Pulsatile infusion of luteinizing hormone-releasing hormone induces precocious puberty (vaginal opening and first ovulation) in the immature female guinea pig

Previously we have hypothesized that an increase in luteinizing hormone-releasing hormone (LHRH) due to hypothalamic maturation is the key factor controlling the onset of puberty. This led to the working hypothesis that precocious puberty would be induced if LHRH is administered with an appropriate protocol. Thus, effects of pulsatile infusion of LHRH on the onset of first vaginal opening and first ovulation in immature female guinea pigs were studied. Luteinizing hormone-releasing hormone in hourly pulses of either 5 ng or 50 ng was infused through a chronically implanted jugular catheter for 9-29 days starting at 20 days of age. For the control experiment saline was infused in a similar manner. Infusion of 5 ng LHRH/h resulted in significantly earlier (P less than 0.001) ages at first vaginal opening (24.7 +/- 0.9 days) and at first ovulation (28.8 +/- 0.9 days) compared to saline controls (first vaginal opening 53.3 +/- 6.8 days; first ovulation 55.2 +/- 6.5 days). Infusion with a 10-fold higher LHRH dose (50 ng/h) also advanced the age at first vaginal opening (25.3 +/- 0.7 days), but precocious ovulation was no longer induced (53.7 +/- 5.3 days). Interestingly, LHRH infusion with the high dose resulted in a prolonged period of vaginal opening and cornification without ovulation. These results indicate that 1) pulsatile infusion of a small amount of LHRH with a constant frequency induces precocious puberty in a laboratory rodent, and 2) infusion of LHRH with a dose higher than the effective dose for the induction of early puberty results in a persistent estrous anovulatory syndrome. Therefore, the present study not only supports our hypothesis that an increase in endogenous LHRH release is responsible for the onset of puberty, but also further suggests that excessive release of LHRH or abnormal patterns of LHRH release may be involved in the etiology of the anovulatory persistent estrus syndrome.     

Gonadotropin-releasing hormone secretion during the postpartum anestrous period of the ewe

An increase in episodic release of LH is putatively the initial event leading to the onset of postpartum ovarian cyclicity in ewes. This experiment was conducted to determine the relationship between hypothalamic release of GnRH and onset of pulsatile secretion of LH during postpartum anestrus. Control ewes (n = 7) were monitored during the postpartum period to determine when normal estrous cycles resumed. In controls, the mean interval from parturition to the first postpartum estrus as indicated by a rise in serum progesterone greater than 1 ng/mg was 25.8 +/- 0.6 days. Additional ewes (n = 4-5) at 3, 7, 14, and 21 days postpartum (+/- 1 day) were surgically fitted with cannula for collection of hypophyseal-portal blood. Hypophyseal-portal and jugular blood samples were collected over a 6- to 7-h period at 10-min intervals. The number of GnRH pulses/6 h increased (p less than 0.05) from Day 3 postpartum (2.2 +/- 0.5) to Days 7 and 14 (3.6 +/- 0.2 and 3.9 +/- 0.4, respectively). A further increase (p less than 0.05) in GnRH pulse frequency was observed at Day 21 postpartum (6.4 +/- 0.4 pulses/6 h). Changes in pulsatile LH release paralleled changes observed in pulsatile GnRH release over Days 3, 7, 14, and 21 postpartum (0.83 +/- 0.3, 2.8 +/- 0.4, 2.9 +/- 0.6, and 4.0 +/- 1.1 pulses/6 h, respectively). GnRH pulse amplitude was higher at Day 21 than at Days 3, 7, or 14 postpartum. These findings suggest that an increase in the frequency of GnRH release promotes the onset of pulsatile LH release during postpartum anestrus in ewes.     

Testosterone administration to ovariectomized female rhesus monkeys (Macaca mulatta) reduces the frequency of pulsatile luteinizing hormone secretion

In the male rhesus monkey testosterone (T) retards the frequency of intermittent LH secretion. The purpose of the present study was to determine whether this action of T is demonstrable in the female. Five ovariectomized rhesus monkeys, bearing indwelling cardiac catheters, were implanted s.c. on one or more occasions with T-containing Silastic capsules. Sequential blood samples were collected for 8 h every 10 min before T treatment and usually at 1, 2, 4, and 8 days thereafter. Plasma LH concentrations were measured in duplicate by radioimmunoassay and subsequently analyzed with a computerized algorithm. Sustained increments in circulating T (5-13 ng/ml) in ovariectomized monkeys resulted in a progressive reduction in LH pulse frequencies from approximately 1 pulse every 60 min before initiation of T treatment to 1 pulse every 100-150 min at 48 h thereafter. In most cases the deceleration in pulsatile gonadotropin secretion continued, and by 4-8 days of T treatment LH pulse frequencies as low as 1 pulse every 5 h were observed. The onset of the T-induced deceleration in LH pulse frequency was generally associated with an increase in LH pulse amplitude and with a decline in mean LH levels. This LH response in the female to T treatment was similar to that previously reported for male castrates.     

