Development and evaluation of an index assessing adherence to the Norwegian food-based dietary guidelines: the Norwegian Dietary Guideline Index (NDGI).

BACKGROUND: Monitoring adherence to the Norwegian food-based dietary guidelines (FBDGs) could provide valuable insight into current and future diet-related health risks. This study aimed to develop and evaluate an index measuring adherence to the Norwegian FBDGs to be used as a compact tool in nutrition surveillance suitable for inclusion in large public health surveys. METHODS: The Norwegian Dietary Guideline Index (NDGI) was designed to reflect adherence to the Norwegian FBDGs on a scale from 0-100, with a higher score indicating better adherence. Dietary intakes were assessed through 19 questions, reflecting 15 dietary components covered by the Norwegian FBDGs. The NDGI was applied and evaluated using nationally representative dietary data from the cross-sectional web-based Norwegian Public Health Survey which included 8,558 adults.​ RESULTS: The population-weighted NDGI score followed a nearly normal distribution with a mean of 65 (SD 11) and range 21-99. Mean scores varied with background factors known to be associated with adherence to a healthy diet; women scored higher than men (67 vs. 64) and the score increased with age, with higher educational attainment (high 69 vs. low 64) and with better self-perceived household economy (good 67 vs. restricted 62). The NDGI captured a variety of dietary patterns that contributed to a healthy diet consistent with the FBDGs. CONCLUSION: The NDGI serve as a compact tool to assess and monitor adherence to the Norwegian FBDGs, to identify target groups for interventions, and to inform priorities in public health policies.​ The tool is flexible to adjustments and may be adaptable to use in other countries or settings with similar dietary guidelines.

How does the updated Nutri-Score discriminate and classify the nutritional quality of foods in a Norwegian setting?

BACKGROUND: The Nutri-Score is a candidate for the harmonized mandatory front-of-pack nutrition label enabling consumers in the European Union to make healthier food choices. Nutri-Score classifies foods (including beverages) from A (high nutritional quality) to E (low nutritional quality) based on the foods' qualifying and disqualifying components. We aimed to evaluate the updated Nutri-Score for foods (2022) and beverages (2023) in a Norwegian setting by exploring its ability to discriminate the nutritional quality of foods within categories. Additionally, we assessed Nutri-Scores' ability to classify foods in accordance with the Norwegian food-based dietary guidelines (FBDGs). METHODS: The updated Nutri-Score was calculated for 1,782 foods in a Norwegian food database. The discriminatory ability of the updated Nutri-Score was considered by exploring the distribution of Nutri-Score within categories of foods using boxplots and frequency tables, and by examining which qualifying and disqualifying components that contributed most to the Nutri-Score class. Accordance with the Norwegian FBDGs was assessed by exploring Nutri-Score for foods specifically mentioned in the guidelines. RESULTS: Overall, the updated Nutri-Score seemed to discriminate the nutritional quality of foods within categories, in a Norwegian setting. The foods' content of salt and the beverages' content of sugar were components contributing the most to Nutri-Scores' discriminatory ability. Furthermore, in most cases the updated Nutri-Score classified foods in accordance with the Norwegian FBDGs. However, there were minor inconsistencies in how Nutri-Score classified certain foods, such as the inabilities to discriminate between full-fat and low-fat/leaner cheeses, cremes and processed meats (sausages), and between whole grain and refined pasta/rice. CONCLUSIONS: We observed an overall acceptable discriminatory performance of the updated Nutri-Score in a Norwegian setting and in most cases the updated Nutri-Score classified foods in accordance with the Norwegian FBDGs. However, minor inconsistencies were observed. Together with the FBDGs, the updated Nutri-Score could be a useful tool in guiding consumers towards healthier food choices in Norway, but consumer evaluations are warranted to fully assess the performance of the updated Nutri-Score in a Norwegian context.

Identification of Sertoli cell-specific transcripts in the mouse testis and the role of FSH and androgen in the control of Sertoli cell activity.

