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Biomedical subjects

H Fox

Publications and source records attributed to H Fox.

324 records · Page 18Linked to original sources

The effects of cigarette smoking on the human placenta: a light and electron microscopic study.

A histological and electronoptical study of placentae from women who smoke cigarettes during pregnancy shows a tendency towards a paucity of vasculosyncytial membranes, villous cytotrophoblastic cell proliferation, focal syncytial necrosis, decreased syncytial pinocytotic and secretory activity, dilatation of syncytial rough endoplasmic reticulum, abnormalities of syncytial microvilli, focal infolding of the free plasma membrane of the syncytiotrophoblast, degeneration of isolated cytotrophoblastic cells, irregular thickening of the trophoblastic basement membrane and degeneration of villous capillary endothelial cells. It is thought that many of these changes are due to placental ischaemia consequent upon nicotine-induced constriction of the uterine vessels; some of the changes cannot be explained on this basis and it is suggested that these may possibly be due either to cadmium toxicity or to accumulation of polycyclic aromatic hydrocarbons. There is apparently some impairment of placental function in cigarette smokers but this is probably offset by the ability of the placenta to repair ischaemic damage and to undergo a compensatory hyperplasia.

Adult↗

The human placenta in idiopathic intrauterine growth retardation: a light and electron microscopic study.

Six placentae from small for gestational age infants were examined by both light and electron microscopy. These were from pregnancies in which all maternal or fetal factors known to be associated with intrauterine growth retardation, including maternal cigarette smoking, were excluded. At the light microscopic level the only significant finding was an excess of villous cytotrophoblastic cells whilst electron microscopy showed these placentae to be characterized by villous cytotrophoblastic hyperplasia, focal syncytial necrosis, microvillous abnormalities, reduced syncytial secretory activity, irregular thickening of the trophoblastic basement membrane and the presence of small fetal villous vessels with multilayered basement membranes. It is thought that most of the observed abnormalities are due to uteroplacental ischaemia and it is possible that the fetal vascular abnormalities are a reflection of the fetal growth retardation. There is little evidence that the functional efficiency of the placenta is impaired in these cases and it is suggested that the principal factor in the pathogenesis of fetal growth retardation is a restriction of nutrient supply to the fetus because of an inadequate degree of physiological change within the maternal spiral vessels.

Adult↗

An immunohistological comparison of the secretory capacity of villous and extravillous trophoblast in the human placenta.

Using an immunoperoxidase technique the localization of hCG, hPL, SP1, PAPP-A and PP5 within villous and extravillous trophoblast has been studied. The villous syncytiotrophoblast appears to be the sole significant source of hCG, SP1, PAPP-A and PP5 but hPL is also present in the infiltrating extravillous trophoblast. Within the interstitial extravillous trophoblast the proportion of cells staining positively for hPL increases progressively as the cells extend deeper into the uterine tissues but all the vascular extravillous trophoblast within the lumina of the spiral arteries stains positively for hPL at all levels within the decidua and inner myometrium. It is not clear why the synthetic capacity of the infiltrating trophoblast is limited to the production of hPL. We suggest that this might be indicative of selectivity of a specific subpopulation of cytotrophoblastic cells. It is unlikely that the physiological effects of infiltrating trophoblast are mediated by hPL, this substance being probably only a marker of a cell population with a particular invasive capacity.

Chorionic Gonadotropin↗

Villitis of unknown aetiology: its incidence and significance in placentae from a British population.

A histological study of 1000 randomly selected placentae from women delivered in Manchester, UK, revealed 136 cases of villitis; this is a higher incidence than that recorded in Australia and North America but lower than that noted in South America. There were no obvious clinical differences between mothers whose placentae showed a villitis and those in a control group whose placentae were free of villitis. As in other studies, there was an association between the presence of a villitis, particularly severe villitis, and fetal intrauterine growth retardation. The nature of this association cannot, however, be clarified until the aetiology of villitis is determined.

Adult↗

The human placenta does not contain lipofuscin pigment.

Autofluorescent granules are present in the villous syncytiotrophoblast of the human placenta, most prominently during the first trimester. These granules differ in both size and hue from classical lipofuscin granules, have different staining characteristics, and are shown by electron microscopy to be syncytial lipid droplets. It is concluded that previous reports of the presence of lipofuscin pigment in the placenta are unfounded.

Cell Survival↗

The placenta in leprosy.

