[Clear cell adenocarcinoma of the cervix uteri].
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Biomedical subjects
Publications and source records attributed to D Douvin.
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Morphological study of the human fetal membranes (at the term of pregnancy) shows that under the amniochorion lies the chorionic cytophoblast, which completely surrounds the amniotic cavity. Chorionic cytotrophoblast as well as parietal decidua persist until full term and remain well-developed. Within trophoblastic cells there are numerous canalicular formations bordered by microvilli resembling those observed between amniotic cells. The authors therefore believe that the circulation of amniotic fluid, after traversing the amnion, will continue through the intercellular canaliculi of the chorionic cytotrophoblast to reach the decidua parietalis. All the components of this complex membrane must play a part in the amniotic fluid circulation.
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Total hepatic inflow occlusion is well tolerated in pigs with normothermia for as long as two hours, provided that splanchnic venous pooling is avoided by active pumping through a splenojugular bypass. Hepatic dysfunction after 60, 90 and, even, 120 minutes of hepatic ischemia is mild and transient. Complete return to normal liver function tests is rapid. Early microscopic alterations of the liver are moderate, and no late abnormalities, such as cirrhosis or vascular changes, were observed one to three months later. Conversely, interruption of hepatic blood flow for three hours is not compatible with life. In this study, a previously unsuspected resistance of the pig liver to warm ischemia is demonstrated. These findings corroborate and extend those of recent clinical studies in which a similar tolerance of the human liver to prolonged normotherthermic ischemia is reported, thus questioning the necessity for deliberate hypothermia in operations involving the liver.
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Total clamping of the hepatic pedicle was performed for a period of two hours in the normothermic pig. During this time an external pulsed spleno-jugular shunt ensured effective-portal decompression. Under such conditions, the biological and histological consequences of this ischaemia were minimal and perfectly compatible with survival. This would suggest that the clinical syndrome of "shock liver" above all reflects splanchnic impairment.
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