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Biomedical subjects

W B Robertson

Publications and source records attributed to W B Robertson.

At least 19 recordsLinked to original sources
PubMed1987

Acute atherosis in preeclampsia: maternal determinants and fetal outcome in the presence of the lesion.

In 39 patients with preeclampsia a detailed analysis of some maternal factors, fetal outcome, and a histologic assessment of the presence or absence of acute atherosis in maternal intrauterine vessels has been done. There was no statistically significant relation between acute atherosis and parity, degree of proteinuria, severity and duration of hypertension, or antihypertensive therapy. These findings do not support a purely hemodynamic pathogenesis for the vasculopathy. Fetal outcome was only marginally worse in the preeclamptic patients who developed acute atherosis.

Acute Disease↗
PubMed1987

Defective haemochorial placentation as a cause of miscarriage: a preliminary study.

The morphology of the placental bed in idiopathic sporadic and recurrent miscarriages was studied and the findings correlated with the fetal chromosomal pattern where possible. Defective development of haemochorial placentation, which was not necessarily linked with fetal chromosomal abnormality, was seen in association with some miscarriages. These preliminary results, not previously demonstrated, strongly support the concept that miscarriages and pregnancies complicated by pre-eclampsia and/or small-for-gestational-age infants may be a continuum of disorders with a similar pathology in the placental bed.

Abortion, Spontaneous↗
PubMed1986

An immunocytochemical study of fetal cells at the maternal-placental interface using monoclonal antibodies to keratins, vimentin and desmin.

The expression of keratin, vimentin and desmin intermediate filaments by cells in the placenta, amniochorion and placental bed at different stages of pregnancy was studied by use of a panel of monoclonal antibodies. All trophoblast subsets express keratin but not vimentin or desmin intermediate filaments at all stages of pregnancy. Differentiation of the various forms of trophoblast probably does not involve qualitative alterations to the keratin pattern of embryonic trophoblast. Amniotic epithelium co-expressed keratin and variable amounts of vimentin while a subset of fetal mesenchyme cells of the amniochorion and chorionic villi were immunolabelled by antibodies to keratin, to vimentin and to desmin, suggesting simultaneous triple co-expression of three intermediate filaments. This finding suggests the identification of a cell population that is analogous to parietal endoderm in some eutherian animals.

Antibodies, Monoclonal↗
PubMed1986

The placental bed biopsy: review from three European centers.

This review derives from extensive experience with the placental bed biopsy technique in three centers over the last 30 years. A placental bed biopsy, usually taken at cesarean section, must include basal decidua and subjacent myometrium from the central zone of the placental site. Attention is drawn specifically to the sampling errors and to the pitfalls in morphologic interpretation of tissues, both maternal and fetal, that are continuously changing throughout the course of pregnancy. The features of the normal placental bed and of vascular lesions in pathologic pregnancies are briefly reviewed. Extension and elaboration of the technique and its more widespread use could contribute to the elucidation of many of the unresolved problems in human pregnancy.

Abortion, Spontaneous↗
PubMed1986

Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants.

An examination of the maternal vascular response to placentation shows that physiological changes in the placental bed normally extend from the decidua into the inner myometrium. In pre-eclampsia and in a proportion of pregnancies with small-for-gestational age infants (SGA) the physiological changes are restricted to the decidual segments alone. In addition, complete absence of physiological changes throughout the entire length of some spiral arteries is seen in pre-eclampsia and SGA. This new observation is confirmed in a study of basal plates of placentas from abnormal pregnancies. Intraluminal endovascular trophoblast may be seen in the placental bed spiral arteries in the third trimester in pre-eclampsia and SGA, a feature not seen beyond the second trimester in normal pregnancy. These findings point to a defect in the normal interaction between migratory trophoblast and maternal uterine tissues in pre-eclampsia and in SGA.

Female↗
PubMed1985

Strongyloidiasis in Canadian Far East war veterans.

A survey was done of Canadians who had been interned by the Japanese during World War II to assess the prevalence of latent infection with Strongyloides stercoralis in this group. Packages containing three mail-in kits and a questionnaire were sent to 992 men, 694 (70%) of whom responded. Larvae were found in the stool specimens of four of the respondents. Examination of stool specimens after formalin-ether concentration was the most successful method of detecting Strongyloides larvae. The Baermann concentration technique yielded negative results in all four men. Three of the four cases of strongyloidiasis were detected after sampling of three fecal specimens. In the fourth case additional specimens were requested on the basis of data derived from the questionnaire. The most frequently cited clinical manifestations were abdominal pain, weight loss, diarrhea and rashes.

Aged↗
PubMed1985

Human cytotrophoblast populations studied by monoclonal antibodies using single and double biotin-avidin-peroxidase immunocytochemistry.

Single and double biotin-avidin-peroxidase immunocytochemical methods in conjunction with an anti-trophoblast monoclonal antibody 18B/A5 and an anti-HLA-A,B,C monoclonal antibody W6/32 were used to study various human trophoblast populations. Several combinations of peroxidase substrates were tried in the double-labeling procedure. It was concluded that the use of 4-chloro-1 naphthol to develop the primary sequence peroxidase and of 3-amino-9-ethyl carbazole for the second sequence peroxidase was the most suitable. The significant findings were: Monoclonal antibody 18B/A5 proved to be a useful marker for villous as well as nonvillous trophoblast, which facilitated the identification of these cells particularly in the placental bed. The expression of MHC Class I antigens was not confined to extravillous trophoblast but these antigens were also demonstrable on the villous cytotrophoblast proliferating to form new primary villi. Double labeling revealed that many of these cells, particularly those furthest away from the mesenchymal core, expressed both trophoblast and HLA antigens as shown by a mixing of the colors produced by the two reaction products. A large number of these HLA-A,B,C, positive trophoblast cells were found to infiltrate deep into the uterine myometrium. The hypothesis was put forward that these fetal cells could be the ones that are responsible for maternal sensitization.