BACKGROUND: The Sertoli cells act to induce testis differentiation and subsequent development in fetal and post-natal life which makes them key to an understanding of testis biology. As a major step towards characterisation of factors involved in Sertoli cell function we have identified Sertoli cell-specific transcripts in the mouse testis and have used the data to identify Sertoli cell-specific transcripts altered in mice lacking follicle-stimulating hormone receptors (FSHRKO) and/or androgen receptors (AR) in the Sertoli cells (SCARKO). RESULTS: Adult iDTR mice were injected with busulfan to ablate the germ cells and 50 days later they were treated with diphtheria toxin (DTX) to ablate the Sertoli cells. RNAseq carried out on testes from control, busulfan-treated and busulfan + DTX-treated mice identified 701 Sertoli-specific transcripts and 4302 germ cell-specific transcripts. This data was mapped against results from microarrays using testicular mRNA from 20 day-old FSHRKO, SCARKO and FSHRKO.SCARKO mice. Results show that of the 534 Sertoli cell-specific transcripts present on the gene chips, 85% were altered in the FSHRKO mice and 94% in the SCARKO mice (mostly reduced in both cases). In the FSHRKO.SCARKO mice additive or synergistic effects were seen for most transcripts. Age-dependent studies on a selected number of Sertoli cell-specific transcripts, showed that the marked effects in the FSHRKO at 20 days had largely disappeared by adulthood although synergistic effects of FSHR and AR knockout were seen. CONCLUSIONS: These studies have identified the Sertoli cell-specific transcriptome in the mouse testis and have shown that most genes in the transcriptome are FSH- and androgen-dependent at puberty although the importance of FSH diminishes towards adulthood.

Pituitary gonadotrophic hormone synthesis, secretion, subunit gene expression and cell structure in normal and follicle-stimulating hormone ß knockout, follicle-stimulating hormone receptor knockout, luteinising hormone receptor knockout, hypogonadal and ovariectomised female mice.

To investigate the relationship between gonadotroph function and ultrastructure, we have compared, in parallel in female mice, the effects of several different mutations that perturb the hypothalamic-pituitary-gonadal axis. Specifically, serum and pituitary gonadotrophin concentrations, gonadotrophin gene expression, gonadotroph structure and number were measured. Follicle-stimulating hormone ß knockout (FSHßKO), follicle-stimulating hormone receptor knockout (FSHRKO), luteinising hormone receptor knockout (LuRKO), hypogonadal (hpg) and ovariectomised mice were compared with control wild-type or heterozygote female mice. Serum levels of LH were elevated in FSHßKO and FSHRKO compared to heterozygote females, reflecting the likely decreased oestrogen production in KO females, as demonstrated by the threadlike uteri and acyclicity. As expected, there was no detectable FSH in the serum or pituitary and an absence of expression of the FSHß subunit gene in FSHßKO mice. However, there was a significant increase in expression of the FSHß and LHß subunit genes in FSHRKO female mice. The morphology of FSHßKO and FSHRKO gonadotrophs was not significantly different from the control, except that secretory granules in FSHRKO gonadotrophs were larger in diameter. In LuRKO and ovariectomised mice, stimulation of LHß and FSHß mRNA, as well as serum protein concentrations, were reflected in subcellular changes in gonadotroph morphology, including more dilated rough endoplasmic reticula and fewer, larger secretory granules. In the gonadotophin-releasing hormone deficient hpg mouse, gonadotrophin mRNA and protein levels were significantly lower than in control mice and gonadotrophs were correspondingly smaller with less abundant endoplasmic reticula and reduced numbers of secretory granules. In summary, major differences in pituitary content and serum concentrations of the gonadotrophins LH and FSH were found between control and mutant female mice. These changes were associated with changes in expression of the gonadotrophin subunit genes and were reflected in the cellular structure and secretory granule appearance within the gonadotroph cells.

An investigation into pituitary gonadotrophic hormone synthesis, secretion, subunit gene expression and cell structure in normal and mutant male mice.

