The Experts below are selected from a list of 294 Experts worldwide ranked by ideXlab platform

Dino A Giussani - One of the best experts on this subject based on the ideXlab platform.

  • the placental phenotype adapts to chronic hypoxia and mitochondria targeted antioxidant mitoq therapy in rat pregnancy
    Reproductive Sciences, 2015
    Co-Authors: A M Nuzzo, Emily J Camm, A N Sferruzziperri, Alessandro Rolfo, Tullia Todros, A Logan, Michael P Murphy, Dino A Giussani
    Abstract:

    Introduction: The placenta responds to adverse environmental conditions, such as Maternal glucorticoid over-exposure and dietary manipulation, by adapting its capacity for substrate transfer to maintain appropriate fetal growth and development (Fowden et al. J Neuroendocrinol 20(4):439, 2008). Comparatively little is known about placental adaptations to hypoxia and/or oxidative stress. Here, we determined the effect of Maternal chronic hypoxia on placental morphology and established whether Maternal Treatment with MitoQ protected against hypoxiainduced alterations in placental structure.

  • vitamin c prevents intrauterine programming of in vivo cardiovascular dysfunction in the rat
    Circulation, 2013
    Co-Authors: Andrew D Kane, Emily J Camm, Emilio A Herrera, Dino A Giussani
    Abstract:

    Background: Fetal hypoxia is common and in vitro evidence supports its role in the programming of adult cardiovascular dysfunction through the generation of oxidative stress. Whether fetal chronic hypoxia programmes alterations in cardiovascular control in vivo, and if these alterations can be prevented by antioxidant Treatment, is unknown. This study investigated the effects of prenatal fetal hypoxia, with and without Maternal supplementation with vitamin C, on basal and stimulated cardiovascular function in vivo in the adult offspring at 4 months of age in the rat. Methods and Results: From days 6 to 20 of pregnancy, Wistar rats were subjected to Normoxia, Hypoxia (13% O2), Hypoxia+Vitamin C (5mg/ml in drinking water) or Normoxia+Vitamin C. At 4 months, male offspring were instrumented under urethane anaesthesia. Basal mean arterial blood pressure, heart rate and heart rate variability (HRV) were assessed, and stimulated baroreflex curves were generated with phenylephrine and sodium nitroprusside. Chronic fetal hypoxia increased the LF/HF HRV ratio and baroreflex gain, effects prevented by vitamin C administration during pregnancy. Conclusions: Chronic intrauterine hypoxia programmes cardiovascular dysfunction in vivo in adult rat offspring; effects ameliorated by Maternal Treatment with vitamin C. The data support a role for fetal chronic hypoxia programming cardiovascular dysfunction in the adult rat offspring in vivo through the generation of oxidative stress in utero.  (Circ J 2013; 77: 2604–2611)

George D. Wendel - One of the best experts on this subject based on the ideXlab platform.

  • Congenital syphilis after Maternal Treatment for syphilis during pregnancy
    American Journal of Obstetrics and Gynecology, 2002
    Co-Authors: Jeanne S. Sheffield, Pablo J. Sánchez, George Morris, Mark Maberry, Fiker Zeray, Donald D. Mcintire, George D. Wendel
    Abstract:

    Abstract OBJECTIVE: The purpose of this study was to characterize pregnancies that were complicated by Maternal syphilis that had been treated before delivery in which the newborn infant was diagnosed with congenital syphilis. STUDY DESIGN: Prospective surveillance from January 1, 1982, to December 31, 1998, involved women who received antenatal Treatment for syphilis. Infants who were born with congenital syphilis were identified by clinical or laboratory criteria. Antepartum factors such as gestational age, time to delivery and VDRL titers were then analyzed and compared with those of women who had been treated and who were delivered of an uninfected infant. The 1:1 match was based on the stage of syphilis and the gestational age at Treatment. RESULTS: Forty-three women who received antepartum therapy for syphilis were delivered of an infant with congenital syphilis. Most of the women had been treated for early syphilis; the mean gestational age at Treatment was 30.3 weeks. Thirty-five percent of the women were treated >30 days before delivery. Fifty-six percent of the infants were preterm. The 1:1 match revealed that Treatment and delivery high VDRL titers, prematurity, and a short interval from Treatment to delivery were significantly different in those infants who were diagnosed with congenital syphilis. CONCLUSION: High VDRL titers at Treatment and delivery, earlier Maternal stage of syphilis, the interval from Treatment to delivery, and delivery of an infant at ≤36 weeks' gestation are associated with the delivery of a congenitally infected neonate after adequate Treatment for Maternal syphilis. (Am J Obstet Gynecol 2002;186:569-73.)