Release of luteinizing hormone and growth hormone after recovery from maximal exercise

Pulsatile properties of luteinizing hormone (LH) and growth hormone (GH) release were evaluated in 19 eumenorrheic untrained females [mean age 31.1 +/- 1.1 yr, height 165.2 +/- 1.4 cm, weight 64.8 +/- 2.1 kg, peak oxygen uptake (Vo2) 41.6 +/- 1.4 (SE) ml.kg-1.min-1] during the early follicular phase of the menstrual cycle (days 3-4 after the onset of menses). Each subject was studied during two consecutive menstrual cycles under each of two conditions in random order: 1) no formal exercise for 72 h (C) and 2) 12-24 h after two maximal exercise bouts (peak Vo2/lactate threshold treadmill evaluation and a 3,200-m time-trial run or a maximal Vo2 inclined treadmill test) performed on consecutive days (EX). Blood sampling was performed every 10 min for 12 h. LH and GH pulsatile parameters were identified and characterized by the Cluster pulse detection algorithm. No significant differences were noted in the number of peaks, peak amplitude, interpeak interval, peak increment, or 12-h integrated concentrations between C and EX for LH or GH. We conclude that maximal exercise protocols typically used for exercise evaluation do not have an effect on the pulsatile characteristics of LH or GH release in untrained women during the early follicular phase of the menstrual cycle if 12-24 h of recovery are allowed before evaluation of the pulsatile secretion of gonadotropins or GH.     

Levels of progesterone and changes in prostaglandin F(2alpha) release during luteolysis and early pregnancy in llamas and the effect of treatment with flunixin meglumine

The secretory patterns of progesterone in relation to concentrations of 15-ketodihydro-PGF(2alpha) (PGFM) during the period of luteolysis or of maternal recognition of pregnancy were determined in the blood of llamas mated either with an intact or a vasectomized male. The ability of flunixin meglumine (FM) to postpone luteolysis in non-pregnant llamas was investigated by injecting the drug intravenously every 6 h at a dose of 2.2 mg/kg from days 6 to 12 post-copulation into a group of non-pregnant llamas. A pulsatile pattern of prostaglandin release was recorded during luteolysis in non-pregnant llamas, giving further support to the hypothesis that PGF(2alpha) is the luteolytic agent in llamas. The mean number of peaks per animal rose from 0.3 on day 7 to 3.8 on day 10 and then declined to 1.1 on day 12 with corresponding mean peak amplitude changing from 465 to 1234 and 566 pmol l(-1), respectively. In pregnant llamas, prostaglandin pulsatile release also occurred. The mean number of peaks per animal rose from 0.4 on day 7 to 0.8 on day 10 and then declined to 0.2 on day 11 and 0.6 on day 12, with corresponding mean peak amplitude changing from 494 to 676, 388 and 547 pmol l(-1), respectively. The transient decrease and subsequent recovery in progesterone concentrations was observed to occur in connection with prostaglandin release during early pregnancy. Oestradiol-17beta plasma peak concentrations attained after luteolysis were significantly higher than those recorded in early pregnant animals (around 30 pmol l(-1) and ll pmol l(-1)). Concentrations of PGFM decreased rapidly after the first administration of FM and remained low throughout the first 2 days of treatment. Thereafter, pulsatile release of prostaglandins started, and luteolysis proceeded; but a delay of 1-1.5 days in the progesterone decline was observed. Thus, it might be suggested that a higher dose and/or a more intensive injection schedule is required in llamas than in other ruminants to prevent luteolysis.     