To investigate brain-pituitary-gonadal inter-relationships, we have compared the effects of mutations that perturb the hypothalamic-pituitary-gonadal axis in male mice. Specifically, serum and pituitary gonadotrophin concentrations, gonadotrophin gene expression, and gonadotroph structure and number were measured. Follicle-stimulating hormone (FSH)ß knockout (FSHßKO), FSH receptor knockout (FSHRKO), luteinising hormone (LH) receptor knockout (LuRKO), hypogonadal (hpg), testicular feminised (tfm) and gonadectomised mice were compared with control wild-type mice or heterozygotes. Serum levels of LH were similar in FSHßKO, FSHRKO and heterozygote males despite decreased androgen production in KO males. As expected, there was no detectable FSH in the serum or pituitary and an absence of expression of the FSHß subunit gene in FSHßKO mice. However, there was a significant increase in expression of the common α and LHß subunit genes in FSHRKO males. The morphology of FSHßKO and FSHRKO gonadotrophs was not significantly different from controls, except that the subpopulation of granules consisting of an electron-dense core and electron-lucent 'halo' was not observed in FSHßKO gonadotrophs and the granules were smaller in diameter. In the gonadotrophin-releasing hormone deficient hpg mouse, gonadotrophin mRNA and hormone levels were significantly lower compared to control mice and gonadotrophs were correspondingly smaller, with less abundant endoplasmic reticulum and reduced secretory granules. In LuRKO, tfm and gonadectomised mice, hyperstimulation of LHß and FSHß mRNA and serum protein concentrations was reflected by subcellular changes in gonadotroph morphology, including more dilated rough endoplasmic reticulum and more secretory granules distributed adjacent to the plasma membrane. In summary, major differences in pituitary content and serum concentrations of the gonadotrophins LH and FSH have been found between normal and mutant male mice. These changes are associated with changes in transcriptional activity of the gonadotrophin subunit genes and are reflected by changes in the cellular structure and secretory granule architecture within the gonadotroph cells.

Direct action through the sertoli cells is essential for androgen stimulation of spermatogenesis.

Androgens act to stimulate spermatogenesis through androgen receptors (ARs) on the Sertoli cells and peritubular myoid cells. Specific ablation of the AR in either cell type will cause a severe disruption of spermatogenesis. To determine whether androgens can stimulate spermatogenesis through direct action on the peritubular myoid cells alone or whether action on the Sertoli cells is essential, we crossed hypogonadal (hpg) mice that lack gonadotrophins and intratesticular androgen with mice lacking ARs either ubiquitously (ARKO) or specifically on the Sertoli cells (SCARKO). These hpg.ARKO and hpg.SCARKO mice were treated with testosterone (T) or dihydrotestosterone (DHT) for 7 d and testicular morphology and cell numbers assessed. Androgen treatment did not affect Sertoli cell numbers in any animal group. Both T and DHT increased numbers of spermatogonia and spermatocytes in hpg mice, but DHT has no effect on germ cell numbers in hpg.SCARKO and hpg.ARKO mice. T increased germ cell numbers in hpg.SCARKO and hpg.ARKO mice, but this was associated with stimulation of FSH release. Results show that androgen stimulation of spermatogenesis requires direct androgen action on the Sertoli cells.

Transcriptional profiling of luteinizing hormone receptor-deficient mice before and after testosterone treatment provides insight into the hormonal control of postnatal testicular development and Leydig cell differentiation.

Luteinizing hormone (LH) is a key regulator of male fertility through its effects on testosterone secretion by Leydig cells. Transcriptional control of this is, however, currently poorly understood. Mice in which the LH receptor is knocked out (LuRKO) show reduced testicular size, reduced testosterone, elevated serum LH, and a spermatogenic arrest that can be rescued by the administration of testosterone. Using genome-wide transcription profiling of LuRKO and control testes during postnatal development and following testosterone treatment, we show that the transcriptional effects of LH insensitivity are biphasic, with an early testosterone-independent phase and a subsequent testosterone-dependent phase. Testosterone rescue re-enables the second, testosterone-dependent phase of the normal prepubertal transcription program and permits the continuation of spermatogenesis. Examination of the earliest responses to testosterone highlights six genes that respond rapidly in a dose-dependent fashion to the androgen and that are therefore candidate regulatory genes associated with the testosterone-driven progression of spermatogenesis. In addition, our transcriptional data suggest a model for the replacement of fetal-type Leydig cells by adult-type cells during testicular development in which a testosterone feedback switch is necessary for adult Leydig cell production. LH signaling affects the timing of the switch but is not a strict requirement for Leydig cell differentiation.

Effect of FSH on testicular morphology and spermatogenesis in gonadotrophin-deficient hypogonadal mice lacking androgen receptors.

