Pulsatile LH secretion in women with premenstrual syndrome (PMS): Evidence for normal neuroregulation of the menstrual cycle

The premenstrual syndrome (PMS) has been proposed to result from excessive exposure to and/or withdrawal of brain opioid activity during the luteal phase. Because hypothalamic opioids are believed to modulate GnRH secretion, in part under the influence of ovarian steroids, we performed longitudinal studies of gonadotropin and ovarian steroid secretion across ovulatory, symptomatic cycles of 17 PMS patients and 8 normal volunteers. Pulsatile LH secretion was measured every 10 min for 8 hr at times when central opioid activity was expected to be low (early follicular phase), high (mid-luteal phase; ML), and declining (late luteal phase). In both subject groups, a cycle-phase effect was observed for LH pulse frequency (p=p=0.002), and for the transverse mean concentrations of LH (p=0.05), FSH (p2) (p=p=p=<0.05). The similar changes in luteal LH pulse frequency fail to provide evidence that GnRH secretion is impaired, thus challenging the view that the neuroregulation of the menstrual cycle in women with PMS is markedly altered.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30073/1/0000443.pd

Congenital adrenal hypoplasia and isolated gonadotropin deficiency

Congenital adrenal hypoplasia with gonadotropin deficiency is a rare X-linked recessive disorder that usually manifests with symptoms of adrenal insufficiency early in infancy. Adequate replacement therapy with glucocorticoids, mineralocorticoids, and salt has resulted in an increased survival. Slow growth and failure to undergo sexual maturation during the adolescent years usually ensues, secondary to hypogonadotropic hypogonadism. The X-linked congenital adrenal hypoplasia locus has been mapped to region Xp21.3-p21.2. Interstitial deletions of the X chromosome overlapping this region have been observed to cause complex clinical problems, with adrenal hypoplasia as a prominent component. Within a family segregating the disease, there is a 50% risk of having an affected male and a 50% risk of having a carrier female; considerations of genetic heterogeneity, possible chromosomal abnormalities, and prenatal diagnostic studies warrant medical genetic evaluations. The following case presentations illustrate the clinical spectrum of this condition.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29244/1/0000300.pd

Ontogenesis of corticotropes and lactotropes in situ in the pituitary gland of the hamster

The development of corticotropes and lactotropes was investigated in the golden Syrian hamster using an anti-porcine ACTH antiserum and a homologous antihamster PRL antiserum. Oval corticotropes were first visible in the ventral region of the pars distalis at 13 days of gestation. By the end of gestation, corticotropes were found throughout the pars distalis and in the pars intermedia. Corticotropes in the pars distalis of postnatal hamsters were either round or irregularly-shaped, often appearing in clusters. Throughout development, corticotropes often appeared to be surrounding other cells. Scarce, very small lactotropes were first observed in the pars distalis of hamsters on the first postnatal day. The number of these cells, which were either round or polyhedral, increased dramatically between 4 and 20 days of postnatal life. These observations indicate that the sequence of appearance of corticotropes and lactotropes in the hamster is similar to that in other species and that lactotropes are confined to the pars distalis of postnatal hamsters.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47682/1/441_2004_Article_BF00218571.pd

Partial trisomy of the long arm of human chromosome 1 as demonstrated by in situ hybridization with 5S ribosomal RNA

In a newborn boy with multiple malformations, a tandem duplication was detected at the distal end of the long arm of one human chromosome 1. The Giemsa bands, 1q31 to 1q43–44, were repeated serially. Since 5S rRNA genes are located at 1q42–43, in situ hybridization of 125 I 5S rRNA with fixed chromosome preparations was used to confirm the chromosomal duplication. The infant exhibited numerous developmental and clinical abnormalities as might be expected with an abnormality of chromosome structure relating to a ribosome component.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47604/1/439_2004_Article_BF00390432.pd

The 2006 Leon and Josephine Winkelman Lecture, University of Michigan School of Social Work