Virginia B. Bowen - One of the best experts on this subject based on the ideXlab platform.

  • Missed Opportunities for Prevention of Congenital Syphilis — United States, 2018
    MMWR. Morbidity and mortality weekly report, 2020
    Co-Authors: Anne Kimball, Hillard Weinstock, Elizabeth Torrone, Kathryn Miele, Laura Bachmann, Phoebe Thorpe, Virginia B. Bowen
    Abstract:

    Congenital syphilis is an infection with Treponema pallidum in an infant or fetus, acquired during pregnancy from a mother with untreated or inadequately treated syphilis. Congenital syphilis can cause miscarriage, stillbirth, or early infant death, and infected infants can experience lifelong physical and neurologic problems. Although timely identification and Treatment of Maternal syphilis during pregnancy can prevent congenital syphilis (1,2), the number of reported congenital syphilis cases in the United States increased 261% during 2013-2018, from 362 to 1,306. Among reported congenital syphilis cases during 2018, a total of 94 resulted in stillbirths or early infant deaths (3). Using 2018 national congenital syphilis surveillance data and a previously developed framework (4), CDC identified missed opportunities for congenital syphilis prevention. Nationally, the most commonly missed prevention opportunities were a lack of adequate Maternal Treatment despite the timely diagnosis of syphilis (30.7%) and a lack of timely prenatal care (28.2%), with variation by geographic region. Congenital syphilis prevention involves syphilis prevention for women and their partners and timely identification and Treatment of pregnant women with syphilis. Preventing continued increases in congenital syphilis requires reducing barriers to family planning and prenatal care, ensuring syphilis screening at the first prenatal visit with rescreening at 28 weeks' gestation and at delivery, as indicated, and adequately treating pregnant women with syphilis (2). Congenital syphilis prevention strategies that implement tailored public health and health care interventions to address missed opportunities can have substantial public health impact.

  • increase in incidence of congenital syphilis united states 2012 2014
    Morbidity and Mortality Weekly Report, 2015
    Co-Authors: Virginia B. Bowen, Elizabeth Torrone, Sarah Kidd, Hillard Weinstock
    Abstract:

    Congenital syphilis (CS) occurs when a mother infected with syphilis transmits the infection to her child during pregnancy. CS can cause severe illness, miscarriage, stillbirth, and early infant death. However, among pregnant women with syphilis who deliver after 20 weeks gestation, Maternal Treatment with penicillin is 98% effective at preventing CS (1). In the United States, the rate of CS decreased during 1991–2005 but increased slightly during 2005–2008 (2). To assess recent trends in CS, CDC analyzed national surveillance data reported during 2008–2014, calculated rates, and described selected characteristics of infants with CS and their mothers. The overall rate of reported CS decreased from 10.5 to 8.4 cases per 100,000 live births during 2008–2012, and then increased to 11.6 cases per 100,000 live births in 2014, the highest CS rate reported since 2001. From 2012 to 2014, reported cases and rates of CS increased across all regions of the United States. To reduce CS, the timely identification of and response to increases in syphilis among women of reproductive age and men who have sex with women are essential. All women should have access to quality prenatal care, including syphilis screening and adequate Treatment, during pregnancy (3).

Hillard Weinstock - One of the best experts on this subject based on the ideXlab platform.

  • Missed Opportunities for Prevention of Congenital Syphilis — United States, 2018
    MMWR. Morbidity and mortality weekly report, 2020
    Co-Authors: Anne Kimball, Hillard Weinstock, Elizabeth Torrone, Kathryn Miele, Laura Bachmann, Phoebe Thorpe, Virginia B. Bowen
    Abstract:

    Congenital syphilis is an infection with Treponema pallidum in an infant or fetus, acquired during pregnancy from a mother with untreated or inadequately treated syphilis. Congenital syphilis can cause miscarriage, stillbirth, or early infant death, and infected infants can experience lifelong physical and neurologic problems. Although timely identification and Treatment of Maternal syphilis during pregnancy can prevent congenital syphilis (1,2), the number of reported congenital syphilis cases in the United States increased 261% during 2013-2018, from 362 to 1,306. Among reported congenital syphilis cases during 2018, a total of 94 resulted in stillbirths or early infant deaths (3). Using 2018 national congenital syphilis surveillance data and a previously developed framework (4), CDC identified missed opportunities for congenital syphilis prevention. Nationally, the most commonly missed prevention opportunities were a lack of adequate Maternal Treatment despite the timely diagnosis of syphilis (30.7%) and a lack of timely prenatal care (28.2%), with variation by geographic region. Congenital syphilis prevention involves syphilis prevention for women and their partners and timely identification and Treatment of pregnant women with syphilis. Preventing continued increases in congenital syphilis requires reducing barriers to family planning and prenatal care, ensuring syphilis screening at the first prenatal visit with rescreening at 28 weeks' gestation and at delivery, as indicated, and adequately treating pregnant women with syphilis (2). Congenital syphilis prevention strategies that implement tailored public health and health care interventions to address missed opportunities can have substantial public health impact.