FSH and androgen act to stimulate and maintain spermatogenesis. FSH acts directly on the Sertoli cells to stimulate germ cell number and acts indirectly to increase androgen production by the Leydig cells. In order to differentiate between the direct effects of FSH on spermatogenesis and those mediated indirectly through androgen action, we have crossed hypogonadal (hpg) mice, which lack gonadotrophins, with mice lacking androgen receptors (AR) either ubiquitously (ARKO) or specifically on the Sertoli cells (SCARKO). These hpg.ARKO and hpg.SCARKO mice were treated with recombinant FSH for 7 days and testicular morphology and cell numbers were assessed. In untreated hpg and hpg.SCARKO mice, germ cell development was limited and did not progress beyond the pachytene stage. In hpg.ARKO mice, testes were smaller with fewer Sertoli cells and germ cells compared to hpg mice. Treatment with FSH had no effect on Sertoli cell number but significantly increased germ cell numbers in all groups. In hpg mice, FSH increased the numbers of spermatogonia and spermatocytes, and induced round spermatid formation. In hpg.SCARKO and hpg.ARKO mice, in contrast, only spermatogonial and spermatocyte numbers were increased with no formation of spermatids. Leydig cell numbers were increased by FSH in hpg and hpg.SCARKO mice but not in hpg.ARKO mice. Results show that in rodents 1) FSH acts to stimulate spermatogenesis through an increase in spermatogonial number and subsequent entry of these cells into meiosis, 2) FSH has no direct effect on the completion of meiosis and 3) FSH effects on Leydig cell number are mediated through interstitial ARs.

Effects of FSH on testicular mRNA transcript levels in the hypogonadal mouse.

FSH acts through the Sertoli cell to ensure normal testicular development and function. To identify transcriptional mechanisms through which FSH acts in the testis, we have treated gonadotrophin-deficient hypogonadal (hpg) mice with recombinant FSH and measured changes in testicular transcript levels using microarrays and real-time PCR 12, 24 and 72 h after the start of treatment. Approximately 400 transcripts were significantly altered at each time point by FSH treatment. At 12 h, there was a clear increase in the levels of a number of known Sertoli cell transcripts (e.g. Fabp5, Lgals1, Tesc, Scara5, Aqp5). Additionally, levels of Leydig cell transcripts were also markedly increased (e.g. Ren1, Cyp17a1, Akr1b7, Star, Nr4a1). This was associated with a small but significant rise in testosterone at 24 and 72 h. At 24 h, androgen-dependent Sertoli cell transcripts were up-regulated (e.g. Rhox5, Drd4, Spinlw1, Tubb3 and Tsx) and this trend continued up to 72 h. By contrast with the somatic cells, only five germ cell transcripts (Dkkl1, Hdc, Pou5f1, Zfp541 and 1700021K02Rik) were altered by FSH within the time-course of the experiment. Analysis of canonical pathways showed that FSH induced a general decline in transcripts related to formation and regulation of tight junctions. Results show that FSH acts directly and indirectly to induce rapid changes in Sertoli cell and Leydig cell transcript levels in the hpg mouse but that effects on germ cell development must occur over a longer time-span.

Role of androgen and gonadotrophins in the development and function of the Sertoli cells and Leydig cells: data from mutant and genetically modified mice.

Development and maintenance of the male phenotype and establishment of fertility are all dependent upon the activity of the Sertoli cells and Leydig cells of the testis. This review examines the regulation and function of these cell during fetal and post-natal development. Fetal Leydig cells are sensitive to both luteinising hormone (LH) and adrenocorticotrophic hormone (ACTH) but Leydig cell function appears normal in fetal mice lacking both hormones or their receptors. Post-natally, the Sertoli cells and Leydig cells are reliant upon the pituitary gonadotrophins. Leydig cells are critically dependent on LH but follicle-stimulating hormone (FSH), presumably acting through the Sertoli cell, can also affect Leydig cell function. Testosterone secreted by the Leydig cells acts with FSH to stimulate Sertoli cell activity and spermatogenesis. Study of animals lacking FSH-receptors and androgen-receptors shows that both hormones can act to maintain the meiotic germ cell population but that androgens are critical for completion of meiosis.

Spermatogenesis and sertoli cell activity in mice lacking sertoli cell receptors for follicle-stimulating hormone and androgen.

