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Male Fetuses (male + fetuse)
Selected AbstractsMaternal and neonatal outcomes of pregnancies complicated by asthma in an Australian populationAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 6 2009Vicki L. CLIFTON Objective:, To determine if there are sex differences in risk and incidence of stillbirth, preterm delivery and small-for-gestational age (SGA) in pregnancies complicated by maternal asthma relative to a non-asthmatic population. Study design:, Univariant and multiple regression analysis of the incidence of preterm delivery, SGA and stillbirth in singleton pregnancies complicated by asthma in Newcastle, NSW, Australia, from 1995 to 1999. Results:, Asthma complicated 12% of all singleton pregnancies. The incidence of preterm delivery was not significantly different between asthmatic (13%) and non-asthmatic (11%) pregnancies. Male fetuses (53%) were more likely to deliver preterm than female fetuses (47%) in both asthmatic and non-asthmatic populations. There were significantly more male neonates of pregnancies complicated by asthma that were SGA at term relative to those of the non-asthmatic population. There were significantly more preterm female neonates that were SGA in pregnancies complicated by asthma relative to those of the non-asthmatic population. Male fetuses were more likely to be associated with a stillbirth in pregnancies complicated by asthma than female fetuses. Conclusion:, The presence of maternal asthma during pregnancy increases the risk of stillbirth for the male fetus and is associated with changes in fetal growth, but does not increase the incidence of a preterm delivery. [source] Antiandrogenic effects of dibutyl phthalate and its metabolite, monobutyl phthalate, in ratsCONGENITAL ANOMALIES, Issue 4 2002Makoto Ema ABSTRACT, Developmental toxicity following administration of dibutyl phthalate (DBF) and its major metabolite, monobutyl phthalate (MBuP), by gavage was determined in Wistar rats. DBF on days 0,8 of pregnancy induced an increase in the incidence of preimplantation loss at 1250 mg/kg and higher and postimplantation loss at 750 mg/kg and higher. MBuP on days 0,8 of pregnancy produced an increase in the incidence of pre-and postimplantation loss at 1000 mg/kg. DBF on days 7,15 of pregnancy caused an increase in the incidence of fetuses with malformations at 750 mg/kg. MBuP on days 7,15 of pregnancy produced an increased incidence of fetuses with malformations at 500 mg/kg and higher. DBF on days 15,17 of pregnancy resulted in a decrease in the anogenital distance (AGD) of male fetuses and increase in the incidence of fetuses with undescended testes at 500 mg/kg and higher. MBuP on days 15,17 of pregnancy caused a decreased male AGD and increased incidence of fetuses with undescended testes at 250 mg/kg and higher. No effect of DBF and MBuP on the AGD was found in female offspring. The spectrum of fetal malformations, dependence of gestational days of treatment on the manifestation of teratogenicity, and alterations in development of the male reproductive system observed after administration of DBF were in good agreement with those observed after administration of MBuP. These findings suggest that MBuP may be responsible for the induction of developmental toxic effects of DBP. The doses that produced a decrease in the AGD and undescended testes in male offspring were lower than those producing maternal toxicity, fetal malformations after administration during major organogenesis, and embryonic loss. The male reproductive system may be more susceptible than other organ systems to DBP and MBuP toxicity after maternal exposure. [source] Intrauterine proximity to male fetuses affects the morphology of the sexually dimorphic nucleus of the preoptic area in the adult rat brainEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2006Minjuan Pei Abstract Previous studies on polytocous rodents have revealed that the fetal intrauterine position influences its later anatomy, physiology, reproductive performance and behavior. To investigate whether the position of a fetus in the uterus modifies the development of the brain, we examined whether the structure of the sexually dimorphic nucleus of the preoptic area (SDN-POA) of rat brains accorded to their intrauterine positions. Brain sections of adult rats gestated between two male fetuses (2M) and between two female fetuses (2F) in the uterus were analysed for their immunoreactivity to calbindin-D28k, which is a marker of the SDN-POA. The SDN-POA volume of the 2M adult males was greater than that of the 2F adult males, whereas the SDN-POA volume of the 2M and 2F adult females showed no significant difference. This result indicated that contiguous male fetuses have a masculinizing effect on the SDN-POA volume of the male. To further examine whether the increment of SDN-POA volume in adulthood was due to exposure to elevated steroid hormones during fetal life, concentrations of testosterone and 17,-estradiol in the brain were measured with 2M and 2F fetuses during gestation, respectively. On gestation day 21, the concentrations of testosterone and 17,-estradiol in the brain were significantly higher in the 2M male rats as compared with the 2F male rats. The results suggested that there was a relationship between the fetal intrauterine position, hormone transfer from adjacent fetuses and the SDN-POA volume in adult rat brains. [source] Differential developmental toxicities of di- n -hexyl phthalate and dicyclohexyl