56 research outputs found
<b>Supplemental Material - Responding to Uncertainty: The Importance of Covertness in Support for Retaliation to Cyber and Kinetic Attacks</b>
Supplemental Material for Responding to Uncertainty: The Importance of Covertness in Support for Retaliation to Cyber and Kinetic Attacks by Michael J. Soules in Journal of Conflict Resolution</p
<b>Supplemental Material - Recruiting Rebels: Introducing the Rebel Appeals and Incentives Dataset</b>
Supplemental Material for Recruiting Rebels: Introducing the Rebel Appeals and Incentives Dataset by Michael J. Soules in Journal of Conflict Resolution</p
Prolactin secretion and corpus luteum function in women with luteal phase deficiency
Luteal phase deficiency (LPD) as a clinical infertility problem is
considered to have a heterogeneous etiology. Hyperprolactinemia has long
been considered a causative factor of LPD. In this context we investigated
PRL secretion in 18 women with LPD. All of the subjects were infertile
with 2 out of phase (greater than 2 days) endometrial biopsies; 10 of the
women also had daily blood samples, this latter subgroup had significantly
decreased integrated luteal phase progesterone (P) levels compared to
normal women with in-phase biopsies. PRL secretion was investigated as
follows: 1) daily blood levels; 2) pulsatile secretion patterns in 3 cycle
phase [early follicular (12 h); late follicular (12 h); midluteal (24 h)],
3) LH-PRL coupling, and 4) nocturnal patterns. Results were compared to
findings in 36 normal women. The mean daily levels of PRL over the
menstrual cycle were not different between the two groups (LPD, 12.1 +/-
1.5; normal, 13.8 +/- 0.8 microgram/L; P = 0.3). There was no correlation
between luteal phase integrated P and PRL levels for either group. There
was a small difference in the PRL pulse amplitude in the early follicular
phase between the LPD and normal women (2.6 +/- 0.3 vs. 5.5 +/- 1.3
micrograms/L; P less than 0.05). There were no significant differences
between groups in PRL pulse frequency or mean level during the 12 or 24 h
in any cycle phase. There was an equivalent amount of LH-PRL pulse
coupling in both groups in all three cycle phases. Diurnal and nocturnal
PRL secretion was studied by breaking the 24 h data (midluteal) into day
(0700-2300 h) and night (2300-0700) segments. Mean PRL levels were higher
at night in both groups (LPD, 15.9 vs. 12.6; normal, 15.4 vs. 9.3
micrograms/L; P less than 0.05), as expected. There were no differences in
nocturnal PRL secretory patterns between the two groups. In summary, we
have serious reservations whether abnormalities in PRL secretion are a
common or integral part of the pathophysiology of LPD. From previous work
we know these subtle abnormalities in PRL secretion in LPD are associated
with definite abnormalities in gonadotropin secretion. We believe these
gonadotropin abnormalities are probably more significant in terms of
decreased P secretion
Abnormal patterns of pulsatile luteinizing hormone in women with luteal phase deficiency
Luteal phase deficiency is usually a problem of inadequate progesterone
production associated with inadequate ovarian follicular development. The
hypothesis that luteal phase deficiency results from an abnormal secretion
pattern of luteinizing hormone (LH) was tested in these women. To this
end, the early follicular LH secretion pattern in four women with luteal
phase deficiency was characterized and compared with patterns in normal
women. Blood samples were obtained through indwelling catheters every ten
minutes for eight hours (10 AM to 6 PM), and plasma levels of LH and FSH
were measured. Luteinizing hormone and FSH secretion profiles were
analyzed for pulse frequency, amplitude, and mean plasma level. A
significantly greater LH pulse frequency in women with luteal phase
deficiency was observed when compared with the frequency in normal
controls (luteal phase deficiency, 10.5 pulses/eight hours; normal, 5.2
pulses/eight hours; P less than or equal to .05). The mean FSH
concentration was less in the women with luteal phase deficiency, but the
level was not significant. These data suggest that the abnormal LH
secretion pattern observed in women with luteal phase deficiency is
responsible for their inadequate luteal phase progesterone secretion and
their infertility