Antibodies, Monoclonal↗
PubMed1985

Abnormal placentation.

It is only relatively recently that attention has been directed to studies of the uterine side of the placenta to look for possible defects that might explain otherwise inexplicable pregnancy complications. Preeclampsia and intrauterine fetal growth retardation are two such disorders, in which new information has come to light by the study of placental bed biopsies and occasional cesarean hysterectomy specimens. It will be less easy to apply these techniques to such problems as spontaneous abortion and antepartum hemorrhage, but reemphasizing what should be the self-evident importance of the establishment and development of the uteroplacental blood supply might help reorient thinking about these and other important complications of pregnancy. Fresh thoughts are required too about the etiology and natural history of ectopic pregnancy, not so much for its own sake but more because of what it tells us about nidation and placentation in general. It is now difficult to insist on stringent criteria for the endometrium in human gestation, with all that this implies for the woman under investigation for infertility, when in some circumstances these criteria are flouted in what should be an alien mucosa. Much more needs to be known about the promotion and control exercised over trophoblastic differentiation and migration and interaction with uterine tissues. The uterus certainly can no longer be considered an immunologically privileged site even were that privilege extended to the fallopian tube and, indeed, to the adnexa generally. The constraining influence of decidua, if indeed it has such a property, requires elucidation; it cannot be fortuitous that only in species with hemochorial placentation, characterized by migratory nonvillous trophoblast, is a true stromal decidua formed. This surely indicates that decidua has a major role to play in negotiating "the treaty of compromise" ultimately signed between fetal and maternal tissues and if such a treaty is not signed, or is broken, defective placentation and its consequences must follow.

Abortion, Spontaneous↗
PubMed1977

Fetal growth retardation and the arteries of the placental bed.

The morphology of the placental bed spiral arteries was studied in 68 pregnancies complicated by fetal growth retardation and in 40 pregnancies with a normally grown fetus. When the birth weight was normal the extent and depth of physiological vascular changes were normal except in those pregnancies complicated by pre-eclampsia. When the birth weight was low and the mothers were normotensive the extent and depth of physiological vascular changes were either normal or restricted, and in all patients with hypertension and a baby with low birth weight the physiological changes were restricted to the decidual segments of the spiral (uteroplacental) arteries. Acute atherosis was only found in pregnancies complicated by hypertension, particularly if there was proteinuria. We do not believe that there exists an arteriopathy which is common to hypertensive and normotensive pregnancies complicated by fetal growth retardation.

Arteries↗
PubMed1976

Pathology of acute myocardial infarction with particular reference to occlusive coronary thrombi.

Analysis of the pathological findings in 500 cases of fatal acute myocardial infarction showed that in 469 this was localized to one transmural area of the left ventricle; in 31 there was diffuse subendocardial necrosis. In the former occlusive coronary thrombus was found in the related artery in 95 per cent of cases. Variation in the percentage of occlusions found was noted between different prosectors and when coronary artery calcification was present. Only 4 of the 31 patients with subendocardial necrosis had recent occlusion; triple vessel disease was common in this group suggesting general failure of coronary perfusion. It is essential in necropsy studies of the relation of coronary thrombosis to myocardial infarction to be sure that muscle necrosis is present, to distinguish the two forms of myocardial necrosis, and to employ a meticulous dissection technique with decalcification of the arteries when necessary.

Acute Disease↗
PubMed1976

Maternal uterine vascular lesions in the hypertensive complications of pregnancy.

To establich hemochorial placentation, the nonvillous trophoblast breaches the spiral arteries in the basal decidua and later migrates down the arteries as far as the parent radial arteries in the myometrium. Interactions between the endovascular trophoblast and the tissues of the maternal vessel wall (physiological changes) adapt these arteries to the uteroplacental arteries, and these large caliber vessels empty into the intervillous space. Loss of reactive musculoelastic vascular tissue results in a lowering of peripheral resistance, permitting a greatly increased blood flow into the intervillous space. In preeclamptic pregnancies, there is inhibition of the secondary endovascular trophoblast migration in the second trimester, so that the myometrial segments of the uteroplacental arteries remain as responseive musculoelastic arteries. With the onset of clinical preeclampsia, acute atherosis, a necrotizing arteriopathy, affects small muscular arteries in the placental bed and arterioles in the decidua vera. When essential hypertension is complicated by preeclampsia, the placental bed arteries show a combination of hyperplastic arteriosclerosis and acute atherosis. There is evidence that the establishment of hemochorial placentation requires controlled immunological reactions between fetal and maternal tissues and that an inappropriate immune response may be involved in the pathogenesis of the arteriopathy of preeclampsia.

Arteries↗
PubMed1975

The ultrastructure of acute atherosis in hypertensive pregnancy.

Acute atherosis of the myometrial segments of the uteroplacental arteries from pre-eclamptic pregnancies was studied by electron microscopy. The lesions in their early stages are characterized by endothelial damage, insudation of plasma constituents into the vessel wall, proliferation of myointimal cells, and medial necrosis. Fat acculumation is seen first in myointimal cells and, later, macrophages engulf the lipid-rich debris released from disintegrating myogenic foam cells. Gross endothelial damage, massive intramural fibrin deposition, luminal thrombosis, and vessel rupture with hemorrhage are epiphenomena.

Arteries↗