Pulsatile infusion of luteinizing hormone-releasing hormone: Effects on luteinizing hormone secretion and ovarian function in prepuberal gilts

Ten intact and hypophysial stalk-transected (HST), prepuberal Yorkshire gilts, 112–160 days old, were subjected to a pulsatile infusion regimen of luteinizing hormone-releasing hormone (LHRH) to investigate secretion profiles of luteinizing hormone (LH) and ovarian function. A catheter was implanted in a common carotid artery and connected to an infusion pump and recycling timer, whereas an indwelling external jugular catheter allowed collection of sequential blood samples for radioimmunoassay of LH and progesterone. In a dose response study, intracarotid injection of 5 μg LHRH induced peak LH release (5.9 ± 0.65 ng/ml; mean ± SE) within 20 min, which was greater (P < 0.001) than during the preinjection period (0.7 ± 0.65 ng/ml). After HST, 5 μg LHRH elicited LH release in only one of three prepuberal gilts. Four intact animals were infused with 5 μg LHRH (in 0.1% gel phosphate buffer saline, PBS) in 0.5-ml pulses (0.1 ml/min) at 1.5-h intervals continuously during 12 days. Daily blood samples were obtained at 20-min intervals 1 h before and 5, 10, 20, 40, 60 and 80 min after one LHRH infusion. Plasma LH release occurred in response to pulsatile LHRH infusion during the 12-day period; circulating LH during 60 min before onset of LHRH infusion was 0.7 ± 0.16 ng/ml compared with 1.3 ± 0.16 ng/ml during 60 min after onset of infusion (P < 0.001). Only one of four intact gilts ovulated, however, in response to LHRH infusion. This animal was 159 days old, and successive estrous cycles did not recur after LHRH infusion was discontinued. Puberal estrus occurred at 252 ± 7 days in these gilts and was confirmed by plasma progesterone levels. These results indicate that intracarotid infusion of 5 μg LHRH elicits LH release in the intact prepuberal gilt, but this dosage is insufficient to cause a consistent response after HST.     

Factors accounting for perinatal occurrence of pulsatile gonadotropin-releasing hormone secretion in vitro in rats

Our aim was to study the inhibitory and facilitatory factors possibly accounting for the undetectable activity of the GnRH pulse generator in late fetal life in vitro and its awakening in early postnatal life. Gamma aminobutyric acid (GABA(A)) receptor antagonism using SR 95 531 did not cause any secretory pulse in fetal explants, whereas a significant stimulation of GnRH pulse frequency was obtained at 5 and 15 days. GnRH secretory response to repeated N-methyl-D-aspartate (NMDA) stimulation showed progressive disappearance, indicating that the inhibitory autofeedback was operating. GnRH release caused by glutamine was respectively 9% and 20% of that evoked by glutamate in fetal and 5-day-old rats whereas both amino acids were equally active at 15 days. Explants obtained after cesarean section performed at onset of labor did not show any secretory pulse, while pulses could be observed with explants obtained 2 h after vaginal delivery. Incubation of fetal explants with oxytocin (10(-8) M) or prostaglandin E2 (PGE2) (10(-6) M) resulted in occurrence of GnRH secretory pulses. A facilitatory effect of the oxytocin was shown to persist on Days 1, 5, and 15 and inhibitory effects of an oxytocin receptor antagonist provided some evidence of endogenous oxytocin involvement. We conclude that, in the fetal rat hypothalamus, GnRH inhibitory autofeedback and GABAergic inputs do not account for the absence of pulsatile GnRH secretion in vitro. A low rate of glutamate biosynthesis from glutamine is a possibly limiting factor. Oxytocin and PGE2 can play a facilitatory role in the postpartal occurrence of pulsatile GnRH secretion.     

Pulsatile GnRH secretion from primary cultures of sheep olfactory placode explants

The aim of this study was to investigate the development of pulsatile GnRH secretion by GnRH neurones in primary cultures of olfactory placodes from ovine embryos. Culture medium was collected every 10 min for 8 h to detect pulsatile secretion. In the first experiment, pulsatile secretion was studied in two different sets of cultures after 17 and 24 days in vitro. In the second experiment, a set of cultures was tested after 10, 17 and 24 days in vitro to investigate the development of pulsatile GnRH secretion in each individual culture. This study demonstrated that (i) primary cultures of GnRH neurones from olfactory explants secreted GnRH in a pulsatile manner and that the frequency and mean interpulse duration were similar to those reported in castrated ewes, and (ii) pulsatile secretion was not present at the beginning of the culture but was observed between 17 and 24 days in vitro, indicating the maturation of individual neurones and the development of their synchronization.     