Eighty-one placentae from women with leprosy and 17 placentae from healthy controls were subjected to a detailed macroscopic, light microscopic, ultrastructural, immunopathological, microbiological and biochemical study. The placental morphology and immunohistology were normal, and there was no morphological evidence of infection of the placenta due to M. leprae. No acid-fast bacilli or acid-fast bacillary granules were seen on light microscopy of any of the placentae from leprous women, although homogenates from two out of seven placentae from women with very active lepromatous leprosy contained acid-fast bacilli in very small numbers. The small placental size of women with leprosy, most marked in those with lepromatous leprosy, appears to be due to a decrease in placental cell size, rather than to a reduced number of cells in the placenta. It is postulated that the small placenta and reduced fetal birth weight observed in lepromatous leprosy are a consequence of depressed maternal immune reactivity.

Complement System Proteins↗

Human placental ultrastructure after in vitro dual perfusion.

Unperfused term placental tissue maintained at 37 degrees C for two hours preserved a major part of its structure while displaying a number of signs of hypoxic damage. Most placentae perfused through maternal and fetal circulations with Krebs-Ringer medium retained their ultrastructural integrity after two or more hours of perfusion.

Female↗

Immunohistochemical localization of follicle-stimulating hormone, luteinizing hormone, growth hormone, adrenocorticotrophic hormone and prolactin in the human placenta.

The sites of localization of luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), adrenocorticotrophic hormone (ACTH) and prolactin (PRL) within placental tissues have been studied by an immunoperoxidase technique. The syncytiotrophoblast is the sole significant site of localization of LH, FSH, GH and ACTH; PRL is found both in syncytiotrophoblast and in decidual cells. It is highly probable that the sites of localization of these peptide hormones represents their sites of synthesis in the placenta and thus that the syncytiotrophoblast is the sole site of synthesis of LH, FSH, LH and ACTH. PRL appears to be synthesized both in syncytiotrophoblast and decidua, but the latter is probably not the major site of synthesis of this hormone. Whether these placental peptide hormones have any physiological role to play during pregnancy or whether the placental capacity to synthesize such hormones is an atavistic phenomenon of no functional importance is currently a moot point.

Adrenocorticotropic Hormone↗

Profiles of cognitive decline in Alzheimer disease.

Most recent studies have used only two observations to estimate the rate of cognitive decline in patients with Alzheimer disease (AD); few have data taken from more than a 2-year period; and none report on autopsy-verified cases. Repeated observations over the complete course of the disease are necessary to quantitatively evaluate hypotheses such as the triphasic linear model of Brooks et al. (1993). The goal of this study is to compare the triphasic linear and quadratic models of decline in a group of 12 AD patients confirmed at autopsy with a group of age- and sex-matched normal control subjects. Both groups were taken from the University of Western Ontario Dementia Study, and the Extended Scale for Dementia was used as the outcome measure. The squared multiple correlation as a measure of goodness of fit suggested the superiority of the more parsimonious quadratic model over the triphasic linear model. Quantitative models more accurately reflect the profiles of change in AD and may prove more sensitive in measuring the effects of drugs on these patterns.

Aged↗

An ultrahistochemical study of the placental content of respiratory enzymes in normal and prolonged pregnancies.

The placental content of malate dehydrogenase and lactate dehydrogenase has been studied at the ultrastructural level. In the trophoblast both enzymes have a predominantly mitochondrial localization although occasional membrane-bound extra-mitochondrial activity is also seen. As compared with the first trimester placenta, there is a highly significant decrease in the activity of both enzymes within the trophoblast at term; this may represent an adaptative change to reduce placental oxygen consumption and increase the amount of oxygen available to the fetus. In prolonged pregnancies, there is a continued decline in trophoblastic malate dehydrogenase activity but the lactate dehydrogenase activity tends to increase, these changes suggesting that there is a switch from oxidative pohosphorylation to anaerobic glycolysis. It is not clear whether this change to a less efficient mode of energy generation is due to an intrinsic ageing change within the trophoblast or is secondary to placental ischaemia.

Animals↗

An identical twin pair discordant for rheumatoid arthritis and ankylosing spondylitis.

Both rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have an increased familial occurrence and each disease is associated with the inheritance of specific HLA antigens. We report a pair of identical twin brothers with discordant disease phenotypes: one developed AS at the age of 26, and the other developed RA at the age of 55. The twins possessed both of the disease susceptibility antigens HLA B27 and DR4. Differences in the twins' environmental exposure are discussed.

Arthritis, Rheumatoid↗