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W Tyson

Publications and source records attributed to W Tyson.

10 recordsLinked to original sources
PubMed2003

Remodelling of uteroplacental arteries is decreased in high altitude placentae.

Uterine blood flow and birth weight are reduced and the risk of pre-eclampsia is increased in high-altitude pregnancies. Since IUGR and pre-eclampsia are associated with reduced invasion and remodelling of maternal spiral arteries we asked whether the terminal ends of uteroplacental arteries located at the maternal-foetal decidual interface evidenced less remodelling in 19 high (3100 m) compared with 13 moderate (1600 m) altitude placentae from normal pregnancies. Previous work has demonstrated marked villous angiogenesis in high altitude placentae. We asked whether such changes are compensatory for reduced modelling and/or whether they contribute to increased birth weight. Placentae were randomly sampled and examined with immunohistochemistry to evaluate vessel remodelling and foetal capillary density. The decidual ends of uteroplacental arteries were 8-fold more likely to be remodelled at 1600 vs. 3100 m (OR=8.1; CI 2.4, 27.0,P< 0.001). There were more than twice as many uteroplacental arteries observed in the high vs. moderate altitude placentae (OR=2.1; CI: 1.3, 3.5, P=0.006). Foetal capillary density was greater at 3100 vs. 1600 m (P< 0.001), but did not relate to remodelling nor to birth weight. In this in vivo model for chronic hypoxia, remodelling is reduced, and villous angiogenesis is not fully compensatory for reduced PO(2).

Adaptation, Physiological↗
PubMed1989

Apparent Smith-Lemli-Opitz syndrome and Miller-Dieker syndrome in a family with segregating translocation t(7;17)(q34;p13.1).

We describe a family in which one male infant presented with Miller-Dieker syndrome and four male relatives had a phenotype similar to the Smith-Lemli-Opitz (SLO) syndrome. High resolution cytogenetic analysis on the child with Miller-Dieker syndrome showed 46,XY,-17,+der17t(7;17)(q34:p13.1). Paternal chromosomes showed a balanced translocation: 46,XY,t(7;17)(q34:p13.1). The paternal grandmother had a history of multiple miscarriages, and a paternal uncle had two sons who died neonatally. Chromosomes on these children and their father had originally been reported as normal. There was also a paternal cousin to the father of the propositus who had had two sons with similar clinical findings. A diagnosis of SLO syndrome was considered. Image enhancement techniques on previous suboptimal preparations on these four children documented the subtle unbalanced translocation 46,XY,-7,+der7t(7;17)(q34:p13.1). Subsequent high resolution analysis on one of these four children who was still living confirmed this chromosome constitution. It is postulated that these apparent SLO cases may represent a contiguous gene syndrome in which SLO or a separate entity closely mimicking the syndrome in included.

Abnormalities, Multiple↗
PubMed1987

Pathologic aspects of fetal death.

The number of autopsies has declined during the past decade; however, repeated studies by pathologists, clinicians, and others have shown its great value in defining disease, quality control, patient and physician education, and providing material for basic research. In recent years financial concerns have added to the decrease in autopsies. Nonetheless, reported studies find perinatal autopsies clinically useful. The authors have attempted to outline an approach to the fetal and neonatal autopsy that minimizes cost and is complete enough to form a basis for making decisions about future pregnancies.

Autopsy↗