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Introduction: It is becoming more evident that hormone balance is not only vital to a healthy lifestyle, but necessary for health, vitality and longevity. Men and women alike suffer from [...]

C-reactive protein (CRP) is a widely used, sensitive biomarker of inflammation. Studies conducted among users of exogenous hormones suggest that estrogen increases CRP, whereas progesterone decreases CRP. Examinations of CRP in normally cycling women suggest the opposite: CRP is negatively associated with endogenous estrogen and positively associated with endogenous progesterone. This work evaluates the association between menstrual cycle-related hormone changes and events (menstruation and ovulation) and CRP. Eight female subjects gave urine and blood samples from twelve days across the menstrual cycle, for a total of eleven cycles. Blood samples were assayed for CRP; urine samples for [beta]-follicle stimulating hormone [beta]FSH), pregnanediol 3-glucuronide (PDG), and estrone glucuronide (E1G). Ovulation day was estimated using hormone levels. Presence or absence of menses was reported by subjects. Analyses were conducted with random-effects linear regression. All cycles were ovulatory; day of ovulation was identified for nine cycles. A ten-fold increase in progesterone was associated with a 23% increase in CRP (P = 0.01), a ten-fold increase in estrogen was associated with a 29% decrease in CRP (P = 0.05), and menses was associated with a 17% increase in CRP (P = 0.18); no association between ovulation or FSH and CRP was found. Hormone changes across the menstrual cycle should be controlled for in future studies of inflammation in reproductive-age women. KEY WORDS inflammation; estrogen; progesterone; biomarker

There are two major subtypes of human breast cancers: the luminal, estrogen, and progesterone receptor-positive, cytokeratin 18-positive (E[R.sup+]P[R.sup+]CK[18.sup+]) subtype, and the basal E[R.sup-]P[R.sup-]CK[18.sup-]CK[5.sup+] subtype. Tumor-initiating cells (CD[44.sup+]) have been described for human breast cancers; whether these are common to the two subtypes is unknown. We have identified a rare population of cells that are both CD[44.sup+] and E[R.sup-]P[R.sup-]CK[5.sup+] in luminal-like E[R.sup+]P[R.sup+] T47D human breast tumor xenografts. The tumor-isolated CD[44.sup+] cell fraction was highly enriched for clonogenic (in vitro culture) and tumorigenic (in vivo reimplantation) cells compared with the CD[44.sup-] cell fraction. Rare E[R.sup-]P[R.sup-]CK[5.sup+] cells were present within CD[44.sup+]-derived colonies. Tumor-isolated cells placed in minimal media also contained rare E[R.sup-]P[R.sup-] CK[5.sup+] cells at early time points ( cancer stem cell | cytokeratin 5 | estrogen receptor | progesterone receptor

August-Copenhagen-Irish (ACI) rats are unique in that the ovaryintact females develop high incidence of mammary cancers induced solely by hormones upon prolonged exposure to high levels of estrogen alone. Studies have also shown that such prolonged exposure to high-dose estrogen results in human-like aneuploid mammary cancers in ovary-intact ACI rats. To determine the role of progesterone in mammary carcinogenesis, six-week-old intact and ovariectomized ACI rats were continuously exposed to low- and high-dose estrogen alone, progesterone alone, low-dose estrogen plus progesterone, and ovariectomized ACI rats with high-dose estrogen plus progesterone. Also, ovariectomized ACI rats were treated with high-dose estrogen plus progesterone plus testosterone to determine the role of the androgen, testosterone, if any, in hormonal mammary carcinogenesis. The results indicate that continuous exposure to high, but not low, concentrations of estrogen alone can induce mammary carcinogenesis in intact but not in ovariectomized rats. Mammary carcinogenesis in ovariectomized ACI rats requires continuous exposure to high concentrations of estrogen and progesterone. The addition of testosterone propionate does not affect tumor incidence in such rats. These results suggest that both ovarian hormones estrogen and progesterone are necessary for mammary carcinogenesis induced solely by hormones in ovariectomized ACI rats. Our results are in agreement with the Women's Health Initiative studies, where treatment of postmenopausal women with estrogen (ERT) alone did not increase the risk of breast cancer, but estrogen and progesterone (HRT) did.

Progesterone and estrogens play key roles in regulating various physiological phenomena related to normal growth, development, and reproduction of domestic animals. This review focuses on the mechanisms by which progesterone and estrogens regulate the reproductive processes in these animals. The majority of research on the actions of progesterone and estrogens on the reproductive systems of cattle, sheep, and pigs has been genomic in nature and represents attempts to better understand how these steroids regulate gene expression. Results of recent research suggest that progesterone and estrogens can alter target cell responses nongenomically via membrane receptors. The characteristics of membrane receptors for progesterone and estrogen in various cell types are described and the intracellular signal pathways defined. Estrogens acting via membrane receptors can suppress LH secretion by gonadotropes and stimulate rapid increases in uterine blood flow. Progesterone acting via a membrane receptor has been shown to inhibit binding of oxytocin to oxytocin receptors in isolated endometrial plasma membranes and stimulate capacitation of spermatozoa. Results of research suggest that progesterone and estrogens can act nongenomically to alter target cell responses in domestic animals. The biological implications of this mode of action in these animals are discussed. Key words: estradiol-17[beta], luteinizing hormone, membrane receptor, oxytocin, progesterone, uterus

Intravaginal impedance (IVI) fluctuates during the goat estrous cycle. To understand which ovarian steroids are responsible for IVI changes and whether IVI variations are associated with precopulatory and copulatory behaviors, 8 ovariectomized females were assigned to 4 treatments in a 4 x 4 Latin square replicated over four 8-d periods. The treatments were as follows: progesterone plus estradiol-17[beta] ([P.sub.4] + [E.sub.2]), oil plus estradiol-17[beta] ([E.sub.2]), progesterone plus oil (P.sub.4]), or oil (OIL). Daily IVI measurements at the vaginocervical junction were taken at 1 and 70 KHz. Progesterone was given on d 2 and 3. Estradiol was given in the evening of d 5. On d 1 to 8, goats were group-exposed to a sexually experienced male and observed for the expression of sexual behaviors. On d 6 and 7, IVI was less when goats received [P.sub.4] + [E.sub.2] or [E.sub.2] compared with goats given [P.sub.4] or OIL (P < 0.05). Impedance measured at 1 kHz tended to remain lower on d 8 in [P.sub.4] + [E.sub.2] treated females compared with those given [P.sub.4] or OIL (P < 0.055). Like previous results, [P.sub.4] + [E.sub.2] or [E.sub.2] treatment induced behavioral estrus; 5 of 8 [P.sub.4] + [E.sub.2]-treated and 5 of 8 [E.sub.2]-treated females were sexually receptive on d 6. On d 7, although IVI remained low and 2 of 8 [P.sub.4] + [E.sub.2]-treated goats and 4 of 8 [E.sub.2]-treated goats remained sexually receptive, no additional females were in estrus. No IVI decreases and no estrous behavior were observed in goats given [P.sub.4] or OIL. This experiment demonstrated that E2 initiates the periestrous drop in IVI, and [P.sub.4] may delay baseline return. Key words: estrogen, estrus, goat, impedance, progesterone, vagina