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Placental Pathology (placental + pathology)
Selected AbstractsCurrent awareness in prenatal diagnosisPRENATAL DIAGNOSIS, Issue 9 2009Article first published online: 28 AUG 200 In order to keep subscribers up-to-date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of prenatal diagnosis. Each bibliography is divided into 21 sections: 1 Reviews; 2 General Interest; 3 Normal Fetal Development; 4 Preimplantation Genetic Diagnosis; 5 First Trimester Diagnosis; 6 Second Trimester Diagnosis; 7 Fetal Imaging: General; Ultrasound; MRI; 8 Maternal Serum Screening for Aneuploidy; 9 Screening for Carriers of Genetic Abnormality; 10 Molecular Cytogenetics: Metaphase Cytogenetics/FISH; Array CGH; 11 Fetal Cells in Maternal Circulation; 12 Fetal DNA/RNA in Maternal Body Fluids; 13 Fetal Therapy; 14 Psychosocial and Ethical Aspects; 15 Epidemiology and Environmental Factors; 16 Developmental and Placental Pathology; 17 Genetic Counseling. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted [source] Current awareness in prenatal diagnosisPRENATAL DIAGNOSIS, Issue 4 2009Article first published online: 30 MAR 200 In order to keep subscribers up-to-date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of prenatal diagnosis. Each bibliography is divided into 20 sections: 1 Reviews; 2 General Interest; 3 Normal Fetal Development; 4 Preimplantation Genetic Diagnosis; 5 First Trimester Diagnosis; 6 Second Trimester Diagnosis; 7 Fetal Imaging: General; Ultrasound; MRI; 8 Maternal Serum Screening for Aneuploidy; 9 Screening for Carriers of Genetic Abnormality; 10 Molecular Cytogenetics: Metaphase Cytogenetics/FISH; Array cGH; 11 Fetal Cells in Maternal Circulation; 12 Fetal DNA/RNA in Maternal Body Fluids; 13 Fetal Therapy; 14 Psychosocial and Ethical Aspects; 15 Epidemiology and Environmental Factors; 16 Developmental and Placental Pathology; 17 Genetic Counseling. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted [source] Current awareness in prenatal diagnosisPRENATAL DIAGNOSIS, Issue 3 2009Article first published online: 26 FEB 200 In order to keep subscribers up-to-date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of prenatal diagnosis. Each bibliography is divided into 20 sections: 1 Reviews; 2 General Interest; 3 Normal Fetal Development; 4 Preimplantation Genetic Diagnosis; 5 First Trimester Diagnosis; 6 Second Trimester Diagnosis; 7 Fetal Imaging: General; Ultrasound; MRI; 8 Maternal Serum Screening for Aneuploidy; 9 Screening for Carriers of Genetic Abnormality; 10 Molecular Cytogenetics: Metaphase Cytogenetics/FISH; Array cGH; 11 Fetal Cells in Maternal Circulation; 12 Fetal DNA/RNA in Maternal Body Fluids; 13 Fetal Therapy; 14 Psychosocial and Ethical Aspects; 15 Epidemiology and Environmental Factors; 16 Developmental and Placental Pathology; 17 Genetic Counseling. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted [source] REVIEW ARTICLE: Placental Apoptosis in Health and DiseaseAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2010Andrew N. Sharp Citation Sharp AN, Heazell AEP, Crocker IP, Mor G. Placental apoptosis in health and disease. Am J Reprod Immunol 2010; 64: 159,169 Apoptosis, programmed cell death, is an essential feature of normal placental development but is exaggerated in association with placental disease. Placental development relies upon effective implantation and invasion of the maternal decidua by the placental trophoblast. In normal pregnancy, trophoblast apoptosis increases with placental growth and advancing gestation. However, apoptosis is notably exaggerated in the pregnancy complications, hydatidiform mole, pre-eclampsia, and intrauterine growth restriction (IUGR). Placental apoptosis may be initiated by a variety of stimuli, including hypoxia and oxidative stress. In common with other cell-types, trophoblast apoptosis follows the extrinsic or intrinsic pathways culminating in the activation of caspases. In contrast, the formation of apoptotic bodies is less clearly identified, but postulated by some to involve the clustering of apoptotic nuclei and liberation of this material into the maternal circulation. In addition to promoting a favorable maternal immune response, the release of this placental-derived material is thought to provoke the endothelial dysfunction of pre-eclampsia. Widespread apoptosis of the syncytiotrophoblast may also impair trophoblast function leading to the reduction in nutrient transport seen in IUGR. A clearer understanding of placental apoptosis and its regulation may provide new insights into placental pathologies, potentially suggesting therapeutic targets. [source] Do maternal- or pregnancy-associated disease states affect blood pressure in the early neonatal period?AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 4 2009Alison L. KENT Background: Placental vascular changes associated with maternal disease states may affect fetal vascular development. There is evidence suggesting that being born prematurely