 15: 1373-1377) and inhibition of this pathway suppresses ovulation (Reich et al., 1983; Prostaglandins 26: 1011-1020). Furthermore, INDO, a cyclooxygenase inhibitor, inhibits 15-lipoxygenase as well as PG synthesis (Tanaka et al., 1989 Endocrinology 15: 1373-1377). The PMSG/hCG prepuberal gilt model was used to investigate the involvement of 15-HETE in the procine ovulatory process, and the effect of INDO on the 15-lipoxygenase pathway. Follicular fluid concentrations of 15-HETE were elevated 40 h post hCG (p $<$ 0.01). The effects of INDO and nordihydroguaiaretic acid (NDGA), an inhibitor of lipoxygenase activity, on ovulation rate, FF 15-HETE and FF PGF$ rm sb{2a}$ were investigated by intraovarian administration of INDO or NDGA. INDO inhibited ovulation rate (p $<$ 0.01) and PGF$ rm sb{2a}$ (p $<$ 0.01) as well as 15-HETE (p $<$ 0.01). NDGA also suppressed ovulation rate (p $<$ 0.01) but did not inhibit 15-HETE or PGF$ rm sb{2a}$ production. In in vitro experiments, 15-HETE production by both granulosa cell (GC) and theca interna cell (TIC) cultures 40 h post hCG was greater (p $<$ 0.01) than at 0 h post hCG. INDO inhibited 15-HETE production in 40 h post hCG TIC cultures (p $<$ 0.01) but not GC cultures, while NDGA inhibited 15-HETE production by both cell types (p $<$ 0.01). These results sugges