phthalate administered orally to ratsJOURNAL OF APPLIED TOXICOLOGY, Issue 6 2009Anne-Marie Saillenfait Abstract The objective of this study was to evaluate the developmental toxic potential of di- n -hexyl phthalate (DnHP) and dicyclohexyl phthalate (DCHP) in rats. Pregnant Sprague,Dawley rats were exposed to DnHP or DCHP at doses of 0 (olive oil), 250, 500 and 750 mg kg,1 per day, by gavage, on gestational days (GD) 6,20. Maternal food consumption and body weight gain were significantly reduced at 750 mg kg,1 per day of DnHP and at the two high doses of DCHP. Slight changes in liver weight associated with peroxisomal enzyme induction were seen in dams treated with DnHP or DCHP. DnHP caused dose-related developmental toxic effects, including marked embryo mortality at 750 mg kg,1 per day, and presence of malformations (mainly cleft palate, eye defects and axial skeleton abnormalities) and significant decreases in fetal weight at 500 and 750 mg kg,1 per day. Significant delay of ossification and increase in the incidence of skeletal variants (e.g. supernumerary lumbar ribs) also appeared at 250 mg kg,1 per day. DCHP produced fetal growth retardation at 750 mg kg,1 per day, as evidenced by significant reduction of fetal weight. DnHP and DCHP induced a significant and dose-related decrease in the anogenital distance of male fetuses at all doses, and there was a significant increase in the incidence of male fetuses with undescended testis at 500 and 750 mg kg,1 per day of DnHP. In conclusion, DnHP showed clear embryolethality and teratogenicity, but not DCHP. There was evidence that both phthalates could alter the development of the male reproductive system after in utero exposure, DnHP being much more potent than DCHP. Copyright © 2009 John Wiley & Sons, Ltd. [source] Prenatal testosterone treatment potentiates the aggression-inhibiting effect of the neurosteroid dehydroepiandrosterone in female miceAGGRESSIVE BEHAVIOR, Issue 2 2001Fabrice Perché Abstract The neurosteroid dehydroepiandrosterone (DHEA) is a powerful inhibitor of aggression in murine models when given for 15 days and potentially may be useful in the management of inappropriate human aggression. Although the biosynthesis and metabolism of DHEA have been described, little is known about the potential effect of the steroidal environment during sexual differentiation on the subsequent response to DHEA. Whether prenatal androgen exposure influences the subsequent response to DHEA was assessed by comparing the effect of DHEA (80 ,g/d) on aggression in female offspring where dams were treated with 1, 10, or 100 ,g of testosterone (T) on days 15 to 18 of gestation (Experiment I) or that developed in different uterine positions (Experiment II). The results showed that DHEA decreased attack behavior in general and that the 100-,g prenatal T treatments enhanced the antiaggressive effect of this neurosteroid. Neither the lower doses of exogenously administered T nor the uterine position led to an enhanced response to DHEA. In addition, whether DHEA produced changes in social and nonsocial activities was examined. In the 100-,g T females, DHEA increased the duration of the former and decreased the frequency and duration of the latter, indicating that it was not a general decrement in behavioral expression that mediated the enhanced response to the antiaggressive effect of DHEA. In the second experiment, DHEA treatment led to increased frequencies of social nonaggressive and nonsocial activities. However, the uterine positions × treatment interactions were not significant, demonstrating that contiguity to male fetuses did not differentially affect the response to DHEA. Aggr. Behav. 27:130,138, 2001. © 2001 Wiley-Liss, Inc. [source] The sex ratio and age-specific male mortality: Evidence for culling in uteroAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 6 2007Tim Bruckner While adverse conditions early in life reportedly predispose individuals to increased mortality in adulthood, controversy remains as to whether exogenous insults in utero, especially among male fetuses, induce similar cohort "damage" in populations. A rival theory postulates that exogenous stressors in gestation may "cull" frail male members of the cohort before birth, leaving a smaller but hardier cohort with improved survival. Recent tests, which use the sex ratio (i.e., the odds of a male live birth) as a gauge of insults inflicted upon cohorts in gestation, support the culled cohort argument. These tests, however, examined only aggregate male lifespan, thereby obscuring potential heterogeneity of both damaged and culled cohorts at specific ages over the life course. Using time-series methods, we explore associations between the sex ratio and cohort male mortality in infancy (before age 1), childhood (1,4 years), youth (5,19 years), adulthood (20,54 years), and old-age (55,79 years). We examine males born in Sweden (1751,1913), Denmark (1835,1913), and England and Wales (1841,1912). Our findings generally support culled cohorts in that male mortality across all ages fell below its expected value among cohorts in which the sex ratio dropped below its expected level. These findings suggest that exogenous shocks to gestation, as measured by a lower than expected sex ratio, may cull males in utero, leaving behind a less frail cohort over the entire life course. Am. J. Hum. Biol., 2007. © 2007 Wiley-Liss, Inc. [source] Fetal sex determination using circulating cell-free fetal DNA (ccffDNA) at 11 to 13 weeks of gestationPRENATAL