Spermatogenesis in the adult male depends on the action of FSH and androgen. Ablation of either hormone has deleterious effects on Sertoli cell function and the progression of germ cells through spermatogenesis. In this study we generated mice lacking both FSH receptors (FSHRKO) and androgen receptors on the Sertoli cell (SCARKO) to examine how FSH and androgen combine to regulate Sertoli cell function and spermatogenesis. Sertoli cell number in FSHRKO-SCARKO mice was reduced by about 50% but was not significantly different from FSHRKO mice. In contrast, total germ cell number in FSHRKO-SCARKO mice was reduced to 2% of control mice (and 20% of SCARKO mice) due to a failure to progress beyond early meiosis. Measurement of Sertoli cell-specific transcript levels showed that about a third were independent of hormonal action on the Sertoli cell, whereas others were predominantly androgen dependent or showed redundant control by FSH and androgen. Results show that FSH and androgen act through redundant, additive, and synergistic regulation of spermatogenesis and Sertoli cell activity. In addition, the Sertoli cell retains a significant capacity for activity, which is independent of direct hormonal regulation.

Age-related uterine and ovarian hypertrophy in FSH receptor knockout and FSHbeta subunit knockout mice.

Female mice in which the gene encoding the follicle-stimulating hormone FSH receptor (FSHR) knockout (KO) or its ligand (FSHbetaKO) have been disrupted were infertile. Ovaries of these mice were significantly smaller than those of heterozygous littermates but significantly larger than those of hypogonadal mice of the same age. Uterine masses in all three mutants were <6 mg, significantly reduced compared with heterozygous mice. At 1 year of age uterine mass had increased to >12 mg in 63% of FSHRKO females and 88% of FSHbetaKO females. Despite the increase in uterine size there was no evidence of contractility: uteri were flaccid and unresponsive to electrical or pharmacological stimulation. In most females in which uterine growth had occurred there was evidence of ovarian growth with hypertrophy of the interstitial tissue, occurrence of ovarian cysts and epithelial and tubular inclusions. There was no evidence of uterine or ovarian hypertrophy in hypogonadal (hpg) mice at any age or in 1 year old females in which the FSH mutations were bred onto the hpg background. There was an inverse correlation of plasma LH concentrations and uterine mass in 1 year old mutant females with uterine hypertrophy. Ovariectomy of both FSHRKO and FSHbetaKO females with large uteri resulted in decreased uterine mass and increased plasma concentration of LH. The number of mice with ovarian pathology, reminiscent of the serous ovarian adenocarcinomas found in humans, was significantly greater in the FSHbetaKO mice, indicating that the presence of an intact FSH receptor on ovarian cells of FSHbetaKO females may allow constitutive basal stimulation of the ovary, which is absent in mice lacking FSH receptors.

The effect of a null mutation in the follicle-stimulating hormone receptor gene on mouse reproduction.

To investigate further brain-pituitary-gonadal interrelationships we have generated mice in which the gene encoding the FSH receptor has been disrupted. Female FSH receptor knockout (FSHRKO) mice were infertile. The ovaries were significantly reduced in size, with follicular development arrested at the preantral stage, but there was evidence of stromal hypertrophy. The vagina was imperforate, and the uterus was atrophic. There was no response to administration of PMSG. Inhibins A and B were undetectable in both the serum and gonads. Compared with those in control animals, serum concentrations of FSH and LH were significantly elevated in mutant females. The pituitary content of FSH, but not LH, was also significantly elevated. Estrogen administration in FSHRKO female mice suppressed serum LH levels to those seen in control mice, whereas FSH levels were reduced by only 50%. Male FSHRKO mice were fertile, although testis weight was significantly reduced. However, testicular inhibin A and B concentrations did not differ from those in normal littermates. Serum levels of FSH and LH were elevated in the null mutant male mice, whereas no differences were found in the pituitary content of these hormones. In conclusion, ovarian follicular development cannot progress beyond the preantral stage without FSH. In the absence of mature follicles ovarian estrogen remains low, and consequently accessory sex tissue growth and negative feedback regulation of gonadotropin secretion are severely compromised. In the male, however, inability to respond to FSH does not impair fertility, although testicular weight is reduced, and feedback regulation of pituitary gonadotropins and intratesticular paracrine interactions may be disturbed.

Interaction of humor and gender in moderating relationships between stress and outcomes.