is associated with a higher blood pressure (BP) in later life. Aim: To determine whether maternal disease state affects BP in the early neonatal period. Methods: Cohort study of neonates admitted to neonatal intensive care unit with exposure to maternal hypertension and diabetes. Inclusion criteria were neonates greater than 27 weeks gestation not ventilated or requiring inotropes for more than 24 h, materna l hypertension (pregnancy induced or essential) or diabetes of any kind requiring treatment, and spontaneous delivery. Exclusion criteria included chromosomal or congenital anomaly and illicit maternal drug use. Oscillometric BP measurements taken until discharge on days 1, 2, 3, 4, 7, 14, 21 and 28. Placental histopathology was performed. Results: One hundred and ninety infants enrolled, 104 in the control and 86 in the study group. Sixty-five infants were born between 28,31 weeks and 125 infants between 32,41 weeks gestation. Those born between 28,31 weeks with a history of diabetes had a statistically higher systolic, mean and diastolic BP throughout the first 28 days of life (P = 0.001; P = 0.007; P = 0.02). Those born between 32,41 weeks gestation with placental pathology associated with altered uteroplacental perfusion had a higher systolic BP (P = 0.005). Conclusions: Maternal- or pregnancy-associated disease states appear to influence BP in the early neonatal period. Diabetes and altered placental perfusion were associated with higher BP readings. Clinical significance of these statistically elevated BPs in the early neonatal period is unknown. [source] Reclassification of unexplained stillbirths using clinical practice guidelinesAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 3 2009Elizabeth HEADLEY Background: Twenty-eight per cent of stillbirths in Australia remain unexplained. A clinical practice guideline (CPG) produced by the Perinatal Society of Australia and New Zealand (PSANZ) Perinatal Mortality Special Interest Group is in use to assist clinicians in the investigation and audit of perinatal deaths. Aims: To describe in a tertiary hospital using the PSANZ stillbirth investigation guidelines: (i) the distribution and classification of stillbirths, and (ii) the compliance with suggested stillbirth core investigations. Methods: Retrospective cohort of all stillbirths delivered between November 2005 and March 2008. Stillbirths were defined as no sign of life on delivery at , 20 weeks gestation or 400 g birthweight if gestation is unknown. Data were collected via the hospital Perinatal Mortality Audit Committee (PMAC). Cause of death was classified by the PSANZ Perinatal Death Classification. Results: There were 86 stillbirths (rate 7.2 per 1000 births). The percentage of unexplained stillbirths was 34% and 13% before and after CPG investigations, respectively. Unexplained stillbirths had the highest compliance with the recommended investigations. The initial cause of death documented on the death certificate was changed by the PMAC in 19 cases. The investigations most likely to prompt a change in the cause of death classification were autopsy and placental pathology. Conclusions: The percentage of unexplained stillbirths is lower than the national average in a hospital using the Perinatal Mortality Audit Guidelines. However, overall compliance is low, suggesting a targeted approach to investigation is used by clinicians despite a policy that aims to be non-selective. Autopsy and placental examination are the most useful investigations in assisting formal classification of cause of death. [source] Monoamniotic twin pregnancies: antenatal management and perinatal results of 19 consecutive casesBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 1 2004Fabien Demaria Objective To describe the obstetric management and perinatal outcome of antenatally diagnosed monoamniotic twin pregnancies (MATP) in a tertiary level maternity unit. Setting Port-Royal Maternity Hospital, Paris, France. Population MATP that progressed beyond 22 weeks seen from 1993 to 2001. Methods A retrospective chart review of all twin pregnancies. Diagnosis of MATP was made by ultrasonography and confirmed by placental pathology. Main outcome measure Perinatal mortality. Results Among the 1242 twins pregnancies delivered during the study period, 19 were monoamniotic. Four fetuses (10% of all births) had malformations. Perinatal mortality was high (n= 12, 32%) because of fetal deaths (nine cases) and very preterm births (three neonatal deaths). No fetal deaths occurred after 29 weeks. Of the 15 women with at least one live fetus before labour, 6 gave birth by vaginal delivery (40%). No obstetric accidents occurred during vaginal deliveries. Conclusion Perinatal mortality of MATP is still very high, even with accurate, early antenatal diagnosis, intensified surveillance and delivery provided in a tertiary level hospital. The main causes of perinatal deaths are cord accidents in utero, congenital anomalies and very preterm births. [source] | ||||||||||