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Takeshi Maruo - One of the best experts on this subject based on the ideXlab platform.
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increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or Intrauterine Growth Retardation
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Naonori Ishihara, Hiroya Matsuo, Homare Murakoshi, Jovelle B Laoagfernandez, Takashi Samoto, Takeshi MaruoAbstract:OBJECTIVE: This study was undertaken to determine whether preeclampsia and Intrauterine Growth Retardation are associated with an increase in placental apoptosis. STUDY DESIGN: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. RESULTS: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and Intrauterine Growth Retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P <.001; Intrauterine Growth Retardation, P <.01). Transmission electron microscopy revealed the appearance of apoptotic nuclei in trophoblasts in severe preeclamptic term placenta. CONCLUSION: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and Intrauterine Growth Retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.
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increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or Intrauterine Growth Retardation
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Naonori Ishihara, Hiroya Matsuo, Homare Murakoshi, Jovelle B Laoagfernandez, Takashi Samoto, Takeshi MaruoAbstract:Abstract Objective: This study was undertaken to determine whether preeclampsia and Intrauterine Growth Retardation are associated with an increase in placental apoptosis. Study Design: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. Results: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and Intrauterine Growth Retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P P Conclusion: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and Intrauterine Growth Retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.(Am J Obstet Gynecol 2002;186:158-66.)
Naonori Ishihara - One of the best experts on this subject based on the ideXlab platform.
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increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or Intrauterine Growth Retardation
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Naonori Ishihara, Hiroya Matsuo, Homare Murakoshi, Jovelle B Laoagfernandez, Takashi Samoto, Takeshi MaruoAbstract:OBJECTIVE: This study was undertaken to determine whether preeclampsia and Intrauterine Growth Retardation are associated with an increase in placental apoptosis. STUDY DESIGN: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. RESULTS: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and Intrauterine Growth Retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P <.001; Intrauterine Growth Retardation, P <.01). Transmission electron microscopy revealed the appearance of apoptotic nuclei in trophoblasts in severe preeclamptic term placenta. CONCLUSION: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and Intrauterine Growth Retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.
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increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or Intrauterine Growth Retardation
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Naonori Ishihara, Hiroya Matsuo, Homare Murakoshi, Jovelle B Laoagfernandez, Takashi Samoto, Takeshi MaruoAbstract:Abstract Objective: This study was undertaken to determine whether preeclampsia and Intrauterine Growth Retardation are associated with an increase in placental apoptosis. Study Design: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. Results: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and Intrauterine Growth Retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P P Conclusion: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and Intrauterine Growth Retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.(Am J Obstet Gynecol 2002;186:158-66.)
Shaul Harel - One of the best experts on this subject based on the ideXlab platform.
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Sleep-wake patterns in children with Intrauterine Growth Retardation.
Journal of child neurology, 2002Co-Authors: Yael Leitner, Aviva Fattal-valevski, Aviva Mimouni Bloch, Avi Sadeh, Orit Neuderfer, Liat Tikotzky, Shaul HarelAbstract:The purpose of this study was to characterize the sleep patterns of children with Intrauterine Growth Retardation, known to be at risk for neurodevelopmental disorders, and seek a possible correlation with behavior, concentration, and attention problems. The sleep patterns of 26 children with Intrauterine Growth Retardation aged 4 to 7 years were compared with those of 47 control children using activity monitors (actigraphs). In addition, data were collected from the parents regarding sleep habits, behavior, concentration, and attention. Children with Intrauterine Growth Retardation aged 4 to 7 years were found to have a tendency toward poorer quality of sleep than their matched controls. This inclination was statistically significant only for one sleep measure, the true sleep time. A tendency toward increased fragmentation of sleep, prolonged waking, and decreased sleep efficiency, although not statistically significant in this study, was demonstrated. Our results showed that 58% of the children with Intrauterine Growth Retardation, compared with 40% of the children in the control group, could be defined as "poor sleepers" (sleep efficiency lower than 90% or three or more waking episodes per night). This disturbed sleep profile is probably an integral part of the neurodevelopmental profile typical of these at-risk children. No significant correlations were found between sleep quality and behavior, concentration, and attention problems.
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experimental Intrauterine Growth Retardation alters renal development
Pediatric Nephrology, 2000Co-Authors: Haim Bassan, Leonor Trejo, Naam Kariv, Merav Bassan, Esther Berger, Aviva Fattal, Illana Gozes, Shaul HarelAbstract:Vascular placental insufficiency is considered a common pathogenic factor in human Intrauterine Growth Retardation (IUGR), resulting in small-for-gestational-age, asymmetric newborns. IUGR neonates experience higher morbidity and mortality rates, as well as a possible contribution towards late sequelae, such as hypertension, and cardiovascular disease in adulthood. To simulate vascular placental insufficiency, an experimental rabbit IUGR model was used. Intrauterine Growth Retardation was achieved by ligation of 25–30% uteroplacental vessels of half of the fetuses during the last third of gestation. Ischemic fetuses were significantly small, asymmetric, and had a disproportionately small body with a relatively large head. The kidneys from all groups were analyzed for relative estimated glomeruli number (REGN) using an unbiased blind design. The glomeruli number was significantly reduced in the asymmetric IUGR rabbit fetuses, probably due to decreased renal vascular supply. Our results support the concept that the reduced number of glomeruli may contribute to impaired renal function, thus predisposing to neonatal renal dysfunction and late sequelae, such as adult hypertension. This study emphasizes the clinical importance of early IUGR diagnosis and prevention.