Corpus luteum insufficiency induced by a rapid gonadotropin-releasing hormone-induced gonadotropin secretion pattern in the follicular phase
The pulse frequency of LH and FSH (and by inference, GnRH) is a major
determinant of the relative baseline plasma levels of LH and FSH. Luteal
phase deficiency has been reported to be associated with increased
gonadotropin pulse frequency and inadequate preovulatory follicular
development. In this study we induced in normal women a supraphysiological
gonadotropin pulse frequency in the follicular phase to determine its
effect on follicular development and corpus luteum function. Specifically,
we tested the hypothesis that a supraphysiological GnRH pulse frequency
would result in deficient luteal phase production of progesterone. The
subjects were six normal ovulatory women (age range, 23-35 yr). They were
initially studied during a control cycle (cycle 1). Then, 25 ng/kg GnRH
was administered iv every 30 min from the early follicular phase of the
next cycle (cycle 2) until ovulation occurred. GnRH administration
resulted in increased follicular phase plasma LH and FSH levels and LH to
FSH ratios, multiple preovulatory follicles (mean, 2.8) with increased
mean integrated estradiol [1302 (pg/mL)day (cycle 1) vs. 2550 (pg/mL)day
(cycle 2); P less than 0.05; 4780 vs. 9360 (pmol/L)day, Systeme
International units], spontaneous ovulation, decreased luteal phase plasma
immunoreactive and bioactive LH levels, decreased luteal phase length
[13.5 days (cycle 1) vs. 8.8 days (cycle 2); P less than 0.05], and
decreased mean integrated progesterone secretion [152 (ng/mL)day (cycle 1)
vs. 66 (ng/mL)day (cycle 2); P less than 0.01; 482 vs. 209 (nmol/L)day,
Systeme International units]. We conclude that high frequency LH and FSH
secretion during the follicular phase can induce inadequate progesterone
secretion during the subsequent luteal phase, and we infer that the
pathophysiological basis for this induced luteal phase deficiency is
decreased LH support of corpus luteum function
The effects of inducing a follicular phase gonadotropin secretory pattern in normal women during the luteal phase
It has been hypothesized that the slowing of the luteinizing hormone (LH)
pulse frequency in the luteal phase may be necessary for the demise of the
corpus luteum, the intercycle rise in baseline follicle-stimulating
hormone (FSH), or ovarian follicular development in the subsequent cycle.
For assessment of the physiologic role of the luteal phase LH pulse
pattern, this pattern was converted to a follicular pattern in six normal
women who used exogenous gonadotropin-releasing hormone administered with
a portable pump (dose 50 to 100 ng/kg subcutaneously every 90 minutes
beginning in the early luteal [n = 3] and midluteal [n = 3] cycle phases).
There was no significant difference between the treated and the subsequent
cycle for luteal progesterone production [186.3 versus 159.0 (ng/ml) day],
preovulatory follicular size (23.1 versus 22.5 mm), estradiol levels,
luteal phase length (15.6 versus 14.3 days), and daily gonadotropin
concentrations including the intercycle FSH rise (160.5 versus 139.1
ng/ml). A follicular phase gonadotropin pulse pattern (increased
frequency, decreased amplitude) in the luteal phase had no discernible
effects on the corpus luteum or on follicular development in the
subsequent cycle
Ovulation induction with pulsatile gonadotropin-releasing hormone: a study of the subcutaneous route of administration
The efficacy of ovulation induction with the use of intermittent
gonadotropin-releasing hormone (GnRH) therapy was examined in seven
infertile women with hypothalamic amenorrhea. GnRH was administered every
90 minutes via the subcutaneous route in doses ranging from 50 to 300
ng/kg. Analysis of the induced gonadotropin pulse pattern revealed normal
to modestly increased luteinizing hormone secretory parameters (e.g.,
pulse amplitude) in six of the seven patients. Six of seven women and 15
of 16 treatment cycles (94%) were ovulatory. The conception rate was 43%
per woman and 19% per cycle. However, detailed hormonal analysis of 13
treatment cycles revealed that only 1 cycle was entirely normal in terms
of duration and/or steroid secretion
Abnormal Patterns of Pulsatile Luteinizing Hormone in Women with Luteal Phase Deficiency
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