Effect of stage of diestrus and number of cloprostenol (ICI 80, 996) injections on intervals to estrus, LH peak and ovulation in heifers

Intervals to the onset of estrus, luteinizing hormone (LH) peak and ovulation were compared in diestrous heifers after each of two cloprostenol treatments. Diestrous heifers were grouped at the first treatment (T1) according to day of the cycle, with heifers on days 5 through 8 designated as early diestrus and heifers on days 9 through 17 designated as late diestrus. Cloprostenol treatment was repeated (T2) 11 days after T1, at which time heifers in both groups were at similar stages of the estrous cycle. Visual observation, identification of the preovulatory LH peak, and rectal palpation were utilized to estimate data parameters. Split-plot analysis of variance showed a significant treatment x group interaction (P < .05). Time from prostaglandin treatment to the onset of estrus was similar for the early diestrous group after T1 (x = 53.1 hours ) and the early and late diestrous groups after T2 (x = 49.4 hours and 45.4 hours respectively). This interval was longer (P < .05) for the late diestrous group after T1 (x = 60.8 hours ) than for either group after T2, but not different from that for the early diestrous group after T1. Serum progesterone concentrations were higher (P < .05) at the time of T1 in the late diestrous group (x = 5.8 ng/ml ) than in the early diestrous group (x = 3.0 ng/ml ) or in either group at the time of T2 (x = 2.8 and 3.2 ng/ml respectively). Over all heifers, the synchrony of the onset of estrus was more precise (P < .05) after T2 than T1. Intervals from the onset of estrus to ovulation were not affected by group or treatment (overall mean = 24.4 +/- 1.0 hours, n = 42). We conclude that different recommendations for appointment artificial insemination (AI) may be indicated depending on the number of prostaglandin injections which are used in a prostaglandin synchronization program prior to insemination.     

Postnatal development of vascularity in the inferior colliculus of the young rat

The inferior colliculus in the rat midbrain is an auditory relay center whose functional maturation occurs postnatally. We examined by morphometry the vascularity and the nuclear profile density of the inferior colliculus in normal young rats at different ages (before and after the onset of auditory input). We also compared this region with a frontal region of the cerebral cortex in 24-day-old rats. The inferior colliculus from aldehyde-perfused Sprague-Dawley rats aged 5, 9, 14, and 24 days was analyzed by light microscopy of semithin plastic sections. The central region (mostly the central nucleus) was sampled at 5 levels representing its entire rostrocaudal extent. Patent-blood-vessel profiles were counted and classified according to their size and profile orientation. Counts of nuclear profiles in the same sections were also made. In the inferior colliculus of rats between 5 and 24 days of age, the small (less than 10-microns diameter) cross-sectioned vessel profiles increased over 6-fold in number per unit area. Correspondingly the vascular volume density, estimated by differential point counting, increased between these ages. However, there was a decrease in the number of neuronal and glial nuclear profiles per unit area, probably because of growth in the volume of the neuronal perikarya and processes, along with cell emigration reported to occur at early postnatal ages. This study has shown that an increase in vascularity in the central region of the rat inferior colliculus continues for up to 2 weeks after the onset of hearing.(ABSTRACT TRUNCATED AT 250 WORDS)     

11-Ketotetranor PGF metabolites,a suitable indicator for measuring prostaglandin release during the normal oestrous cycle and early pregnancy in the goat

Peripheral plasma levels of 15-ketodihydro-PGF_2α, 11-ketotetranor PGF metabolites and progesterone were measured during normal oestrous cycle and early pregnancy in six goats. The does were synchronized before the start of the study by means of 10 mg of PGF_2α. Blood samples were collected twice daily until day 12 of the oestrous cycle and subsequently every 3 h until the onset of oestrus, at which time the does were mated. The blood sampling protocol was repeated until day 28 of pregnancy. High pulsatile peaks of 15-ketodihydro-PGF_2α and 11-ketotetranor PGF metabolites were observed during the last days of the oestrous cycle, indicating PGF_2α releases. This coincided with a fall in progesterone levels. During early pregnancy no such peaks of prostaglandin metabolites were recorded and high levels of progesterone were maintained. In the goat, analysis of the 11-ketotetranor PGF metabolites seems to be a better indicator of PGF_2α release than the analysis of 15-ketodihydro-PGF_2α. The former metabolites are more long-lived in the circulation and are thus easier to detect.     