The Leon and Josephine Winkelman Memorial Lecture was established at the U-M School of Social Work by the Winkelman brothers (Stanley J., John H., Frederick R., and Henry R.) as a memorial to their parents. The lecture provides a forum for presenting new and emerging knowledge from the social sciences and helping professions, and discussion of the application of that knowledge to the development of social policy, the organization and management of social welfare services, and the delivery of social work services. The selection of topics and scholars reflects the interdisciplinary character of the lecture. This is in keeping with the representation of several disciplines in the Social Work faculty, the School's links with social sciences through its interdisciplinary Joint Doctoral Program in Social Work and Social Science, and the School's collaborations with the School of Public Health, the Medical Center, and the Institute of Gerontology.The Leon and Josephine Winkelman Family; School of Social Work; alumni, faculty, and friends of the School of Social Workhttp://deepblue.lib.umich.edu/bitstream/2027.42/49492/3/2006 Winkelman Lecture Kelch.pd

Testicular responsiveness to human chorionic gonadotrophin in growth hormone deficient pre-pubertal boys: lack of effect of replacement therapy

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/74977/1/j.1365-2605.1982.tb00246.x.pd

Dissociation of lutropin-induced loss of testicular lutropin receptors and lutropin-induced desensitization of testosterone synthesis

The relationship between changes in testicular lutropin receptors, as measured by specific binding of 125I-labeled human chorionic gonadotropin, and testosterone synthesis in response to lutropin (testicular responsiveness) was studied in intact and hypophysectomized rats. Administration of a single 200-[mu]g dose of ovine lutropin to intact rats results at 3 days in a 58% decrease in lutropin receptors associated with a parallel decrease in testicular responsiveness. A single 30-[mu]g dose of lutropin to intact rats resulted in a comparable decrease in lutropin receptors with a transient increase in testicular responsiveness. Rats receiving twice-daily injections of 15 [mu]g lutropin for 10 days exhibited a 48% decrease in lutropin receptors by day 3 which persisted during the 10-day treatment period, but was accompanied by a progressive increase in testicular responsiveness to lutropin. Hypophysectomy resulted in an 80% loss of receptors and a 72% loss in responsiveness 7 days after surgery. Daily treatment with lutropin initiated immediately following surgery resulted in a further dose-dependent decrease in lutropin receptors and a dose-dependent increase in testicular responsiveness. Loss of lutropin receptors was not due to occupancy of the receptor by exogenous lutropin. These studies demonstrate a dissociation between the negative regulation of lutropin receptors and testicular responsiveness to lutropin. Furthermore, the studies in hypophysectomized rats indicate that lutropin is the only hormone essential for maintenance of steroidogenesis and that this is independent of lutropin receptor concentration.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/22603/1/0000152.pd

EFFECTS OF CHANGING GONADOTROPHIN-RELEASING HORMONE PULSE FREQUENCY ON GONADOTROPHIN SECRETION IN MEN

To investigate the effects of alterations in GnRH pulse frequency on gonadotro-phin secretion, we administered low dose GnRH pulses (25 ng/kg) at hourly or 2-hourly frequencies to eight normal men. All subjects received GnRH pulses i.v. every 2 h for 88 h. Following this, exogenous GnRH was discontinued in four normal men (Group A, GnRH withdrawal), and the frequency of GnRH injections was increased to one pulse every hour for 24 h in the other four normal men (Group B, hourly GnRH). Blood samples were obtained every 20 min for LH and FSH and every 12 h for testosterone (T) and oestradiol (E2). Plasma LH increased in all subjects during injection of GnRH pulses every 2h. Withdrawal of GnRH pulses in Group A men was accompanied by a fall in mean LH, reductions in LH pulse amplitude (X¯± SEM: control 6.5±1.0; GnRH withdrawal 4.0 ± 0.5 mlU/ml) and pulse frequency (control 5.5 ± 0.2; GnRH withdrawal 3.5 ± 0.7 pulses/12 h), and an increase in plasma E 2 (control 122 ± 15; GnRH withdrawal 340 ± 37 pmol/l). Gonadotrophin responses to GnRH (25 ng/kg) were normal when tested 32 h after GnRH withdrawal. Injection of hourly GnRH pulses in Group B men was accompanied by a time-dependent change in mean LH, which transiently rose, then fell, and subsequently rose to a plateau during the second 12 h period of hourly GnRH. The final rise in LH was accompanied by an increase in LH frequency to 11.8 ± 0.3 pulses/12 h. These data suggest that: (1) increases in gonadal steroids decrease LH secretion by reducing the amplitude and frequency of endogenous GnRH pulses; and (2) the normal adult male pituitary requires approximately 12 h to initiate a sustained increase in LH secretion in response to a doubling in GnRH pulse frequency.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71865/1/j.1365-2265.1988.tb03857.x.pd