DIAGNOSIS, Issue 10 2010Ranjit Akolekar Abstract Objective To examine the performance of a mass spectrometry-based detection platform using three Y-chromosome sequences for fetal sex determination from circulating cell-free fetal DNA (ccffDNA) in maternal blood in the first trimester of pregnancy. Methods We extracted ccffDNA for the determination of fetal sex from stored maternal plasma obtained at 11 to 13 weeks' gestation from singleton pregnancies with documented fetal gender. Mass spectrometry was used to examine 236 specimens for the presence of three Y-chromosome sequences (SRY, DBY and TTTY2). The sample was classified as male, female or inconclusive depending on the detection of three, one/none and two sequences, respectively. Results Three (1.3%) of the 236 cases were classified as invalid due to the absence of a well-defined spectral peak for TGIF and 22 (9.3%) were reported as inconclusive. In the 211 cases with a valid result, the fetal sex was correctly identified in 90 of 91 male babies and 119 of 120 female babies giving an accuracy of 99.1% and sensitivity and specificity for prediction of male fetuses of 98.9 and 99.2%, respectively. Conclusion Fetal sex determination can be accurately determined from maternal ccffDNA in the first trimester of pregnancy using mass spectrometry analysis. Copyright © 2010 John Wiley & Sons, Ltd. [source] Fetal cells in maternal plasma are found in a late state of apoptosisPRENATAL DIAGNOSIS, Issue 9 2004Aggeliki Kolialexi Abstract Objective The present study was designed to give possible answers to some of the discrepancies regarding the presence or not of intact fetal cells in maternal plasma during pregnancy. Materials and Methods 12-mL peripheral blood was collected from 33 pregnant women in the second trimester: 6 mL was harvested by 3-step Percoll gradient centrifugation and plasma cells were analyzed by FISH with X/Y chromosome specific probes. From the remaining 6 mL, plasma-derived cells were isolated with three different gradient centrifugation protocols and apoptosis was determined following EthBr staining. Results The number of cells recovered ranged from 900 to 3000. At least one Y positive signal was seen in 12 out of 17 cases with male fetuses at a frequency of 0.12% (range 0.05,0.27%). No XY cells were detected in the plasma of women carrying female fetuses. Hybridization efficiency was <60%. EthBr staining demonstrated that the majority of these cells were in their late apoptosis. Conclusion Our findings confirm the presence of intact fetal apoptotic cells in maternal plasma; however, their late apoptotic state and the low number does not as yet encourage their use in clinical practice. Copyright © 2004 John Wiley & Sons, Ltd. [source] Hydrops fetalis in three male fetuses of a female with incontinentia pigmentiPRENATAL DIAGNOSIS, Issue 12 2001Andreas Dufke Abstract Objectives Careful investigation of hydrops fetalis (HF) is important with regard to genetic counselling and prenatal diagnosis. HF is known to be associated with various genetic disorders. To date there has been only one report of a male fetus in whom incontinentia pigmenti (IP) was associated with generalised oedema. We describe a family who had a girl with clinical signs of IP after three consecutive miscarriages of three male fetuses due to HF. Results Molecular genetic analysis showed a mutation in the NEMO/IKK, gene in the girl and the mother, which confirmed the diagnosis of IP in both cases. In the two fetuses that could be investigated, inheritance of the affected maternal X chromosome could be demonstrated retrospectively by linkage analysis. Conclusion The present findings suggest that IP might be an X-linked dominant trait causing HF in male fetuses. In cases of recurrent HF in male fetuses, minimal signs of IP in the maternal line should therefore be carefully investigated in order to be able to perform mutational analysis and to offer appropriate genetic counselling. Copyright © 2001 John Wiley & Sons, Ltd. [source] The effect of oestrogen and testosterone on the urethral seam of the developing male mouse genital tubercleBJU INTERNATIONAL, Issue 9 2003S. Yucel OBJECTIVES To describe the effects of exogenous oestrogens and androgens on urethral formation in the mouse, as the development of the mouse and human urethra have significant similarities, and understanding normal male urethral development may help to identify the causes of abnormal development, e.g. hypospadias. MATERIALS AND METHODS Timed-pregnant C57/6 mice were exposed to synthetic oestrogens and androgens. The morphology of the genital tubercles was examined histologically and with three-dimensional computer reconstruction. Specific attention was focused on the developing urethral seam. RESULTS Microscopic serial analysis confirmed the presence of an arrest in seam formation in about half of oestrogen-treated male fetuses. In contrast, there was acceleration of urethral fold fusion and a longer urethral tube in those treated with androgens. Oestrogen-treated fetuses had a thin periurethral spongiosa, in contrast to androgen-treated fetuses which developed a thicker periurethral spongiosa. The effect of oestrogens on seam area formation did not depend on the dose, but in contrast, in the androgen-treated fetuses it was. CONCLUSION Oestrogens and androgens have a direct effect on the fusion of the urethral fold that leads to seam formation. Normal urethral development depends on the delicate balance of these complementary hormones. [source] | |||||||||||||