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Six-year follow-up of children with Intrauterine Growth Retardation: long-term, prospective study.
Journal of child neurology, 2000Co-Authors: Yael Leitner, Aviva Fattal-valevski, Miriam Kutai, Ariel J. Jaffa, Ariel Many, Ronny Geva, Haim Bassan, Edith Posner, Shaul HarelAbstract:This prospective study was designed to characterize the neurodevelopmental and cognitive difficulties specific to children with Intrauterine Growth Retardation and to detect early clinical predictors of these difficulties. Eighty-one children with Intrauterine Growth Retardation were monitored up to 6 to 7 years of age using biometric parameters, perinatal risk questionnaires, and detailed neurodevelopmental and cognitive assessments. Forty-one children served as age-matched, appropriate for gestational age controls. A significant difference in Growth parameters (P < .001), neurodevelopmental score (P < .05), and IQ (P < .05) was found between the children with Intrauterine Growth Retardation and controls. A specific profile of difficulties in coordination, lateralization, spatial and graphomotor skills, and abundance of associated movements is typical of the children with Intrauterine Growth Retardation and hints at possible later learning disabilities. The clinical parameters best predicting neurodevelo...
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Neurodevelopmental outcome in children with Intrauterine Growth Retardation: a 3-year follow-up.
Journal of child neurology, 1999Co-Authors: Aviva Fattal-valevski, Yael Leitner, Miriam Kutai, Edith Tal-posener, Abraham Tomer, Deborah Lieberman, Ariel J. Jaffa, Ariel Many, Shaul HarelAbstract:The study was designed to detect early clinical predictors of developmental outcome in children with Intrauterine Growth Retardation. Eighty-five children with Intrauterine Growth Retardation were followed up prospectively to 3 years of age, using biometric parameters, perinatal risk questionnaires, and neurodevelopmental evaluations. Forty-two children served as controls. A significant difference in neurodevelopmental score at 3 years of age was noted between the Intrauterine Growth Retardation and control groups (P < .001). In the Intrauterine Growth Retardation group, the clinical parameters that most significantly correlated with outcome were cephalization index (head circumference:birthweight ratio), neonatal risk score, and birthweight. The best predictor of 3-year outcome was the cephalization index (P < .01). The children with Intrauterine Growth Retardation with neonatal complications had significantly lower IQ scores (P < .05) and a poorer neurodevelopmental outcome (P < .01) than those without complications. Children with Intrauterine Growth Retardation are at higher risk for developmental disabilities than are controls, especially in the presence of neonatal complications and a high cephalization index.
Hiroya Matsuo - One of the best experts on this subject based on the ideXlab platform.
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increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or Intrauterine Growth Retardation
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Naonori Ishihara, Hiroya Matsuo, Homare Murakoshi, Jovelle B Laoagfernandez, Takashi Samoto, Takeshi MaruoAbstract:OBJECTIVE: This study was undertaken to determine whether preeclampsia and Intrauterine Growth Retardation are associated with an increase in placental apoptosis. STUDY DESIGN: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. RESULTS: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and Intrauterine Growth Retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P <.001; Intrauterine Growth Retardation, P <.01). Transmission electron microscopy revealed the appearance of apoptotic nuclei in trophoblasts in severe preeclamptic term placenta. CONCLUSION: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and Intrauterine Growth Retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.
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increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or Intrauterine Growth Retardation
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Naonori Ishihara, Hiroya Matsuo, Homare Murakoshi, Jovelle B Laoagfernandez, Takashi Samoto, Takeshi MaruoAbstract:Abstract Objective: This study was undertaken to determine whether preeclampsia and Intrauterine Growth Retardation are associated with an increase in placental apoptosis. Study Design: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. Results: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and Intrauterine Growth Retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P P Conclusion: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and Intrauterine Growth Retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.(Am J Obstet Gynecol 2002;186:158-66.)
Homare Murakoshi - One of the best experts on this subject based on the ideXlab platform.
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increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or Intrauterine Growth Retardation
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Naonori Ishihara, Hiroya Matsuo, Homare Murakoshi, Jovelle B Laoagfernandez, Takashi Samoto, Takeshi MaruoAbstract:OBJECTIVE: This study was undertaken to determine whether preeclampsia and Intrauterine Growth Retardation are associated with an increase in placental apoptosis. STUDY DESIGN: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. RESULTS: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and Intrauterine Growth Retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P <.001; Intrauterine Growth Retardation, P <.01). Transmission electron microscopy revealed the appearance of apoptotic nuclei in trophoblasts in severe preeclamptic term placenta. CONCLUSION: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and Intrauterine Growth Retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.
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increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or Intrauterine Growth Retardation
American Journal of Obstetrics and Gynecology, 2002Co-Authors: Naonori Ishihara, Hiroya Matsuo, Homare Murakoshi, Jovelle B Laoagfernandez, Takashi Samoto, Takeshi MaruoAbstract:Abstract Objective: This study was undertaken to determine whether preeclampsia and Intrauterine Growth Retardation are associated with an increase in placental apoptosis. Study Design: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. Results: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or Intrauterine Growth Retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and Intrauterine Growth Retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P P Conclusion: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and Intrauterine Growth Retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.(Am J Obstet Gynecol 2002;186:158-66.)