  • increase in incidence of congenital syphilis united states 2012 2014
    Morbidity and Mortality Weekly Report, 2015
    Co-Authors: Virginia B. Bowen, Elizabeth Torrone, Sarah Kidd, Hillard Weinstock
    Abstract:

    Congenital syphilis (CS) occurs when a mother infected with syphilis transmits the infection to her child during pregnancy. CS can cause severe illness, miscarriage, stillbirth, and early infant death. However, among pregnant women with syphilis who deliver after 20 weeks gestation, Maternal Treatment with penicillin is 98% effective at preventing CS (1). In the United States, the rate of CS decreased during 1991–2005 but increased slightly during 2005–2008 (2). To assess recent trends in CS, CDC analyzed national surveillance data reported during 2008–2014, calculated rates, and described selected characteristics of infants with CS and their mothers. The overall rate of reported CS decreased from 10.5 to 8.4 cases per 100,000 live births during 2008–2012, and then increased to 11.6 cases per 100,000 live births in 2014, the highest CS rate reported since 2001. From 2012 to 2014, reported cases and rates of CS increased across all regions of the United States. To reduce CS, the timely identification of and response to increases in syphilis among women of reproductive age and men who have sex with women are essential. All women should have access to quality prenatal care, including syphilis screening and adequate Treatment, during pregnancy (3).

Mary J. Druse - One of the best experts on this subject based on the ideXlab platform.

  • Effects of ethanol and ipsapirone on the development of midline raphe glial cells and astrocytes.
    Alcohol (Fayetteville N.Y.), 2003
    Co-Authors: Nuzhath F Tajuddin, Jason L. Eriksen, Luisa A. Orrico, Mary J. Druse
    Abstract:

    Abstract Previously, results of studies from our laboratory have shown that the offspring of ethanol-fed female rats have a significant decrease in serotonin (5-HT) neurons and glia that contain S100B, an essential trophic factor for the development of 5-HT neurons. The deficiency of S100B-immunopositive glia was detected during the vulnerable period in 5-HT neuron development and in brain areas proximal to these neurons. The reductions of both 5-HT neurons and S100B-positive glia were prevented by Maternal Treatment with a 5-HT 1A agonist (i.e., ipsapirone or buspirone). In the current study, we investigated whether the offspring of ethanol-fed rats had a general decrease in the density of glial cells in the brain areas that contain 5-HT neurons, and we determined whether these changes were prevented by Maternal Treatment with ipsapirone between gestational days (GDs) 13 and 20. We estimated the density of vimentin-positive glia of the midline raphe glial structure (MRGS) at GD 20 and postnatal day (PND) 5 and of glial fibrillary acidic protein (GFAP)–positive astrocytes proximal to the dorsal and median raphe at PNDs 5 and 19. The results of this study provide evidence that in utero ethanol exposure is associated with a reduced density of GFAP-immunopositive astrocytes proximal to the dorsal and median raphe. Maternal ipsapirone Treatment significantly increased astroglial density in the dorsal raphe at PNDs 5 and 19 and in the median raphe at PND 5, such that it either prevented (dorsal raphe, PNDs 5 and 19) or blunted (median raphe, PND 5) the effects of ethanol.