This study is an examination of the interaction of humor and gender in moderating relationships among perceived stress, anxiety, and physical symptoms. Introductory psychology students (70 women, 61 men) completed self-report scales measuring perceived stress, humor, and symptomology. Multiple regression analyses revealed a moderating effect for humor between stress and anxiety, but only for men. When humor was low, a positive relationship was obtained between stress and anxiety; no relationship existed when humor was high. No gender differences were found in the significant moderating effect of humor between stress and physical symptoms. When humor was low, stress was related to physical symptoms; no relationship was found when humor was high. Overall, the findings supported humor as a moderator of stress; gender differences also existed for some outcomes.

The role of self-esteem in typical and atypical changes in expectations.

Self-esteem was explored as a factor in appropriate (typical) and inappropriate (atypical) changes in performance expectations across trials of a nonthreatening success condition vs. a threatening failure condition. Participants (51 women, 45 men) were randomly assigned to one of the conditions and completed a self-esteem scale and 8 trials of a timed digit-substitution task. Moderated multiple regression revealed significant interactions between self-esteem and condition for typical and atypical changes. A significant positive relationship between self-esteem and typical changes was found under success and between self-esteem and atypical changes under failure. Differences between conditions were evident only for high self-esteem, with greater typical changes for success and greater atypical changes for failure.

Low birth weight and interactions between traditional risk factors.

The effects of traditional risk factors on low birth weight were examined, using logistic regression analyses and adjusting for interactions between multiple factors. Data for 11,936 births were obtained from a state birth cohort file. The effect for maternal ethnicity was dependent on education and marital status; the effect of marital status was dependent on ethnicity, medical risk, and level of prenatal care; and the effect of prenatal care was dependent on marital status. Results suggest that examining only main effects and ignoring interactions can produce overgeneralized conclusions about the influence of individual risk factors on low birth weight.

Maternal characteristics and inadequate prenatal care.

This study examined the effects of traditional risk factors on receipt of inadequate prenatal care when controlling for interactions of multiple factors. Birth certificate data on 11,936 births were obtained from a state birth cohort file. A logistic regression model indicated significant interactions between maternal ethnicity (black vs white), marital status, and education in the prediction of inadequate prenatal care. Examining only main effects and ignoring interactions can produce oversimplified conclusions about individual risk factors.

Self-esteem moderator or mediator between perceived stress and expectancy of success.

Relationships between perceived stress, self-esteem, and expectancy of success were examined, and the moderating and mediating effects of self-esteem between perceived stress and expectancy of success were explored. Participants (48 women, 27 men) completed self-rating scales measuring perceived stress, self-esteem, and expectancy of success. Negative relationships were obtained between perceived stress and self-esteem and between perceived stress and expectancy of success. Self-esteem and expectancy of success were positively associated. Moderated multiple regression analysis yielded no moderating effect of self-esteem between perceived stress and expectancy of success; however, a moderating effect of self-esteem was obtained using regression techniques.

A demonstration program for homeless male alcohol and other drug abusers.

The National Institute on Alcohol Abuse and Alcoholism, in consultation with the National Institute on Drug Abuse, awarded nine demonstration grants in 1988 for community-based programs addressing issues of the homeless alcohol and other drug (AOD) abusers. Project Connect in Louisville, Kentucky, was one of the nine demonstration grants. The three-year project was designed to address a multitude of needs of the homeless male AOD abuser, including housing, medical, employment/economic, and social support, in addition to treatment for AOD abuse. The present article details the evolution and implementation of Project Connect and describes characteristics of the target population. In addition, the article presents issues and problems that surfaced during program implementation in order to assist other communities that are considering similar programs for their homeless populations.

The concentrations of prostaglandins in endometrium during the menstrual cycle in women with measured menstrual blood loss.

The concentrations of PGF2 alpha, PGE2 and 6-oxo-PGF1 alpha were measured in human uterine tissues during the menstrual cycle. The concentrations of all PGs in endometrium were greater than in myometrium. PGF2 alpha, which was found in the greatest concentrations, was high in the mid-secretory phase in both endometrium and myometrium. The concentration of PGE2 did not vary during the menstrual cycle in either tissue. The biosynthetic capacity of endometrium to produce both PGF2 alpha and PGE2 was significantly greater in the mid than the late secretory phase in the presence of exogenous arachidonic acid. Also, in spite of low endogenous concentrations, both endometrium and myometrium were able to produce significant amounts of 6-oxo-PGF1 alpha during a 30 minute incubation. The possible significance of this late secretory decline in the capacity of the endometrium to produce PGF2 alpha and PGE2 is discussed.