Effect of pulsatile or continuous administration of pituitary-derived chicken growth hormone (p-cGH) on lipid metabolism in broiler pullets.

1. The effects of pulsatile and continuous intravenous administration of exogenous, pituitary-derived chicken growth hormone (p-cGH) on lipid metabolism and endocrine/metabolite levels of broiler-strain pullets were studied. 2. Eight-week-old pullets were administered p-cGH or vehicle over a 10 min period every 90 min for 7 days. 3. Pullets were also administered the same daily amount (123 micrograms/kg of body weight/day) continuously for 7 days. 4. Feed intake, body weight gain, in vitro lipogenesis and hepatic enzyme activities were determined with certain hormones identified with the control of growth. 5. Pulsatile p-cGH administration for 7 days lacked effect on weight gain, feed efficiency, muscle or bone development. 6. Abdominal fat pad size was decreased (P less than 0.05) by pulsatile but not continuous administration of p-cGH. Pulsatile p-cGH administration also decreased (P less than 0.05) in vitro lipogenesis. Liver malic enzyme and isocitrate dehydrogenase activities were increased (P less than 0.05) by pulsatile but not continuous administration of p-cGH. In contrast, glutamic oxaloacetic transaminase activity was increased by a continuous infusion of p-cGH. 7. Plasma concentrations of T4 corticosterone and triglycerides were decreased (P less than 0.05) by a pulsatile but not a constant infusion of p-cGH. 8. Plasma T3 and GH were increased (P less than 0.05) by pulsatile p-cGH compared to both a continuous infusion of p-cGH and the saline controls. 9. This study is the first to prove that in the broiler chicken, the pattern of exogenous p-cGH administration is a factor influencing in vitro responses to the hormone.     

Pathogenesis of age dependent paralysis by a temperature sensitive mutant (tsl) of Moloney murine leukemia virus-TB.

The tsl mutant of Moloney murine leukemia virus-TB produces neurological disease leading to fatal hind limb paralysis when inoculated in newborn BALB/c mice. The present study was under taken to assess the role of T and B lymphocytes in age dependent resistance to tsl induced paralysis in BALB/c mice. The adoptive transfer of non-immune splenic unseparated lymphoid cells, T cells and B cells and tsl immune B cells and T cells to newborn BALB/c mice infected with tsl did not prevent the development of paralysis. However, adoptive transfer of immune splenic unseparated lymphoid cells and immune T cells delayed the onset of paralysis by 5 to 10 days as compared to the mice which did not receive the immune lymphocytes. Athymic BALB/c nude mice inoculated with tsl at days 1 and 10 after birth failed to develop the paralytic disease. Transfer of tsl neutralising antibody also delayed the onset of paralysis. Mice (10 days old) treated with cyclophosphamide, cyclosporine A, cortisone acetate and anti-T cell serum when inoculated with tsl also did not develop neurological disease. The results suggest that age related resistance to neurological disease may not be associated with B cell mediated immunity.     

Effect of alterations in pulsatile luteinizing hormone release on ovarian follicular atresia and steroid secretion on diestrus 1 in the rat estrous cycle

This study examined the importance of pulsatile luteinizing hormone (LH) release on diestrus 1 (D1; metestrus) in the rat estrous cycle to ovarian follicular development and estradiol (E2) secretion. Single injections of a luteinizing hormone-releasing hormone (LHRH) antagonist given at -7.5 h prior to the onset of a 3-h blood sampling period on D1 reduced mean blood LH levels by decreasing LH pulse amplitude, while frequency was not altered. Sequential injections at -7.5 and -3.5 h completely eliminated pulsatile LH secretion. Neither treatment altered the total number of follicles/ovary greater than 150 mu in diameter, the number of follicles in any size group between 150 and 551 mu, or plasma E2, progesterone, or follicle-stimulating hormone (FSH) levels. However, both treatments with LHRH antagonist significantly increased the percentage of atretic follicles in the ovary. These data indicate that: 1) pulsatile LH release is an important factor in determining the rate at which follicles undergo atresia on D1; 2) reductions in LH pulse amplitude alone are sufficient to increase the rate of follicular atresia on D1; 3) an absence of pulsatile LH release for a period of up to 10 h on D1 is not sufficient to produce a decline in ovarian E2 secretion, most likely because the atretic process was in its early stages and had not yet affected a sufficient number of E2-secreting granulosa cells to reduce the follicle's capacity to secrete E2; and 4) suppression or elimination of pulsatile LH release on D1 is not associated with diminished FSH secretion.     