  • A persistent deficit of serotonin neurons in the offspring of ethanol-fed dams: protective effects of Maternal ipsapirone Treatment.
    Brain research. Developmental brain research, 2001
    Co-Authors: Nuzhath F Tajuddin, Mary J. Druse
    Abstract:

    Abstract An earlier study from this laboratory found a significant reduction in the density of serotonin (5-HT) neurons in the dorsal and median raphe and in the B9 complex of postnatal day 5 (PN5) offspring of female rats that consumed ethanol on a chronic basis prior to parturition. In addition, we demonstrated that Maternal Treatment with the 5-HT 1A agonist ipsapirone (3 mg/kg) prevented the ethanol-associated reduction in 5-HT neurons. The present investigation examined whether there was a persistent deficit of 5-HT-immunopositive neurons in the dorsal and median raphe of the offspring of ethanol-fed dams. We also evaluated whether a lower ipsapirone dose (1 mg/kg) was protective to developing 5-HT neurons in the offspring of ethanol-fed dams. The offspring of ethanol-fed dams exhibited an apparent lasting reduction in the density of 5-HT neurons in the dorsal and median raphe. The density of 5-HT neurons in control offspring was comparable at PN5 and PN19, but at both ages the offspring of ethanol-fed dams had a significant deficit of 5-HT neurons in the dorsal and median raphe. The lack of recovery in the density of 5-HT-immunopositive neurons in the offspring of ethanol-fed dams between PN5 and PN19 suggests and that the reduction was long lasting. The protective effects of ipsapirone appeared to be dose dependent. The density of 5-HT neurons in the dorsal and median raphe of PN5 (prior study) and PN19 offspring of ethanol-fed dams that were treated with 3 mg/kg of ipsapirone between gestational day 13 (G13) and G20 was comparable to that of control offspring. However, the effects of Maternal Treatment of ethanol-fed dams with the 1 mg/kg dose were variable, and some abnormalities were detected in the offspring of ipsapirone-treated control dams.

  • potential involvement of s100b in the protective effects of a serotonin 1a agonist on ethanol treated astrocytes
    Developmental Brain Research, 2001
    Co-Authors: Jason L. Eriksen, Mary J. Druse
    Abstract:

    Abstract Previously, this laboratory found that the offspring of rats that consumed ethanol on a chronic basis prior to parturition exhibited a significant reduction in serotonin (5-HT) neurons and in astrocytes proximal to these neurons. This laboratory also showed that Maternal Treatment with a 5-HT1A agonist during the latter part of gestation prevented the reduction of 5-HT neurons and most of the astrocyte abnormalities. The present in vitro studies extended our prior in vivo work by examining the potential involvement of S100B with the protective effects of a 5-HT1A agonist, i.e., buspirone, on astrocytes. Astrocyte cultures were either maintained in chemically defined media in the presence and absence of ethanol and buspirone or in conditioned media that was generated by ethanol- and buspirone-treated astrocytes. A mouse monoclonal antibody to S100B was used to assess the potential involvement of S100B with the protective effects of buspirone. Additional in vitro studies measured the direct effects of S100B and ethanol on astrocyte proliferation. These investigations demonstrate that in vitro ethanol exposure reduces the number of astrocytes, and that Treatment with the 5-HT1A agonist buspirone prevents the ethanol-associated reduction in astrocyte number. The protective effects of buspirone appear to be mediated by factors that are secreted by astrocytes; such factors likely include S100B. In addition, added S100B prevents an ethanol-associated reduction in [3H]-thymidine incorporation into proliferating astrocytes.

  • in utero ethanol exposure decreased the density of serotonin neurons Maternal ipsapirone Treatment exerted a protective effect
    Developmental Brain Research, 1999
    Co-Authors: Nuzhath F Tajuddin, Mary J. Druse
    Abstract:

    Abstract Prior studies from this laboratory showed that in utero ethanol exposure severely retards the development of the serotonin (5-HT) system; we demonstrated a reduced concentration of 5-HT and 5-HT reuptake sites and alterations in the concentration of 5-HT 1A receptors in ethanol-exposed offspring. These investigations also found that Maternal Treatment with a 5-HT 1A agonist, buspirone, prevented most of the ethanol-associated damage to the developing 5-HT system. In the present investigation, we investigated whether the ethanol-associated changes in the 5-HT system are due to a reduction of 5-HT neurons and whether any changes in the density of 5-HT neurons can be prevented by Maternal Treatment with another 5-HT 1A agonist, ipsapirone. Using immunocytochemistry, we found that in utero ethanol exposure reduced the density of 5-HT immunopositive neurons in the dorsal raphe, median raphe and B9 neurons of postnatal day 5 (PN5) rats. In all three brain areas, the offspring of ethanol-fed, saline-treated dams exhibited a 28%–40% reduction in 5-HT neurons. Ipsapirone prevented the ethanol-induced reduction in 5-HT immunopositive neurons in the dorsal raphe, median raphe and B9 neurons. In the dorsal and median raphe of control offspring, ipsapirone did not alter the concentration of 5-HT neurons. However, this drug did reduce 5-HT neurons in the B9 region of the offspring of control-fed rats.