Talk:Third Trimester: Difference between revisions

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==2012==
==2012==
===Third-trimester pregnancy complications===
Prim Care. 2012 Mar;39(1):95-113.
Newfield E.
Source
Department of Obstetrics and Gynecology, Contra Costa Regional Medical Center, 2500 Alhambra Avenue, Martinez, CA 94543, USA. dr.emily.newfield@gmail.com
Abstract
Complications arising in the third trimester often challenge the clinician to balance the concern for maternal well-being with the consequences of infant prematurity. The most serious and challenging antepartum issues relate to preterm labor and birth, hypertensive disorders, and bleeding events. This article guides the practitioner through decision-making and management of these problems.
Copyright © 2012 Elsevier Inc. All rights reserved.
PMID 22309584
http://www.primarycare.theclinics.com/article/S0095-4543(11)00092-3/abstract


===A morphometric study of suprarenal gland development in the fetal period===
===A morphometric study of suprarenal gland development in the fetal period===

Revision as of 10:58, 22 March 2012

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Cite this page: Hill, M.A. (2024, April 25) Embryology Third Trimester. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Third_Trimester

2012

Third-trimester pregnancy complications

Prim Care. 2012 Mar;39(1):95-113.

Newfield E. Source Department of Obstetrics and Gynecology, Contra Costa Regional Medical Center, 2500 Alhambra Avenue, Martinez, CA 94543, USA. dr.emily.newfield@gmail.com

Abstract

Complications arising in the third trimester often challenge the clinician to balance the concern for maternal well-being with the consequences of infant prematurity. The most serious and challenging antepartum issues relate to preterm labor and birth, hypertensive disorders, and bleeding events. This article guides the practitioner through decision-making and management of these problems. Copyright © 2012 Elsevier Inc. All rights reserved.

PMID 22309584

http://www.primarycare.theclinics.com/article/S0095-4543(11)00092-3/abstract


A morphometric study of suprarenal gland development in the fetal period

Surg Radiol Anat. 2012 Mar 20. [Epub ahead of print]

Ozgüner G, Sulak O, Koyuncu E. Source Department of Anatomy, Faculty of Medicine, Suleyman Demirel University, 32260, Isparta, Turkey, ozgunerg@hotmail.com.

Abstract

PURPOSE: The present study's purpose was to examine the morphometric development of the suprarenal gland using anatomic dissection methods during the fetal period. METHODS: This study was performed on 172 human fetuses (76 males and 96 females) and 344 fetal suprarenal glands obtained from ages 9-40 weeks of gestation with no external pathology or anomaly. Fetuses were divided into 4 groups between gestational ages as follows: Group 1, 9-12 weeks (first trimester); Group 2, 13-25 weeks (second trimester); Group 3, 26-37 weeks (third trimester); and Group 4, 38-40 weeks (full term). Also, the fetuses were grouped into monthly cohorts: 9-12 weeks 3rd month, 13-16 weeks 4th month, 17-20 weeks 5th month, 21-24 weeks 6th month, 25-28 weeks 7th month, 29-32 weeks 8th month, 33-36 weeks 9th month, and 37-40 weeks 10th month. The suprarenal glands were dissected in the abdominal cavity. The dimensions (width, length, and thickness), volumes and weights of the suprarenal glands were evaluated. The ratio of the fetal suprarenal gland weight/fetal body weight, the ratio of the fetal suprarenal gland volume/fetal kidney volume, and the ratio of the fetal suprarenal gland dimensions/fetal kidney dimensions were evaluated. RESULTS: Mean values and standard deviations of all parameters according to gestational weeks and trimesters were calculated. It is found that all parameters increase with gestational age. There was significant correlation between gestational age and all parameters (p < 0.001). No significant differences were observed between sexes for any of the parameters (p > 0.05). There was no difference between the right and left sides of parameters except the thickness of the suprarenal glands. The left suprarenal glands were thicker than the right. The ratio of suprarenal volumes to kidney volumes was determined, and we observed that the ratio decreased during the fetal period. CONCLUSIONS: We believe that the results obtained from this study will be beneficial in understanding the development of suprarenal glands and also contribute to future studies in obstetrics, perinatology, and fetopathology.

PMID 22430763


Acute and Long-Term Purkinje Cell Loss Following a Single Ethanol Binge During the Early Third Trimester Equivalent in the Rat

Alcohol Clin Exp Res. 2012 Mar 8. doi: 10.1111/j.1530-0277.2012.01743.x. [Epub ahead of print]

Idrus NM, Napper RM. Source Department of Anatomy and Structural Biology, University of Otago, Dunedin, New Zealand. Abstract BACKGROUND: In the rat, binge-like ethanol (EtOH) exposure during the early neonatal period (a developmental period equivalent to the human third trimester) can result in a permanent deficit of cerebellar Purkinje cells (Pcells). However, the consequences of a moderate binge alcohol exposure on a single day during this postnatal period have not been established. This is an issue of importance as many pregnant women binge drink periodically at social drinking levels. This study aimed to identify both the acute and long-term effects of exposure to a single alcohol binge that achieved a mean peak blood EtOH concentration of approximately 250 mg/dl during early postnatal life using a rat model of fetal alcohol spectrum disorders. METHODS: Acute apoptotic Pcell death 10 hours after a moderate dose binge EtOH exposure from postnatal days (PDs) 0 to 10 was assessed using active caspase-3 immunolabeling. Acute Pcell apoptosis was quantified in cerebellar vermal lobules I-X using the physical disector method. Long-term effects were assessed at PD 60 using stereological methods to determine total Pcell numbers in the vermis, lobule III, and lobule IX, following a moderate dose binge EtOH exposure at PDs 0, 2, or 4. RESULTS: Acute apoptosis was induced by EtOH on PDs 1 to 8 in a time and lobular-dependent manner. For EtOH exposure on PD 2, significant long-term Pcell loss occurred in lobule III. EtOH exposure on PD 4 resulted in significant long-term Pcell loss throughout the entire vermis. CONCLUSIONS: These results indicate that a single, early EtOH episode of moderate dose can create significant and permanent Pcell loss in the developing cerebellum. Copyright © 2012 by the Research Society on Alcoholism.

PMID 22404759