The possible involvement of oscillatory cAMP signaling in multicellular morphogenesis of the cellular slime molds

The involvement of pulsatile chemoattractant emission and signal relay in aggregation and multicellular morphogenesis of a variety of cellular slime mold species was investigated. The species differ from each other in the developmental stage when pulsatile signaling first becomes evident. In D. discoideum, D. mucoroides, and D. purpureum pulsatile signal emission starts in the preaggregative field. In D. vinaceo-fuscum, D. mexicanum, P. violaceum, and P. pallidum the aggregation centers shifts from continuous to pulsatile secretion of chemoattractant during the aggregation process. In D. minutum pulsatile signaling starts after the completion of aggregation and slightly before the onset of culmination. Tip formation is a consequence of continued attraction of amoebae inside the aggregate to the center of signal emission. The occurrence of pulsatile signaling at an early stage of development is correlated with the capacity of the tip (signaling center) to organize a relatively large number of cells into a single fruiting body. Several lines of evidence suggest that cAMP is probably involved in the coordination of morphogenetic movement in the multicellular stage of all investigated species.     

Effects of pulsation frequency and endothelial integrity on enhanced arterial transmural filtration produced by pulsatile pressure

The role of the endothelium in regulating transmural fluid filtration into the artery wall under pulsatile pressure and the effects of changes in pulsatile frequency on filtration have received little attention. Previous experiments (Alberding JP, Baldwin AL, Barton JK, and Wiley E. Am J Physiol Heart Circ Physiol 286: H1827-H1835, 2004) demonstrated significantly increased filtration after initial onset of pulsatile pressure compared with that predicted by using parameters measured under steady pressure. To determine the role of the endothelium in this phenomenon, the following experiments were performed on five New Zealand White rabbits (anesthetized with 30 mg/kg pentobarbital sodium). One of each pair of carotid arteries was deendothelialized, and filtration measurements under steady and pulsatile pressure were compared with those made in intact vessels (Alberding JP, Baldwin AL, Barton JK, and Wiley E. Am J Physiol Heart Circ Physiol 286: H1827-H1835, 2004). To determine the effect of increasing pulsatile frequency on arterial filtration, transmural filtration was measured by using pulsatile pressure frequencies of 1 Hz, followed by 2 Hz, in another set of intact arteries (6 arteries and 3 animals). For deendothelialized vessels, the initial increase in filtration after onset of pulsatility was similar to that observed in intact vessels, but the subsequent reduction in filtration was less abrupt. When pulsatile frequency was increased from 1 to 2 Hz in intact arteries, an initial increase in filtration was observed, similar to that obtained after onset of pulsatile pressure subsequent to a steady pressure. The observed responses of arteries to pulsatile pressure, with and without endothelium, or undergoing a frequency change, suggest a dynamic role for the endothelium in regulating transvascular transport in vivo.     

Proestrous hormonal changes preceding the onset of ovulatory failure in lightly androgenized female rats

Proestrous hormonal profiles were characterized in lightly androgenized female rats prior to the onset of the delayed anovulatory syndrome (DAS). In these females, ovulatory failure and persistent vaginal estrus (PVE) occur at a very early age. Female Sprague-Dawley rats were injected with 10 micrograms testosterone propionate (TP) on postnatal Day 5. Control rats were untreated. All animals were weaned at 21 days of age, and following the onset of puberty, estrous cyclicity was monitored by vaginal smear. Rats showing regular 4-day cycles were used. Between 50-70 days of age, intra-atrial cannulae were implanted on a morning of proestrus (0700-0900 h) and blood was sampled at 2-h intervals from 1000 to 2000 h. Additional samples were taken at 0.5-h intervals from 1600 to 1800 h. Plasma was assayed for luteinizing hormone (LH), follicle-stimulating hormone (FSH) and progesterone (P) by radioimmunoassay (RIA). All animals were monitored for the onset of PVE or other alterations in estrous cyclicity. Females treated neonatally with TP that subsequently showed PVE by 150 days of age (PRE DAS) displayed a reduced peak amplitude (P less than 0.01) and delay in onset (1600 vs. 1400 h) of LH but not FSH secretion, when compared to controls. Females treated neonatally with TP that did not enter PVE by 150 days of age (No DAS) also showed a delayed rise in LH when compared to controls. However, the amplitude of LH secretion was not different from controls or PRE DAS females.(ABSTRACT TRUNCATED AT 250 WORDS)     

The influence of hosts, temperature and food sources on the longevity of Trichogramma platneri

Feeding experiments were conducted with Trichogramma platneri Nagarkatti (Hymenoptera: Trichogrammatidae) reared from the Angoumois grain moth, Sitotroga cerealella (Oliver) (Lepidoptera: Gelechiidae). T. platneri provisioned with host eggs do not live any longer than T. platneri without host eggs. Longevity of T. platneri is inversely related to temperature declining from 53 days at 10 °C to 3 days at 35 °C for honey-fed parasitoids and from 9 days at 10 °C to 1 day at 35 °C for unfed parasitoids. Sugar sources are necessary to prolong longevity of T. platneri, but a source of amino acid did not promote longevity. Honey solutions greater than 10%, and 43% fructose and sucrose solutions increased longevity 10–13 fold to 15–20 days in comparison to water when fed daily to T. platneri. Parasitoids fed only at the onset of the trial had greater longevity than unfed parasitoids but had a shorter longevity than parasitoids fed daily, due to the evaporation of the sugar solutions and consumption of the honey. Aphid honeydew is a suitable field-available sugar source supporting longevity up to 10 days, but is not as good as other sugar sources. Stabilizing additives did not reduce evaporation of a dilute sugar solution nor prolong longevity of T. platneri. Simulating a daily dew fall by misting vials, to redissolve the crystallized food residues left after providing food at the onset of the trial, failed to increase parasitoid longevity.     

In vitro flow dynamics of four prosthetic aortic valves: a comparative analysis

The velocity fields downstream of four prosthetic heart valves were mapped in vitro over the entire cross-section of a model aortic root using laser Doppler anemometry. THe Bj?rk-Shiley 60 degrees convexo-concave tilting disc valve, the Smeloff-Cutter caged ball valve, the St. Jude Medical bileaflet valve, and the Ionescu-Shiley standard bioprosthesis were examined under both steady and pulsatile flows. Velocity profiles under steady flow conditions were a good approximation for pulsatile profiles only during midsystole. The pulsatile flow characteristics of the four valves showed variation in large scale flow structures. Comparison of the valves according to pressure drop, shear stress and maximum velocities are also provided.     

Analytical construct of reversible desensitization of pituitary-testicular signaling: illustrative application in aging

Luteinizing hormone (LH) administered in pharmacological amounts downregulates Leydig cell steroidogenesis. Whether reversible downregulation of physiological gonadotropin drive operates in vivo is unknown. Most of the analytical models of dose-response functions that have been constructed are biased by the assumption that no downregulation exists. The present study employs a new analytical platform to quantify potential (but not required) pulsatile cycles of LH-testosterone (T) dose-response stimulation, desensitization, and recovery (pulse-by-pulse hysteresis) in 26 healthy men sampled every 10 min for 24 h. A sensitivity-downregulation hysteresis construct predicted marked hysteresis with a median time delay to LH dose-response inflection within individual T pulses of 23 min and with median T pulse onset and recovery LH sensitivities of 1.1 and 0.10 slope unit, respectively (P < 0.001). A potency-downregulation model yielded median estimates of one-half maximally stimulatory LH concentrations (EC(50) values) of 0.66 and 7.5 IU/l for onset and recovery, respectively (P < 0.001). An efficacy-downregulation formulation of hysteresis forecasts median LH efficacies of 20 and 8.3 ng·dl(-1)·min(-1) for onset and offset of T secretory burst, respectively (P = 0.002). Segmentation of the LH-T data by age suggested greater sensitivity, higher EC(50) (increased LH potency), and markedly (2.7-fold) attenuated LH efficacy in older individuals. Each of the three hysteresis models yielded a marked (P < 0.005) reduction in estimated model residual error compared with no hysteresis. In summary, model-based analyses allowing for (but not requiring) reversible pituitary-gonadal effector-response downregulation are consistent with a hypothesis of recurrent, brief cycles of LH-dependent stimulation, desensitization, and recovery of pulsatile T secretion in vivo and an age-associated reduction of LH efficacy. Prospective studies would be required to prove this aging effect.